Accession Organism Samples Type Platform Title Year Summary Link Paper_title Journal Impact factor 2018 doi or pubmed id All references Type of molecule BioProject link (NCBI) BioProject link (EBI) SRA All protocols GSE117322 Homo sapiens 6 Expression profiling by high throughput sequencing GPL16791 Identification of the role of polydom in neurofibromas 2018-07-18 Dermal neurofibromas in von Recklinghausen's disease (vRD) develop in the dermis. Therefore, we hypothesized that a dermal niche exists that promotes the development of dermal neurofibromas in subjects with vRD. We focused on polydom, a ligand for integrin α9β1 and known as a factor expressed in the nerve tissue of mice and human breast cancer and lung cancer, which is expressed around nerve tissue. There were fewer polydom-positive fibroblasts in dermal tissue surrounding neurofibromas than in the dermis of normal skin. However, the expression level of polydom mRNA was significantly higher in neurofibroma tissue than control tissue. In addition, quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis of RNA purified from primary cultured dermal neurofibroma cells demonstrated that polydom mRNA expression was significantly higher in cells derived from the matrix of raised-type neurofibromas compared to normal human dermal fibroblasts. To investigate the role of polydom, RNA sequencing was used to compare the gene expression between cultured cells derived from dermal neurofibroma surrounding tissue with and without polydom knockdown. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE117322 Expression of polydom in dermal neurofibroma and surrounding dermis in von Recklinghausen's disease. Journal of dermatological science 3.986 https://doi.org/10.1016/j.jdermsci.2019.09.005 {Journal of dermatological science (3.986): 10.1016/j.jdermsci.2019.09.005} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA481758 https://www.ebi.ac.uk/ena/browser/view/PRJNA481758 https://www.ncbi.nlm.nih.gov/sra?term=SRP154361 [Overal design]We performed an RNA sequencing used to compare the gene expression between cultured cells derived from dermal neurofibroma surrounding tissue with and without polydom knockdown in triplicates.; [Treatment]'Primary cultured cells from the matrix of neurofibromas (8×104/1.5 ml) were seeded on 6-well dishes 1 day prior to transfection. Cells were transfected with 30 nM polydom or control siRNAs (QIAGEN, Hilden, Germany) using RNAi MAX (Invitrogen, Carlsbad, California, USA). The culture medium was replaced 6 h later. One day after transfection, total RNA was purified.'; [Growth]'None'; [Extraction]'Total RNA was extracted from primary cultured cells treated for 6 h with mock, 5 ng/ml β-estradiol (SIGMA-ALDRICH, St. Louis, Missouri, USA), 10 ng/ml TGF-β1 (R&D SYSTEMS, Minneapolis, Minnesota, USA), 5 μM ITD1 (TOCRIS, Avonmouth, Bristol, BS11 9QD United Kingdom), or siRNA (QIAGEN) using the Maxwell 16 LEV simply RNA Tissue kit (Promega, Madison, WI).\nLibrary preparation was performed using a TruSeq stranded mRNA sample prep kit (Illumina, San Diego, CA) according to the manufacturer’s instructions.'; [Cell type]'fibroblasts surrounding neurofibromas''cell type: fibroblasts surrounding neurofibromas; gender: female; age: 36; type: trunk; ', 'cell type: fibroblasts surrounding neurofibromas; gender: female; age: 56; type: upper limb; ', 'cell type: fibroblasts surrounding neurofibromas; gender: male; age: 52; type: trunk; ' GSE31604 Homo sapiens 30 Expression profiling by array GPL6480 Human breast cancer cell lines: vehicle vs. BMP7 incubation 2011-08-23 Bone morphogenetic proteins (BMPs) are members of the TGF-β superfamily of growth factors. They are known for their roles in regulation of osteogenesis and developmental processes and, in recent years, evidence has accumulated of their crucial functions in tumor biology. BMP7, in particular, has been implicated in breast cancer. However, little is known about BMP target genes in the context of tumor. We therefore explored the effects of BMP7 treatment on global gene transcription in five breast cancer cell lines during a 6-point time series. Data analysis included hierarchical clustering of differentially expressed genes, gene ontology enrichment analyses and model based clustering of temporal data. BMP7 had a strong effect on gene expression. The cellular functions most strongly affected were regulation of transcription and development. The observed transcriptional response followed a temporal sequence. Hierarchical clustering revealed distinct differences in the response of individual cell lines to BMP7, but also highlighted a synexpression group of genes. Finally, this study provides a list of potential novel BMP target genes relevant in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE31604 Analysis of BMP4 and BMP7 signaling in breast cancer cells unveils time-dependent transcription patterns and highlights a common synexpression group of genes. BMC medical genomics 2.568 https://doi.org/10.1186/1755-8794-4-80 {BMC medical genomics (2.568): 10.1186/1755-8794-4-80} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA154999 https://www.ebi.ac.uk/ena/browser/view/PRJNA154999 None [Overal design]Two-condition experiment, vehicle-treated vs. BMP7-treated. Five cell lines were tested at six time points each, what makes a total of 30 samples. RNA samples from three biological replicates were pooled before hybridization.; [Treatment]'Cells were seeded on 24-well plates, allowed to adhere for 24h, and treated with vehicle for 30min, 1h, 3h, 6h, 12h and 24h. Experiments were performed in triplicate and collected cells were pooled.', 'Cells were seeded on 24-well plates, allowed to adhere for 24h, and treated with recombinant human BMP7 protein for 30min, 1h, 3h, 6h, 12h and 24h. Experiments were performed in triplicate and collected cells were pooled.'; [Growth]'None'; [Extraction]'Total RNA was extracted using the RNeasy Mini Kit (Qiagen, Valencia, CA) and the quality of RNA was validated using the Agilent RNA 6000 Nano Kit (Agilent Technologies, Palo Alto, CA, USA).'; [Cell type]'Source: ''cell line: HCC1954; agent: vehicle; time point: 30min; ', 'cell line: HCC1954; agent: BMP7; time point: 30min; ', 'cell line: HCC1954; agent: vehicle; time point: 1h; ', 'cell line: HCC1954; agent: BMP7; time point: 1h; ', 'cell line: HCC1954; agent: vehicle; time point: 3h; ', 'cell line: HCC1954; agent: BMP7; time point: 3h; ', 'cell line: HCC1954; agent: vehicle; time point: 6h; ', 'cell line: HCC1954; agent: BMP7; time point: 6h; ', 'cell line: HCC1954; agent: vehicle; time point: 12h; ', 'cell line: HCC1954; agent: BMP7; time point: 12h; ', 'cell line: HCC1954; agent: vehicle; time point: 24h; ', 'cell line: HCC1954; agent: BMP7; time point: 24h; ', 'cell line: MDA-MB-231; agent: vehicle; time point: 30min; ', 'cell line: MDA-MB-231; agent: BMP7; time point: 30min; ', 'cell line: MDA-MB-231; agent: vehicle; time point: 1h; ', 'cell line: MDA-MB-231; agent: BMP7; time point: 1h; ', 'cell line: MDA-MB-231; agent: vehicle; time point: 3h; ', 'cell line: MDA-MB-231; agent: BMP7; time point: 3h; ', 'cell line: MDA-MB-231; agent: vehicle; time point: 6h; ', 'cell line: MDA-MB-231; agent: BMP7; time point: 6h; ', 'cell line: MDA-MB-231; agent: vehicle; time point: 12h; ', 'cell line: MDA-MB-231; agent: BMP7; time point: 12h; ', 'cell line: MDA-MB-231; agent: vehicle; time point: 24h; ', 'cell line: MDA-MB-231; agent: BMP7; time point: 24h; ', 'cell line: MDA-MB-361; agent: vehicle; time point: 30min; ', 'cell line: MDA-MB-361; agent: BMP7; time point: 30min; ', 'cell line: MDA-MB-361; agent: vehicle; time point: 1h; ', 'cell line: MDA-MB-361; agent: BMP7; time point: 1h; ', 'cell line: MDA-MB-361; agent: vehicle; time point: 3h; ', 'cell line: MDA-MB-361; agent: BMP7; time point: 3h; ', 'cell line: MDA-MB-361; agent: vehicle; time point: 6h; ', 'cell line: MDA-MB-361; agent: BMP7; time point: 6h; ', 'cell line: MDA-MB-361; agent: vehicle; time point: 12h; ', 'cell line: MDA-MB-361; agent: BMP7; time point: 12h; ', 'cell line: MDA-MB-361; agent: vehicle; time point: 24h; ', 'cell line: MDA-MB-361; agent: BMP7; time point: 24h; ', 'cell line: T-47-D; agent: vehicle; time point: 30min; ', 'cell line: T-47-D; agent: BMP7; time point: 30min; ', 'cell line: T-47-D; agent: vehicle; time point: 1h; ', 'cell line: T-47-D; agent: BMP7; time point: 1h; ', 'cell line: T-47-D; agent: vehicle; time point: 3h; ', 'cell line: T-47-D; agent: BMP7; time point: 3h; ', 'cell line: T-47-D; agent: vehicle; time point: 6h; ', 'cell line: T-47-D; agent: BMP7; time point: 6h; ', 'cell line: T-47-D; agent: vehicle; time point: 12h; ', 'cell line: T-47-D; agent: BMP7; time point: 12h; ', 'cell line: T-47-D; agent: vehicle; time point: 24h; ', 'cell line: T-47-D; agent: BMP7; time point: 24h; ', 'cell line: ZR-75-30; agent: vehicle; time point: 30min; ', 'cell line: ZR-75-30; agent: BMP7; time point: 30min; ', 'cell line: ZR-75-30; agent: vehicle; time point: 1h; ', 'cell line: ZR-75-30; agent: BMP7; time point: 1h; ', 'cell line: ZR-75-30; agent: vehicle; time point: 3h; ', 'cell line: ZR-75-30; agent: BMP7; time point: 3h; ', 'cell line: ZR-75-30; agent: vehicle; time point: 6h; ', 'cell line: ZR-75-30; agent: BMP7; time point: 6h; ', 'cell line: ZR-75-30; agent: vehicle; time point: 12h; ', 'cell line: ZR-75-30; agent: BMP7; time point: 12h; ', 'cell line: ZR-75-30; agent: vehicle; time point: 24h; ', 'cell line: ZR-75-30; agent: BMP7; time point: 24h; ' GSE157284 Homo sapiens 82 Expression profiling by array GPL570 Gene expression profiles of PD-L1 SP142 expression in triple-negative breast cancer 2020-09-01 The SP142 PD-L1 assay is a companion diagnostic for atezolizumab in metastatic triple-negative breast cancer (TNBC). The VENTANA SP142 assay was used to identify PD-L1 expression from TMA slides where PD-L1-positivity for an individual sample was defined as ≥1% of tumor-infiltrating immune cells as having PD-L1 expression. The PD-L1-positive gene signature consisted of 94 immune-related genes. The PD-L1-positive signature was predictive of pathologic complete response and survival outcome in multiple TNBC cohorts. In other malignancies treated with ICIs, the PD-L1-positive signature was associated with response and improved survival. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE157284 Clinical and genomic assessment of PD-L1 SP142 expression in triple-negative breast cancer. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-021-06193-9 {Breast cancer research and treatment (3.471): 10.1007/s10549-021-06193-9} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA660764 https://www.ebi.ac.uk/ena/browser/view/PRJNA660764 None [Overal design]We prospectively collected tumor tissues from specimens of surgically resected breast cancer at the Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea, between July 1997 and December 2007. A total of 84 patients with triple negative breast cancer were enrolled for gene expression profiling.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was isolated from tissues with TRIzol (Life Technologies, NY) reagent according to the manufacturer’s protocol. RNA quality and integrity were confirmed by electrophoresis on agarose gel stained with ethidium bromide and examined under ultraviolet light.'; [Cell type]'Source: ''sp142 pd-l1: negative; age: 48; ajcc stage: 4; vital status: death; ', 'sp142 pd-l1: negative; age: 61; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: positive; age: 69; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 51; ajcc stage: 3; vital status: death; ', 'sp142 pd-l1: negative; age: 34; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: positive; age: 37; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 36; ajcc stage: 2; vital status: death; ', 'sp142 pd-l1: negative; age: 32; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: positive; age: 64; ajcc stage: NA; vital status: NA; ', 'sp142 pd-l1: negative; age: 65; ajcc stage: 1; vital status: death; ', 'sp142 pd-l1: negative; age: 31; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 47; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 48; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 29; ajcc stage: 3; vital status: death; ', 'sp142 pd-l1: negative; age: 67; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 56; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 34; ajcc stage: 3; vital status: alive; ', 'sp142 pd-l1: positive; age: 64; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 61; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 35; ajcc stage: 2; vital status: death; ', 'sp142 pd-l1: negative; age: 37; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 48; ajcc stage: 3; vital status: alive; ', 'sp142 pd-l1: negative; age: 45; ajcc stage: 1; vital status: death; ', 'sp142 pd-l1: negative; age: 28; ajcc stage: 3; vital status: alive; ', 'sp142 pd-l1: negative; age: 53; ajcc stage: 3; vital status: death; ', 'sp142 pd-l1: negative; age: 60; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 56; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 40; ajcc stage: 3; vital status: death; ', 'sp142 pd-l1: negative; age: 78; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 65; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 45; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 41; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: positive; age: 73; ajcc stage: 1; vital status: death; ', 'sp142 pd-l1: positive; age: 46; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 57; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 32; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 50; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: positive; age: 63; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 40; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 58; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: positive; age: 50; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: positive; age: 45; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 35; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 41; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: positive; age: 54; ajcc stage: 1; vital status: NA; ', 'sp142 pd-l1: negative; age: 60; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: positive; age: 40; ajcc stage: 3; vital status: alive; ', 'sp142 pd-l1: positive; age: 35; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 56; ajcc stage: 4; vital status: death; ', 'sp142 pd-l1: positive; age: 42; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: positive; age: 34; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 46; ajcc stage: 3; vital status: alive; ', 'sp142 pd-l1: positive; age: 53; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: positive; age: 76; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 76; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 72; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 42; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 51; ajcc stage: NA; vital status: alive; ', 'sp142 pd-l1: negative; age: 38; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: positive; age: 54; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: positive; age: 34; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 36; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: positive; age: 53; ajcc stage: 1; vital status: NA; ', 'sp142 pd-l1: positive; age: 59; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: positive; age: 72; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: positive; age: 54; ajcc stage: 1; vital status: alive; ', 'sp142 pd-l1: negative; age: 54; ajcc stage: 2; vital status: alive; ', 'sp142 pd-l1: negative; age: 53; ajcc stage: 4; vital status: death; ', 'sp142 pd-l1: negative; age: 51; ajcc stage: 1; vital status: alive; ' GSE63958 Homo sapiens 10 Expression profiling by array GPL10904 TRPM7 maintains mesenchymal phenotype of breast cancer cells by tensional regulation of SOX4 2014-12-08 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE63958 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA269596 https://www.ebi.ac.uk/ena/browser/view/PRJNA269596 None [Overal design]Refer to individual Series; [Treatment]'Transduced with scrambled or TRPM7 shRNA', 'Transduced with scrambled or SOX4 shRNA'; [Growth]'Cultured in DMEM supplemented with Glutamax, 10% fetal bovine serum and 1% pen/strep'; [Extraction]'RNA was extracted with RNeasy Minikit (Qiagen), followed by clean-up and DNase I treatment in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'breast cancer''cell line: MDA-231; cell type: breast cancer; transduced with: scrambled shRNA; ', 'cell line: MDA-231; cell type: breast cancer; transduced with: TRPM7 shRNA; ', 'cell line: MDA-231; cell type: breast cancer; transduced with: SOX4 shRNA; ' GSE115696 Homo sapiens 27 Methylation profiling by high throughput sequencing GPL16791 DNA methylatioin analysis of breast cancer cell lines with TET1 knockout 2018-06-12 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115696 TET1-Mediated Hypomethylation Activates Oncogenic Signaling in Triple-Negative Breast Cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-17-2082 {Cancer research (8.378): 10.1158/0008-5472.CAN-17-2082} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA475775 https://www.ebi.ac.uk/ena/browser/view/PRJNA475775 None [Overal design]Refer to individual Series; [Treatment]'gRNAs targeting 3 different TET1 exons were cloned into the Lenti CRISPR V2 plasmid. gRNAs targeted exon 6 (KO-1), exon 3 (KO-2) and exon 11 (KO-3). Lentiviruses were generated using HEK293T cells by transfecting with packaging plasmid (psPAX2, Addgene 12260), envelope plasmid (pMD2.G, Addgene 12259) and lenti-CRISPR V2 plasmid (Addgene 52961). Cells were transfected using Lipofectamine 2000. Viral supernatant was collected at 48 and 72 hours, filtered with 0.45µm membrane and incubated on MDA-MB-231 cells for 7 hours in the presence of polybrene (6µg/mL, Millipore). We puromycin selected (1µg/mL) the cells for three days, followed by single cell cloning using serial dilution in 96 well plates. After selection, cells were maintained in normal media supplemented with 0.25 µg/mL puromycin.', 'gRNAs targeting 2 different TET1 exons were cloned into the Lenti CRISPR V2 plasmid. gRNAs targeted exon 11 (ATTCCCCGAATCAAGCGGAA, KO-1 and KO-2) and exon 3 (AAGTTTTAAAGGTAATCAGC, KO-3). Lentiviruses were generated using HEK293T cells by transfecting with packaging plasmid (psPAX2, Addgene 12260), envelope plasmid (pMD2.G, Addgene 12259) and lenti-CRISPR V2 plasmid (Addgene 52961). Cells were transfected using Lipofectamine 2000. Viral supernatant was collected at 48 and 72 hours, filtered with 0.45µm membrane and incubated on Hs578T cells for 7 hours in the presence of polybrene (6µg/mL, Millipore). We puromycin selected (1µg/mL) the cells for three days, followed by single cell cloning using serial dilution in 96 well plates. After selection, cells were maintained in normal media supplemented with 0.25 µg/mL puromycin.'; [Growth]'MDA-MB-231 cells were cultured in DMEM medium with 10% fetal bovine serum', 'Hs578T cells were cultured in DMEM medium with 10% fetal bovine serum'; [Extraction]'Genomic DNA was extracted using Puregene Gentra DNA extraction protocol.\nGenomic DNA extracted from tissue samples was spiked with methylation standards and sequentially digested with two restriction endonucleases recognizing CCCGGG sites in DNA. SmaI cleaved only unmethylated sites resulting in blunt ended fragments starting with 5’-GGG. Next, XmaI cleaved the remaining methylated sites creating 5’-CmeCGG overhang sequences. Exonuclease-deficient Klenow fragment DNA polymerase was then used to fill in the 3’ recesses left by XmaI and add 3’-dA overhangs to the ends of all fragments. Thus, specific signatures 5’-GGG and 5’-CCGGG were created at unmethylated and methylated CpG sites, respectively. Illumina sequencing adapters were then ligated to the enzyme-treated DNA; sequencing libraries were generated according to Illumina protocols and run on an Illumina HiSeq 2500 instrument at Fox Chase Cancer Center Genomics facility. Sequencing data were aligned to the rat genome (rn4), and the reads with unmethylated and methylated signatures were counted at individual CCCGGG sites. Methylation levels were calculated as the ratio of reads with the methylated signature to all reads mapping to each respective site. DNA methylation values at individual CpG sites were adjusted based on spiked in standards and filtered for the minimum sequencing depth of 100 reads.', "DNA isolation: The pellet was lysed in the solution containing 2% sodium dodecyl sulphate and 25 mM EDTA. Proteins were precipitated by adding 1/3 volume of 10 M ammonium acetate and removed as a pellet by centrifugation. DNA was precipitated from the supernatant with isopropanol, washed with 70% ethanol and dissolved in TE (10 mM TRIS pH 8.0, 1 mM EDTA).\nTwo micrograms of genomic DNA spiked with 5 methylation standards with defined methylation levels were digested with 20 units of SmaI endonuclease (NEB) for 8 hours at 25°C. Subsequently, 20 units of XmaI endonuclease (NEB) were added and the digestion was continued for an additional 16 hours at 37°C. Digested DNA with methylation-specific signatures at the ends of restriction fragments was end repaired using dCTP, dGTP and dATP (0.4 mM final concentration of each) and 15 units of Klenow Fragment (3'>5' exonuclease deficient) DNA polymerase (NEB).\nIllumina paired end (Quail et al. 2008) or barcoded Truseq (Illumina, San Diego, CA) sequencing adapters were then ligated at 10:1 adapter:fragment ratio using Rapid T4 DNA ligase (Enzymatics, Beverly, MA). The ligation mix was size selected by electrophoresis in 2% agarose. Two slices corresponding to 250-350 bp and 350-500 bp sizes based on a 100 bp DNA ladder (NEB) were cut out and DNA was extracted from agarose. DNA eluted from the slices was separately amplified with Illumina paired end PCR primers (Quail et al. 2008) using iProof high-fidelity DNA polymerase (Bio-Rad Laboratories, Hercules, CA) and 18 cycles of amplification. Resulting sequencing libraries were purified with AMPure magnetic beads (Agencourt, Beverly, MA)."; [Cell type]'Triple negative breast cancer cell line', 'Source: ''cell type: Triple negative breast cancer cell line; age: adult; genotype/variation: Empty vector single clone 1; ', 'cell type: Triple negative breast cancer cell line; age: adult; genotype/variation: Empty vector single clone 2; ', 'cell type: Triple negative breast cancer cell line; age: adult; genotype/variation: Empty vector single clone 3; ', 'cell type: Triple negative breast cancer cell line; age: adult; genotype/variation: TET1 KO_1 single clone (gRNA targeting exon 6); ', 'cell type: Triple negative breast cancer cell line; age: adult; genotype/variation: TET1 KO_2 single clone (gRNA targeting exon 3); ', 'cell type: Triple negative breast cancer cell line; age: adult; genotype/variation: TET1 KO_3 single clone (gRNA targeting exon 11); ', 'cell type: Triple negative breast cancer cell line; age: adult; genotype/variation: Empty vector pooled cells 1; ', 'cell type: Triple negative breast cancer cell line; age: adult; genotype/variation: Empty vector pooled cells 2; ', 'cell type: Triple negative breast cancer cell line; age: adult; genotype/variation: Empty vector pooled cells 3; ', 'cell line: Hs578T; phenotype: Triple negative breast cancer cell line; age: adult; genotype/variation: Empty vector single clone B5; ', 'cell line: Hs578T; phenotype: Triple negative breast cancer cell line; age: adult; genotype/variation: Empty vector single clone C5; ', 'cell line: Hs578T; phenotype: Triple negative breast cancer cell line; age: adult; genotype/variation: Empty vector single clone D5; ', 'cell line: Hs578T; phenotype: Triple negative breast cancer cell line; age: adult; genotype/variation: TET1 KO_1 single clone Both_B5 (gRNA ATTCCCCGAATCAAGCGGAA targeting exon 11); ', 'cell line: Hs578T; phenotype: Triple negative breast cancer cell line; age: adult; genotype/variation: TET1 KO_1 single clone Both_C6 (gRNA ATTCCCCGAATCAAGCGGAA targeting exon 11); ', 'cell line: Hs578T; phenotype: Triple negative breast cancer cell line; age: adult; genotype/variation: TET1 KO_3 single clone 13_D8 (gRNA AAGTTTTAAAGGTAATCAGC targeting exon 3); ' GSE104076 Homo sapiens 8 Non-coding RNA profiling by array GPL18044 Determination of trastuzumab responsive microRNAs in SKBR3 and BT474 cells. 2017-09-20 To develop gene-miRNA and pathway-miRNA networks in trastuzumab treatment, we performed a recent miRNA microarray profiling in trastuzumab treated/untreated SKBR3 and BT474 cell lines. The cells were plated at a starting density of 2 millions in 100 mm cell culture dishes and then, they were treated with 6 ug/mL trastuzumab and PBS in two replicates. Total RNA was isolated with the TRIzol reagent (Invitrogen) according to the manufacturer's instructions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE104076 Construction of miRNA-miRNA networks revealing the complexity of miRNA-mediated mechanisms in trastuzumab treated breast cancer cell lines. PloS one 2.776 https://doi.org/10.1371/journal.pone.0185558 {PloS one (2.776): 10.1371/journal.pone.0185558} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA408159 https://www.ebi.ac.uk/ena/browser/view/PRJNA408159 None [Overal design]RNA samples were isolated after 144h trastuzumab treatment. A total of 4 samples from BT474 cells (2 from trastuzumab treated and 2 from PBS treated) and 4 samples from SKBR3 cells (2 from trastuzumab treated and 2 from PBS treated) were analyzed.; [Treatment]'SKBR3 and BT474 cells were plated at a starting density of 2 x 106 in 100 mm cell culture plates. BT474 and SKBR3 cells were treated with 6 µg/mL trastuzumab and/or PBS as control within two biological replicates for 144 hours. The media were changed in every 72 hours.'; [Growth]'HER2+ breast cancer cell lines BT474 (HTB-20) and SKBR3 (HTB-30) were purchased from the American Type Culture Collection (ATCC). SKBR3 cells were maintained in Mc Coy’s 5A medium (Lonza) with L-glutamine containing 10% fetal bovine serum (FBS), 1% penicillin-streptomycin. BT474 cells were maintained in RPMI 1640 medium with L-glutamine (Lonza) supplemented with 10% FBS, 1% penicillin-streptomycin and 2% bovine insulin. The cell lines were cultured in a humidified air supplemented with 5% CO2 at 37°C.'; [Extraction]"Total RNA was isolated with the TRIzol reagent (Invitrogen) according to the manufacturer's instructions. Absorption at 260 nm and 280 nm was measured for the determination of RNA purity."; [Cell type]'HER2+ breast cancer cell line''cell line: BT474; cell type: HER2+ breast cancer cell line; receptor: ER+, HER2+, PR+; treated with: PBS for 144 hrs; ', 'cell line: BT474; cell type: HER2+ breast cancer cell line; receptor: ER+, HER2+, PR+; treated with: 6 ug/mL trastuzumab for 144 hrs; ', 'cell line: SKBR3; cell type: HER2+ breast cancer cell line; receptor: ER-, HER2+, PR+; treated with: PBS for 144 hrs; ', 'cell line: SKBR3; cell type: HER2+ breast cancer cell line; receptor: ER-, HER2+, PR+; treated with: 6 ug/mL trastuzumab for 144 hrs; ' GSE130572 Homo sapiens 2 Expression profiling by high throughput sequencing GPL20795 POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [PTX3_OE] 2019-05-01 We conduct transcriptome comparison of control and PTX3-overexpressed HMLER cells to gain genomic insights on the biological processes that PTX3 is involved in breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130572 SH3RF3 promotes breast cancer stem-like properties via JNK activation and PTX3 upregulation. Nature communications 11.878 https://doi.org/10.1038/s41467-020-16051-9 {Nature communications (11.878): 10.1038/s41467-020-16051-9} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA540670 https://www.ebi.ac.uk/ena/browser/view/PRJNA540670 https://www.ncbi.nlm.nih.gov/sra?term=SRP194401 [Overal design]In the study presented here, PTX3 was overexpressed in the HMLER breast cancer cells. RNA sequencing profiling of mRNA levels was performed in the control and overexpression cells.; [Treatment]'no treatment.'; [Growth]'MEGM'; [Extraction]'Trizol reagent was used to extract RNA, then total RNA was subjected to Hiseq PE150 RNA-Seq.\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'epithelial-like''cell type: epithelial-like; genotype/variation: control; cell line: HMLER; ', 'cell type: epithelial-like; genotype/variation: PTX3-overexpressed; cell line: HMLER; ' GSE84071 Homo sapiens 3 Genome binding/occupancy profiling by genome tiling array GPL15975 ChIP-on-chip from MDA-MB-231 cells with PHF1, CUL4B and PRMT5 2016-07-06 It has been reported that PHF1, CUL4B and PRMT5 all play important roles in epigenetic regulation. We reported that PHF1, CRL4B and PRMT5 may act as a complex in transcriptional regulation and have a vital effect in breast cancer progression. So we performed ChIP-on-chip assays to find unique promoters co-targeted by PHF1, CUL4B and PRMT5. PHF1, CUL4B and PRMT5 have a predominant cooperation, at least in MDA-MB-231 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE84071 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA327931 https://www.ebi.ac.uk/ena/browser/view/PRJNA327931 None [Overal design]comparison of PHF1, CUL4B and PRMT5 target genes; [Treatment]'1x10E7 cells were collected for ChIP assay per antibody'; [Growth]"MDA-MB-231 cell lines were maintained in Dulbecco's modified Eagle's medium (DMEM) (Gibco, Invitrogen). All media contained 10% fetal bovine serum (FBS), 100 units/ml penicillin, and 100 mg/ml streptomycin (Gibco BRL)."; [Extraction]'1x10E7 cells were washed twice with PBS and cross-linked with 1% formaldehyde at room temperature for 10 min. Cells then were rinsed with ice-cold PBS twice and collected into 100 mM Tris-HCl (pH 9.4), 10 mM DTT and incubated for 15 min at 30°C and centrifuged for 5 min at 2000 g. Cells were washed sequentially with 1 ml of ice-cold PBS, buffer I (0.25% Triton X-100, 10 mM EDTA, 0.5 mM EGTA, 10 mM HEPES, pH 6.5), and buffer II (200 mM NaCl, 1 mM EDTA, 0.5 mM EGTA, 10 mM HEPES, pH 6.5). Cells were then resuspended in 0.3 ml of lysis buffer (1% SDS, 10 mM EDTA, 50 mM Tris-HCl, pH 8.1, 1× protease inhibitor cocktail (Roche Molecular Biochemicals, Indianapolis, IN) and sonicated three times for 10 s each at the maximum setting (Fisher Sonic Dismembrator, Model 300) followed by centrifugation for 10 min. Supernatants were collected and diluted in buffer (1% Triton X-100, 2 mM EDTA, 150 mM NaCl, 20 mM Tris-HCl, pH 8.1) followed by immunoclearing with 2 μg sheared salmon sperm DNA, 20 μl preimmune serum and protein A-sepharose (45 μl of 50% slurry in 10 mM Tris-HCl, pH 8.1, 1 mM EDTA) for 2 hr at 4°C. Immunoprecipitation was performed for 6 hr or overnight at 4°C with specific antibodies. After immunoprecipitation, 45 μl protein A-Sepharose and 2 μg of salmon sperm DNA were added and the incubation was continued for another 1 hr. Precipitates were washed sequentially for 10 min each in TSE I (0.1% SDS, 1% Triton X-100, 2 mM EDTA, 20 mM Tris-HCl, pH 8.1, 150 mM NaCl), TSE II (0.1% SDS, 1% Triton X-100, 2 mM EDTA, 20 mM Tris-HCl, pH 8.1, 500 mM NaCl), and buffer III (0.25 M LiCl, 1% NP-40, 1% deoxycholate, 1 mM EDTA, 10 mM Tris-HCl, pH 8.1). Precipitates were then washed three times with TE buffer and extracted three times with 1% SDS, 0.1 M NaHCO3. Eluates were pooled and heated at 65°C for at least 6 hr to reverse the formaldehyde cross-linking. DNA fragments were purified with a QIAquick Spin Kit (Qiagen, CA). For PCR, 1 μl from a 50 μl DNA extraction and 21–25 cycles of amplification were used.'; [Cell type]'Source: ''cell line: MDA-MB-231; chip antibody: PHF1; chip antibody vendor: abcam; chip antibody cat. #: ab80042; chip antibody lot #: GR37656-1; ', 'cell line: MDA-MB-231; chip antibody: none, input DNA; ', 'cell line: MDA-MB-231; chip antibody: CUL4B; chip antibody vendor: sigma-aldrich; chip antibody cat. #: C9995; chip antibody lot #: 128K4864; ', 'cell line: MDA-MB-231; chip antibody: PRMT5; chip antibody vendor: abcam; chip antibody cat. #: ab109451; chip antibody lot #: GR125109-4; ' GSE48566 Mus musculus 267 Expression profiling by array GPL6246 Expression data from mammary tumors from MOLF/Ei x PyMT mouse crosses and Diversity Outcross x PyMT mouse crosses 2013-07-05 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48566 Aicardi-Goutières syndrome gene Rnaseh2c is a metastasis susceptibility gene in breast cancer. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1008020 {PloS one (2.776) doi:10.1371/journal.pone.0072287}; {PLoS genetics (5.224) doi:10.1371/journal.pgen.1008020}; {PLoS genetics (5.224) doi:10.1371/journal.pgen.1005989}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA210664 https://www.ebi.ac.uk/ena/browser/view/PRJNA210664 None [Overal design]Refer to individual Series; [Treatment]'No treatment was performed.'; [Growth]'Tumors were permitted to grow until animal neared humane endpoints. Tumors were harvested, snap frozen and stored at -80oC until RNA extraction.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 1491; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3275; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3276; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3402; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3493; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3497; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3498; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3508; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3533; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3536; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3544; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3594; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3595; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3598; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3790; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3803; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3792; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3807; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3832; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3872; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3874; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3878; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3942; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3943; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3945; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 3947; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4021; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4025; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4028; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4140; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4143; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4158; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4161; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4174; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4175; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4180; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4183; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4256; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4258; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4263; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4273; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4275; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4277; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4278; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4295; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4299; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4310; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4312; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4333; ', 'strain/background: MOLF/Ei x PyMT; 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tissue: mammary tumor; mouse id: 4360; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4363; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4367; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4374; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4375; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4376; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4379; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4380; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4382; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4385; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4540; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4546; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4567; ', 'strain/background: MOLF/Ei x PyMT; 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tissue: mammary tumor; mouse id: 4488; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4492; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4511; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4516; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4547; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4638; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4386; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4392; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4403; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4413; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4433; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4434; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4435; ', 'strain/background: MOLF/Ei x PyMT; 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tissue: mammary tumor; mouse id: 4525; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4529; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4532; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4533; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4534; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4537; ', 'strain/background: MOLF/Ei x PyMT; tissue: mammary tumor; mouse id: 4539; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14087; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14264; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14227; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14176; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14273; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14056; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13955; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14267; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14095; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14249; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14266; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14247; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14233; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14015; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14091; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14149; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14061; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14141; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14064; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14121; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14078; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13960; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14089; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14103; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14127; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14182; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14051; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14048; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14024; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14118; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14271; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14098; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14086; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14199; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14090; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14052; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14128; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14125; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14110; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13953; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14261; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14028; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14198; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13976; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14150; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14077; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14185; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14021; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13948; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13950; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13951; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13956; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13958; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13973; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13974; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13975; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13981; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13983; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13986; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13987; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13998; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13999; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14000; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14001; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14002; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14005; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14018r; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14022r; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14026; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14027; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14032; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14033; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14037; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14043; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14044; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14050; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14050r; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14055; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14058; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14072; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14083; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14085; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14094; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14099; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14106; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14122; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14124; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14126; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14148; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14151; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14170; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14187; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14189; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14190; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14195; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14200; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14201; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14223; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14224; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14231; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14248; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14250; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14251; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14252r; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14253r; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14260; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14262; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14272; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14275; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14280; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14281; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14282; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14286; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14287; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14289; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14290; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14291; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14295; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14306; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14308; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14309; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14311; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14312; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14320; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14322; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14327; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14328; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14329; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14352; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14352r; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14354; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14356; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14358; ' GSE131980 Mus musculus; Homo sapiens 23 Genome variation profiling by high throughput sequencing GPL21290; GPL21493 Acquired resistance to combined BET and CDK4/6 inhibition in triple-negative breast cancer [Exome] 2019-05-30 BET inhibitors are promising therapeutic agents for the treatment of triple-negative breast cancer (TNBC), but the rapid emergence of resistance necessitates investigation of combination therapies and their effects on tumor evolution. Here, we show that palbociclib, a CDK4/6 inhibitor, and paclitaxel, a microtubule inhibitor, synergize with the BET inhibitor JQ1 in TNBC lines. High-complexity DNA barcoding and mathematical modeling indicate a high rate of de novo acquired resistance to these drugs relative to pre-existing resistance. We demonstrate that the combination of JQ1 and palbociclib induces cell division errors, which can increase the chance of developing aneuploidy. Characterizing acquired resistance to combination treatment at single cell level shows heterogeneous mechanisms including activation of G1-S and senescence pathways. Our results establish a rationale for further investigation of combined BET and CDK4/6 inhibition in TNBC and suggest novel mechanisms of action for these drugs, and new vulnerabilities in cells after emergence of resistance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131980 Acquired resistance to combined BET and CDK4/6 inhibition in triple-negative breast cancer. Nature communications 11.878 https://doi.org/10.1038/s41467-020-16170-3 {Nature communications (11.878): 10.1038/s41467-020-16170-3} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA545506 https://www.ebi.ac.uk/ena/browser/view/PRJNA545506 https://www.ncbi.nlm.nih.gov/sra?term=SRP199905 [Overal design]Exome-seq of SUM159 breast cancer cell line treated in vitro with JQ1, palbociclib, paclitaxel, and combinations; [Treatment]'Cells were grown in vitro in the presence of DMSO, JQ1 (100 nM), paclitaxel (0.6 nM), palbociclib (160 nM), JQ1+paclitaxel, or JQ1+palbociclib, in triplicates, for up to 18 passages. Mice were treated for up to 2 weeks with vehicle, JQ1 (30-50 mg/kg daily), palbociclib (75 mg/kg daily), paclitaxel (10 mg/kg twice weekly), JQ1+palbociclib, or JQ1+paclitaxel, or for 1 week with JQ1 followed by 1 week with paclitaxel, 1 week with paclitaxel followed by 1 week with JQ1, or 1 week with JQ1+paclitaxel followed by 1 week with vehicle, with 5 mice per group.'; [Growth]'Cells were lentivirally infected with the ClonTracer barcode library (Bhang et al., 2015). Barcoded cells were passaged in vitro in the presence of drug or injected orthotopically into mammary fat pads of NOG mice to produce xenografts.'; [Extraction]'DNA was extracted from frozen cultured cells and xenografts using the AllPrep DNA/RNA Mini Kit or the QIAamp DNA Mini Kit (Qiagen). Equal amounts of DNA were pooled from replicates for library construction.\nDNA was fragmented to 250 bp (Covaris ultrasonication) and further purified using Agencourt AMPure XP beads. Size-selected DNA was ligated to sequencing adaptors with sample-specific barcodes using the KAPA Hyper Prep Kit. Libraries were pooled and sequenced on an Illumina MiSeq nano flow cell to estimate the library DNA concentration based on the number of barcode reads per sample. Libraries were pooled and captured using SureSelectXT Human All Exon v5 (Agilent) in 7 x 3-plex and 1 x 2-plex. Captures were performed using the SureSelectXT Reagent Kit (Agilent).'; [Cell type]'Source: ''cell line: SUM159; treatment: pre-treatment; ', 'cell line: SUM159; treatment: DMSO; ', 'cell line: SUM159; treatment: paclitaxel; ', 'cell line: SUM159; treatment: JQ1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; ', 'cell line: SUM159; treatment: palbociclib; ', 'cell line: SUM159; treatment: JQ1+palbociclib; ', 'cell line: SUM159; treatment: vehicle; ', 'cell line: SUM159; treatment: JQ1->paclitaxel; ', 'cell line: SUM159; treatment: paclitaxel->JQ1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel->vehicle; ', 'cell line: NOD.Cg-Prkdcscid Il2rgtm1Sug/JicTac (NOG); treatment: N/A; ', 'cell line: CEPH1408 cells; treatment: N/A; ' GSE27444 Homo sapiens 14 Expression profiling by array GPL570 Expression data from zinc-finger-transcription-factor-induced Fulvestrant-Resistant MCF7 Cell Lines 2011-02-22 Multiple gene expression studies have demonstrated that breast cancer biological diversity is associated with distinct transcriptional programs. Transcription factors, because of their unique ability to coordinate the expression of multiple genes, are speculated to play a role in generating phenotypic plasticity associated with cancer progression including acquired drug resistance. Combinatorial libraries of artificial zinc-finger transcription factors (ZF-TFs) provide a robust means for inducing and understanding various functional components of the cancer phenotype. Herein, we utilized combinatorial ZF-TF library technology to better understand how breast cancer cells acquire resistance to a fulvestrant, a clinically important anti-endocrine therapeutic agent. We isolated six ZF-TF library members capable of inducing stable, long-term anti-endocrine drug-resistance in two independent estrogen receptor positive breast cancer cell lines. Comparative gene expression profile analysis of the ZF-TF-transduced breast cancer cell lines revealed a 72-gene cluster that constituted a common signature for the fulvestrant-resistance phenotype. Pathway enrichment-analysis of gene expression data revealed that the ZF-TF-induced fulvestrant resistance is associated with an estrogen receptor negative-like gene set and four unique myb-regulated gene sets. Furthermore, we identified a set of genes strongly expressed in the ZF-TF-induced fulvestrant-resistant cells that was correlated with a lower probability of distant metastasis-free or death-from-relapse-free survival of breast cancer patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE27444 Induction of stable drug resistance in human breast cancer cells using a combinatorial zinc finger transcription factor library. PloS one 2.776 https://doi.org/10.1371/journal.pone.0021112 {PloS one (2.776): 10.1371/journal.pone.0021112} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA137069 https://www.ebi.ac.uk/ena/browser/view/PRJNA137069 None [Overal design]MCF7-R73 cells, a monoclonal MCF7 subline that is highly sensitive to fulvestrant-induced cytocidal activity, underwent retroviral transduction with the zinc finger transcription factor (ZF-TF) activator library or with a control plasmid encoding only the NF-kB p65 activation domain. Both populations of cells were enriched for transduced cells by selecting for growth in puromycin and for fulvestrant-resistant cells by selecting with 100 nM fulvestrant. After 6 weeks of continuous treatment with fulvestrant, hundreds of drug-resistant colonies emerged from the population of cells infected with the ZF-TF activator library. By contrast, as expected, the control MCF7cell line transduced by NF-kB p65-only underwent massive cell death resulting in the complete absence of resistant colonies. DNA encoding the zinc-finger arrays was rescued by PCR from genomic DNA of pooled fulvestrant-resistant cells. The sequences of the ZF-TFs were determined and 46 unique ZF-TF clones identified. These 46 unique ZF-TFs were re-cloned into the retroviral vector and converted into clonal virus stocks that were used to transduce MCF7-R73 cells. These 46 retrovirally transduced cell populations were then challenged with fulvestrant. As compared with the control MCF-238 cells, MCF7-R73 cells transduced with six unique ZF-TFs demonstrated survival and growth in the presence of 100nM fulvestrant.; [Treatment]'293T cells were seeded at 5 x 105 cells per 10 cm culture dish, transfected with 3.2 μg of ZT-TF p65 activator library DNA and 2.4μg and 0.8μg of PMD-MLV and PMD-G plasmid DNA using Fugene 6 according to the manufacture’s protocol and retroviral supernatant harvested 48 hrs later. MCF7-R73 cells (6 x105 per 10 cm plate) were infected with 1.33 x 105 ZF-TF retrovirions in media containing polybrene. Two days post-infection the cells were exposed to puromycin (0.4mg/ml), and three days later were subjected to continuous combined puromycin and fulvestrant (100nM) selection for an additional 42 days. Retroviral DNA was recovered by PCR, subcloned into the pDONOR plasmid using Gateway technology (Invitrogen), and subject to DNA sequencing that revealed 46 unique ZF-TF arrays. The 46 ZF-TFs were re-cloned into the retroviral destination plasmid using Gateway technology, 46 ZF-TF retroviral supernatants generated, and MCF-R73 cells infected and subjected to puromycin and fulvestrant selection. Six unique ZF-TFs conferred drug resistance in the presence of continuous fulvestrant exposure. A control MCF7 cell line (MCF7-R238) was generated by infecting MCF7-R73 cells with a retrovirus bearing the p65 activation domain only. T47D cells were infected with the six unique ZF-TF bearing retroviruses and subjected to fulvestrant exposure as described for the MCF7 cells.'; [Growth]'MCF7-R73 cells, a clonal isolate derived from the MCF7 cell line were kindly provided by Dr. Toshi Shioda (MGH, Charlestown, MA) and maintained in a xenoestrogen controlled environment as described in Coser KR, Wittner BS, Rosenthal NF, Collins SC, Melas A, et al. (2009) Antiestrogen-resistant subclones of MCF-7 human breast cancer cells are derived from a common monoclonal drug-resistant progenitor, Proc Natl Acad Sci U S A 106: 14536-14541'; [Extraction]'QIAGEN RNeasy protocol and reagents for extraction of total RNA'; [Cell type]'Source: ''retroviral transduction: control; ', 'retroviral transduction: zinc finger transcription factor 115; ', 'retroviral transduction: zinc finger transcription factor 19; ', 'retroviral transduction: zinc finger transcription factor 64; ', 'retroviral transduction: zinc finger transcription factor 70; ', 'retroviral transduction: zinc finger transcription factor 7; ', 'retroviral transduction: zinc finger transcription factor 83; ' GSE27820 Homo sapiens 3 Expression profiling by array GPL570 Expression data from active human umbilical cord mesenchymal stem cell (active HUMSC) and inactive human umbilical cord mesenchymal stem cell (inactive HUMSC) 2011-03-08 Active HUMSC with distinct binding rate to MDA MB-231 breast cancer cells, distinct ability in suppressing tumorigenesis,distinct cell in cell features and distinct features under TEM then inactive HUMSC We used microarrays to detail the difference gene expression between active HUMSC and inactive HUMSC https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE27820 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA137909 https://www.ebi.ac.uk/ena/browser/view/PRJNA137909 None [Overal design]HUMSC with high MDA MB-231 breast cancer cells suppression rate was selective as active HUMSC and HUMSC with low MDA MB-231 breast cancer cells suppression rate was selective as inactive HUMSC; [Treatment]'UCHY was UC cells but cultured in 2% O2 incubator at 37℃ for 3 days'; [Growth]'HST and UC were cultured in 5% CO2 incubator at 37℃.'; [Extraction]"Qiagene RNeasy mini kit extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'mesenchymal stem cell (HUMSC)''tissue: umbilical cord; cell type: mesenchymal stem cell (HUMSC); tumor suppression: low; ', 'tissue: umbilical cord; cell type: mesenchymal stem cell (HUMSC); tumor suppression: high; ', 'tissue: umbilical cord; cell type: mesenchymal stem cell (HUMSC); tumor suppression: high; growth condition: hypoxia; ' GSE66647 Homo sapiens 168 Protein profiling by protein array GPL19861 RPPA_RATHER_ILC 2015-03-06 Invasive lobular carcinoma (ILC) is the second most frequent histological breast cancer subtype after invasive ductal carcinoma (IDC), accounting for 5-15% of all breast cancers. Although clinical outcomes of ILC and IDC seem similar, the molecular processes underlying ILC are still largely unknown. To explore this, we have performed a comprehensive proteomics analysis of a large ILC patient cohort. These data are generated in the context of the RATHER consortium (http://www.ratherproject.com/) https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE66647 None None None None None 'protein' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA277536 https://www.ebi.ac.uk/ena/browser/view/PRJNA277536 None [Overal design]Fresh frozen tissue sections from 118 ILCs with a median clinical follow-up of 6.8 years were lysed and printed on protein arrays. Each sample was printed in 5 serial dilutions and each dilution was printed twice on the arrays. Arrays were hybridized with 168 specific primary antibodies against the kinome and cancer-related proteins.; [Treatment]'None'; [Growth]'None'; [Extraction]'Three sections of fresh frozen tissue were lysed in hot Laemmli buffer (50 mM Tris pH =6.8, 2% SDS, 5% glycerol, 2 mM DTT, 2.5 mM EDTA, 2.5 mM EGTA, 1x HALT Phosphatase inhibitor (Perbio 78420), Protease inhibitor cocktail complete MINI EDTA-free (Roche 1836170, 1 tablet/10 mL), 2 mM Na3VO4 and 10 mM NaF) and boiled for 10 min at 100°C. Samples were sonicated in a waterbath for 1-2min to break the DNA and spinned for 10 min at 13000 rpm. Supernatant was snapfrozen and protein concentration was measured (BCA reducing agents compatible kit, Pierce, Ref 23252).'; [Cell type]'Source: ''antibody vendor/catalog#: CST 4058; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 4056; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9154; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9126; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Abcam ab51089; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Abcam ab109268; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3358; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 1596-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9272; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 2212; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: BD610181; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9102; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 2862; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 9284; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 9212; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 4631; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3050; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9251; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 2215; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: BD 558686; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: BD 610627; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: Chemicon MAB4331; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3009 (C42B5); source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 4764 (C22B4); source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Upstate (M07-702); source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 2271-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9452; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 2527; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3033; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 1673-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: non-commercial; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 2532; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 2708; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Upstate M04-392; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9106; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9152; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 9559; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9188S; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9554; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Abcam ab51032; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 1696-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3270; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 4035 (C8F7); source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 2347; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 3312; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 2197; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Santa-Cruz sc-8408 (G-4); source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3232; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 9743; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 1871-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 2255-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 1826-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9132; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 9134; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 1718-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3230; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 5482; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9282; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 1051-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3174; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 8955; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 2326-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 1077-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 2822; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 9308; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 2223-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 2243; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Upstate (M05-907); source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9286; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9309 (4H1); source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: BD610445; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: BD610016; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 2402 (G31); source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: BD610177; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: BD611105; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: Lab Vision MS-432-P1 (Ab11); source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: BD 612685; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: R&D BBA10; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3131; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 2202-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 1524-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Santa-Cruz sc-03 (1005); source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 4407; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3974; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 3285; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 9467; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Santa-Cruz sc-285; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 4791; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Abcam ab11175; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 3489; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Santa-Cruz sc-10 (C-12); source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 2370; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Santa-Cruz sc-7883 (H-273); source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Upstate (M06-248); source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 2655; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 2241; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 3311; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 3141; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 3682; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 3061; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 1483-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 2163-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3723; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 1991-1; ab53290; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9510; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 8644; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3090 (H364); source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 3122; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 2105; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 9172; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 1735-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 2060-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 4911S; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 1613-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3591; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 5558; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 1647-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 1091-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 2250-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3692; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 3691; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 3592; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 1487-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Santa-Cruzsc-7291; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: BD610051; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: DakoM7240; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: BD610623; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: Upstate (M05-908); source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3440; source of antibody: Mouse; clonality: Monoclonal; ', 'antibody vendor/catalog#: Abcam ab2893; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Signalway 11238-1; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 1652-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 1653-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9145; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3556; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 2825-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 5528; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 3296-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Upstate (M06-668); source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 1611-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 1574-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9582; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 2231-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Upstate (M06-638); source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Novus NB100-92662; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 2066-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 2109; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 3517-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 1823-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 1303-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Novus NB100-82260; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 1688-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 8562; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: Epitomics 2258-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 2883; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3745; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 8155; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 5651; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 4176; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 2017; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 9331; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: Epitomics 2309-1; source of antibody: Rabbit; clonality: Monoclonal; ', 'antibody vendor/catalog#: CST 3427; source of antibody: Rabbit; clonality: Polyclonal; ', 'antibody vendor/catalog#: CST 2565; source of antibody: Rabbit; clonality: Monoclonal; ' GSE38959 Homo sapiens 47 Expression profiling by array GPL4133 Gene expression profiling of triple negative breast cancer, normal ductal cells, and normal tissues 2012-06-27 To identify novel molecular targets for triple negative breast cancer (TNBC), we have employed whole genome microarray expression profiling. We purified 30 surgically resected breast cancer tissue diagnosed triple negative by means of immunohistochemical staining and 13 normal mammary ductal cells with lasermicrobeam microdissection system (PALM MicroBeam, Carl Zeiss MicroImaging Co., Ltd), performed whole human genome microarray, and compared gene expression levels of TNBC, normal mammary ductal cells, and normal vital organs to develop molecular targets with a minimum risk. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE38959 Molecular features of triple negative breast cancer cells by genome-wide gene expression profiling analysis. International journal of oncology 3.571 https://doi.org/10.3892/ijo.2012.1744 {International journal of oncology (3.571): 10.3892/ijo.2012.1744} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA169423 https://www.ebi.ac.uk/ena/browser/view/PRJNA169423 None [Overal design]Gene expression levels of 30 TNBC, 13 normal mammary ductal cells, and 4 normal vital tissues were evaluated. to clarify the molecular mechanism involved in TNBC, we analyzed gene expression profiles of 30 TNBC as well as 13 normal epithelial ductal cells purified by laser microbeam microdissection, and identified 301 transcripts that were significantly up-regulated and 321 transcripts that were significantly down-regulated in TNBC. In addition, gene-expression profiles analysis of normal human vital organs including heart, lung, liver, and kidney allowed us to identify 90 cancer-specific genes involved in breast carcinogenesis such as NEK2, PBK, DTL, MELK and GPSM2. Among them, we focused on cell cycle regulators, asp (abnormal spindle) homolog, microcephaly associated (Drosophila) (ASPM) and centromere protein K (CENPK) as novel therapeutic targets for TNBC.; [Treatment]'None'; [Growth]'None'; [Extraction]'We purified 30 TNBC, 13 normal ductal cells using lasermicrobeam microdissection system (PALM MicroBeam, Carl Zeiss MicroImaging Co., Ltd) in accordance with the manufacturer’s guidance. Dissected cancer and normal ductal cells were dissolved in RLT lysis buffer (QIAGEN, Maryland, CA) containing 1% β-mercaptoethanol. The extracted total RNAs were purified with RNeasy Mini Kit (QIAGEN, Velanica, CA) according to the manufacture’s protocol. For RNA amplification and labeling, we used Agilent Low-Input QuickAmp labeling kit according to the manufacture’s guidance. Briefly, 100 ng of total RNA of each sample was amplified T7-RNA polymerase and simultaneously incorporated Cy3-labeled CTP.'; [Cell type]'triple negative breast cancer cells', 'mammary gland ductal cells', 'Source: ''disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 49; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 55; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 37; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 61; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 32; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 53; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 70; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 80; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 54; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 41; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 59; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 69; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 28; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 36; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 44; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 60; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 45; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 64; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 52; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 42; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 63; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 39; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 50; ', 'disease state: triple negative breast cancer; cell type: triple negative breast cancer cells; gender: female; age (y): 46; ', 'disease state: normal; cell type: mammary gland ductal cells; gender: female; age (y): 55; ', 'disease state: normal; cell type: mammary gland ductal cells; gender: female; age (y): 52; ', 'disease state: normal; cell type: mammary gland ductal cells; gender: female; age (y): 35; ', 'disease state: normal; cell type: mammary gland ductal cells; gender: female; age (y): 42; ', 'disease state: normal; cell type: mammary gland ductal cells; gender: female; age (y): 79; ', 'disease state: normal; cell type: mammary gland ductal cells; gender: female; age (y): 59; ', 'disease state: normal; cell type: mammary gland ductal cells; gender: female; age (y): 58; ', 'disease state: normal; cell type: mammary gland ductal cells; gender: female; age (y): 50; ', 'disease state: normal; cell type: mammary gland ductal cells; gender: female; age (y): 57; ', 'disease state: normal; tissue: whole heart tissue; sample type: commercially available (Clonetech); ', 'disease state: normal; tissue: whole lung tissue; sample type: commercially available (Clonetech); ', 'disease state: normal; tissue: whole liver tissue; sample type: commercially available (Clonetech); ', 'disease state: normal; tissue: whole kidney tissue; sample type: commercially available (Clonetech); ' GSE148089 Homo sapiens 16 Expression profiling by array GPL17586 Fra-2 overexpression upregulates pro-metastatic cell-adhesion molecules, promotes pulmonary metastasis and reduces survival in a spontaneous xenograft model of human breast cancer 2020-04-05 The effect of Fra-2 overexpression in two stable Fra-2 overexpressing clones of the human breast cancer cell line MDA-MB-231 on survival and metastatic load was studied after subcutaneous injection into scid and E- and P-selectin deficient scid (select) mice. To identify Fra-2 target genes, we performed cDNA microarrays with mRNA isolated from xenograft tumour tissue. Fra-2 overexpression lead to a significantly shorter overall survival and a higher amount of spontaneous metastases in scid mouse lungs and compared to select mice indicating that Fra-2 regulates selectin binding sites on the tumour cell surface, which directly influence overall survival. By using cDNA microarray analysis of resected primary tumours a multitude of deregulated genes, which are known to be involved in metastasis formation https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148089 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA623184 https://www.ebi.ac.uk/ena/browser/view/PRJNA623184 None [Overal design]The cells of two clones of MDA-MB231 line with Fra-2 overexpression (clone 1 and clone 2) as well as control cells were injected subcutaneously into scid mice and E- and P-selectin double knock-out scid mice (select). mRNA was isolated from xenograft tumour tissue (three tumours per group) and analyzed using Affimetrix transcriptome arrays.; [Treatment]'No further treatment was administered.'; [Growth]'Cells were adjusted to 5 x 106 ml-1 medium. 200 µl of this suspension were injected subcutaneously between the scapulae of each mouse. When the primary tumours had reached maximum 20% of the body weight of the animal at the beginning of the experiment or ulcerated, the mice were terminally narcotized, sacrificed by cardiocentesis and cervical dislocation.'; [Extraction]'The total RNA was isolated using QIAzol Lysis Reagent (Qiagen, Hilden, Germany) and the miRNeasy Mini Kit (Qiagen, Hilden, Germany), according to manufacturer`s instruction.'; [Cell type]'Source: ''origin: Xenograft; strain: scid; cell transfection: pIRES; ', 'origin: Xenograft; strain: E- and P-selectin deficient scid; cell transfection: pIRES; ', 'origin: Xenograft; strain: scid; cell transfection: Fra-2-pIRES; fra-2 overexpressing clone: clone 1; ', 'origin: Xenograft; strain: E- and P-selectin deficient scid; cell transfection: Fra-2-pIRES; fra-2 overexpressing clone: clone 1; ', 'origin: Xenograft; strain: scid; cell transfection: Fra-2-pIRES; fra-2 overexpressing clone: clone 2; ', 'origin: Xenograft; strain: E- and P-selectin deficient scid; cell transfection: Fra-2-pIRES; fra-2 overexpressing clone: clone 2; ' GSE140060 Homo sapiens 7 Genome binding/occupancy profiling by high throughput sequencing GPL9052; GPL18573 Genome wide analysis of PAX2 chromatin interaction in MCF-7 cell 2019-11-07 The aim of the study is to understand the role of the transcription factor PAX2 in estrogen receptor positive breast cancer cell line by using ChIP-seq. MCF-7-PAX2 stable cells were cultured in full media and treated with doxycycline (50ng/ml) for 16 hours to induce overexpression of PAX2-HA protein. Then cells were treated with 4-OH-tamoxifen (1μM) for 6 hours. All 3 treatments (Veh, Dox, DoxTam) were performed in duplicates. After treatments, cells were collected for ChIP experiment with HA antibody. ChIP-seq libraries were sequenced and data analysis showed almost no binding in Veh treatment, indicating low backgroud and good quality of the data. PAX transcription factor motif were enriched in PAX2 peaks, indicating the reliability of the data. When crossing the ChIP-seq data with genes regulated by PAX2 in MCF-7, we could observe high level binding of PAX2 to prmoters of PAX2 up-regulated genes and the center of intergenic transcripts induced by PAX2, suggesting the role of PAX2 in regulating transcription activation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE140060 The proapoptotic gene interferon regulatory factor-1 mediates the antiproliferative outcome of paired box 2 gene and tamoxifen. Oncogene 6.634 https://doi.org/10.1038/s41388-020-01435-4 {Oncogene (6.634): 10.1038/s41388-020-01435-4} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA588153 https://www.ebi.ac.uk/ena/browser/view/PRJNA588153 https://www.ncbi.nlm.nih.gov/sra?term=SRP229065 [Overal design]PAX2 genome interaction mapping in MCF-7 cells treated with doxycycline (50ng/ml) alone, or in combination with tamoxifen (1uM). Whole experiment include 2 replicates of each treatments, a Veh control (no PAX2-HA overexpression), and input samples.; [Treatment]'Cells were treated with doxycycline (50ng/ml) to induce PAX2 oeverexpresson, followed by tamoxifen (1uM) treatment for 6 hours.'; [Growth]'MCF-7 cells were cultured in DMEM with 5% FBS'; [Extraction]'MCF-7 chromatin was sonicated and PAX2 bond genomic regions were isolated by using HA tag antibody.\nLibraries were prepared by Norwegian sequencing centre and CRUK genomics core facility'; [Cell type]'Breast adenocarcinoma''cell type: Breast adenocarcinoma; gender: Female; chip antibody: HA tag (abcam: ab9110); cell line: MCF-7; agent: doxycycline; ', 'cell type: Breast adenocarcinoma; gender: Female; chip antibody: HA tag (abcam: ab9110); cell line: MCF-7; agent: doxycycline+ tamoxifen; ', 'cell type: Breast adenocarcinoma; gender: Female; chip antibody: HA tag (abcam: ab9110); cell line: MCF-7; agent: Veh; ', 'cell type: Breast adenocarcinoma; gender: Female; chip antibody: none; cell line: MCF-7; agent: doxycycline; ', 'cell type: Breast adenocarcinoma; gender: Female; chip antibody: none; cell line: MCF-7; agent: doxycycline+ tamoxifen; ' GSE59590 Homo sapiens 175 Expression profiling by array GPL17518 Gene and microRNA expression profiling of breast tumors from Chinese and Italian women [gene] 2014-07-18 Gene and miRNA profiles from a unique Chinese/Caucasian trans-ethnic collection of breast cancer from Shanghai (China) and Milan (Italy) were compared using an unsupervised approach that identified similar clusters of correlated features in Chinese and Caucasian datasets. Partition of gene expression data using previously published gene signatures, such as the PAM50 intrinsic gene list and the extracellular matrix (ECM) genes, revealed Chinese and Caucasian subgroups with equivalent gene and miRNA expression profiles. A significant reduction of Luminal-A tumors was observed in the Chinese series. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59590 Molecular portrait of breast cancer in China reveals comprehensive transcriptomic likeness to Caucasian breast cancer and low prevalence of luminal A subtype. Cancer medicine 3.357 https://doi.org/10.1002/cam4.442 {Cancer medicine (3.357): 10.1002/cam4.442} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA255673 https://www.ebi.ac.uk/ena/browser/view/PRJNA255673 None [Overal design]Tissue samples from 78 Chinese (Han Chinese) and 97 Italian (South Europe Caucasian) consecutive primary breast tumors were subjected to gene and miRNA profiling. Tissue specimens, initially collected respectively in the Chinese and Italian hospitals, were all stored, randomly processed and analyzed in identical experimental conditions in the Italian center to minimize pre-analytical, instrumental and computational variability, enabling direct comparison of gene and miRNA profiles from the two groups.; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was extracted using the miRNeasy Mini Kit (Qiagen) and treated with RNase-free DNase to remove genomic DNA traces using the RNeasy Mini Kit (Qiagen) according to the manufacturer's instructions."; [Cell type]'Source: ''tissue: breast tumor; age (years): 53; gender: female; nationality: China; grade: III; size (cm): 2.5; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 43; gender: female; nationality: China; grade: III; size (cm): 2; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 38; gender: female; nationality: China; grade: III; size (cm): 2.6; lymph node status: 1; er status: 0; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 43; gender: female; nationality: China; grade: II; size (cm): 2; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: ERBB2; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 67; gender: female; nationality: China; grade: II; size (cm): 1.2; lymph node status: 0; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: ERBB2; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 71; gender: female; nationality: China; grade: III; size (cm): 3; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 75; gender: female; nationality: China; grade: II; size (cm): 4; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 60; gender: female; nationality: China; grade: II; size (cm): 2.2; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 55; gender: female; nationality: China; grade: II; size (cm): 2; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 52; gender: female; nationality: China; grade: II; size (cm): 3.5; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 44; gender: female; nationality: China; grade: NA; size (cm): 2.5; lymph node status: 1; er status: 0; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 62; gender: female; nationality: China; grade: II; size (cm): 2.5; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 50; gender: female; nationality: China; grade: III; size (cm): 2.5; lymph node status: 1; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 42; gender: female; nationality: China; grade: II; size (cm): 2.5; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 56; gender: female; nationality: China; grade: II; size (cm): 2; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 45; gender: female; nationality: China; grade: II; size (cm): 2.5; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 63; gender: female; nationality: China; grade: II; size (cm): 2.7; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 59; gender: female; nationality: China; grade: NA; size (cm): 1.6; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 48; gender: female; nationality: China; grade: II; size (cm): 2.5; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 64; gender: female; nationality: China; grade: III; size (cm): 3.7; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 75; gender: female; nationality: China; grade: II; size (cm): 2.3; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 48; gender: female; nationality: China; grade: II; size (cm): 2; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 46; gender: female; nationality: China; grade: II; size (cm): 2.5; lymph node status: 1; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 37; gender: female; nationality: China; grade: II; size (cm): 1.2; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 70; gender: female; nationality: China; grade: II; size (cm): 2; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 57; gender: female; nationality: China; grade: II; size (cm): 3.5; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 48; gender: female; nationality: China; grade: NA; size (cm): 2.8; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 46; gender: female; nationality: China; grade: II; size (cm): 4; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 52; gender: female; nationality: China; grade: III; size (cm): 2; lymph node status: NA; er status: 0; pgr status: 0; erbb2 status: 1; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 76; gender: female; nationality: China; grade: III; size (cm): 2.5; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 1; pam50 subtype: luminal-B; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 47; gender: female; nationality: China; grade: II; size (cm): 4; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 1; er status gene: 0; erbb2 status gene: 0; pam50 subtype: ERBB2; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 55; gender: female; nationality: China; grade: III; size (cm): 2.8; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 50; gender: female; nationality: China; grade: III; size (cm): 2.5; lymph node status: NA; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 47; gender: female; nationality: China; grade: III; size (cm): 7; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 54; gender: female; nationality: China; grade: NA; size (cm): 4; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 45; gender: female; nationality: China; grade: III; size (cm): 4; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 1; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 67; gender: female; nationality: China; grade: III; size (cm): 1.4; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 56; gender: female; nationality: China; grade: II; size (cm): 2; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 66; gender: female; nationality: China; grade: III; size (cm): 1.4; lymph node status: 1; er status: 1; pgr status: 0; erbb2 status: 1; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 50; gender: female; nationality: China; grade: II; size (cm): 2.8; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 56; gender: female; nationality: China; grade: II; size (cm): 2; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 1; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 43; gender: female; nationality: China; grade: NA; size (cm): 3; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 1; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 43; gender: female; nationality: China; grade: II; size (cm): 3; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 45; gender: female; nationality: China; grade: II; size (cm): 4; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 44; gender: female; nationality: China; grade: II; size (cm): 5; lymph node status: 1; er status: 0; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 71; gender: female; nationality: China; grade: NA; size (cm): 1.8; lymph node status: 1; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 49; gender: female; nationality: China; grade: II; size (cm): 3; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: ERBB2; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 40; gender: female; nationality: China; grade: NA; size (cm): 1.5; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 43; gender: female; nationality: China; grade: II; size (cm): 2.4; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 45; gender: female; nationality: China; grade: III; size (cm): 2.2; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: ERBB2; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 44; gender: female; nationality: China; grade: II; size (cm): 1.2; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 56; gender: female; nationality: China; grade: II; size (cm): 2; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 1; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 48; gender: female; nationality: China; grade: III; size (cm): 2; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 37; gender: female; nationality: China; grade: NA; size (cm): 3; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 76; gender: female; nationality: China; grade: III; size (cm): 1.8; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 32; gender: female; nationality: China; grade: NA; size (cm): 4; lymph node status: 0; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 58; gender: female; nationality: China; grade: II; size (cm): 3; lymph node status: 0; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 48; gender: female; nationality: China; grade: III; size (cm): 2.2; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 1; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 44; gender: female; nationality: China; grade: II; size (cm): 2; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 57; gender: female; nationality: China; grade: III; size (cm): 3; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 1; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 38; gender: female; nationality: China; grade: III; size (cm): 4.5; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 64; gender: female; nationality: China; grade: II; size (cm): 1.5; lymph node status: 0; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 63; gender: female; nationality: China; grade: NA; size (cm): 2.3; lymph node status: NA; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 57; gender: female; nationality: China; grade: NA; size (cm): 3; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 36; gender: female; nationality: China; grade: II; size (cm): 2; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 49; gender: female; nationality: China; grade: II; size (cm): 4; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 53; gender: female; nationality: China; grade: II; size (cm): 2.2; lymph node status: NA; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: ERBB2; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 75; gender: female; nationality: China; grade: III; size (cm): 1.5; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 51; gender: female; nationality: China; grade: II; size (cm): 1.5; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 45; gender: female; nationality: China; grade: II; size (cm): 2.2; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 1; er status gene: 0; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 53; gender: female; nationality: China; grade: NA; size (cm): 1.5; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 58; gender: female; nationality: China; grade: III; size (cm): 1.5; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 78; gender: female; nationality: China; grade: II; size (cm): 3; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: ERBB2; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 45; gender: female; nationality: China; grade: III; size (cm): 1.8; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 45; gender: female; nationality: China; grade: III; size (cm): 2; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 37; gender: female; nationality: China; grade: III; size (cm): 2; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 1; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 43; gender: female; nationality: China; grade: III; size (cm): 3.5; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 60; gender: female; nationality: Italy; grade: II; size (cm): 1.5; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 83; gender: female; nationality: Italy; grade: III; size (cm): 1.4; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 69; gender: female; nationality: Italy; grade: III; size (cm): 2.2; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 85; gender: female; nationality: Italy; grade: II; size (cm): 0.9; lymph node status: 1; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 78; gender: female; nationality: Italy; grade: II; size (cm): 2.5; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 1; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 77; gender: female; nationality: Italy; grade: III; size (cm): 3.5; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 52; gender: female; nationality: Italy; grade: III; size (cm): 0.4; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 42; gender: female; nationality: Italy; grade: II; size (cm): 1.4; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 57; gender: female; nationality: Italy; grade: III; size (cm): 1.7; lymph node status: 1; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 47; gender: female; nationality: Italy; grade: III; size (cm): 3; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 76; gender: female; nationality: Italy; grade: III; size (cm): 3.5; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 57; gender: female; nationality: Italy; grade: III; size (cm): 1.1; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 54; gender: female; nationality: Italy; grade: II; size (cm): 2; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 44; gender: female; nationality: Italy; grade: III; size (cm): 3.6; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 85; gender: female; nationality: Italy; grade: II; size (cm): 1.7; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 45; gender: female; nationality: Italy; grade: II; size (cm): 2.2; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 51; gender: female; nationality: Italy; grade: II; size (cm): 1; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 79; gender: female; nationality: Italy; grade: II; size (cm): 0.7; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 36; gender: female; nationality: Italy; grade: II; size (cm): 1.8; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 1; er status gene: 1; erbb2 status gene: 1; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 67; gender: female; nationality: Italy; grade: III; size (cm): 1.5; lymph node status: 1; er status: 0; pgr status: 1; erbb2 status: 1; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 69; gender: female; nationality: Italy; grade: III; size (cm): 2; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 47; gender: female; nationality: Italy; grade: III; size (cm): 2.2; lymph node status: 0; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 70; gender: female; nationality: Italy; grade: III; size (cm): 2.2; lymph node status: NA; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 48; gender: female; nationality: Italy; grade: II; size (cm): 1.4; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 71; gender: female; nationality: Italy; grade: III; size (cm): 1.5; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 76; gender: female; nationality: Italy; grade: NA; size (cm): 4; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 64; gender: female; nationality: Italy; grade: II; size (cm): 1.5; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 65; gender: female; nationality: Italy; grade: III; size (cm): 1; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 63; gender: female; nationality: Italy; grade: III; size (cm): 3; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 74; gender: female; nationality: Italy; grade: II; size (cm): 1.9; lymph node status: 0; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 44; gender: female; nationality: Italy; grade: II; size (cm): 1.5; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 35; gender: female; nationality: Italy; grade: II; size (cm): 2.5; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 38; gender: female; nationality: Italy; grade: II; size (cm): 2.6; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 74; gender: female; nationality: Italy; grade: III; size (cm): 11; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 67; gender: female; nationality: Italy; grade: NA; size (cm): 1.7; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 37; gender: female; nationality: Italy; grade: III; size (cm): 2; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 77; gender: female; nationality: Italy; grade: II; size (cm): 2.2; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 46; gender: female; nationality: Italy; grade: III; size (cm): 1.3; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 1; er status gene: 1; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 59; gender: female; nationality: Italy; grade: III; size (cm): 1.7; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 47; gender: female; nationality: Italy; grade: II; size (cm): 0.9; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 1; er status gene: 0; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 39; gender: female; nationality: Italy; grade: II; size (cm): 1.4; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 60; gender: female; nationality: Italy; grade: II; size (cm): 4; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 77; gender: female; nationality: Italy; grade: III; size (cm): 3.6; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 39; gender: female; nationality: Italy; grade: III; size (cm): 3.6; lymph node status: NA; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 65; gender: female; nationality: Italy; grade: II; size (cm): 1.7; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 1; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 47; gender: female; nationality: Italy; grade: III; size (cm): 5; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 50; gender: female; nationality: Italy; grade: III; size (cm): 2.1; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 1; er status gene: 1; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 48; gender: female; nationality: Italy; grade: II; size (cm): 2.4; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 61; gender: female; nationality: Italy; grade: II; size (cm): 2.1; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 82; gender: female; nationality: Italy; grade: II; size (cm): 1.5; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 84; gender: female; nationality: Italy; grade: II; size (cm): 3; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: undetermined; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 51; gender: female; nationality: Italy; grade: II; size (cm): 1.3; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 66; gender: female; nationality: Italy; grade: II; size (cm): 2.2; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 57; gender: female; nationality: Italy; grade: III; size (cm): 2; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 1; er status gene: 0; erbb2 status gene: 0; pam50 subtype: ERBB2; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 53; gender: female; nationality: Italy; grade: III; size (cm): 1.5; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 1; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 76; gender: female; nationality: Italy; grade: III; size (cm): 4; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 62; gender: female; nationality: Italy; grade: III; size (cm): 2.5; lymph node status: 0; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 64; gender: female; nationality: Italy; grade: III; size (cm): 1.7; lymph node status: 0; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 56; gender: female; nationality: Italy; grade: II; size (cm): 2.3; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 73; gender: female; nationality: Italy; grade: II; size (cm): 2; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 38; gender: female; nationality: Italy; grade: II; size (cm): 9; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 62; gender: female; nationality: Italy; grade: II; size (cm): 0.9; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 50; gender: female; nationality: Italy; grade: NA; size (cm): 6; lymph node status: 0; er status: 1; pgr status: 0; erbb2 status: 1; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 38; gender: female; nationality: Italy; grade: III; size (cm): NA; lymph node status: NA; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 63; gender: female; nationality: Italy; grade: III; size (cm): 2; lymph node status: 1; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 76; gender: female; nationality: Italy; grade: III; size (cm): 2.6; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 1; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 76; gender: female; nationality: Italy; grade: III; size (cm): 2; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 1; er status gene: 1; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 56; gender: female; nationality: Italy; grade: II; size (cm): 1.8; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 75; gender: female; nationality: Italy; grade: II; size (cm): 2.6; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 79; gender: female; nationality: Italy; grade: II; size (cm): 1.8; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 49; gender: female; nationality: Italy; grade: II; size (cm): 1.3; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 50; gender: female; nationality: Italy; grade: II; size (cm): 2.5; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 68; gender: female; nationality: Italy; grade: II; size (cm): 1.7; lymph node status: NA; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 72; gender: female; nationality: Italy; grade: II; size (cm): 2; lymph node status: 0; er status: 0; pgr status: 1; erbb2 status: 1; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 75; gender: female; nationality: Italy; grade: III; size (cm): 3; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 79; gender: female; nationality: Italy; grade: II; size (cm): 1.8; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 44; gender: female; nationality: Italy; grade: II; size (cm): 0.9; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 52; gender: female; nationality: Italy; grade: III; size (cm): 2.5; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 58; gender: female; nationality: Italy; grade: III; size (cm): 2.2; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 1; er status gene: 0; erbb2 status gene: 1; pam50 subtype: ERBB2; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 43; gender: female; nationality: Italy; grade: III; size (cm): 1; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 49; gender: female; nationality: Italy; grade: III; size (cm): 6; lymph node status: 1; er status: 0; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 71; gender: female; nationality: Italy; grade: III; size (cm): 1.5; lymph node status: 1; er status: 0; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: ERBB2; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 61; gender: female; nationality: Italy; grade: III; size (cm): 2; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 60; gender: female; nationality: Italy; grade: II; size (cm): 2.1; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 81; gender: female; nationality: Italy; grade: III; size (cm): 2.3; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 55; gender: female; nationality: Italy; grade: II; size (cm): 4.5; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 43; gender: female; nationality: Italy; grade: II; size (cm): 1.4; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 64; gender: female; nationality: Italy; grade: II; size (cm): 2.5; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 56; gender: female; nationality: Italy; grade: III; size (cm): 2.8; lymph node status: NA; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 50; gender: female; nationality: Italy; grade: III; size (cm): 2.2; lymph node status: 0; er status: 0; pgr status: 1; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 37; gender: female; nationality: Italy; grade: III; size (cm): 3; lymph node status: 1; er status: 1; pgr status: 0; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: ECM3; ', 'tissue: breast tumor; age (years): 75; gender: female; nationality: Italy; grade: II; size (cm): 5; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 45; gender: female; nationality: Italy; grade: III; size (cm): 5; lymph node status: 1; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 64; gender: female; nationality: Italy; grade: III; size (cm): 2.5; lymph node status: 0; er status: 0; pgr status: 0; erbb2 status: 0; er status gene: 0; erbb2 status gene: 0; pam50 subtype: basal; ecm1/3 subtype: ECM1; ', 'tissue: breast tumor; age (years): 39; gender: female; nationality: Italy; grade: III; size (cm): 1.3; lymph node status: 0; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 77; gender: female; nationality: Italy; grade: III; size (cm): 2.8; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-B; ecm1/3 subtype: undetermined; ', 'tissue: breast tumor; age (years): 84; gender: female; nationality: Italy; grade: II; size (cm): NA; lymph node status: 1; er status: 1; pgr status: 1; erbb2 status: 0; er status gene: 1; erbb2 status gene: 0; pam50 subtype: luminal-A; ecm1/3 subtype: undetermined; ' GSE98210 Homo sapiens 19 Expression profiling by high throughput sequencing GPL18573 Alternative splicing regulated by QKI and RBFOX1 promotes the mesenchymal cell state in breast cancer 2017-04-25 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98210 An alternative splicing switch in FLNB promotes the mesenchymal cell state in human breast cancer. eLife 7.551 https://doi.org/10.7554/eLife.37184 {eLife (7.551): 10.7554/eLife.37184} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA384253 https://www.ebi.ac.uk/ena/browser/view/PRJNA384253 None [Overal design]Refer to individual Series; [Treatment]'None', 'UV crosslinking (254nm) at 400mJ/cm^2'; [Growth]'None'; [Extraction]"Total RNA was extracted from cells usingthe RNeasy Mini Kit (Qiagen)\nLibraries were constructed using the Nextera unstranded mRNA protocol according to the manufacturer's instructions (Illumina)", 'Immunoprecipitation of RNA-protein complexes and purification of RNA were done as described in the ENCODE eCLIP protocol (Van Nostrand et al. 2016, PMID: 27018577 and ENCODE).\nLibraries were constructed as described in the ENCODE eCLIP protocol (Van Nostrand et al 2016, PMID: 27018577), with slight modifications as described in Li et al (submitted).'; [Cell type]'Immortalized mammary epithelial cells (HME)''cell type: Immortalized mammary epithelial cells (HME); genotype/variation: overexpressing negative control protein EGFP; ', 'cell type: Immortalized mammary epithelial cells (HME); genotype/variation: overexpressing negative control protein HcRed; ', 'cell type: Immortalized mammary epithelial cells (HME); genotype/variation: overexpressing candidate ORF QKI; ', 'cell type: Immortalized mammary epithelial cells (HME); genotype/variation: overexpressing candidate ORF RBFOX1; ', 'cell type: Immortalized mammary epithelial cells (HME); genotype/variation: overexpressing candidate ORF SNAI1; ', 'cell type: Immortalized mammary epithelial cells (HME); genotype/variation: stably overexpressing V5-tagged QKI; treated with: UV crosslinking at 254nm with 400mJ/cm^2; ', 'cell type: Immortalized mammary epithelial cells (HME); genotype/variation: stably overexpressing V5-tagged RBFOX1; treated with: UV crosslinking at 254nm with 400mJ/cm^2; ' GSE68050 Homo sapiens 6 Expression profiling by array GPL10558 Linker histone H1.2 establishes chromatin comapction and gene silencing through recognition of H3K27me3 2015-04-20 Linker histone H1 is a protein component of chromatin and has been linked to chromatin compaction and global gene silencing.It has been sugegsted that H1 plays a significant role, regulating a relatively small number of genes. Here we show that H1.2- a variant of H1 subtype is recruited to chromatin region and is dependent on EZH2-mediated H3K27me3. Therefore a Gene expression array analysis was carried out with H1.2 as well as EZH2 knockout MCF7 cells to confirm the interlationship of H1.2 and EZH2 activity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE68050 Linker histone H1.2 establishes chromatin compaction and gene silencing through recognition of H3K27me3. Scientific reports 4.011 https://doi.org/10.1038/srep16714 {Scientific reports (4.011): 10.1038/srep16714} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA281624 https://www.ebi.ac.uk/ena/browser/view/PRJNA281624 None [Overal design]Total RNA was isolated from MCF7 cells in which EZH2 and H1.2 genes have been depleted along with the wild type cells to study the differential regulation of various genes in each case.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyzer.'; [Cell type]'Source: ''cell line: Breast cancer cell line MCF7; genotype/variation: Control; ', 'cell line: Breast cancer cell line MCF7; genotype/variation: EZH2 KO; ', 'cell line: Breast cancer cell line MCF7; genotype/variation: H1.2 KO; ' GSE30037 Homo sapiens 9 Expression profiling by array GPL6244 TFPI alpha and beta regulate mRNAs involved in cancer biology and in the immune system 2011-06-16 Emerging evidences indicate a new role of TFPI in cancer biology. We recently reported that both isoforms of TFPI induced apoptosis and inhibited proliferation of cancer cells. The signaling pathway(s) mediating the effects of TFPI is, however, presently still unclear. Our goal was to further investigate the cellular processes affected by TFPI and to get insight into the molecular mechanisms involved in the effects of TFPI, using a global gene expression study approach. TFPIa or TFPIb cDNA were transfected into SK-BR-3 breast cancer cells for stable overexpression. Global mRNA and microRNA (miRNA) expressions were measured and functional annotation of the differentially expressed genes and miRNAs according to gene ontology terms was conducted. Selected results were validated using qRT-PCR and Western blot. Overexpression of TFPIa or TFPIb resulted in a 6.4- and 17-fold increase in TFPI protein levels, respectively. A total of 242 and 801 mRNA transcripts and 120 and 46 miRNAs were differentially expressed in cells overexpressing TFPIa or TFPIb, respectively. Overexpression of either isoform significantly affected the expression of genes involved in cell development (apoptosis, cell movement, migration, invasion, colony formation, growth, and adhesion) and immune response. Network analyses revealed biological interactions between these genes and implied that several of the genes may be involved in both processes. Functional cluster analyses indicated altered activity of the epidermal growth factor receptor (EGFR), small GTPases, and the NFkB and JAK/STAT cascades. Integrated mRNA-miRNA analyses showed that up to 46 and 252 genes differentially expressed in cells overexpressing TFPIa or TFPIb, respectively, may have been regulated by miRNAs. Overexpression of TFPI in breast cancer cells affected the expression of mRNAs and miRNAs involved in processes facilitating cancer cell growth and immunologic response, probably by signal transduction involving the EGFR pathway. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE30037 TFPI alpha and beta regulate mRNAs and microRNAs involved in cancer biology and in the immune system in breast cancer cells. PloS one 2.776 https://doi.org/10.1371/journal.pone.0047184 {PloS one (2.776): 10.1371/journal.pone.0047184} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA144065 https://www.ebi.ac.uk/ena/browser/view/PRJNA144065 None [Overal design]Total RNA was isolated from SK-BR-3 breast cancer cells stably transfected with TFPIalpha or TFPIbeta cDNA, or with an empty vector for control. RNA was obtained from three independent isolations, yielding three biological replicates of each of the three samples. Mean expression data from cells overexpressing TFPIalpha or TFPIbeta were compared to mean data from cells transfected with an empty vector.; [Treatment]'Cells had been stably tranfected with pcDNA3.1/V5/His-pTOPO vectors containing TFPIalpha or TFPIbeta cDNA, or empty vectors, and selected using puromycin (2mg/ul)'; [Growth]'SK-BR-3 cells were grown in RPMI1640 containing phenol red and 2 mM L-glutamine, supplemented with 10% heat inactivated FBS. Cells were cultured at 37 °C in an incubator with a humidified atmosphere and 5% CO2.'; [Extraction]'Total RNA was isolated using the miRVANA miRNA isolation kit, following the manufacturers descriptions for extraction of total RNA'; [Cell type]'Source: ''tissue: tumor; cell line: SK-BR-3; origin: luminal-like; transfector: TFPI alpha; ', 'tissue: tumor; cell line: SK-BR-3; origin: luminal-like; transfector: TFPI beta; ', 'tissue: tumor; cell line: SK-BR-3; origin: luminal-like; transfector: empty vector; ' GSE135710 Mus musculus; Homo sapiens 4 Expression profiling by high throughput sequencing GPL20795; GPL21273 Single-cell RNA-seq of B cell polustion in breast cancer patients 2019-08-12 Re-education of immune cells in tumor microenvironment is required for optimal treatment outcome. The prevailing notion is that B cells, a major immune cell type in tumors, are immunosuppressive and pro-tumoral. However, why B cells inhibit tumor progression in certain contexts remains unexplained. By single cell dissection of B cell heterogeneity in longitudinal samples of breast cancer patients before and after neoadjuvant chemotherapy, we revealed a distinct subset of B cells emerges after chemotherapy, which is predictive for therapeutic efficacy and prognosis in multiple patient cohorts. Using three immunocompetent mouse models, our in vivo experiments faithfully recapitulated the subset switch of human tumor-infiltrating B cells during chemotherapy. Employing B-specific deletion and adoptive transfer experiment, we showed that ICOSL in this B cell subset boosts anti-tumor immunity by enhancing the ratio of effector and regulatory T cells. The signature of ICOSL+ B cell subset is imprinted by complement-CR2 signaling, which is triggered by chemotherapy-induced immunogenic tumor cell death. Moreover, by screening the cell line encyclopedia, we identified CD55, a complement inhibitory protein, determines the dual roles of B cells in the response of various malignancies to chemotherapy. Collectively, our study demonstrates a critical role of B cell subset switch in chemotherapy response and have implications for designing novel therapeutic approaches. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE135710 Complement Signals Determine Opposite Effects of B Cells in Chemotherapy-Induced Immunity. Cell 36.216 https://doi.org/10.1016/j.cell.2020.02.015 {Cell (36.216): 10.1016/j.cell.2020.02.015} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA559817 https://www.ebi.ac.uk/ena/browser/view/PRJNA559817 https://www.ncbi.nlm.nih.gov/sra?term=SRP218090 [Overal design]Two experimental conditions: before and after neoadjuvant chemotherapy (NAC); [Treatment]'Sample 2 derived from patients who received four cycles of neoadjuvant chemotherapy.', 'Sample derived from inoculated tumor of C57/BL6 mice treated by PBS/Dox.'; [Growth]'None'; [Extraction]'Cells were isolated from breast tumor tissues of breast cancer patients by flow cytometry.\nScRNA-seq libraries were constructed using Chromium Single Cell 3’ Reagent Kits v3 (10× GENOMICS) according to the manufacturer’s protocol.', 'Cells were isolated from inoculated tumor tissues of C57/BL6 mice treated by PBS/Dox using flow cytometry.\nScRNA-seq libraries were constructed using Chromium Single Cell 3’ Reagent Kits v3 (10× GENOMICS) according to the manufacturer’s protocol.'; [Cell type]'B cells''cell type: B cells; tissue: breast tumor tissues; ', 'strain: C57/BL6; treatment: PBS; tissue: Inoculated tumor tissues; cell type: B cells; ', 'strain: C57/BL6; treatment: Dox; tissue: Inoculated tumor tissues; cell type: B cells; ' GSE68694 Homo sapiens 6 Expression profiling by array GPL570 A Preclinical Model for ERα-Positive Breast Cancer Points to the Epithelial Microenvironment as Determinant of Luminal Phenotype and Hormone Response [MCF7] 2015-05-08 A high percentage of potential oncology drugs fail in clinical trials, partly because preclinical models used to test them are inadequate. Breast cancer is the leading cause of cancer-related death among women worldwide but we lack appropriate in vivo models for the ER+ subtypes, which represent more than 75% of all cases. We address these issues by xenografting tumor cells to their site of origin, the milk ducts. All ER+ cell lines and patient-derived xenografts grow mimicking their clinical counterparts. Disease progresses with invasion and metastasis, which become amenable to study. The action of hormones, important in breast carcinogenesis, can now be studied in a relevant context. Importantly, these open opportunities for development and evaluation of therapies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE68694 A Preclinical Model for ERα-Positive Breast Cancer Points to the Epithelial Microenvironment as Determinant of Luminal Phenotype and Hormone Response. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2016.02.002 {Cancer cell (23.916): 10.1016/j.ccell.2016.02.002} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA283486 https://www.ebi.ac.uk/ena/browser/view/PRJNA283486 None [Overal design]Eight- to twelve-week-old female SCID Beige mice (Charles River) were injected with 2x10e5 MCF7-DsRed/luc2 cells (n=3) either into the mammary fat pad or 5x10e4 MCF7-DsRed/luc2 cells intraductally (n=3). Xenografted MCF7 were FACS sorting based on DsRed expression; total RNA was extracted using Trizol Reagent (Invitrogen), purified with the miRNeasy Mini Kit (Qiagen), quantity and quality were assessed by NanoDrop®ND-1000 spectrophotometer and RNA 6000 NanoChips with the Agilent 2100 Bioanalyzer (Agilent, Palo Alto, USA). Only samples with RIN score >7.0 were included. For each sample, 300 ng of total RNA were amplified using the message amp II enhanced kit (AM1791, Ambion). 12.5 μg of biotin-labelled cRNA were chemically fragmented. Affymetrix GeneChip Human Genome U133A 2.0 Arrays (Affymetrix, Santa Clara, CA, USA) were hybridized with 11μg of fragmented target, at 45°C for 17 hours, washed and stained according to Affymetrix GeneChip® Expression Analysis Manual (Fluidics protocol FS450_0007). Arrays were scanned using the GeneChip Scanner 3000 7G (Affymetrix) and raw data was extracted from the scanned images and analyzed with the Affymetrix Power Tools software package (Affymetrix). All statistical analyses were performed using R and Bioconductor packages (http://www.Bioconductor.org). Hybridization quality was assessed using the Expression Console software (Affymetrix). Normalized expression signals were calculated from Affymetrix CEL files using RMA. Differential hybridized features were identified using Bioconductor package “limma” that implements linear models for microarray data (Smyth, 2004). P values were adjusted for multiple testing with Benjamini and Hochberg’s method to control false discovery rate (FDR) (Benjamini et al., 2001). Probe sets showing ≥2-fold change and a FDR ≤0.05 were considered significant.; [Treatment]'None'; [Growth]'None'; [Extraction]'Xenografted MCF7 were FACS sorting based on DsRED expression; total RNA was extracted using Trizol Reagent (Invitrogen), purified with the miRNeasy Mini Kit (Qiagen), and quantity and quality were assessed by NanoDrop®ND-1000 spectrophotometer and RNA 6000 NanoChips with the Agilent 2100 Bioanalyzer (Agilent, Palo Alto, USA). Only samples with RIN score >7.0 were included.'; [Cell type]'xenografted, FACS-sorted MCF7''source cell type: MCF7-DsRED/luc2 cells; host strain info: 8-12 wk-old female SCID Beige mice; sample group: fat pad xenograft; cell type: xenografted, FACS-sorted MCF7; ', 'source cell type: MCF7-DsRED/luc2 cells; host strain info: 8-12 wk-old female SCID Beige mice; sample group: intraductal xenograft; cell type: xenografted, FACS-sorted MCF7; ' GSE116907 Homo sapiens 12 Expression profiling by high throughput sequencing GPL18573 Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination (RNAseq) 2018-07-10 Three triple negative breast cancer cell lines (MDAMB231, SUM159, and HCC1806) were treated with small molecule inhibitors (JQ1, BET bromodomain inhibitor; GSK2801, BAZ2A/B bromodomain inhibitor) alone and in combination for 72 hours https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE116907 GSK2801, a BAZ2/BRD9 Bromodomain Inhibitor, Synergizes with BET Inhibitors to Induce Apoptosis in Triple-Negative Breast Cancer. Molecular cancer research : MCR 4.484 https://doi.org/10.1158/1541-7786.MCR-18-1121 {Molecular cancer research : MCR (4.484): 10.1158/1541-7786.MCR-18-1121} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA480603 https://www.ebi.ac.uk/ena/browser/view/PRJNA480603 https://www.ncbi.nlm.nih.gov/sra?term=SRP153037 [Overal design]12 experimental samples; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was isolated using Qiagen RNeasy Plus kit.\n4 µg total RNA and 10 cycles of amplification were used for libraries constructed with KAPA Stranded mRNAseq kit.'; [Cell type]'Source: ''cell line: SUM159; treatment: DMSO 72hr; culture media: DMEM/F12 1:1 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: SUM159; treatment: 300nM JQ1 72hr; culture media: DMEM/F12 1:1 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: SUM159; treatment: 10uM GSK2801 72hr; culture media: DMEM/F12 1:1 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: SUM159; treatment: 300nM JQ1 and 10uM GSK2801 72hr; culture media: DMEM/F12 1:1 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: MDAMB231; treatment: DMSO 72hr; culture media: DMEM/F12 1:1 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: MDAMB231; treatment: 100nM JQ1 72hr; culture media: DMEM/F12 1:1 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: MDAMB231; treatment: 10uM GSK2801 72hr; culture media: DMEM/F12 1:1 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: MDAMB231; treatment: 100nM JQ1 and 10uM GSK2801 72hr; culture media: DMEM/F12 1:1 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: HCC1806; treatment: DMSO 72hr; culture media: RPMI 1640 supplemented with 10% FBS; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: HCC1806; treatment: 500nM JQ1 72hr; culture media: RPMI 1640 supplemented with 10% FBS; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: HCC1806; treatment: 10uM GSK2801 72hr; culture media: RPMI 1640 supplemented with 10% FBS; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: HCC1806; treatment: 500nM JQ1 and 10uM GSK2801 72hr; culture media: RPMI 1640 supplemented with 10% FBS; library preparation kit: Illumina TruSeq RNA library kit v2; ' GSE104984 Homo sapiens 5 Other GPL11154 KDM5B links cellular transcriptome heterogeneity to therapy resistance (Exome-Seq) 2017-10-15 The KDM5B histone H3 lysine 4 (H3K4) demethylase has been implicated in therapy resistance in multiple cancer types including breast cancer, but the underlying mechanism is poorly defined. Here we show that inhibition of KDM5B activity increases sensitivity to anti-estrogens by modulating estrogen-receptor (ER) signaling. Conversely, acquired resistance to KDM5 inhibitors leads to gain of ER chromatin binding and estrogen-independent growth. Sequencing of barcoded cell populations and mathematical modeling demonstrate selection for pre-existent genetically distinct endocrine-resistant cells, while resistance to KDM5 inhibitors is a switch to an acquired epigenetic state. Rare resistant cells can already be detected by single cell RNA-seq prior to treatment. Inhibition of KDM5B in luminal ER+ cells increases H3K4me3 broad domains at promoters and decreases cellular transcriptional heterogeneity. Higher transcriptome heterogeneity is associated with higher KDM5B levels and poor prognosis in ER+ luminal breast tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE104984 KDM5 Histone Demethylase Activity Links Cellular Transcriptomic Heterogeneity to Therapeutic Resistance. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2018.10.014 {Cancer cell (23.916): 10.1016/j.ccell.2018.10.014} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA414330 https://www.ebi.ac.uk/ena/browser/view/PRJNA414330 https://www.ncbi.nlm.nih.gov/sra?term=SRP119969 [Overal design]Exome-seq of parental and multiple resistant breast cancer cell lines; [Treatment]'None'; [Growth]'MCF7, C70R and C49R cells were cultured in DMEM supplemented with 10% FBS, 1% penicillin/streptomycin and 10 μg ml−1 insulin. FULVR and TAMR cells are cultured in RPMI without phenol red supplemented with 10% charcoal-stripped FBS, 1% penicillin/streptomycin and 10 μg ml−1 insulin.'; [Extraction]'Genomic DNA was extracted from the frozen cell populations with a QIAamp DNA Mini Kit (Qiagen).\nSequencing libraries were prepared as previously described (Brastianos et al., 2013). Briefly, gDNA from five cell lines and one human CEPH normal (http://hapmap.ncbi.nlm.nih.gov/citinghapmap.html.en) were fragmented to 250 bp using Adaptive Focused Acoustics (AFA) ultra-sonication (Covaris Inc., Woburn, MA) and further purified using Agencourt AMPure XP beads (Beckman Coulter, Inc., Indianapolis, IN). A total of 50 ng of size-selected DNA was ligated to DNA barcoded adaptors during library preparation (KAPA HTP DNA Library Preparation Kit, KK8234, Kapa Biosystems, Inc., Wilmington, MA). Each library was made with sample-specific barcodes and quantified using an Illumina MiSeq Nano flow cell (Illumina Inc., San Diego, CA). For exome enrichment, the 6 libraries were pooled in 3 x 2-plex to a total of 750 ng per pool, and exonic regions were captured with the SureSelect Target Enrichment system using the Human All Exon V5 hybrid capture kit (Agilent Technologies, Santa Clara, CA). All captures were further pooled and sequenced in two lanes of the HiSeq 2500 system in Rapid Run Mode (Illumina Inc., San Diego, CA).\nExome-seq'; [Cell type]'Source: ''cell line: MCF7; treatment_time: None; ', 'cell line: Fulvestrant resistant MCF7; treatment_time: None; ', 'cell line: Tamoxifen resistant MCF7; treatment_time: None; ', 'cell line: C49 resistant MCF7; treatment_time: None; ', 'cell line: C70 resistant MCF7; treatment_time: None; ' GSE108979 Homo sapiens 21 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Identification of the ER-beta cistrome in ER-beta expressing MDA-MB-231 cells [ChIP-seq] 2018-01-09 We have utilized ChIPseq to identify the ER-beta cistrome in ER-beta expressing MDA-MB-231 triple negative breast cancer cells. ER-beta has been identified as a tumor suppressor in breast cancer and recent reports have demonstrated that ER-beta protein is detectable at moderate to high levels in approximately 30% of triple negative breast tumors. Increased expression of ER-beta in triple negative breast cancer has also been reported to be associated with improved recurrence-free survival. Treatment of ER-beta expressing triple negative breast cancer cells with estrogen, or the ER-beta selective agonist, LY500307, results in decreased cell proliferation, invasion and migration. To begin to identify the molecular mechanisms by which ER-beta elicits tumor suppressive effects in triple negative breast cancer, we performed ChIPseq studies and identified the genome-wide binding sites for ER-beta following exposure to 1nM estrogen or 10nM LY500307 for 3 hours. Over 28,000 and 10,000 unique ER-beta binding sites were identifed in response to these two ligands respectively. The top transcription factor motifs identified under both treatment conditions were estrogen response elements and AP1 response elements. The majority of ER-beta binding sites were found at enhancer regions located within introns or intergenic chromatin regions followed by gene promoters. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE108979 ERβ-mediated induction of cystatins results in suppression of TGFβ signaling and inhibition of triple-negative breast cancer metastasis. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1807751115 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1807751115} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA429300 https://www.ebi.ac.uk/ena/browser/view/PRJNA429300 https://www.ncbi.nlm.nih.gov/sra?term=SRP128615 [Overal design]Examination of ER-beta binding sites in ER-beta expressing MDA-MB-231 cells. ER-beta immunoprecipitations were carried out using a Flag-specific antibody (M2). All treatment conditions were conducted in triplicate and data were normalized using input controls and compared to vehicle treated cells.; [Treatment]'MDA-MB-231-ER-beta cells were plated in 15 cm dishes and allowed to grow to approximately 80% confluence in DMEM/F12 medium containing 10% charcoal stripped FBS and Doxycycline (100 ng/ml, to induce ER-beta expression). Cells were subsequently treated in triplicate with ethanol vehicle, 1 nM estradiol or 10 nM LY500307 for 3 hours.'; [Growth]'Doxycycline-inducible ER-beta expressing MDA-MB-231cells were maintained in phenol red-free DMEM/F12 medium supplemented with 10% fetal bovine serum (FBS), 1% antibiotic-antimycotic (AA), 5 mg/L blasticidin S and 500 mg/L zeocin.'; [Extraction]"Nuclear lysates were prepared and ER-beta bound chromatin was purified using the Flag-specific antibody.\nDNA was prepared for Illumina sequencing on the HiSeq 2500 using the ThruPLEX DNA-seq kit according to the manufacturer's instructions."; [Cell type]'Triple Negative Breast Cancer Cell Line''cell line: MDA-MB-231-ER-beta; cell type: Triple Negative Breast Cancer Cell Line; passages: 20-25; treated with: ethanol vehicle for 3 h; chip antibody: Flag (Sigma, M2); ', 'cell line: MDA-MB-231-ER-beta; cell type: Triple Negative Breast Cancer Cell Line; passages: 20-25; treated with: 1 nM estradiol for 3 h; chip antibody: Flag (Sigma, M2); ', 'cell line: MDA-MB-231-ER-beta; cell type: Triple Negative Breast Cancer Cell Line; passages: 20-25; treated with: 10 nM LY500307 for 3 h; chip antibody: Flag (Sigma, M2); ', 'cell line: MDA-MB-231-ER-beta; cell type: Triple Negative Breast Cancer Cell Line; passages: 20-25; treated with: ethanol vehicle for 3 h; chip antibody: None; ', 'cell line: MDA-MB-231-ER-beta; cell type: Triple Negative Breast Cancer Cell Line; passages: 20-25; treated with: 1 nM estradiol for 3 h; chip antibody: None; ', 'cell line: MDA-MB-231-ER-beta; cell type: Triple Negative Breast Cancer Cell Line; passages: 20-25; treated with: 10 nM LY500307 for 3 h; chip antibody: None; ' GSE10099 Homo sapiens 626 Genome variation profiling by SNP array GPL2004; GPL2005 Multi-dimensional genomic analysis in breast cancer patients 2008-01-08 Multi-dimensional genomic analysis identifies a class of breast cancer patients with high metastatic outcome and differential response to chemotherapeutic drugs The application of multi-dimensional genomic analyses might provide a more refined risk assessment of breast tumor aggressiveness and improve the selection of patients for personalized medicine. Our study demonstrates the feasibility of using CNAs to predict patient outcome. In combination with gene expression profiles, the clinical implication for such prognostic assays is the identification of breast cancer patients at different risks and sensitivities to chemotherapeutic drugs. Keywords: survival time https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE10099 Copy number alterations that predict metastatic capability of human breast cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-08-4596 {Cancer research (8.378): 10.1158/0008-5472.CAN-08-4596} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA108245 https://www.ebi.ac.uk/ena/browser/view/PRJNA108245 None [Overal design]try to find the association between genomic DNA copy number changes with breast cancer patients survival time.; [Treatment]'None'; [Growth]'None'; [Extraction]'QIAamp DNA mini kit according to the manufacturer'; [Cell type]'Source: ''sample_id: 34; age: 47; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 100; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 843; age: 60; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Neg; survival time (months): 110; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 856; age: 45; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 88; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 900; age: 64; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 108; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 91; age: 55; stage.t: T1; differentiation: moderate; er: Pos; menopause: post; pr: Neg; survival time (months): 20; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 273; age: 39; stage.t: T2; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 81; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 540; age: 66; stage.t: T2; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 49; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 550; age: 71; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 58; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 141; age: 74; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 25; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 237; age: 41; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Neg; survival time (months): 19; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 239; age: 71; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Neg; survival time (months): 35; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 240; age: 40; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 36; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 241; age: 56; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Neg; survival time (months): 17; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 244; age: 58; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 39; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 606; age: 43; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 66; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 611; age: 43; stage.t: T1; differentiation: moderate; er: Pos; menopause: pre; pr: Neg; survival time (months): 75; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 612; age: 47; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 92; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 613; age: 71; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 93; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 614; age: 47; stage.t: T1; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 88; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 615; age: 64; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 92; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 616; age: 46; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 88; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 5; age: 47; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 118; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 19; age: 66; stage.t: T2; differentiation: NA; er: Pos; menopause: post; pr: Neg; survival time (months): 32; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 40; age: 74; stage.t: T2; differentiation: moderate; er: Pos; menopause: post; pr: Pos; survival time (months): 102; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 205; age: 47; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 23; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 44; age: 71; stage.t: T2; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 169; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 62; age: 47; stage.t: T1; differentiation: moderate; er: Pos; menopause: pre; pr: Pos; survival time (months): 108; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 63; age: 49; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 14; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 81; age: 29; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Neg; survival time (months): 11; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 86; age: 55; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Neg; survival time (months): 104; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 9; age: 62; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Neg; survival time (months): 125; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 11; age: 69; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Neg; survival time (months): 109; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 15; age: 44; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 99; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 33; age: 69; stage.t: T2; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 7; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 39; age: 38; stage.t: T2; differentiation: poor; er: Pos; menopause: pre; pr: Neg; survival time (months): 43; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 72; age: 40; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 134; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 75; age: 63; stage.t: T1; differentiation: moderate; er: Pos; menopause: post; pr: Neg; survival time (months): 15; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 137; age: 69; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 32; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 49; age: 32; stage.t: T2; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 28; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 913; age: 73; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Neg; survival time (months): 80; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 200; age: 68; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 108; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 126; age: 49; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 37; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 125; age: 54; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Neg; survival time (months): 93; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 258; age: 47; stage.t: T2; differentiation: moderate; er: Pos; menopause: pre; pr: Pos; survival time (months): 9; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 899; age: 71; stage.t: T2; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 86; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 416; age: 66; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 60; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 130; age: 55; stage.t: T1; 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status (0=no relapse, 1=relapse): 0; ', 'sample_id: 276; age: 47; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 54; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 277; age: 80; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 79; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 278; age: 38; stage.t: T2; differentiation: moderate; er: Pos; menopause: pre; pr: Neg; survival time (months): 50; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 696; age: 48; stage.t: T1; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 51; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 284; age: 62; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 72; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 285; age: 46; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 51; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 286; age: 68; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: NA; survival time (months): 107; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 288; age: 62; stage.t: T1; differentiation: moderate; er: Pos; menopause: post; pr: NA; survival time (months): 71; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 290; age: 54; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: NA; survival time (months): 100; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 600; age: 57; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: NA; survival time (months): 66; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 601; age: 50; stage.t: T1; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 52; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 602; age: 40; stage.t: T2; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 57; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 605; age: 78; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Neg; survival time (months): 57; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 620; age: 72; stage.t: T2; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 62; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 703; age: 43; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 61; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 625; age: 61; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Neg; survival time (months): 72; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 627; age: 38; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 113; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 629; age: 44; stage.t: T1; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 131; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 630; age: 45; stage.t: T2; 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pr: Neg; survival time (months): 109; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 760; age: 79; stage.t: T2; differentiation: moderate; er: Pos; menopause: post; pr: Pos; survival time (months): 98; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 762; age: 46; stage.t: T2; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 116; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 765; age: 62; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Neg; survival time (months): 147; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 767; age: 60; stage.t: T1; differentiation: moderate; er: Pos; menopause: post; pr: Pos; survival time (months): 134; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 768; age: 50; stage.t: T1; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 129; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 769; age: 68; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Neg; survival time (months): 84; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 891; age: 74; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 112; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 772; age: 44; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Neg; survival time (months): 108; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 778; age: 66; stage.t: T2; differentiation: moderate; er: Pos; menopause: post; pr: Pos; survival time (months): 104; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 779; age: 50; stage.t: T1; differentiation: moderate; er: Pos; menopause: pre; pr: Pos; survival time (months): 137; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 785; age: 73; stage.t: T2; differentiation: moderate; er: Pos; menopause: post; pr: Pos; survival time (months): 138; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 787; age: 73; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Neg; 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status (0=no relapse, 1=relapse): 0; ', 'sample_id: 797; age: 46; stage.t: T1; differentiation: moderate; er: Pos; menopause: pre; pr: Pos; survival time (months): 122; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 798; age: 48; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 132; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 804; age: 37; stage.t: T1; differentiation: moderate; er: Pos; menopause: pre; pr: NA; survival time (months): 121; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 903; age: 63; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 110; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 808; age: 66; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 110; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 809; age: 43; stage.t: T2; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 107; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 810; age: 57; stage.t: T1; differentiation: moderate; er: Pos; menopause: post; pr: Pos; survival time (months): 84; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 815; age: 56; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 107; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 817; age: 61; stage.t: T3; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 108; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 820; age: 64; stage.t: T2; differentiation: NA; er: Pos; menopause: post; pr: Neg; survival time (months): 116; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 836; age: 73; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 84; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 841; age: 61; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 96; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 845; age: 42; stage.t: T1; differentiation: NA; er: Pos; menopause: pre; pr: Neg; survival time (months): 109; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 847; age: 45; stage.t: T1; differentiation: moderate; er: Pos; menopause: pre; pr: Neg; survival time (months): 105; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 848; age: 72; stage.t: T1; differentiation: moderate; er: Pos; menopause: post; pr: Pos; survival time (months): 86; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 849; age: 73; stage.t: T2; differentiation: NA; er: Pos; menopause: post; pr: Neg; survival time (months): 88; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 851; age: 46; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 92; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 852; age: 44; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 113; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 909; age: 44; stage.t: T2; differentiation: moderate; er: Pos; menopause: pre; pr: Neg; survival time (months): 109; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 861; age: 61; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 95; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 863; age: 63; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 107; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 865; age: 44; stage.t: T1; differentiation: moderate; er: Pos; menopause: pre; pr: Pos; survival time (months): 92; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 866; age: 38; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 75; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 867; age: 75; stage.t: T2; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 55; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 868; age: 52; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 77; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 712; age: 70; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Neg; survival time (months): 86; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 714; age: 54; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 157; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 870; age: 60; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 56; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 871; age: 40; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 71; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 873; age: 62; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 59; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 874; age: 52; stage.t: T2; differentiation: moderate; er: Pos; 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status (0=no relapse, 1=relapse): 0; ', 'sample_id: 82; age: 47; stage.t: T1; differentiation: moderate; er: Pos; menopause: pre; pr: Pos; survival time (months): 143; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 57; age: 53; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 20; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 28; age: 42; stage.t: T2; differentiation: good; er: Pos; menopause: pre; pr: Neg; survival time (months): 155; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 18; age: 32; stage.t: T2; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 34; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 21; age: 46; stage.t: T1; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 14; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 99; age: 80; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 107; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 105; age: 50; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 99; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 67; age: 32; stage.t: T2; differentiation: poor; er: Pos; menopause: pre; pr: Neg; survival time (months): 19; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 114; age: 62; stage.t: T2; differentiation: moderate; er: Pos; menopause: post; pr: Pos; survival time (months): 86; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 122; age: 54; stage.t: T1; differentiation: moderate; er: Pos; menopause: pre; pr: Neg; survival time (months): 104; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 89; age: 51; stage.t: T2; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 2; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 104; age: 53; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 11; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 139; age: 47; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 111; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 106; age: 46; stage.t: T1; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 40; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 108; age: 66; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Neg; survival time (months): 28; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 110; age: 73; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 8; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 32; age: 44; stage.t: T2; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 84; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 50; age: 53; stage.t: T1; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 125; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 54; age: 47; stage.t: T1; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 144; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 56; age: 52; stage.t: T1; differentiation: NA; er: Pos; menopause: post; pr: Pos; survival time (months): 153; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 68; age: 49; stage.t: T2; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 112; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 41; age: 46; stage.t: T3; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 25; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 88; age: 55; stage.t: T1; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 98; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 103; age: 41; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Pos; survival time (months): 97; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 115; age: 61; stage.t: T2; differentiation: poor; er: Pos; menopause: post; pr: Pos; survival time (months): 15; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 728; age: 83; stage.t: T2; differentiation: moderate; er: Pos; menopause: post; pr: Pos; survival time (months): 105; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 737; age: 61; stage.t: T1; differentiation: moderate; er: Pos; menopause: post; pr: Pos; survival time (months): 123; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 233; age: 37; stage.t: T3; differentiation: NA; er: Pos; menopause: pre; pr: Pos; survival time (months): 5; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 213; age: 32; stage.t: T1; differentiation: poor; er: Pos; menopause: pre; pr: Neg; survival time (months): 16; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 48; age: 29; stage.t: T2; differentiation: poor; er: Pos; menopause: pre; pr: Neg; survival time (months): 101; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 292; age: 67; stage.t: T2; differentiation: moderate; er: Neg; 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survival time (months): 106; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 8; age: 70; stage.t: Tx; differentiation: NA; er: Neg; menopause: post; pr: Pos; survival time (months): 37; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 38; age: 42; stage.t: T2; differentiation: moderate; er: Neg; menopause: pre; pr: Neg; survival time (months): 133; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 204; age: 66; stage.t: T1; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 24; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 71; age: 52; stage.t: T1; differentiation: NA; er: Neg; menopause: pre; pr: Neg; survival time (months): 12; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 79; age: 41; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 32; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 96; age: 58; stage.t: T1; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 30; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 113; age: 47; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 101; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 64; age: 47; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Pos; survival time (months): 134; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 74; age: 70; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 90; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 78; age: 28; stage.t: T2; differentiation: moderate; er: Neg; menopause: pre; pr: Pos; survival time (months): 152; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 84; age: 66; stage.t: T1; differentiation: poor; er: Neg; menopause: post; pr: Pos; survival time (months): 114; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 55; age: 54; stage.t: T1; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 11; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 136; age: 69; stage.t: T1; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 25; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 65; age: 58; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 9; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 215; age: 53; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 6; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 255; age: 48; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 6; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 259; age: 69; stage.t: T1; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 14; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 260; age: 52; stage.t: T2; differentiation: NA; er: Neg; menopause: post; pr: Pos; survival time (months): 29; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 261; age: 69; stage.t: T1; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 18; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 263; age: 42; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 32; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 264; age: 57; stage.t: T1; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 33; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 265; age: 50; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Pos; survival time (months): 66; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 267; age: 83; stage.t: T4; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 59; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 268; age: 48; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Pos; survival time (months): 82; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 275; age: 40; stage.t: T1; 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er: Neg; menopause: post; pr: Neg; survival time (months): 120; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 777; age: 68; stage.t: T1; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 153; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 780; age: 72; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 124; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 782; age: 43; stage.t: T2; differentiation: NA; er: Neg; menopause: pre; pr: Pos; survival time (months): 148; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 894; age: 43; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 123; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 805; age: 36; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 103; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 806; age: 44; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; 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status (0=no relapse, 1=relapse): 0; ', 'sample_id: 855; age: 71; stage.t: T2; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 88; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 857; age: 38; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Pos; survival time (months): 98; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 862; age: 43; stage.t: T1; differentiation: moderate; er: Neg; menopause: pre; pr: Neg; survival time (months): 87; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 864; age: 60; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 87; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 713; age: 52; stage.t: T1; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 156; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 879; age: 39; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: NA; survival time (months): 108; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 3; age: 36; stage.t: T2; differentiation: NA; er: Neg; menopause: pre; pr: Neg; survival time (months): 101; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 90; age: 41; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 108; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 94; age: 58; stage.t: T2; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 109; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 121; age: 46; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 23; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 118; age: 78; stage.t: T2; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 95; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 14; age: 68; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 14; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 29; age: 42; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 25; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 37; age: 62; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 7; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 61; age: 27; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 11; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 20; age: 34; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Pos; survival time (months): 128; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 111; age: 60; stage.t: T2; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 98; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 93; age: 37; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 48; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 112; age: 47; stage.t: T1; differentiation: NA; er: Neg; menopause: pre; pr: Neg; survival time (months): 17; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 216; age: 46; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 13; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 621; age: 47; stage.t: T1; differentiation: good; er: Neg; menopause: pre; pr: Neg; survival time (months): 80; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 100; age: 48; stage.t: T1; differentiation: moderate; er: Neg; menopause: pre; pr: Neg; survival time (months): 39; status (0=no relapse, 1=relapse): 1; ', 'sample_id: 107; age: 53; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 94; status (0=no relapse, 1=relapse): 0; ', 'sample_id: 98; age: 53; stage.t: T1; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 14; status (0=no relapse, 1=relapse): 1; ', 'sample_id: JA.1821; age: 58; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 88; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1828; age: 61; stage.t: T2; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 103; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.812; age: 38; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 117; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1853; age: 45; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 63; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1858; age: 39; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 89; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.401; age: 70; stage.t: T3; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 12; status (0=no relapse, 1=relapse): 1; ', 'sample_id: JA.1412; age: 47; stage.t: T2; differentiation: NA; er: Neg; menopause: pre; pr: Neg; survival time (months): 128; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1593; age: 63; stage.t: T1; differentiation: moderate; er: Neg; menopause: post; pr: Neg; survival time (months): 127; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1571; age: 58; stage.t: T1; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 76; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1939; age: 33; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 152; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.872; age: 67; stage.t: T1; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 69; status (0=no relapse, 1=relapse): 1; ', 'sample_id: JA.1568; age: 60; stage.t: T1; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 115; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1482; age: 63; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 86; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1535; age: 74; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 42; status (0=no relapse, 1=relapse): 1; ', 'sample_id: JA.076; age: 53; stage.t: T1; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 136; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1524; age: 82; stage.t: T3; differentiation: moderate; er: Neg; menopause: post; pr: Neg; survival time (months): 68; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1501; age: 40; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 74; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.746; age: 42; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 123; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1487; age: 74; stage.t: T1; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 71; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1650; age: 57; stage.t: T1; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 88; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.282; age: 55; stage.t: T1; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 83; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1069; age: 32; stage.t: T2; differentiation: NA; er: Neg; menopause: pre; pr: Neg; survival time (months): 24; status (0=no relapse, 1=relapse): 1; ', 'sample_id: JA.1938; age: 38; stage.t: T2; differentiation: NA; er: Neg; menopause: pre; pr: Neg; survival time (months): 90; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1455; age: 63; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 64; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.941; age: 34; stage.t: T2; differentiation: NA; er: Neg; menopause: pre; pr: Neg; survival time (months): 87; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.243; age: 43; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 10; status (0=no relapse, 1=relapse): 1; ', 'sample_id: JA.1966; age: 57; stage.t: T2; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 61; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1967; age: 40; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 80; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1978; age: 50; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 6 9; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.245; age: 38; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 22; status (0=no relapse, 1=relapse): 1; ', 'sample_id: JA.248; age: 49; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 29; status (0=no relapse, 1=relapse): 1; ', 'sample_id: JA.632; age: 69; stage.t: T4; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 61; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1222; age: 35; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 7; status (0=no relapse, 1=relapse): 1; ', 'sample_id: JA.2001; age: 39; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 4; status (0=no relapse, 1=relapse): 1; ', 'sample_id: JA.2007; age: 59; stage.t: T2; differentiation: NA; er: Neg; menopause: post; pr: Neg; survival time (months): 91; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1060; age: 38; stage.t: T1; differentiation: NA; er: Neg; menopause: pre; pr: Neg; survival time (months): 71; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.120; age: 48; stage.t: T3; differentiation: moderate; er: Neg; menopause: pre; pr: Neg; survival time (months): 96; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.2025; age: 73; stage.t: T2; differentiation: poor; er: Neg; menopause: post; pr: Neg; survival time (months): 83; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.2038; age: 46; stage.t: T1; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 102; status (0=no relapse, 1=relapse): 0; ', 'sample_id: JA.1563; age: 40; stage.t: T2; differentiation: poor; er: Neg; menopause: pre; pr: Neg; survival time (months): 103; status (0=no relapse, 1=relapse): 0; ' GSE69397 Mus musculus; Homo sapiens 23 Expression profiling by array GPL20258; GPL20265 A mutation in the viral sensor 2’-5’-oligoadenylate synthetase 2 causes failure of lactation. 2015-05-29 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE69397 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA285358 https://www.ebi.ac.uk/ena/browser/view/PRJNA285358 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'wt/wt or mt/mt mice were time mated, and mammary glands were collected at day 18 of pregnancy or 2 days after parturition (2 dpp) and snap frozen in liquid N2.'; [Extraction]'Total RNA was isolated using Trizol reagent (Gibco/Invitrogen, Vic) and measured on the 2100 Bioanalyzer (Agilent).'; [Cell type]'Source: ''strain/background: C57BL/6 and CBA/CaJ; genotype/variation: WT; gender: female; tissue: mammary gland; time point: 18dpc; ', 'strain/background: C57BL/6 and CBA/CaJ; genotype/variation: WT; gender: female; tissue: mammary gland; time point: 2dpp; ', 'strain/background: C57BL/6 and CBA/CaJ; genotype/variation: Oas2 mutant; gender: female; tissue: mammary gland; time point: 18dpc; ', 'strain/background: C57BL/6 and CBA/CaJ; genotype/variation: Oas2 mutant; gender: female; tissue: mammary gland; time point: 2dpp; ', 'cell line: T47D; cell line type: luminal-like breast cancer; mouse oas2 expression: WT; doxycycline: -DOX; ', 'cell line: T47D; cell line type: luminal-like breast cancer; mouse oas2 expression: WT; doxycycline: +DOX; ', 'cell line: T47D; cell line type: luminal-like breast cancer; mouse oas2 expression: mutant Oas2; doxycycline: -DOX; ', 'cell line: T47D; cell line type: luminal-like breast cancer; mouse oas2 expression: mutant Oas2; doxycycline: +DOX; ' GSE48927 Homo sapiens 125 Expression profiling by array GPL10558 Over-expression of FGFR2b from a tetracycline-inducible expression vector 2013-07-16 Genome-wide association studies for breast cancer have identified over 80 different risk regions in the genome, with the FGFR2 locus consistently identified as the most strongly associated locus. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Here we use a systems biology approach to elucidate the regulatory networks operating in breast cancer and examine the role of FGFR2 in mediating risk. Using model systems we identify FGFR2-regulated genes and, combining variant set enrichment and eQTL analysis, show that these are preferentially linked to breast cancer risk loci. Our results support the concept that cancer-risk associated genes cluster in pathways https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48927 Master regulators of FGFR2 signalling and breast cancer risk. Nature communications 11.878 https://doi.org/10.1038/ncomms3464 {Nature communications (11.878): 10.1038/ncomms3464} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA212327 https://www.ebi.ac.uk/ena/browser/view/PRJNA212327 None [Overal design]The data consists of 125 microarray samples from MCF-7 cells treated under different conditions, at 5 time points (0, 3, 6, 12 and 24 h) in order to perturb FGFR2 signalling by overexpressing the full length FGFR2b from a tetracycline-inducible expression vector. The data have been pre-processed in R using the beadarray package, and are presented in the form of log2 expression values. The experiment was carried out on 11 Humanv4 BeadChips using 12 samples per BeadChip. The original arrays contains 48324 features, with a mean of 22 beads per feature (Standard Deviation of 5); [Treatment]'Estrogen deprived cells were stimulated with 1nM estradiol (Sigma); 100ng/mL FGF10 (Invitrogen). FGFR2b over-expression was induced by tetracycline (final concentration of 1mg/mL)'; [Growth]'MCF7 human breast cancer cells were cultured in DMEM supplemented with 10% HI-FCS and antibiotics. Cell synchronisation via estrogen deprivation was carried out for at least 3 days in phenol red-free DMEM (Invitrogen) supplemented with 5% charcoal dextran-treated HI-FBS (Hyclone) and 1% penicillin-streptomycin. All cells were grown at 37oC in 5% CO2. The FGFR2b tetracycline-inducible over-expression MCF7 line was established by double-transfection of FspI-linearised F2b-pcDNA4/TO and pcDNA6/TR in a 1:5 ratio by DNA weight. Single cell clones were expanded under selection using 500μg/mL Zeocin and 3μg/mL blasticidin. Tetracycline induction of FGFR2b expression was confirmed by Western blot'; [Extraction]'RNA was extracted using the miRNeasy spin column kit (Qiagen) and quality checked using an RNA 6000 Nano chip on a 2100 Bioanalyser (Agilent). 250ng RNA (RIN>7) was used for cRNA amplification and labelling using the Illumina TotalPrep-96 kit (Ambion 4397949)'; [Cell type]'Source: ''cell line: MCF-7; group: MinusTet; treatment duration (hs): 0; ', 'cell line: MCF-7; group: MinusTet; treatment duration (hs): 3; ', 'cell line: MCF-7; group: MinusTet; treatment duration (hs): 6; ', 'cell line: MCF-7; group: MinusTet; treatment duration (hs): 12; ', 'cell line: MCF-7; group: MinusTet; treatment duration (hs): 24; ', 'cell line: MCF-7; group: PlusTet; treatment duration (hs): 0; ', 'cell line: MCF-7; group: PlusTet; treatment duration (hs): 3; ', 'cell line: MCF-7; group: PlusTet; treatment duration (hs): 6; ', 'cell line: MCF-7; group: PlusTet; treatment duration (hs): 12; ', 'cell line: MCF-7; group: PlusTet; treatment duration (hs): 24; ' GSE71071 Mus musculus 5 Genome variation profiling by genome tiling array GPL4092 Genomic profiling of murine mammary tumors identifies potential personalized drug targets for p53-deficient mammary cancers 2015-07-18 Breast cancer is the second leading cause of cancer related death in American women. Patient care is complicated by inherent tumor heterogeneity that can be classified into at least six intrinsic subtypes. While targeted treatments are standard of care for most subtypes, there remains a clinical need for targeted therapies against basal-like tumors that are typically ‘triple negative breast cancers’. As such, the molecular mechanisms underlying basal-like tumors are under intense investigation to identify genetic drivers and possible drug targets of this subtype. Somatic p53 mutations are one of the most common genetic events in basal-like breast tumors. This genetic foundation primes cells to accumulate secondary genetic aberrations, a subset of which is predicted to promote tumorigenesis. To identify additional drivers of basal-like tumors, a comparative study between human and murine tumors was performed utilizing a p53null mammary transplant murine model. The p53null mammary transplant murine model produced a genomically diverse set of tumors, a subset of which we show resemble the human basal-like subtype. Microarray and sequencing technologies were used to interrogate the secondary genetic aberrations of these murine tumors which were then compared to human basal-like tumors to highlight conserved features. Of the ‘omic’ datasets analyzed, DNA copy number variation produced the largest number of conserved candidate driver genes. These candidate gene lists were further filtered using a DNA-RNA Pearson correlation cutoff of 0.5 and a requirement that the gene was deemed essential in at least one human basal-like cell line from a genome-wide RNA-mediated interference screen database. These steps highlighted seven potential driver genes that are at amplified loci in both murine and human basal-like tumors: Atp11a, Col4a2, Cul4a, Lamp1, Met, Pnpla6, and Tubgcp3. Inhibition of Met using Crizotinib caused Met amplified tumors to regress, confirming that this genetic event is a driver in a subset of p53null transplant mammary tumors. This study identifies MET as a driver of basal-like murine tumors, thus identifying a shared potential driver of human basal-like breast cancer. Our results also highlight the importance of comparative genomic studies for discovering drug targets and for providing models to study whether patient populations are likely to respond to selective targeted treatments. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE71071 Genomic profiling of murine mammary tumors identifies potential personalized drug targets for p53-deficient mammary cancers. Disease models & mechanisms 4.028 https://doi.org/10.1242/dmm.025239 {Disease models & mechanisms (4.028): 10.1242/dmm.025239} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA290272 https://www.ebi.ac.uk/ena/browser/view/PRJNA290272 None [Overal design]Agilent CGH microarrays were performed comparing DNA from BALB/c p53null mammary transplant tumors to DNA from FVB wild-type mice; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA isolated using a Qiagen Blood and Tissue Kit'; [Cell type]'Source: ''sample_source: FVB DNA Reference; ', 'sample_source: BALB/c p53null mammary transplant line: 2350R; sample type: Mammary tumor DNA; tissue: mammary tumor; ', 'sample_source: BALB/c p53null mammary transplant line: 2397L; sample type: Mammary tumor DNA; tissue: mammary tumor; ', 'sample_source: BALB/c p53null mammary transplant line: 2374L; sample type: Mammary tumor DNA; tissue: mammary tumor; ', 'sample_source: BALB/c p53null mammary transplant line: 2245R; sample type: Mammary tumor DNA; tissue: mammary tumor; ', 'sample_source: BALB/c p53null mammary transplant line: 2374R; sample type: Mammary tumor DNA; tissue: mammary tumor; ' GSE135353 Mus musculus 27 Expression profiling by high throughput sequencing GPL13112 Myocardial Infarction accelerates breast cancer via innate immune reprogramming (RNA-seq) 2019-08-04 Disruptions of systemic homeostasis have emerged as critical regulators of cancer. Recent studies indicate that chronic or acute host stressors (e.g., obesity1, surgery2) alter cancer pathogenesis. Many cancer patients, particularly those with breast cancer, are at increased risk for cardiovascular disease due to treatment toxicity and resulting changes in lifestyle behaviors3-5. While elevated risk and incidence of cardiovascular events in breast cancer is well-established, whether such events impact cancer pathogenesis is not known. Herein, we show that an incident myocardial infarction (MI or heart attack) accelerates breast cancer outgrowth and cancer-specific mortality in mice and humans. In mouse models of breast cancer, MI epigenetically reprogrammed Ly6Chigh monocytes in the bone marrow reservoir to an immunosuppressive phenotype that was maintained at the transcriptional level in monocytes in the circulation and tumor. In parallel, MI increased circulating Ly6Chigh monocyte levels and recruitment to tumors, and depletion of these cells abrogated MI-induced tumor growth. Furthermore, evaluation of the relationship between a new onset post-diagnosis cardiovascular event and cancer outcomes in early-stage breast cancer patients revealed increased risk of recurrence and cancer-specific death, highlighting the clinical relevance of our findings. Collectively, our results demonstrate that MI induces alterations to systemic homeostasis, triggering cross-disease communication that accelerates breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE135353 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA558550 https://www.ebi.ac.uk/ena/browser/view/PRJNA558550 None [Overal design]Bulk RNA sequencing; [Treatment]'None'; [Growth]'None'; [Extraction]'Cells were flow sorted and RNA was harvested with trizol LS. NEBNext Ultra RNA library prep with rRNA depletion was used with 50-100 ng of total RNA for the construction of sequencing libraries.\nNEBNext Ultra RNA library prep with rRNA depletion (New England Biolabs)'; [Cell type]'Source: ''strain: C57BL/6J; age: 11-15 weeks; treatment: E0771 tumor implantation + LAD ligation (surgical myocardial infarction); ', 'strain: C57BL/6J; age: 11-15 weeks; treatment: E0771 tumor implantation + SHAM surgery; ' GSE110626 Homo sapiens 21 Expression profiling by high throughput sequencing GPL16791 RNA sequencing data from triple-negative breast cancer patient-derived xenografts (PDX) 2018-02-14 RNAseq was performed on WHIM2 and WHIM30 PDX mammary tumors, brain metastases, and single cell suspensions over time. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE110626 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA434130 https://www.ebi.ac.uk/ena/browser/view/PRJNA434130 https://www.ncbi.nlm.nih.gov/sra?term=SRP132889 [Overal design]Comparison of gene expression profiles between two PDX models of triple-negative breast cancer, and between primary tumors, cell suspensions, and brain metastases within the PDX lines.; [Treatment]'None'; [Growth]'WHIM2 and WHIM30 mammary tumors were grown in NSG mice. WHIM2 and WHIM30 brain metastases were generated in NSG mice by intracardiac injection. WHIM2 and WHIM30 cell suspensions were generated from mammary tumor tissue removed from mice. Cells were collected immediately after processing (day 0) and also grown in suspension culture and collected after one week (day 7) for RNA isolation.'; [Extraction]'RNA was harvested from tissue/cell samples using the Qiagen Rneasy Mini Kit.\nKAPA Stranded mRNA-Seq Kit was used for library preparation.'; [Cell type]'Source: ''histologic subtype: Triple-negative; intrinsic subtype: Basal-like; model type: Patient-derived xenograft; tissue: WHIM2 mammary gland tumor; ', 'histologic subtype: Triple-negative; intrinsic subtype: Basal-like; model type: Patient-derived xenograft; tissue: WHIM2 day 0 single cell suspension; ', 'histologic subtype: Triple-negative; intrinsic subtype: Basal-like; model type: Patient-derived xenograft; tissue: WHIM2 day 7 single cell suspension; ', 'histologic subtype: Triple-negative; intrinsic subtype: Basal-like; model type: Patient-derived xenograft; tissue: WHIM2 brain metastasis; ', 'histologic subtype: Triple-negative; intrinsic subtype: Basal-like; model type: Patient-derived xenograft; tissue: WHIM30 mammary gland tumor; ', 'histologic subtype: Triple-negative; intrinsic subtype: Basal-like; model type: Patient-derived xenograft; tissue: WHIM30 day 0 single cell suspension; ', 'histologic subtype: Triple-negative; intrinsic subtype: Basal-like; model type: Patient-derived xenograft; tissue: WHIM30 day 7 single cell suspension; ', 'histologic subtype: Triple-negative; intrinsic subtype: Basal-like; model type: Patient-derived xenograft; tissue: WHIM30 brain metastasis; ' GSE51687 Homo sapiens 20 Other GPL10999 Estrogen induces global reorganization of chromatin structure in human breast cancer cells 2013-10-24 In the cell nucleus, each chromosome is confined to a chromosome territory. This spatial organization of chromosomes plays a crucial role in gene regulation and genome stability. Recently an additional level of organization has been discovered at the chromosome scale: the spatial segregation into open and closed chromatin to form two genome-wide compartments. Although considerable progress has been made in our knowledge of chromatin organization, a fundamental issue remains the understanding of its dynamic, especially in cancer. To address this issue, we performed genome-wide mapping of intra- and interchromosomal interactions (Hi-C) over the time after estrogen (E2) stimulation of breast cancer cells. To biologically interpret these interactions, we integrated with estrogen receptor alpha (ER alpha) binding events, gene expression and multiple epigenetic marks. We show that E2 induces a global reorganization of genome. More specifically, gene-rich chromosomes as well as areas of open and highly transcribed chromatins are moved spatially closer, thus enabling genes to share transcriptional machinery and regulatory elements. At a lower scale, differentially interacting loci are enriched for cancer proliferation and E2 related genes. We also observe that these differentially interacting loci are correlated with higher ER alpha binding events and gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE51687 Estrogen induces global reorganization of chromatin structure in human breast cancer cells. PloS one 2.776 https://doi.org/10.1371/journal.pone.0113354 {PloS one (2.776): 10.1371/journal.pone.0113354} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA224561 https://www.ebi.ac.uk/ena/browser/view/PRJNA224561 https://www.ncbi.nlm.nih.gov/sra?term=SRP031901 [Overal design]5 time points: before E2 (0h) and after E2 (0.5h, 1h, 4h and 24h). For each time point, there are two lanes per sample and two biological replicate samples. Please note that a processed data file corresponds to the merging of 2 replicates, and that there are 2 lanes per replicates (4 files in total per processed data file). Information about data merging is provided in the title of the sample. For instance : 0h_replicate_1_lane 1 0h_replicate_1_lane 2 0h_replicate_2_lane_1 0h_replicate_2_lane_2 are merged to generate the processed data hic_0h-all-1M.IC.csv.gz. Several bin sizes are provided for the same processed data: hic_0h-all-1M.IC.csv.gz hic_0h-all-2M.IC.csv.gz hic_0h-all-4M.IC.csv.gz hic_0h-all-500k.IC.csv.gz are the same processed data, but with different bin sizes.; [Treatment]'After 48 hours of hormone deprivation in 5% charcoal-dextran stripped serum media (no phenol red), cells were stimulated with 70 nM estrogen (E2) for various times: before (0) or after 0.5, 1, 4 and 24 hours of stimulation.'; [Growth]'MCF-7 breast cancer cell line, obtained from the American Type Culture Collection, was maintained in phenol red-free medium.'; [Extraction]"Briefly, cells were fixed with 1% formaldehyde. Chromatin was digested with HindIII (NEB, Ipswich, MA). DNA ends of digested chromatin were marked by biotin-14-dCTP (Invitrogen, Carlsbad, CA) following blunt-end ligation with T4 DNA ligase in diluted condition. Ligated DNA was then de-crosslinked and purified by phenol extraction procedures. Biotin-14-dCTP at non-ligated DNA ends was removed with exonuclease activity of T4 DNA polymerase. Ligated DNA was then applied to paired-end sequencing by using the Illumina sequencing technology platform (Genome Analyzer IIx, Illumina).\nSample preparation for paired-end sequencing was performed following the manufacturer's instructions. Briefly, ligated DNA (5 microg) was sheared to a size of 300-500 basepairs by a nebulizer supplied with the Illumina paired-end sample preparation kit. Fragmented DNA was end-paired using T4 DNA polymerase and Klenow polymerase with T4 polynucleotide kinase to phosphorylate the 5' ends. A 3' overhang was created using a 3'-5' exonuclease-deficient Klenow fragment, and then subjected to immunoprecipitation by Dynabeads MyOne Streptavin C1 Beads (Invitrogen) in DNA LoBind tubes (Eppendorf, Westbury, NY) with ligation of Illumina paired-end adaptor oligonucleotides. The ligation mixtures were electrophoresed on E-gel SizeSelect 2% pre-cast agarose gels (Invitrogen) to collect 250-bp fragments. Size-selected DNA fragments were enriched with Illumina paired-end primers by a 15-cycle PCR reaction. DNA samples (20 nM per sample), quantified by an Agilent Bioanalyzer, were loaded onto the paired-end flowcell of Genome Analyzer IIx (GAIIx) in the supplied cluster station according to the manufacturer's protocol. Clusters of PCR colonies were then sequenced on GAIIx with 51-bp per read."; [Cell type]'breast cancer cells''cell line: MCF-7; cell type: breast cancer cells; time point: before (0h) estrogen (E2) stimulation; ', 'cell line: MCF-7; cell type: breast cancer cells; time point: after 0.5h of estrogen (E2) stimulation; ', 'cell line: MCF-7; cell type: breast cancer cells; time point: after 1h of estrogen (E2) stimulation; ', 'cell line: MCF-7; cell type: breast cancer cells; time point: after 4h of estrogen (E2) stimulation; ', 'cell line: MCF-7; cell type: breast cancer cells; time point: after 24h of estrogen (E2) stimulation; ' GSE17155 Homo sapiens 38 Non-coding RNA profiling by array GPL8871 MicroRNA expression profiling of male breast cancer 2009-07-16 To test the hypothesis that there is a specific miRNA expression signature which characterizes male breast cancers, we performed miRNA microarray analysis in a series of male breast cancers and compared them to cases of male gynecomastia and female breast cancers https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17155 MicroRNA expression profiling of male breast cancer. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr2348 {Breast cancer research : BCR (5.676): 10.1186/bcr2348} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA119757 https://www.ebi.ac.uk/ena/browser/view/PRJNA119757 None [Overal design]miRNA microarray analysis was performed in a series of 23 male breast cancers, 5 cases of gynecomastia and 10 female ductal breast carcinomas; [Treatment]'None'; [Growth]'None'; [Extraction]'Four 15 μm sections were obtained from each case. Tissue sections were deparaffinized with xylene at 50°C for 3 minutes. Total RNA extraction was undertaken using the RecoverAll kit (Ambion Inc, Austin, Tex) according to manufacturer’s instructions.'; [Cell type]'Source: ''tissue: primary breast cancer; histology: ductal carcinoma; sex: Male; ', 'tissue: gynecomastia; histology: gynecomastia; sex: Male; ', 'tissue: primary breast cancer; histology: ductal carcinoma; sex: Female; ' GSE48213 Homo sapiens 56 Expression profiling by high throughput sequencing GPL10999 Transcriptional profiling of a breast cancer cell line panel using RNAseq technology 2013-06-21 56 breast cancer cell lines were profiled to identify patterns of gene expression associated with subtype and response to therapeutic compounds. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48213 Modeling precision treatment of breast cancer. Genome biology 14.028 https://doi.org/10.1186/gb-2013-14-10-r110 {Genome biology (14.028): 10.1186/gb-2013-14-10-r110} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA210428 https://www.ebi.ac.uk/ena/browser/view/PRJNA210428 https://www.ncbi.nlm.nih.gov/sra?term=SRP026537 [Overal design]Cell lines were profiled in their baseline, unperturbed state.; [Treatment]'None'; [Growth]'Cells in exponential growth phase'; [Extraction]"Qiagen RNAeasy\nRNAseq libraries for transcriptome analysis were prepared using the TruSeq RNA Sample Preparation Kit (Illumina) and Agilent Automation NGS system per manufacturers' instructions. Sample prep began with 1 _g of total RNA from each sample. Poly-A RNA was purified from the sample with oligo dT magnetic beads, and the poly(A) RNA was fragmented with divalent cations. Fragmented poly-A RNA was converted into cDNA through reverse transcription and were repaired using T4 DNA polymerase, Klenow polymerase, and T4 polynucleotide kinase. 3' A-tailing with exo-minus Klenow polymerase was followed by ligation of Illumina paired-end oligo adapters to the cDNA fragment. Ligated DNA was PCR amplified for 15 cycles and purified using AMPure XP beads. After purification of the PCR products with AMPure XP beads, the quality and quantity of the resulting libraries were analyzed using an Agilent Bioanalyzer High Sensitivity chip."; [Cell type]'breast cancer', 'breast cancer cell line''cell line: 184A1; cell type: breast cancer; subtype: Non-malignant; ', 'cell line: 184B5; cell type: breast cancer; subtype: Non-malignant; ', 'cell line: 21MT1; cell type: breast cancer; subtype: Basal; ', 'cell line: 21MT2; cell type: breast cancer; subtype: Basal; ', 'cell line: 21NT; cell type: breast cancer; subtype: Basal; ', 'cell line: 21PT; cell type: breast cancer; subtype: Basal; ', 'cell line: 600MPE; cell type: breast cancer; subtype: Luminal; ', 'cell line: AU565; cell type: breast cancer; subtype: Luminal; ', 'cell line: BT474; cell type: breast cancer; subtype: Luminal; ', 'cell line: BT483; cell type: breast cancer; subtype: Luminal; ', 'cell line: BT549; cell type: breast cancer; subtype: Claudin-low; ', 'cell line: CAMA1; cell type: breast cancer; subtype: Luminal; ', 'cell line: EFM192A; cell type: breast cancer; subtype: Luminal; ', 'cell line: EFM192B; cell type: breast cancer; subtype: Luminal; ', 'cell line: EFM192C; cell type: breast cancer; subtype: Luminal; ', 'cell line: HCC1143; cell type: breast cancer; subtype: Basal; ', 'cell line: HCC1395; cell type: breast cancer; subtype: Claudin-low; ', 'cell line: HCC1419; cell type: breast cancer; subtype: Luminal; ', 'cell line: HCC1428; cell type: breast cancer; subtype: Luminal; ', 'cell line: HCC1569; cell type: breast cancer; subtype: Basal; ', 'cell line: HCC1599; cell type: breast cancer; subtype: Basal; ', 'cell line: HCC1806; cell type: breast cancer; subtype: Basal; ', 'cell line: HCC1937; cell type: breast cancer; subtype: Basal; ', 'cell line: HCC1954; cell type: breast cancer; subtype: Basal; ', 'cell line: HCC202; cell type: breast cancer; subtype: Luminal; ', 'cell line: HCC2218; cell type: breast cancer; subtype: Luminal; ', 'cell line: HCC3153; cell type: breast cancer; subtype: Basal; ', 'cell line: HCC38; cell type: breast cancer; subtype: Claudin-low; ', 'cell line: HCC70; cell type: breast cancer; subtype: Basal; ', 'cell line: HS578T; cell type: breast cancer; subtype: Claudin-low; ', 'cell line: JIMT1; cell type: breast cancer; subtype: Basal; ', 'cell line: LY2; cell type: breast cancer; subtype: Luminal; ', 'cell line: MB157; cell type: breast cancer; subtype: unknown; ', 'cell line: MCF10A; cell type: breast cancer; subtype: Non-malignant; ', 'cell line: MCF10F; cell type: breast cancer; subtype: Non-malignant; ', 'cell line: MCF12A; cell type: breast cancer; subtype: Non-malignant; ', 'cell line: MCF7; cell type: breast cancer; subtype: Luminal; ', 'cell line: MDAMB134VI; cell type: breast cancer; subtype: Luminal; ', 'cell line: MDAMB175; cell type: breast cancer; subtype: Luminal; ', 'cell line: MDAMB231; cell type: breast cancer; subtype: Claudin-low; ', 'cell line: MDAMB361; cell type: breast cancer; subtype: Luminal; ', 'cell line: MX1; cell type: breast cancer; subtype: unknown; ', 'cell line: SKBR3; cell type: breast cancer; subtype: Luminal; ', 'cell line: SUM1315; cell type: breast cancer; subtype: Claudin-low; ', 'cell line: SUM149PT; cell type: breast cancer; subtype: Basal; ', 'cell line: SUM225CWN; cell type: breast cancer; subtype: Luminal; ', 'cell line: SUM229PE; cell type: breast cancer; subtype: unknown; ', 'cell line: SUM52PE; cell type: breast cancer; subtype: Luminal; ', 'cell line: T47D; cell type: breast cancer; subtype: Luminal; ', 'cell line: T47D Kbluc; cell type: breast cancer; subtype: unknown; ', 'cell line: UACC812; cell type: breast cancer; subtype: Luminal; ', 'cell line: UACC893; cell type: breast cancer; subtype: Luminal; ', 'cell line: ZR751; cell type: breast cancer; subtype: Luminal; ', 'cell line: ZR7530; cell type: breast cancer; subtype: Luminal; ', 'cell line: ZR75B; cell type: breast cancer; subtype: Luminal; ', 'cell line: MDAMB453; cell type: breast cancer cell line; subtype: Luminal; ' GSE56579 Homo sapiens 12 Expression profiling by array GPL6480 Gene expression profiling upon PI3K inhibition using different inhibitors 2014-04-07 Activation of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway is one the most frequent genetic events in human cancer. Therefore, the development of PI3K inhibitors has attracted much attention. We previously described the pyrazolopyrimidine derivative ETP-45658 as a potent inhibitor of PI3K p110α in vitro and in vivo. Here we report the gene expression signatures of MCF7 cells treated with ETP-45658 or the reference PI3K inhibitor PI-103. Both compounds potently inhibited proliferation of a wide range of human cancer cells. ETP-45658 most potently suppressed the growth of PIK3CA (E545K)-mutated MCF7 breast cancer cells. Treatment with ETP-45658 or PI-103 resulted in a time and concentration-dependent decrease in phosphorylation of AKT Ser473 in MCF7 cells. We conducted microarray analysis examining the gene expression profile in MCF7 cells at six hours post ETP-45658 or PI-103 incubation. Both compounds induced the expression of negative cell cycle regulators including Cyclin G2, p27kip1 and ING4 and decreased positive regulators such as Cyclin D1 without significantly affecting the expression of pro-apoptotic genes. We found FOXO transcription factor binding sites over-represented in both up- and down-regulated genes but not in those without significant changes. The expression of the breast cancer tumor suppressor Nischarin was found to be induced by ETP-45658 but not after PI-103 treatment while several genes differentially expressed specifically after ETP-45658 treatment are functionally associated with the focal adhesion pathway. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE56579 A novel phosphatidylinositol 3-kinase (PI3K) inhibitor directs a potent FOXO-dependent, p53-independent cell cycle arrest phenotype characterized by the differential induction of a subset of FOXO-regulated genes. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-014-0482-y {Breast cancer research : BCR (5.676): 10.1186/s13058-014-0482-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA243974 https://www.ebi.ac.uk/ena/browser/view/PRJNA243974 None [Overal design]Twelve samples have been analyzed in six different conditions. Two replicates have been included for each condition.; [Treatment]'Add DMSO or PI3K inhibitors in DMSO'; [Growth]'RPMI/10%FBS/antibiotics-antimycotics'; [Extraction]'Total RNA was prepared from cell lysates using the RNeasy total RNA Mini kit (Qiagen, Courtaboeuf, France), according to the manufacturer’s protocol. The amount and purity of total RNA was determined using the NanoDrop and the integrity of the RNA was assessed using a 2100 Bioanalyzer (Agilent Technologies).'; [Cell type]'human breast adenocarcinoma cell''cell line: MCF7; cell type: human breast adenocarcinoma cell; cell line source: 69-year-old female; treated with: DMSO for 6hrs; ', 'cell line: MCF7; cell type: human breast adenocarcinoma cell; cell line source: 69-year-old female; treated with: ETP-45658 for 6hrs; ', 'cell line: MCF7; cell type: human breast adenocarcinoma cell; cell line source: 69-year-old female; treated with: reference PI3K inhibitor PI-103 for 6hrs; ' GSE103023 Homo sapiens 24 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Estrogen receptor ChIP-seq in response to mTOR inhibition 2017-08-24 We have used ChIP-seq to profile binding of the estrogen receptor (ER) to chromatin in response to two mTOR inhibitors, i.e. everolimus (RAD001) and vistusertib (AZD2014). Two hours of treatment with these inhibitors significantly affected mTOR signaling, but surprisingly did not affect binding of ER to chromatin. This suggests that these mTOR inhibitors work through largely ER-independent mechanisms. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE103023 Combined Inhibition of mTOR and CDK4/6 Is Required for Optimal Blockade of E2F Function and Long-term Growth Inhibition in Estrogen Receptor-positive Breast Cancer. Molecular cancer therapeutics 4.856 https://doi.org/10.1158/1535-7163.MCT-17-0537 {Molecular cancer therapeutics (4.856): 10.1158/1535-7163.MCT-17-0537} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA399833 https://www.ebi.ac.uk/ena/browser/view/PRJNA399833 https://www.ncbi.nlm.nih.gov/sra?term=SRP116074 [Overal design]Estrogen receptor ChIP-seq was performed on chromatin from asynchronous MCF7 cells in full estrogenic media treated for 2 hours with vehicle, everolimus, or vistusertib.; [Treatment]'Asynchronous cells were treated for 2 hours with vehicle (DMSO), 500nM RAD001, or 500nM AZD2014'; [Growth]'MCF7 cells were grown in DMEM supplemented with 10% FBS, 1%pen/strep, 2mM L-glutamine.'; [Extraction]"Cells were crosslinked for 10min using 1% formaldehyde. After sonication, chromatin immunoprecipitation was performed using a polyclonal ERa antibody over night. After decrosslinking at 65 C over night followed by RNase A and proteinase K treatment, immunoprecipitated DNA was purified by phenol-chloroform extraction.\nDNA was prepared for Illumina sequencing on the HiSeq 2500 using the ThruPLEX DNA-seq kit according to the manufacturer's instructions."; [Cell type]'Breast cancer''cell type: Breast cancer; passages: p19; cell line: MCF7; chip antibody: ERa sc-543; agent: No treatment; ', 'cell type: Breast cancer; passages: p19; cell line: MCF7; chip antibody: ERa sc-543; agent: Treatment with RAD001; ', 'cell type: Breast cancer; passages: p19; cell line: MCF7; chip antibody: ERa sc-543; agent: Treatment with AZD201; ', 'cell type: Breast cancer; passages: p19; cell line: MCF7; chip antibody: Input; agent: No treatment; ', 'cell type: Breast cancer; passages: p19; cell line: MCF7; chip antibody: Input; agent: Treatment with RAD001; ', 'cell type: Breast cancer; passages: p19; cell line: MCF7; chip antibody: Input; agent: Treatment with AZD201; ', 'cell type: Breast cancer; passages: p20; cell line: MCF7; chip antibody: ERa sc-543; agent: No treatment; ', 'cell type: Breast cancer; passages: p20; cell line: MCF7; chip antibody: ERa sc-543; agent: Treatment with RAD001; ', 'cell type: Breast cancer; passages: p20; cell line: MCF7; chip antibody: ERa sc-543; agent: Treatment with AZD201; ', 'cell type: Breast cancer; passages: p20; cell line: MCF7; chip antibody: Input; agent: No treatment; ', 'cell type: Breast cancer; passages: p20; cell line: MCF7; chip antibody: Input; agent: Treatment with RAD001; ', 'cell type: Breast cancer; passages: p20; cell line: MCF7; chip antibody: Input; agent: Treatment with AZD201; ', 'cell type: Breast cancer; passages: p21; cell line: MCF7; chip antibody: ERa sc-543; agent: No treatment; ', 'cell type: Breast cancer; passages: p21; cell line: MCF7; chip antibody: ERa sc-543; agent: Treatment with RAD001; ', 'cell type: Breast cancer; passages: p21; cell line: MCF7; chip antibody: ERa sc-543; agent: Treatment with AZD201; ', 'cell type: Breast cancer; passages: p21; cell line: MCF7; chip antibody: Input; agent: No treatment; ', 'cell type: Breast cancer; passages: p21; cell line: MCF7; chip antibody: Input; agent: Treatment with RAD001; ', 'cell type: Breast cancer; passages: p21; cell line: MCF7; chip antibody: Input; agent: Treatment with AZD201; ', 'cell type: Breast cancer; passages: p22; cell line: MCF7; chip antibody: ERa sc-543; agent: No treatment; ', 'cell type: Breast cancer; passages: p22; cell line: MCF7; chip antibody: ERa sc-543; agent: Treatment with RAD001; ', 'cell type: Breast cancer; passages: p22; cell line: MCF7; chip antibody: ERa sc-543; agent: Treatment with AZD201; ', 'cell type: Breast cancer; passages: p22; cell line: MCF7; chip antibody: Input; agent: No treatment; ', 'cell type: Breast cancer; passages: p22; cell line: MCF7; chip antibody: Input; agent: Treatment with RAD001; ', 'cell type: Breast cancer; passages: p22; cell line: MCF7; chip antibody: Input; agent: Treatment with AZD201; ' GSE124393 Homo sapiens 6 Expression profiling by high throughput sequencing GPL20301 LARP7 is a substrate of BRCA1 that regulats genome instability and tumorigenesis 2018-12-26 Impaired DNA repair leads to cancer, aging and many genetic diseases. However, understanding of the complexity of DNA is far from complete, resulting in the failure of therapies using genotoxic reagents. Here, we found that LARP7, an RNA-binding protein known to stabilize 7SK RNA, was degraded after DNA injury caused by ionizing radiation and chemotherapy. The LARP7 degradation was catalyzed by an E3 ligase complex of BRCA1 and BARD1 that was triggered by ATM-mediated phosphorylation. LARP7 depletion caused transcriptional repression of the cell cycle regulators CCNB1, CCNB2 and CDK1; this repression arrested cells before the G2/M DNA damage checkpoint and reduced BRCA2 phosphorylation, therefore enhancing Rad51 recruitment and ultimately ensuring the homologous repair of damaged DNA. Importantly, the increased DNA damage repair capacity induced by LARP7 depletion caused resistance to ionizing radiation and CDDP treatment in both wild-type and BRCA1-mutant breast cancer cells and in mouse xenografts. Such resistance also contributed to reduced relapse-free survival rates in breast cancer patients with low levels of LARP7 after chemotherapy. Taken together, the results of this study show that LARP7 coordinates cell cycle progression and faithful DNA repair. We suggest that this mechanism could be exploited to prevent tumorigenesis and improve the effectiveness of cancer therapies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124393 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA511893 https://www.ebi.ac.uk/ena/browser/view/PRJNA511893 https://www.ncbi.nlm.nih.gov/sra?term=SRP174498 [Overal design]RNA-seq on wild-type MEFs, LARP7-/- MEFs, and two breast cancer cell lines (MDA-MB-231 and HCC1937) with or without siLARP7 treatment.; [Treatment]'For siRNA experiment, 10ng/ml siRNA was used.'; [Growth]'MDA-MB-231 cells provided by Dr. Sean Li (Harvard University) were grown in L-15 medium (Gibco) and 10% fetal bovine serum. HCC1937 cells purchased from Cell Bank of Shanghai Institutes for Biological Sciences were grown in RPMI 1640 medium (Gibco) supplemented with NaHCO3 1.5 g/L, glucose 2.5 g/L, Sodium Pyruvate 0.11 g/L, and 10% fetal bovine serum. MEF cells were purified from LARP7+/+ or LARP7-/- embryos at the age of E13.5 and used for experiments with passages between 1-6, and were cultured in DMEM with 10% fetal bovine serum.'; [Extraction]'Total RNA was purified by using RNeasy miniprep kit (Qiagen) with an on-column DNAseI digestion protocol to eliminate the residual DNA.\nRNA-seq protocol followed NEBNext® UltraTM RNA library Prep Kit for Illumina (NEB).'; [Cell type]'Source: ''cell line: MEF; genotype/variation: LARP7-/-; ', 'cell line: MEF; genotype/variation: wild-type; ', 'cell line: MDA-MB-231; sirna: siLARP7; ', 'cell line: MDA-MB-231; sirna: siNC; ', 'cell line: HCC1937; sirna: siLARP7; ', 'cell line: HCC1937; sirna: siNC; ' GSE104974 Homo sapiens 60 Expression profiling by array; Expression profiling by high throughput sequencing GPL11154; GPL24082 Comparison of RNA-seq and Microarray Platforms for Splice Event Detection using a Cross-Platform Algorithm 2017-10-14 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE104974 Comparison of RNA-seq and microarray platforms for splice event detection using a cross-platform algorithm. BMC genomics 3.501 https://doi.org/10.1186/s12864-018-5082-2 {BMC genomics (3.501): 10.1186/s12864-018-5082-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA414289 https://www.ebi.ac.uk/ena/browser/view/PRJNA414289 None [Overal design]Refer to individual Series; [Treatment]'To induce splicing events, cells were grown to ~70% confluence and treated with 1µM CX-4945 or DMSO during 12 hours in a total of 5 replicates per condition'; [Growth]'All cell lines were grown according to the suppliers’ recommendation'; [Extraction]"Total RNAs were isolated using the RNeasy Mini Kit (Qiagen, Germantown, MD) according to the manufacturer's protocol", "Total RNAs were isolated using the RNeasy Mini Kit (Qiagen, Germantown, MD) according to the manufacturer's protocol\nRNAseq was performed in the Center for Cooperative Research in Biosciences (CICBiogune) using the Illumina HiSeq2000 sequencing technology, HiSeq Flow Cell v3 and TruSeq SBS Kit v3. 2ug of RNA of each sample was sent for this purpose. The run type was strand specific, multiplexed with paired-end reads of 100 nucleotides each. The amount of RNA for hybridization and validation purposes was 5 ug."; [Cell type]'Source: ', 'Triple Negative Breast Cancer Cell Line''cell line: SUM149; agent: DMSO; ', 'cell line: SUM149; agent: CX4945; ', 'cell line: MDA231; agent: DMSO; ', 'cell line: MDA 231; agent: CX4945; ', 'cell line: MDA231; agent: CX4945; ', 'cell line: MDA468; agent: DMSO; ', 'cell line: MDA468; agent: CX4945; ', 'cell line: MDA-MB-231; cell type: Triple Negative Breast Cancer Cell Line; agent: CX4945; ', 'cell line: MDA-MB-231; cell type: Triple Negative Breast Cancer Cell Line; agent: DMSO; ', 'cell line: MDA-MB-468; cell type: Triple Negative Breast Cancer Cell Line; agent: CX4945; ', 'cell line: MDA-MB-468; cell type: Triple Negative Breast Cancer Cell Line; agent: DMSO; ', 'cell line: SUM-149; cell type: Triple Negative Breast Cancer Cell Line; agent: CX4945; ', 'cell line: SUM-149; cell type: Triple Negative Breast Cancer Cell Line; agent: DMSO; ' GSE82058 Homo sapiens 12 Expression profiling by array GPL10558 Transcriptomics response to miR-644 overexpression in three breast cancer cell lines 2016-05-31 The goal of the study is to investigate the effect of microRNA-644 overexpression by chemical mimics on gene expression in breast cancer cell lines. To this purpose control and microRNA-644 mimics are used to transfect MDA-MB-231 cells, SK-BR-3 cells, and MCF-7 cells respectively. Transcriptomics profiling was performed with Illumina HumanHT-12 V4.0 BeadChip microarray. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE82058 The miR-644a/CTBP1/p53 axis suppresses drug resistance by simultaneous inhibition of cell survival and epithelial-mesenchymal transition in breast cancer. Oncotarget None https://doi.org/10.18632/oncotarget.10489 {Oncotarget (None): 10.18632/oncotarget.10489} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA323851 https://www.ebi.ac.uk/ena/browser/view/PRJNA323851 None [Overal design]Three cell lines are treated with scramble microRNA mimic (control herein) and microRNA-644 mimic (miR-644 herein), with two replicates per condition. mRNA expression is compared between miR-644 and control treatment within each cell line, respectively.; [Treatment]'Scramble control and miR-644 mimic was transfected using lipofectamin.'; [Growth]"SK-BR-3 cells were cultured in McCoy's 5a medium (GIBCO BRL). MDA-MB-231 cells were cultured in Leibovitz's L-15 medium (Sigma). MCF-7 cells were cultured in Eagle's Minimial essential medium, All media were supplemented with 50 U/mL penicillin, 50 μg/mL streptomycin sulphate, 1% non-essential amino acids and 10% fetal bovine serum (all media and supplements from Gibco BRL). Additionally, 2.2 g/L sodium bicarbonate was supplemented for MDA-MB-231 cells. In media for MCF-7 cells we added 0.01 mg/mL bovine insulin. The cells were incubated at 37°C with 5% CO2 and split 2–3 times per week in a 1:3 ratio for no more than 20 passages. All cell lines were validated by genotyping."; [Extraction]"Total RNA was isolated according to the manufacturer's protocol using the RNeasy Mini Kit (Qiagen)."; [Cell type]'Source: ''cell line: MDA-MB-231; microrna mimic: control; ', 'cell line: MDA-MB-231; microrna mimic: miR-644; ', 'cell line: SK-BR-3; microrna mimic: control; ', 'cell line: SK-BR-3; microrna mimic: miR-644; ', 'cell line: MCF-7; microrna mimic: control; ', 'cell line: MCF-7; microrna mimic: miR-644; ' GSE107176 Homo sapiens 57 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL18573 Polycomb complexes associate with enhancers to promote oncogenic transcriptional programs in cancer 2017-11-20 The Polycomb repressive complexes PRC1 and PRC2 play an essential role in cell fate decisions, embryonic development and gene regulation. While the functions of PRC2 in cancer are under intense study, the function of PRC1 in cancer remains largely unexplored. Here, we show that RNF2, the gene encoding RING1B, and canonical PRC1 (cPRC1) genes are amplified and overexpressed in breast cancer. Specifically, in estrogen receptor positive (ER+) breast cancer cells, cPRC1 is functionally associated with enhancers and genes regulated by ERa, while in triple negative breast cancer (TNBC) cells, a different cPRC1 variant is recruited to enhancers and promoters occupied by the bromodomain protein BRD4. Mechanistically, cPRC1 complexes are recruited to active enhancers independently of PRC2 and RING1B enzymatic activity. Moreover, RING1B has a dual role in regulating enhancer activity and gene transcription as it is recruited to enhancers to maintain and promote gene expression of breast cancer oncogenes. We also show that RING1B regulates chromatin accessibility of oncogenic transcription factors. Finally, we provide evidence that association of PRC1 to active enhancers is not restricted to breast cancer, demonstrating that RING1B recruitment to transcriptionally active sites occurs in multiple cancer types. Our work highlights a non-classical function of cPRC1 complexes in regulating specific oncogenic programs in cancer through its association with enhancer regions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE107176 Polycomb complexes associate with enhancers and promote oncogenic transcriptional programs in cancer through multiple mechanisms. Nature communications 11.878 https://doi.org/10.1038/s41467-018-05728-x {Nature communications (11.878): 10.1038/s41467-018-05728-x} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA419210 https://www.ebi.ac.uk/ena/browser/view/PRJNA419210 https://www.ncbi.nlm.nih.gov/sra?term=SRP125328 [Overal design]ChIP-seq of RING1B, H3K27me3, H2AK119ub1, H3K4me3, and H3K27ac in iPSCs, MCF10A, MDA-MB-231 and T47D; PCGF2 and H3K36me3 in MCF10A, MDA-MB-231, and T47D; H3K4me1 in MDA-MB-231 and T47D; ERa in T47D; and BRD4 in MDA-MB-231. RNA-seq of RING1B-depleted MDA-MB-231, T47D, and SKBR3 in duplicates. ATAC-seq of RING1B-depleted MDA-MB-231 and T47D in duplicates.; [Treatment]'None'; [Growth]'Human iPSCs were maintained in complete feeder-free mTESR1 culture medium (STEMCELL Technologies cat# 85850) on matrigel-coated plates (Corning ca# 354277) at 37°C with 5% CO2. The culture medium was changed daily and colonies were enzymatically passaged with StemPro Accutaste cell dissociation reagent (Thermo Fisher Scientific cat# A1110501) at a 1:4-1:6 split ratio every 4-7 days. DMEM/F-12 media (STEMCELL Technologies cat# 36254) was used to detach colonies. ROCK inhibitor Y-27632 (STEMCELL Technologies cat# 72302) was used in every split and when cells were thawed from liquid nitrogen. If identified, spontaneously differentiated cells were mechanically removed prior to passaging.', 'MCF10A were maintained at 37°C with 5% CO2 and passaged every 2-3 days at a 1:3 split ratio, according to ATCC recommendations. Complete culture media comprised of DMEM/Ham’s F-12 (1:1) that was supplemented with 5% horse serum, 10ng/ml EGF (Thermo Fisher Scientific cat# PHG0311), 50ng/ml cholera toxin (Sigma-Aldrich cat# C8052), 10μg/ml insulin (Sigma-Aldrich cat# 91077C), 500ng/ml hydrocortisone (Sigma-Aldrich cat# H0888), 1x penicillin/streptomycin, and 1x glutamax.', 'MDA-MB-231 were maintained at 37°C with 5% CO2 and passaged every 2-3 days at a 1:3 split ratio, according to ATCC recommendations. Complete culture media comprised of DMEM that was supplemented with 10% FBS, 1x penicillin/streptomycin, and 1x glutamax.', 'T47D were maintained at 37°C with 5% CO2 and passaged every 2-3 days at a 1:3 split ratio, according to ATCC recommendations. Complete culture media comprised of RPMI-1640 that was supplemented with 10% FBS,10μg/ml insulin (Sigma-Aldrich cat# 91077C), 1x penicillin/streptomycin, and 1x glutamax.', "SKBR3 were maintained at 37°C with 5% CO2 and passaged every 2-3 days at a 1:3 split ratio, according to ATCC recommendations. Complete culture media comprised of McCoy's 5a Medium Modified that was supplemented with 10% FBS, 1x penicillin/streptomycin, and 1x glutamax."; [Extraction]'Cells were grown to 80% confluence on 150cm plates and processed using the High Sensitivity ChIP-IT Kit (Active Motif cat #53040).\nImmunoprecipitated DNA was used to generate libraries using the NEBNext Ultra DNA Library Prep Kit for Illumina (New England Biolabs cat# 7370) following the manufacturer’s instructions.', 'Cells were grown to 80% confluence on 150cm plates and fixed with 1% formaldehyde (Sigma-Aldrich cat# 252549) added directly to culture media for 15min shaking gently at RT. During crosslinking, 1.25M glycine solution (10X) was prepared, then added to plates at a final concentration of 0.125M for 5min shaking gently at RT. The supernatant was aspirated, cells washed 1x with PBS, and harvested on ice using cell scrapers into 15ml sonication tubes (Diagenode cat# C01020031). Cells were pelleted at 2000rpm for 3min at 4°C, washed 1x with 10ml cold PBS, and pelleted once more. Cell pellet was resuspended in 1.3ml cold ChIP Buffer (2 volumes of SDS ChIP Buffer [100mM NaCl, 50mM Tris-HCl pH 8.1, 5mM EDTA pH 8.0, 0.5% SDS] with 1 volume TXT ChIP Buffer [100mM Tris-HCl pH 8.6, 100mM NaCl, 5mM EDTA pH 8.0, 5% Triton X-100]). Cells were then sonicated on a Bioruptor Pico at 4°C for 10min of 30’’ ON-OFF cycles. After sonication, samples were centrifuged at maximum speed for 15min at 4°C and supernatant transferred to a new 1.5ml microtube. To check sonication efficiency, 20µl of sonicated samples was transferred to a new microtube with 80µl PBS and incubated at 65°C for 3hr on an Eppendorf Thermomixer shaking at 1000rpm to decrosslink. DNA was purified with the QIAquick PCR Purification Kit (Qiagen cat# 28106) and eluted in 30µl H2O. 6µl of orange DNA dye was added and 12µl and 24µl of each sample were run in a 1% agarose gel at 100V for 15min and imaged on a Bio-rad ChemiDoc XRS+. Protein concentration in sonicated samples was measured by Bradford assay, and 200µg of total protein was transferred to a 1.5ml LoBind tube (Eppendorf cat# 0030108051) and brought up to 500µl final volume with ChIP buffer. 5µl was removed as input material (1%) and placed in a separate microtube at 4°C. 2µg antibody was used for each histone ChIP (see Key Resources table for list of antibodies). The samples were rotated end-to-end overnight at 4°C. Protein A sepharose beads (GE Healthcare cat# 17528001) were washed 3x with ChIP buffer and 30µl bead slurry was added to each sample. Samples were incubated with beads for 2hr at 4°C rotating end-to-end. Following incubation, samples were centrifuged at 2000rpm for 3min at 4°C, washed 2x with ChIP Low Salt Buffer (50mM HEPES pH7.5, 140mM NaCl, 1% Triton X-100, 1x protease inhibitors), and 1x with ChIP High Salt Buffer (50mM HEPES pH7.5, 500mM NaCl, 1% Triton X-100, 1x protease inhibitors). Beads were dried after the last wash with a 28G needle fitted to a 1ml syringe. Elution Buffer (1% SDS, 0.1M sodium carbonate) was prepared fresh before use and 110µl was added to each sample and 95µl to each input sample that was previously set aside. To elute immunocomplexes from beads, samples were incubated at 65°C for 3hr on an Eppendorf Thermomixer shaking at 1000rpm. Tubes were centrifuged for 3min at 2000rpm at RT and 100µl of supernatant was transferred to a new tube, being careful not to aspirate beads. DNA purification was performed with the QIAquick PCR Purification Kit (Qiagen cat# 28106) and eluted in 60µl H2O and quantified by Qubit.\nImmunoprecipitated DNA was used to generate libraries using the NEBNext Ultra DNA Library Prep Kit for Illumina (New England Biolabs cat# 7370) following the manufacturer’s instructions.', "RNA was isolated from fresh or frozen cell pellets using TRIzol reagent (Thermo Fisher Scientific cat# 15596018) according to manufacturer's instructions.\nRibosomal RNA was removed using the NEBNext rRNA Depletion Kit (New England Biolabs cat# E6310) starting with 1µg total RNA and following the manufacturer’s instructions. Ribo-depleted RNA was then further processed with the NEBNext Ultra Directional RNA Library Prep Kit for Illumina (New England Biolabs cat# E7420) for library preparation following the manufacturer’s instructions.", 'Cells were grown to 80% confluence on 150cm plates and fixed with 1% formaldehyde (Sigma-Aldrich cat# 252549) added directly to culture media for 15min shaking gently at RT. During crosslinking, 1.25M glycine solution (10X) was prepared, then added to plates at a final concentration of 0.125M for 5min shaking gently at RT. The supernatant was aspirated, cells washed 1x with PBS, and harvested on ice using cell scrapers into 15ml sonication tubes (Diagenode cat# C01020031). Cells were pelleted at 2000rpm for 3min at 4°C, washed 1x with 10ml cold PBS, and pelleted once more. Cell pellet was resuspended in 1.3ml cold ChIP Buffer (2 volumes of SDS ChIP Buffer [100mM NaCl, 50mM Tris-HCl pH 8.1, 5mM EDTA pH 8.0, 0.5% SDS] with 1 volume TXT ChIP Buffer [100mM Tris-HCl pH 8.6, 100mM NaCl, 5mM EDTA pH 8.0, 5% Triton X-100]). Cells were then sonicated on a Bioruptor Pico at 4°C for 20min of 30’’ ON-OFF cycles. After sonication, samples were centrifuged at maximum speed for 15min at 4°C and supernatant transferred to a new 1.5ml microtube. To check sonication efficiency, 20µl of sonicated samples was transferred to a new microtube with 80µl PBS and incubated at 65°C for 3hr on an Eppendorf Thermomixer shaking at 1000rpm to decrosslink. DNA was purified with the QIAquick PCR Purification Kit (Qiagen cat# 28106) and eluted in 30µl H2O. 6µl of orange DNA dye was added and 12µl and 24µl of each sample were run in a 1% agarose gel at 100V for 15min and imaged on a Bio-rad ChemiDoc XRS+. Protein concentration in sonicated samples was measured by Bradford assay, and 200µg of total protein was transferred to a 1.5ml LoBind tube (Eppendorf cat# 0030108051) and brought up to 500µl final volume with ChIP buffer. 5µl was removed as input material (1%) and placed in a separate microtube at 4°C. 2µg antibody was used for each histone ChIP (see Key Resources table for list of antibodies). The samples were rotated end-to-end overnight at 4°C. Protein A sepharose beads (GE Healthcare cat# 17528001) were washed 3x with ChIP buffer and 30µl bead slurry was added to each sample. Samples were incubated with beads for 2hr at 4°C rotating end-to-end. Following incubation, samples were centrifuged at 2000rpm for 3min at 4°C, washed 2x with ChIP Low Salt Buffer (50mM HEPES pH7.5, 140mM NaCl, 1% Triton X-100, 1x protease inhibitors), and 1x with ChIP High Salt Buffer (50mM HEPES pH7.5, 500mM NaCl, 1% Triton X-100, 1x protease inhibitors). Beads were dried after the last wash with a 28G needle fitted to a 1ml syringe. Elution Buffer (1% SDS, 0.1M sodium carbonate) was prepared fresh before use and 110µl was added to each sample and 95µl to each input sample that was previously set aside. To elute immunocomplexes from beads, samples were incubated at 65°C for 3hr on an Eppendorf Thermomixer shaking at 1000rpm. Tubes were centrifuged for 3min at 2000rpm at RT and 100µl of supernatant was transferred to a new tube, being careful not to aspirate beads. DNA purification was performed with the QIAquick PCR Purification Kit (Qiagen cat# 28106) and eluted in 60µl H2O and quantified by Qubit.\nImmunoprecipitated DNA was used to generate libraries using the NEBNext Ultra DNA Library Prep Kit for Illumina (New England Biolabs cat# 7370) following the manufacturer’s instructions.', 'ATAC-seq experiments were performed as previously described (Buenrostro et al., 2013) with the following modifications: 25,000 cells for each cell line were used to perform the transposon reaction. Samples were purified with a MinElute Reaction Cleanup kit (Qiagen cat# 28206) and DNA eluted in 13μl of EB Buffer.\nTo calculate the number of cycles for library amplification, 2μl of transposed DNA were amplified by qPCR for a total of 25 cycles. The 10μl qPCR reaction was set up as follows: 2μl of transposed DNA, 0.3μl 25μM Ad1_noMX, 0.3μl 25μM Ad2.X (custom oligos synthesized by Integrated DNA Technologies), 5μl NEBNext High-Fidelity 2X PCR Master Mix (New England BioLabs, #M0541S), 0.1μl 100X SYBR Green I (10,000X stock from Invitrogen, #S7563) and 2.3μl nuclease-free water with the following program on a Bio-Rad CFX96 Optics Module Thermal Cycler machine: 1) 72°C for 5 minutes, 2) 98°C for 30 seconds, 3) 98°C for 10 seconds, 63°C for 30 seconds and 72°C for 30 seconds, 25 cycles, 4) 72°C for 1 minute, and 5) hold at 10°C. The Ct value of each sample reflects the number of PCR cycles for optimal amplification in the linear range of the reaction. A 50ul PCR reaction was then set up as follows: 10μl transposed DNA, 1.5μl 25μM Ad1_noMX, 1.5 μl 25μM Ad2.X (unique for each sample), 12μl of nuclease free water, and 25μl NEBNext High-Fidelity 2X PCR Master Mix with the same program as for the qPCR, but substituting the cycle number with the Ct-value obtained from the qPCR reaction. The PCR was performed on a Bio-Rad C1000 Touch Thermal Cycler. After PCR, the 50μl reactions were cleaned up and size selected by adding 25 μl of AMPure XP beads (Beckman Coulter #A63881) to remove fragments higher than 800bp. The supernatant was transferred to a new tube and 65μl of AMPure XP beads were added to remove fragments smaller than 100bp, then washed twice with freshly prepared 80% ethanol and eluted in 25μl of water. To determine the average fragment size of each library, samples were run through a High-sensitivity DNA screentape (Agilent Technologies cat# 5067-5584) following the manufacturer’s instructions on an Agilent Technologies 2200 TapeStation machine. To determine the concentration of each library, Qubit dsDNA high sensitivity reagents (Thermo Fisher Scientific cat# Q32851) were used following the manufacturer’s instructions on a Qubit 3 fluorometer.'; [Cell type]'Heart-derived sendai virus reprogrammed induced pluripotent stem cell', 'Mammary gland fibrocystic disease epithelial cells', 'Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site', 'Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site''cell line: iPSC; cell type: Heart-derived sendai virus reprogrammed induced pluripotent stem cell; cell source: ATCC #ACS-1021; modifications: Parental cells; ', 'cell line: iPSC; cell type: Heart-derived sendai virus reprogrammed induced pluripotent stem cell; cell source: ATCC #ACS-1021; modifications: Parental cells; chip antibody: Homemade (ref. Morey et al., Cell Stem Cell, 2015); ', 'cell line: iPSC; cell type: Heart-derived sendai virus reprogrammed induced pluripotent stem cell; cell source: ATCC #ACS-1021; modifications: Parental cells; chip antibody: Active Motif # 39155; ', 'cell line: iPSC; cell type: Heart-derived sendai virus reprogrammed induced pluripotent stem cell; cell source: ATCC #ACS-1021; modifications: Parental cells; chip antibody: Cell Signaling # 8240; ', 'cell line: iPSC; cell type: Heart-derived sendai virus reprogrammed induced pluripotent stem cell; cell source: ATCC #ACS-1021; modifications: Parental cells; chip antibody: Diagenode # C15410003; ', 'cell line: iPSC; cell type: Heart-derived sendai virus reprogrammed induced pluripotent stem cell; cell source: ATCC #ACS-1021; modifications: Parental cells; chip antibody: Abcam # ab4729; ', 'cell line: MCF10A; cell type: Mammary gland fibrocystic disease epithelial cells; cell source: ATCC #CRL-10317; modifications: Parental cells; ', 'cell line: MCF10A; cell type: Mammary gland fibrocystic disease epithelial cells; cell source: ATCC #CRL-10317; modifications: Parental cells; chip antibody: Homemade (ref. Morey et al., Cell Stem Cell, 2015); ', 'cell line: MCF10A; cell type: Mammary gland fibrocystic disease epithelial cells; cell source: ATCC #CRL-10317; modifications: Parental cells; chip antibody: Active Motif # 39155; ', 'cell line: MCF10A; cell type: Mammary gland fibrocystic disease epithelial cells; cell source: ATCC #CRL-10317; modifications: Parental cells; chip antibody: Cell Signaling # 8240; ', 'cell line: MCF10A; cell type: Mammary gland fibrocystic disease epithelial cells; cell source: ATCC #CRL-10317; modifications: Parental cells; chip antibody: Diagenode # C15410003; ', 'cell line: MCF10A; cell type: Mammary gland fibrocystic disease epithelial cells; cell source: ATCC #CRL-10317; modifications: Parental cells; chip antibody: Abcam # ab4729; ', 'cell line: MCF10A; cell type: Mammary gland fibrocystic disease epithelial cells; cell source: ATCC #CRL-10317; modifications: Parental cells; chip antibody: Abcam # ab9050; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: Parental cells; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: Parental cells; chip antibody: Active Motif # 39663; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: Parental cells; chip antibody: Active Motif # 39155; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: Parental cells; chip antibody: Cell Signaling # 8240; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: Parental cells; chip antibody: Diagenode # C15410003; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: Parental cells; chip antibody: Abcam # ab4729; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: Parental cells; chip antibody: Abcam # ab9050; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: Parental cells; chip antibody: Santa Cruz # sc-10744 X; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: Parental cells; chip antibody: Diagenode # C15410194; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: Parental cells; chip antibody: Bethyl Laboratories # A301-985A100; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: pLKO_shCTR stable cells; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: pLKO_shRING1B stable cells; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: siCTR transiently transfected cells; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: siRING1B transiently transfected cells; ', 'cell line: MDA-MB-231; cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-26; modifications: siRING1B transiently transfected cells; chip antibody: N/A; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: Parental cells; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: Parental cells; chip antibody: Active Motif # 39663; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: Parental cells; chip antibody: Active Motif # 39155; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: Parental cells; chip antibody: Cell Signaling # 8240; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: Parental cells; chip antibody: Diagenode # C15410003; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: Parental cells; chip antibody: Abcam # ab4729; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: Parental cells; chip antibody: Abcam # ab9050; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: Parental cells; chip antibody: Santa Cruz # sc-10744 X; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: Parental cells; chip antibody: Diagenode # C15410194; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: Parental cells; chip antibody: Diagenode # C15100066; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: pLKO_shCTR stable cells; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: pLKO_shRING1B stable cells; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: siCTR transiently transfected cells; ', 'cell line: T47D; cell type: Mammary gland ductal carcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-133; modifications: siRING1B transiently transfected cells; ', 'cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-30; modifications: pLKO_shCTR stable cells; ', 'cell type: Mammary gland adenocarcarcinoma epithelial cells derived from metastatic site; cell source: ATCC #HTB-30; modifications: pLKO_shRING1B stable cells; ' GSE160001 Homo sapiens 12 Expression profiling by high throughput sequencing GPL18573 FOXA1-dependent responses of the HER2+ SKBR-3 cell line to lapatinib 2020-10-23 SKBR-3 HER2+ breast cancer cells were treated with 25 nM Dharmacon siGENOME non-targeting (NT) siRNA control pool or siRNA pool targeting FOXA1 for 48h, then treated with either DMSO or 300nM lapatinib for 24h. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE160001 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA671641 https://www.ebi.ac.uk/ena/browser/view/PRJNA671641 https://www.ncbi.nlm.nih.gov/sra?term=SRP288463 [Overal design]12 experimental samples; [Treatment]'RPMI supplemented with 10% FBS'; [Growth]'None'; [Extraction]'Total RNA was isolated using Qiagen RNeasy Plus kit.\n4 ug total RNA and 10 cycles of amplification were used for libraries constructed with KAPA Stranded mRNAseq kit.'; [Cell type]'Source: ''cell line: SKBR-3 HER2+; treatment: non-targeting (NT) siRNA control pool for 48h, then treated with DMSO for 24h; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: SKBR-3 HER2+; treatment: non-targeting (NT) siRNA control pool for 48h, then treated with 300nM lapatinib for 24h; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: SKBR-3 HER2+; treatment: FOXA1 siRNA pool for 48h, then treated with DMSO for 24h; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'treatment: FOXA1 siRNA pool for 48h, then treated with DMSO for 24h; library preparation kit: Illumina TruSeq RNA library kit v2; cell line: SKBR-3 HER2+; ', 'treatment: FOXA1 siRNA pool for 48h, then treated with 300nM lapatinib for 24h; library preparation kit: Illumina TruSeq RNA library kit v2; cell line: SKBR-3 HER2+; ' GSE93757 Homo sapiens 16 Genome binding/occupancy profiling by high throughput sequencing GPL11154 UBR7 is a novel E3 ubiquitin ligase for H2BK120 and acts as a tumor-suppressor in breast cancer [ChIP-Seq] 2017-01-18 Plant Homeo Domain (PHD) is a versatile chromatin reader/effector module which recognizes methylated, acetylated or unmodified histone substrates and regulates cellular gene expression programs. Although PHD domains shows selective epigenetic recognition of methylated, acetylated and unmodified histone substrates, there has been no previous report on its catalytic function regulating malignant transformation of cells. Here we report that PHD finger of UBR7 (Ubiquitin Protein Ligase E3 Component N-Recognin 7 (Putative)), in isolation or in context of full length protein, harbors E3 ubiquitin ligase activity towards monoubiquitination of histone H2B at lysine 120 . Knockdown of UBR7 in MCF10a and breast cancer cells decreased H2BK120ub both at the global levels and on specific genes. Conversely, overexpression of wild type, but not catalytic mutant, rescued H2BK120ub levels. Low UBR7 expression was associated with basal-like and triple negative breast cancers as well as showed poor expression in metastatic tumors. Consistently, UBR7 loss resulted in invasion properties, induced epithelial-to-mesenchymal transition and promoted metastasis. Conversely, ectopic expression of UBR7 reduced cell growth, invasion and tumor growth in mouse fat pad. Mechanistically, UBR7 reduced H2BK120ub gene body of cell-adhesion related genes as well as gene expression including on CDH4 gene. Importantly, rebuilding CDH4 levels rescued invasion phenotypes seen in UBR7-low cells. Collectively, our results establish that UBR7 PHD has novel H2B ubiquitin ligase activity and it suppresses tumor growth in basal-like breast cancers. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93757 Atypical plant homeodomain of UBR7 functions as an H2BK120Ub ligase and breast tumor suppressor. Nature communications 11.878 https://doi.org/10.1038/s41467-019-08986-5 {Nature communications (11.878): 10.1038/s41467-019-08986-5} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA362302 https://www.ebi.ac.uk/ena/browser/view/PRJNA362302 https://www.ncbi.nlm.nih.gov/sra?term=SRP096947 [Overal design]Examination of 7 different histone modifications in Wild Type and UBR7-shRNA MCF10A Cell Line; [Treatment]'shRNA plasmids for UBR7 with pLKO.1-puro backbone (Sigma Aldrich) were screened for efficient knock-down.Two out seven shRNAs were selected for subsequent experiments. Four micrograms of shRNA and packaging vectors were transfected as described previously (ref). Cells were selected using puromycin (10 μg / ml) (Sigma) for 3days.'; [Growth]'MCF10A cells were maintained in DMEM / Ham’s F12 supplemented with 5% horse serum (Gibco), EGF, insulin, hydrocortisone, cholera toxin (Sigma) and 1% antibiotic-antimycotic.'; [Extraction]'Histone-DNA complexes were isolated using antibodies described from Control and UBR7-shRNA sonicated nuclei.\nLibraries for Illumina sequencing were generated following the New England BioLabs NEBNext Ultra DNA Library Prep Kit protocol. A total of 10x cycles were used during PCR amplification for the generation of all ChIP-seq libraries. Amplified ChIP DNA was purified using double-sided AMPure XP to retain fragments ~200 to 500bp and quantified using the Qubit 2000 and Bioanalyzer 1000 before multiplexing.'; [Cell type]'Human mammary epithelial cell line''cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H2BK120ub Millipore 17-650; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H3K4me1 Abcam ab8895; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H3K9me3 Abcam ab8898; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H3K27ac Abcam ab4729; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H3K79me2 Abcam ab3594; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H3K4me3 Abcam/Millipore ab; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H3K27me3 Abcam ab6002; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: none (input); ' GSE92477 Homo sapiens 10 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Chromatin state upon MSK1 downregulation by shRNA in dormant bone metastatic (DBM) cells. 2016-12-15 For many breast cancer (BCa) patients, symptomatic bone metastases appear after years or even decades of latency. How metastatic cells disseminate, and how micromet­astatic lesions remain dormant and undetectable, are major questions in cancer research. Here we identify and func­tionally analyse a molecular mechanism involved in the bone metastatic latency of estrogen receptor (ER)+ BCa. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE92477 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA357643 https://www.ebi.ac.uk/ena/browser/view/PRJNA357643 https://www.ncbi.nlm.nih.gov/sra?term=SRP095215 [Overal design]ChIP-sequencing was performed on DBM shCTRL and DBM shMSK1 cells using antibodies recognizing 4 chromatin marks at histone H3 (H3K9ac, H3K9me3, H3K27ac, H3K27me3).; [Treatment]'none'; [Growth]'Cells were grown in DMEM 4,5g/L D-glucose medium supplemeted with 10% FBS, 50 U/ml penicilin, 50μg/ml streptomycin and 5% glutamine.'; [Extraction]"Lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with indicated antibody\nLibraries for sequencing were prepared using NEBNext Ultra DNA Library Prep Kit for Illumina (E7370L) following the manufacturer's instructions."; [Cell type]'Source: ''transfection: shCTRL; chip antibody: H3K9ac (Abcam, ab4441); ', 'transfection: shCTRL; chip antibody: H3K9me3 (Abcam, ab8898); ', 'transfection: shCTRL; chip antibody: H3K27ac (Merck Millipore, 07-360); ', 'transfection: shCTRL; chip antibody: H3K27me3 (Abcam, ab6002); ', 'transfection: shCTRL; chip antibody: none; ', 'transfection: shMSK1; chip antibody: H3K9ac (Abcam, ab4441); ', 'transfection: shMSK1; chip antibody: H3K9me3 (Abcam, ab8898); ', 'transfection: shMSK1; chip antibody: H3K27ac (Merck Millipore, 07-360); ', 'transfection: shMSK1; chip antibody: H3K27me3 (Abcam, ab6002); ', 'transfection: shMSK1; chip antibody: none; ' GSE93336 Homo sapiens 8 Expression profiling by array GPL13667 FFPE samples profiled on HG-U219 array with Nugen's Ovation® FFPE WTA System and EncoreTM Biotin Module 2017-01-09 The reliability of differential expression analysis on FFPE expression profiles from Affymetrix arrays is questionable, due to the wide range of percent-present values reported in studies which profiled FFPE samples on Affymetrix arrays. Moreover the validity of externally defined gene-modules in FFPE microarray expression profiles is unknown. Using eight breast cancer tumors with available frozen and FFPE samples, five sample-matched data sets were generated from different combination of Affymetrix arrays, amplification-and-labeling kit and sample preservation method. The reliability of differential expression analysis was investigated by developing de novo ER/HER2 pathway gene-modules from matched data sets and validating it on external data set using ROC analysis. Spearman's rank correlation coefficient of module scores between matched FFPE-frozen expression profiles was used to measure reliability of externally defined gene-modules in FFPE expression profiles. Independent of array/amplification-kit/sample preservation method used, de novo ER/HER2 gene-modules derived from all matching data sets showed similar prediction performance during independent validation (AUC range; ER: 0.92-0.95, HER2: 0.88-0.91), except for de novo HER2 gene-module derived from FFPE data set with 3'IVT kit (AUC: 0.67-0.72). Further not all gene-module based biological signals present in frozen expression profiles can be recovered from matching FFPE microarray expression profiles using the currently available FFPE specific sample preparation kits. The gene-module based biological signal extracted from FFPE RNA, using microarrays, may not be as reliable as that from their frozen counterpart, if the sample preparation protocol used with FFPE RNA failed to recover relevant genes involved in the biological signal. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93336 Feasibility of developing reliable gene expression modules from FFPE derived RNA profiled on Affymetrix arrays. PloS one 2.776 https://doi.org/10.1371/journal.pone.0203346 {PloS one (2.776): 10.1371/journal.pone.0203346} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA360632 https://www.ebi.ac.uk/ena/browser/view/PRJNA360632 None [Overal design]RNAs were extracted from eight FFPE preserved breast cancers. RNAs were amplified and labeled using Nugen's Ovation® FFPE WTA System and EncoreTM Biotin Module, and profiled on Affymetrix® HG-U219 Array Plate according to Affymetrix's standard procedure.; [Treatment]'NA'; [Growth]'NA'; [Extraction]'Total RNA from FFPE sections was extracted using miRNeasy FFPE kit according to Qiagen recommendation.'; [Cell type]'Source: ''tissue: breast tumor; er status: negative; her2 status: negative; tissue preservation method: FFPE; ', 'tissue: breast tumor; er status: positive; her2 status: negative; tissue preservation method: FFPE; ', 'tissue: breast tumor; er status: negative; her2 status: positive; tissue preservation method: FFPE; ', 'tissue: breast tumor; er status: positive; her2 status: positive; tissue preservation method: FFPE; ' GSE15026 Homo sapiens 30 Expression profiling by array GPL570 Expression data from breast cancer cell lines with various colony-forming ability 2009-02-26 Cultured cancer cells exhibit substantial phenotypic heterogeneity when measured in a variety of ways such as sensitivity to drugs or the capacity to grow under various conditions. Among these, the ability to exhibit anchorage-independent cell growth (colony forming capacity in semisolid media), has been considered to be fundamental in cancer biology, because it has been connected with tumor cell aggressiveness in vivo such as tumorigenic and metastatic potentials, and also utilized as a marker for in vitro transformation. Although multiple genetic factors for anchorage-independence have been identified, the molecular basis for this capacity is still largely unknown. To investigate the molecular mechanisms underlying anchorage independent cell growth, we have used genome-wide DNA microarray studies to develop an expression signature associated with this phenotype. Using this signature, we identify a program of activated mitochondrial biogenesis associated with the phenotype of anchorage-independent growth and importantly, we demonstrate that this phenotype predicts potential for metastasis in primary breast and lung tumors. Keywords: Breast cancer cell lines with various colony-forming ability https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15026 Anchorage-independent cell growth signature identifies tumors with metastatic potential. Oncogene 6.634 https://doi.org/10.1038/onc.2009.139 {Oncogene (6.634): 10.1038/onc.2009.139} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA123207 https://www.ebi.ac.uk/ena/browser/view/PRJNA123207 None [Overal design]To develop an expression signature reflecting the capacity for anchorage-independent cell growth, we first carried out colony formation assays with 19 breast cancer cell lines in suspension culture dish with methyl-cellulose containing media. Starting with 20,000 plated cells, five cell lines (MDA-MB-361, HCC38, ZR75, Hs578T and BT483) gave rise to less than 20 colonies, while 8 cell lines (MCF7, MDA-MB-231, BT20, SKBR3, MDA-MB-435s, T47D and BT474) showed formation of more than 500 colonies. The rest of the cell lines showed an intermediate phenotype in colony forming ability (20-200 colonies; HCC1143, HCC1806, HCC1428, MDA-MB-453, CAMA1, BT549 and MDA-MB-157). Among 19 cell lines, 11 cell lines have duplicates of expression data in a different batch. We removed the batch effect of this Affymetrix expression data using ComBat according to the instruction of http://statistics.byu.edu/johnson/ComBat/Abstract.html. Therefore, this dataset is a combined and standardized data that are originally RMA formatted.; [Treatment]'None'; [Growth]'None'; [Extraction]"Snap-frozen samples in liquid nitrogen were used for extraction. Total RNA was extracted by Qiagen RNEasy kit according to the manufacturer's instructions."; [Cell type]'Breast Cancer''cell line: T47D; cell type: Breast Cancer; colony number: 6586.666667; batch: 1; ', 'cell line: BT20; cell type: Breast Cancer; colony number: 1564.333333; batch: 1; ', 'cell line: BT483; cell type: Breast Cancer; colony number: 13; batch: 1; ', 'cell line: ZR75; cell type: Breast Cancer; colony number: 3.333333333; batch: 1; ', 'cell line: MDA-MB-435s; cell type: Breast Cancer; colony number: 4950.666667; batch: 1; ', 'cell line: MCF7; cell type: Breast Cancer; colony number: 632.6666667; batch: 1; ', 'cell line: MDA-MB-231; cell type: Breast Cancer; colony number: 1088; batch: 1; ', 'cell line: BT474; cell type: Breast Cancer; colony number: 6898.333333; batch: 1; ', 'cell line: BT549; cell type: Breast Cancer; colony number: 80.33333333; batch: 1; ', 'cell line: SKBR3; cell type: Breast Cancer; colony number: 3601; batch: 1; ', 'cell line: MDA-MB-361; cell type: Breast Cancer; colony number: 0; batch: 1; ', 'cell line: BT20; cell type: Breast Cancer; colony number: 1564.333333; batch: 2; ', 'cell line: BT474; cell type: Breast Cancer; colony number: 6898.333333; batch: 2; ', 'cell line: MCF7; cell type: Breast Cancer; colony number: 632.6666667; batch: 2; ', 'cell line: Hs578T; cell type: Breast Cancer; colony number: 6; batch: 2; ', 'cell line: CAMA1; cell type: Breast Cancer; colony number: 73.33333333; batch: 2; ', 'cell line: MDA-MB-361; cell type: Breast Cancer; colony number: 0; batch: 2; ', 'cell line: MDA-MB-157; cell type: Breast Cancer; colony number: 158; batch: 2; ', 'cell line: BT483; cell type: Breast Cancer; colony number: 13; batch: 2; ', 'cell line: BT549; cell type: Breast Cancer; colony number: 80.33333333; batch: 2; ', 'cell line: SKBR3; cell type: Breast Cancer; colony number: 3601; batch: 2; ', 'cell line: T47D; cell type: Breast Cancer; colony number: 6586.666667; batch: 2; ', 'cell line: ZR75; cell type: Breast Cancer; colony number: 3.333333333; batch: 2; ', 'cell line: HCC1143; cell type: Breast Cancer; colony number: 48.6666666666667; batch: 2; ', 'cell line: HCC1806; cell type: Breast Cancer; colony number: 51; batch: 2; ', 'cell line: HCC1428; cell type: Breast Cancer; colony number: 56; batch: 2; ', 'cell line: HCC38; cell type: Breast Cancer; colony number: 0; batch: 2; ', 'cell line: MDA-MB-435s; cell type: Breast Cancer; colony number: 4950.666667; batch: 2; ', 'cell line: MDA-MB-231; cell type: Breast Cancer; colony number: 1088; batch: 2; ', 'cell line: MDA-MB-453; cell type: Breast Cancer; colony number: 68.66666667; batch: 2; ' GSE30731 Homo sapiens 4 Expression profiling by array GPL6848 CrkII transgene induces atypical mammary gland development and tumorigenesis 2011-07-18 The v-Crk protein was originally isolated as the oncogene fusion product of the CT10 chicken retrovirus. Cellular homologues of v-Crk include Crk, which encodes two alternatively spliced proteins (CrkI and CrkII), and CrkL. Though CrkI/II proteins are elevated in several types of cancer, including breast, the question of whether these Crk adaptor proteins can promote breast cancer has not been addressed. We created a transgenic mouse model that allows the expression of CrkII through the hormonally responsive mouse mammary tumor virus promoter. During puberty, transgenic mice were found to have delayed ductal outgrowth, characterized by increased collagen surrounding the terminal end buds. In post-pubertal mice, precocious ductal branching was observed and associated with increased proliferation. Focal mammary tumors appeared in a subset of animals, with a latency of approximately 15 months. Mouse mammary tumor virus/CrkII tumors showed high levels of Crk protein as well as various cytokeratin markers characteristic of their respective tumor pathologies. This study demonstrates that the precise expression of CrkII is critical for integrating signals for ductal outgrowth and branching morphogenesis during mammary gland development. Furthermore, this study provides evidence for a potential role of CrkII in integrating signals for breast cancer progression in vivo, which has important implications for elevated CrkII observed in human cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE30731 CrkII transgene induces atypical mammary gland development and tumorigenesis. The American journal of pathology 3.762 https://doi.org/10.2353/ajpath.2010.090383 {The American journal of pathology (3.762): 10.2353/ajpath.2010.090383} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA144353 https://www.ebi.ac.uk/ena/browser/view/PRJNA144353 None [Overal design]Two T47D-CrkII samples vs two T47D samples.; [Treatment]'None'; [Growth]'ES cells were kept in an undifferentiated, pluripotent state by using 1000 IU/ml leukemia inhibitory factor (LIF; Chemicon, ESGRO, ESG1107), and grown on top of murine embryonic fibroblasts feeder layer inactivated by 10 ug/ml of mitomycin C (Sigma, St. L)'; [Extraction]"Total RNA extracted using Trizol following manufacturer's instructions"; [Cell type]'T47D Cell', 'Source: ', 'T47D-CrkII Cell''cell type: T47D Cell; ', 'reference: Universal Human Refence RNA; ', 'cell type: T47D-CrkII Cell; ' GSE5927 Homo sapiens 41 Genome variation profiling by SNP array GPL2005 SNP expression data from breast cancer 2006-09-28 SNP Expression profiling of human breast cancer: 29 tumor samples, 4 pure normal breat samples and 8 lymphocytes samples Keywords: Human Cancer https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE5927 Targets of genome copy number reduction in primary breast cancers identified by integrative genomics. Genes, chromosomes & cancer 2.940 https://doi.org/10.1002/gcc.20411 {Genes, chromosomes & cancer (2.940): 10.1002/gcc.20411} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA97373 https://www.ebi.ac.uk/ena/browser/view/PRJNA97373 None [Overal design]In the operating theater, morphologically visible tumors were removed by surgery and examined by a surgical pathologist to confirm the presence of cancer cells by cryosections. The tissue samples were divided into discrete aliquots, flash frozen and subsequently stored in liquid nitrogen. Pure normal breast tissues are got from costmetic surgery and pure lymphocytes samples are from donators.; [Treatment]'None'; [Growth]'None'; [Extraction]"Qiagen DNA extraction kit was used according to the manufacturer's instructions."; [Cell type]'Source: ''Tissue: Breast; ', 'Tissue: lymphocytes; ' GSE106200 synthetic construct; Homo sapiens 20 Expression profiling by array; Non-coding RNA profiling by array GPL570; GPL19117 RNA differencial expression data between scrambled siRNA-treated mice and HN1L siRNA-treated mice tumor samples 2017-10-26 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE106200 HN1L Promotes Triple-Negative Breast Cancer Stem Cells through LEPR-STAT3 Pathway. Stem cell reports 5.499 https://doi.org/10.1016/j.stemcr.2017.11.010 {Stem cell reports (5.499): 10.1016/j.stemcr.2017.11.010} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA415905 https://www.ebi.ac.uk/ena/browser/view/PRJNA415905 None [Overal design]Refer to individual Series; [Treatment]'Groups (0) and (1) (n=10) were treated with 5 µg/mouse DOPC nanoliposomal siRNA IP injection twice a week for 3 weeks. Mice were sacrificed on day 21. Tumors were harvested and snap frozen.'; [Growth]'In docetaxel-resistant BCM2665 PDX xenografts, tumors were transplanted into the mammary fat pad of SCID-Beige mice. Mice were randomized into 5 groups when tumor volume reached 150-200mm3: (0)scrambled siRNA, (1)HN1L siRNA.'; [Extraction]'Extraction of total RNA from each frozen tumor sample was performed using RNeasy Mini kit from Qiagen following manufacturer instruction.', 'Extraction of miRNA from each frozen tumor sample was performed using miRNeasy Mini kit from Qiagen following manufacturer instruction.'; [Cell type]'Source: ''tissue: breast cancer tumor tissue; genotype: Triple-negative breast cancer; xenograft type: BCM2665; ' GSE89093 Homo sapiens 92 Methylation profiling by array GPL13534 DNA methylome analysis of human peripheral blood samples in cancer discordant monozygotic twin-pairs 2016-10-24 Genome wide DNA methylation profiling with the HumanMethylation450 BeadChip (450k) of peripheral blood samples of 46 adult female monozygotic twin-pairs obtained at the same time point. Samples included 41 healthy females (not diagnosed with cancer to date) paired with their co-twin diagnosed with cancer within a 5 year window around the time of sampling as well as 5 extra pairs with a co-twin diagnosed with cancer within 11 to 5 years prior to blood sampling. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE89093 Integrative DNA methylome analysis of pan-cancer biomarkers in cancer discordant monozygotic twin-pairs. Clinical epigenetics 5.496 https://doi.org/10.1186/s13148-016-0172-y {Clinical epigenetics (5.496): 10.1186/s13148-016-0172-y} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA350276 https://www.ebi.ac.uk/ena/browser/view/PRJNA350276 None [Overal design]Bisulphite converted DNA from the 92 samples were hybridised to the Illumina HumanMethylation450 BeadChip; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was extracted and purified from peripheral blood samples'; [Cell type]'Source: ''tissue: peripheral blood; twin pair id: pair_38; age at blood sample: 73.14; gender: female; beadchip and order on beadchip (sentrix id): 6042308041_R02C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -3.36; ', 'tissue: peripheral blood; twin pair id: pair_43; age at blood sample: 65.18; gender: female; beadchip and order on beadchip (sentrix id): 6055432089_R01C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -2.35; cancer location: endometrium; icd information: Malignt neoplasm of endometrium; histology: Adenocarcinoma NOS; ', 'tissue: peripheral blood; twin pair id: pair_43; age at blood sample: 65.18; gender: female; beadchip and order on beadchip (sentrix id): 6055432089_R02C01; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -2.35; ', 'tissue: peripheral blood; twin pair id: pair_17; age at blood sample: 75.7; gender: female; beadchip and order on beadchip (sentrix id): 6055432099_R05C01; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -4.55; ', 'tissue: peripheral blood; twin pair id: pair_17; age at blood sample: 75.7; gender: female; beadchip and order on beadchip (sentrix id): 6055432099_R06C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -4.55; cancer location: breast; icd information: Malignt neoplasm of lower-outer quadrant of breast; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_46; age at blood sample: 49.1; gender: female; beadchip and order on beadchip (sentrix id): 6055432102_R06C02; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.13; ', 'tissue: peripheral blood; twin pair id: pair_46; age at blood sample: 49.1; gender: female; beadchip and order on beadchip (sentrix id): 6055432120_R02C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.13; cancer location: melanoma; icd information: Malignt melanoma of trunk; histology: Malignt melanoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_38; age at blood sample: 73.14; gender: female; beadchip and order on beadchip (sentrix id): 6055432120_R03C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -3.36; cancer location: colon; icd information: Malignt neoplasm of colon, unspecified; histology: Adenocarcinoma NOS; ', 'tissue: peripheral blood; twin pair id: pair_45; age at blood sample: 62.89; gender: female; beadchip and order on beadchip (sentrix id): 6055432139_R02C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -4.24; cancer location: breast; icd information: Malignt neoplasm of overlapping sites of breast; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_45; age at blood sample: 62.89; gender: female; beadchip and order on beadchip (sentrix id): 6055432139_R03C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -4.24; ', 'tissue: peripheral blood; twin pair id: pair_20; age at blood sample: 67.58; gender: female; beadchip and order on beadchip (sentrix id): 6055432144_R05C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -2.74; cancer location: colon; icd information: Malignt neoplasm of rectum; histology: Mucin-producing adenocarcinoma; ', 'tissue: peripheral blood; twin pair id: pair_20; age at blood sample: 67.58; gender: female; beadchip and order on beadchip (sentrix id): 6055432144_R06C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -2.74; ', 'tissue: peripheral blood; twin pair id: pair_4; age at blood sample: 42.55; gender: female; beadchip and order on beadchip (sentrix id): 6055432155_R02C01; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -0.91; ', 'tissue: peripheral blood; twin pair id: pair_33; age at blood sample: 49.4; gender: female; beadchip and order on beadchip (sentrix id): 6055432155_R02C02; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 6.15; ', 'tissue: peripheral blood; twin pair id: pair_4; age at blood sample: 42.55; gender: female; beadchip and order on beadchip (sentrix id): 6055432155_R03C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -0.91; cancer location: cervix; icd information: Malignt neoplasm of endocervix; histology: Adenocarcinoma NOS; ', 'tissue: peripheral blood; twin pair id: pair_33; age at blood sample: 49.4; gender: female; beadchip and order on beadchip (sentrix id): 6055432155_R05C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 6.15; cancer location: breast; icd information: Malignt neoplasm of central portion of breast; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_18; age at blood sample: 59.6; gender: female; beadchip and order on beadchip (sentrix id): 6055432168_R01C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.98; cancer location: colon; icd information: Malignt neoplasm of rectosigmoid junction; histology: Adenocarcinoma NOS; ', 'tissue: peripheral blood; twin pair id: pair_18; age at blood sample: 59.6; gender: female; beadchip and order on beadchip (sentrix id): 6055432168_R03C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.98; ', 'tissue: peripheral blood; twin pair id: pair_13; age at blood sample: 50.3; gender: female; beadchip and order on beadchip (sentrix id): 6057825027_R06C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.6; ', 'tissue: peripheral blood; twin pair id: pair_13; age at blood sample: 50.3; gender: female; beadchip and order on beadchip (sentrix id): 6057825033_R01C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.6; cancer location: breast; icd information: Malignt neoplasm of breast of unspecified site; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_22; age at blood sample: 56.87; gender: female; beadchip and order on beadchip (sentrix id): 6057825040_R05C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.64; cancer location: breast; icd information: Malignt neoplasm of upper-outer quadrant of breast; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_22; age at blood sample: 56.87; gender: female; beadchip and order on beadchip (sentrix id): 6057825040_R06C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.64; ', 'tissue: peripheral blood; twin pair id: pair_24; age at blood sample: 68.13; gender: female; beadchip and order on beadchip (sentrix id): 6057825042_R02C02; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 2.09; ', 'tissue: peripheral blood; twin pair id: pair_24; age at blood sample: 68.13; gender: female; beadchip and order on beadchip (sentrix id): 6057825046_R06C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 2.09; cancer location: melanoma; icd information: Malignt melanoma of upper limb, including shoulder; histology: Malignt melanoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_2; age at blood sample: 71.5; gender: female; beadchip and order on beadchip (sentrix id): 6929742017_R01C02; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 2.08; ', 'tissue: peripheral blood; twin pair id: pair_1; age at blood sample: 62.6; gender: female; beadchip and order on beadchip (sentrix id): 6929742017_R02C02; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 12.85; ', 'tissue: peripheral blood; twin pair id: pair_1; age at blood sample: 62.6; gender: female; beadchip and order on beadchip (sentrix id): 6929742017_R03C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 12.85; cancer location: colon; icd information: Malignt neoplasm of splenic flexure; histology: Mucinous adenocarcinoma; ', 'tissue: peripheral blood; twin pair id: pair_25; age at blood sample: 78.7; gender: female; beadchip and order on beadchip (sentrix id): 6929742023_R03C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 3.87; cancer location: breast; icd information: Malignt neoplasm of breast of unspecified site; histology: Intraductal papillary adenocarcinoma with invasion; ', 'tissue: peripheral blood; twin pair id: pair_25; age at blood sample: 78.7; gender: female; beadchip and order on beadchip (sentrix id): 6929742023_R04C02; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 3.87; ', 'tissue: peripheral blood; twin pair id: pair_11; age at blood sample: 59.4; gender: female; beadchip and order on beadchip (sentrix id): 6929742053_R04C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -4.48; cancer location: colon; icd information: Malignt neoplasm of sigmoid colon; histology: Adenocarcinoma NOS; ', 'tissue: peripheral blood; twin pair id: pair_11; age at blood sample: 59.4; gender: female; beadchip and order on beadchip (sentrix id): 6929742053_R05C01; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -4.48; ', 'tissue: peripheral blood; twin pair id: pair_27; age at blood sample: 53.4; gender: female; beadchip and order on beadchip (sentrix id): 6929742055_R03C02; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 4.16; ', 'tissue: peripheral blood; twin pair id: pair_27; age at blood sample: 53.4; gender: female; beadchip and order on beadchip (sentrix id): 6929742055_R04C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 4.16; cancer location: colon; icd information: Malignt neoplasm of sigmoid colon; histology: Adenocarcinoma NOS; ', 'tissue: peripheral blood; twin pair id: pair_6; age at blood sample: 38.1; gender: female; beadchip and order on beadchip (sentrix id): 6929742055_R05C01; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 5.39; ', 'tissue: peripheral blood; twin pair id: pair_6; age at blood sample: 38.1; gender: female; beadchip and order on beadchip (sentrix id): 6929742055_R06C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 5.39; cancer location: breast; icd information: Malignt neoplasm of breast of unspecified site; histology: Carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_3; age at blood sample: 59.2; gender: female; beadchip and order on beadchip (sentrix id): 6929742058_R03C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 3.29; cancer location: breast; icd information: Malignt neoplasm of breast of unspecified site; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_21; age at blood sample: 65; gender: female; beadchip and order on beadchip (sentrix id): 6929742058_R06C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 8.32; cancer location: colon; icd information: Malignt neoplasm of sigmoid colon; histology: Adenocarcinoma NOS; ', 'tissue: peripheral blood; twin pair id: pair_26; age at blood sample: 67.9; gender: female; beadchip and order on beadchip (sentrix id): 6929742080_R03C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -3.34; cancer location: breast; icd information: Malignt neoplasm of central portion of breast; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_34; age at blood sample: 45.4; gender: female; beadchip and order on beadchip (sentrix id): 6929793004_R02C01; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -2.41; ', 'tissue: peripheral blood; twin pair id: pair_34; age at blood sample: 45.4; gender: female; beadchip and order on beadchip (sentrix id): 6929793004_R03C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -2.41; cancer location: breast; icd information: Malignt neoplasm of breast of unspecified site; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_36; age at blood sample: 77.7; gender: female; beadchip and order on beadchip (sentrix id): 6929793004_R04C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.64; ', 'tissue: peripheral blood; twin pair id: pair_36; age at blood sample: 77.7; gender: female; beadchip and order on beadchip (sentrix id): 6929793004_R05C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.64; cancer location: melanoma; icd information: Malignt melanoma of upper limb, including shoulder; histology: Superficial spreading melanoma; ', 'tissue: peripheral blood; twin pair id: pair_39; age at blood sample: 56; gender: female; beadchip and order on beadchip (sentrix id): 6929793024_R02C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -3.85; cancer location: breast; icd information: Malignt neoplasm of upper-outer quadrant of breast; histology: Tubular adenocarcinoma; ', 'tissue: peripheral blood; twin pair id: pair_39; age at blood sample: 56; gender: female; beadchip and order on beadchip (sentrix id): 6929793024_R03C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -3.85; ', 'tissue: peripheral blood; twin pair id: pair_41; age at blood sample: 58.3; gender: female; beadchip and order on beadchip (sentrix id): 6929793024_R04C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.89; cancer location: breast; icd information: Malignt neoplasm of breast of unspecified site; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_41; age at blood sample: 58.3; gender: female; beadchip and order on beadchip (sentrix id): 6929793024_R05C02; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.89; ', 'tissue: peripheral blood; twin pair id: pair_35; age at blood sample: 71.3; gender: female; beadchip and order on beadchip (sentrix id): 6929793033_R02C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -2.25; ', 'tissue: peripheral blood; twin pair id: pair_35; age at blood sample: 71.3; gender: female; beadchip and order on beadchip (sentrix id): 6929793033_R03C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -2.25; cancer location: gland_thyroid; icd information: Malignt neoplasm of thyroid gland; histology: Papillary adenocarcinoma; ', 'tissue: peripheral blood; twin pair id: pair_42; age at blood sample: 68.1; gender: female; beadchip and order on beadchip (sentrix id): 6929793055_R03C01; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.23; ', 'tissue: peripheral blood; twin pair id: pair_42; age at blood sample: 68.1; gender: female; beadchip and order on beadchip (sentrix id): 6929793055_R04C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.23; cancer location: pancreas; icd information: Malignt neoplasm of head of pancreas; histology: Carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_31; age at blood sample: 51.8; gender: female; beadchip and order on beadchip (sentrix id): 6929793055_R05C01; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.19; ', 'tissue: peripheral blood; twin pair id: pair_31; age at blood sample: 51.8; gender: female; beadchip and order on beadchip (sentrix id): 6929793055_R06C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.19; cancer location: breast; icd information: Malignt neoplasm of upper-inner quadrant of breast; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_30; age at blood sample: 61.1; gender: female; beadchip and order on beadchip (sentrix id): 6929793057_R01C01; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -4.37; ', 'tissue: peripheral blood; twin pair id: pair_32; age at blood sample: 59.9; gender: female; beadchip and order on beadchip (sentrix id): 6929793103_R01C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -4.78; cancer location: colon; icd information: Malignt neoplasm of sigmoid colon; histology: Adenocarcinoma NOS; ', 'tissue: peripheral blood; twin pair id: pair_32; age at blood sample: 59.9; gender: female; beadchip and order on beadchip (sentrix id): 6929793103_R06C01; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -4.78; ', 'tissue: peripheral blood; twin pair id: pair_40; age at blood sample: 61.1; gender: female; beadchip and order on beadchip (sentrix id): 6929793103_R06C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -0.84; ', 'tissue: peripheral blood; twin pair id: pair_12; age at blood sample: 62.2; gender: female; beadchip and order on beadchip (sentrix id): 6929793109_R01C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 3.73; cancer location: breast; icd information: Intraductal carcinoma in situ of breast; histology: Carcinoma in situ NOS; ', 'tissue: peripheral blood; twin pair id: pair_12; age at blood sample: 62.2; gender: female; beadchip and order on beadchip (sentrix id): 6929793109_R02C01; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 3.73; ', 'tissue: peripheral blood; twin pair id: pair_30; age at blood sample: 61.1; gender: female; beadchip and order on beadchip (sentrix id): 6929793109_R06C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -4.37; cancer location: colon; icd information: Malignt neoplasm of rectum; histology: Mucinous adenocarcinoma; ', 'tissue: peripheral blood; twin pair id: pair_15; age at blood sample: 69.7; gender: female; beadchip and order on beadchip (sentrix id): 6929793118_R05C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.46; ', 'tissue: peripheral blood; twin pair id: pair_15; age at blood sample: 69.7; gender: female; beadchip and order on beadchip (sentrix id): 6929793118_R06C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.46; cancer location: breast; icd information: Malignt neoplasm of breast of unspecified site; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_28; age at blood sample: 58.7; gender: female; beadchip and order on beadchip (sentrix id): 6929793124_R01C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -0.77; cancer location: colon; icd information: Malignt neoplasm of rectosigmoid junction; histology: Adenocarcinoma NOS; ', 'tissue: peripheral blood; twin pair id: pair_28; age at blood sample: 58.7; gender: female; beadchip and order on beadchip (sentrix id): 6929793124_R02C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -0.77; ', 'tissue: peripheral blood; twin pair id: pair_9; age at blood sample: 64.3; gender: female; beadchip and order on beadchip (sentrix id): 6929793124_R05C01; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.04; ', 'tissue: peripheral blood; twin pair id: pair_29; age at blood sample: 41.5; gender: female; beadchip and order on beadchip (sentrix id): 6929793124_R05C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -2.6; ', 'tissue: peripheral blood; twin pair id: pair_9; age at blood sample: 64.3; gender: female; beadchip and order on beadchip (sentrix id): 6929793124_R06C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.04; cancer location: breast; icd information: Malignt neoplasm of upper-outer quadrant of breast; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_29; age at blood sample: 41.5; gender: female; beadchip and order on beadchip (sentrix id): 6929793124_R06C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -2.6; cancer location: breast; icd information: Malignt neoplasm of breast of unspecified site; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_8; age at blood sample: 71.1; gender: female; beadchip and order on beadchip (sentrix id): 6929793126_R04C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.12; cancer location: colon; icd information: Malignt neoplasm of sigmoid colon; histology: Adenocarcinoma NOS; ', 'tissue: peripheral blood; twin pair id: pair_8; age at blood sample: 71.1; gender: female; beadchip and order on beadchip (sentrix id): 6929793126_R05C01; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.12; ', 'tissue: peripheral blood; twin pair id: pair_16; age at blood sample: 62.7; gender: female; beadchip and order on beadchip (sentrix id): 6929793137_R03C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.79; cancer location: breast; icd information: Malignt neoplasm of breast of unspecified site; histology: Neoplasm, malignt; ', 'tissue: peripheral blood; twin pair id: pair_16; age at blood sample: 62.7; gender: female; beadchip and order on beadchip (sentrix id): 6929793137_R04C01; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -1.79; ', 'tissue: peripheral blood; twin pair id: pair_37; age at blood sample: 70.3; gender: female; beadchip and order on beadchip (sentrix id): 6929793141_R01C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 1.95; cancer location: ovary; icd information: Malignt neoplasm of ovary; histology: Serous cystadenocarcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_37; age at blood sample: 70.3; gender: female; beadchip and order on beadchip (sentrix id): 6929793141_R02C01; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 1.95; ', 'tissue: peripheral blood; twin pair id: pair_5; age at blood sample: 58.6; gender: female; beadchip and order on beadchip (sentrix id): 6929793141_R04C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.35; cancer location: breast; icd information: Malignt neoplasm of lower-outer quadrant of breast; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_5; age at blood sample: 58.6; gender: female; beadchip and order on beadchip (sentrix id): 6929793141_R05C02; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.35; ', 'tissue: peripheral blood; twin pair id: pair_19; age at blood sample: 73.3; gender: female; beadchip and order on beadchip (sentrix id): 6929793167_R03C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 1.02; cancer location: breast; icd information: Malignt neoplasm of breast of unspecified site; histology: Infiltrating duct and lobular carcinoma; ', 'tissue: peripheral blood; twin pair id: pair_26; age at blood sample: 67.9; gender: female; beadchip and order on beadchip (sentrix id): 6929806004_R02C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -3.34; ', 'tissue: peripheral blood; twin pair id: pair_44; age at blood sample: 72.9; gender: female; beadchip and order on beadchip (sentrix id): 6929806011_R03C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -0.94; ', 'tissue: peripheral blood; twin pair id: pair_44; age at blood sample: 72.9; gender: female; beadchip and order on beadchip (sentrix id): 6929806011_R04C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -0.94; cancer location: breast; icd information: Malignt neoplasm of breast of unspecified site; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_7; age at blood sample: 44; gender: female; beadchip and order on beadchip (sentrix id): 6929806011_R05C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.1; cancer location: breast; icd information: Intraductal carcinoma in situ of breast; histology: Intraductal carcinoma, noninfiltrating; ', 'tissue: peripheral blood; twin pair id: pair_7; age at blood sample: 44; gender: female; beadchip and order on beadchip (sentrix id): 6929806011_R06C02; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.1; ', 'tissue: peripheral blood; twin pair id: pair_23; age at blood sample: 56.6; gender: female; beadchip and order on beadchip (sentrix id): 6929806049_R02C01; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 6.62; ', 'tissue: peripheral blood; twin pair id: pair_23; age at blood sample: 56.6; gender: female; beadchip and order on beadchip (sentrix id): 6929806049_R03C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 6.62; cancer location: breast; icd information: Malignt neoplasm of upper-outer quadrant of breast; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_40; age at blood sample: 61.1; gender: female; beadchip and order on beadchip (sentrix id): 6929806054_R01C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -0.84; cancer location: breast; icd information: Intraductal carcinoma in situ of breast; histology: Carcinoma in situ NOS; ', 'tissue: peripheral blood; twin pair id: pair_10; age at blood sample: 59.5; gender: female; beadchip and order on beadchip (sentrix id): 6929806054_R04C02; cancer status: healthy; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -2.07; ', 'tissue: peripheral blood; twin pair id: pair_10; age at blood sample: 59.5; gender: female; beadchip and order on beadchip (sentrix id): 6929806054_R05C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: After; age at diagnosis minus age at blood sampling: -2.07; cancer location: breast; icd information: Malignt neoplasm of overlapping sites of breast; histology: Lobular carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_21; age at blood sample: 65; gender: female; beadchip and order on beadchip (sentrix id): 6929806056_R01C02; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 8.32; ', 'tissue: peripheral blood; twin pair id: pair_19; age at blood sample: 73.3; gender: female; beadchip and order on beadchip (sentrix id): 6929806056_R05C02; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 1.02; ', 'tissue: peripheral blood; twin pair id: pair_3; age at blood sample: 59.2; gender: female; beadchip and order on beadchip (sentrix id): 6929806056_R06C01; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 3.29; ', 'tissue: peripheral blood; twin pair id: pair_14; age at blood sample: 50.7; gender: female; beadchip and order on beadchip (sentrix id): 6929806058_R04C01; cancer status: healthy; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.99; ', 'tissue: peripheral blood; twin pair id: pair_14; age at blood sample: 50.7; gender: female; beadchip and order on beadchip (sentrix id): 6929806058_R05C01; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 0.99; cancer location: breast; icd information: Malignt neoplasm of upper-outer quadrant of breast; histology: Infiltrating duct carcinoma, NOS; ', 'tissue: peripheral blood; twin pair id: pair_2; age at blood sample: 71.5; gender: female; beadchip and order on beadchip (sentrix id): 6929806078_R06C02; cancer status: cancer-diagnosis; age at blood sampling vs age at diagnosis: Before; age at diagnosis minus age at blood sampling: 2.08; cancer location: colon; icd information: Malignt neoplasm of colon, unspecified; histology: Adenocarcinoma NOS; ' GSE23610 Homo sapiens 24 Expression profiling by array GPL570 Gene expression profiles of MCF-7 cells treated with Si-Wu-Tang, estradiol and ferulic acid 2010-08-13 Traditional Chinese medicines (TCM), usually composed of a mixture of components, may simultaneously target multiple genes/pathways and thus achieve superior efficacy for complex diseases such as cancer. To identify novel mechanisms of action and potential health benefits for a TCM formula Si-Wu-Tang (SWT) widely used for women’s health, we obtained the DNA microarray expression profiles for SWT, its active component ferulic acid, and estradiol in human breast cancer cell line MCF-7 and analyzed the gene expression signatures associated with each treatment using the “Connectivity Map” (cMAP). This study indicates that DNA microarray profiling analysis and cMAP data mining provide a powerful approach to discover unknown mechanisms of actions and identify potential new health benefits for TCM. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23610 Discovery of molecular mechanisms of traditional Chinese medicinal formula Si-Wu-Tang using gene expression microarray and connectivity map. PloS one 2.776 https://doi.org/10.1371/journal.pone.0018278 {PloS one (2.776): 10.1371/journal.pone.0018278} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA129951 https://www.ebi.ac.uk/ena/browser/view/PRJNA129951 None [Overal design]We profiled the gene expression of MCF-7 cell lines to SWT, its active component FA, as well as estradiol using Affymetrix human genome U133 plus 2.0 arrays. The data set includes profiles for 24 samples, divided into eight groups of treatment: 0.001% DMSO used as the vehicle control (C), 0.1 µM estradiol (EM), FA at three concentrations (0.1, 1, and 10 µM) (FL, FM and FH) and SWT at three concentrations (0.0256, 0.256, and 2.56 mg/ml) (SL, SM and SH). For each treatment group, 3 biological replicates were included, resulting in 24 (8 groups × 3 replicates/group) RNA samples.; [Treatment]'The MCF-7 cells were incubated with hormone free medium and treated by 0.001% DMSO (control group), 0.1 µM 17 β-estradiol, 0.1, 1 or 10 µM of ferulic acid (equivalent to 0.0194, 0.194, and 1.94 mg/ml), 0.0256, 0.256, and 2.56 mg/ml SWT for 6 hours.'; [Growth]'The MCF-7 cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% fetal bovine serum (FBS), 1% non-essential amino acids, 100 unit/mL penicillin, 100 μg/mL streptomycin, 1 mM sodium pyruvate, and 2 mM L-glutamine in an atmosphere of 5% CO2 at 37 °C.'; [Extraction]'RNA was extracted using QIAGEN RNeasy Mini Kit, following the manufacturer’s protocol.'; [Cell type]'Source: ''cell line: breast cancer cell line MCF-7; treatment: DMSO treated; ', 'cell line: breast cancer cell line MCF-7; treatment: Estradiol treated; ', 'cell line: breast cancer cell line MCF-7; treatment: Ferulic acid treated; ', 'cell line: breast cancer cell line MCF-7; treatment: Si-Wu-Tang treated; ' GSE26998 Homo sapiens 8 Expression profiling by array GPL201 HSD17B14 induction in breast cancer cell lines 2011-02-01 The 17beta-hydroxy steroid dehydrogenase family is involved in the fine tuning of conversion of different substances such as steroids, retenoids and fatty acids. The expression of HSD17B14 has been correlated to better prognosis in breast cancer. The function of HSD17B14 is still not known, but it may convert estradiol to estrone. We transfected breast cancer cell lines with a HSD17B14-containing plasmid and compared with mock-transfected samples. The influence on global gene expression was examined with microarrays. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26998 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA136939 https://www.ebi.ac.uk/ena/browser/view/PRJNA136939 None [Overal design]The breast cancer cell lines SKBR3 and ZR75-1 were transfected with a HSD17B14-containing plasmid or a plasmid without insertion as control. This was performed in duplicates. The cells were harvested after 48 hours, and RNA was extracted and hybridized on Affymetrix microarrays.; [Treatment]'Twenty-four hours after seeding, the cells were transfected with a HSD17B14-plasmid, using FuGene-6 transfection reagent . Control cells were incubated with the same amount of a vector missing the HSD17B14 insert. 48 hours after transfection, cells were harvested and immediately prepared for RNA isolation.'; [Growth]'Breast cancer cell lines SKBR3 and ZR75-1 were cultured in phenol-red free Optimem-I supplemented with 4% foetal bovine serum and incubated at 37°C in 5% CO2.'; [Extraction]"RNA was prepared using Trizol following the manufacturer's instructions. RNA was cleaned using the RNeasy MinElute Cleanup Kit according to the manufacturer’s protocol. RNA preparations were thereafter quantified and qualitatively evaluated using the Agilent 2100 Bioanalyzer."; [Cell type]'breast cancer''cell line: ZR75-1; cell type: breast cancer; er status: ER +; transfection: HSD17B14; ', 'cell line: ZR75-1; cell type: breast cancer; er status: ER +; transfection: mock; ', 'cell line: SKBR3; cell type: breast cancer; er status: ER -; transfection: HSD17B14; ', 'cell line: SKBR3; cell type: breast cancer; er status: ER -; transfection: mock; ' GSE155688 Homo sapiens 6 Expression profiling by high throughput sequencing GPL18573 CCM3 is a gatekeeper in focal adhesions regulating mechanotransduction and YAP/TAZ signalling 2020-08-04 We report that loss of CCM3/PDCD10 in fibroblasts induces FAK/Src-paxillin signalling driving actomyosin-dependent mechanotransduction leading to YAP/TAZ signalling. In vivo, loss of CCM3 in fibroblasts drives excessive tissue remodelling leading to the dissemination of breast cancer cells to distant organs. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE155688 CCM3 is a gatekeeper in focal adhesions regulating mechanotransduction and YAP/TAZ signalling. Nature cell biology 17.728 https://doi.org/10.1038/s41556-021-00702-0 {Nature cell biology (17.728): 10.1038/s41556-021-00702-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA655226 https://www.ebi.ac.uk/ena/browser/view/PRJNA655226 https://www.ncbi.nlm.nih.gov/sra?term=SRP275829 [Overal design]Examination of the varying RNA levels in control human vulval cancer-associated fibroblasts versus CCM3-depleted cells; [Treatment]'Cells were transfected using Dharmafect 4 reagent for siControl (Ctr) and siCCM3 (PDCD10).'; [Growth]'Cells were maintained in DMEM high glucose with 10% FBS, 1% Pen-strep, and insulin-tranferrin-selenium supplement, at 37℃, 5% CO2.'; [Extraction]'Cells were harvested 72 hours post-transfection using RNeasy kit (Qiagen) and treated with DNase I.\nLibrary was prepared according to TruSeq® Stranded mRNA Sample Preparation Guide (Part # 15031047 Rev.\xa0E) Modification of “Enrich DNA Fragment” step: from 15 to 13 PCR cycles.'; [Cell type]'Human vulval carcinoma-associated fibroblasts, hTERT-immortalised''cell type: Human vulval carcinoma-associated fibroblasts, hTERT-immortalised; sirna: siCCM3; genotype/variation: CCM3-depleted; ', 'cell type: Human vulval carcinoma-associated fibroblasts, hTERT-immortalised; sirna: siControl; genotype/variation: control; ' GSE9483 Homo sapiens 13 Expression profiling by array GPL6071 Molecular Profiling of BRCA1-and BRCA2-associated Breast Cancers 2007-10-31 Molecular Profiling of BRCA1-and BRCA2-associated Breast Cancers Identifies FGFR2 as a Gene More Highly Expressed in BRCA2-associated Tumors BRCA1- and BRCA2-associated tumors have many morphologic characteristics in common, but appear to have distinct molecular signatures. BRCA1-associated tumors are predominantly basal-like cancers, whereas BRCA2-associated tumors have a predominant luminal-like phenotype. These two molecular signatures reflect in part the two cell types, basal/myoepithelial and luminal, found in the terminal duct lobular unit of the breast. To elucidate novel genes involved in these two spectra of breast cancer tumorigenesis we performed global gene expression analysis on breast tumors from germline BRCA1 and BRCA2 mutation carriers. Breast tumor RNAs from 7 germline BRCA1 and 6 germline BRCA2 carriers were profiled using UHN human 19K cDNA microarrays. Supervised univariate analyses were conducted to identify genes differentially expressed between BRCA1 and BRCA2-associated tumors. Selected discriminatory genes were validated using real time reverse transcription polymerase chain reaction (RT-PCR) in the tumor RNAs, and/or by immunohistochemistry (IHC) or by in situ hybridization (ISH) on tissue microarrays (TMAs) containing an independent set of 58 BRCA1 and 64 BRCA2-associated tumors. Genes more highly expressed in BRCA1-associated tumors included stathmin/oncoprotein 18, osteopontin, TGFß2 and Jagged 1 in addition to genes previously identified as characteristic of basal-like breast cancers. Genes more highly expressed in BRCA2-associated tumors had functions related to transcription, signal transduction (particularly MAPK signaling), cell proliferation, cell adhesion and extracellular matrix remodeling. BRCA2-associated cancers were characterized by the higher relative expression of amongst others, FGF1 and FGFR2. Tissue microarrays were used to validate the expression of FGFR2 protein by immunohistochemistry and Jagged 1 expression by in situ hybridization. BRCA2-associated cancers expressed higher levels of FGFR2 protein than BRCA1-associated cancers (p=0.004); whereas BRCA1-associated tumors exhibited elevated levels of Jagged1 mRNA compared to BRCA2-associated cancers (p=0.02). FGFR2 and FGF1 were more highly expressed in BRCA2-associated cancers compared with BRCA1-associated breast cancers, suggesting the existence of an autocrine or paracrine stimulatory loop. In addition to corroborating the basal-like signature of BRCA1-associated tumors, we identified osteopontin, stathmin/oncoprotein 18, TGFβ2, and Jagged 1 as being more highly expressed in BRCA1-associated tumors. Keywords: Gene expression profiling, genetic comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE9483 Expression profiling of familial breast cancers demonstrates higher expression of FGFR2 in BRCA2-associated tumors. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-008-0087-1 {Breast cancer research and treatment (3.471): 10.1007/s10549-008-0087-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA103261 https://www.ebi.ac.uk/ena/browser/view/PRJNA103261 None [Overal design]13 tumor samples: 7 BRCA1 and 6 BRCA2, no replicates, there is a reference sample, 2 dye-swaps for the tumor samples 1693-BRCA1 and 4324-BRCA2); [Treatment]'None'; [Growth]'None'; [Extraction]'RNA Extraction & Reverse Transcription: Total RNA from flash-frozen tumor samples was extracted using Trizol according to manufacturer’s instructions (Life Technologies). The purity of RNA was confirmed by A260/A280 ratio of 1.8-2.2, while the integrity of RNA was verified by 1% agarose gel electrophoresis. RNA from each tumor sample, as well as reference RNA that is composed of 13 pooled cell lines, were reverse-transcribed to generate complementary DNA. In brief, 5 μg of mRNA was first combined with 1.5 μl of 100 pmol/μl AncT mRNA primer (Qiagen), 8 μl of 5x first strand buffer, and 4 μl of 100 mM DTT, to a total volume of 34.35 μl, and incubated at 65oC for 5 minutes, followed by 47oC for 5 minutes. While at 47oC, the following reagents were added to each of the reaction and were incubated for two hours: 1 μl of dGTP, dATP, dCTP mix (20 mM each), 1.3 μl of 5mM dTTP, 1.35 μl of 10 mM aa-dUTP, 2 μl of 200 units/μl superscript III reverse transcriptase (Invitrogen), in a total volume of 40 μl. Each of the reactions were stopped and hydrolyzed by adding 4 μl of 50 mM EDTA and 2 μl of 10N NaOH and incubated at 65oC for 20 minutes, followed by neutralization with the addition of 4 μl of 5 M acetic acid. Reaction purifications were performed using PCR purification kit (Qiagen) to remove all traces of tris, thus preventing reaction of the amine groups on tris with monofunctional NHS-ester of the Cyanine dye. Samples were then vacuumed-dried, and stored at –20oC until ready for labeling.'; [Cell type]'Source: ''Mutation: 5382insC; type: Ductal and No special type; agedx: 44; grade: 3; Lymphatic Invasion: no; ER: equivocal; PR: positive; ', 'NTERA-2 (Human testis cancer teratoma derived cell line), Hs578T (Human breast carcinosarcoma), HepG2 (Human Hepatoblastoma), Ht1080 (Human Fibrosarcoma), SW872 (Human Liposarcoma), T47D (Human mammary gland ductal carcinoma derived from pleural effusion), MCF-12A (Human mammary gland: epithelial mucin), Fetal Normal Muscle Cells, Colo-205 (Human colorectal adenocarcinoma), MOLT-4 (Human T lymphoblast acute lymphoblastic leukemia), RPMI 8226 (Human plasmocytoma myeloma), SK-MEL-28 (Human skin. Malignant melanoma) ,SKOV3 (Human ovary adenocarcinoma); ', 'Mutation: 5293delAAAG; type: Ductal and No special type; agedx: 30; grade: 3; Lymphatic Invasion: yes; ER: negative; PR: not available; ', 'Mutation: 6174delT; type: Ductal and No special type; agedx: 46; grade: 3; Lymphatic Invasion: yes; ER: positive; PR: positive; ', 'Mutation: 4603G-T; type: Ductal and No special type; agedx: 33; grade: 3; Lymphatic Invasion: not available; ER: negative; PR: positive; ', 'Mutation: 185delAG; type: Ductal and No special type; agedx: 32; grade: 3; Lymphatic Invasion: yes; ER: negative; PR: equivocal; ', 'Mutation: 6764insA; type: Ductal and No special type; agedx: 75; grade: 3; Lymphatic Invasion: yes; ER: positive; PR: equivocal; ', 'Mutation: 2457C-T; type: Ductal and No special type; agedx: 50; grade: 3; Lymphatic Invasion: no; ER: negative; PR: negative; ', 'Mutation: 9132delC; type: Ductal and No special type; agedx: 34; grade: 3; Lymphatic Invasion: yes; ER: positive; PR: positive; ', 'Mutation: 185delAG; type: Ductal and No special type; agedx: 40; grade: 3; Lymphatic Invasion: no; ER: equivocal; PR: positive; ', 'Mutation: 8765delAG; type: Ductal and No special type; agedx: 44; grade: 3; Lymphatic Invasion: present; ER: negative; PR: positive; ', 'Mutation: 185delAG; type: Ductal and No special type; agedx: 35; grade: 3; Lymphatic Invasion: no; ER: not available; PR: negative; ', 'Mutation: 8765delAG; type: Ductal and No special type; agedx: 58; grade: 3; Lymphatic Invasion: yes; ER: negative; PR: negative; ', 'Mutation: IVS16+3 A-C; type: Ductal and No special type; agedx: 44; grade: 3; Lymphatic Invasion: no; ER: negative; PR: negative; ' GSE8871 Homo sapiens 8 Expression profiling by array GPL887 Human Breast Cancer Cell Lines: Control vs. Fn14 or Luciferase siRNA Treated 2007-08-24 We performed gene expression profiling on the MDA-MB-231 and MDA-MB-436 human breast cancer cell lines following siRNA-mediated inhibition of Fn14 expression as an approach to identify the mechanistic basis for Fn14 regulation of invasive capacity. Keywords: siRNA-mediated inhibition https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE8871 The fibroblast growth factor-inducible 14 receptor is highly expressed in HER2-positive breast tumors and regulates breast cancer cell invasive capacity. Molecular cancer research : MCR 4.484 https://doi.org/10.1158/1541-7786.MCR-08-0005 {Molecular cancer research : MCR (4.484): 10.1158/1541-7786.MCR-08-0005} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA102239 https://www.ebi.ac.uk/ena/browser/view/PRJNA102239 None [Overal design]Each cell lines was transfected with etiher an Fn14 or firefly luciferase-specific (GL2) siRNA, with untreated cells used as a reference. 2 biological replicates were performed for each array, independently grown, treated and harvested.; [Treatment]'Both Fn14 and GL2 siRNA were transfected at a concentration of 60 nmol/L using Lipofectamine 2000 (Invitrogen). Cells were then incubated for 16hrs prior to lysate collection.'; [Growth]'Both cell lines were grown at 37ºC with constant humidity and 5% CO2 using RPMI-1640 media supplimented with 10% fetal bovine serum (Invitrogen).'; [Extraction]'Total RNA was collected in Trizol and exctrated using the Qiagen Rneasy mini kit.'; [Cell type]'Source: ''' GSE148623 Homo sapiens 43 Expression profiling by high throughput sequencing GPL16791; GPL24676 Network-based assessment of HDAC6 activity is highly predictive of pre-clinical and clinical responses to the HDAC6 inhibitor ricolinostat [high throughput sequencing] 2020-04-14 Despite the anticancer activity of pan-histone deacetylase (HDAC) inhibitors, their clinical use has been limited due to toxicity. However, the development of more specific inhibitors that selectively inhibit individual HDACs is emerging as a novel and well-tolerated alternative. Here, we present the results of the first clinical trial evaluating the activity of ricolinostat (the leading HDAC6 inhibitor) in breast cancer (BC) patients. We have developed a computational network-based algorithm to evaluate the activity of the HDAC6 protein, based on the enrichment of its transcriptional targets in differentially expressed genes (HDAC6 score). Through preclinical in vitro and in vivo studies, we confirmed that the HDAC6 score can stratify the sensitivity of BC cells to ricolinostat treatment and may thus have value as a predictive biomarker. Moreover, analysis of ~3,000 primary human breast cancers showed that ~30% of them present high HDAC6 scores. Based on these results, we designed a phase Ib clinical trial to evaluate the activity of ricolinostat plus nab-paclitaxel in metastatic BC patients. Study results showed that the two agents can be safely combined, that clinical activity is identified specifically in patients with HR+/HER2- disease, and that the HDAC6 score was predictive of response. Expansion of our analysis to other tumor types identified multiple cohorts enriched in high HDAC6 score samples. These results suggest that the HDAC6 score may provide an effective predictive biomarker of ricolinostat sensitivity in multiple human cancers. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148623 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA625217 https://www.ebi.ac.uk/ena/browser/view/PRJNA625217 https://www.ncbi.nlm.nih.gov/sra?term=SRP256322 [Overal design]Gene expression profiles of 1) 10 formalin fixed parafilm embedded biopsy samples from 10 patients of ductal breast cancer who were treated with HDAC6 inhibitor ricolinostat; and 2) 4 breast cancer cell lines treated by ricolinostat for 6 hours and 24 hours and by tunicamycin for 18 hours.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted from 11 ductal breast cancer tissues and 32 breast cancer cell line samples. Ribosomal RNA were further removed.\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'Source: ''tissue: ductal breast cancer; subtype: HR+/HER2-; response: Non-responder; progression-free survival indicator: 1; progression-free survival: 2.53 months; ', 'tissue: ductal breast cancer; subtype: HR+/HER2-; response: Responder; progression-free survival indicator: 0; progression-free survival: 5.03 months; ', 'tissue: ductal breast cancer; subtype: TNBC; response: Non-responder; progression-free survival indicator: 1; progression-free survival: 1.84 months; ', 'tissue: ductal breast cancer; subtype: TNBC; response: Non-responder; progression-free survival indicator: 1; progression-free survival: 1.08 months; ', 'tissue: ductal breast cancer; subtype: TNBC; response: Responder; progression-free survival indicator: 1; progression-free survival: 20.28 months; ', 'tissue: ductal breast cancer; subtype: HR+/HER2-; response: Responder; progression-free survival indicator: 1; progression-free survival: 11.41 months; ', 'tissue: ductal breast cancer; subtype: HR+/HER2-; response: Responder; progression-free survival indicator: 1; progression-free survival: 6.51 months; ', 'tissue: ductal breast cancer; subtype: HR+/HER2-; response: Responder; progression-free survival indicator: 1; progression-free survival: 4.47 months; ', 'tissue: ductal breast cancer; subtype: HR+/HER2-; response: Responder; progression-free survival indicator: 0; progression-free survival: 2.76 months; ', 'tissue: ductal breast cancer; subtype: HR+/HER2-; response: Responder; progression-free survival indicator: 1; progression-free survival: 5.19 months; ', 'cell line: MDA-MB-453; subtype: Luminal; response: Sensitive; treatment: Vehicle; ', 'cell line: MDA-MB-453; subtype: Luminal; response: Sensitive; treatment: Ricolinostat; time: 6hrs; ', 'cell line: MDA-MB-453; subtype: Luminal; response: Sensitive; treatment: Ricolinostat; time: 24hrs; ', 'cell line: MDA-MB-453; subtype: Luminal; response: Sensitive; treatment: Tunicamycin; time: 18hrs; ', 'cell line: SK-BR-3; subtype: Luminal; response: Sensitive; treatment: Vehicle; ', 'cell line: SK-BR-3; subtype: Luminal; response: Sensitive; treatment: Ricolinostat; time: 6hrs; ', 'cell line: SK-BR-3; subtype: Luminal; response: Sensitive; treatment: Ricolinostat; time: 24hrs; ', 'cell line: SK-BR-3; subtype: Luminal; response: Sensitive; treatment: Tunicamycin; time: 18hrs; ', 'cell line: MDA-MB-436; subtype: Basal B; response: Resistant; treatment: Vehicle; ', 'cell line: MDA-MB-436; subtype: Basal B; response: Resistant; treatment: Ricolinostat; time: 6hrs; ', 'cell line: MDA-MB-436; subtype: Basal B; response: Resistant; treatment: Ricolinostat; time: 24hrs; ', 'cell line: MDA-MB-436; subtype: Basal B; response: Resistant; treatment: Tunicamycin; time: 18hrs; ', 'cell line: MDA-MB-468; subtype: Basal A; response: Resistant; treatment: Vehicle; ', 'cell line: MDA-MB-468; subtype: Basal A; response: Resistant; treatment: Ricolinostat; time: 6hrs; ', 'cell line: MDA-MB-468; subtype: Basal A; response: Resistant; treatment: Ricolinostat; time: 24hrs; ', 'cell line: MDA-MB-468; subtype: Basal A; response: Resistant; treatment: Tunicamycin; time: 18hrs; ' GSE134876 Homo sapiens 8 Expression profiling by high throughput sequencing GPL11154 Reciprocal regulation of EGR1 and EZH2 in breast cancer cells 2019-07-25 We found that EGR1 stimulates the expression of EZH2, which in turn inhibited the expression of EGR1 through a silencer region and deletion of the silencer resulted in upregulation of EGR1, which reduced the malignancy of breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE134876 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA556677 https://www.ebi.ac.uk/ena/browser/view/PRJNA556677 https://www.ncbi.nlm.nih.gov/sra?term=SRP216394 [Overal design]RNA sequencing of MDA-MB-231 and MCF-7 with wildtype and silencer knockout. Two clones of silencer knockout were included.; [Treatment]'We used CRISPR-Cas9 system to delete 1780 bp fragment of the silencer region and transfected the PX459-sgRNAs to MDA-MB-231 and MCF-7 cells. After 48h, the cells were selected with 1ug/ml puromacin to get positive clones.'; [Growth]'MDA-MB-231 and MCF-7 cells were cultured at 37 °C in DMEM supplemented with 10% fetal bovine serum (Invitrogen) in an incubator with 5% CO2.'; [Extraction]'Cells were harvested at desired time points for total RNA isolation using RNeasy Mini kit (Qiagen).\nRNA-seq library was prepared using the VAHTS Total RNA-seq (H/M/R) Library Prep Kit for Illumina.'; [Cell type]'Source: ''strain: MCF-7; genotype: WT; ', 'strain: MCF-7; genotype: Silencer KO; ', 'strain: MDA-MB-231; genotype: WT; ', 'strain: MDA-MB-231; genotype: Silencer KO; ' GSE31003 Homo sapiens 20 Expression profiling by array GPL4133 FOXA1 actively represses the molecular phenotype of basal breast cancers. 2011-07-27 Breast cancer is a heterogeneous disease comprised of at least five major subtypes. Luminal subtype tumors confer a more favorable patient prognosis, which is in part, attributed to the Estrogen Receptor-α (ER) positivity and anti-hormone responsiveness of these tumors. Expression of the forkhead box transcription factor, FOXA1, also correlates with the luminal subtype and patient survival, but is present in a subset of ER-negative tumors. Similarly, FOXA1 is consistently expressed in luminal breast cancer cell lines even in the absence of ER. In contrast, basal breast cancer cell lines do not express FOXA1, and loss of FOXA1 in luminal cells increases migration and invasion, characteristics of the basal subtype. To delineate an ER-independent role for FOXA1 in maintaining the luminal phenotype, and hence a more favorable prognosis, we performed cDNA microarray analyses on luminal FOXA1-positive, ER-positive (MCF7, T47D) and FOXA1-positive, ER-negative (MDA-MB-453, SKBR3) cell lines in the presence or absence of transient FOXA1 silencing. This resulted in three FOXA1 transcriptomes: (1) a luminal-signature (consistent across cell lines), (2) an ER-positive signature (restricted to MCF7 and T47D) and (3) an ER-negative signature (restricted to MDA-MB-453 and SKBR3). Use of Gene Set Enrichment Analyses (GSEA) as a phenotyping tool revealed that FOXA1 silencing resulted in a transcriptome shift from luminal to basal gene expression signatures. FOXA1 binds to both luminal and basal genes within luminal breast cancer cells, suggesting that it not only transactivates luminal genes, but also represses basal-associated genes. From these results we conclude that FOXA1 controls plasticity between basal and luminal cells, playing a dominant role in repressing the basal phenotype, and thus tumor aggressiveness, in luminal breast cancer cells. Although it has been proposed that FOXA1-targeting agents may be useful for treating luminal tumors, these data suggest that this approach may promote transitions toward a more aggressive cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE31003 FOXA1 represses the molecular phenotype of basal breast cancer cells. Oncogene 6.634 https://doi.org/10.1038/onc.2012.62 {Oncogene (6.634): 10.1038/onc.2012.62} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA146339 https://www.ebi.ac.uk/ena/browser/view/PRJNA146339 None [Overal design]FOXA1 siRNA treated breast cell lines compared directly to nonspecific siRNA treated cell lines using Agilent 4X44 microarrays.; [Treatment]'None'; [Growth]'All cell lines were obtained from ATCC. MCF7 and MDA-MB-453 cells were grown in DMEM (Mediatech); T47D cells in RPMI 1640 (Gibco); SKBR3 cells in McCoy’s 5A (Sigma). Media was supplemented with 10% FBS and 1% Penicillin-Streptamycin (Invitrogen). Cells were seeded in 100 mm dishes to be 30-50% confluent upon transfection. siRNA targeting firefly luciferase mRNA (siCONTROL Non-targeting siRNA #2, Dharmacon, herein described as NT) or human FOXA1 mRNA (siGENOME M-010319-01 and -04, Dharmacon) were transfected in OPTI-MEM media (Invitrogen) using Lipfectamine 2000 (Invitrogen) to a final concentration of 100 nM. Culture media was changed to complete growth medium after 24 hours. Cells were harvested at 36 or 72 hours post-transfection.'; [Extraction]'Total RNA was isolated using TRIzol Reagent (Invitrogen), treated with DNAse I (DNA-free, Ambion), and cDNA produced using SuperScript II Reverse Transcriptase (Invitrogen).'; [Cell type]'Source: ''cell line: MCF7; tissue: breast cancer cell line; treatment: Non-targeting siRNA for 36hrs; ', 'cell line: MCF7; tissue: breast cancer cell line; treatment: FOXA1 siRNA for 36hrs; ', 'cell line: MCF7; tissue: breast cancer cell line; treatment: Non-targeting siRNA for 72hrs; ', 'cell line: MCF7; tissue: breast cancer cell line; treatment: FOXA1 siRNA for 72hrs; ', 'cell line: T47D; tissue: breast cancer cell line; treatment: Non-targeting siRNA for 36hrs; ', 'cell line: T47D; tissue: breast cancer cell line; treatment: FOXA1 siRNA for 36hrs; ', 'cell line: T47D; tissue: breast cancer cell line; treatment: Non-targeting siRNA for 72hrs; ', 'cell line: T47D; tissue: breast cancer cell line; treatment: FOXA1 siRNA for 72hrs; ', 'cell line: MB453; tissue: breast cancer cell line; treatment: Non-targeting siRNA for 36hrs; ', 'cell line: MB453; tissue: breast cancer cell line; treatment: FOXA1 siRNA for 36hrs; ', 'cell line: MB453; tissue: breast cancer cell line; treatment: Non-targeting siRNA for 72hrs; ', 'cell line: MB453; tissue: breast cancer cell line; treatment: FOXA1 siRNA for 72hrs; ', 'cell line: SKBR3; tissue: breast cancer cell line; treatment: Non-targeting siRNA for 36hrs; ', 'cell line: SKBR3; tissue: breast cancer cell line; treatment: FOXA1 siRNA for 36hrs; ', 'cell line: SKBR3; tissue: breast cancer cell line; treatment: Non-targeting siRNA for 72hrs; ', 'cell line: SKBR3; tissue: breast cancer cell line; treatment: FOXA1 siRNA for 72hrs; ' GSE58845 Homo sapiens 2 Non-coding RNA profiling by array GPL16593 miRNA profiling of MCF7 autocrine hGH 2014-06-26 MicroRNAs are widely expressed in the normal pubertal mammary gland and orchestrate mammary gland development by regulating cell proliferation, differentiation, apoptosis, and metabolism. Although human Growth hormone(hGH) plays fundamental roles in normal mammary gland development and elevated autocrine hGH levels have been documented to contribute to breast cancer, whether hGH should influence the expression pattern and the functional roles of miRNAs in this context remain unknown.This study explores the effects of autocrine hGH on microRNA expression in MCF7 cell. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58845 Autocrine/Paracrine Human Growth Hormone-stimulated MicroRNA 96-182-183 Cluster Promotes Epithelial-Mesenchymal Transition and Invasion in Breast Cancer. The Journal of biological chemistry 4.106 https://doi.org/10.1074/jbc.M115.653261 {The Journal of biological chemistry (4.106): 10.1074/jbc.M115.653261} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA253691 https://www.ebi.ac.uk/ena/browser/view/PRJNA253691 None [Overal design]MCF7 cells with stably integrated hGH and Mut hGH were cultured for a total of 24 h in serum-free medium before processing for RNA preparation. Total miRNA was isolated, labeled and hybridized to the miRNA microarray as described by the manufacturer (Invitrogen). The hybridized slides were then analyzed on a GenePix scanner.; [Treatment]'MCF-MUT and MCF-hGH were cultured for a total of 24 h in serum-free medium before processing for RNA preparation.'; [Growth]'MCF7-MUT and MCF7-hGH were cultured at 37 °C in 5% CO2 in completed RPMI-1640 medium supplemented with 10% heat-inactivated fetal bovine serum.'; [Extraction]'The total RNA and miRNA was isolated from cells by using the TRIzol Reagent (Life Technologies) and mirVana(TM) Isolation Kit (Invitrogen).'; [Cell type]'Breast cancer''cell line: MCF7; cell type: Breast cancer; transfection: pMT-MUT hGH; ', 'cell line: MCF7; cell type: Breast cancer; transfection: pMT-hGH; ' GSE131027 Homo sapiens 92 Expression profiling by array GPL570 High frequency of pathogenic germline variants in genes associated with homologous recombination repair in patients with advanced solid cancers 2019-05-10 We identified pathogenic and likely pathogenic variants in 17.8% of the patients within a wide range of cancer types. In particular, mesothelioma, ovarian cancer, cervical cancer, urothelial cancer, and cancer of unknown primary origin displayed high frequencies of pathogenic variants. In total, 22 BRCA1 and BRCA2 germline variant were identified in 12 different cancer types, of which 10 (45%) variants were not previously identified in these patients. Pathogenic germline variants were predominantly found in DNA repair pathways; approximately half of the variants were within genes involved in homologous recombination repair. Loss of heterozygosity and somatic second hits were identified in several of these genes, supporting possible causality for cancer development. A potential treatment target based on pathogenic germline variant could be suggested in 25 patients (4%). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131027 High frequency of pathogenic germline variants within homologous recombination repair in patients with advanced cancer. NPJ genomic medicine 4.422 https://doi.org/10.1038/s41525-019-0087-6 {NPJ genomic medicine (4.422): 10.1038/s41525-019-0087-6} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA542341 https://www.ebi.ac.uk/ena/browser/view/PRJNA542341 None [Overal design]investigation of expression features related to Class 4 and 5 germline mutations in cancer patients; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen manufactures procedure automatized on QiaCube for DNA and RNA isolation. RNA quality and quantity was controled by BioAnalyzer and Nanodrop.'; [Cell type]'Source: ''tissue: tumor biopsy; cancer: Breast cancer; mutated gene: ATR; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: FAN1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: ERCC3; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Bile duct cancer; mutated gene: FANCD2; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Mesothelioma; mutated gene: BAP1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Urothelial cancer; mutated gene: DDB2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Pancreatic cancer; mutated gene: TP53; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Melanoma; mutated gene: ATM; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: CHEK1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Breast cancer; mutated gene: BRCA1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: WRN; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Hepatocellular carcinoma; mutated gene: CHEK2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Ovarian cancer; mutated gene: BRCA2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Mesothelioma; mutated gene: BRCA2; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Cervical cancer; mutated gene: XPC; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Mesothelioma; mutated gene: FANCD2; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Pancreatic cancer; mutated gene: PALB2; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Head and Neck cancer; mutated gene: ABRAXAS1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: CHEK2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: BRCA2; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Sarcoma; mutated gene: WRN; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: CHEK2; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Cervical cancer; mutated gene: NBN; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Pancreatic cancer; mutated gene: BLM; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Prostate cancer; mutated gene: BRCA2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: FAM111B; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Adenoid cystic carcinoma; mutated gene: BRCA1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Head and Neck cancer; mutated gene: FANCA; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Sarcoma; mutated gene: CHEK1; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Ovarian cancer; mutated gene: BRCA1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Mesothelioma; mutated gene: FANCA; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Pancreatic cancer; mutated gene: MLH1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Ovarian cancer; mutated gene: BRCA2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: NSCLC; mutated gene: CHEK2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Ovarian cancer; mutated gene: ATM; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Bile duct cancer; mutated gene: BRIP1; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: CHEK2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Oesophageal cancer; mutated gene: ATM; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Breast cancer; mutated gene: BRCA2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Breast cancer; mutated gene: BRCA2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Thymoma; mutated gene: BLM; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Bile duct cancer; mutated gene: ATM; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Breast cancer; mutated gene: BRCA2; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Others; mutated gene: IPMK; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Breast cancer; mutated gene: CHEK1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Urothelial cancer; mutated gene: BRCA2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Breast cancer; mutated gene: CHEK2; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: CUP; mutated gene: RECQL; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Breast cancer; mutated gene: FAN1; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Pancreatic cancer; mutated gene: RAD50; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Mesothelioma; mutated gene: FANCM; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: BLM; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Ovarian cancer; mutated gene: ATR; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Melanoma; mutated gene: BAP1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Bile duct cancer; mutated gene: BRCA1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Sarcoma; mutated gene: XPC; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: NSCLC; mutated gene: NBN; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Cervical cancer; mutated gene: XPC; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Urothelial cancer; mutated gene: GALNT12; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Breast cancer; mutated gene: SMAD9; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Breast cancer; mutated gene: ERCC2; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: FANCD2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: BRIP1; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Renal cell carcinoma; mutated gene: CHEK2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: BLM; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Mesothelioma; mutated gene: FANCC; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Gastric cancer; mutated gene: GALNT12; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: CUP; mutated gene: BRCA2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: NF1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Renal cell carcinoma; mutated gene: SEC23B; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Pancreatic cancer; mutated gene: FANCM; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: FANCA; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Cervical cancer; mutated gene: CHEK2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: NSCLC; mutated gene: BLM; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Neuroendocrine cancer; mutated gene: ERCC3; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP sensitive; ', 'tissue: tumor biopsy; cancer: Prostate cancer; mutated gene: FAN1; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Ovarian cancer; mutated gene: MRE11; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Mesothelioma; mutated gene: XPC; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: vulvovaginal; mutated gene: PMS2; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: ATM; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Bile duct cancer; mutated gene: PALB2; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Prostate cancer; mutated gene: NBN; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: CEP57; predicted: HRDEXP: NO_HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: CDH1; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ', 'tissue: tumor biopsy; cancer: Colorectal cancer; mutated gene: FANCM; predicted: HRDEXP: HRD; parp predicted: kmeans-2: PARP insensitive; ' GSE131097 Homo sapiens 61 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Synthetic lethal and resistance interactions with BET bromodomain inhibitors [ChIP-Seq] 2019-05-13 BET bromodomain inhibitors (BBDI) are promising therapeutic agents in triple-negative breast cancer (TNBC). However, not all tumors respond and acquired resistance emerges rapidly even in the responders. Using CRISPR and small molecule inhibitor screens combined with comprehensive molecular profiling of BBDI response and resistance in TNBC cell lines, we identified numerous synthetic lethal interactions with BBDIs as well as genes that when deleted confer resistance. The most prominent and consistent synergy was observed with CDK4/6 inhibitors and paclitaxel. We also uncovered functional similarities and differences between BBD proteins BRD2, BRD4, and BRD7, whereas deletion of BRD2 and BRD4 enhances sensitivity to BBDIs, BRD7 loss leads to resistance. Lastly, single cell RNA-seq and cellular barcoding analysis of BBDI responses in sensitive and resistant cell lines highlight heterogeneity among samples and demonstrate that BBDI resistance can be both pre-existing and acquired. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131097 Synthetic Lethal and Resistance Interactions with BET Bromodomain Inhibitors in Triple-Negative Breast Cancer. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2020.04.027 {Molecular cell (14.548): 10.1016/j.molcel.2020.04.027} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA542646 https://www.ebi.ac.uk/ena/browser/view/PRJNA542646 https://www.ncbi.nlm.nih.gov/sra?term=SRP198256 [Overal design]ChIP-Seq of parental and JQ1 resistant breast cancer cell lines; [Treatment]'SUM149, SUM159, SUM149R, SUM159R cells were incubated for 12 hr with JQ1 or DMSO treatment.'; [Growth]'SUM149, SUM159, SUM149R, SUM159R cells were grown in SUM Medium'; [Extraction]'Cells (1x107) were grown in SUM Medium. The media were then removed and replaced with media containing 1% formaldehyde (EM grade; tebu-bio) and crosslinked for 8 min. Crosslinking was quenched by adding glycine to a final concentration of 0.2 M. The cells were washed with ice-cold PBS, harvested in PBS, and the cell pellet was washed with PBS. The nuclear fraction was extracted by first resuspending the pellet in 10 ml of LB1 buffer (50mM HEPES-KOH [pH 7.5], 140mMNaCl, 1mMEDTA, 10% glycerol, 0.5% NP-40 or Igepal CA-630, and 0.25% Triton X-100) for 10 min at 4\uf0b0C. Cells were pelleted, resuspended in 10 ml of LB2 buffer (10 mM Tris-HCL [pH 8.0], 200 mM NaCl, 1 mM EDTA, and 0.5 mM EGTA), and mixed for 5 min. Cells were pelleted and resuspended in 1ml LB3 buffer (10 mM Tris-HCl [pH 7.4], 1 mM EDTA, 0.1%SDS, 1%Triton X-100, 0.1% Na-deoxycholate, 1Mm DTT, 0.25% N-lauroylsarcosine, protease inhibitors and phosphatase inhibitors) and sonicated in a covaris sonicator for 10 min. A total of 30 \uf06dl of 5M Nacl was added, and lysate was centrifuged for 10 min at 20,000 rcf to purify the debris. The supernatant was then incubated with 50 \uf06dl of magnetic beads (Life Technologies) prebound with 20 \uf06dg BRD4 antibody (Bethyl, A301-985A), and immunoprecipitation (IP) was conducted overnight in the cold room. The beads were washed ten times in 1 ml of RIPA buffer and twice in 100mM ammonium hydrogen carbonate (AMBIC) solution. DNA was eluted in elution buffer (50 mM Tris-HCl pH 8, 10 mM EDTA, and 1% SDS). Cross-links were reversed overnight at 65\uf0b0C. RNA and protein were digested with 0.2 mg/mL RNase A for 2 hr followed by 0.2 mg/mL Proteinase K for 1 hr. DNA was purified with phenol chloroform extraction and ethanol precipitation.\nChIP-seq libraries were prepared using the Rubicon ThruPLEX DNA-seq Kit from 1 ng of purified ChIP DNA or input DNA according to the manufacturer’s protocol.', 'Cells were grown in SUM Medium. The media were then removed and replaced with media containing 1% formaldehyde (EM grade; tebu-bio) and crosslinked for 8 min. Crosslinking was quenched by adding glycine to a final concentration of 0.2 M. The cells were washed with ice-cold PBS, harvested in PBS, and the cell pellet was washed with PBS. The nuclear fraction was extracted by first resuspending the pellet in 10 ml of LB1 buffer (50mM HEPES-KOH [pH 7.5], 140mMNaCl, 1mMEDTA, 10% glycerol, 0.5% NP-40 or Igepal CA-630, and 0.25% Triton X-100) for 10 min at 4\uf0b0C. Cells were pelleted, resuspended in 10 ml of LB2 buffer (10 mM Tris-HCL [pH 8.0], 200 mM NaCl, 1 mM EDTA, and 0.5 mM EGTA), and mixed for 5 min. Cells were pelleted and resuspended in 1ml LB3 buffer (10 mM Tris-HCl [pH 7.4], 1 mM EDTA, 0.1%SDS, 1%Triton X-100, 0.1% Na-deoxycholate, 1Mm DTT, 0.25% N-lauroylsarcosine, protease inhibitors and phosphatase inhibitors) and sonicated in a covaris sonicator for 10 min. A total of 30 \uf06dl of 5M Nacl was added, and lysate was centrifuged for 10 min at 20,000 rcf to purify the debris. The supernatant was then incubated with 50 \uf06dl of magnetic beads (Life Technologies) prebound with 20 \uf06dg BRD4 antibody (Bethyl, A301-985A), and immunoprecipitation (IP) was conducted overnight in the cold room. The beads were washed ten times in 1 ml of RIPA buffer and twice in 100mM ammonium hydrogen carbonate (AMBIC) solution. DNA was eluted in elution buffer (50 mM Tris-HCl pH 8, 10 mM EDTA, and 1% SDS). Cross-links were reversed overnight at 65\uf0b0C. RNA and protein were digested with 0.2 mg/mL RNase A for 2 hr followed by 0.2 mg/mL Proteinase K for 1 hr. DNA was purified with phenol chloroform extraction and ethanol precipitation.\nChIP-seq libraries were prepared using the Rubicon ThruPLEX DNA-seq Kit from 1 ng of purified ChIP DNA or input DNA according to the manufacturer’s protocol.'; [Cell type]'Source: ''cell line: SUM159; antibody: anti-BRD7 (Cell Signaling, 14910); treatment: DMSO; replicate: 1; ', 'cell line: SUM159; antibody: anti-BRD7 (Cell Signaling, 14910); treatment: JQ1; replicate: 1; ', 'cell line: SUM159; antibody: anti-BRD7 (Cell Signaling, 14910); treatment: JQ1; replicate: 2; ', 'cell line: SUM159; antibody: -; treatment: -; replicate: -; ', 'cell line: SUM159R; antibody: anti-BRD7 (Cell Signaling, 14910); treatment: DMSO; replicate: 1; ', 'cell line: SUM159R; antibody: anti-BRD7 (Cell Signaling, 14910); treatment: DMSO; replicate: 2; ', 'cell line: SUM159R; antibody: anti-BRD7 (Cell Signaling, 14910); treatment: JQ1; replicate: 1; ', 'cell line: SUM159R; antibody: anti-BRD7 (Cell Signaling, 14910); treatment: JQ1; replicate: 2; ', 'cell line: SUM159R; antibody: -; treatment: -; replicate: -; ', 'cell line: SUM149; antibody: anti-BRD2 (Cell signaling, 5848); treatment: DMSO; replicate: 1; ', 'cell line: SUM149; antibody: anti-BRD2 (Cell signaling, 5848); treatment: DMSO; replicate: 2; ', 'cell line: SUM149; antibody: anti-BRD4 (Bethyl, A301-985A); treatment: DMSO; replicate: 1; ', 'cell line: SUM149; antibody: anti-H3K27ac (Abcam, ab4729); treatment: DMSO; replicate: 1; ', 'cell line: SUM149; antibody: -; treatment: -; replicate: -; ', 'cell line: SUM149; antibody: anti-BRD2 (Cell signaling, 5848); treatment: JQ1; replicate: 1; ', 'cell line: SUM149; antibody: anti-BRD2 (Cell signaling, 5848); treatment: JQ1; replicate: 2; ', 'cell line: SUM149; antibody: anti-BRD4 (Bethyl, A301-985A); treatment: JQ1; replicate: 1; ', 'cell line: SUM149; antibody: anti-H3K27ac (Abcam, ab4729); treatment: JQ1; replicate: 1; ', 'cell line: SUM149R; antibody: anti-BRD2 (Cell signaling, 5848); treatment: DMSO; replicate: 1; ', 'cell line: SUM149R; antibody: anti-BRD2 (Cell signaling, 5848); treatment: DMSO; replicate: 2; ', 'cell line: SUM149R; antibody: anti-BRD4 (Bethyl, A301-985A); treatment: DMSO; replicate: 1; ', 'cell line: SUM149R; antibody: anti-H3K27ac (Abcam, ab4729); treatment: DMSO; replicate: 1; ', 'cell line: SUM149R; antibody: -; treatment: -; replicate: -; ', 'cell line: SUM149R; antibody: anti-BRD2 (Cell signaling, 5848); treatment: JQ1; replicate: 1; ', 'cell line: SUM149R; antibody: anti-BRD2 (Cell signaling, 5848); treatment: JQ1; replicate: 2; ', 'cell line: SUM149R; antibody: anti-BRD4 (Bethyl, A301-985A); treatment: JQ1; replicate: 1; ', 'cell line: SUM149R; antibody: anti-H3K27ac (Abcam, ab4729); treatment: JQ1; replicate: 1; ', 'cell line: SUM159; antibody: anti-BRD2 (Cell signaling, 5848); treatment: DMSO; replicate: 1; ', 'cell line: SUM159; antibody: anti-BRD2 (Cell signaling, 5848); treatment: DMSO; replicate: 2; ', 'cell line: SUM159; antibody: anti-BRD4 (Bethyl, A301-985A); treatment: DMSO; replicate: 1; ', 'cell line: SUM159; antibody: anti-BRD4 (Bethyl, A301-985A); treatment: DMSO; replicate: 2; ', 'cell line: SUM159; antibody: anti-H3K27ac (Abcam, ab4729); treatment: -; replicate: 1; ', 'cell line: SUM159; antibody: anti-BRD2 (Cell signaling, 5848); treatment: JQ1; replicate: 1; ', 'cell line: SUM159; antibody: anti-BRD2 (Cell signaling, 5848); treatment: JQ1; replicate: 2; ', 'cell line: SUM159; antibody: anti-BRD4 (Bethyl, A301-985A); treatment: JQ1; replicate: 1; ', 'cell line: SUM159; antibody: anti-BRD4 (Bethyl, A301-985A); treatment: JQ1; replicate: 2; ', 'cell line: SUM159R; antibody: anti-BRD2 (Cell signaling, 5848); treatment: DMSO; replicate: 1; ', 'cell line: SUM159R; antibody: anti-BRD2 (Cell signaling, 5848); treatment: DMSO; replicate: 2; ', 'cell line: SUM159R; antibody: anti-BRD4 (Bethyl, A301-985A); treatment: DMSO; replicate: 1; ', 'cell line: SUM159R; antibody: anti-BRD4 (Bethyl, A301-985A); treatment: DMSO; replicate: 2; ', 'cell line: SUM159R; antibody: anti-H3K27ac (Abcam, ab4729); treatment: -; replicate: 1; ', 'cell line: SUM159R; antibody: anti-BRD2 (Cell signaling, 5848); treatment: JQ1; replicate: 1; ', 'cell line: SUM159R; antibody: anti-BRD2 (Cell signaling, 5848); treatment: JQ1; replicate: 2; ', 'cell line: SUM159R; antibody: anti-BRD4 (Bethyl, A301-985A); treatment: JQ1; replicate: 1; ', 'cell line: SUM159R; antibody: anti-BRD4 (Bethyl, A301-985A); treatment: JQ1; replicate: 2; ', 'cell line: SUM159; antibody: none; brd7 status: Wild type; number of cells: 10 million cells; ', 'cell line: SUM159; antibody: none; brd7 status: Wild type; number of cells: 40 million cells; ', 'cell line: SUM159; antibody: BRD4 (Bethyl, A301-985A); brd7 status: Wild type; number of cells: 40 million cells; ', 'cell line: SUM159; antibody: histone H3K27ac (Abcam, ab4729); brd7 status: Wild type; number of cells: 10 million cells; ', 'cell line: SUM159; antibody: histone H3K27me3 (Cell Signaling, 9733); brd7 status: Wild type; number of cells: 10 million cells; ', 'cell line: SUM159; antibody: histone H3K4me3 (Abcam, ab1012); brd7 status: Wild type; number of cells: 10 million cells; ', 'cell line: SUM159; antibody: none; brd7 status: Knockout; number of cells: 10 million cells; ', 'cell line: SUM159; antibody: none; brd7 status: Knockout; number of cells: 40 million cells; ', 'cell line: SUM159; antibody: BRD4 (Bethyl, A301-985A); brd7 status: Knockout; number of cells: 40 million cells; ', 'cell line: SUM159; antibody: histone H3K27ac (Abcam, ab4729); brd7 status: Knockout; number of cells: 10 million cells; ', 'cell line: SUM159; antibody: histone H3K27me3 (Cell Signaling, 9733); brd7 status: Knockout; number of cells: 10 million cells; ', 'cell line: SUM159; antibody: histone H3K4me3 (Abcam, ab1012); brd7 status: Knockout; number of cells: 10 million cells; ' GSE81146 Mus musculus 2 Expression profiling by array GPL1261 Gene expression signatures for B cells from tumor draining lymph node and normal lymph node 2016-05-05 To determine the different gene signatures between B lymphocytes from tumor draining lymph node (DLN) and normal lymph node (NLN), we have employed gene microarray as a discovery platform to identify gene signatures of tumor-educated B cells in DLN from tumor-bearing mice, taking NLN from normal mice as a control. We subcutaneously inoculated Balb/c mice with breast cancer cell line 4T1. Two weeks later, DLN was harvest and B cells were purified as descript in “treatment protocol”. From gene microarray, we found that B cells in DLN showed quite different transcript profiles from that in NLN. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE81146 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA320737 https://www.ebi.ac.uk/ena/browser/view/PRJNA320737 None [Overal design]Examination of different gene signatures between B cells from tumor draining lymph node and normal lymph node; [Treatment]'We subcutaneously inoculated Balb/c mice with breast cancer cell line 4T1. DLN was harvest two weeks later. To purify B cells, single-cell suspensions from DLN and NLN were stained with antibodies, and CD3- CD19+ cells were sorted using a MoFlo XDP flow cytometer (Beckman-Coulter) with purities of >95%.'; [Growth]'None'; [Extraction]'Total RNA of parietal cortex of the patient was extracted with RNeasy Mini Kit (Qiagen), according to the manufacturer’s instruction.'; [Cell type]'B cell''cell type: B cell; strain: Balb/c; ' GSE13553 Mus musculus 10 Expression profiling by array GPL1261 The effect of dietary CLA on mammary tumorigenesis 2008-11-10 Conjugated linoleic acid (CLA), a class of fatty acids found in beef and dairy products, has been shown to inhibit tumorigenesis in a variety of cancer model systems. Based on previously well-documented anti-tumor activity of CLA in rodent models of breast cancer, a pilot study was initiated to examine the effect of dietary CLA in a well-established transgenic model of breast cancer. Western blots were performed for the detection of AKT, c-Src, ERK1/2, and Cdc24. CLA significantly increased tumor burden (p<0.1) independent of an increase in oncogenic signaling. Mammary gland whole mounts indicated a loss of mammary adipose and extensive epithelial expansion in CLA-treated animals. Microarray analysis indicated a significant reduction in cytoskeletal related genes with at least a two-fold decrease in five out of six CLA-fed animals compared to untreated controls. Reduction of Cdc42, a key regulator of cell adhesion and cytoskeletal arrangements, was confirmed at the protein level by western blot (p<0.01). These findings suggest that dietary CLA may advance the malignant phenotype by promoting a loss of cell polarity and adhesion in the mammary gland epithelium. This action may have serious clinical implications for a subset high-risk population and warrants further investigation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE13553 Pilot study on the effects of dietary conjugated linoleic acid on tumorigenesis and gene expression in PyMT transgenic mice. Carcinogenesis 4.004 https://doi.org/10.1093/carcin/bgq148 {Carcinogenesis (4.004): 10.1093/carcin/bgq148} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA110737 https://www.ebi.ac.uk/ena/browser/view/PRJNA110737 None [Overal design]Virgin, four-week-old PyV-mT mice were administered a diet of a mixed-isomer CLA formulation (1% wt/wt) (N=6) or control AIN96G diet (N=5) for four weeks. Measurements of food disappearance, weights and palpations were recorded weekly. All animals were euthanized at eight weeks of age. Formalin-fixed, paraffin-embedded mammary gland tissue was used for H&E and trichrome staining and immunohistochemistry for Ki67. Tissue levels of CLA were measured by gas chromatography. Thoracic mammary glands were fixed in glacial acetic acid:ethanol and carmine stained. cDNA microarray was performed on RNA from 6 CLA-fed mice and 4 control mice using the Affymetrix 430 2.0 mouse genome chips.; [Treatment]'PyV-MT expressing female mice were fed a diet supplemented with 1% conjugated linoleic acid or control chow for 4 weeks. Animals were euthanized at 8 weeks of age and mammary glands were collected for RNA processing.'; [Growth]'None'; [Extraction]'Mammary glands were collected according to standard necropsis procedures. Tissue was stored in RNAlater (Sigma, St. Louis, MO) until processing. RNA was obtained using Qiagen RNeasy (Valencia CA) and stored in -80 degrees Celsius.'; [Cell type]'Source: ''Strain: FVB/PyV-Mt; Age: 8 weeks; Sex: Female; Parity: No; Tissue: Mammary gland; ' GSE121119 Homo sapiens 16 Expression profiling by high throughput sequencing GPL19415 Using a xenograft model and RNA-seq to differentiate between the tumour and tumour microenvironment transcriptome 2018-10-11 In addition to the tumour cells, breast tumours contain other cell types such as fibroblasts, adipocytes, inflammatory and immune cells. Together with the extracellular matrix, these non-tumour cells compose the tumour microenvironment (TME). Complex interactions occur between tumour cells and the TME that can inhibit or stimulate tumour cell growth, metastasis and/or chemoresistance. While treatment of tumours with chemotherapeutic agents such as Abraxane, leads to apoptosis of tumour cells, it can also have consequences for the cellular makeup and transcriptional profile of the TME and these, like the increased infiltration of macrophages, may have detrimental effects. Transcriptome profiling of whole tumours from mice injected with tumour cell lines and treated with combinations of chemotherapeutic drugs has provided novel insights into pathways affected by different agents and diagnostic signatures. However, differences in the cellular composition of tumours from treated mice can have confounding effects and increase variation in whole tumour transcriptomes. To be able to examine the effects of co-treatment of Abraxane with another drug, we performed RNA-seq on tumours from mice injected with the human breast cancer cell line MDA-MB-231. We then separated reads mapped to the human and mouse genomes in silico, creating tumour and TME transcriptomes for control, Abraxane, drug and combination treated mice. Separation of the tumour and TME profiles revealed that while in the tumour cells, co-addition of the drug potentiated Abraxane’s inhibitory effect on cell cycle genes and promotional effect on antigen presentation genes, in the TME it inhibited genes involved in the inflammation and migration responses and promoted genes involved in lipid and xenobiotic metabolism. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE121119 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA495798 https://www.ebi.ac.uk/ena/browser/view/PRJNA495798 https://www.ncbi.nlm.nih.gov/sra?term=SRP165188 [Overal design]4 mice per treatment. 4 treatments. Paired end RNA-seq; [Treatment]'MDA-MB-231 Cells 2 x 10^6 in 50µl (50:50 PBS:Matrigel) were transplanted subcutaneously into the mammary fat pads of balb/c nude mice and 50 days later the tumour was excised from the sacrificed mouse.'; [Growth]'None'; [Extraction]'The tumor tissues were collected in Allprotect tissue reagent kit and then processed using the Rneasy Microarray Tissue Mini Kit according to manufacturer’s protocol (tissues were lysed mechanically using the Tissue Lyser II).\nLibraries were constructed with theTruSeq mRNA Paired-End kit per manufacturers instructions.'; [Cell type]'Source: ''cell line: MDA-MB-231; host mouse strain: balb/c nude; tissue: mammary gland; ' GSE156676 Homo sapiens 8 Protein profiling by protein array GPL29056 PTK6 domain mutants modulates action in Triple-negative breast cancer 2020-08-22 Protein tyrosine kinase 6 (PTK6; also called Brk) is overexpressed in 86% of breast cancer patients; high PTK6 expression predicts poor outcome. We reported PTK6 induction by HIF/GR complexes in response to either cellular or host stress. However, PTK6-driven signaling events in the context of TNBC remain undefined. In a mouse model of TNBC, manipulation of PTK6 levels (i.e. via knock-out or add-back) had little effect on primary tumor volume but altered lung metastasis. To delineate the mechanisms of PTK6 downstream signaling, we created kinase-dead (KM) and kinase-intact domain structure mutants of PTK6 via in frame deletions of the N-terminal SH3 or SH2 domains. While the PTK6 kinase domain contributed to soft-agar colony formation, PTK6 kinase activity was entirely dispensable for cell migration. Specifically, TNBC models expressing a PTK6 variant lacking the SH2 domain (SH2-del PTK6) were unresponsive to growth factor-stimulated cell motility relative to SH3-del, KM or wild-type PTK6 controls. Reverse phase protein array (RPPA) revealed that while intact PTK6 mediates spheroid formation via p38 MAPK signaling, the SH2 domain of PTK6 limits this biology, and instead mediates TNBC cell motility via activation of the RhoA and/or AhR signaling pathways. Inhibition of RhoA and/or AhR blocked TNBC cell migration as well as the branching/invasive morphology of PTK6+/AhR+ primary breast tumor tissue organoids. Inhibition of RhoA also enhanced paclitaxel cytotoxicity in TNBC cells, including in a taxane-refractory TNBC model. Together, these studies reveal that the SH2-domain of PTK6 is a potent effector of advanced cancer phenotypes in TNBC and identify RhoA and AhR as novel therapeutic targets in PTK6+ breast tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE156676 Breast Tumor Kinase (Brk/PTK6) Mediates Advanced Cancer Phenotypes via SH2-Domain Dependent Activation of RhoA and Aryl Hydrocarbon Receptor (AhR) Signaling. Molecular cancer research : MCR 4.484 https://doi.org/10.1158/1541-7786.MCR-20-0295 {Molecular cancer research : MCR (4.484): 10.1158/1541-7786.MCR-20-0295} 'protein' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA658686 https://www.ebi.ac.uk/ena/browser/view/PRJNA658686 None [Overal design]Examination of the effect of HGF in TNBC cell line MDA-MB-231 with mutation in the ptk6 protein.; [Treatment]'Cells were treated with vehicle treatment or either 50 ng/mL of HGF for 6 hrs.'; [Growth]'MDA-MB-231 expressing either wt-GR or S134A-GR were serum starved in IMEM containing 1% DCC for 18 hrs.'; [Extraction]'Total protein was extracted with RIPA-lysis buffer and stained slides qauntification was doned by Array-Pro-Analyzer'; [Cell type]'Source: ''ptk6-status: WT-PTK6; treatment: Vehicle; cell line: MDA-MB-231; ', 'ptk6-status: WT-PTK6; treatment: HGF; cell line: MDA-MB-231; ', 'ptk6-status: SH2-deleted; treatment: Vehicle; cell line: MDA-MB-231; ', 'ptk6-status: SH2-deleted; treatment: HGF; cell line: MDA-MB-231; ', 'ptk6-status: KM-PTK6; treatment: Vehicle; cell line: MDA-MB-231; ', 'ptk6-status: KM-PTK6; treatment: HGF; cell line: MDA-MB-231; ', 'ptk6-status: PTK6-KO; treatment: Vehicle; cell line: MDA-MB-231; ', 'ptk6-status: PTK6-KO; treatment: HGF; cell line: MDA-MB-231; ' GSE78753 Homo sapiens 18 Expression profiling by array GPL570 A Preclinical Model for ERα-Positive Breast Cancer Points to the Epithelial Microenvironment as Determinant of Luminal Phenotype and Hormone Response 2016-02-29 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE78753 A Preclinical Model for ERα-Positive Breast Cancer Points to the Epithelial Microenvironment as Determinant of Luminal Phenotype and Hormone Response. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2016.02.002 {Cancer cell (23.916): 10.1016/j.ccell.2016.02.002} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA313431 https://www.ebi.ac.uk/ena/browser/view/PRJNA313431 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'Xenografted MCF7 were FACS sorting based on DsRED expression; total RNA was extracted using Trizol Reagent (Invitrogen), purified with the miRNeasy Mini Kit (Qiagen), and quantity and quality were assessed by NanoDrop®ND-1000 spectrophotometer and RNA 6000 NanoChips with the Agilent 2100 Bioanalyzer (Agilent, Palo Alto, USA). Only samples with RIN score >7.0 were included.', 'Xenografted BT20 or HCC1806 were sorted by FACS based on DsRed expression; total RNA was extracted using Trizol Reagent (Invitrogen), purified with the miRNeasy Mini Kit (Qiagen), and quantity and quality were assessed by NanoDrop®ND-1000 spectrophotometer and RNA 6000 NanoChips with the Agilent 2100 Bioanalyzer (Agilent, Palo Alto, USA). Only samples with RIN score >7.0 were included.'; [Cell type]'xenografted, FACS-sorted MCF7', 'Source: ''source cell type: MCF7-DsRED/luc2 cells; host strain info: 8-12 wk-old female SCID Beige mice; sample group: fat pad xenograft; cell type: xenografted, FACS-sorted MCF7; ', 'source cell type: MCF7-DsRED/luc2 cells; host strain info: 8-12 wk-old female SCID Beige mice; sample group: intraductal xenograft; cell type: xenografted, FACS-sorted MCF7; ', 'tissue: fat pad xenograft; ', 'tissue: intraductal xenograft; ' GSE15749 Homo sapiens 4 Expression profiling by array GPL570 Gene expression-based dentification of microRNA-9-3 target genes in breast epithelial cells 2009-04-20 In current study, DES could effectively suppress the expression of miR-9-3 through the ERa-dependent epigenetic machinery in MDECs and MCF-7 cells. We want to figure out the biological significance and the potential targets of miR-9-3 and the related signaling cascades. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15749 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA116891 https://www.ebi.ac.uk/ena/browser/view/PRJNA116891 None [Overal design]MCF-7 cells were transfected with two pre-designed maturated mimics of miR-9-3, miR-9 and miR-9*. After 48hr of transfection, total RNA was collected for gene expression analysis to figure out the potential targets of miR-9-3.; [Treatment]'None'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''tissue: breast cancer cell line; genotype: ERa-positive; treatment: control; ', 'tissue: breast cancer cell line; genotype: ERa-positive; treatment: miR-9 transfection; ', 'tissue: breast cancer cell line; genotype: ERa-positive; treatment: miR-9* transfection; ' GSE130852 Homo sapiens 12 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL18573 MCF-7 as a model for functional analysis of breast cancer risk variants 2019-05-07 Here we report how the ER+ cell line MCF-7 can be used to inform risk mechanisms for BCa. We identified active regulatory elements (enhancers, promoters, and chromatin organizing elements) by histone H3K27 acetylation and CTCF occupancy and determined the enrichment of risk variants at these sites. We measured gene expression via RNA-seq. After intersection with GWAS risk variants we found 39 enhancers and 15 CTCF occupancy sites that, between them, overlapped 96 BCa credible risk variants at 42 loci. These risk enhancers likely regulate the expression of dozens of genes, which are enriched for GO categories including estrogen and prolactin signaling. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130852 MCF-7 as a Model for Functional Analysis of Breast Cancer Risk Variants. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 5.057 https://doi.org/10.1158/1055-9965.EPI-19-0066 {Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology (5.057): 10.1158/1055-9965.EPI-19-0066} 'polyA RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA541872 https://www.ebi.ac.uk/ena/browser/view/PRJNA541872 https://www.ncbi.nlm.nih.gov/sra?term=SRP197070 [Overal design]Two WT MCF-7 samples were used for CTCF ChIP-seq and two for H3k27Ac ChIP-Seq. 8 samples in 2 separate batches, were used for RNA-Seq. These data were compared with publically available data for MCF-7 and HMEC.; [Treatment]'For ChIP we followed previously published protocols from Rhie et al (20) with slight modifications. Roughly 30-40 x 106 cells were used per ChIP. Upon reaching 70-80% confluency, cells were directly fixed in T75 flasks by adding 16% formaldehyde to the culture medium to a final concentration of 1%. The reaction was quenched for 5 minutes at room temperature with 10X (1.15 M) glycine. Using a Bioruptor Pico (Diagenode, Cat # B01060001) the isolated chromatin was sonicated for 30 second on and 30 second off cycles to yield DNA fragments between 200 and 500 base pairs. 100 ug of sonicated chromatin was used for immunoprecipitation and 1 ug (1%) was used for the input control. To probe for CTCF or H3K27ac, samples were incubated at 4 °C overnight with a primary antibody [CTCF: Cell Signaling monoclonal (D31H2), Cat# 3418; H3K27ac: Active Motif, Cat #39133] or an IgG control (Sigma, Cat # R9133). A/G magnetic beads (Pierce, Cat # 88802) were then incubated with the samples for 2 hours at 4 °C. Following this incubation, the beads were washed with a series of buffers of varying salt concentrations before overnight elution at 67 °C. The ChIP, IgG, and Input samples were all purified using a QIAprep Spin Miniprep Kit (Qiagen, Cat # 27104).'; [Growth]'MCF-7 cells were obtained from ATCC and cultured in DMEM (ATCC, cat # 30-2003) supplemented with 10% FBS and 0.01 mg/ml human recombinant insulin (Gibco, ref # 12585-014). They were incubated in a humidified 37°C, 5% CO2 incubator. For routine passaging, cells were grown in T25 and T75 culture flasks and passaged using 0.25% Trypsin/EDTA.'; [Extraction]'100 ug of sonicated chromatin was used for immunoprecipitation and 1 ug (1%) was used for the input control.\nLibraries for input and IP samples were prepared by the Van Andel Genomics Core from 10 ng of input material and all available IP material using the KAPA Hyper Prep Kit (v5.16) (Kapa Biosystems, Wilmington, MA USA). Prior to PCR amplification, end-repaired and Atailed DNA fragments were ligated to Bio Scientific NEXTflex Adapters (Bio Scientific, Austin, TX, USA). The quality and quantity of the finished libraries were assessed using a combination of Agilent DNA High Sensitivity chip (Agilent Technologies, Inc.), QuantiFluor dsDNA System (Promega Corp., Madison, WI, USA), and Kapa Illumina Library Quantification qPCR assays (Kapa Biosystems). Sequencing (75 bp, single end) was performed on an Illumina NextSeq 500 sequencer using a 75-bp sequencing kit (v2) (Illumina Inc., San Diego, CA, USA). Base calling used Illumina NextSeq Control Software (NCS) v2.0, and the output of NCS was demultiplexed and converted to FastQ format with Illumina Bcl2fastq v1.9.0.\nRNA was isolated using a Qiagen RNeasy mini kit (Cat # 74104). Paired-end mRNA libraries were then prepared.\nLibraries were prepared by the Van Andel Research Institute Genomics Core from 1 μg of material using the KAPA Stranded mRNAseq Kit (v4.16) (Kapa Biosystems, Wilmington, MA USA). RNA was sheared to 250–300 bp. Prior to PCR amplification, cDNA fragments were ligated to Bio Scientific NEXTflex Adapters (Bioo Scientific, Austin, TX, USA). The quality and quantity of the finished libraries were assessed using a combination of Agilent DNA High Sensitivity chip (Agilent Technologies, Inc.), QuantiFluor dsDNA System (Promega Corp., Madison, WI, USA), and Kapa Illumina Library Quantification qPCR assays (Kapa Biosystems).'; [Cell type]'Source: ''general: luminal epithelial breast cancer line; ER+, PR+/-, HER2-; Sex: female; passages: 23; sample type: WT, treated with CRISPR/Cas9 -> no insertion; ', 'general: luminal epithelial breast cancer line; ER+, PR+/-, HER2-; Sex: female; passages: 20; sample type: WT, treated with CRISPR/Cas9 -> no insertion; ', 'general: luminal epithelial breast cancer line; ER+, PR+/-, HER2-; Sex: female; passages: 21; sample type: WT, treated with CRISPR/Cas9 -> no insertion; ', 'general: luminal epithelial breast cancer line; ER+, PR+/-, HER2-; Sex: female; passages: 11; sample type: WT; ', 'general: luminal epithelial breast cancer line; ER+, PR+/-, HER2-; Sex: female; passages: 13; sample type: WT; ', 'general: luminal epithelial breast cancer line; ER+, PR+/-, HER2-; Sex: female; passages: 7 to 13; sample type: WT; antibody: H3k27Ac; ', 'general: luminal epithelial breast cancer line; ER+, PR+/-, HER2-; Sex: female; passages: 7 to 13; sample type: WT; antibody: CTCF; ' GSE142268 Homo sapiens 9 Expression profiling by high throughput sequencing GPL24676 Expression of ncRNAs on the DLK1-DIO3 locus is associated with basel and mesenchymal phenotype in breast epithelial progenitor cells 2019-12-18 Epithelial-to-mesenchymal transition (EMT) and its reversed process mesenchymal-to-epithelial transition (MET) play a critical role in epithelial plasticity during development and cancer progression. Among important regulators of these cellular processes are non-coding RNAs (ncRNAs). The imprinted DLK1-DIO3 locus, containing numerous maternally expressed ncRNAs including the lncRNA maternally expressed gene 3 (MEG3) and a cluster of over 50 miRNAs, has been shown to be a modulator of stemness in embryonic stem cells and in cancer progression, potentially through the tumor suppressor role of MEG3. In this study we analyzed the expression pattern and functional role of ncRNAs from the DLK1-DIO3 locus in epithelial plasticity of the breast. We studied their expression in various cell types of breast tissue and revisit the role of the locus in EMT/MET using a breast epithelial progenitor cell line (D492) and its isogenic mesenchymal derivative (D492M). Marked upregulation of ncRNAs from the DLK1-DIO3 locus was seen after EMT induction in two cell line models of EMT. In addition, the expression of MEG3 and the maternally expressed ncRNAs was higher in stromal cells compared to epithelial cell types in primary breast tissue. We also show that expression of MEG3 is concomitant with the expression of the ncRNAs from the DLK1-DIO3 locus and its expression is therefore likely indicative of activation of all ncRNAs at the locus. MEG3 expression is correlated with stromal markers in normal tissue and breast cancer tissue and negatively correlated with the survival of breast cancer patients in two different cohorts. Overexpression of MEG3 using CRISPR activation in a breast epithelial cell line induced partial EMT and enriched for a basal-like phenotype. Conversely, knock down of MEG3 using CRISPR inhibition in a mesenchymal cell line reduced the mesenchymal and basal-like phenotype of the cell line. In summary our study shows that maternally expressed ncRNAs are markers of EMT and suggests that MEG3 is a novel regulator of EMT/MET in breast tissue. Nevertheless, further studies are needed to fully dissect the molecular pathways influenced by non-coding RNAs at the DLK1-DIO3 locus in breast tissue. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE142268 Expression of ncRNAs on the DLK1-DIO3 Locus Is Associated With Basal and Mesenchymal Phenotype in Breast Epithelial Progenitor Cells. Frontiers in cell and developmental biology 5.206 https://doi.org/10.3389/fcell.2020.00461 {Frontiers in cell and developmental biology (5.206): 10.3389/fcell.2020.00461} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA596443 https://www.ebi.ac.uk/ena/browser/view/PRJNA596443 https://www.ncbi.nlm.nih.gov/sra?term=SRP238079 [Overal design]A total of ten samples were analyzed: Five replicates from D492M KD ctrl and five replicates from D492M KD MEG3. However, sample no. 5 from D492M KD ctrl was omitted due to high deviation from the outher four samples.; [Treatment]'None'; [Growth]'D492M was cultured in H14 medium (DMEM:F12 supplemented with 50 IU/ml penicillin, 50 ug/ml streptomycin, 250 ng/ml insulin, 10 ug/ml transferrin, 2.6 ng/ml sodium selenite, 0.1 nM estradiol, 0.5 ug/ml hydrocortisone, 5 ug/ml prolactin and 10 ng/ml EGF), in flasks coated with collagen I. Media was changed three times a week.'; [Extraction]"RNA was extracted using a Tri-Reagent standard protocol\nLibraries were prepared according to Illumina's instructions"; [Cell type]'Breast epithelial cell line (D492) mesenchymal derivative (D492M)''passages: 21; cell type: Breast epithelial cell line (D492) mesenchymal derivative (D492M); genotype: control; ', 'passages: 21; cell type: Breast epithelial cell line (D492) mesenchymal derivative (D492M); genotype: MEG3 knockdown; ' GSE84594 Homo sapiens 14 Genome binding/occupancy profiling by high throughput sequencing; Other GPL11154 Regulation of KMT2D by PI(3)K/AKT signalling orchestrates oestrogen receptor mediated transcriptional activation in breast cancer 2016-07-19 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE84594 PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D. Science (New York, N.Y.) 41.037 https://doi.org/10.1126/science.aah6893 {Science (New York, N.Y.) (41.037): 10.1126/science.aah6893} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA330537 https://www.ebi.ac.uk/ena/browser/view/PRJNA330537 None [Overal design]Refer to individual Series; [Treatment]'50,000 T47D cells were treated with DMSO or BYL719 1μM for 24hr.', '10 milion T47D cells were treated with DMSO or BYL719 1μM for 24hr.'; [Growth]'T47D cells were maintained in RPMI 1640 with 10% FBS, 1% L-glutamine and 1% penicillin-streptomycin.'; [Extraction]"50,000 T47D cells were dissociated with acutase treatment and lysed with double the concentration of IGEPAL (0.2%) for successful library preparation.\nATAC-seq libraries were prepared using Illumina's TruSeq ChIP sample prep.Libraries were validated using the Agient Technologies 2100 Bioanalyzer and Qubit high sensitivity assay.", "Cells were lysed and sonicated leading to a DNA average size of 200bp. Protein G dynabeads were pre-incubated with 5μg of ER alpha (sc-543) or FOXA1 (ab5089) with pre cleared chromatin. The complexes were reverse cross-linked and DNA was purified.\nChIP-seq libraries were prepared using 10 ng of DNA and Illumina's TruSeq ChIP sample prep.Libraries were validated using the Agient Technologies 2100 Bioanalyzer and Qubit high sensitivity assay."; [Cell type]'Source: ''tissue: breast; cell line: T47D; passages: 5 to 10; ', 'cell line: T47D; passages: 5 to 10; ', 'cell line: T47D; passages: 5 to 10; chip-antibody: ER alpha (sc543) Santa Cruz; ', 'cell line: T47D; passages: 5 to 10; chip-antibody: FOXA1 (ab5089) Abcam; ' GSE102412 Homo sapiens 25 Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing GPL9052; GPL23126 ERα and AP-1 coordinate transcription and tamoxifen response in ERα-positive breast cancer 2017-08-09 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE102412 c-Jun/AP-1 overexpression reprograms ERα signaling related to tamoxifen response in ERα-positive breast cancer. Oncogene 6.634 https://doi.org/10.1038/s41388-018-0165-8 {Oncogene (6.634): 10.1038/s41388-018-0165-8} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA397705 https://www.ebi.ac.uk/ena/browser/view/PRJNA397705 None [Overal design]Refer to individual Series; [Treatment]'Cells were cultured in steroid depleted media for 72 h and treated with ethnaol, 10 nM 17β-estradiol or 1μM Tamoxifen for 24 h.', 'Cells were cultured in steroid depleted media for 72 h and treated with ethanol, 10 nM 17β-estradiol or 1μM Tamoxifen for 1 h. Cells were fixed with 1% formaldehyde for 10 minutes, then glycine-quenched and harvested'; [Growth]'MCF-7/c-Jun +Tet cells were maintained in DMEM supplemented with 10% FBS containing media in presence of 2μg/ml tetracycline.MCF-7/c-Jun -Tet cells were maintained in 10% FBS containing media in absence of tetracycline.', 'Cells were maintained in DMEM supplemented with 10% FBS containing media in absence of tetracycline.'; [Extraction]'Total RNA was extracted using RNeasy Mini Kit (Qiagen, Valencia, CA).', 'Lysates were clarified from sonicated nuclei, c-Jun and ERα complexes were isolated with antibody.\nChIP-seq libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ', 'ERalpha-positive breast cancer cells''treatment: vehicle; ', 'treatment: E2; ', 'treatment: Tamoxifen; ', 'cell line: MCF-7; cell type: ERalpha-positive breast cancer cells; chip antibody: c-Jun (H-79, Santa Cruz); ', 'cell line: MCF-7; cell type: ERalpha-positive breast cancer cells; chip antibody: ERalpha (H-20, Santa Cruz); ', 'cell line: MCF-7; cell type: ERalpha-positive breast cancer cells; chip antibody: none; ' GSE9205 Homo sapiens 5 Genome variation profiling by array GPL5620 Role of CSN5 in breast cancer (array CGH) 2007-10-01 CSN5 has been implicated as a candidate oncogene in human breast cancers by genetic linkage with activation of the poor-prognosis, wound response gene expression signature. CSN5 is a subunit of the eight-protein COP9 signalosome, a signaling complex with multiple biochemical activities; the mechanism of CSN5 action in cancer development remains poorly understood. Here we show that CSN5 isopeptidase activity is essential for breast epithelial transformation and progression. Amplification of CSN5 is required for transformation of primary human breast epithelial cells by defined oncogenes. The transforming effects of CSN5 require CSN subunits for assembly of the full COP9 signalosome and the isopeptidase activity of CSN5, which potentiates the transcriptional activity of MYC. Transgenic inhibition of CSN5 isopeptidase activity blocks breast cancer progression evoked by MYC and RAS in vivo. These results highlight CSN5 isopeptidase activity in breast cancer progression, suggesting it as a therapeutic target in aggressive human breast cancers. A strain or line experiment design type assays differences between multiple strains, cultivars, serovars, isolates, lines from organisms of a single species. Keywords: strain_or_line_design https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE9205 CSN5 isopeptidase activity links COP9 signalosome activation to breast cancer progression. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-07-3060 {Cancer research (8.378): 10.1158/0008-5472.CAN-07-3060} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA105249 https://www.ebi.ac.uk/ena/browser/view/PRJNA105249 None [Overal design]Computed; [Treatment]'None'; [Growth]'None'; [Extraction]'not provided'; [Cell type]'Source: ''' GSE130364 Homo sapiens 19 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Genomic binding profiles for ZNF165, ZNF446, and SMAD3 in triple-negative breast cancer 2019-04-26 The testis protein ZNF165 is aberrantly expressed in triple-negative breast cancer (TNBC), where it modulates TGFβ signaling to promote tumor growth and survival. To investigate whether ZNF165 functions in this capacity via cooperation with SMAD3, a canonical TGFβ-induced transcription factor, we performed ChIP-seq for both factors in TNBC cell lines (WHIM12 and SUM159). Additionally, we established genomic binding profiles for ZNF446, a previously uncharacterized transcription factor that we have identified as a member of a ZNF165-SMAD3 complex. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130364 The testis protein ZNF165 is a SMAD3 cofactor that coordinates oncogenic TGFβ signaling in triple-negative breast cancer. eLife 7.551 https://doi.org/10.7554/eLife.57679 {eLife (7.551): 10.7554/eLife.57679} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA539904 https://www.ebi.ac.uk/ena/browser/view/PRJNA539904 https://www.ncbi.nlm.nih.gov/sra?term=SRP193960 [Overal design]ChIP-seq for ZNF165, ZNF446, and SMAD3 in WHIM12 and/or SUM159 cells; [Treatment]'None'; [Growth]"Cells were grown to ~90% confluency on 150mm plates prior to harvesting. WHIM12 cells were cultured in MEM supplemented with 10% FBS. SUM159 cells were cultured in Ham's F-12 supplemented with 5% FBS, 1 μg/mL hydrocortisone, and 5 μg/mL insulin."; [Extraction]"Cells were crosslinked with 1% formaldehyde for 15 min at 37°C. Crosslinking was quenched with 0.125 M glycine for 5 min at 4°C, followed by multiple washes with cold PBS. Nuclei were harvested via hypotonic lysis and subjected to sonication in a lysis buffer containing 1% SDS. Sheared chromatin lysates were then pre-cleared with Protein A/G agarose beads for 1 hour, followed by immunoprecipitation with appropriate antibody overnight at 4°C. Protein A/G agarose beads blocked with BSA were added to lysates for 2 hours the next day, followed by extensive washes. Protein/DNA complexes were eluted from the beads with 100 mM NaHCO3 and 1% SDS, and de-crosslinking was carried out overnight at 65°C. RNA and protein were digested with RNase A and Proteinase K, respectively. DNA was purified using phenol/chloroform/isoamyl alcohol (25:24:1) and precipitated overnight at -20°C.\nLibraries of ChIP DNA were prepared using the KAPA Hyper Prep Kit (KAPA Biosystems) according to manufacturer's instructions, and samples were multiplexed with Illumina adapters (NEB)."; [Cell type]'triple-negative breast cancer''cell line: SUM159; cell type: triple-negative breast cancer; chip antibody: input; ', 'cell line: SUM159; cell type: triple-negative breast cancer; chip antibody: SMAD3 (Abcam, ab28379); ', 'cell line: WHIM12; cell type: triple-negative breast cancer; chip antibody: input; ', 'cell line: WHIM12; cell type: triple-negative breast cancer; chip antibody: SMAD3 (Abcam, ab28379); ', 'cell line: SUM159; cell type: triple-negative breast cancer; chip antibody: V5 (Abcam, ab9116); ', 'cell line: WHIM12; cell type: triple-negative breast cancer; chip antibody: V5 (Abcam, ab9116); ' GSE128790 Homo sapiens 112 Other; Expression profiling by high throughput sequencing GPL18573 GTO sequencing of Human Cell Lines [cell line GTO-seq] 2019-03-25 We first validated the robustness and high throughput capability of the GTO protocol in multiple cell lines. The key step to success of GTO is determining the optimum number of cycles for first amplification of cDNA. This step needs to be result in a balance between cDNA and gDNA reads so that the gene expression profiles generated are good while not comprimising on the CNA profile quality. This validation was done in SKBR3, A375 and BT549 cell lines. They were then compared to 315A control diploid cell line also processed by the GTO method. The scRNAseq and scDNAseq data generated by GTO was alsocompared to bulk RNAseq and DNAseq data generated in triplicates for each cell line by traditional methods. After the method was tested in cell lines, we next applied the method to mouse models to understand tumor biology. The mouse model we used here is an orthotopic transplantation model of pancreatic cancer in syngenic mice. EGFP positive KPC 1199 tumor cells were injected into the pancreas of adult wild-type mice to generate primary tumors in pancreas and metastases in liver, spleen, peritoneum and kidneys. These primary tumors and mets were then extracted and dissociated into single cell suspensions. The single cell suspensions were analyzed by flow cytometry with antibodies against CD45, Epcam and for endogeneous GFP to isolate single stromal and tumor cells. These cells were then processed by GTP protocol to analyze gDNA by CNV profiles and RNA through read counts from the same cell. To validate our data and also have controls, we generated scRNAseq gene expression data and scDNAseq CNA profiles from the 2D cells at the same passage number at which they were injected into the mice. The scRNAseq data was generated using Fluidigm C1 machine on theie medium IFC for mRNA seq according to user manual instructions. The scDNAseq data for CNA profiles was generated by sorting single nuclei into PCR plates and then using SeqXE kit from Sigma Aldrich for Whole genome amplification using their instructions again. The data analysis was done similar to scRNAseq or scDNAseq data from GTO. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE128790 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA528898 https://www.ebi.ac.uk/ena/browser/view/PRJNA528898 https://www.ncbi.nlm.nih.gov/sra?term=SRP189327 [Overal design]In this study we describe a new method for GTO (Genomics Transcriptomics One-Tube) that allows for simeltaneous sequencing of RNA and DNA from a single cell in the same tube. This method relies on dual amplification. The first amplification is done immediately after the mRNA is transcribed to cDNA using SMART-Seq2 protocol (Picelli et al., 2014) to increase the level of cDNA to that comparable to gDNA. The second amplification with universal primers from SeqXE kit for whole genome amplification (from Sigma Aldrich) amplifies the cDNA and gDNA fragments to amounts required for library preparation. The reads generated from this mixed library are separated bioinformatically to exonic and nonexonic reads depending on where they align in the reference genome to generate the RNAseq and DNAseq data respectively. We present data generated from single in-vitro cells of multiple cell lines (A375, BT549, SKBR3, 315A) and also from single in-vivo cells isolated from tumors of an orthotopic tranplantation mouse model of pancreatic cancer (using KPC1199-EGFP cell line). GTO sequencing to analyze RNA and DNA from single cell; [Treatment]'No treatment'; [Growth]'Cells were cultured in respective media at 37C, 5% CO2'; [Extraction]'Cells were trypsinized, diluted to 1000cells/ml and handpicked as single cells in 10x Lysis buffer\nSingle cells isolated into 10x Lysis Buffer with Rnase inhibitor were processed for mRNA transcription for first strand synthesis and cDNA amplification following SMART-Seq2 protocol. Samples were then treated ionically to fragment gDNA and cDNA to 400-700bp fragments. Later gDNA was amplified using SeqXE kit from Sigma Aldirch using manufacturer instructions. Libraries were made by end repair, Adenylation, Adapter ligation and PCR steps.'; [Cell type]'Source: ''cell line: A375_Melanoma cancer cell line; cell line source: Skin; culture type: Adherent cell line; media: DMEM with 10% FBS and 1% Pencillin/Streptomycin; molecule type: genomic DNA and mRNA; ', 'cell line: BT549_Triple negative breast cancer cell line; cell line source: Breast; culture type: Adherent cell line; media: RPMI with 10% FBS and 1% Pencillin/Streptomycin; molecule type: genomic DNA and mRNA; ', 'cell line: SKBR3_Her2 overexpresson breast cancer cell line; cell line source: Breast; culture type: Adherent cell line; media: DMEM with 10% FBS and 1% Pencillin/Streptomycin; molecule type: genomic DNA and mRNA; ', 'cell line: 315A_Diploid lymphoblastoid cell line; cell line source: Lymphoblastoid; culture type: Suspension cell line; media: RPMI with 10% FBS and 1% Pencillin/Streptomycin; molecule type: genomic DNA and mRNA; ' GSE44203 Homo sapiens 12 Expression profiling by array GPL14951 Transcription factor activator protein 2C (TFAP2C) regulates luminal differentiation in mammary development and carcinogenesis 2013-02-08 Molecular subtypes of breast cancer are characterized by patterns of gene expression, which can be used to predict response to therapy and overall clinical outcome. The luminal breast cancer subtypes are defined by the expression of ER-alpha (ERa) and a set of ERa-associated genes. The transcription factor activator protein 2C (TFAP2C, AP-2C, AP-2g) transcription factor plays a critical role in regulating cell growth and differentiation during ectodermal development and has been implicated in the regulation of ERa and other luminal-associated genes in breast cancer. While TFAP2C has been established as a prognostic factor in human breast cancer, the role of TFAP2C in development of the luminal epithelial cells in the normal mammary gland and in breast cancer have remained elusive. Herein, we demonstrate a critical role of TFAP2C in maintaining the luminal differentiation phenotype during normal mammary development and in luminal breast carcinoma cell lines. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE44203 TFAP2C governs the luminal epithelial phenotype in mammary development and carcinogenesis. Oncogene 6.634 https://doi.org/10.1038/onc.2013.569 {Oncogene (6.634): 10.1038/onc.2013.569} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA189059 https://www.ebi.ac.uk/ena/browser/view/PRJNA189059 None [Overal design]Total RNA from MCF7 cells with and without knockdown of TFAP2c. 3 biological replicates, with 2 technical replicates each, were performed for each sample type.; [Treatment]'In order to constantly knockdown TFAP2C expression in the MCF7 cell line, commercially available MISSION shRNA Lentiviral Particles based on pLKO.1-puro vector containing shRNA targeting TFAP2C (Cat# TRCN0000019745) and Non-Mammalian shRNA Control (Cat# SHC002) were used (Sigma-Aldrich, St. Louis, MO, USA).'; [Growth]'The MCF7 cell line was obtained from the American Type Culture Collection and grown in appropriate medium at 37 oC in a humidified 5% CO2 incubator.'; [Extraction]"For RNA isolation, the mirVana Isolation kit № AM1560 (Ambion, USA) was used without enrichment. All procedures were done according to the manufacturer's protocol. All required RNA sample preparations, the subsequent hybridization and performing microarray analysis were done at the University of Iowa DNA Facility according to the manufacturer's recommended protocols."; [Cell type]'Source: ''cell line: MCF7; shRNA: control; ', 'cell line: MCF7; shRNA: TFAP2C; ' GSE114082 Homo sapiens 34 Expression profiling by array GPL14951 Gene expression profiling of primary HER2-positive breast cancers before and after brief exposure to single agent neoadjuvant trastuzumab 2018-05-06 Tumor incisional biopsies were obtained at baseline and after brief-exposure to single-agent trastuzumab from patients enrolled on the TRastuzumab-UPfront-in-HER2-positive-locally-advanced- BC (TRUP) window-of-opportunity trial. Gene expression profiling was conducted on these tumor biopsies to identify transcriptional features at baseline and changes upon brief-exposure to trastuzumab associated with response to short term trastuzumab and the complete pre-operative therapy https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE114082 Early immune modulation by single-agent trastuzumab as a marker of trastuzumab benefit. British journal of cancer 5.416 https://doi.org/10.1038/s41416-018-0318-0 {British journal of cancer (5.416): 10.1038/s41416-018-0318-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA464245 https://www.ebi.ac.uk/ena/browser/view/PRJNA464245 None [Overal design]Gene expression profiling was performed using RNA from frozen core biopsies from 17 patients with primary HER2-positive (HER2+) tumors before and after brief-exposure treatment with single agent neoadjuvant trastuzumab.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with QIAGEN FFPE RNeasy mini kit in accordance with the prescribed protocol provided with the kit.'; [Cell type]'Source: ''patient id: 1; time: Pre; tumor size: T2; lymph node status: pos; estrogen receptor: neg; progesteron receptor: neg; grade: II; clinical dimension: 35; ki67 %: 40; ', 'patient id: 1; time: Post; tumor size: T2; lymph node status: pos; estrogen receptor: neg; progesteron receptor: neg; grade: II; clinical dimension: 26; ki67 %: 35; ', 'patient id: 2; time: Pre; tumor size: T2; lymph node status: neg; estrogen receptor: pos; progesteron receptor: neg; grade: II; clinical dimension: 31; ki67 %: 12; ', 'patient id: 2; time: Post; tumor size: T2; lymph node status: neg; estrogen receptor: pos; progesteron receptor: neg; grade: II; clinical dimension: 25; ki67 %: 10; ', 'patient id: 3; time: Pre; tumor size: T2; lymph node status: pos; estrogen receptor: neg; progesteron receptor: neg; grade: III; clinical dimension: 35; ki67 %: 30; ', 'patient id: 3; time: Post; tumor size: T2; lymph node status: pos; estrogen receptor: neg; progesteron receptor: neg; grade: III; clinical dimension: NA; ki67 %: NA; ', 'patient id: 4; time: Pre; tumor size: T2; lymph node status: neg; estrogen receptor: neg; progesteron receptor: neg; grade: III; clinical dimension: 40; ki67 %: 35; ', 'patient id: 4; time: Post; tumor size: T2; lymph node status: neg; estrogen receptor: neg; progesteron receptor: neg; grade: III; clinical dimension: 10; ki67 %: 35; ', 'patient id: 5; time: Pre; tumor size: T2; lymph node status: neg; estrogen receptor: neg; progesteron receptor: neg; grade: III; clinical dimension: 30; ki67 %: 40; ', 'patient id: 5; time: Post; tumor size: T2; lymph node status: neg; estrogen receptor: neg; progesteron receptor: neg; grade: III; clinical dimension: 22; ki67 %: 20; ', 'patient id: 6; time: Pre; tumor size: T4; lymph node status: NA; estrogen receptor: pos; progesteron receptor: pos; grade: III; clinical dimension: 35; ki67 %: 50; ', 'patient id: 6; time: Post; tumor size: T4; lymph node status: NA; estrogen receptor: pos; progesteron receptor: pos; grade: III; clinical dimension: 40; ki67 %: 40; ', 'patient id: 7; time: Pre; tumor size: T3; lymph node status: NA; estrogen receptor: neg; progesteron receptor: neg; grade: II; clinical dimension: 30; ki67 %: 20; ', 'patient id: 7; time: Post; tumor size: T3; lymph node status: NA; estrogen receptor: neg; progesteron receptor: neg; grade: II; clinical dimension: 25; ki67 %: 0; ', 'patient id: 8; time: Pre; tumor size: T2; lymph node status: neg; estrogen receptor: pos; progesteron receptor: neg; grade: III; clinical dimension: 30; ki67 %: 25; ', 'patient id: 8; time: Post; tumor size: T2; lymph node status: neg; estrogen receptor: pos; progesteron receptor: neg; grade: III; clinical dimension: 22; ki67 %: 0; ', 'patient id: 9; time: Pre; tumor size: T2; lymph node status: pos; estrogen receptor: neg; progesteron receptor: neg; grade: III; clinical dimension: 40; ki67 %: 15; ', 'patient id: 9; time: Post; tumor size: T2; lymph node status: pos; estrogen receptor: neg; progesteron receptor: neg; grade: III; clinical dimension: 10; ki67 %: 0; ', 'patient id: 10; time: Pre; tumor size: T2; lymph node status: neg; estrogen receptor: pos; progesteron receptor: neg; grade: II; clinical dimension: 20; ki67 %: 22; ', 'patient id: 10; time: Post; tumor size: T2; lymph node status: neg; estrogen receptor: pos; progesteron receptor: neg; grade: II; clinical dimension: 34; ki67 %: 12; ', 'patient id: 11; time: Pre; tumor size: T1; lymph node status: neg; estrogen receptor: pos; progesteron receptor: neg; grade: II; clinical dimension: 18; ki67 %: 5; ', 'patient id: 11; time: Post; tumor size: T1; lymph node status: neg; estrogen receptor: pos; progesteron receptor: neg; grade: II; clinical dimension: 0; ki67 %: 0; ', 'patient id: 12; time: Pre; tumor size: T3; lymph node status: pos; estrogen receptor: neg; progesteron receptor: neg; grade: III; clinical dimension: 60; ki67 %: 23; ', 'patient id: 12; time: Post; tumor size: T3; lymph node status: pos; estrogen receptor: neg; progesteron receptor: neg; grade: III; clinical dimension: 30; ki67 %: 30; ', 'patient id: 13; time: Pre; tumor size: T3; lymph node status: pos; estrogen receptor: neg; progesteron receptor: neg; grade: III; clinical dimension: 20; ki67 %: 28; ', 'patient id: 13; time: Post; tumor size: T3; lymph node status: pos; estrogen receptor: neg; progesteron receptor: neg; grade: III; clinical dimension: 35; ki67 %: 20; ', 'patient id: 14; time: Pre; tumor size: T3; lymph node status: neg; estrogen receptor: neg; progesteron receptor: pos; grade: III; clinical dimension: 60; ki67 %: 80; ', 'patient id: 14; time: Post; tumor size: T3; lymph node status: neg; estrogen receptor: neg; progesteron receptor: pos; grade: III; clinical dimension: 40; ki67 %: 60; ', 'patient id: 15; time: Pre; tumor size: T3; lymph node status: neg; estrogen receptor: pos; progesteron receptor: pos; grade: III; clinical dimension: 80; ki67 %: 28; ', 'patient id: 15; time: Post; tumor size: T3; lymph node status: neg; estrogen receptor: pos; progesteron receptor: pos; grade: III; clinical dimension: 60; ki67 %: 20; ', 'patient id: 16; time: Pre; tumor size: T2; lymph node status: pos; estrogen receptor: pos; progesteron receptor: pos; grade: III; clinical dimension: 40; ki67 %: 30; ', 'patient id: 16; time: Post; tumor size: T2; lymph node status: pos; estrogen receptor: pos; progesteron receptor: pos; grade: III; clinical dimension: 50; ki67 %: 18; ', 'patient id: 17; time: Pre; tumor size: T3; lymph node status: neg; estrogen receptor: pos; progesteron receptor: neg; grade: III; clinical dimension: 80; ki67 %: 50; ', 'patient id: 17; time: Post; tumor size: T3; lymph node status: neg; estrogen receptor: pos; progesteron receptor: neg; grade: III; clinical dimension: 90; ki67 %: 50; ' GSE15746 Homo sapiens 52 Methylation profiling by genome tiling array GPL8459 Methylation detection Oligonucleotide Microarray Analysis: high resolution method for CpG island methylation detection 1 2009-04-20 Methylation of CpG islands associated with genes can affect the expression of the proximal gene, and methylation of non associated CpG islands correlates to genomic instability. This epigenetic modification has been shown to be important in many pathologies, from development and disease to cancer. We report the development of a novel high-resolution microarray that detects the methylation status of over 25,000 CpG islands in the human genome. Experiments were performed to demonstrate low system noise in the methodology and that the array probes have a high signal to noise ratio. Methylation measurements between different cell lines were validated demonstrating the accuracy of measurement. We then identified alterations in CpG islands, both those associated with gene promoters, as well as non-promoter associated islands in a set of breast and ovarian tumors. We demonstrate that this methodology accurately identifies methylation profiles in cancer and in principle it can differentiate any CpG methylation alterations and can be adapted to analyze other species. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15746 Methylation detection oligonucleotide microarray analysis: a high-resolution method for detection of CpG island methylation. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkp413 {Nucleic acids research (11.147): 10.1093/nar/gkp413} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA123031 https://www.ebi.ac.uk/ena/browser/view/PRJNA123031 None [Overal design]We have developed a method to profile genome wide methylation. 12 breast normal samples and matching tumors from these individuals and an additional 28 tumor samples from other individuals were analyzed for CpG methylation. After inter array normalization, the tumor samples were taken together and the methylation compared to that of the normal samples to identify regions of the CpG islands that are significantly altered between the two datasets. Some of these regions were validated for their methylation as a proof of principle for the method.; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA was extracted by first homeginizing tumor in lysis buffer and incubating for 60 minutes followed by 3 phenol extractions and precipitiation.'; [Cell type]'Source: ''tissue: breast; disease state: tumor; ', 'tissue: breast; disease state: normal; ' GSE123366 Mus musculus 7 Expression profiling by high throughput sequencing GPL17021 Single-cell transcriptomic analysis of mammary tumors reveals distinct patterns of hierarchical and subtype heterogeneity 2018-12-05 Breast cancer stem cells (BCSCs) contribute to intra-tumoral heterogeneity and therapeutic resistance. However, the binary concept of universal BCSCs co-existing with bulk tumor cells is over-simplified. Through single-cell RNA-sequencing, we found that Neu, PyMT and BRCA1-null mammary tumors each corresponded to a spectrum of minimally overlapping cell differentiation states without a universal BCSC population. Instead, our analyses revealed that these tumors contained distinct lineage-specific tumor propagating cells (TPCs) and this is reflective of the self-sustaining capabilities of lineage-specific stem/progenitor cells in the mammary epithelial hierarchy. By understanding the respective tumor hierarchies, we were able to identify CD14 as a TPC marker in the Neu tumor. Additionally, single-cell breast cancer subtype stratification revealed the co-existence of multiple breast cancer subtypes within tumors. Collectively, our findings emphasize the need to account for lineage-specific TPCs and the hierarchical composition within breast tumors, as these heterogenous sub-populations can have differential therapeutic susceptibilities. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE123366 Single-cell RNA-sequencing reveals distinct patterns of cell state heterogeneity in mouse models of breast cancer. eLife 7.551 https://doi.org/10.7554/eLife.58810 {eLife (7.551): 10.7554/eLife.58810} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA508501 https://www.ebi.ac.uk/ena/browser/view/PRJNA508501 https://www.ncbi.nlm.nih.gov/sra?term=SRP173246 [Overal design]We compared the gene expression profile at single-cell level of four breast tumor models in mice.; [Treatment]'Tumors were not treated and were harvested when the size was about 1000mm3.'; [Growth]'Tumor cells derived from primary tumors were cultured in DMEM/F12 supplemented with 10% FBS, 10ng/ml EGF, 20μgml insulin and 50units/ml penicillin-streptomycin. 4T1 cells were obtained from ATCC and cultured in DMEM supplemented with 10% FBS. 4T1 cells were transduced with pLenti-GFP (LTV-400, Cell Biolabs) before transplantation experiments. FF99WT cells were derived from an autochthonous MMTV-PyMT tumor with FIP200 floxed alleles (essentially wild-type without Cre recombinase). FF99WT cells were used to generate the PyMT transplant tumor that was analyzed by scRNA-seq. The Neu and BRCA1-null tumors were endogeneous spontaneous mammary tumors for MMTV-Neu and Brca1 F/F; Trp53 F/F; K14-Cre mice respectively.', 'Tumor cells derived from primary tumors were cultured in DMEM/F12 supplemented with 10% FBS, 10ng/ml EGF, 20μgml insulin and 50units/ml penicillin-streptomycin. 4T1 cells were obtained from ATCC and cultured in DMEM supplemented with 10% FBS. 4T1 cells were transduced with pLenti-GFP (LTV-400, Cell Biolabs) before transplantation experiments. FF99WT cells were derived from an autochthonous MMTV-PyMT tumor with FIP200 floxed alleles62 (essentially wild-type without Cre recombinase). FF99WT cells were used to generate the PyMT transplant tumor that was analyzed by scRNA-seq. N148 cells were derived from the autochthonous MMTV-Neu tumor with FIP200 floxed alleles (essentially wild-type without Cre recombinase) that was analyzed by sc-RNAseq.'; [Extraction]'Dissected primary tumors were cut and minced and then incubated in DMEM/F12 supplemented with 5% FBS, 1x antibiotic-antimycotics, gentamycin (20 µg/mL) (all from Invitrogen), collagenase (300 units/mL), and hyaluronidase (100 units/mL) (Worthington Biomedical) for 2 hours at 37 oC. They were then centrifuged at 400 g for 5 minutes, and the pellets were washed with PBS, and suspended in 0.05% trypsin/0.025% EDTA (Invitrogen) before incubated for 5 minutes at 37 oC. An equal volume of DMEM/F12 containing 5% FBS and DNase I (20 units/ml, Roche) was then added to stop the digestion. After filtering through a 40µm nylon mesh (BD Biosciences), the cells were collected by centrifugation at 400g for 5 min and re-suspended in ACK lysis buffer (Invitrogen) to lyse red blood cells. Tumor single-cell suspensions were incubated with CD24-PE (553262, BD Biosciences), CD31-APC (102410, Biolegend), CD45-APC (103112, Biolegend), Ter119-APC (116212, Biolegend) according to manufacturer’s instructions for 20 minutes at 40C. Following that, cells were then rinsed and resuspended in HBSS before sorting or analysis by FACSAria or FACSCanto instruments (BD Biosciences). CD24+ Lin- (Ter119-, CD31-, CD45-) were sorted for single-cell analysis.\nSingle-cell cDNA libraries were prepared using the 10x Chromium single-cell kit (3’ gene expression platform version 2 chemistry) according to manufacturer’s instructions for each tumor separately.', 'Dissected primary tumors were cut and minced and then incubated in DMEM/F12 supplemented with 5% FBS, 1x antibiotic-antimycotics, gentamycin (20 µg/mL) (all from Invitrogen), collagenase (300 units/mL), and hyaluronidase (100 units/mL) (Worthington Biomedical) for 2 hours at 37 oC. They were then centrifuged at 400 g for 5 minutes, and the pellets were washed with PBS, and suspended in 0.05% trypsin/0.025% EDTA (Invitrogen) before incubated for 5 minutes at 37 oC. An equal volume of DMEM/F12 containing 5% FBS and DNase I (20 units/ml, Roche) was then added to stop the digestion. After filtering through a 40µm nylon mesh (BD Biosciences), the cells were collected by centrifugation at 400g for 5 min and re-suspended in ACK lysis buffer (Invitrogen) to lyse red blood cells. Tumor single-cell suspensions were incubated with CD24-PE (553262, BD Biosciences), CD31-APC (102410, Biolegend), CD45-APC (103112, Biolegend), Ter119-APC (116212, Biolegend) according to manufacturer’s instructions for 20 minutes at 40C. Following that, cells were then rinsed and resuspended in HBSS before sorting or analysis by FACSAria or FACSCanto instruments (BD Biosciences). For isolation of CD14+ cells, CD14-APC/Cy7 (123317, Biolegend) antibody was used.\nSingle-cell cDNA libraries were prepared using the 10x Chromium single-cell kit (3’ gene expression platform version 2 chemistry) according to manufacturer’s instructions for each tumor separately.'; [Cell type]'Source: ''developmental stage: Adult; breast tumor model: 4T1 mammary tumor; tissue: Mammary gland tumor; strain: BALB/C; ', 'developmental stage: Adult; breast tumor model: BRCA1null mammary tumor; tissue: Mammary gland tumor; strain: FVB/NJ; ', 'developmental stage: Adult; breast tumor model: MMTV-PyMT driven tumor; tissue: Mammary gland tumor; strain: FVB/NJ; ', 'developmental stage: Adult; breast tumor model: MMTV-Neu driven tumor; tissue: Mammary gland tumor; strain: FVB/NJ; ', 'developmental stage: Adult; tissue: Mammary gland tumor; breast tumor model: MMTV-PyMT driven tumor; strain: FVB/NJ; ' GSE9742 Homo sapiens 9 Expression profiling by array GPL6171 The microRNAs miR-373 and miR-520c promote tumor migration, invasion and metastasis 2007-11-30 MicroRNAs (miRNAs) are single-stranded noncoding RNAs that play important roles in many biological processes. Although the oncogenic and tumor suppressive functions of several miRNAs have been characterized, the role of miRNAs in mediating tumor metastasis was only recently addressed and still remain largely unexplored. To identify potential metastasis-promoting miRNAs, we set up a genetic screen using a non-metastatic human breast tumor cell line that was transduced with a miRNA expression library and subjected to a trans-well migration assay. We found human miR-373 and 520c to stimulate cancer cell migration as well as tumor cell invasion in vitro and in vivo, and that certain cancer cell lines depend on endogenous miR-373 activity to migrate efficiently. Mechanistically, the migration phenotype of miR-373 and miR-520c can be explained by their suppression of CD44 expression. Finally, we found significant up-regulation of miR-373 expression in clinical breast cancer primary and metastasis samples that inversely correlated with CD44 expression. Taken together, our study indicates that miRNAs are involved in tumor migration and invasion and implicates miR-373 and conceivably miR-520c as metastasis-promoting miRNAs. Keywords: human breast cancer cell MCF7 vs MCF7 expressing miR-373 vs MCF7 expressing miR-520c https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE9742 The microRNAs miR-373 and miR-520c promote tumour invasion and metastasis. Nature cell biology 17.728 https://doi.org/10.1038/ncb1681 {Nature cell biology (17.728): 10.1038/ncb1681} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA103659 https://www.ebi.ac.uk/ena/browser/view/PRJNA103659 None [Overal design]Illumina human v6 array was used for MCF7 cells, MCF7 cells stably expressing miR-373 and MCF7 cells stably expressing miR-520c. Triplicate samples were used to performe gene expression analysis on each cell lines.; [Treatment]'None'; [Growth]'None'; [Extraction]'total RNA'; [Cell type]'Source: ''' GSE69893 Homo sapiens 12 Expression profiling by array GPL10558 AKT antagonist AZD5363 influences estrogen receptor function in endocrine resistant breast cancer and synergizes with fulvestrant (ICI182780) in vivo 2015-06-15 Phosphoinositide-3-kinase/protein-kinaseB/mammalian target of rapamycin (PI3K/AKT/mTOR) signalling plays an important role in breast cancer (BC). Its interaction with estrogen receptor (ER) signalling becomes more complex and inter-dependent with acquired endocrine resistance. Targeting mTOR combined with endocrine therapy has shown clinical utility, however, a negative feedback-loop exists downstream of PI3K/AKT/mTOR. Direct blockade of AKT together with endocrine therapy may improve BC treatment. AZD5363, a novel pan-AKT kinase catalytic inhibitor, was examined in a panel of ER+ BC cell lines (MCF7, HCC1428, T47D, ZR75.1) adapted to long-term-estrogen-deprivation (LTED) or tamoxifen (TamR). AZD5363 caused a dose-dependent decrease in proliferation in all cell lines tested (GI50<500nM) except HCC1428 and HCC1428-LTED. T47D-LTED and ZR75-LTED were the most sensitive of the lines (GI50~100nM). AZD5363 re-sensitised TamR cells to tamoxifen and acted synergistically with fulvestrant. AZD5363 decreased p-AKT/mTOR targets leading to a reduction in ERα-mediated transcription in a context specific manner and concomitant decrease in recruitment of ER and CREB-binding protein (CBP) to estrogen-response-elements located on the TFF1, PGR and GREB1 promoters. Furthermore, AZD5363 reduced expression of cell-cycle-regulatory proteins. Global gene expression highlighted ERBB2-ERBB3, ERK5 and IGF1 signaling pathways driven by MYC as potential feedback-loops. Combined treatment with AZD5363 and fulvestrant showed synergy in an ER+ patient derived xenograft and delayed tumour progression post-cessation of therapy. These data support the combination of AZD5363 with fulvestrant as a potential therapy for BC that is sensitive or resistant to E-deprivation or tamoxifen and that activated AKT is a determinant of response, supporting the need for clinical evaluation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE69893 AKT Antagonist AZD5363 Influences Estrogen Receptor Function in Endocrine-Resistant Breast Cancer and Synergizes with Fulvestrant (ICI182780) In Vivo. Molecular cancer therapeutics 4.856 https://doi.org/10.1158/1535-7163.MCT-15-0143 {Molecular cancer therapeutics (4.856): 10.1158/1535-7163.MCT-15-0143} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA287034 https://www.ebi.ac.uk/ena/browser/view/PRJNA287034 None [Overal design]Cell lines were treated in biological triplicates in the absence of estrogen with or without AZD5363 for 24hours in order to identify gene changes associated with perturbation of AKT signalling; [Treatment]'None'; [Growth]'None'; [Extraction]"mRNA from treated cells was extracted with RNeasy Mini Kit (Qiagen), as per the manufacturer's instructions, and quantification performed using the Agilent 2100 Bioanalyzer (Expert Software version B.02.03) with RNA Nano LabChip Kits (Agilent Technologies)."; [Cell type]'Source: ''compound: Mutant PIK3CA, sensitive to estrogen deprivation; cell line: MCF7; ', 'compound: Mutant PIK3CA, sensitive to estrogen deprivation, treated with AKT inhibitor (AZD5363); cell line: MCF7; ', 'compound: LTED- Mutant PIK3CA, resistant to estrogen deprivation; cell line: MCF7; ', 'compound: LTED+AZD5363- Mutant PIK3CA, resistant to estrogen deprivation, treated with AKT inhibitor (AZD5363); cell line: MCF7; ' GSE105402 Homo sapiens 18 Expression profiling by array GPL17586 Cdk4-inhibitor induces tumor regression of Bladder cancer in vivo 2017-10-20 Cdk4/6 inhibitors have shown to increase overall survival in hormone-positive breast tumors, but whether other solid tumors could respond to these inhibitors has not yet defined. Here we show that Palbociclib (a Cdk4/6 specific inhibitor in clinic use) treatment exerts antiproliferative effects in vivo using a bladder cancer cell lines. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE105402 CDK4/6 Inhibitor as a Novel Therapeutic Approach for Advanced Bladder Cancer Independently of RB1 Status. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-18-0685 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-18-0685} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA415124 https://www.ebi.ac.uk/ena/browser/view/PRJNA415124 None [Overal design]Gene expression was compared between bladder cancer cell lines with the same cell lines treated with Cdk4-inhibitor (IC50); [Treatment]'Control (PBS-treated) and palbociclib-treated (IC50) RT112, J82 and 5637 cells, were analyzed. Cell pool transcriptomes were obtained from 3 different p100 dishes grown to 70-80% confluence.'; [Growth]"The bladder cancer cell lines were maintained in Dulbecco's Modified Eagle Medium GlutaMAX™ (Gibco-BRL Life Technologies) with 10% fetal bovine serum (Hyclone) and 1% antibiotic-antimycotic (Gibco-BRL Life Technologies) at 37°C in a humidified atmosphere of 5% CO2."; [Extraction]"Extraction of total RNA was performed using miRNeasy Mini Kit (Qiagen) according to the manufacturer's instructions."; [Cell type]'Bladder cell line''cell line: J82; cell type: Bladder cell line; treated with: PBS (control); ', 'cell line: J82; cell type: Bladder cell line; treated with: palbociclib (IC50); ', 'cell line: RT112; cell type: Bladder cell line; treated with: PBS (control); ', 'cell line: RT112; cell type: Bladder cell line; treated with: palbociclib (IC50); ', 'cell line: 5637; cell type: Bladder cell line; treated with: PBS (control); ', 'cell line: 5637; cell type: Bladder cell line; treated with: palbociclib (IC50); ' GSE116874 Homo sapiens 14 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Oncogenic Notch promotes long-range regulatory interactions within hyperconnected 3D cliques [Rec1_ChIP-seq] 2018-07-10 Purpose: To investigate the impact of oncogenic Notch on the 3D genome organization of cancer cells. Methods: We generated cohesin HiChIP and 1D epigenomic data sets in two different Notch-dependent cancer cell types, triple-negative breast cancer (TNBC) and mantle cell lymphoma (MCL), in the Notch-on and -off states. Results: We report here that Notch transcription complexes control their direct target genes through two distinct regulatory modes: either through existing loops or by facilitating new long-range regulatory interactions. This combination of pre-existing and Notch-promoted loops coalesce enhancers and promoters to form highly interacting clusters, termed “3D cliques”. Notch preferentially activates enhancers and promotes looping interactions within highly connected 3D cliques that regulate key oncogenes. Conclusions: These observations suggest a general mechanism that oncogenic transcription factors can exploit to regulate the transcriptional outputs of cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE116874 Oncogenic Notch Promotes Long-Range Regulatory Interactions within Hyperconnected 3D Cliques. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2019.01.006 {Molecular cell (14.548): 10.1016/j.molcel.2019.01.006} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA480474 https://www.ebi.ac.uk/ena/browser/view/PRJNA480474 https://www.ncbi.nlm.nih.gov/sra?term=SRP152963 [Overal design]ChIP-seq, RNA-seq and HiChIP in Notch-on, -off, -recovery conditions in TNBC and MCL cell lines to profile Notch transcriptional complex binding, histone modification, Notch target genes and contact between regulatory elements.; [Treatment]'Cells were treated with the GSI compound E (1 μM, Calbiochem cat# 565790) for 72 hours, washed, and then cultured for 5 hours in media containing 1μM GSI (mock washout) or DMSO (washout) as previously described (Weng et al., 2006).'; [Growth]'Rec-1 (male) cells were grown in RPMI 1640 (Corning, cat# 10-040-CM) supplemented with 10% fetal bovine serum (Hyclone, cat# SH30070.03), 2 mM L-glutamine (Corning, cat# 25-005-CI), 100 U/mL and 100 μg/mL penicillin/streptomycin (Corning, cat# 30-002-CI), 100 mM nonessential amino acids (Gibco, cat# 11140-050), 1mM sodium pyruvate (Gibco, cat#11360-070) and 0.1mM of 2-mercaptoethanol (Sigma, cat# M6250).'; [Extraction]'ChIP-seq was performed as previously described (Ryan et al., 2017). Briefly, chromatin samples prepared from appropriate number of fixed cells (10^7 for histone modifications and 4 x 10^7 for transcription factors) were sonicated and cleared with recombinant protein G–conjugated Agarose beads (Invitrogen, cat# 15920-010) and subsequently immunoprecipitated with antibodies recognizing Notch1 (Wang et al., 2014), RBPJ (D10A4) (CST, cat# 5313), H3K27ac (Active Motif, cat# 39133), H3K27me3 (EMD Millipore cat# 07-449), H3K4me1 (Abcam, cat# ab8895), Smc1a (Bethyl, cat# A300-055A) and CTCF (EMD Millipore cat# 07-729). Antibody-chromatin complexes were captured with recombinant protein G–conjugated Agarose beads, washed with Low Salt Wash Buffer, High Salt Wash Buffer, LiCl Wash Buffer and TE buffer with 50mM NaCl and eluted. Input sample was prepared by the same approach without immunoprecipitation. After reversal of cross-linking, RNase and Proteinase K (Invitrogen, cat# 25530-049) treatment were performed and DNA was purified with QIAquick PCR Purification Kit (Qiagen, cat# 28106).\nLibraries were then prepared using the NEBNext Ultra II DNA library Prep Kit for Illumina (NEB, cat# E7645S). Two replicates were performed for each condition. Indexed libraries were validated for quality and size distribution using a TapeStation 2200 (Agilent). Single end sequencing (75 bp) or Paired-end sequencing (38 bp+38 bp) was performed on a NextSeq 550.', 'ChIP-seq was performed as previously described (Ryan et al., 2017). Briefly, chromatin samples prepared from appropriate number of fixed cells (107 for histone modifications and 4 x 107 for transcription factors) were sonicated and cleared with recombinant protein G–conjugated Agarose beads (Invitrogen, cat# 15920-010) and subsequently immunoprecipitated with antibodies recognizing Notch1 (Wang et al., 2014), RBPJ (D10A4) (CST, cat# 5313), H3K27ac (Active Motif, cat# 39133), H3K27me3 (EMD Millipore cat# 07-449), H3K4me1 (Abcam, cat# ab8895), Smc1a (Bethyl, cat# A300-055A) and CTCF (EMD Millipore cat# 07-729). Antibody-chromatin complexes were captured with recombinant protein G–conjugated Agarose beads, washed with Low Salt Wash Buffer, High Salt Wash Buffer, LiCl Wash Buffer and TE buffer with 50mM NaCl and eluted. Input sample was prepared by the same approach without immunoprecipitation. After reversal of cross-linking, RNase and Proteinase K (Invitrogen, cat# 25530-049) treatment were performed and DNA was purified with QIAquick PCR Purification Kit (Qiagen, cat# 28106).\nLibraries were then prepared using the NEBNext Ultra II DNA library Prep Kit for Illumina (NEB, cat# E7645S). Two replicates were performed for each condition. Indexed libraries were validated for quality and size distribution using a TapeStation 2200 (Agilent). Single end sequencing (75 bp) or Paired-end sequencing (38 bp+38 bp) was performed on a NextSeq 550.'; [Cell type]'Mantle cell lymphoma cell line''cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: H3K27me3; drug treatment: GSI-washout; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: H3K27me3; drug treatment: GSI-mock-washout; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: H3K27ac; drug treatment: GSI-washout; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: H3K27ac; drug treatment: GSI-mock-washout; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: input; drug treatment: untreated; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: input; drug treatment: GSI-mock-washout; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: input; drug treatment: GSI-washout; ' GSE52629 Homo sapiens 11 Expression profiling by array GPL6947 Tumorigenic-enriched (TE) and lung-metastatic (LM) derivatives and parental populations from the breast cancer MDA-MB-231 and CN34 cell lines 2013-11-21 The LM2 derivative cell line is described in Minn et al. Nature 2005. The LM1a derivative cell line is described in Tavazoie et al. Nature 2008. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE52629 Identification of molecular determinants of primary and metastatic tumour re-initiation in breast cancer. Nature cell biology 17.728 https://doi.org/10.1038/ncb3148 {Nature cell biology (17.728): 10.1038/ncb3148} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA229498 https://www.ebi.ac.uk/ena/browser/view/PRJNA229498 None [Overal design]Tumorigenic-enriched (TE) and lung-metastatic (LM) derivatives and their respective parental populations, from the breast cancer MDA-MB-231 and CN34 cell lines were transcriptomically compared in order to identify candidate regulators of breast cancer tumor re-initiation.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA from multiple cell lines was extracted using the MiRvana RNA isolation kit (AM1560, Applied Biosystems)'; [Cell type]'breast cancer''cell line: MDA-MB-231; population: parental; cell type: breast cancer; ', 'cell line: MDA-MB-231; population: tumorigenic-enriched; cell type: breast cancer; ', 'cell line: MDA-MB-231; population: lung-metastatic; cell type: breast cancer; ', 'cell line: CN34; population: parental; cell type: breast cancer; ', 'cell line: CN34; population: tumorigenic-enriched; cell type: breast cancer; ', 'cell line: CN34; population: lung-metastatic; cell type: breast cancer; ' GSE89333 Homo sapiens 4 Expression profiling by array GPL570 Downregulation of Cholinergic Receptor Alpha 5 (CHRNA5) in MCF7 breast cancer cells 2016-10-31 Cholinergic Receptor Nicotinic Alpha 5 (CHRNA5), an important susceptibility locus for nicotine addiction and lung cancer, is not well studied in breast cancer. In our study, CHRNA5 was transiently depleted in MCF7 cells and transcriptomic changes were compared to siRNA controls. We for the first time showed by microarray analysis that silencing of CHRNA5 in MCF7 breast cancer cells, downregulated genes involved in the cell cycle and proliferation while resulting in reduced cell viability, DNA synthesis and G1 growth arrest. In addition, simultaneous treatment of CHRNA5 siRNA and topoisomerase inhibitors showed an important role of CHRNA5 in increased drug sensitivity. Phalloidin stained CHRNA5 siRNA treated cells on the other hand exhibited a distinct cellular morphotype with increased cellular extensions and a transcriptome characterized by mixed expression of epithelial-mesenchymal genes. Through bioinformatics analysis of the public transcriptome data we demonstrated a strong positive association of expression signature of CHRNA5 RNAi with that of a differentiated cell as well as hormone starvation. Hence, our study implicates CHRNA5 as an antiproliferative differentiation marker in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE89333 Cholinergic Receptor Nicotinic Alpha 5 (CHRNA5) RNAi is associated with cell cycle inhibition, apoptosis, DNA damage response and drug sensitivity in breast cancer. PloS one 2.776 https://doi.org/10.1371/journal.pone.0208982 {PloS one (2.776): 10.1371/journal.pone.0208982} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA351830 https://www.ebi.ac.uk/ena/browser/view/PRJNA351830 None [Overal design]MCF7 cells were seeded in 6-well plates. After 24 h, cells were treated either with 10nM of siRNA against several CHRNA5 spliced variants (FlexiTube, SI03051111, Qiagen) or the respective negative controls (AllStars Negative Control siRNA, 1027280, Qiagen) using HiPerFect transfection reagent (301704, Qiagen). Treatments were performed for 72h (3 days) after which RNA was extracted. Experiments were performed using two biological replicas. Affymetrix HGU133 Plus 2 platform was used for expression profiling of siRNA treated and corresponding siRNA control exposed MCF7 cells, according to the manufacturer’s protocols.; [Treatment]'After 24 hours, cells were treated either with 10nM of siRNA against several CHRNA5 spliced variants (FlexiTube, SI03051111, Qiagen) or the respective negative control siRNA at the same concentration (AllStars Negative Control siRNA, 1027280, Qiagen) using 12 µl of HiPerFect transfection reagent (301704, Qiagen).'; [Growth]'2 x 10^5 MCF7 cells were seeded in each well of the 6-well plates.'; [Extraction]'1 µg RNA was isolated using RNeasy Mini kit (74104, Qiagen, Hamburg, Germany) according to the manufacturer’s protocols.'; [Cell type]'breast cancer''cell line: MCF-7; cell type: breast cancer; group: Control siRNA; ', 'cell line: MCF-7; cell type: breast cancer; group: CHRNA5 siRNA treatment; ' GSE49345 Homo sapiens 21 Expression profiling by array; Genome binding/occupancy profiling by genome tiling array; Genome binding/occupancy profiling by high throughput sequencing GPL11154; GPL13607; GPL15802 Genomic distribution of human histone H1 subtypes 2013-07-30 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE49345 Mapping of six somatic linker histone H1 variants in human breast cancer cells uncovers specific features of H1.2. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gku079 {Nucleic acids research (11.147) doi:10.1093/nar/gku079}; {The Journal of biological chemistry (None) doi:10.1074/jbc.M114.617324}; 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA213705 https://www.ebi.ac.uk/ena/browser/view/PRJNA213705 None [Overal design]Refer to individual Series; [Treatment]'None', 'no treatment'; [Growth]'T47D-MTVL (RPMI 1640 medium + 10%FBS, 1% glutamine, 1% penicillin/streptomycin)', 'RPMI 1640 medium + 10%FBS, 1%glutamine, 1%penicillin/streptomycin', 'DMEM GlutaMax medium + 10%FBS, 1%penicillin/streptomycin'; [Extraction]"Total RNA was extracted using High Pure RNA isolation kit (Roche) according to the manufacturer's instructions. cDNA was obtained from 100 ng of total RNA using SuperScript VILO cDNA synthesis (Invitrogen). High RNA integrity was assessed by Bioanalyzer nano 6000 assay with RIN numbers 9.5 fopr T47D_r1 and 9.2 for T47D_r2", 'T47D-MTVL or HeLa cells cells were fixed using 1% formaldehyde, harvested and sonicated using a Diagenode Bioruptor to generate chromatin fragments between 200 and 500 bp. To perform the chromatin immunoprecipitation, 30 µg of chromatin was immunoprecipitated overnight using the indicated antibody. Rabbit IgG (Santa Cruz Biothechnology) was used as a control for nonspecific interaction of DNA. Input was prepared with 10% of the chromatin material used for an immunoprecipitation. Immunocomplexes were recovered using Protein A magnetic beads from Millipore. Beads with bound antibody/protein/DNA complexes were washed, decross-linked at 65ºC overnight and immunoprecipitated DNA was recovered using the IPure Kit from Diagenode.', 'T47D-MTVL cells were fixed using 1% formaldehyde, harvested and sonicated using a Diagenode Bioruptor to generate chromatin fragments between 200 and 500 bp. To perform the chromatin immunoprecipitation, 30 µg of chromatin was immunoprecipitated overnight using the indicated antibody. Rabbit IgG (Santa Cruz Biothechnology) was used as a control for nonspecific interaction of DNA. Input was prepared with 10% of the chromatin material used for an immunoprecipitation. Immunocomplexes were recovered using Protein A magnetic beads from Millipore. Beads with bound antibody/protein/DNA complexes were washed, decross-linked at 65ºC overnight and immunoprecipitated DNA was recovered using the IPure Kit from Diagenode.\nDNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''gender: female; tissue: breast cancer ductal carcinoma; cell line: T47D-MTVL; ', 'cell line: T47D-MTVL; stably overexpressing: H1.0-HA; gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-HA (Abcam 9110); ', 'cell line: T47D-MTVL; stably overexpressing: H1.0; gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'cell line: T47D-MTVL; stably overexpressing: H1.2-HA; gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H1.2 (Abcam 4086); ', 'cell line: T47D-MTVL; stably overexpressing: H1.2; gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'cell line: T47D-MTVL; gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H1.2 (Abcam 4086); ', 'cell line: T47D-MTVL; gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'cell line: T47D-MTVL; stably overexpressing: H1.3-HA; gender: female; tissue: breast cancer ductal carcinoma; antibody: H1.3-HA histone protein immunoprecipitated DNA; ', 'cell line: T47D-MTVL; stably overexpressing: H1.3; gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'cell line: T47D-MTVL; stably overexpressing: H1.4-HA; gender: female; tissue: breast cancer ductal carcinoma; antibody: H1.4-HA histone protein immunoprecipitated DNA; ', 'cell line: T47D-MTVL; stably overexpressing: H1.4; gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'cell line: T47D-MTVL; stably overexpressing: H1.5-HA; gender: female; tissue: breast cancer ductal carcinoma; antibody: H1.5-HA histone protein immunoprecipitated DNA; ', 'cell line: T47D-MTVL; stably overexpressing: H1.5; gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'cell line: T47D-MTVL; gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H1X (Abcam 31972); ', 'cell line: T47D-MTVL; gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H3 (Abcam 1791); ', 'cell line: HeLa; gender: female; tissue: cervical cancer; antibody: anti-H1.2 (Abcam 4086); ', 'cell line: HeLa; gender: female; tissue: cervical cancer; antibody: none; ', 'cell line: HeLa; gender: female; tissue: cervical cancer; antibody: anti-H1X (Abcam 31972); ', 'gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-HA (Abcam 9110); ', 'gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H1.2 (Abcam 4086); ', 'gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H1X (Abcam 31972); ', 'gender: female; tissue: breast cancer ductal carcinoma; antibody: H1.4-HA histone protein immunoprecipitated DNA; ', 'gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H3 (Abcam 1791); ' GSE13293 Homo sapiens 210 Expression profiling by array GPL7384; GPL7392; GPL7393 Parity and the genomic signature in the Human Breast 2008-10-21 Case-control study for the analysis of the gene expression profile of epithelial cells microdissected from normal breast tissues obtained from 17 parous and 7 nulliparous women free of breast pathology (controls), and 39 parous and 8 nulliparous women with history of breast cancer (cases). Keywords: genetic modifications https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE13293 Full-term pregnancy induces a specific genomic signature in the human breast. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 5.057 https://doi.org/10.1158/1055-9965.EPI-07-0678 {Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology (5.057): 10.1158/1055-9965.EPI-07-0678} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA109621 https://www.ebi.ac.uk/ena/browser/view/PRJNA109621 None [Overal design]Four-condition experiment: nulliparous case, nulliparous control, parous case and parous control labeled with Cy5 and Universal human reference used as a common reference labeled with Cy3. Moderated t statistic was used as the basic statistic for significance analysis; it was computed for each probe and for each contrast. False discovery rate was controlled using the Benjamini and Hochberg. All genes with P value below a threshold of 0.05 were selected as differentially expressed, maintaining the proportion of false discoveries in the selected group below the threshold value, in this case 5%. Breast 11 parous control HuII, Breast 28 parous case HuII, and Breast 62 nulliparous control HuIII excluded: raw data is missing; [Treatment]'None'; [Growth]'None'; [Extraction]"From laser capture microdissection samples the RNA was extracted using TRIzol according with manufacturer's protocol", 'not applicable'; [Cell type]'Source: ''Age at diagnosis: 50; Age at first birth: 33; Parity status: Parous control; Breast biopsy diagnosis: Fibrocystic changes; ', '', 'Age at diagnosis: 59; Age at first birth: 25; Parity status: Parous control; Breast biopsy diagnosis: Ductal hyperplasia; ', 'Age at diagnosis: 55; Age at first birth: 22; Parity status: Parous control; Breast biopsy diagnosis: Fibroadenoma; ', 'Age at diagnosis: 61; Age at first birth: 25; Parity status: Parous control; Breast biopsy diagnosis: Fibrocystic changes; ', 'Age at diagnosis: 55; Age at first birth: 17; Parity status: Parous control; Breast biopsy diagnosis: Ductal hyperplasia, mild; ', 'Age at diagnosis: 61; Age at first birth: 34; Parity status: Parous control; Breast biopsy diagnosis: Fibroadenoma, adenosis; ', 'Age at diagnosis: 52; Age at first birth: 31; Parity status: Parous control; Breast biopsy diagnosis: Adenosis, ductal ectasia; ', 'Age at diagnosis: 77; Age at first birth: 23; Parity status: Parous control; Breast biopsy diagnosis: Apocrine metaplasia; ', 'Age at diagnosis: 64; Age at first birth: 27; Parity status: Parous control; Breast biopsy diagnosis: Adenosis; ', 'Age at diagnosis: 71; Age at first birth: 24; Parity status: Parous control; Breast biopsy diagnosis: Adenosis; ', 'Age at diagnosis: 59; Age at first birth: 20; Parity status: Parous control; Breast biopsy diagnosis: Papilloma; ', 'Age at diagnosis: 63; Age at first birth: 18; Parity status: Parous control; Breast biopsy diagnosis: Ductal hyperplasia, mild; ', 'Age at diagnosis: 61; Age at first birth: 21; Parity status: Parous control; Breast biopsy diagnosis: Stromal fibrosis; ', 'Age at diagnosis: 77; Age at first birth: 21; Parity status: Parous control; Breast biopsy diagnosis: Adenosis; ', 'Age at diagnosis: 78; Age at first birth: 24; Parity status: Parous control; Breast biopsy diagnosis: Adenosis; ', 'Age at diagnosis: 72; Age at first birth: 27; Parity status: Parous control; Breast biopsy diagnosis: Adenosis; ', 'Age at diagnosis: 60; Age at first birth: 20; Parity status: Parous control; Breast biopsy diagnosis: Benign breast disease; ', 'Age at diagnosis: 71; Age at first birth: 17; Parity status: Parous case; Breast biopsy diagnosis: Invasive Ductal carcinoma; ', 'Age at diagnosis: 61; Age at first birth: 26; Parity status: Parous case; Breast biopsy diagnosis: Invasive Ductal Carcinoma; ', 'Age at diagnosis: 55; Age at first birth: 26; Parity status: Parous case; Breast biopsy diagnosis: Invasive Ductal and lobular carcinoma; ', 'Age at diagnosis: 60; Age at first birth: 25; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 72; Age at first birth: 19; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 57; Age at first birth: 19; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 74; Age at first birth: 26; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal and lobular carcinoma; ', 'Age at diagnosis: 75; Age at first birth: 26; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 75; Age at first birth: 25; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 76; Age at first birth: 20; Parity status: Parous case; Breast biopsy diagnosis: Mucinous adenocarcinoma; ', 'Age at diagnosis: 78; Age at first birth: 23; Parity status: Parous case; Breast biopsy diagnosis: Mucinous adenocarcinoma; ', 'Age at diagnosis: 59; Age at first birth: 28; Parity status: Parous case; Breast biopsy diagnosis: Invasive Ductal carcinoma and DCIS; ', 'Age at diagnosis: 76; Age at first birth: 26; Parity status: Parous case; Breast biopsy diagnosis: Invasive Ductal carcinoma; ', 'Age at diagnosis: 84; Age at first birth: 31; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 67; Age at first birth: 24; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 55; Age at first birth: 29; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma and DCIS; ', 'Age at diagnosis: 75; Age at first birth: 27; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma and DCIS; ', 'Age at diagnosis: 65; Age at first birth: 23; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 74; Age at first birth: 25; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 62; Age at first birth: 28; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma and DCIS; ', 'Age at diagnosis: 65; Age at first birth: 26; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 81; Age at first birth: 25; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma and DCIS; ', 'Age at diagnosis: 56; Age at first birth: 32; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma and DCIS; ', 'Age at diagnosis: 82; Age at first birth: 30; Parity status: Parous case; Breast biopsy diagnosis: Invasive lobular carcinoma; ', 'Age at diagnosis: 65; Age at first birth: 30; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 76; Age at first birth: 20; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma and DCIS; ', 'Age at diagnosis: 79; Age at first birth: 28; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 82; Age at first birth: 21; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 58; Age at first birth: 26; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 73; Age at first birth: 26; Parity status: Parous case; Breast biopsy diagnosis: Invasive lobular carcinoma and LCIS; ', 'Age at diagnosis: 70; Age at first birth: 23; Parity status: Parous case; Breast biopsy diagnosis: Invasive lobular carcinoma; ', 'Age at diagnosis: 92; Age at first birth: 19; Parity status: Parous case; Breast biopsy diagnosis: Invasive lobular Carcinoma; ', 'Age at diagnosis: 70; Age at first birth: 25; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 60; Age at first birth: 31; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma and DCIS; ', 'Age at diagnosis: 61; Age at first birth: 19; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 60; Age at first birth: 16; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 66; Age at first birth: 30; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma and DCIS; ', 'Age at diagnosis: 63; Age at first birth: 28; Parity status: Parous case; Breast biopsy diagnosis: Invasive ductal carcinoma and DCIS; ', 'Age at diagnosis: 65; Age at first birth: N/A; Parity status: Nulliparous control; Breast biopsy diagnosis: Adenosis; ', 'Age at diagnosis: 62; Age at first birth: N/A; Parity status: Nulliparous control; Breast biopsy diagnosis: Fibroadenoma; ', 'Age at diagnosis: 58; Age at first birth: N/A; Parity status: Nulliparous control; Breast biopsy diagnosis: Papilloma; ', 'Age at diagnosis: 51; Age at first birth: N/A; Parity status: Nulliparous control; Breast biopsy diagnosis: Fibroadenoma, papilloma; ', 'Age at diagnosis: 53; Age at first birth: N/A; Parity status: Nulliparous control; Breast biopsy diagnosis: Stromal fibrosis; ', 'Age at diagnosis: 50; Age at first birth: N/A; Parity status: Nulliparous control; Breast biopsy diagnosis: Apocrine metaplasia, stromal fibrosis; ', 'Age at diagnosis: 58; Age at first birth: N/A; Parity status: Nulliparous control; Breast biopsy diagnosis: Adenosis; ', 'Age at diagnosis: 53; Age at first birth: N/A; Parity status: Nulliparous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 68; Age at first birth: N/A; Parity status: Nulliparous case; Breast biopsy diagnosis: Invasive ductal and lobular carcinoma; ', 'Age at diagnosis: 77; Age at first birth: N/A; Parity status: Nulliparous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 74; Age at first birth: N/A; Parity status: Nulliparous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 87; Age at first birth: N/A; Parity status: Nulliparous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 57; Age at first birth: N/A; Parity status: Nulliparous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ', 'Age at diagnosis: 57; Age at first birth: N/A; Parity status: Nulliparous case; Breast biopsy diagnosis: Invasive lobular carcinoma; ', 'Age at diagnosis: 55; Age at first birth: N/A; Parity status: Nulliparous case; Breast biopsy diagnosis: Invasive ductal carcinoma; ' GSE141987 Homo sapiens 8 Expression profiling by high throughput sequencing GPL20301; GPL21290 The dual function of JmjC domain-containing protein KDM5C in both gene transcriptional activation and repression promotes breast cancer cell growth and tumorigenesis [RNA-seq] 2019-12-13 Emerging evidence suggested that epigenetic regulators can exhibit both co-activator and co-repressor activities in gene transcriptional regulation and disease development, such as cancer. However, how these dual activities are regulated and coordinated in cellular contexts remains elusive. Here, we reported that KDM5C, a repressive histone demethylase, is unexpectedly required for estrogen/estrogen receptor alpha (ERa)-induced gene transcriptional activation to promote cell proliferation, while it suppresses the expression of type I interferons (IFNs) and interferon-stimulated genes (ISGs) to escape from immuno-surveillance. KDM5C-interacting protein, ZMYND8, is found to be accompanied with KDM5C in regulation of both subsets of genes. Mechanistically, during estrogen/ERa-induced gene transcriptional activation, ERa interacts and recruits KDM5C/ZMYND8 to active enhancers, where ERa masks KDM5C’s demethylase activity towards H3K4me2/3, converting KDM5C from a co-repressor to a co-activator. Furthermore, KDM5C and ZMYND8 are found to recruit the P-TEFb complex in a cooperative manner to activate estrogen/ERa-target genes. In contrast, KDM5C/ZMYND8 represses type I IFNs and ISGs through directly interfering TBK1 phosphorylation in an enzymatic-dependent manner. The combinatory effects of KDM5C’s dual activities in regulation of genes involved in both cell proliferation and immuno-escape lead to breast cancer cell proliferation in vitro and xenograft growth in mice. Taken together, we revealed a mechanism by which a repressive epigenetic regulator can be converted to a co-activator under specific signal cues to regulate specific gene programs, and the dual nature as both a co-repressor and co-activator together contributes to cancer development. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE141987 The Dual Function of KDM5C in Both Gene Transcriptional Activation and Repression Promotes Breast Cancer Cell Growth and Tumorigenesis. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 15.804 https://doi.org/10.1002/advs.202004635 {Advanced science (Weinheim, Baden-Wurttemberg, Germany) (15.804): 10.1002/advs.202004635} 'total RNA', 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA595509 https://www.ebi.ac.uk/ena/browser/view/PRJNA595509 https://www.ncbi.nlm.nih.gov/sra?term=SRP237512 [Overal design]RNA-seq performed in this study was designed to understand the molecular mechanisms underlying KDM5C in gene transcription regulation.; [Treatment]'Before experiment, MCF-7 cells were knockdown by siRNA(CTL) or siRNA specifically targeting KDM5C or ZMYND8 and medium was changed to phenol red free DMEM plus 5% charcoal-stripped FBS and 1% penncilin and streptomycin. On the second day, cells were treated with the same way as described above and maintained for another two days, followed by treatemnt of either 100nM 17-β-estrodial or ethanol for 6hrs.'; [Growth]'MCF-7 cells were cultured in DMEM medium supplemented with 10% FBS and 1%penicillin and streptomycin'; [Extraction]'Total RNA was isolated using RNeasy Mini Kit (Qiagen) following the manufacturer’s protocol. DNase I in column digestion was included to ensure the RNA quality.\nRNA library preparation was performed by using NEBNext® Ultra™ Directional RNA Library Prep Kit for Illumina (E7420L). Paired-end sequencing was performed with Illumina HiSeq platform at RiboBio Co., Ltd. or Amogene Biotech Co., Ltd.'; [Cell type]'Source: ''cell line: Michigan Cancer Foundation-7 (MCF-7) cells; genotype/varaition: siCTL; treatment: control; ', 'cell line: Michigan Cancer Foundation-7 (MCF-7) cells; genotype/varaition: siCTL; treatment: E2; ', 'cell line: Michigan Cancer Foundation-7 (MCF-7) cells; genotype/varaition: siKDM5C; treatment: control; ', 'cell line: Michigan Cancer Foundation-7 (MCF-7) cells; genotype/varaition: siKDM5C; treatment: E2; ' GSE135204 Homo sapiens 15 Expression profiling by array GPL17692 Transcriptomic profiling of breast cancer cells incubated in vitro with surgical wound fluids from patients with breast cancer 2019-07-31 Transcriptomic profiling of breast cancer cells incubated in vitro with surgical wound fluids from patients with breast cancer reveals similarities in the biological response induced by intraoperative radiation therapy and the radiation-induced bystander effect In patients with breast cancer who undergo breast-conserving surgery (BCS), more than 90% of local recurrences occur in the same quadrant as the primary cancer. Surgical wound fluids (SWF) are believed to play a role in this process by inducing an inflammatory process in the scar tissue area. Despite strong clinical data demonstrating the benefits of intraoperative radiotherapy (IORT), the biological basis underlying this process remains poorly understood. Ionizing radiation (IR) directly affects cells by damaging DNA, thereby altering the cell phenotype. IR direct effects cancer cells and also influences unirradiated cells located nearby, a phenomenon known as the radiation-induced bystander effect (RIBE), significantly modifying the tumour microenvironment. We hypothesized that SWF obtained from patients after breast-conserving surgery (BCS) and IORT would induce a radiobiological response (due to RIBE) in unirradiated cells, thereby modifying their phenotype. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE135204 Surgical Wound Fluids from Patients with Breast Cancer Reveal Similarities in the Biological Response Induced by Intraoperative Radiation Therapy and the Radiation-Induced Bystander Effect-Transcriptomic Approach. International journal of molecular sciences 4.183 https://doi.org/10.3390/ijms21031159 {International journal of molecular sciences (4.183): 10.3390/ijms21031159} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA557716 https://www.ebi.ac.uk/ena/browser/view/PRJNA557716 None [Overal design]To confirm this hypothesis, breast cancer cells were incubated with SWF collected from patients after BCS 1) without IORT (WF group), 2) with IORT (RT-WF group), and 3) WF with conditioned medium from irradiated cells (WF+RIBE group) and then subjected to microarray analysis. We performed gene set enrichment analysis to determine the biological processes present in these cells.; [Treatment]'Shortly, MDA-MB-468 cells were irradiated in suspension. A total dose of 10 Gy was administered at approximately 2.5 Gy/min using GammaCell® 1000 Elite (BestTheratronics Ltd, Canada) using a Caesium-137 source. After irradiation, the cells were cultured for 24h and then the RIBE medium was collected, sterile-filtered, and stored at − 80 °C. MDA-MB-468 cells were incubated with SWF obtained from the two study groups (RT-WF and WF groups). In all cases, the wound fluid was conditioned in DMEM without fetal bovine serum (FBS). The WF and RT-WF groups both contained 10% WF, which were conditioned in DMEM without FBS, as stated above. A third group of cells was conditioned in 5% RIBE and 5% WF (WF+RIBE).'; [Growth]'Cells were cultured in a humidified atmosphere with 5% carbon dioxide at 37°C in Dulbecco modified Eagle medium supplemented with 10% fetal bovine serum and 1% penicillin/streptomycin 10,000 U/ml .'; [Extraction]'Total RNA was purified using Direct-zol™ RNA MiniPrep (Zymo Research; Irvine, CA, USA) according to the manufacturer’s instructions.'; [Cell type]'human breast cancer cell line''cell line: MDA-MB-468; cell type: human breast cancer cell line; ' GSE41922 Homo sapiens 54 Expression profiling by RT-PCR; Non-coding RNA profiling by array GPL16224 Clinical Utility of Circulating MicroRNA Signatures for Breast Cancer Diagnosis (RT-PCR) 2012-10-30 Purpose: There is a quest for novel non-invasive diagnostic markers for the detection of breast cancer. The goal of this study is to identify circulating microRNA signatures using a cohort of Asian Chinese breast cancer patients, and to compare microRNA profiles between tumour and serum samples. Experimental design: MicroRNAs from paired breast cancer tumours, normal tissue and serum samples derived from 32 patients were comprehensively profiled using microarrays (1300 microRNAs against tumour and normal tissues) or LNA RT-PCR panels (742 microRNAs against serum samples). Serum samples from healthy individuals (n=22) were also employed as normal controls. Significant serum microRNAs, identified by logistic regression, were validated in an independent set of serum samples from patients (n=82) and healthy controls (n=53). Results: The 20 most significant microRNAs differentially expressed in breast cancer tumours included miR-21, miR-10b, and miR-145, previously shown to be dysregulated in breast cancer. Interestingly, 16 of the 20 most significant microRNAs differentially expressed in serum samples were novel. MiR-1, miR-92a, miR-133a and miR-133b were identified as the most important diagnostic markers, and were successfully validated; receiver operating characteristic curves derived from combinations of these microRNAs exhibited areas under the curves of 0.944-0.946. Only seven microRNAs were overexpressed in both tumours and serum, suggesting that microRNAs may be released into the serum selectively. Conclusion: The clinical employment of microRNA signatures as a non-invasive diagnostic strategy is promising, but should be further validated for different subtypes of breast cancers. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41922 Identification of circulating microRNA signatures for breast cancer detection. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-12-3401 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-12-3401} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA179165 https://www.ebi.ac.uk/ena/browser/view/PRJNA179165 None [Overal design]Blood samples were collected in Becton Dickinson (Franklin Lakes, NJ) Vacutainer SST tubes. Serum was harvested by centrifugation at 2200g after allowing blood to clot for 30mins. 32 patient samples and 22 samples from healthy controls were obtained for profiling. Sera samples were stored at -80oC.; [Treatment]'Serum samples'; [Growth]'None'; [Extraction]"RNA was extracted using miRNeasy (Qiagen) following the manufacturer's recommendations."; [Cell type]'Source: ''estrogen receptor: +; her2: na; node positivity: +; age: 69; disease state: Breast cancer; ', 'estrogen receptor: +; her2: na; node positivity: -; age: 54; disease state: Breast cancer; ', 'estrogen receptor: -; her2: na; node positivity: +; age: 48; disease state: Breast cancer; ', 'estrogen receptor: +; her2: na; node positivity: +; age: 41; disease state: Breast cancer; ', 'estrogen receptor: +; her2: -; node positivity: -; age: 47; disease state: Breast cancer; ', 'estrogen receptor: -; her2: na; node positivity: +; age: 59; disease state: Breast cancer; ', 'estrogen receptor: +; her2: -; node positivity: -; age: 68; disease state: Breast cancer; ', 'estrogen receptor: -; her2: +; node positivity: -; age: 36; disease state: Breast cancer; ', 'estrogen receptor: +; her2: -; node positivity: -; age: 43; disease state: Breast cancer; ', 'estrogen receptor: +; her2: +; node positivity: -; age: 37; disease state: Breast cancer; ', 'estrogen receptor: +; her2: -; node positivity: +; age: 44; disease state: Breast cancer; ', 'estrogen receptor: +; her2: -; node positivity: +; age: 28; disease state: Breast cancer; ', 'estrogen receptor: +; her2: -; node positivity: +; age: 41; disease state: Breast cancer; ', 'estrogen receptor: -; her2: +; node positivity: +; age: 46; disease state: Breast cancer; ', 'estrogen receptor: +; her2: +; node positivity: +; age: 48; disease state: Breast cancer; ', 'estrogen receptor: -; her2: +; node positivity: +; age: 38; disease state: Breast cancer; ', 'estrogen receptor: -; her2: +; node positivity: +; age: 58; disease state: Breast cancer; ', 'estrogen receptor: +; her2: -; node positivity: +; age: 47; disease state: Breast cancer; ', 'estrogen receptor: +; her2: +; node positivity: -; age: 39; disease state: Breast cancer; ', 'estrogen receptor: +; her2: +; node positivity: +; age: 43; disease state: Breast cancer; ', 'estrogen receptor: -; her2: na; node positivity: -; age: 79; disease state: Breast cancer; ', 'estrogen receptor: +; her2: +; node positivity: +; age: 50; disease state: Breast cancer; ', 'estrogen receptor: +; her2: -; node positivity: +; age: 71; disease state: Breast cancer; ', 'estrogen receptor: +; her2: +; node positivity: +; age: 65; disease state: Breast cancer; ', 'estrogen receptor: -; her2: -; node positivity: -; age: 65; disease state: Breast cancer; ', 'estrogen receptor: +; her2: +; node positivity: +; age: 49; disease state: Breast cancer; ', 'estrogen receptor: +; her2: -; node positivity: +; age: 49; disease state: Breast cancer; ', 'estrogen receptor: +; her2: +; node positivity: -; age: 42; disease state: Breast cancer; ', 'estrogen receptor: +; her2: +; node positivity: -; age: 81; disease state: Breast cancer; ', 'estrogen receptor: +; her2: +; node positivity: +; age: 36; disease state: Breast cancer; ', 'estrogen receptor: -; her2: -; node positivity: +; age: 37; disease state: Breast cancer; ', 'estrogen receptor: +; her2: na; node positivity: +; age: 49; disease state: Breast cancer; ', 'age: 42; disease state: Healthy volunteer; ', 'age: 52; disease state: Healthy volunteer; ', 'age: 40; disease state: Healthy volunteer; ', 'age: 45; disease state: Healthy volunteer; ', 'age: 43; disease state: Healthy volunteer; ', 'age: 61; disease state: Healthy volunteer; ', 'age: 44; disease state: Healthy volunteer; ', 'age: 47; disease state: Healthy volunteer; ', 'age: 57; disease state: Healthy volunteer; ', 'age: 39; disease state: Healthy volunteer; ', 'age: 46; disease state: Healthy volunteer; ', 'age: 54; disease state: Healthy volunteer; ', 'age: 50; disease state: Healthy volunteer; ', 'age: 55; disease state: Healthy volunteer; ', 'age: 53; disease state: Healthy volunteer; ' GSE8140 Homo sapiens 14 Expression profiling by array GPL570 Expression data from MCF7 wt xenografts 2007-06-15 To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). Another group received ED plus the antiestrogen fulvestrant (MCF7 wt only). Tumors with acquired or de novo resistance to these endocrine therapies were profiled for mRNA expression using Affymetrix Genechip arrays. Keywords: multiple group comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE8140 Development of resistance to targeted therapies transforms the clinically associated molecular profile subtype of breast tumor xenografts. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-08-1404 {Cancer research (8.378): 10.1158/0008-5472.CAN-08-1404} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA105411 https://www.ebi.ac.uk/ena/browser/view/PRJNA105411 None [Overal design]MCF7 xenografts were established in ovariectomized five to six week-old nu/nu athymic nude mice supplemented with 0.25 mg 21 day release estrogen pellets by inoculating subcutaneously (s.c.) 5E-6 cells. When tumors reached the size of 150-200 mm3 (3-5 weeks), the animals were randomly allocated to continued estrogen (E2), continued estrogen with gefitinib (E2+G; 100mg/kg, 5 days/week), estrogen withdrawal alone (ED; by removal of the estrogen pellets), and estrogen withdrawal plus tamoxifen citrate (Tam; 500 microg/animal s.c. in peanut oil, 5 days/week), with either gefitinib (Tam+G; 100mg/kg, 5 days/week) or vehicle (1% Tween 80) administered via gavage, as well as estrogen withdrawal plus fulvestrant (ICI 182,780) in the MCF7 wt model (Fulv; 5mg/mouse s.c. once weekly), and estrogen withdrawal with gefitinib (ED+G). Tumors were harvested for molecular studies when they became resistant to treatment and reached the size of 1000 mm3 (n=7).; [Treatment]'None'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was carried out using EZ1 RNA universal tissue kit with BioRobot EZ1 workstation according to the manufacturer's instructions."; [Cell type]'Source: ''' GSE128676 Homo sapiens 4 Other GPL21290 Genome-wide chromatin interactions identify characteristic promoter-distal loops 2019-03-21 We developed a novel computational model, HiSIF (Hi-C Significant Interacting Fragments), which uses a Poisson Mixture Model (PMM) with a power-law decay background. We compared its performance to some existing programs with publicly available Hi-C data, and then applied it to in situ Hi-C data in breast cancer sensitive and resistant cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE128676 The 3D genomic landscape of differential response to EGFR/HER2 inhibition in endocrine-resistant breast cancer cells. Biochimica et biophysica acta. Gene regulatory mechanisms 4.599 https://doi.org/10.1016/j.bbagrm.2020.194631 {Biochimica et biophysica acta. Gene regulatory mechanisms (4.599): 10.1016/j.bbagrm.2020.194631} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA528483 https://www.ebi.ac.uk/ena/browser/view/PRJNA528483 https://www.ncbi.nlm.nih.gov/sra?term=SRP189090 [Overal design]In this study, we tested the model in our newly generated Hi-C data in three ERα positive breast cancer cell lines, MCF7, tamoxifen-resistant MCF7 (MCF7-TamR) (MCF7 and MCF7-TamR data have been deposited in GEO under accession number GSE108787), T47D and tamoxifen-resistant T47D (T47D-TamR), ZR75-1 and tamoxifen-resistant ZR75-1 (ZR75-1-TamR).; [Treatment]'Untreated'; [Growth]'Routine cell media for all cell lines, respectively.'; [Extraction]'Extraction of cell nucleus and DNA were performed as described (Rao et al. 2014).\nIn situ Hi-C was performed as described (Rao et al. 2014).'; [Cell type]'immortalized breast epithelial cell line''cell line background: T47D; cell type: immortalized breast epithelial cell line; phenotype: control; parental; analysis: in situ Hi-C; ', 'cell line background: T47D; cell type: immortalized breast epithelial cell line; phenotype: Tamoxifen Resistant; analysis: in situ Hi-C; ', 'cell line background: ZR75-1; cell type: immortalized breast epithelial cell line; phenotype: control; parental; analysis: in situ Hi-C; ', 'cell line background: ZR75-1; cell type: immortalized breast epithelial cell line; phenotype: Tamoxifen Resistant; analysis: in situ Hi-C; ' GSE111188 Homo sapiens 9 Expression profiling by high throughput sequencing GPL18573 Transcriptome-wide HITS-CLIP of Quaking (QKI) in TGF-Beta-treated HMLE (Mesenchymal-like) cells 2018-02-27 Members of the miR-200 family are critical gatekeepers of the epithelial state, restraining expression of pro-mesenchymal genes that drive epithelial-mesenchymal transition (EMT) and contribute to metastatic cancer progression. Here, we show that miR-200c and another epithelial-enriched miRNA, miR-375, exert widespread control of alternative splicing in cancer cells. This is achieved by their strong suppression of the RNA binding protein Quaking (QKI), which is required to mediate the splicing changes regulated by these miRNAs. During EMT, QKI-5 directly binds to and regulates hundreds of alternative splicing events and exerts pleiotropic effects, such as increasing cell migration and invasion and restraining tumour growth, without appreciably affecting mRNA levels. QKI-5 is both necessary and sufficient to direct EMT alternative splicing changes, and this splicing signature is broadly conserved across many epithelial-derived cancer types. Importantly, several actin cytoskeleton-associated genes are directly targeted both by QKI and miR-200c, revealing coordinated control of alternative splicing and mRNA abundance during EMT. These findings demonstrate the existence of a miR-200/miR-375/QKI axis that impacts cancer-associated epithelial cell plasticity through widespread control of alternative splicing. The purpose of the CLIP experiment was to determine direct targets of QKI. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE111188 miR-200/375 control epithelial plasticity-associated alternative splicing by repressing the RNA-binding protein Quaking. The EMBO journal 11.227 https://doi.org/10.15252/embj.201899016 {The EMBO journal (11.227): 10.15252/embj.201899016} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA436149 https://www.ebi.ac.uk/ena/browser/view/PRJNA436149 https://www.ncbi.nlm.nih.gov/sra?term=SRP133593 [Overal design]9 samples: 7 technical replicates of QKI immunoprecipitation, 2 technical replicates of size-matched input samples (controls); [Treatment]'HMLE cells (Mani, Guo et al., 2008) were cultured in HuMEC ready media (ThermoFisher) and induced to undergo EMT by transferring to DMEM: F12 media (1:1) supplemented with 10 μg/ml insulin, 20 ng/ml EGF, 0.5 μg/ml hydrocortisone, 5% fetal calf serum (FCS) and treating with 2.5 ng/ml of TGF-β1 (R&D) for at least 14 days. MesHMLE cells, which are derived from HMLE from prolonged treatment with TGF-β1 (Mani et al., 2008), were maintained in EMT-inducing media without additional TGF-β1.'; [Growth]'Human breast cancer cell lines were cultured as described previously (Gregory et al., 2008).'; [Extraction]'The QKI-CLIP method was adapted from published methods (Jensen & Darnell, 2008), incorporating modifications from eCLIP (Van Nostrand, Pratt et al., 2016) and iCLIP (Sutandy, Hildebrandt et al., 2016). UV crosslinking and preparation of lysates: MesHMLE cells were grown in 100mm plates to ~90% confluency, rinsed once with ice-cold PBS, and irradiated with 600 mJ/cm2 in ice-cold PBS using a UV Stratalinker-1800 (Agilent). Cells were collected by scraping, washed in PBS, and stored at -80°C as one pellet per plate. Each pellet was resuspended using 200 µl of 1 X QLB (1 X PBS, 0.3% SDS, 0.5% deoxycholate, 0.5% Igepal, EDTA-free Complete protease inhibitor cocktail (PIC; Roche, 11873580001) for 15 min on ice to liberate QKI from high molecular weight complexes, followed by addition of 400 µl of 1 X QDB (1 X PBS, 0.5% deoxycholate, 0.5% Igepal, PIC) and trituration by passing through a 21G needle and syringe 5 times. DNA was digested with 20 µl RQ1 DNAse (Promega, M6101) at 37°C for 10 min on a Thermomixer (750 rpm, Eppendorf). RNA was partially digested with RNase 1 (ThermoFisher, AM2295) by adding 6 µl of 1:50 diluted RNase 1 in 1 X PBS at 37°C for 5 min on a Thermomixer (750 rpm), then returned to ice. Lysates were centrifuged at 21,000 x g for 20 min at 4°C and supernatant transferred to a fresh tube. Immunoprecipitation: QKI-RNA complexes were immunoprecipitated using a QKI5 specific antibody (Bethyl, A300-183A) with a rabbit IgG antibody (Santa Cruz sc-2027) used as a control (Appendix Supplementary Methods Figure S1B,C). Antibodies (5 µg) were conjugated to 100 µl protein A Dynabeads (ThermoFisher, 10002D) in PBS-Tw (1 X PBS, 0.05% Tween-20) for 45 min and washed three times with 1 X PXL (1 X PBS, 0.1% SDS, 0.5% sodium deoxycholate, 0.5% Igepal) before resuspending the beads with 500 µl of prepared lysate and rotating for 2 hr at 4°C. A further 2% of IP input lysate was set aside to be used as a size-matched input (SMin) as in van Nostrand et al 2016 (Van Nostrand, Pratt et al., 2016). Bound QKI-5-RNA complexes were washed twice each consecutively with ice cold 1 X PXL, 5 X PXL (5 X PBS, 0.1% SDS, 0.5% sodium deoxycholate, 0.5% Igepal), and 1 X PNK (50 mM Tris-Cl pH 7.5, 10 mM MgCl2, and 0.5% Igepal). 3’ end dephosphorylation and 3’ linker ligation: Beads were first treated with T4 PNK (NEB, M0201L; 20 U in 80 µl reaction volume) in the absence of ATP at 37°C, 850 rpm for 20 min, to dephosphorylate 3’ RNA ends followed by washes with 1 X PNK, 5 X PXL, and two washes with 1 X PNK at 4°C. The 3’ preadenylated linker (NEBNext 3’SR adaptor for Illumina) was ligated to the RNA fragments on bead using RNA ligase I (NEB M0437M; 75 U in a 30 µl reaction volume, 15% PEG8000, 2.5% DMSO, 0.25 µM adaptor) in the absence of ATP at 22°C, 75 min with periodic mixing. Beads were washed with 1 X PNK, 1 X PNK + EGTA (50 mM Tris-Cl pH 7.5, 20 mM EGTA, and 0.5% Igepal), 5 X PXL, and two washes with 1X PNK at 4°C. Twenty percent of beads were removed and labelled with P32 \uf067-ATP using T4 PNK (according to Sutandy et al 2016 (Sutandy, Hildebrandt et al., 2016)), washed then recombined with the unlabelled fraction to track the RNA in subsequent steps. SDS PAGE, nitrocellulose transfer, and RNA extraction and size purification: QKI-5-RNA complexes were eluted with 40 µl 1 X Bolt LDS sample buffer (ThermoFisher) without reducing agent at 70°C for 10 min on a Thermomixer (1200 rpm). Samples were separated through Bolt 10% Bis-tris Plus gels (ThermoFisher) using Bolt MOPS SDS running buffer at 165 V for 47 min. Complexes were then transferred to nitrocellulose (Schleicher&Schuell, BA-85) by wet transfer using 1 X Bolt transfer buffer with 10% methanol (Appendix Supplementary Methods Figure S1D).Filters were placed on a phosphor screen and exposed using a Typhoon imager (GE). Nitrocellulose was cut as marked in Appendix Supplementary Methods Figure S1E and the RNA extracted by proteinase K digestion (2 mg/mL proteinase K, 100 mM Tris-HCl pH 7.5, 50 mM NaCl, 10 mM EDTA, 0.2% SDS) at 50°C for 60 min on a Thermomixer (1200 rpm) followed by extraction with acid phenol (ThermoFisher, AM9712) and precipitation with 1:1 isopropanol:ethanol. RNA was pelleted by centrifugation then separated on a 15% denaturing polyacrylamide gel (1:19 acrylamide, 1 X TBE, 7 M urea). The wet gel was wrapped in plastic wrap and exposed to a phosphor screen and imaged using a Typhoon. Gel slices were cut as marked in Appendix Supplementary Methods Figure S1F and the RNA eluted by the “crush and soak” method as previously described (Jensen & Darnell, 2008). Size match input controls (SMin) were prepared essentially as preciously described (Van Nostrand et al., 2016) with the addition of RNA size selection alongside the QKI-associated RNA fragments.\nReverse transcription, 5’ linker ligation and amplification were performed essentially as previously described (Van Nostrand et al., 2016) but using a custom synthesized 5’ linker (IDT, 5’SRdeg /5Phos/NN NNN NNN NNG ATC GTC GGA CTG TAG AAC TCT GAA C/3SpC3/), and SR-RT primer for reverse transcription (IDT, AGACGTGTGCTCTTCCGATCT). Products were amplified for 17 (CLIP) or 9 (SMin) cycles using a common forward primer (NEBNext SR primer for Illumina) and barcoded reverse primers for each sample (NEBNext Index primers for Illumina). PCR products were purified using Qiagen Qiaquick PCR purification kit, separated on a 10% acrylamide (29:1) TBE non-denaturing gel, stained with SYBR Gold nucleic acid gel stain (ThermoFisher) and imaged on a ChemiDoc (BioRad). Products corresponding to an insert size of ~30 – 70 nt were excised from the gel as shown in Appendix Supplementary Methods Figure S1G and extracted by the “crush and soak” method as previously described (Jensen & Darnell, 2008). Library quality and quantity was assessed by Bioanalyzer (Agilent), Qubit (ThermoFisher) and qPCR, pooled and sequenced on an Illumina NextSeq 500 (1 x 75bp).\nRNA-seq of UV cross-linked Immuno-precipitated RNA (HITS-CLIP)'; [Cell type]'Breast cancer''cell line: Mesenchymal-like HMLE cells; cell type: Breast cancer; immunoprecipitation antibody: QKI5 specific antibody (Bethyl, A300-183A); ', 'cell line: Mesenchymal-like HMLE cells; cell type: Breast cancer; immunoprecipitation antibody: None; ' GSE11294 Homo sapiens 16 Expression profiling by array GPL5953 T47D_MTVL_H1.2sh or T47D_MTVL_controlsh 2008-04-29 H1.2 (and control) knock-down cell lines were established from T47D-MTVL cells: Human breast cancer cell line T47D modified to contain one stably integrated copy of Luciferase reporter gene driven by the Mouse Mammary Tumor Virus promoter, named T47D-MTVL (Truss, M., J. Bartsch, A. Schelbert, R. J. Hache, and M. Beato. 1995). Initially, a cell line expressing the Dox-responsive KRAB repressor and RedFP (ptTR-KRAB-Red) was generated. Then, this cell line was infected with viruses for expression of the different H1 variants shRNAs (pLVTHM). The inducible knocked-down cell lines were sorted in a FACSvantageSE (Becton Dickinson) for RedFP-positive and GFP-positive fluorescence after 3 days of Dox treatment. Then cells were amplified in the absence of Dox until an experiment was performed. Plasmids for the lentivirus vector-mediated drug-inducible RNA interference system (pLVTHM, ptTR-KRAB-Red, pCMC-R8.91 and pMD.G) were provided by D. Trono (University of Geneva) (Wiznerowicz M & Trono D (2003) Conditional suppression of cellular genes: lentivirus vector-mediated drug-inducible RNA interference. J Virol 77: 8957-8961). Keywords: Gene expression - T47D-MTVL-control sh/sh H1.2 +/- Dox induction https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE11294 Histone H1 depletion triggers an interferon response in cancer cells via activation of heterochromatic repeats. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkx746 {PLoS genetics (5.224) doi:10.1371/journal.pgen.1000227}; {Nucleic acids research (11.147) doi:10.1093/nar/gkx746}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA106713 https://www.ebi.ac.uk/ena/browser/view/PRJNA106713 None [Overal design]4 biological replicates are included of each sample: Control sh samples are treated with/without Dox H1.2 sh samples are treated with/without Dox Cell line sample was labeled with Cy5 and hybridized against Universal Human Reference RNA (Stratagene) labeled with Cy3.; [Treatment]'Along a 6-day treatment with Dox, cells were passaged at day 3. Serum-containing media was replaced with serum-free media at day 4 for growth arrest.', 'none'; [Growth]'These cell lines were grown in RPMI 1640 medium, supplemented with 10% FBS, 2mM L-glutamine, 100 U/ml penicillin, and 100µg/ml streptomycin. Doxicycline (Sigma) was added at 2.5 µg/ml when indicated.', 'none'; [Extraction]'RNeasy mini kit (QUIAGEN, cat.no. 74104)\nQuality assesment of Total RNA samples were analyzed using the Agilent Bioanalyzer 2100 and the RNA 6000 LabChip Kit (Agilent) with the Eukaryote Total RNA Nano Assay.', 'none'; [Cell type]'Source: ''H1.2 (and control) knock-down cell lines were established from T47D-MTVL cells: Human breast cancer cell line T47D modified to contain one stably integrated copy of Luciferase reporter gene driven by the Mouse Mammary Tumor Virus promoter, named T47D-MTVL (Truss, M., J. Bartsch, A. Schelbert, R. J. Hache, and M. Beato. 1995).; Initially, a cell line expressing the Dox-responsive KRAB repressor and RedFP (ptTR-KRAB-Red) was generated. Then, this cell line was infected with viruses for expression of the different H1 variants shRNAs (pLVTHM). The inducible knocked-down cell lines were sorted in a FACSvantageSE (Becton Dickinson) for RedFP-positive and GFP-positive fluorescence after 3 days of Dox treatment. Then cells were amplified in the absence of Dox until an experiment was performed. Plasmids for the lentivirus vector-mediated drug-inducible RNA interference system (pLVTHM, ptTR-KRAB-Red, pCMC-R8.91 and pMD.G) were provided by D. Trono (University of Geneva) (Wiznerowicz M & Trono D (2003) Conditional suppression of cellular genes: lentivirus vector-mediated drug-inducible RNA interference. J Virol 77: 8957-8961).; ', '' GSE90564 Homo sapiens 38 Expression profiling by array GPL13607 Paclitaxel resistance in triple negative breast cancer involves novel functional genomic aberrations in the ABCB1 gene. 2016-11-27 Five Triple Negative Breast Cancer cell lines were exposed to increasing concentration of Paclitaxel untill they acquired resistance. In order to identify changes in gene expression associated with resistance to PTX, we performed gene expression profiling on parental and resistant cell lines. Of ~22000 genes surveyed by microarray analysis, 5.0%, 3.7%, 9.0%, 7.3%, and 5.4% of the genes showed changes in expression of 2-fold or greater (p value < 0.05) in BT20, SUM149, MDA-MB-231, MDA-MB-436 and MDA-MB-468 cell lines, respectively. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE90564 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA355042 https://www.ebi.ac.uk/ena/browser/view/PRJNA355042 None [Overal design]Parental and resistant cells growing were seeded at a density of 0.8x106 per well in 6 well-plates and incubated without drug for 24 hours. Cells were harvested and total RNA from parental and resistant cell lines were extracted using the AllPrep DNA/RNA Mini kit. Four independent RNA extraction from different cell passage was performed for all cell lines except for MDA-MB-468. Three independent replicate is presented for MDA-MB-468 P and MDA-MB-468 R. .; [Treatment]'None'; [Growth]'Parental and resistant cells were seeded at a density of 1x106 per well in 6 well-plates and incubated without drug for 24 hours'; [Extraction]'Cells were harvested and total RNA from parental and resistant cell lines were extracted simultaneously using the AllPrep DNA/RNA Mini kit (Qiagen, Canada). The quality of RNA was determined with the NanoDrop™ spectrophotometer (ND-1000) (Wilmington, DE, USA). All RNA samples with A260/A280 ratio higher than 1.8 and DNA with A260/A280 ratio higher than 2 were selected for further analysis. The RNA integrity number (RIN) was measured with a 2100 Bioanalyzer (Agilent\xa0Technologies, Santa Clara, CA, USA). RNA with RIN higher than 8 qualified forgene expression profiling.'; [Cell type]'Breast Cancer Cell Line''cell line: BT20; cell type: Breast Cancer Cell Line; treated with: none (parental); ', 'cell line: BT20; cell type: Breast Cancer Cell Line; treated with: Paclitaxel; ', 'cell line: SUM149; cell type: Breast Cancer Cell Line; treated with: none (parental); ', 'cell line: SUM149; cell type: Breast Cancer Cell Line; treated with: Paclitaxel; ', 'cell line: MDA-MB-231; cell type: Breast Cancer Cell Line; treated with: none (parental); ', 'cell line: MDA-MB-231; cell type: Breast Cancer Cell Line; treated with: Paclitaxel; ', 'cell line: MDA-MB-436; cell type: Breast Cancer Cell Line; treated with: none (parental); ', 'cell line: MDA-MB-436; cell type: Breast Cancer Cell Line; treated with: Paclitaxel; ', 'cell line: MDA-MB-468; cell type: Breast Cancer Cell Line; treated with: none (parental); ', 'cell line: MDA-MB-468; cell type: Breast Cancer Cell Line; treated with: Paclitaxel; ' GSE128018 Homo sapiens 27 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Androgen Receptor is a Backdoor Inhibitor of Wildtype and Mutant Estrogen Receptors in Refractory Hormone Receptor-Positive Breast Cancers 2019-03-07 Ligand-activated AR inhibits wildtype and mutant-refractory ER activity in PDXs by reprogramming the ER and FOXA1 cistrome and rendering tumor-growth inhibition. These findings suggest that ligand-activated AR may function as a backdoor inhibitor of ER and that AR agonists may offer a safe and effective treatment for ER-positive breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE128018 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA526053 https://www.ebi.ac.uk/ena/browser/view/PRJNA526053 https://www.ncbi.nlm.nih.gov/sra?term=SRP187889 [Overal design]Tumor xenograft PDX models: AR, ER, and FOXA1 ChIP-Seq; [Treatment]'Vehicle (DMSO+PEG-300 15:85): Enobosarm (10 mg/kg): Oral treatment'; [Growth]'1 mm3 tumor fragments were implanted under the mammary fat pad. Once the tumors reach 100-200 mm3, the animals were randomized and treated with vehicle or enobosarm (10 mg/kg orally). After 30 days of treatment, the animals were sacrificed and the tumors were excised and flash frozen.'; [Extraction]'Tumors were harvested, flash frozen and sectioned. Chromatin was extracted using an SDS based sonication protocol and immunoprecipitated.\nDNA libraries were prepared using Swift Accel-NGS 2S Plus kit in an automated platform'; [Cell type]'Source: ''tissue: tumor tissue; chip antibody: AR; chip antibody vendor: Spring Bioscience; chip antibody cat.#: E2724; chip antibody lot/batch#: 160627LVB; ', 'tissue: tumor tissue; chip antibody: FOXA1; chip antibody vendor: abcam,abcam; chip antibody cat.#: 5089, 23738; chip antibody lot/batch#: gr122110-14, gr292351-2; ', 'tissue: tumor tissue; chip antibody: ER; chip antibody vendor: Santa Cruz Biotechnology, Thermo; chip antibody cat.#: sc-543, MS-315-P1ABX; chip antibody lot/batch#: c2114, 315X1510A; ', 'tissue: tumor tissue; chip antibody: input; ' GSE54505 Homo sapiens 6 Expression profiling by high throughput sequencing GPL11154 TWIST1-induced microRNA-424 drives an intermediate epithelial-to-mesenchymal transition that opposes metastasis 2014-01-29 Epithelial-to-mesenchymal transition (EMT) is a dynamic process that relies on cellular plasticity; an EMT/MET axis is critical for metastatic colonization of carcinomas. Unlike epithelial programming, regulation of mesenchymal programming is not well understood in EMT. Here we describe the first microRNA that enhances exclusively mesenchymal programming. We demonstrate that microRNA-424 is up-regulated early during a TWIST1/SNAI1-induced EMT, and that it causes cells to express mesenchymal genes without affecting epithelial genes, resulting in a mixed/intermediate EMT. Further, microRNA-424 increases motility, decreases adhesion and induces a growth arrest, changes associated with a complete EMT. Patient microRNA-424 levels positively associate with TWIST1/2 and EMT-like gene signatures and is increased in primary tumors versus matched normal breast. However, microRNA-424 is down-regulated in metastases versus matched primary tumors. Correspondingly, microRNA-424 decreases tumor initiation and is post-transcriptionally down-regulated in macrometastases in mice. RNA-seq identified microRNA-424 regulates numerous genes associated with EMT and breast cancer stemness including the novel miR-424 target, TGFBR3, which regulates mesenchymal phenotypes without influencing miR-424 effects on tumor-initiating phenotypes; instead, we show that ERK signaling is critical for such tumor-initiating effects of miR-424. These findings suggest microRNA-424 plays distinct roles downstream of EMT-inducing factors, facilitating earlier stages, but repressing later stages, of metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54505 TWIST1-Induced miR-424 Reversibly Drives Mesenchymal Programming while Inhibiting Tumor Initiation. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-14-2394 {Cancer research (8.378): 10.1158/0008-5472.CAN-14-2394} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA236738 https://www.ebi.ac.uk/ena/browser/view/PRJNA236738 https://www.ncbi.nlm.nih.gov/sra?term=SRP036035 [Overal design]Examination of mRNA levels in MCF12A human breast cell lines that stably over-expressed miR-424 or an empty vector (EV) control. Each group has three replicates.; [Treatment]'None'; [Growth]'10^5 MCF12A cells stably over-expressing miR-424 or an empty vector (EV) control were grown in triplicate for 48 hours.'; [Extraction]"Total RNA was extracted and mRNA isolated using the miRNeasy Kit (Qiagen) according to manufacturer's instructions.\nRNA libraries were prepared for sequencing using TruSEQ RNA Sample Prep v2 using standard Illumina protocols."; [Cell type]'breast cancer cancer cell line''cell line: MCF12A; cell type: breast cancer cancer cell line; stable expression: empty vector; ', 'cell line: MCF12A; cell type: breast cancer cancer cell line; stable expression: miR-424 over-expressed; ' GSE113198 Homo sapiens 325 Expression profiling by high throughput sequencing GPL16791 Single Cell RNA sequencing of Adult Human Breast Epithelial Cells [C1_Individual_3] 2018-04-16 Breast cancer arises from breast epithelial cells that acquire genetic alterations leading to subsequent loss of tissue homeostasis. Several distinct epithelial subpopulations have been proposed, but complete understanding of the spectrum of heterogeneity and differentiation hierarchy in the human breast remains elusive. Here, we used single-cell mRNA sequencing (scRNAseq) to profile the transcriptomes of 25,790 primary human breast epithelial cells isolated from reduction mammoplasties of seven individuals. Unbiased clustering analysis reveals the existence of three distinct epithelial cell populations, one basal and two luminal cell types, which we identify as secretory L1- and hormone-responsive L2-type cells. Pseudotemporal reconstruction of differentiation trajectories produc one continuous lineage hierarchy that closely connects the basal lineage to the two differentiated luminal branches. Our comprehensive cell atlas provides novel insights into cellular blueprint of the human breast epithelium and will form the foundation to understand how the system goes awry during breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113198 Profiling human breast epithelial cells using single cell RNA sequencing identifies cell diversity. Nature communications 11.878 https://doi.org/10.1038/s41467-018-04334-1 {Nature communications (11.878) doi:10.1038/s41467-018-04334-1}; {Communications biology (None) doi:10.1038/s42003-019-0554-8}; 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA450412 https://www.ebi.ac.uk/ena/browser/view/PRJNA450412 https://www.ncbi.nlm.nih.gov/sra?term=SRP140536 [Overal design]Microfluidics-enabled Single Cell RNA sequencing libraries were generated for 3 adult human women using the Fluidigm C1 and sequenced on the Illumina HighSeq 2500; [Treatment]'Samples were washed in PBS (Corning 21-031-CV) and mechanically dissociated using a razor blade. Dissociated samples were digested overnight in DMEM (Corning 10-013-CV) with Collagenase Type I, 2 mg/mL (Life Technologies 17100-017). Viable organoids were separated using differential centrifugation and viably frozen in 50% FBS (Omega Scientific FB-12), 40% DMEM, and 10% DMSO (Sigma-Aldrich D8418) by volume.'; [Growth]'None'; [Extraction]'Viable organoids were thawed and washed using DMEM, and digested with 0.05% trypsin (Corning 25-052-CI) containing DNase (Sigma Aldrich D4263-5VL) to generate single cell suspension. Cells were stained for FACS using fluorescently labeled antibodies for CD31 (eBiosciences 48-0319-42), CD45 (eBiosciences 48-9459-42), EpCAM (eBiosciences 50-9326-42), CD49f (eBiosciences 12-0495-82), SytoxBlue (Life Technologies S34857). We only proceeded with samples showing at least 80% viability as measured using SytoxBlue in FACS\nSorted cells were washed and resuspended at a concentration of approximately 500 cells/µl. For microfluidics-enabled scRNAseq, cell suspensions were mixed with Fluidigm C1 Suspension Reagents (Fluidigm 100-5315) at a ratio of 8:2 before loading mix onto C1 chip (Fluidigm 100-5760). Bright field images of captured cells were collected using a Keyence BZ-X710 microscope (Keyence Corporation, Itasca, Illinois, USA). Single-cell RNA isolation and amplification were performed using the Fluidigm C1 Single Cell Auto Prep IFC following the Fluidigm Protocol: 100-7168 I1. RNA spike-in controls were omitted. cDNA library preparation were performed following the Fluidigm C1 Protocol: 100-7168 I1. Reagents Kits v2 User Guide: CG00052 Rev B. Quantification of cDNA libraries was performed using Qubit dsDNA HS Assay Kit (Life Technologies Q32851) and high-sensitivity DNA chips (Agilent. 5067-4626). Quantification of library construction was performed using KAPA qPCR (Kapa Biosystems KK4824). For microfluidics-enabled scRNAseq libraries, we generally multiplexed 96 cells per lane on an Illumina HiSeq2500 resulting in a calculated depth of ~1.6 million reads per cell (Illumina Rapid PE kit v2 402-4002 and Rapid SBS kit v2 FC 401-4022).'; [Cell type]'Source: ''Sex: female; tissue: Adult Human Breast Epithelium; location: Basal; ', 'Sex: female; tissue: Adult Human Breast Epithelium; location: Luminal; ' GSE109522 Mus musculus 2 Expression profiling by high throughput sequencing GPL21103 Per2 regulation of mammary gland development and branching morphogenesis via cell fate determination 2018-01-23 Circadian rhythms play key roles in daily physiological functions, development, and cancer. Period 2 (PER2) is a repressive element which inhibits transcription activated by positive clock elements resulting in diurnal cycling of genes. Here we show, that outside of time keeping, PER2 has a non-circadian function that is critical to mammary gland development. Virgin Per2 deficient mice, Per2ldc, have underdeveloped glands containing fewer bifurcations and terminal ducts. Using a transplantation model, we show that these changes are intrinsic to the gland and furthermore identify changes in cell fate commitment. Per2ldc mouse mammary glands have a luminal/basal bi-potent phenotype in cells of the ductal epithelium. We identified co-localization of E-cadherin and Keratin 14 in luminal cells and decreased p63 staining and gene expression in myoepithelial cells. Moreover, Per2ldc mice overexpress SLUG, which is related to mammary stem cell maintenance and EMT. Similar results were demonstrated using MCF10A and shPER2 MCF10A cell lines. Collectively this study reveals a critical non-circadian function of PER2 in mammary gland development, validates the Per2ldc model, and describes a potential role for PER2 in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE109522 PER2 regulation of mammary gland development. Development (Cambridge, England) 5.763 https://doi.org/10.1242/dev.157966 {Development (Cambridge, England) (5.763): 10.1242/dev.157966} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA431294 https://www.ebi.ac.uk/ena/browser/view/PRJNA431294 https://www.ncbi.nlm.nih.gov/sra?term=SRP131155 [Overal design]Analysis of RNA expression from wild type and Per2ldc mice; [Treatment]'None'; [Growth]'None'; [Extraction]'Mouse mammary glands were harvested from virgin WT (n=3) and Per2ldc (n=4) mice followed by a primary mammary epithelial cell isolation. Glands were homogenized on a 10cm plate using scalpels and digested in DMEM/F12 containing 10% FBS and 2mg/ml collagenase A for 30 min at 37°C. Samples were then treated with DNAseI and pulse spins performed to remove red blood cells. RNA was isolated from MECs using the High Pure RNA Isolation Kit (Roche, Mannheim, Germany).\nIllumina true seq'; [Cell type]'mammary epithleial cells', 'mammary epithelial cells''genotype/variation: Wild Type; tissue: Mammary gland; cell type: mammary epithleial cells; ', 'genotype/variation: Per2ldc; tissue: Mammary gland; cell type: mammary epithelial cells; ' GSE54497 Homo sapiens 116 Expression profiling by array; Non-coding RNA profiling by array GPL6947; GPL8178 Molecular diversity of breast cancers at the time of endocrine resistance 2014-01-29 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54497 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA236645 https://www.ebi.ac.uk/ena/browser/view/PRJNA236645 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]"RNA was extracted using miRNEasy Qiagen kits, followed by DNase treatment in accordance with the manufactirer's recommendations. Quality control was performed with NanoDrop and Agilent Bioanalyser.", 'RNA was extracted using miRNEasy Qiagen kits. Quality control was performed with NanoDrop and Agilent Bioanalyser.'; [Cell type]'Source: ''tissue: Clinical biopsy of breast cancer; ', 'tissue: Clinical biopsy of breast cancer; molecule subtype: microRNA; ' GSE51689 Homo sapiens 12 Non-coding RNA profiling by array GPL17840 MicroRNA-769-3p down-regulated NDRG1 and enhanced apoptosis in MCF-7 during reoxygenation. 2013-10-24 In this study, breast cancer MCF-7 cells were cultured under 0.5% oxygen for 24 h followed by 24 h of reoxygenation. Cells was harvested at 0, 1, 12, and 24 h during reoxygenation, and examined the miRNA profile by Nanostring nCounter. Forty-three miRNAs had dramatic changes as compared with 0 h upon reoxygenation, with 63% (n=27) of the miRNAs up-regulated upon reoxygenation. Among these miRNAs, miR-769-3p, which was down-regulated in MCF-7 upon reoxygenation, was chosen for further investigation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE51689 MicroRNA-769-3p down-regulates NDRG1 and enhances apoptosis in MCF-7 cells during reoxygenation. Scientific reports 4.011 https://doi.org/10.1038/srep05908 {Scientific reports (4.011): 10.1038/srep05908} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA224566 https://www.ebi.ac.uk/ena/browser/view/PRJNA224566 None [Overal design]The hypothesis was that the down-regulation of NDRG1 upon reoxygenation was regulated by miRNAs. To examine wether miRNAs regulate NDRG1 under 0.5% O2 concentrations, the miRNA expression profiles of MCF-7 cells under reoxygenation were examined. Cells were harvested at 0 (hypoxia control), 1, 12, and 24 h upon reoxygenation. Each profile was done in triplicate. The genomic profile of miRNAs was measured using NanoString nCounter® miRNA Expression Assays.; [Treatment]'0.5% O2 hypoxia and reoxygenation.'; [Growth]'Culture withDMEM medium.'; [Extraction]'Total RNA from the cells were isolated using TRIzol® reagent (Invitrogen, Calsbad, CA) and purified with RNeasy® mini kits (Qiagen).'; [Cell type]'Breast ductal carcinoma''cell line: MCF-7; cell type: Breast ductal carcinoma; time point: 0h (hypoxia control); ', 'cell line: MCF-7; cell type: Breast ductal carcinoma; time point: 1h upon reoxygenation; ', 'cell line: MCF-7; cell type: Breast ductal carcinoma; time point: 12h upon reoxygenation; ', 'cell line: MCF-7; cell type: Breast ductal carcinoma; time point: 24 h upon reoxygenation; ' GSE23640 Homo sapiens 14 Expression profiling by array GPL570 Gene-expression profile of breast cancer cell lines and sorted breast cancer epithelial cells 2010-08-16 Most of the breast cancer samples used in clinical research contain multiple cell types other than epithelial cells alone. The non-epithelial cell types have have a substantial effect on the gene expression-profile, which is used to define molecular subtypes of the tumours. The purpose of this data set is to retrieve gene-expression profile within tumour epithelial cells. We collected 9 breast cancer epithelial cell lines and 5 tumour sampes from which epithelial cells were sorted and enriched using BerEp4 antibody coated beads. We profiled the mRNA expression level of these samples and classified probe sets into epithelial genes which were those genes with present calls in at least 50% of the samples. Then we derived an 23-gene signature based on only the epithelial genes to stratify breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23640 Minimising immunohistochemical false negative ER classification using a complementary 23 gene expression signature of ER status. PloS one 2.776 https://doi.org/10.1371/journal.pone.0015031 {PloS one (2.776): 10.1371/journal.pone.0015031} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA130949 https://www.ebi.ac.uk/ena/browser/view/PRJNA130949 None [Overal design]Gene-expression profile analysis of 9 breast cancer epithelial cell lines and 5 tumour epithelium samples purified using BerEp4 antibody coated beads.; [Treatment]'Primary tumor samples were collagenase digested then sorted for epithelial cells using BerEp4 antibody coated magnetic beads'; [Growth]'None'; [Extraction]'Isolation of RNA was performed using the Trizol method (Invitrogen) according to the manufacturers instructions and was purified using RNeasy mini-columns (Qiagen, Valencia, CA). The quality of the RNA obtained from each tumour sample was assessed based on the RNA profile generated by the bioanalyzer (Agilent Inc)olation of RNA was performed using the Trizol method (Invitrogen) according to the manufacturers instructions and was purified using RNeasy mini-columns (Qiagen, Valencia, CA). The quality of the RNA obtained from each tumour sample was assessed based on the RNA profile generated by the bioanalyzer (Agilent Inc).'; [Cell type]'Breast cancer cell line', 'sorted breast tumor epithelium''cell type: Breast cancer cell line; genotype: B1germ; invasive tumour type: Ductal; invasive b-r grade: III; er status: pos; pr status: neg; her2 status: neg; ', 'cell type: Breast cancer cell line; genotype: wt; invasive tumour type: Ductal; invasive b-r grade: III; er status: neg; pr status: neg; her2 status: neg; ', 'cell type: Breast cancer cell line; genotype: wt; invasive tumour type: Ductal; invasive b-r grade: III; er status: neg; pr status: neg; her2 status: pos; ', 'cell type: Breast cancer cell line; genotype: wt; invasive tumour type: Ductal; invasive b-r grade: II; er status: neg; pr status: pos; her2 status: neg; ', 'cell type: Breast cancer cell line; genotype: wt; invasive tumour type: Ductal; invasive b-r grade: III; er status: neg; pr status: pos; her2 status: pos; ', 'cell type: Breast cancer cell line; genotype: B1germ; invasive tumour type: Ductal; invasive b-r grade: III; er status: neg; pr status: neg; her2 status: neg; ', 'cell type: Breast cancer cell line; genotype: B2som; invasive tumour type: Ductal; invasive b-r grade: III; er status: neg; pr status: neg; her2 status: neg; ', 'cell type: Breast cancer cell line; genotype: wt; invasive tumour type: Unknown; invasive b-r grade: Unknown; er status: pos; pr status: pos; her2 status: neg; ', 'cell type: sorted breast tumor epithelium; genotype: Unknown; invasive tumour type: Ductal; invasive b-r grade: I; er status: pos; pr status: pos; her2 status: neg; ', 'cell type: sorted breast tumor epithelium; genotype: Unknown; invasive tumour type: Ductal; invasive b-r grade: III; er status: pos; pr status: pos; her2 status: neg; ', 'cell type: sorted breast tumor epithelium; genotype: Unknown; invasive tumour type: M; invasive b-r grade: II; er status: pos; pr status: pos; her2 status: neg; ', 'cell type: sorted breast tumor epithelium; genotype: Unknown; invasive tumour type: Ductal; invasive b-r grade: II; er status: pos; pr status: neg; her2 status: neg; ' GSE152203 Homo sapiens 18 Genome binding/occupancy profiling by high throughput sequencing GPL11154 STAT3 and GR cooperate to drive basal-like triple negative breast cancer gene expression and proliferation 2020-06-10 Breast cancers can be divided into subtypes with different prognoses and treatment responses based on global gene expression differences. This study utilized integrated analysis of DNA methylation, chromatin accessibility, transcription factor binding, and gene expression in large collections of breast cancer cell lines and patient tumors to identify transcription factors responsible for the basal-like gene expression program. The results of this study indicate that glucocorticoid receptor (GR) and signal transducer and activator of transcription 3 (STAT3) bind to the same genomic regulatory regions that are specifically open and unmethylated in basal-like breast cancer. These transcription factors cooperate to regulate expression of hundreds of genes in the basal-like gene expression signature and these downstream genes are associated with poor prognosis in patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE152203 STAT3 and GR Cooperate to Drive Gene Expression and Growth of Basal-Like Triple-Negative Breast Cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-20-1379 {Cancer research (8.378): 10.1158/0008-5472.CAN-20-1379} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA638631 https://www.ebi.ac.uk/ena/browser/view/PRJNA638631 https://www.ncbi.nlm.nih.gov/sra?term=SRP266791 [Overal design]Transcription factor ChIP-seq for GR and STAT3 was performed in TNBC cell lines, SUM159, MDA-MB-231, HCC1937, HCC70, HCC1187, and luminal cell lines MDA-MB-361, BT-474, MDA-MB-453, and MCF-7. STAT3 and GR ChIP-seq was performed after 1hr vehicle control induction (ethanol) and 100nM Dexamethasone induction respectively.; [Treatment]'None'; [Growth]'The following cell lines: MDA-MB-231, MDA-MB-361 , MDA-MB-453, were cultured in DMEM media (Gibco, ThermoFisher Scientific, Waltham, MA) supplemented with 10% fetal bovine serum (Hyclone, GE Healthcare, Logan, UT), 1 mM sodium pyruvate, and non-essential amino acids (Gibco). HCC70, HCC1187, HCC1937 were cultured in RPMI media (Gibco), supplemented with 10% fetal bovine serum (Hyclone), 10 mM HEPES (Sigma-Aldrich, St. Louis, MO), 1 mM sodium pyruvate (Gibco), and 4.5 g/l glucose (Sigma-Aldrich). BT474 were cultured in RPMI, 10% fetal bovine serum, 10 mM HEPES, 1mM sodium pyruvate, 4.5g/l glucose, 10µg/ml insulin. MCF-7 cells were cultured in EMEM, 10% fetal bovine serum, 1mM sodium pyruvate, non-essential amino acids and 10µg/ml insulin. SUM159 cells were cultured in Ham’s F12, 5% fetal bovine serum, 1µg/ml hydrocortisone, and 5µg/ml insulin. Cells were passaged and harvested at 80% confluence.'; [Extraction]'For ChIP experiments, protein-DNA complexes were covalently cross-linked by incubating cells in 1% formaldehyde for 10 min at room temperature. Cells were incubated with 0.125 M glycine for 5 min, to quench cross-linking reaction. Cells were washed and scraped with PBS (pH 7.4) (Lonza). Cells were lysed with Farnham Lysis Buffer (5mM PIPES at pH 8.0, 85 mM KCl, 0.5% NP-40) containing protease inhibitor (Roche). Cell lysate was centrifuged at 2,000 rpm for 5 min at 4 °C. The crude nuclear extract contained in the supernatant was stored at −80 °C.\nChIP-seq libraries were constructed as described here: https://www.encodeproject.org/documents/df9dd0ec-c1cf-4391-a745-a933ab1af7a7/@@download/attachment/Myers_Lab_ChIP-seq_Protocol_v042211.pdf'; [Cell type]'Source: ''chip antibody: sc-482; treatment: EtOH; cell line: BT474; ', 'chip antibody: sc-482; treatment: EtOH; cell line: HCC1187; ', 'chip antibody: sc-482; treatment: EtOH; cell line: HCC1937; ', 'chip antibody: sc-482; treatment: EtOH; cell line: HCC70; ', 'chip antibody: sc-482; treatment: EtOH; cell line: MCF7; ', 'chip antibody: sc-482; treatment: EtOH; cell line: MDA-MB-231; ', 'chip antibody: sc-482; treatment: EtOH; cell line: MDA-MB-361; ', 'chip antibody: sc-482; treatment: EtOH; cell line: MDA-MB-453; ', 'chip antibody: sc-482; treatment: EtOH; cell line: SUM159; ', 'chip antibody: sc-1003; treatment: 100nM dexamethasone; cell line: BT474; ', 'chip antibody: sc-1003; treatment: 100nM dexamethasone; cell line: HCC1187; ', 'chip antibody: sc-1003; treatment: 100nM dexamethasone; cell line: HCC1937; ', 'chip antibody: sc-1003; treatment: 100nM dexamethasone; cell line: HCC70; ', 'chip antibody: sc-1003; treatment: 100nM dexamethasone; cell line: MCF-7; ', 'chip antibody: sc-1003; treatment: 100nM dexamethasone; cell line: MDA-MB-231; ', 'chip antibody: sc-1003; treatment: 100nM dexamethasone; cell line: MDA-MB-361; ', 'chip antibody: sc-1003; treatment: 100nM dexamethasone; cell line: MDA-MB-453; ', 'chip antibody: sc-1003; treatment: 100nM dexamethasone; cell line: SUM159; ' GSE95302 Homo sapiens 33 Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL11154; GPL16791 DNA structure-specific endonuclease FEN1 as a novel drug target in tamoxifen resistant breast cancer. 2017-02-23 Estrogen receptor α (ERα) is a key transcriptional regulator in the majority of breast cancers. ERα-positive patients are frequently treated with tamoxifen, but resistance is common. In this study, we refined a previously identified 111-gene outcome prediction-classifier, revealing FEN1 as the strongest determining factor in ERα-positive patient prognostication. FEN1 levels were predictive of outcome in tamoxifen-treated patients, and FEN1 played a causal role in ERα-driven cell growth. FEN1 impacted the transcriptional-activity of ERα by facilitating coactivator recruitment to the ERα transcriptional complex. FEN1 blockade induced proteasome-mediated degradation of activated ERα, resulting in loss of ERα-driven gene expression and eradicated tumor cell proliferation. Finally, a high-throughput 465,195 compound screen identified a novel FEN1 inhibitor, which effectively blocked ERα-function and inhibited proliferation of tamoxifen-resistant cell lines as well as ex-vivo cultured ERα-positive breast tumors. Collectively, these results provide therapeutic proof-of-principle for FEN1 blockade in tamoxifen-resistant breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95302 None None None None None 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA376593 https://www.ebi.ac.uk/ena/browser/view/PRJNA376593 https://www.ncbi.nlm.nih.gov/sra?term=SRP100642 [Overal design]RNA-seq and Chip-seq of ERα, FOXA1, XRCC1, PCNA, POLII, PARP1, XRCC1, BRG1 and FAIRE-seq in MCF-7 cells treated with siRNAs or FEN1 inhibitor RRBS of MCF-7 cells treated -+ 45 min E2 -+ FEN1 inhibitor; [Treatment]'Hormone treatments consisted of solvent Dimethylsulfoxide (DMSO) or 10nM of estradiol. Additionally cells were pretreated with 100nM of the FEN1 inhibitor prior to hormone treatment. For knockdown experiments 25nM of single or pooled duplexes of siRNA against FEN1 (Dharmacon MU-010344-01) or a non-targeting control pool (Dharmacon, D-001206-14-20) were transfected with Dharmafect according to manufactures protocol.'; [Growth]'MCF-7were cultured in DMEM medium in the presence of 10% FBS and antibiotics (penicillin, streptavidin). For hormone deficient conditions, cells were deprived of hormone for 72 hours, by culturing in phenol-red-free DMEM containing 5% charcoal-treated serum, antibiotics and supplemented with L-glutamine, prior to hormone treatment.'; [Extraction]'ChIP experiments were performed as described previously (Zwart et al., 2011).\nChIP DNA was amplified as described (Jansen et al., 2013). Sequences were generated by the Illumina Hiseq 2000 genome analyser (using 51 or 65 bp reads), and aligned to the Human Reference Genome (assembly hg19, February 2009).', 'ChIP experiments were performed as described previously (Zwart et al., 2011).\nChIP DNA was amplified as described (Jansen et al., 2013). Sequences were generated by theHiSeq 2500 High Output Mode, and aligned to the Human Reference Genome (assembly hg19, February 2009).', 'Libraries were generated with the Illumina TruSeq RNA Library Preparation kit (RS-122-2001/2, Illumina Inc.) and sequenced on a HiSeq 2500 (using 65bp reads)'; [Cell type]'Source: ''treatment: ERα siControl; ', 'treatment: ERα siFEN1; ', 'treatment: FOXA1 siControl; ', 'treatment: FOXA1 siFEN1; ', 'treatment: FAIRE siControl; ', 'treatment: FAIRE siFEN1; ', 'treatment: ERα 10 min E2 vehicle; ', 'treatment: ERα 10 min E2 FEN1 inhibitor; ', 'treatment: XRCC1 10 min E2; ', 'treatment: PARP1 30 min E2 vehicle; ', 'treatment: PARP1 30 min E2 FEN1 inhibitor; ', 'treatment: BRG1 control; ', 'treatment: BRG1 fen1 inhibitor; ', 'cell line: MCF-7; ' GSE128460 Homo sapiens 117 Genome binding/occupancy profiling by high throughput sequencing; Other; Expression profiling by high throughput sequencing GPL18573; GPL21290 Enhancer reprogramming driven by high-order assemblies of transcription factors promotes phenotypic plasticity and breast cancer endocrine resistance 2019-03-18 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE128460 Enhancer reprogramming driven by high-order assemblies of transcription factors promotes phenotypic plasticity and breast cancer endocrine resistance. Nature cell biology 17.728 https://doi.org/10.1038/s41556-020-0514-z {Nature cell biology (17.728): 10.1038/s41556-020-0514-z} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA527786 https://www.ebi.ac.uk/ena/browser/view/PRJNA527786 None [Overal design]Refer to individual Series; [Treatment]'None', 'For knockdown of GATA3 or JUN, MCF7 parental or TamR cells were infected with shRNA lentiviruses and selected by puromycin (1 μg/ml) for 3 days to establish GATA3 knockdown MCF7 parental or JUN knockdown TamR stable cell lines. For the Dox-inducible GATA3, JUN-overexpressing cell lines, GATA3 and JUN cDNAs (Open Biosystems) were cloned into the pInducer 20 destination vector (Meerbrey et al., 2011) using the Gateway system (Invitrogen). Lentivirus was produced in 293T cells and used to infect cells in media containing polybrene (8 μg/ml). Cells were selected for 4 days by 500 μg/mL G418 (Invitrogen) after virus infection to get inducible overexperssion stable lines. To induce GATA3 or JUN protein expression, 1 μg/ml doxycycline was added into culture media for about 48 h before collection for experiments. For knockdown of GATA3 and overexpression of JUN in MCF7 parental cells at the same time, Dox-inducible JUN-overexpressing MCF7 parental stable cell line was further infected with shGATA3 lentiviruses and selected by puromycin (1 μg/ml) for 24 h, then 1 μg/ml doxycycline was added into culture media to induce JUN overexpression for about 48 h before collection for experiments.', 'For knockdown of GATA3, T47D cells were infected with shRNA lentiviruses and selected by puromycin (1 μg/ml) for 3 days to establish GATA3 knockdown T47D stable cell lines. For the Dox-inducible JUN-overexpressing cell lines, JUN cDNAs (Open Biosystems) were cloned into the pInducer 20 destination vector (Meerbrey et al., 2011) using the Gateway system (Invitrogen). Lentivirus was produced in 293T cells and used to infect cells in media containing polybrene (8 μg/ml). Cells were selected for 4 days by 500 μg/mL G418 (Invitrogen) after virus infection to get inducible overexperssion stable lines. To induce JUN protein expression, 1 μg/ml doxycycline was added into culture media for about 48 h before collection for experiments. For knockdown of GATA3 and overexpression of JUN in T47D cells at the same time, Dox-inducible JUN-overexpressing T47D stable cell line was further infected with shGATA3 lentiviruses and selected by puromycin (1 μg/ml) for 24 h, then 1 μg/ml doxycycline was added into culture media to induce JUN overexpression for about 48 h before collection for experiments.', 'For knockdown of GATA3, T47D or ZR75-1 cells were infected with shRNA lentiviruses and selected by puromycin (1 μg/ml) for 3 days to establish GATA3 knockdown T47D or ZR75-1 stable cell lines. For the Dox-inducible JUN-overexpressing cell lines, JUN cDNAs (Open Biosystems) were cloned into the pInducer 20 destination vector (Meerbrey et al., 2011) using the Gateway system (Invitrogen). Lentivirus was produced in 293T cells and used to infect cells in media containing polybrene (8 μg/ml). Cells were selected for 4 days by 500 μg/mL G418 (Invitrogen) after virus infection to get inducible overexperssion stable lines. To induce JUN protein expression, 1 μg/ml doxycycline was added into culture media for about 48 h before collection for experiments. For knockdown of GATA3 and overexpression of JUN in T47D or ZR75-1 cells at the same time, Dox-inducible JUN-overexpressing T47D or ZR75-1 stable cell line was further infected with shGATA3 lentiviruses and selected by puromycin (1 μg/ml) for 24 h, then 1 μg/ml doxycycline was added into culture media to induce JUN overexpression for about 48 h before collection for experiments.'; [Growth]'MCF7 parental cells were maintained in RPMI/1640 supplemented with 10% heat-inactivated FBS (Sigma) and 1% penicillin-streptomycin (P/S). The TamR cells were kept in phenol-red free RPMI/1640 medium supplemented with 10% heat-inactivated charcoal-stripped-FBS and 1% P/S with the addition of 100 nM 4-hydroxytamoxifen (4-OHT, H7904, Sigma). All cells were kept at 37 °C in a humified incubator with 5% CO2.', 'MCF7 and T47D parental cells were maintained in RPMI/1640 supplemented with 10% heat-inactivated FBS (Sigma) and 1% penicillin-streptomycin (P/S). The TamR cells were kept in phenol-red free RPMI/1640 medium supplemented with 10% heat-inactivated charcoal-stripped-FBS and 1% P/S with the addition of 100 nM 4-hydroxytamoxifen (4-OHT, H7904, Sigma). All cells were kept at 37 °C in a humified incubator with 5% CO2.', 'T47D and ZR75-1 cells were maintained in RPMI/1640 supplemented with 10% heat-inactivated FBS (Sigma) and 1% penicillin-streptomycin (P/S). All cells were kept at 37 °C in a humified incubator with 5% CO2.', 'T47D cells were maintained in RPMI/1640 supplemented with 10% heat-inactivated FBS (Sigma) and 1% penicillin-streptomycin (P/S). All cells were kept at 37 °C in a humified incubator with 5% CO2.', 'T47D cells were maintained in RPMI/1640 supplemented with 10% heat-inactivated FBS (Sigma) and 1% penicillin-streptomycin (P/S). All cells were kept at 37 °C in a humified incubator with 5% CO2. The hormone-independent HBCx-124 ED PDX was established from a HBCx-124 xenograft that escaped after 3 months of estrogen deprivation (ED).'; [Extraction]'50,000 cells were harvested for each condition. After purification of nuclei, transposition was performed with Tn5 transposase from Nextera DNA Library Prep Kit (Illumina, catalog # FC-121-1030). ATAC-seq library prep was performed as in Buenrostro et al, 2015. Libraries were sequenced with Mid 75bp PE on Illumina NextSeq 500 (4 samples in one lane).', 'Lysates were clarified from sonicated nuclei and protein-DNA complexes were isolated with antibody.\nThe extracted ChIP DNA was ligated to specific adaptors using KAPA LTP Library Preparation Kit (KK8230) or KAPA Hyper Prep Kit (KK8504), according to the manufacturer’s instructions.', 'Cells were subjected to nuclear run-on for 5minutes at 30°C with BrU labeling. The run-on RNAs were pull down by BrU beads and subjected to library preparation for deep sequencing.\nWe followed a previous published protocol (Ingolia et al., 2009 Science; Wang et al., 2011 Nature). Briefly, the run-on RNA were first added with a polyA tracts by RNA polyA polymerase. This polyA tail enables the run-on RNA to be reverse transcribed into single strand cDNA by Reverse Transcriptase. The cDNA was circularized by CircLigase (Epicentre) and re-linearized by APE I, subsequently subjected to PCR amplification and deep sequencing.', 'Total RNA was extracted by RNeasy Mini Kit from Qiagen(Cat no 74106).\nRNA-seq library were prepared by the KAPA RNA HyperPrep Kits with RiboErase (KK8560) or KAPA mRNA HyperPrep Kit (KK8580), according to the manufacturer’s instructions.', 'Lysates were clarified from sonicated nuclei and protein-DNA complexes were isolated with antibody.\nThe extracted ChIP DNA was ligated to specific adaptors using KAPA Hyper Prep Kit (KK8504), according to the manufacturer’s instructions.', 'Total RNA was extracted by RNeasy Mini Kit from Qiagen(Cat no 74106).\nRNA-seq library were prepared by the KAPA mRNA HyperPrep Kit (KK8580), according to the manufacturer’s instructions.'; [Cell type]'Source: ''cell line: MCF7; growth protocol: control (parental cell); ', 'cell line: MCF7; growth protocol: TamR; ', 'cell line: MCF7; growth protocol: control (parental cell); growth medium: Full media; chip antibody: ERalpha (Santa Cruz, sc-543); ', 'cell line: MCF7; growth protocol: TamR; growth medium: Full media; chip antibody: ERalpha (Santa Cruz, sc-543); ', 'cell line: MCF7; growth protocol: control (parental cell); growth medium: Full media; chip antibody: H3K4me1(Abcam, ab8895); ', 'cell line: MCF7; growth protocol: control (parental cell); growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: TamR; growth medium: Full media; chip antibody: H3K4me1(Abcam, ab8895); ', 'cell line: MCF7; growth protocol: TamR; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: control (parental cell); growth medium: Full media; chip antibody: Input; ', 'cell line: MCF7; growth protocol: TamR; growth medium: Full media; chip antibody: Input; ', 'cell line: MCF7; growth protocol: control (parental cell); growth medium: Full media; chip antibody: FOXA1(Abcam, ab5068); ', 'cell line: MCF7; growth protocol: TamR; growth medium: Full media; chip antibody: FOXA1(Abcam, ab5068); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with Control shRNA (scramble); growth medium: Full media; chip antibody: ERalpha (Santa Cruz, sc-543); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with JUN shRNA(sh9591); growth medium: Full media; chip antibody: ERalpha (Santa Cruz, sc-543); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with Control shRNA (scramble); growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with JUN shRNA(sh9591); growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 cells were infected with Control shRNA (scramble); growth medium: Full media; chip antibody: ERalpha (Santa Cruz, sc-543); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 cells were infected with GATA3 shRNA(sh9301); growth medium: Full media; chip antibody: ERalpha (Santa Cruz, sc-543); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 cells were infected with Control shRNA (scramble); growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 cells were infected with GATA3 shRNA(sh9301); growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: control (parental cell); growth medium: Full media; chip antibody: P300(Santa Cruz, sc-585); ', 'cell line: MCF7; growth protocol: TamR; growth medium: Full media; chip antibody: P300(Santa Cruz, sc-585); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 parental cells with DOX-inducible expression of JUN-without DOX treatment; growth medium: Full media; chip antibody: ERalpha (Santa Cruz, sc-543); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 parental cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; chip antibody: ERalpha (Santa Cruz, sc-543); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells with DOX-inducible expression of GATA3-without DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells with DOX-inducible expression of GATA3-with DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 parental cells with DOX-inducible expression of JUN-without DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 parental cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with Control shRNA (scramble); growth medium: Full media; chip antibody: ARID1B(Bethyl, A301-046A); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with JUN shRNA(sh9591); growth medium: Full media; chip antibody: ARID1B(Bethyl, A301-046A); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with Control shRNA (scramble); growth medium: Full media; chip antibody: BRG1(Abcam, ab4081); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with JUN shRNA(sh9591); growth medium: Full media; chip antibody: BRG1(Abcam, ab4081); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with Control shRNA (scramble); growth medium: Full media; chip antibody: P300(Active motif, 61401); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with JUN shRNA(sh9591); growth medium: Full media; chip antibody: P300(Active motif, 61401); ', 'cell line: MCF7; growth protocol: control (parental cell); growth medium: Full media; chip antibody: GATA3 (Cell Signaling, CST5852); ', 'cell line: MCF7; growth protocol: TamR; growth medium: Full media; chip antibody: GATA3 (Cell Signaling, CST5852); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: Control shRNA (scramble) for MCF7 parental cells with DOX-inducible expression of JUN-without DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: Control shRNA (scramble) for MCF7 parental cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: GATA3 shRNA (sh9301) for MCF7 parental cells with DOX-inducible expression of JUN-without DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: GATA3 shRNA (sh9301) for MCF7 parental cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: MCF7; growth protocol: control (parental cell); growth medium: Full media; chip antibody: JUN (Cell Signaling, CST9165); ', 'cell line: MCF7; growth protocol: TamR; growth medium: Full media; chip antibody: JUN (Cell Signaling, CST9165); ', 'cell line: MCF7; growth protocol: control (parental cell); growth medium: Full media; chip antibody: JUN (BD, 610326); ', 'cell line: MCF7; growth protocol: TamR; growth medium: Full media; chip antibody: JUN (BD, 610326); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: Full media for MCF7-P; ', 'cell line: MCF7; growth protocol: TamR; treatment: Full media for MCF7-TamR (100nM 4_OHT); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: Control shRNA (scramble) for MCF7 parental cells with DOX-inducible expression of JUN-without DOX treatment; ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: Control shRNA (scramble) for MCF7 parental cells with DOX-inducible expression of JUN-with DOX treatment; ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: GATA3 shRNA (sh9301) for MCF7 parental cells with DOX-inducible expression of JUN-without DOX treatment; ', 'cell line: MCF7; growth protocol: TamR; treatment: GATA3 shRNA (sh9301) for MCF7 parental cells with DOX-inducible expression of JUN-with DOX treatment; ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: TamR as a reference; ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 cells were infected with Control shRNA (scramble); ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 cells were infected with GATA3 shRNA(sh9301); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with Control shRNA (scramble); ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with JUN shRNA(sh9591); ', 'cell line: MCF7; growth protocol: control (parental cell); growth medium: Full media; ', 'cell line: MCF7; growth protocol: TamR; growth medium: Full media; ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 cells were infected with Control shRNA (scramble); growth medium: Full media; ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 cells were infected with GATA3 shRNA(sh9301); growth medium: Full media; ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with Control shRNA (scramble); growth medium: Full media; ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR cells were infected with JUN shRNA(sh9591); growth medium: Full media; ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 parental cells with DOX-inducible expression of JUN-without DOX treatment; growth medium: Full media; ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: MCF7 parental cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: Control shRNA (scramble) for MCF7 parental cells with DOX-inducible expression of JUN-without DOX treatment; growth medium: Full media; ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: Control shRNA (scramble) for MCF7 parental cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: GATA3 shRNA (sh9301) for MCF7 parental cells with DOX-inducible expression of JUN-without DOX treatment; growth medium: Full media; ', 'cell line: MCF7; growth protocol: control (parental cell); treatment: GATA3 shRNA (sh9301) for MCF7 parental cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; ', 'cell line: MCF7; growth protocol: TamR; treatment: TamR as a reference; growth medium: Full media; ', 'cell line: MCF7; growth protocol: resistant cell; ', 'cell line: T47D; growth protocol: control (parental cell); ', 'cell line: T47D; growth protocol: resistant cell; ', 'cell line: T47D; ', 'cell line: T47D; treatment: Control shRNA (scramble) for T47D cells with DOX-inducible expression of JUN-without DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: T47D; treatment: Control shRNA (scramble) for T47D cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', '', 'cell line: T47D; treatment: GATA3 shRNA (sh9301) for T47D cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: ZR75-1; treatment: Control shRNA (scramble) for ZR75-1 cells with DOX-inducible expression of JUN-without DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: ZR75-1; treatment: Control shRNA (scramble) for ZR75-1 cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: ZR75-1; treatment: GATA3 shRNA (sh9301) for ZR75-1 cells with DOX-inducible expression of JUN-without DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: ZR75-1; treatment: GATA3 shRNA (sh9301) for ZR75-1 cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; chip antibody: H3K27ac(Abcam, ab4729); ', 'cell line: T47D; treatment: Control shRNA (scramble) for T47D cells with DOX-inducible expression of JUN-without DOX treatment; ', 'cell line: T47D; treatment: Control shRNA (scramble) for T47D cells with DOX-inducible expression of JUN-with DOX treatment; ', 'cell line: T47D; treatment: GATA3 shRNA (sh9301) for T47D cells with DOX-inducible expression of JUN-without DOX treatment; ', 'cell line: T47D; treatment: GATA3 shRNA (sh9301) for T47D cells with DOX-inducible expression of JUN-with DOX treatment; ', 'cell line: PDX; treatment: Estrogen supplementation; growth medium: Full media; ', 'cell line: PDX; treatment: Estrogen deprivation; growth medium: Full media; ', 'cell line: T47D; treatment: Control shRNA (scramble) for T47D cells with DOX-inducible expression of JUN-without DOX treatment; growth medium: Full media; ', 'cell line: T47D; treatment: Control shRNA (scramble) for T47D cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; ', 'cell line: T47D; treatment: GATA3 shRNA (sh9301) for T47D cells with DOX-inducible expression of JUN-without DOX treatment; growth medium: Full media; ', 'cell line: T47D; treatment: GATA3 shRNA (sh9301) for T47D cells with DOX-inducible expression of JUN-with DOX treatment; growth medium: Full media; ' GSE111329 Mus musculus 4 Expression profiling by high throughput sequencing GPL16417 Knockdown of the Prolactin Receptor Inhibits Recruitment of Tregs and their Promotion of EMT in a Syngeneic Breast Cancer Model 2018-03-02 The clinical relevance and prognostic significance of tumor-infiltrating Tregs in different types of cancers makes them appealing therapeutic targets. However, while effective at inhibiting cancer progression, immunotherapeutics targeting Treg function have adverse effects in a substantial proportion of patients, ranging from mild inflammatory disorders to frank autoimmune disease. Here, we report that systemic knockdown of the long form of the prolactin receptor (LFPRLR) inhibits recruitment of Tregs to primary tumors and, importantly, metastasis-promoting activities of tumor Tregs, with no change in the production of TGFβ or IL-10 by tumor Tregs or the ability of peripheral Tregs to suppress anti-CD3/CD28-stimulated effector cell proliferation. Knockdown of the LFPRLR was accomplished using a derivatized DNA splice-modulating oligomer and outcome was assessed in the highly-metastatic, syngeneic, orthotopic 4T1-Balb/c immune-competent breast cancer model. We conclude that knockdown of the LFPRLR produces a more functionally-specific anti-cancer effect in Tregs, suggesting promise as a future therapeutic approach. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE111329 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA436638 https://www.ebi.ac.uk/ena/browser/view/PRJNA436638 https://www.ncbi.nlm.nih.gov/sra?term=SRP133813 [Overal design]mice were orthotopically injected with 4T1 breast cancer cells treated with other control splice modulating oligomer or LFPRLR splice modulating oligomer for 12 days. Whole tumor or sorted tumor Tregs were collected and the gene expression was analyzed by RNAseq between the control and LFPRLR treated mice. N=6 in each group.; [Treatment]'mice were orthotopically injected with 4T1 breast cancer cells treated with other control splice modulating oligomer or LFPRLR splice modulating oligomer for 12 days. Whole tumor or sorted tumor Tregs were collected and the gene expression was analyzed by RNAseq between the control and LFPRLR treated mice. N=6 in each group.'; [Growth]'None'; [Extraction]"Total RNA was extracted using Trizol followed by rRNA depletion (NEB)\ncDNA library was constructed as described in manufacturer's instruction (Kapa Biosystems)"; [Cell type]'Source: ''strain: Balb/c; injected with: 4T1 breast cancer cells treated with other control splice modulating oligomer; tissue: mammary; tissue/cell subtype: whole tumor; ', 'strain: Balb/c; injected with: 4T1 breast cancer cells treated with LFPRLR splice modulating oligomer; tissue: mammary; tissue/cell subtype: whole tumor; ', 'strain: Balb/c; injected with: 4T1 breast cancer cells treated with other control splice modulating oligomer; tissue: mammary; tissue/cell subtype: sorted tumor Tregs; ', 'strain: Balb/c; injected with: 4T1 breast cancer cells treated with LFPRLR splice modulating oligomer; tissue: mammary; tissue/cell subtype: sorted tumor Tregs; ' GSE26771 Mus musculus 12 Expression profiling by array GPL1261 Expression data from primary mammary epithelial cells expressing ectopic p190B RhoGAP 2011-01-20 P190B RhoGAP is required for mammary gland development, and its overexpression disrupts mammary gland branching morphogenesis. To better understand the mechanisms by which p190B regulates mammary gland development we performed gene expression microarray analysis on mammary epithelial cells isolated from p190B overexpressing transgenic mice compared to control mice. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26771 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA136301 https://www.ebi.ac.uk/ena/browser/view/PRJNA136301 None [Overal design]The mice used in this study were previously developed to inducibly overexpress p190B selectively in the mammary gland (Vargo-Gogola 2006). FVB/N mice carrying the MMTV-rtTA and TetO-p190B-IRES-luciferase transgenes or the MMTV-rtTA transgene only (Gunther EJ, FASEB) were fed doxycycline (Dox) chow (2 g/kg) for 7 d prior to removal of mammary glands and isolation of primary mammary epithelial cells at 6 weeks of age.; [Treatment]'mammary epithelial cells were isolated as previously described (McHenry PR et al., 2010, Breast Cancer Research)'; [Growth]'5 week old female mice were treated for 7 days with doxycycline containing chow (2 g/kg)'; [Extraction]"Trizol extraction of total RNA followed by purification using a RNeasy column according to manufacturer's instructions."; [Cell type]'Source: ''strain: FVB/N; genotype/variation: MMTV-rtTA; gender: female; ', 'strain: FVB/N; genotype/variation: MMTV-rtTA/TetO-p190B; gender: female; ' GSE65616 Homo sapiens 24 Expression profiling by array GPL10558 RUNX1 and RUNX2 responsiveness in MCF7 breast cancer cells: relationship to estrogen signaling 2015-02-04 Comparative analysis of RUNX1 and RUNX2 responsiveness in the presence or absence of E2 https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE65616 RUNX1 prevents oestrogen-mediated AXIN1 suppression and β-catenin activation in ER-positive breast cancer. Nature communications 11.878 https://doi.org/10.1038/ncomms10751 {Nature communications (11.878): 10.1038/ncomms10751} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA274487 https://www.ebi.ac.uk/ena/browser/view/PRJNA274487 None [Overal design]RUNX1 was constitutively silenced in MCF7 cells, and kept in charcoal stripped serum for 48h prior to dox inducible re-expression of RUNX1 in MCF7/Rx1dox, or expression of RUNX2 in MCF7/Rx2dox cells. Global gene expression was profiled to define genes regulated by estradiol, RUNX1 (or RUNX2) or both.; [Treatment]'treated with 500 ng/ml doxycycline and/or 10nM E2'; [Growth]'cells were grown in phenol red free DMEM containing 10% charcoal stripped serum'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''cell line: MCF7, with dox inducible RUNX1 expression; treatment: Veh; ', 'cell line: MCF7, with dox inducible RUNX1 expression; treatment: Dox; ', 'cell line: MCF7, with dox inducible RUNX1 expression; treatment: E2; ', 'cell line: MCF7, with dox inducible RUNX1 expression; treatment: Dox+E2; ', 'cell line: MCF7, with dox inducible RUNX2 expression; treatment: Veh; ', 'cell line: MCF7, with dox inducible RUNX2 expression; treatment: Dox; ', 'cell line: MCF7, with dox inducible RUNX2 expression; treatment: E2; ', 'cell line: MCF7, with dox inducible RUNX2 expression; treatment: Dox+E2; ' GSE54582 Mus musculus 222 Expression profiling by array GPL6246 Transcriptomic analysis of mammary tumors from MMTV-ErbB2 transgenic mice 2014-01-31 The tyrosine kinase ErbB2 positive breast tumors have more aggressive tumor growth, poorer clinical outcome, and more resistance to radiotherapy, chemotherapy and hormone therapy. A humanized anti-ErbB2 monoclonal antibody Herceptin and a small molecules inhibitor Lapatinib were developed and approved by FDA to treat patients with ErbB2 amplification and overexpression. Unfortunately, most ErbB2+ breast cancers do not respond to Herceptin and Lapatinib, and the majority of responders become resistant within 12 months of initial therapy (defined as secondary drug resistance). Such differences in response to Lapatinib treatment is contributed by substantial heterogeneity within ErbB2+ breast cancers. To address this possibility, we carried out transcriptomic analysis of mammary tumors from genetically diverse MMTV-ErbB2 mice. This will help us to have a better understanding of the heterogeneous response to ErbB2 targeted therapy and permit us to design better and more individualized (personalized) treatment strategies for human ErbB2 positive breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54582 Unraveling heterogeneous susceptibility and the evolution of breast cancer using a systems biology approach. Genome biology 14.028 https://doi.org/10.1186/s13059-015-0599-z {Genome biology (14.028): 10.1186/s13059-015-0599-z} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA237109 https://www.ebi.ac.uk/ena/browser/view/PRJNA237109 None [Overal design]214 MMTV-ErbB2 mammary tumors and 8 normal mammary glands were analyzed by Affymetrix microarrays.; [Treatment]'None'; [Growth]'spontaneous mammary tumors from genetically diverse MMTV-ErbB2 mice'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''tissue: mammary tumor; genotype: MMTV-ErbB2; genetic background: F1Bx: (C57BL/6 x FVB/N) x FVB/N; ', 'tissue: mammary tumor; genotype: MMTV-ErbB2; genetic background: F1: C57BL/6 x FVB/N; ', 'tissue: mammary tumor; genotype: MMTV-ErbB2; genetic background: FVB/N; ', 'tissue: Normal mammary gland; genotype: MMTV-ErbB2; genetic background: F1: C57BL/6 x FVB/N; ', 'tissue: Normal mammary gland; genotype: MMTV-ErbB2; genetic background: FVB/N; ', 'tissue: Normal mammary gland; genotype: Wild type; genetic background: F1: C57BL/6 x FVB/N; ' GSE59872 Mus musculus 25 Expression profiling by array GPL6246 Gene expression profiling of Lgr5-creERT2/PIK3CA H1047R and K8-creERT2/PIK3CA H1047R-evoked mammary tumors 2014-07-29 This study examined the gene expression profile of mammary tumors derived from Lgr5- and K8-positive cell-of-origins https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59872 PIK3CA(H1047R) induces multipotency and multi-lineage mammary tumours. Nature 43.070 https://doi.org/10.1038/nature14669 {Nature (43.070): 10.1038/nature14669} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA256962 https://www.ebi.ac.uk/ena/browser/view/PRJNA256962 None [Overal design]Mammary tumors and reference mammary glands from control mice were collected, cryo-homogenized, total RNA was isolated and analyzed by microarray (total 25 samples).; [Treatment]'Adult (7-8 week old) mice were injected with Tamoxifen to induce PIK3CA H1047R expression. After tumor development, tumors were collected and cryo-homogenized.'; [Growth]'tumor cells from Lgr5-creERT2/PIK3CA H1047R (mixed background FVB/C57/BL6) and K8-creERT2/PIK3CA H1047R (mixed background FVB/CD1) animals'; [Extraction]'Trizol method'; [Cell type]'Source: ''strain: mixed background FVB/CD1; genotype/variation: K8-creERT2/PIK3CA H1047R; tissue: mammary tumor; ', 'strain: mixed background FVB/C57/BL6; genotype/variation: Lgr5-creERT2/PIK3CA H1047R; tissue: mammary tumor; ', 'strain: mixed background FVB/C57/BL6; genotype/variation: Lgr5-creERT2 ctrl; tissue: mammary gland; ', 'strain: mixed background FVB/CD1; genotype/variation: K8-creERT2 ctrl; tissue: mammary gland; ' GSE32350 Homo sapiens 23 Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing GPL6244; GPL9052 Methylation specifies distinct estrogen-induced binding site repertoires of CBP to chromatin 2011-09-23 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32350 Methylation specifies distinct estrogen-induced binding site repertoires of CBP to chromatin. Genes & development 8.990 https://doi.org/10.1101/gad.619211 {Genes & development (8.990): 10.1101/gad.619211} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA147247 https://www.ebi.ac.uk/ena/browser/view/PRJNA147247 None [Overal design]Refer to individual Series; [Treatment]'H3396 cells were cultured in charcoal stripped medium for 72 hours before treatment for 1h, 2h, 6h and 24h with 1.10-8 M estrogen or vehicle control', 'Before 1h of estrogen or ethanol treatment, H3396 cells were cultured in charcol stripped medium for 72h'; [Growth]'H3396 cells were maintained in RPMI 1640 supplemented with 10 mM HEPES, 10% fetal bovine serum (FBS), and antibiotics.'; [Extraction]'Total RNA was isolated with GenEluteTM Mammalian Total RNA Miniprep Kit (RTN 350) from Sigma according to the manufacturer’s instructions', 'ChIP assays were performed according to standard protocols'; [Cell type]'Source: ''cell line: H3396; treatment: estrogen; time: 0 h; ', 'cell line: H3396; treatment: estrogen; time: 1 h; ', 'cell line: H3396; treatment: estrogen; time: 2 h; ', 'cell line: H3396; treatment: estrogen; time: 6 h; ', 'cell line: H3396; treatment: estrogen; time: 24 h; ', 'cell line: H3396 cells; treatment: estrogen; comment: Santa Cruz: CBP (A22); chip antibody: CBP; chip antibody manufacturer: Santa Cruz; chip antibody catalog #: A22; ', 'cell line: H3396 cells; treatment: ethanol; comment: Santa Cruz: CBP (A22); chip antibody: CBP; chip antibody manufacturer: Santa Cruz; chip antibody catalog #: A22; ', 'cell line: H3396 cells; treatment: estrogen; comment: In house Rabbit polyclonal: peptide MGP(Rme2a)AASPMC; chip antibody: peptide MGP(Rme2a)AASPMC; chip antibody manufacturer: In house; ', 'cell line: H3396 cells; treatment: estrogen; comment: In house Rabbit polyclonal: peptide ISPS(Rme2a)MPQPC; chip antibody: CBPR768m peptide ISPS(Rme2a)MPQPC; chip antibody manufacturer: In house; ', 'cell line: H3396 cells; treatment: ethanol; comment: In house Rabbit polyclonal: peptide ISPS(Rme2a)MPQPC; chip antibody: CBPR768m peptide ISPS(Rme2a)MPQPC; chip antibody manufacturer: In house; ', 'cell line: H3396 cells; treatment: estrogen; comment: In house Rabbit polyclonal: peptide AGVP(Rme2a)PGVPC; chip antibody: CBPR2151m peptide AGVP(Rme2a)PGVPC; chip antibody manufacturer: In house; ', 'cell line: H3396 cells; treatment: ethanol; comment: In house Rabbit polyclonal: peptide AGVP(Rme2a)PGVPC; chip antibody: CBPR2151m peptide AGVP(Rme2a)PGVPC; chip antibody manufacturer: In house; ', 'cell line: H3396 cells; treatment: estrogen; comment: Santa Cruz: ERa (HC20); chip antibody: ERa; chip antibody manufacturer: Santa Cruz; chip antibody catalog #: HC20; ', 'cell line: H3396 cells; treatment: ethanol; comment: Santa Cruz: ERa (HC20); chip antibody: ERa; chip antibody manufacturer: Santa Cruz; chip antibody catalog #: HC20; ', 'cell line: H3396 cells; treatment: estrogen; comment: In house Rabbit polyclonal: Total H3/H4 acetylated; chip antibody: H3/H4 acetylated; chip antibody manufacturer: In house; ', 'cell line: H3396 cells; treatment: estrogen; comment: Abcam: H3K18ac (ab1191); chip antibody: H3K18ac; chip antibody manufacturer: Abcam; chip antibody catalog #: ab1191; ', 'cell line: H3396 cells; treatment: ethanol; comment: Abcam: H3K18ac (ab1191); chip antibody: H3K18ac; chip antibody manufacturer: Abcam; chip antibody catalog #: ab1191; ', 'cell line: H3396 cells; treatment: estrogen; comment: In house Mouse: 7C2 Clone; chip antibody: PolII 7C2 clone; chip antibody manufacturer: In house; ', 'cell line: H3396 cells; treatment: ethanol; comment: In house Mouse: 7C2 Clone; chip antibody: PolII 7C2 clone; chip antibody manufacturer: In house; ', 'cell line: H3396 cells; treatment: estrogen; comment: Santa Cruz: RAC3 (M397); chip antibody: RAC3; chip antibody manufacturer: Santa Cruz; chip antibody catalog #: M397; ', 'cell line: H3396 cells; treatment: estrogen; comment: In house Rabbit polyclonal: aa. 595-608; chip antibody: CARM1 aa. 595-608; chip antibody manufacturer: In house; ', 'cell line: H3396 cells; treatment: ethanol; comment: In house Rabbit polyclonal: aa. 595-608; chip antibody: CARM1 aa. 595-608; chip antibody manufacturer: In house; ', 'cell line: H3396 cells; treatment: estrogen; chip antibody: none; ' GSE72249 Homo sapiens 45 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Characterization of ER, GR, and FoxA1 binding patterns in breast cancer cells treated with either Dex or E2 2015-08-20 The estrogen receptor (ER), glucocorticoid receptor (GR), and forkhead box protein 1 (FoxA1) are significant factors in breast cancer progression. FoxA1 is well-established as a pioneer factor for steroid receptor recruitment to chromatin. Here we show that ER and GR have the ability to alter the genomic response of FoxA1 to specific binding sites within the genome. These findings alter the classical understood mechanism of FoxA1 establishing a dynamic transcription factor that can be regulated by hormones. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72249 Steroid Receptors Reprogram FoxA1 Occupancy through Dynamic Chromatin Transitions. Cell 36.216 https://doi.org/10.1016/j.cell.2016.02.067 {Cell (36.216): 10.1016/j.cell.2016.02.067} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA293471 https://www.ebi.ac.uk/ena/browser/view/PRJNA293471 https://www.ncbi.nlm.nih.gov/sra?term=SRP062679 [Overal design]We examined the ER and GR mediated affects on FoxA1 binding patterms; [Treatment]'Cells were plated for experiments in phenol red free growth medium supplemented with 10% charcoal-dextran serum twenty-four hours before hormone treatment. Cells were left untreated or induced with 100nM dexamethasone or 100nM estradiol for 30 minutes.'; [Growth]'see additional columns of the SAMPLES section'; [Extraction]'Lysates were clarified from sonicated nuclei and GR/DNA, ER/DNA, of FoxA1/DNA complexes were isolated with antibody.'; [Cell type]'Pleural effusion from an adenocarcinoma of the breast', 'Ascites from a ductal carcinoma of the breast', 'Pleural effusion from a ductal carcinoma of the breast''cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: Dexamethasone and 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: Dexamethasone and 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: Dexamethasone and 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ' GSE33487 Homo sapiens 8 Expression profiling by array GPL10332 Chemokine expressions in breast cancer patients 2011-11-04 Our aim was to evaluate the expression of chemokines in breast cancers before treatment to identify a molecular signature that could distinguish between women with or without cancer. We identified a panel of chemokines clearly deregulated in breast cancer that could be further investigated for prospective novel markers or therapeutically approaches. Samples for gene expression were obtained during surgical resection and after macroscopic pathological assessment. Laser-capture microdissection was used to select and procure only the desired cell types (malignant groups of cells or normal mammary acini), under direct microscopic visualization https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE33487 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA148733 https://www.ebi.ac.uk/ena/browser/view/PRJNA148733 None [Overal design]Chemokine expression profiles using cDNA microarray was evaluated on homogenous, laser-capture microdissected breast cancer specimens before treatment.; [Treatment]'Fresh samples were obtained during surgical resection and after macroscopic pathological assessment. Prelevated tissues (0.5 – 1/0.5 cm) were preserved in tubes with RNAlater solution, (Ambion, Applied Biosystems, Germany) for 24 hours at +4°C and then frozen at -80°C. Corresponding non-lesional tissues removed from the same patients served as normal controls and were treated in similar manner.'; [Growth]'None'; [Extraction]'Laser-capture microdissection was used to select and procure only the desired cell types (malignant groups of cells or normal mammary acini), under direct microscopic visualization, using an UV cutting system (mmi SmartCut Plus, MMI Molecular Machines and Industries, Glattburg, Switzerland) with an Olympus microscope. RNA was extracted with RNAqueous-Micro kit (Ambion, Applied Biosystems, Germany) following exactly the manufacturer protocol for microdissected cells. RNA concentration and purity were quantified spectrophotometrically (NanoDrop ND1000) and the quality of RNA was evaluated on RNA electrophoregrams generated by the Agilent 2100 Bioanalyzer (Agilent Technologies, Massy, France). RNA was stored at -80°C until further gene expression analyses.'; [Cell type]'normal mammary acini', 'malignant cells''tissue: Breast cancer surgical resection; cell type: normal mammary acini; gender: female; age: 43; ', 'tissue: Breast cancer surgical resection; cell type: malignant cells; gender: female; age: 43; ', 'tissue: Breast cancer surgical resection; cell type: normal mammary acini; gender: female; age: 35; ', 'tissue: Breast cancer surgical resection; cell type: malignant cells; gender: female; age: 35; ', 'tissue: Breast cancer surgical resection; cell type: malignant cells; gender: female; age: 70; ', 'tissue: Breast cancer surgical resection; cell type: malignant cells; gender: female; age: 72; ', 'tissue: Breast cancer surgical resection; cell type: malignant cells; gender: female; age: 68; ', 'tissue: Breast cancer surgical resection; cell type: malignant cells; gender: female; age: 64; ' GSE144260 Homo sapiens 6 Expression profiling by array GPL15207 Expression data from MM231 and MM231-FGD5-cas9 breast cancer cells 2020-01-26 To identify the differiational genes and pathways in MM231 and MM231-FGD5-cas9, we examined the microarray gene expression profile of MM231 breast cancer cells vs FGD5-cas9 cells. Ectopic expression or activation of EGFR is found in most TNBCs, and EGFR inhibitors can suppress TNBC growth in vitro. However, these agents exhibit limited efficacy in TNBC patients, possibly due to the nonkinase oncogenic functions of EGFR and the compensatory effects of other oncogenic activities following anti-EGFR therapy. Here, we identified a positive correlation between EGFR and FGD5 expression in TNBC samples. FGD5 deletion attenuated TNBC initiation and progression by decreasing EGFR stability and expression. Moreover, the proteins involved in mutual compensation of EGFR signaling were significantly downregulated in FGD5-deleted TNBC cells. Mechanistically, FGD5 interacted with EGFR to maintain EGFR stability by impeding EGFR ubiquitylation and degradation mediated by the E3 ligase ITCH; disrupting the FGD5-EGFR interaction accelerated EGFR degradation and produced robust anti-TNBC activity. Our study shows that targeted degradation of EGFR through disrupting the FGD5-EGFR interaction is a promising therapeutic strategy for the TNBC subtype of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144260 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA603236 https://www.ebi.ac.uk/ena/browser/view/PRJNA603236 None [Overal design]Total RNA of MM231 and MM231-FGD5-cas9 breast cancer cells were obtained, and RNA quantity and quality were measured by NanoDrop ND-1000. RNA microarrays were performed.; [Treatment]'None'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''tissue: breast cancer; cell line: MDA-MB 231; ' GSE55534 Homo sapiens 15 Expression profiling by high throughput sequencing GPL11154 Rate of elongation by RNA polymerase II is influenced by specific gene features and histone modifications 2014-03-03 The rate of transcription elongation plays important roles in the timing of expression of full-length transcripts as well as for the regulation of alternative splicing. In this study we coupled Bru-Seq technology with 5,6-dichlorobenzimidazole 1-β-D-ribofuranoside (DRB) to estimate the elongation rates of over 2,000 individual genes in human cells. This technique, BruDRB-Seq, revealed gene-specific differences in elongation rates with a median rate of around 1.5 kb/min. We found that genes with fast elongation rates showed higher densities of H3K79m2 and H4K20me1 marks compared to slower elongating genes. Furthermore, fast elongation rates had a positive correlation with gene length, low complexity DNA sequence and distance from nearest active transcription unit. Features that negatively correlated with elongation rate included exon density and the number of LINE sequences in the gene. The BruDRB-Seq technique offers new opportunities to interrogate mechanisms of regulation of transcription elongation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55534 Rate of elongation by RNA polymerase II is associated with specific gene features and epigenetic modifications. Genome research 9.944 https://doi.org/10.1101/gr.171405.113 {Genome research (9.944): 10.1101/gr.171405.113} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA239893 https://www.ebi.ac.uk/ena/browser/view/PRJNA239893 https://www.ncbi.nlm.nih.gov/sra?term=SRP039359 [Overal design]Measurement of RNA Pol II elogation rate. Normal fibroblasts (HF1 and TM), Cockayne syndrome group B fibroblasts, K562 and MCF-7 cells were exposed to DRB for 60 minutes, after which a washout was performed. Nascent RNA was labeled using bromouridine for 10 minutes immediately after the washout. The genomic region extending from actice Trancription Start Sites was used to determine the gene's elongation rate. Please note that the nf_0h_3* samples are duplicated sample records of GSM1062445 and GSM1062446, for the convenient retrieval of the complete raw data from SRA.; [Treatment]'In the DRB treated samples, the drug 5,6-dichloro-1-bold beta-D-ribofuranosylbenzimidazole (DRB, Sigma) is added to the media to a final concentration of 100 μM and cells are incubated for a determined period of time at 37 ̊C. After the incubation with DRB, the cells were washed with PBS twice and nascent RNA was labeled in conditioned media containing 2 mM bromouridine (Bru) (Aldrich) for 10 min at 37°C. The cells were then directly lysed in TRIzol reagent (Invitrogen). K562 cells were grown in suspension so these cells were quickly spun down before being lysed in TRIzol. In the samples nfDRB0m1 and csbDRB0m1, the labeling with Bru is carried out in the presence of DRB.'; [Growth]'Human fibroblasts (HF1, TM and CS-B) were grown in MEM supplemented with 10% FBS, L-glutamine, vitamin mix and antibiotics. K562 human leukemia cells were grown in IMDM supplemented with 10% FBS supplemented with penicillin and streptomycin. MCF-7 human breast cancer cells were grown in high-glucose RPMI supplemented with 10% FBS.'; [Extraction]'Total RNA was isolated by using TRIzol reagent (Invitrogen), and Bru-labeled RNA was isolated from the total RNA by incubation with anti-BrdU antibodies (BD Biosciences) conjugated to magnetic beads (Dynabeads, Goat anti-Mouse IgG; Invitrogen) under gentle agitation at room temperature for 1 h. For more detail, see Paulsen et. al 2013\nBru-labeled RNA was mixed with first strand buffer and random primers and fragmented by heating at 85 ̊C for 10 minutes. The first strand cDNA was then synthesized, in the presence of Actinomycin D to result in strand specific reads (only applicable to certain samples as indicated in sample table above). After purifying the first strand cDNA using AMPure RNAclean beads (Beckman Coulter), the second strand cDNA was synthesized. The resulting cDNA was purified with AMPure XP beads, after which the Illumina TruSeq RNA Sample Prep Kit was used to repair the cDNA ends, adenylate and ligate adaptors to the cDNA. The samples were then run on a 3% agarose gel and size-selected by excising gel slices in the 300bp region. These gel slices were purified using the QIAEX II Gel Extraction Kit (Qiagen) and then the Illumina TruSeq Kit PCR reagents were used to enrich the DNA fragments. After a final purification using AMPure XP beads, the quality and concentration of the DNA libraries were determined using an Agilent Bioanalyzer.'; [Cell type]'Foreskin fibroblasts (HF1)', 'Cockayne syndrome group B fibroblasts', 'Fibroblast (TM)', 'K562', 'MCF-7''cell type: Foreskin fibroblasts (HF1); drb exposure time: 0 minutes; bromouridine labeling start: NA; bromouridine labeling time: 30 minutes; treatment group: Control; exogenous dna: NA; ', 'cell type: Foreskin fibroblasts (HF1); drb exposure time: 60 minutes; bromouridine labeling start: 10 minutes prior to washout; bromouridine labeling time: 10 minutes; treatment group: DRB exposure; exogenous dna: NA; ', 'cell type: Foreskin fibroblasts (HF1); drb exposure time: 60 minutes; bromouridine labeling start: Immediately after washout; bromouridine labeling time: 10 minutes; treatment group: DRB exposure; exogenous dna: NA; ', 'cell type: Foreskin fibroblasts (HF1); drb exposure time: 60 minutes; bromouridine labeling start: 10 minutes after washout; bromouridine labeling time: 10 minutes; treatment group: DRB exposure; exogenous dna: NA; ', 'cell type: Cockayne syndrome group B fibroblasts; drb exposure time: 0 minutes; bromouridine labeling start: NA; bromouridine labeling time: 10 minutes; treatment group: Control; exogenous dna: NA; ', 'cell type: Cockayne syndrome group B fibroblasts; drb exposure time: 60 minutes; bromouridine labeling start: 10 minutes prior to washout; bromouridine labeling time: 10 minutes; treatment group: DRB exposure; exogenous dna: NA; ', 'cell type: Cockayne syndrome group B fibroblasts; drb exposure time: 60 minutes; bromouridine labeling start: Immediately after washout; bromouridine labeling time: 10 minutes; treatment group: DRB exposure; exogenous dna: NA; ', 'cell type: Cockayne syndrome group B fibroblasts; drb exposure time: 60 minutes; bromouridine labeling start: 10 minutes after washout; bromouridine labeling time: 10 minutes; treatment group: DRB exposure; exogenous dna: NA; ', 'cell type: Fibroblast (TM); drb exposure time: 0 minutes; bromouridine labeling start: NA; bromouridine labeling time: 30 minutes; treatment group: Control; exogenous dna: empty vector; ', 'cell type: Fibroblast (TM); drb exposure time: 60 minutes; bromouridine labeling start: Immediately after washout; bromouridine labeling time: 10 minutes; treatment group: DRB exposure; exogenous dna: empty vector; ', 'cell type: K562; drb exposure time: 0 minutes; bromouridine labeling start: NA; bromouridine labeling time: 10 minutes; treatment group: Control; exogenous dna: NA; ', 'cell type: K562; drb exposure time: 60 minutes; bromouridine labeling start: Immediately after washout; bromouridine labeling time: 10 minutes; treatment group: DRB exposure; exogenous dna: NA; ', 'cell type: MCF-7; drb exposure time: 0 minutes; bromouridine labeling start: NA; bromouridine labeling time: 10 minutes; treatment group: Control; exogenous dna: NA; ', 'cell type: MCF-7; drb exposure time: 60 minutes; bromouridine labeling start: Immediately after washout; bromouridine labeling time: 10 minutes; treatment group: DRB exposure; exogenous dna: NA; ' GSE90582 Homo sapiens 4 Expression profiling by array GPL17077 Gene expression profiling of LRRC26-depleted HCC70 cells 2016-11-28 To serach gene expression change under knockdown of LRRC26, Leucin Rich Repeat Containing 26 in human triple negative breast cancer cells HCC70, we performed genome-wide DNA microarray analysis and compared the expression levels of control-siRNA treated cells and LRRC26-siRNA treates cells at 48 to 72 h after siRNA transfection https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE90582 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA355115 https://www.ebi.ac.uk/ena/browser/view/PRJNA355115 None [Overal design]HCC70 cells were transfected with 10 nM of siRNA for EGFP(control) and LRRC26. After 48 hr and 72 h, cells were harvested and RNA was purified for microarray analysis.; [Treatment]"Cells were seeded at a density 2×10^5/well onto 6-well plate folllowed by transfection of 10 nM siEGFP (SIGMA) or siLRRC26 (Darmacon) using Lipofectamine RNAiMAX (Life Technologies) according to manufacture's guidance."; [Growth]'Human triple negative breast cancer cells HCC70 was maintained in RPMI-1640 medium containing 10% FBS and antibiotics/antimycotics.'; [Extraction]'After 48 and 72 h of siRNA transfection, total RNA was extracted using NucleoSpin RNA kit (TaKaRa Bio) according to the instructions. This included an on-column DNase digestion with the RNase-free Dnase (TaKaRa Bio)'; [Cell type]'triple negative breast cancer cell line''cell line: HCC70; cell type: triple negative breast cancer cell line; transfected with: 10 nM of siRNA for EGFP (control); time point: 48hrs post-transfection; ', 'cell line: HCC70; cell type: triple negative breast cancer cell line; transfected with: 10 nM of siRNA for LRRC26; time point: 48hrs post-transfection; ', 'cell line: HCC70; cell type: triple negative breast cancer cell line; transfected with: 10 nM of siRNA for EGFP (control); time point: 72hrs post-transfection; ', 'cell line: HCC70; cell type: triple negative breast cancer cell line; transfected with: 10 nM of siRNA for LRRC26; time point: 72hrs post-transfection; ' GSE114787 Mus musculus 6 Expression profiling by array GPL16570 Microarray expression profiling data for Trp53/Brca1-null mammary tumors derived from K8+ luminal cells 2018-05-22 BRCA1 mutation-carriers are predisposed to develop Basal-like breast cancer (BLBC), and p53 mutations are present in the majority of human BLBC cases, suggesting loss of these two tumor suppressors play key roles in development of BLBC. Recent studies suggest that the majority of human breast cancers, including BLBC, may originate from mammary epithelial cells (MECs) in the luminal lineage. However, how loss of p53 and BRCA1 contributes to development of BLBC from luminal MECs remains largely elusive. We developed a novel genetic targeting and lineage tracing approach based on intraductal injection of Cre-expressing adenovirus under the control of the pan-luminal Keratin 8 (K8) promoter (Ad-K8-Cre). We performed intraductal injection of Ad-K8-Cre to female mice carrying conditional knockout alleles of Brca1 and Trp53. The injected females developed mammary tumors within 12 months after injection. Microarray expression profiling of these tumors showed that they most closely resembled human BLBC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE114787 Inadequate DNA Damage Repair Promotes Mammary Transdifferentiation, Leading to BRCA1 Breast Cancer. Cell 36.216 https://doi.org/10.1016/j.cell.2019.06.002 {Cell (36.216): 10.1016/j.cell.2019.06.002} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA472622 https://www.ebi.ac.uk/ena/browser/view/PRJNA472622 None [Overal design]Total RNAs from YFP+ wild-type luminal mammary epithelial cells (i.e., cells of origin) sorted from Rosa26-Stop-YFP female mice 10-14 days after intraductal induction of Ad-K8-Cre adenovirus, or from mammary tumors developed in Trp53L/L;Brca1L/L females several months after intraductal injection of Ad-K8-Cre, were prepared and subjected to microarray expression profiling.; [Treatment]'Wild-type luminal mammary epithelial cells were obtained from Rosa26-Stop-YFP female mice 10-14 days after intraductal injection of Ad-K8-Cre; Trp53/Brca1-null mammary tumors were obtained from Trp53L/L;Brca1L/L females several months after intraductal injection of Ad-K8-Cre.'; [Growth]'Wild-type luminal mammary epithelial cells were sorted from Rosa26-Stop-YFP female mice after Ad-K8-Cre injection; Trp53/Brca1-null mammary tumors were collected from Trp53L/L;Brca1L/L female mice after Ad-K8-Cre injection.'; [Extraction]"RNeasy kit (Qiagen, #73504) was used on wild-type luminal mammary epithelial cells or Trp53/Brca1-null mammary tumors according to manufacturer's protocol"; [Cell type]'luminal mammary epithelial cells', 'mammary tumor''tissue: mammary gland; cell type: luminal mammary epithelial cells; genotype: wildtype; ', 'tissue: mammary gland; cell type: mammary tumor; genotype: Trp53L/L;Brca1L/L; ' GSE108308 Homo sapiens 12 Expression profiling by high throughput sequencing GPL18573 A cell-permeable stapled peptide inhibitor of the estrogen receptor/coactivator interaction 2017-12-19 We and others have proposed that coactivator binding inhibitors, which block the interaction of estrogen receptor and steroid receptor coactivators, may represent a potential class of new breast cancer therapeutics. The development of coactivator binding inhibitors has been limited, however, because many of the current molecules which are active in in vitro and biochemical assays are not active in cell-based assays. Our goal in this work was to prepare a coactivator binding inhibitor active in cellular models of breast cancer. To accomplish this, we used molecular dynamics simulations to convert a high-affinity stapled peptide with poor cell permeability into R4K1, a cell-penetrating stapled peptide. R4K1 displays high binding affinity for estrogen receptor ɑ, inhibits the formation of estrogen receptor/coactivator complexes, and distributes throughout the cell with a high percentage of nuclear localization. R4K1 represses native gene transcription mediated by estrogen receptor ɑ and inhibits proliferation of estradiol-stimulated MCF-7 cells. Using RNA-Seq, we demonstrate that almost all of the effects of R4K1 on global gene transcription are estrogen receptor-associated. This chemical probe provides a significant proof-of-concept for preparing cell-permeable stapled peptide inhibitors of the estrogen receptor/coactivator interaction. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE108308 A Cell-Permeable Stapled Peptide Inhibitor of the Estrogen Receptor/Coactivator Interaction. ACS chemical biology 4.374 https://doi.org/10.1021/acschembio.7b01016 {ACS chemical biology (4.374): 10.1021/acschembio.7b01016} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA423076 https://www.ebi.ac.uk/ena/browser/view/PRJNA423076 https://www.ncbi.nlm.nih.gov/sra?term=SRP127178 [Overal design]mRNA profiles were generated for MCF-7 cells under six conditions. Experiments were performed in duplicate. Conditions: 1)vehicle treated (DMSO control), 2) estradiol (10 nM), 3) 4-hydroxytamoxifen (1 μM), 4) estradiol (10 nM) + 4-hydroxytamoxifen (1 μM), 5) R4K1 stapled peptide (15 μM), 6) estradiol (10 nM) + R4k1 (15 μM).; [Treatment]'MCF-7 cells were seeded at a density of 150K celsl/well in 6 well plates in treatment media (phenol red-free RPMI 1640 media supplemented with 5% charcoal–dextran–stripped fetal bovine serum for at least 48 hrs. The cells were incubated overnight (24hr) with the stapled peptides (15 μM). The following day cells were treated with E2 (10 nM) or 4OHT (1 μM) for 2hr and for the E2 and 4OHT treated cells the cells were pretreated with 4OHT for 2hrs'; [Growth]'Human MCF-7 were grown in Roswell Park Memorial Institute (RPMI) media supplemented with 10% fetal bovine serum (FBS), 1% non-essential amino acids, 2 mM L-glutamine, 1% antibiotics penicillin-streptomycin, and 6 ng/ml human recombinant insulin at 37 ˚C in 5% CO2 (T75 flasks).'; [Extraction]'Total RNA was isolated using Trizol. RNA samples were DNase treated and purified using the RNA Clean and Concentrator-5 kit (Zymo Research). All samples were quantified using the NanoDrop 1000 instrument (Thermo Fisher Scientific). RNA quality was analyzed on a TapeStation RNA tape (Agilent).\n500ng total RNA from each sample was used as input for library prep, using the QuantSeq 3’ mRNA-Seq Library Prep kit (Lexogen). The protocol was followed as written. In brief, the RNA underwent oligo dT priming, reverse transcription, removal of the RNA template, and second strand synthesis via random priming, resulting in double-stranded libraries. Illumina indexes were then incorporated during 16 cycles of PCR amplification. Library yields were assessed with the Qubit dsDNA HS reagent (Invitrogen), and TapeStation D1000 tape (Invitrogen)'; [Cell type]'Breast cancer cell''cell type: Breast cancer cell; cell line: MCF-7; treatment: vehicle; ', 'cell type: Breast cancer cell; cell line: MCF-7; treatment: estradiol (10 nM); ', 'cell type: Breast cancer cell; cell line: MCF-7; treatment: 4-hydroxytamoxifen (1 μM); ', 'cell type: Breast cancer cell; cell line: MCF-7; treatment: estradiol (10 nM) + 4-hydroxytamoxifen (1 μM); ', 'cell type: Breast cancer cell; cell line: MCF-7; treatment: R4K1 stapled peptide (15 μM); ', 'cell type: Breast cancer cell; cell line: MCF-7; treatment: estradiol (10 nM) + R4k1 (15 μM); ' GSE75876 Homo sapiens 3 Genome binding/occupancy profiling by high throughput sequencing GPL11154 The PGC-1α/ERRα Axis Represses One-Carbon Metabolism and Promotes Sensitivity to Anti-Folate Therapy in Breast Cancer [ChIP-Seq] 2015-12-10 Reprogramming of cellular metabolism plays a central role in fuelling malignant transformation, and AMPK as well as the PGC-1α/ERRα axis are key regulators of this process. Intersection of gene expression and binding event datasets in breast cancer cells shows that activation of AMPK significantly increases the expression of PGC-1α/ERRα and promotes the binding of ERRα to its cognate sites. Unexpectedly, the data also reveal that ERRα, in concert with PGC-1α, negatively regulates the expression of several one-carbon metabolism genes resulting in substantial perturbations in purine biosynthesis. This PGC-1α/ERRα-mediated repression of one-carbon metabolism promotes the sensitivity of breast cancer cells and tumors to the anti-folate drug methotrexate. These data implicate the PGC-1α/ERRα axis as a core regulatory node of folate cycle metabolism and further suggest that activators of AMPK could be used to modulate this pathway in cancer. We used microarrays to detail the global programme of gene expression following AMPK activation by AICAR in BT474 breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE75876 The PGC-1α/ERRα Axis Represses One-Carbon Metabolism and Promotes Sensitivity to Anti-folate Therapy in Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2015.12.086 {Cell reports (7.815): 10.1016/j.celrep.2015.12.086} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA305586 https://www.ebi.ac.uk/ena/browser/view/PRJNA305586 https://www.ncbi.nlm.nih.gov/sra?term=SRP067217 [Overal design]BT474 breast cancer cells were treated for 24h with vehicle or the AMPK activator AICAR and RNA was then purified for microarray analysis. Experiments were performed in duplicate for each condition.; [Treatment]'Reagents were simply added to the media for cell treatment in regular 6cm culture dish.'; [Growth]'Cells were cultured in regular DMEM. 24h after seeding, media was changed and fresh media with vehicle or AICAR 0.5mM'; [Extraction]'After 90min treatment with vehicle or AICAR, nuclei were isolated and subjected to chromatin immunoprecipitation. Following ERRa ChIP, genomic DNA was purified with QIAGEN DNA extraction kit.\nLibraries were performed at the Génome Québec Innovation Centre (McGill University) using standard protocol for HiSeq - Illumina Single reads 50bp sequencing lane'; [Cell type]'Source: ''cell line: BT474; tissue type: Breast tumor; chip antibody: ERRa; ', 'cell line: BT474; tissue type: Breast tumor; chip antibody: none; ' GSE51280 Homo sapiens 24 Expression profiling by array GPL17590 TBCRC 018: Phase II study of iniparib in combination with irinotecan to treat progressive triple negative breast cancer brain metastases 2013-09-30 Approximately half of women diagnosed with advanced triple negative breast cancer (TNBC) will develop brain metastases, of which the majority will have uncontrolled extracranial disease. While local therapies to treat brain metastases are standardly prescribed, survival remains less than 6 months. This phase II, multi-center trial evaluated efficacy of irinotecan and iniparib, anti-cancer agents with activity in TNBC and known to cross the blood brain barrier, among 34 patients with new or progressive TNBC brain metastases. While time to progression was short (2.1 months), 27% of patients experienced intracranial clinical benefit and therapy was well-tolerated. Correlative studies illustrate partial response was associated with germline BRCA mutation status and high tumor expression of proliferation genes and signatures. To our knowledge, this is the first study showing feasibility of enrolling patients with progressive TNBC brain metastases to a systemic therapy and lays the groundwork for future studies to treat this devastating disease. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE51280 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA222298 https://www.ebi.ac.uk/ena/browser/view/PRJNA222298 None [Overal design]24 tumor FFPE samples of this trial, representing 21 individual patients, were gene expression profiled. Expression of 128 selected genes was evaluated, including 5 HK genes.; [Treatment]'NA'; [Growth]'NA'; [Extraction]'Total RNA was isolated from FFPE tissue using ROCHE High Pure FFPE Kit'; [Cell type]'Source: ''pam50_call: Basal; pam50_rorp: 64.1575285879344; pam50_prolif: 0.411892990219305; age: 58; bestresponse: Progression; mrivolume: 19.9401840490798; clinicalbenefit: 0; ', 'pam50_call: Her2; pam50_rorp: 64.9965395734681; pam50_prolif: 0.3930475796958; age: 58; bestresponse: Progression; mrivolume: 19.9401840490798; clinicalbenefit: 1; ', 'pam50_call: Basal; pam50_rorp: 66.0786754349165; pam50_prolif: 0.482793017643962; age: 46; bestresponse: Not Evaluable; mrivolume: NA; clinicalbenefit: 0; ', 'pam50_call: Normal; pam50_rorp: 34.2394917431213; pam50_prolif: -0.0810720895187054; age: 36; bestresponse: Stable Disease; mrivolume: NA; clinicalbenefit: 1; ', 'pam50_call: Basal; pam50_rorp: 47.0523456762771; pam50_prolif: 0.136878577392338; age: 45; bestresponse: Stable Disease; mrivolume: -0.631578947368421; clinicalbenefit: 1; ', 'pam50_call: Basal; pam50_rorp: 53.1100654864079; pam50_prolif: 0.217317121314651; age: 42; bestresponse: Stable Disease; mrivolume: -0.8848; clinicalbenefit: 0; ', 'pam50_call: Basal; pam50_rorp: 68.7228506095727; pam50_prolif: 0.50314394835253; age: 44; bestresponse: Stable Disease; mrivolume: NA; clinicalbenefit: 1; ', 'pam50_call: Basal; pam50_rorp: 63.0567646721144; pam50_prolif: 0.436369566772639; age: 45; bestresponse: Stable Disease; mrivolume: -0.243045387994144; clinicalbenefit: 0; ', 'pam50_call: Basal; pam50_rorp: 41.4399667524861; pam50_prolif: 0.00450809313086506; age: 40; bestresponse: Progression; mrivolume: -0.0478287677265922; clinicalbenefit: 0; ', 'pam50_call: Normal; pam50_rorp: 26.905490839174; pam50_prolif: -0.230856430861373; age: 60; bestresponse: Progression; mrivolume: 1.17903142709943; clinicalbenefit: 0; ', 'pam50_call: Normal; pam50_rorp: 35.2806549158355; pam50_prolif: -0.113209912331369; age: 54; bestresponse: Stable Disease; mrivolume: -0.688098159509203; clinicalbenefit: 0; ', 'pam50_call: Basal; pam50_rorp: 43.4785706072395; pam50_prolif: 0.0343575671489145; age: 48; bestresponse: Partial Response; mrivolume: -0.820270824784571; clinicalbenefit: 1; ', 'pam50_call: Basal; pam50_rorp: 41.3435711671781; pam50_prolif: 0.0206792309460348; age: 39; bestresponse: Progression; mrivolume: NA; clinicalbenefit: 0; ', 'pam50_call: Basal; pam50_rorp: 58.259776831237; pam50_prolif: 0.383580607392828; age: 48; bestresponse: Partial Response; mrivolume: -0.820270824784571; clinicalbenefit: 1; ', 'pam50_call: Basal; pam50_rorp: 59.7080085472356; pam50_prolif: 0.350462482409633; age: 39; bestresponse: Progression; mrivolume: 0.103448275862069; clinicalbenefit: 0; ', 'pam50_call: Basal; pam50_rorp: 58.1883183202087; pam50_prolif: 0.375902801982387; age: 47; bestresponse: Partial Response; mrivolume: -0.968064516129032; clinicalbenefit: 1; ', 'pam50_call: Basal; pam50_rorp: 44.0106637326909; pam50_prolif: 0.0785656341565354; age: 55; bestresponse: Stable Disease; mrivolume: -0.37102158913866; clinicalbenefit: 0; ', 'pam50_call: Basal; pam50_rorp: 35.2292453555182; pam50_prolif: -0.0987701562474437; age: 43; bestresponse: Progression; mrivolume: -0.0380434782608695; clinicalbenefit: 0; ', 'pam50_call: Basal; pam50_rorp: 65.9492591138158; pam50_prolif: 0.517551082649686; age: 37; bestresponse: Not Evaluable; mrivolume: NA; clinicalbenefit: 0; ', 'pam50_call: Basal; pam50_rorp: 43.3835758433837; pam50_prolif: 0.0497168744446408; age: 71; bestresponse: Stable Disease; mrivolume: -0.266666666666667; clinicalbenefit: 1; ', 'pam50_call: Basal; pam50_rorp: 69.1453418332275; pam50_prolif: 0.496690910092923; age: 50; bestresponse: Partial Response; mrivolume: 0.0304316831683169; clinicalbenefit: 1; ', 'pam50_call: Basal; pam50_rorp: 55.2741590855233; pam50_prolif: 0.319681035022153; age: 36; bestresponse: Stable Disease; mrivolume: NA; clinicalbenefit: 1; ', 'pam50_call: Her2; pam50_rorp: 41.8276532262478; pam50_prolif: -0.067957330183548; age: 80; bestresponse: Stable Disease; mrivolume: -0.061874431301183; clinicalbenefit: 1; ', 'pam50_call: Basal; pam50_rorp: 58.1640043537194; pam50_prolif: 0.3633555733447; age: 53; bestresponse: Partial Response; mrivolume: -0.811255411255411; clinicalbenefit: 1; ' GSE19295 Homo sapiens 8 Expression profiling by array GPL571 HER2 and EGFR dependent activation of RalA in breast cancer 2009-12-03 Activated HER2 and EGFR stimulate the Ras small GTPases, which in turn primarily activate the MAPK, PI3K-Akt and RalGEF-Ral pathways. While activation of the MAPK and PI3K-Akt pathways downstream of HER2 and EGFR promote mammary tumorigenesis, little is known regarding the role of the RalGEF-Ral pathway. RalGEFs convert the small GTPases RalA and RalB to an active GTP-bound state. Of the two proteins, only activated RalA is transforming, while RalB is more important for cell motility, and hence we investigated the role of RalA in HER2-overexpressing and EGFR-positive breast cancer. We now report that shRNA-mediated knockdown of RalA reduced the in vitro transformed growth and in vivo tumorigenic growth of MDA-MB-231 human breast cancer cells, while knockdown of RalB reduced migration and invasion. Lastly, we demonstrate that expression of activated HER2 increases RalA-GTP levels, and that a number of genes associated with activated RalA are elevated in tumor compared to normal mammary tissue. Taken together, these results suggest a possible role for RalA in mammary tumorigenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE19295 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA120877 https://www.ebi.ac.uk/ena/browser/view/PRJNA120877 None [Overal design]Four independent cultures of HEK-HT cells stably infected with a retrovirus confirmed to expressed RalAQ72L and four independent cultures of HEK-HT cells stably infected with a control retrovirus RalA activation expression analysis; [Treatment]'None'; [Growth]'HEK-HT cells expressing empty vector or RalAQ72L were grown to 90% confluency in DMEM-H containing 10% FBS and 1x penstrep. When 90% confluency was reached, cells were washed with PBS two times and then grown in DMEM-H without FBS for 48 hours'; [Extraction]'Cells were collected and total RNA was isolated using RNAzol B reagent and chloroform. RNA was precipiated with isoproponal, washed in 75% ethanol, and resuspended in DEPC water.'; [Cell type]'Source: ''culture condition: penstrep; cell line: HEK-HT; ' GSE33038 Mus musculus 6 Expression profiling by array GPL13502 Involuted normal mammary gland in WAP-SV40 transgenic mice [gene expression] 2011-10-18 Transgenic expression in mice of two synergistically acting SV40 early region encoded proteins, large (LT) and small (sT) tumor antigens, in the mammary epithelium recapitulates loss of p53 and Rb function and deregulation of PP2A-controlled mitogenic pathways in human breast cancer. In primiparous mice, WAP-promoter driven expression of SV40 proteins induces well and poorly differentiated mammary adenocarcinomas. We performed a correlative aCGH and gene expression analysis of 25 monofocal tumors, representing four histopathological grades, to explore the molecular traits of SV40-induced mammary tumors and to emphasize the relevance of this tumor model for human breast tumorigenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE33038 Low-grade and high-grade mammary carcinomas in WAP-T transgenic mice are independent entities distinguished by Met expression. International journal of cancer 4.982 https://doi.org/10.1002/ijc.27783 {International journal of cancer (4.982): 10.1002/ijc.27783} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA149535 https://www.ebi.ac.uk/ena/browser/view/PRJNA149535 None [Overal design]Gene expression analysis of 6 involuted normal mammary gland 30 days post weaning in WAP-SV40 T1 and BALB/c samples.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted using Trizol Reagent (Invitrogen) followed by DNA digestion (TURBO DNA-free; Ambion) according to the manufacturer’s instructions. Total RNA from tumor samples and normal mammary gland was cleaned up using RNeasy mini kit according to the manufacturer’s instructions (Qiagen).'; [Cell type]'Source: ''strain: BALB/c; transgenic line: WAP-T1; tissue: involuted normal mammary gland; time: 30 days post weaning; ', 'strain: BALB/c; tissue: involuted normal mammary gland; time: 30 days post weaning; ' GSE99512 Homo sapiens 4 Expression profiling by array GPL17692 Study of gene targets regulated by oncogenic PIK3CA and/or Her2 2017-05-31 Mutant PIK3CA and Her2 genes are oncogenic and their co-existence in breast cancer has been well identified. However, the gene targets and cell signalling pathway regulated by mutant PIK3CA, Her2 and both of PIK3CA and Her2 have not been well studied. We established stable cell models through transfecting mutant PIK3CA, Her2 and both mutant PIK3CA and Her2 into MCF10A cells and performed Affymetrix microarray to identify downstream target genes controlled by either mutant PIK3CA, Her2 or both PIK3CA and Her2. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99512 Cooperative oncogenic effect and cell signaling crosstalk of co‑occurring HER2 and mutant PIK3CA in mammary epithelial cells. International journal of oncology 3.571 https://doi.org/10.3892/ijo.2017.4108 {International journal of oncology (3.571): 10.3892/ijo.2017.4108} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA388678 https://www.ebi.ac.uk/ena/browser/view/PRJNA388678 None [Overal design]RNA was extracted from 4 cell models (MCF10A/LacZ, MCF10A/Her2, MCF10A/mutant PIK3CA, and MCF10A/Her2+mutant PIK3CA) and purified using the RNeasy plus miniKit. Affymetrix microarray was performed and downstream target genes controlled by either mutant PIK3CA, Her2 or both PIK3CA and Her2 were identified. We also analyzed the cell signaling pathways enrichment.; [Treatment]'We did not perform any treatment on these cells.'; [Growth]'All four cell models ((MCF10A/LacZ, MCF10A/Her2, MCF10A/mutant PIK3CA, and MCF10A/Her2+mutant PIK3CA) were cultured in SFIHE medium in 37C with 5% CO2.'; [Extraction]'RNA was extracted and purified using the RNeasy plus mini kit.'; [Cell type]'Source: ''cell line: MCF10A; stable transfection: LacZ; ', 'cell line: MCF10A; stable transfection: Her2; ', 'cell line: MCF10A; stable transfection: PIK3CA-H1047R; ', 'cell line: MCF10A; stable transfection: Her2 and PIK3CA-H1047R; ' GSE138407 Homo sapiens 6 Expression profiling by array GPL23159 Peptidylarginine deiminase IV (PADI4) has a novel tumor cell-autonomous suppressor role in regulating breast cancer stem cells [Array] 2019-10-03 Peptidylarginine deiminases (PADIs) catalyze post-translational modification of many target proteins and have been suggested to play a role in carcinogenesis. Since citrullination of histones by PADI4 was recently implicated in regulating embryonic stem and hematopoietic progenitor cells, here we investigated a possible role for PADI4 in regulating breast cancer stem cells. We showed by genetic and pharmacologic approaches that PADI4 activity limits the number of cancer stem cells (CSCs) in vitro and in vivo in multiple breast cancer models. A gene signature reflecting tumor cell-autonomous PADI4 inhibition is associated with poor outcome in human breast cancer datasets, consistent with a tumor suppressive role for PADI4. Mechanistically, PADI4 inhibition resulted in a global redistribution of histone H3 with accumulation around transcriptional start sites. Interestingly, epigenetic effects of PADI4 on the bulk tumor cell population did not explain the CSC phenotype. However, in sorted tumor cell populations, PADI4 down-regulated expression of the master transcription factors of stemness, NANOG and POU5F1, specifically in the cancer stem cell compartment, by reducing the transcriptionally activating H3R17me2a histone mark at those loci. This effect was not seen in the non-stem cells. Our findings reveal a novel role for PADI4 as a tumor suppressor in regulating breast cancer stem cells, and provide insights into context-specific effects of PADI4 in epigenetic modulation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE138407 Peptidylarginine Deiminase IV Regulates Breast Cancer Stem Cells via a Novel Tumor Cell-Autonomous Suppressor Role. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-19-3018 {Cancer research (8.378): 10.1158/0008-5472.CAN-19-3018} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA575748 https://www.ebi.ac.uk/ena/browser/view/PRJNA575748 None [Overal design]MCF10Ca1h cells were transduced with a lentiviral control shRNA (shCON) or PADI4 knockdown (sh80) and selected with puromycin.; [Treatment]'MCF10Ca1h cells were transduced with a lentiviral control shRNA (shCON) or PADI4 knockdown (sh80) and selected with puromycin.'; [Growth]'MCF10Ca1h cells were cultured in DMEM/F12 media supplemmented with 5% horse serum.'; [Extraction]'Total RNA was extracted using TRIzol reagent (Ambion) and analyzed for quality with the Agilent 2100 Bioanalyzer system.'; [Cell type]'Source: ''cell line: MCF10Ca1h human breast cancer cell line; genotype: control shRNA; ', 'cell line: MCF10Ca1h human breast cancer cell line; genotype: PADI4 knockdown; ' GSE144927 Homo sapiens 4 Genome binding/occupancy profiling by high throughput sequencing GPL21290 Epigenomics-Based Identification of Estrogen-regulated Long Noncoding RNAs in ER+ Breast Cancer 2020-02-07 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144927 Epigenomics-based identification of oestrogen-regulated long noncoding RNAs in ER+ breast cancer. RNA biology 5.477 https://doi.org/10.1080/15476286.2020.1777769 {RNA biology (5.477): 10.1080/15476286.2020.1777769} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA605352 https://www.ebi.ac.uk/ena/browser/view/PRJNA605352 None [Overal design]Refer to individual Series; [Treatment]'Before experiment, the MCF7 cells were hormone-stripped in phenol red-free DMEM medium plus 5% charcoal-treated FBS for 3 days, followed by treatemnt of either 100 nM 17β-estrodial (E2) or ethanol as vehcile control for 1hr.'; [Growth]'MCF7 obtained from ATCC were cultured in DMEM media supplemented with 10% FBS in a 5% CO2 humidified incubator at 37°C.'; [Extraction]'20,000 cells were harvested for each condition. After purification of nuclei, transposition was performed with Tn5 transposase from Nextera DNA Library Prep Kit (Illumina, catalog # FC-121-1030). ATAC-seq library prep was performed as in Buenrostro et al, 2015.', 'Lysates were clarified from sonicated nuclei and protein-DNA complexes were isolated with antibody.\nThe extracted ChIP DNA was ligated to specific adaptors using KAPA Hyper Prep Kit (KK8504), according to the manufacturer’s instructions.'; [Cell type]'Source: ''cell line: MCF7; treatment: Vehicle (one hour); ', 'cell line: MCF7; treatment: E2 (one hour); ', 'cell line: MCF7; treatment: Vehicle (one hour); chip antibody: ARID1B(Bethyl, A301-046A); ', 'cell line: MCF7; treatment: E2 (one hour); chip antibody: ARID1B(Bethyl, A301-046A); ' GSE50104 Homo sapiens 10 Protein profiling by protein array GPL17612 Targeted inhibition of human breast cancer cell line selected as model system of ERBB2-positive breast cancer [RPPA-Shortterm-BT474] 2013-08-22 EGFR-inhibition is required for targeted therapies of ERBB2-positive/EGFR high breast cancer. Approximately 30% of human ERBB2-positive breast tumors also express EGFR. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50104 Boolean ErbB network reconstructions and perturbation simulations reveal individual drug response in different breast cancer cell lines. BMC systems biology 2.048 https://doi.org/10.1186/1752-0509-8-75 {BMC systems biology (2.048): 10.1186/1752-0509-8-75} 'protein' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA216094 https://www.ebi.ac.uk/ena/browser/view/PRJNA216094 None [Overal design]Three targeted therapeutics (erlotinib, pertuzumab, trastuzumab) and two ligands (EGF, HRG) were analyzed in all possible combinations. Each experiment involving inhibition with targeted drugs was performed in three, and measurements without inhibitors were performed in five biological replicates. This resulted in 780 samples. Incubation with therapeutics only and dilution series of control lysated were included as controls.; [Treatment]'The inhibitors trastuzumab (10 ng/µL), pertuzumab (10 ng/µL), and erlotinib (1 µM) (Roche, Penzberg, Germany) were added to cells in starvation medium either alone or in combinations 1 h prior to stimulation with EGF or HRG (5 nM) for 0, 4, 8, 12, 16, 20, 30, 40, 50 and 60 min. After stimulation, medium was removed and ice-cold PBS was added to the plates.'; [Growth]'Cells were seeded in 6-well plates and serum-starved for 24h.'; [Extraction]'Medium was replaced by ice-cold PBS, transferred on ice, and cells were harvested by scraping in M-PER lysis buffer (Pierce, Bonn, Germany) containing protease inhibitor Complete Mini and phosphatase inhibitor PhosSTOP (Roche, Mannheim, Germany). Cells were lyzed for 20 min on an end-over-end shaker and lysates were cleared at 13,000 rpm for 10 min by centrifugation.'; [Cell type]'Source: ''protein target: phospho-ERK1/2; phospho site: T202Y204; antibody id: CST 9106, 4370; ', 'protein target: phospho-AKT; phospho site: S473; antibody id: CST 9271; ', 'protein target: phospho-p70S6K; phospho site: T389; antibody id: CST 9206; ', 'protein target: phospho-ERBB1; phospho site: Y1086; antibody id: CST 2220; ', 'protein target: phospho-ERBB2; phospho site: Y1221Y1222; antibody id: CST 2243; ', 'protein target: phospho-MEK1/2; phospho site: S217S221; antibody id: Sigma M7683; ', 'protein target: phospho-PLCgamma; phospho site: S1248; antibody id: CST 4510; ', 'protein target: phospho-PKCalpha; phospho site: S657Y658, S657; antibody id: Abcam ab23513, Millipore 06-822; ', 'protein target: phospho-mTOR; phospho site: S2481; antibody id: Millipore 09-343; ', 'protein target: phospho-ERBB3; phospho site: Y1289; antibody id: CST 4791; ' GSE71139 Homo sapiens 8 Expression profiling by high throughput sequencing GPL9115 RNA-sequencing of tamoxifen resistant LY2 cells transfected with siRNA-HOXC11. 2015-07-21 To assess the global effects of HOXC11 in endocrine resistant breast cancer cells we performed RNA-seq on LY2 cells which were transfected with either siRNA targeting HOXC11 (siHOXC11) or a scrambled negative control siRNA (scrHOXC11) in the presence of 4-OH-tamoxifen (10-8M). Knockdown was verified by Taq-man qRT-PCR prior to library preparation. RNA (10µg) was extracted using an Oligotex mRNA kit (Qiagen) as per manufacturer’s instructions (n=4). RNA was reverse transcribed followed by mRNA library preparation and sequencing based on a protocol outlined by Wilhelm et al., 2010. Sequencing was performed on an Illumina Genome Analyzer II (GAII) (54 million reads per sample on average). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE71139 Prosaposin activates the androgen receptor and potentiates resistance to endocrine treatment in breast cancer. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-015-0636-6 {Breast cancer research : BCR (5.676): 10.1186/s13058-015-0636-6} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA290630 https://www.ebi.ac.uk/ena/browser/view/PRJNA290630 https://www.ncbi.nlm.nih.gov/sra?term=SRP061430 [Overal design]Silencing of HOXC11 in tamoxifen resistant LY2 cells to identify putative HOXC11 target genes.; [Treatment]'LY2 cells were seeded at a density of 2.5x10e5 and incubated overnight under standard conditions. HOXC11 was silenced by transient transfection using an experimentally verified pool of siRNA (Flexitube, Qiagen, UK) (2μg siRNA/6well)\xa0. All transfections were carried out using Lipofectamine 2000 transfection reagent according to manufacturer’s instructions (Invitrogen, UK) and a non-targeting siRNA negative control (Ambion, UK) was used as a control for all siRNA experiments. Both siRNA and scambled controls were treated with tamoxifen (10-8M) (24 hours) before cells were pelleted and RNA extracted,'; [Growth]'MCF7-derived LY2 (Bronzert et al., 1985) were maintained in phenol red-free Eagle’s minimum essential medium with 2 mM L-glutamine and supplemented with charcoal dextran stripped fetal bovine serum, 10% (Invitrogen, Paisley, UK).'; [Extraction]"RNA was extracted using an RNeasy (Qiagen, UK) according to manufacturer's instractions.\xa0\nLibraries were perepared according to standard Illumina protocols. Four independent biological libraries were prepared for each sample to facilitate the expression detection and variance estimation. Multiplexing was achieved using in-house designed barcoding adapters Four biological replicates of either siHOXC11 or scrHOXC11 sample were sequenced on a flow cell. Two replicates, one from each sample, were multiplexed and loaded on a single lane."; [Cell type]'Source: ''origin: breast epithelial; sirna: scrambled CONTROL; cell line: MCF7-derived LY2; ', 'origin: breast epithelial; sirna: siRNA-HOXC11; cell line: MCF7-derived LY2; ' GSE89216 Homo sapiens 8 Expression profiling by array GPL16686 Identification of resistance mechanisms to anti-HER2 antibody in breast cancer cell line BT-474 2016-10-26 Background: The addition of the anti-HER2 antibody pertuzumab to trastuzumab/chemotherapy treatment in HER2+ breast cancer significantly improves clinical outcome. Concomitantly, the drug-antibody conjugate T-DM1 (trastuzumab-emantasine) has demonstrated efficacy, at least equal, to the combination of trastuzumab/chemotherapy. Scientific, economic and health challenges emerge from the clinical use of these novel anti-HER2 antibodies, aimed to identify new resistance mechanisms and to select the target breast cancer population. Objectives: (1) To identify primary resistance mechanisms to anti-HER2 antibodies trastuzumab, pertuzumab, and to the combined trastuzumab/pertuzumab or pertuzumab/T-DM1 therapy, (2) To identify acquired resistance mechanisms to anti-HER2 antibodies trastuzumab, pertuzumab, and to the combined trastuzumab/pertuzumab or pertuzumab/T-DM1 therapy, (3) To develop new combinations of anti-HER2 antibodies with other targeted therapies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE89216 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA350699 https://www.ebi.ac.uk/ena/browser/view/PRJNA350699 None [Overal design]Samples: Breast cancer cell line BT-474. Treatments: trastuzumab-conditioned cultures. Control samples: same cell lines with no treatment. Triplicates.; [Treatment]'The trastuzumab-conditioned BT-474.R cell lines were established by culturing the BT-474 cell line in the appropriate media supplemented with 15 μg/ml of recombinant humanized monoclonal HER2 antibody, trastuzumab (Herceptin, Genentech, USA). Trastuzumab was dissolved in sterile water at a stock concentration of 20 mg/ml. Resistant populations were obtained for the four cell lines through lifetime exposure to the drug for a minimum of 8 months.'; [Growth]'BT-474 cells were maintained in DMEM-F12 supplemented with 10% heat-inactivated fetal bovine serum (FBS), 2 mmol/L glutamine, and 1% penicillin G-streptomycin.'; [Extraction]'RNeasy mini Kit (Qiagen)'; [Cell type]'Source: ''cell line: BT-474; ' GSE12970 Homo sapiens 46 Expression profiling by array GPL96; GPL570 TPO mimetics study 2008-09-29 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE12970 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA112577 https://www.ebi.ac.uk/ena/browser/view/PRJNA112577 None [Overal design]Refer to individual Series; [Treatment]'MDA-MB-231cells were exposed to regimens on a 10-day cycle: a 3-day treatment with 30 nM paclitaxel and followed by a 7-day exposure to control medium. Paclitaxel resistant MDA-MB-231 cells (MDA-PR) were established within 8 cycles of such treatment (80 days). When these MDA-PR cells were then treated with the combination of 30 nM paclitaxel ( 3 days on and 7 days off) and 1 µM Targretin (10 days on) in a new 10-day cycle for 3 months, MDA-PR cells became re-sensitized to paclitaxel again.', 'Two million cells from each donor were subcultured at 500,000 cells per well of six-well culture dishes in IMDM with 20% FBS, rhSCF at 100 ng/mL, and either 100 ng/mL rhTPO, 1 µM LGD4665, or equivalent volume of vehicle and incubated at 37°C in 5% CO2 for five days.', 'Purified human bone marrow CD34+ cells were cultured with rhSCF at 100 ng/mL, and either 100 ng/mL TPO, 3 µM eltrombopag, or 1 µM LGD-4665 for 10 days. The mature megakaryocytes were enriched using anti-CD61 Miltenyi beads, and FACS analysis showed that more than 90% of the purified cells were CD61+ cells.'; [Growth]'The human breast cancer cell line MDA-MB-231 was obtained from American Type Culture Collection (Manassas, VA), and MDA-MB-231cells were routinely cultured in RPMI 1640 supplemented with 10% fetal bovine serum and 2 mM glutamine in 5% CO2.', 'Human bone marrow hematopoietic CD34+ cells derived from five healthy donors were characterized for viability (90%-95% by Trypan blue dye exclusion) and CD34 expression (> 95% CD34+ by flow cytometry).', 'Human bone marrows from healthy donors were used to purifiy CD34+ cells, and cells were then cultured with rhSCF at 100 ng/mL, and either 100 ng/mL TPO, 3 µM eltrombopag, or 1 µM LGD-4665 for 10 days.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions.", 'Total RNA was isolated with RNA was isolated using RNeasy mini kit from Qiagen', 'Total RNA was isolated with Versagene RNA Cell Kit from Gentra Systems.'; [Cell type]'Source: ''' GSE17646 Homo sapiens 8 Non-coding RNA profiling by array GPL9039 Identification of Recurrence-Related microRNAs in the Bone Marrow of Breast Cancer Patients 2009-08-14 MicroRNA microarray analysis was performed to compare microRNA levels in bone marrow from 4 breast cancer patients with recurrent disease and 4 patients without recurrence. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17646 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA118593 https://www.ebi.ac.uk/ena/browser/view/PRJNA118593 None [Overal design]To achieve this goal, we used microRNA microarray analysis to compare microRNA expression in bone marrow from breast cancer patients with and without disease recurrence.; [Treatment]'None'; [Growth]'None'; [Extraction]'ISOGEN, reagent for RNA extraction manufactured by Nippon Gene Co. Ltd.'; [Cell type]'Source: ''tissue: bone marrow; age: 36y; size of tumor (t factor): T1 (<2cm); number of lymph node metastasis: 0; stage of disease: 1; recurrence and site: -; clinical outcome: alive; follow up period (months): 90; ', 'tissue: bone marrow; age: 65y; size of tumor (t factor): T1 (<2cm); number of lymph node metastasis: 0; stage of disease: 1; recurrence and site: -; clinical outcome: alive; follow up period (months): 49; ', 'tissue: bone marrow; age: 73y; size of tumor (t factor): T1 (<2cm); number of lymph node metastasis: 0; stage of disease: 1; recurrence and site: -; clinical outcome: alive; follow up period (months): 52; ', 'tissue: bone marrow; age: 64y; size of tumor (t factor): T1 (<2cm); number of lymph node metastasis: 0; stage of disease: 1; recurrence and site: -; clinical outcome: alive; follow up period (months): 48; ', 'tissue: bone marrow; age: 54y; size of tumor (t factor): T2 (2cm5cm); number of lymph node metastasis: 20; stage of disease: 3; recurrence and site: skin; clinical outcome: alive; disease free interval (months): 1; follow up period (months): 27; ', 'tissue: bone marrow; age: 56y; size of tumor (t factor): T1 (<2cm); number of lymph node metastasis: 10; stage of disease: 2; recurrence and site: liver; clinical outcome: cancer death; disease free interval (months): 12; follow up period (months): 29; ', 'tissue: bone marrow; age: 61y; size of tumor (t factor): T1 (<2cm); number of lymph node metastasis: 14; stage of disease: 2; recurrence and site: lymph node; clinical outcome: cancer death; disease free interval (months): 15; follow up period (months): 26; ' GSE17820 Homo sapiens 12 Expression profiling by array GPL7363 HuR differentially regulates unique subsets of mRNAs in estrogen receptor negative and positive breast cancer 2009-08-26 Analysis of RNA immunoprecipitation of HuR, a RNA binding protein (RBP), in breast cancer cell lines. This approach, utilizing RNA immunoprecipitation hybridized to microarray (RIP-Chip), provides global identification of putative endogenous mRNA targets of different RBPs. HuR is an RBP that binds to the AU-rich (ARE) regions of labile mRNAs, such as proto-oncogenes, facilitating their translation into protein. HuR has been shown to play a role in cancer progression and elevated levels of cytoplasmic HuR directly correlate with increased invasiveness and poor prognosis for many cancers, including those of the breast. We used HuR RIP-Chip as a comprehensive and systematic method to survey breast cancer target genes in both MCF-7 (estrogen receptor positive, ER+) and MDA-MB-231 (estrogen receptor negative, ER-) breast cancer cell lines. We identified unique subsets of HuR associated mRNAs found individually or in both cell types. Two novel HuR targets, CD-9 and CALM-2, were identified and validated by quantitative RT-PCR and biotin pulldown analysis. Our findings reveal that the differential regulation of these two cancer-related genes by HuR was contingent upon the cellular environment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17820 The RNA binding protein HuR differentially regulates unique subsets of mRNAs in estrogen receptor negative and estrogen receptor positive breast cancer. BMC cancer 2.933 https://doi.org/10.1186/1471-2407-10-126 {BMC cancer (2.933): 10.1186/1471-2407-10-126} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA120039 https://www.ebi.ac.uk/ena/browser/view/PRJNA120039 None [Overal design]RNA immunoprecipitation of the HuR RNA binding protein by 3A2 antibody and IgG (control) from two human breast cancer cell lines, MCF-7 and MDA-MB-231 .; [Treatment]'None'; [Growth]'None'; [Extraction]'HuR Immunoprecipitations (RIP-Chip): Cell lysates were prepared from exponentially growing MB-231 and MCF-7 cells. Equal amounts of protein lysates were used (100-300μg). HuR monoclonal antibody 3A2 or isotype control IgG1 were pre-coated onto protein A Sepharose beads (PAS) and extensively washed. Lysates from each cell line initially were pre-absorbed with 30 μg of IgG1 and then removed by addition of PAS beads. Individual pull downs were performed at 4°C for only 1-2 hr to minimize potential re-assortment of mRNAs.'; [Cell type]'Source: ''ip: 3A2; er status: -; cell line: MDA-MB-231; ', 'ip: 3A2; er status: +; cell line: MCF-7; ', 'ip: IgG; er status: +; cell line: MCF-7; ', 'ip: IgG; er status: -; cell line: MDA-MB-231; ' GSE127885 Homo sapiens 6 Expression profiling by array GPL1930 Human tumor cell lines treated with 5AZA-dC vs control untreated cells. 2019-03-05 Equal amounts of test and reference cDNA Cy-labeled mRNA targets were competitively hybridized against a customized cDNA platform with 4,608 ORESTES (open reading frame expressed sequences tags) representing human genes. With this microarray experiment, we found that N-Myc downstream-regulated gene 4 (NDRG4) is silenced in tumor cells and acts as a mechanistic biomarker of metastasis in ductal invasive breast tumors. While aberrant NDRG4 silencing, by DNA hypermethylation, is significantly associated with the development of metastatic disease, downregulation of NDRG4 transcription and protein expression is functionally associated with enhanced lymph node adhesion and cell mobility. Based on following functional assays, we show that silencing of NDRG4 modulates integrin signaling by assembling β1-integrins into large punctate clusters at the leading edge of tumor cells to promote an “adhesive switch,” decreasing cell adhesion to fibronectin and increasing cell adhesion and migration towards vitronectin, an important component of human lymph nodes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE127885 NDRG4 promoter hypermethylation is a mechanistic biomarker associated with metastatic progression in breast cancer patients. NPJ breast cancer 32.43 https://doi.org/10.1038/s41523-019-0106-x {NPJ breast cancer (32.43): 10.1038/s41523-019-0106-x} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA525694 https://www.ebi.ac.uk/ena/browser/view/PRJNA525694 None [Overal design]Two condition experiments: untreated (Mock) vs 5Aza-dC treated cells (T1) (1uM, 6 days). Three tested human tumor cell lines: MCF-7 (breast cancer), MDA-MB231 (breast cancer) and MDA-MB435 (melanoma) and one cell line used as reference: non-tumor human mammary epithelial cell line HB4a. Two replicates per array. ---------------------------------------- The author is unable to extract data from the TIFF files thus this record is incomplete.; [Treatment]'Tumor cell lines (MCF-7, MDA-MB231 and MDA-MB435) growing under optimal conditions were treated with 1uM 5Aza-dC for 6 days (T1 samples).'; [Growth]'Tumor cell lines (MCF-7, MDA-MB231 and MDA-MB435) and nontumor mammary epithleial cell line (HB4a) were maintained subconfluent at 37oC, under 5% CO2, in defined media. Cell lines are negative for micoplasma.'; [Extraction]'Total RNA from cultured cells was isolated using CsCl gradient as described by Glisin and colleagues (Glisin V et al., Biochemistry 1974; 13:2633-2637).'; [Cell type]'Source: ''culture conditions: MCF-7 cells were maintained in RPMI 1640 supplemented with 10% fetal bovine serum (FBS), insulin (5 ug/ml) and L-glutamine (1%).; tissue: Breast; ', 'culture conditions: HB4a cells were maintained at 37oC, under 5% CO2, in RPMI 1640 supplemented with 10% fetal bovine serum (FBS), insulin (5 ug/ml), L-glutamine (1%) and hydrocortisone (5 ug/ml).; ', 'culture conditions: MCF-7 cells were cultured in conventional conditions plus 1uM 5-Aza-dC for 6 days.; tissue: Breast; ', 'culture conditions: MDA-MB231 cells were maintained in RPMI 1640 supplemented with 10% fetal bovine serum (FBS) and 1% L-glutamine.; tissue: Breast; ', 'culture conditions: MDA-MB231 cells were cultured in conventional conditions plus 1uM 5-Aza-dC for 6 days.; tissue: Breast; ', 'culture conditions: MDA-MB435 cells were maintained in RPMI 1640 supplemented with 10% fetal bovine serum (FBS) and 1% L-glutamine.; tissue: Melanoma; ', 'culture conditions: MDA-MB435 cells were cultured in conventional conditions plus 1uM 5-Aza-dC for 6 days.; tissue: Melanoma; ' GSE6861 Homo sapiens 161 Expression profiling by array GPL1352 Prediction of breast cancer pathological complete response to anthracycline/taxane chemotherapy. 2007-01-25 EORTC 10994 phase III breast cancer clinical trial comparing FEC (5-fluorouracil, cyclophosphamide, epirubicin) with ET (epirubicin, docetaxel). 161 needle biopsies of locally advanced or large operable breast tumours were hybridised to Affymetrix X3P chips. The array data from the ER negative tumours (28/65 pathological CR in the FEC arm, 27/59 pathological CR in the ET arm) were used to validate the cell line-based chemotherapy response predictors developed by the Potti/Nevins group at Duke University (doi:10.1038/nm1491). Keywords: Tumour profiling https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE6861 Disequilibrium of BMP2 levels in the breast stem cell niche launches epithelial transformation by overamplifying BMPR1B cell response. Stem cell reports 5.499 https://doi.org/10.1016/j.stemcr.2014.12.007 {The Lancet. Oncology (None) doi:10.1016/S1470-2045(07)70345-5}; {Stem cell reports (5.499) doi:10.1016/j.stemcr.2014.12.007}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA99107 https://www.ebi.ac.uk/ena/browser/view/PRJNA99107 None [Overal design]We analyzed 161 arrays of breast carcinoma.; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen RNeasy Mini Kit'; [Cell type]'Source: ''' GSE116868 Homo sapiens 25 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Oncogenic Notch promotes long-range regulatory interactions within hyperconnected 3D cliques [MB157_ChIP-seq] 2018-07-10 Purpose: To investigate the impact of oncogenic Notch on the 3D genome organization of cancer cells. Methods: We generated cohesin HiChIP and 1D epigenomic data sets in two different Notch-dependent cancer cell types, triple-negative breast cancer (TNBC) and mantle cell lymphoma (MCL), in the Notch-on and -off states. Results: We report here that Notch transcription complexes control their direct target genes through two distinct regulatory modes: either through existing loops or by facilitating new long-range regulatory interactions. This combination of pre-existing and Notch-promoted loops coalesce enhancers and promoters to form highly interacting clusters, termed “3D cliques”. Notch preferentially activates enhancers and promotes looping interactions within highly connected 3D cliques that regulate key oncogenes. Conclusions: These observations suggest a general mechanism that oncogenic transcription factors can exploit to regulate the transcriptional outputs of cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE116868 Oncogenic Notch Promotes Long-Range Regulatory Interactions within Hyperconnected 3D Cliques. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2019.01.006 {Molecular cell (14.548): 10.1016/j.molcel.2019.01.006} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA480472 https://www.ebi.ac.uk/ena/browser/view/PRJNA480472 https://www.ncbi.nlm.nih.gov/sra?term=SRP152956 [Overal design]ChIP-seq, RNA-seq and HiChIP in Notch-on, -off, -recovery conditions in TNBC and MCL cell lines to profile Notch transcriptional complex binding, histone modification, Notch target genes and contact between regulatory elements.; [Treatment]'Cells were treated with the GSI compound E (1 μM, Calbiochem cat# 565790) for 72 hours, washed, and then cultured for 5 hours in media containing 1μM GSI (mock washout) or DMSO (washout) as previously described (Weng et al., 2006).', 'Untreated.'; [Growth]'MB157 (female) cells were grown in DMEM (Corning, cat# 10-013-CV) supplemented with 10% fetal bovine serum (Hyclone, cat# SH30070.03) and 100 U/mL and 100 μg/mL penicillin/streptomycin (Corning, cat# 30-002-CI). When passaged cells were detached with 0.25% trypsin, EDTA-free (Gibco, cat# 15090-046) to avoid activation of Notch signaling.'; [Extraction]'ChIP-seq was performed as previously described (Ryan et al., 2017). Briefly, chromatin samples prepared from appropriate number of fixed cells (10^7 for histone modifications and 4 x 10^7 for transcription factors) were sonicated and cleared with recombinant protein G–conjugated Agarose beads (Invitrogen, cat# 15920-010) and subsequently immunoprecipitated with antibodies recognizing Notch1 (Wang et al., 2014), RBPJ (D10A4) (CST, cat# 5313), H3K27ac (Active Motif, cat# 39133), H3K27me3 (EMD Millipore cat# 07-449), H3K4me1 (Abcam, cat# ab8895), Smc1a (Bethyl, cat# A300-055A) and CTCF (EMD Millipore cat# 07-729). Antibody-chromatin complexes were captured with recombinant protein G–conjugated Agarose beads, washed with Low Salt Wash Buffer, High Salt Wash Buffer, LiCl Wash Buffer and TE buffer with 50mM NaCl and eluted. Input sample was prepared by the same approach without immunoprecipitation. After reversal of cross-linking, RNase and Proteinase K (Invitrogen, cat# 25530-049) treatment were performed and DNA was purified with QIAquick PCR Purification Kit (Qiagen, cat# 28106).\nLibraries were then prepared using the NEBNext Ultra II DNA library Prep Kit for Illumina (NEB, cat# E7645S). Two replicates were performed for each condition. Indexed libraries were validated for quality and size distribution using a TapeStation 2200 (Agilent). Single end sequencing (75 bp) or Paired-end sequencing (38 bp+38 bp) was performed on a NextSeq 550.', 'ChIP-seq was performed as previously described (Ryan et al., 2017). Briefly, chromatin samples prepared from appropriate number of fixed cells (107 for histone modifications and 4 x 107 for transcription factors) were sonicated and cleared with recombinant protein G–conjugated Agarose beads (Invitrogen, cat# 15920-010) and subsequently immunoprecipitated with antibodies recognizing Notch1 (Wang et al., 2014), RBPJ (D10A4) (CST, cat# 5313), H3K27ac (Active Motif, cat# 39133), H3K27me3 (EMD Millipore cat# 07-449), H3K4me1 (Abcam, cat# ab8895), Smc1a (Bethyl, cat# A300-055A) and CTCF (EMD Millipore cat# 07-729). Antibody-chromatin complexes were captured with recombinant protein G–conjugated Agarose beads, washed with Low Salt Wash Buffer, High Salt Wash Buffer, LiCl Wash Buffer and TE buffer with 50mM NaCl and eluted. Input sample was prepared by the same approach without immunoprecipitation. After reversal of cross-linking, RNase and Proteinase K (Invitrogen, cat# 25530-049) treatment were performed and DNA was purified with QIAquick PCR Purification Kit (Qiagen, cat# 28106).\nLibraries were then prepared using the NEBNext Ultra II DNA library Prep Kit for Illumina (NEB, cat# E7645S). Two replicates were performed for each condition. Indexed libraries were validated for quality and size distribution using a TapeStation 2200 (Agilent). Single end sequencing (75 bp) or Paired-end sequencing (38 bp+38 bp) was performed on a NextSeq 550.'; [Cell type]'Triple-negative breast cancer cell line''cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: H3K27ac; drug treatment: GSI-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: H3K27ac; drug treatment: GSI-mock-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: H3K4me1; drug treatment: GSI-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: H3K4me1; drug treatment: GSI-mock-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: H3K27me3; drug treatment: GSI-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: H3K27me3; drug treatment: GSI-mock-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: NICD1; drug treatment: GSI-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: NICD1; drug treatment: GSI-mock-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: RBPJ; drug treatment: GSI-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: RBPJ; drug treatment: GSI-mock-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: SMC1a; drug treatment: untreated; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: CTCF; drug treatment: untreated; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: input; drug treatment: untreated; ' GSE112756 Homo sapiens 61 Genome variation profiling by array GPL6359 DNA profiling of EpCAM-positive cells in bone marrow of early breast cancer (EBC) patients 2018-04-05 Parallel DNA and RNA profiling of EpCAM-positive cells in bone marrow and primary tumor tissue with positive disseminated tumor cell (DTC) count via immunomagnetic Enrichment/Flow Cytometry (IE/FC) of metastatic breast cancer (MBC) patients confirm their malignant nature We developed a novel approach to isolate tumor cells with high purity from bone marrow which was subjected to immunomagnetic enrichment using EpCAM beads followed by fluorescence activated cell sorting (IE/FACS) to isolate EpCAM-positive cells away from leukocytes (CD45+). For DNA profiling, sorted cells were subjected to BAC array comparative genomic hybridization analysis following whole genome amplification. For RNA profiling, QPCR analysis was performed on sixty four (64) cancer-related genes using Taqman® low density arrays. For non-tumor controls, RNA profiling was performed on matched leukocytes (CD45+) isolated from the same enriched bone marrow samples. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112756 Genomic and expression profiling reveal molecular heterogeneity of disseminated tumor cells in bone marrow of early breast cancer. NPJ breast cancer 32.43 https://doi.org/10.1038/s41523-018-0083-5 {NPJ breast cancer (32.43): 10.1038/s41523-018-0083-5} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA448907 https://www.ebi.ac.uk/ena/browser/view/PRJNA448907 None [Overal design]Bone marrow aspirates were collected from early breast cancer patients. Disseminated tumor cells (DTCs) were enumerated via immunomagnetic enrichment followed by flow cytometry (IE/FC). For patients considered positive for DTCs, the remaining volume of bone marrow sample was subjected to IE/FACS to isolate DTCs for gene expression (QPCR) and copy number analysis. Differential gene expression analysis between EPCAM-positive cells and matched leukocytes confirmed the up-regulation of EPCAM and other genes including MUC1 (adjusted p <0.05). In addition, EPCAM-positive cells showed a significant down-regulation of the leukocyte-specific marker PTPRC (encodes CD45). Matched primary tumor samples from a subset of patients were subjected to copy number analysis. Genomic profiling of DTCs revealed fewer aberrations compared to matched primary tumors.; [Treatment]'Array CGH experiments of Circulating Tumor, Primary Tumor, or cell line genomic DNA as test samples and normal human genomic DNA as reference sample.'; [Growth]'None'; [Extraction]'Magnetic beads coated with EpCAM mAb are used to enrich for tumor cells and then subjected to FACS analysis using differentially labeled mAbs to distinguish tumor cells (EpCAM+) from leukocytes (CD45+) during sorting. Using this protocol, we isolated small pools of highly purified CTCs from breast cancer patients. DNA from Tumor cells sorted in 10µL of TE was amplified using the GenomePlex® Single Cell Whole Genome Amplification Kit (Sigma-Aldrich) according to manufacturer’s protocol. The approach was evaluated using breast tumor cell model systems, BT474 and MCF7, and CTCs metastatic breast cancer (MBC) patients. Microdissection and DNA extraction of archival formalin-fixed paraffin-embedded (FFPE) primary tumor were done as previously described in Waldman FM, DeVries S, Chew KL, Moore DH, 2nd, Kerlikowske K, Ljung BM. Chromosomal alterations in ductal carcinomas in situ and their in situ recurrences. J Natl Cancer Inst 2000;92(4):313-20.'; [Cell type]'Source: ''cancer type: Breast cancer; tumor stage: Early Breast Cancer; gender: Female; source tissue: Bone Marrow; source cell type: Disseminated Tumor Cells; ', 'sample type: Whole genome amplified reference male genomic DNA; ', 'cancer type: Breast cancer; tumor stage: Early Breast Cancer; gender: Female; source tissue: Breast; source cell type: Primary Tumor; ', 'cancer type: Breast cancer; tumor stage: Early Breast Cancer; gender: Female; source tissue: Breast; source cell type: Lymph Node; ' GSE24079 Homo sapiens 53 Expression profiling by array GPL10904 Differential gene expression in circulating leukocytes from breast cancer patients treated with Cognitive Behavioral Stress Management 2010-09-10 Gene expression profiling was carried out on peripheral blood mononuclear cell mRNA samples collected from 53 female breast cancer patients at 6- or 12-month follow-ups in a randomized controlled trial of Cognitive Behavioral Stress Management or an active control condition. The primary research question is whether gene expression differs in patients treated with Cogntive Behavioral Stress Management vs control conditions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24079 Cognitive-behavioral stress management reverses anxiety-related leukocyte transcriptional dynamics. Biological psychiatry 11.501 https://doi.org/10.1016/j.biopsych.2011.10.007 {Biological psychiatry (11.501): 10.1016/j.biopsych.2011.10.007} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA130205 https://www.ebi.ac.uk/ena/browser/view/PRJNA130205 None [Overal design]Gene expression profiling was carried out on peripheral blood mononuclear cell mRNA samples collected from 53 female breast cancer patients at 6- or 12-month follow-ups in a randomized controlled trial of Cognitive Behavioral Stress Management or an active control condition. The primary research question is whether gene expression differs in patients treated with Cogntive Behavioral Stress Management vs control conditions. Risk prediction; [Treatment]'None'; [Growth]'None'; [Extraction]'Human peripheral blood leukocytes were isolated and total RNA was extracted using Qiagen RNEasy.'; [Cell type]'peripheral blood mononuclear cell''treatment: Cognitive behavioral stress management-12 mo; cell type: peripheral blood mononuclear cell; disease state: breast cancer; gender: female; ', 'treatment: Cognitive behavioral stress management-6 mo; cell type: peripheral blood mononuclear cell; disease state: breast cancer; gender: female; ', 'treatment: Control-12 mo; cell type: peripheral blood mononuclear cell; disease state: breast cancer; gender: female; ', 'treatment: Control-6 mo; cell type: peripheral blood mononuclear cell; disease state: breast cancer; gender: female; ' GSE17072 Homo sapiens 20 Expression profiling by array GPL6884 Normal human mammary tissues from BRCA1 mutation carriers, non-BRCA1/2 mutation carriers and normal women 2009-07-13 Gene expression profiles of normal human mammary tissue from BRCA1 mutation carriers, non-BRCA1/2 mutation carriers and normal women. RNA was prepared from normal breast tissue (confirmed by pathology) from reduction mammoplasties (n=5) and prophylactic mastectomies of known BRCA1 (n=7) and non-BRCA1/2 mutation carriers (n=8). non-BRCA1/2 carriers were individuals with a strong family history of breast cancer (kConFab Category 1 (http://www.kconfab.org/Collection/Eligibility.shtml) where no mutation in BRCA1 or BRCA2 has been identified in the family by high sensitivity testing (http://www.kconfab.org/Progress/Sensitivity.shtml) of any individual affected by breast or ovarian cancer. Normal breast samples refer to reduction mammoplasty specimens, where family history is generally not known. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17072 Aberrant luminal progenitors as the candidate target population for basal tumor development in BRCA1 mutation carriers. Nature medicine 30.641 https://doi.org/10.1038/nm.2000 {Nature medicine (30.641): 10.1038/nm.2000} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA119809 https://www.ebi.ac.uk/ena/browser/view/PRJNA119809 None [Overal design]Microarray expression profiles were obtained from whole pre-neoplastic breast tissue from three categories of patient, as described in the summary. Samples were checked for keratin gene expression levels as a marker for epithelium tissue, and a number of samples were removed because two or more keratin genes lacked detectable expression (BeadStudio detection p-value 0.01). One other sample was removed because its expression profile appeared abnormal. Out of 36 samples initially profiled, 20 passed the quality filters and were used for the final analysis.; [Treatment]'Not applicable'; [Growth]'Not applicable'; [Extraction]'RNA from sorted cell populations were prepared with the RNeasy Micro kit (Qiagen). RNA quality was ascertained using the Agilent Bioanalyser 2100 with the NanoChip protocol.'; [Cell type]'Source: ''tissue: Preneoplastic breast tissue; gender: female; mutation: Normal; hybridization date: 10-31-08; beadchip barcode: 4380071031; beadchip section: A; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: BRCA1; hybridization date: 10-31-08; beadchip barcode: 4380071031; beadchip section: B; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: non-BRCA1/2 mutation; hybridization date: 10-31-08; beadchip barcode: 4380071031; beadchip section: C; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: Normal; hybridization date: 10-31-08; beadchip barcode: 4380071031; beadchip section: E; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: BRCA1; hybridization date: 10-31-08; beadchip barcode: 4380071010; beadchip section: A; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: BRCA1; hybridization date: 10-31-08; beadchip barcode: 4380071010; beadchip section: B; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: non-BRCA1/2 mutation; hybridization date: 10-31-08; beadchip barcode: 4380071010; beadchip section: C; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: Normal; hybridization date: 10-31-08; beadchip barcode: 4380071010; beadchip section: F; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: BRCA1; hybridization date: 10-31-08; beadchip barcode: 4380071008; beadchip section: A; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: non-BRCA1/2 mutation; hybridization date: 10-31-08; beadchip barcode: 4380071008; beadchip section: C; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: non-BRCA1/2 mutation; hybridization date: 10-31-08; beadchip barcode: 4380071008; beadchip section: D; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: Normal; hybridization date: 10-31-08; beadchip barcode: 4380071008; beadchip section: E; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: Normal; hybridization date: 10-31-08; beadchip barcode: 4380071008; beadchip section: F; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: non-BRCA1/2 mutation; hybridization date: 2-18-09; beadchip barcode: 4634617015; beadchip section: F; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: BRCA1; hybridization date: 2-18-09; beadchip barcode: 4634617009; beadchip section: C; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: BRCA1; hybridization date: 2-18-09; beadchip barcode: 4634617009; beadchip section: D; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: non-BRCA1/2 mutation; hybridization date: 2-18-09; beadchip barcode: 4634617009; beadchip section: E; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: BRCA1; hybridization date: 2-18-09; beadchip barcode: 4634617027; beadchip section: C; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: non-BRCA1/2 mutation; hybridization date: 2-18-09; beadchip barcode: 4634617027; beadchip section: E; ', 'tissue: Preneoplastic breast tissue; gender: female; mutation: non-BRCA1/2 mutation; hybridization date: 2-18-09; beadchip barcode: 4632486019; beadchip section: C; ' GSE13905 Homo sapiens 2 Genome binding/occupancy profiling by array GPL7765 Profiling the target genes for ZIP repressor in MCF-7 2008-12-10 Using ChIP-DSL technology from Aviva Systems Biology to find out the whole genome targets for ZIP transcription repressor https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE13905 ZIP: a novel transcription repressor, represses EGFR oncogene and suppresses breast carcinogenesis. The EMBO journal 11.227 https://doi.org/10.1038/emboj.2009.211 {The EMBO journal (11.227): 10.1038/emboj.2009.211} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA110319 https://www.ebi.ac.uk/ena/browser/view/PRJNA110319 None [Overal design]We analyzed arrays using specific ZIP antibody and negative control to acquire the enriched ratio of each gene; [Treatment]'None'; [Growth]'None'; [Extraction]'common cell lysate'; [Cell type]'Source: ''' GSE103646 Rattus norvegicus 20 Expression profiling by high throughput sequencing GPL20084 Differential gene regulation and tumor inhibitory activities of alpha-, delta- and gamma-tocopherols in estrogen-mediated mammary carcinogenesis 2017-09-08 Purpose: Examination of different forms of tocopherol treatment in mammary tumorigenesis by comparing NGS-derived transcriptome profiling (RNA-seq) Methods: Use of cDNA library construction and Illumina sequencing (NextGen 75 bp pair-end) and quality control using FastQC. Results: Differential transcriptome profiling of mammary tumors between different forms of tocopherol treatment was observed. Conclusions: Our study represents the first detailed analysis of mammary tumor transcriptomes with different tocopherol treatment generated by RNA-seq technology. The optimized data analysis reported here should provide a framework for comparative investigations of expression profiles with tocopherols. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE103646 Differential Gene Regulation and Tumor-Inhibitory Activities of Alpha-, Delta-, and Gamma-Tocopherols in Estrogen-Mediated Mammary Carcinogenesis. Cancer prevention research (Philadelphia, Pa.) 3.866 https://doi.org/10.1158/1940-6207.CAPR-17-0190 {Cancer prevention research (Philadelphia, Pa.) (3.866): 10.1158/1940-6207.CAPR-17-0190} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA403841 https://www.ebi.ac.uk/ena/browser/view/PRJNA403841 https://www.ncbi.nlm.nih.gov/sra?term=SRP117172 [Overal design]mRNA profiles of mammary tumors from ACI rats treated with different tocopherols for 30 weeks were generated by cDNA library construction/illumina sequencing; [Treatment]'Rats are treated with 0.2% δ-T, 0.2% γ-T, 0.2% α-T, or 0.2% γ-TmT for 30 weeks'; [Growth]'None'; [Extraction]'Mammary tumors were removed, flash frozen on dry ice, and RNA was harvested using Trizol reagent. Illumina TruSeq RNA Sample Prep Kit (Cat#FC-122-1001) was used with 1 ug of total RNA for the construction of sequencing libraries.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''strain: ACI; tissue: Mammary tumor; age: 40 weeks old; ' GSE60323 Homo sapiens 4 Expression profiling by array GPL16686 Effect of knock down of LASP-1 on basal-like breast cancer cells (MDA-MB-231) 2014-08-11 Nuclear LASP-1 has a direct correlation with the overall survival of breast cancer patients. Gene expression analysis of MDA-MB-231S (sorted for high surface expression of CXCR4) and MDA-Bone-Un (Mouse bone metastasized MDA-MB-231 cells) human basal-like breast cancer cells cultured in 3D-Matrigel was performed. Changes in transcript levels of key microRNAs 29B1 and 29B2, miRLet7F1, miR519A1, MMP9, MMP1, FAM75D4, Interferons a7 and a17, Glycine receptor a3, CADM2 and claudin12 https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60323 LASP-1: a nuclear hub for the UHRF1-DNMT1-G9a-Snail1 complex. Oncogene 6.634 https://doi.org/10.1038/onc.2015.166 {Oncogene (6.634): 10.1038/onc.2015.166} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA258029 https://www.ebi.ac.uk/ena/browser/view/PRJNA258029 None [Overal design]Non-silencing (control) and LASP-1 knock down MDA-MB-231-S and MDA-Bone-Un cells were cultured on 3D-Matrigel, total RNA was extracted and analyzed - 1 biological replicate each; [Treatment]'Not applicable'; [Growth]'MDA-MB-231S and MDA-Bone-Un breast cancer cells (Non-silencing and LASP-1 knock down) were cultured on growth factor reduced Matrigel for 3 days to form stellate clusters.'; [Extraction]'Total RNA from MDA-MB-231S and MDA-Bone-Un stellate clusters was quantitated using the QuBit RNA assay and were run on the Agilent Bioanalyzer.'; [Cell type]'Basal-like breast cells''cell line: MDA-MB-231-S; cell type: Basal-like breast cells; ', 'cell line: MDA-Bone-Un; cell type: Basal-like breast cells; ' GSE46214 Homo sapiens 4 Expression profiling by array GPL570 DLC1 Suppresses Breast Cancer Bone Metastasis 2013-04-19 The skeleton is the most common metastasis site of breast cancer cells and the molecular underpinning of this process is incompletely understood. The tumor suppressor gene deleted in liver cancer-1 (DLC1) encodes a multi-domain protein including a RhoGTPase activating protein (RhoGAP) domain and has been reported to suppress the lung colonization of breast cancer cells. However, the role of DLC1 in breast cancer bone metastasis and the importance of RhoGAP-dependent and -independent pathways in this process remain unclear. Here, we showed that DLC1 silencing is linked to enhanced bone-tropism of breast cancer cell lines and poor prognosis of clinical samples. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE46214 DLC1-dependent parathyroid hormone-like hormone inhibition suppresses breast cancer bone metastasis. The Journal of clinical investigation 12.282 https://doi.org/10.1172/JCI71812 {The Journal of clinical investigation (12.282): 10.1172/JCI71812} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA198082 https://www.ebi.ac.uk/ena/browser/view/PRJNA198082 None [Overal design]In the study presented here, DLC1 was overexpressed in the SCP2 breast cancer cells, and the control SCP2 and overexpression cells were treated with TGFbeta. Microarray profiling of mRNA levels was performed in the control and overexpression cells with or without TGFbeta treatment.; [Treatment]'None'; [Growth]'None'; [Extraction]'Cancer Cells were cultured and harvested with trypsinization. RNA was extracted with Trizol.'; [Cell type]'breast cancer''cell line: SCP2; cell type: breast cancer; ' GSE100553 Mus musculus 20 Expression profiling by high throughput sequencing GPL17021; GPL19057 A critical role of histone deacetylases, Mbd3/NuRD and Tet2 in epithelial-mesenchymal cell plasticity and in tumor invasion and metastasis 2017-06-27 We have generated and employed reversible and irreversible EMT models of murine breast cancer cells to identify the key players establishing cell state transitions during a reversible and an irreversible EMT. We demonstrate that the Mbd3/NuRD complex, involving histone deacetylases (HDACs) and Tet2 hydroxylase, acts as an epigenetic block in epithelial-mesenchymal plasticity. These epigenetic modifiers keep breast cancer cells in a stable mesenchymal state, and their pharmacological inhibition or genetic ablation leads to a mesenchymal-epithelial transition (MET) and represses primary tumor growth and metastasis formation of highly aggressive, mesenchymal breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE100553 Histone deacetylases, Mbd3/NuRD, and Tet2 hydroxylase are crucial regulators of epithelial-mesenchymal plasticity and tumor metastasis. Oncogene 6.634 https://doi.org/10.1038/s41388-019-1081-2 {Oncogene (6.634): 10.1038/s41388-019-1081-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA392104 https://www.ebi.ac.uk/ena/browser/view/PRJNA392104 https://www.ncbi.nlm.nih.gov/sra?term=SRP110598 [Overal design]We performed RNA-sequencing of 2 replicates of each treatment and cell line; [Treatment]'Cells were treated with 2µM CI994 for 72 hours.'; [Growth]'Py2T cells and M clone cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with glutamine, penicillin, streptomycin and 10% FBS (Sigma-Aldrich). Py2T cells were treated with 2ng/ml TGFb1 and the medium was replenished every 3 days. All cells were cultured at 37°C with 5% CO2 in a humid incubator.'; [Extraction]'Total RNA was isolated from cells of 2 independent experiments using the miRNeasy mini kit (217004, Qiagen) according to the manufacturer’s instruction.\n200ng of RNA was utilized for library preparation with the TruSeq Stranded Total RNA LT Sample Prep Kit (Illumina).'; [Cell type]'Py2T LT', 'M1', 'M2', 'M3''cell type: Py2T LT; tissue: Breast cancer; strain: MMTV-PyMT; ', 'cell type: M1; tissue: Breast cancer; strain: MMTV-PyMT; ', 'cell type: M2; tissue: Breast cancer; strain: MMTV-PyMT; ', 'cell type: M3; tissue: Breast cancer; strain: MMTV-PyMT; ' GSE48652 Homo sapiens 21 Expression profiling by array GPL10558 Capturing drug responses by quantitative promoter activity profiling 2013-07-09 Quantitative analysis of cellular responses to signaling inhibitors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48652 Capturing drug responses by quantitative promoter activity profiling. CPT: pharmacometrics & systems pharmacology 3.370 https://doi.org/10.1038/psp.2013.53 {CPT: pharmacometrics & systems pharmacology (3.370): 10.1038/psp.2013.53} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA210934 https://www.ebi.ac.uk/ena/browser/view/PRJNA210934 None [Overal design]Total RNA obtained from MCF7 human breast cancer cell lines treated with 1uM gefitinib, 500nM U0126 or 10nM wortmannin for 6hr.; [Treatment]'Medium was switched to DMEM supplemented with 2% FBS and the cultures were maintained overnight, and the drug was added and incubated for 6hr.'; [Growth]'The MCF7 was obtained from the American Type Culture Collection and maintained in DMEM supplemented with 10% FBS.'; [Extraction]'RNA was isolated using the miRNeasy Mini kit (QIAGEN) in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''cell line: MCF7 breast cancer; treatment: Control; ', 'cell line: MCF7 breast cancer; treatment: Gefitinib; ', 'cell line: MCF7 breast cancer; treatment: U0126; ', 'cell line: MCF7 breast cancer; treatment: Wortmannin; ', 'cell line: MCF7 breast cancer; treatment: Gefitinib + U0126; ', 'cell line: MCF7 breast cancer; treatment: Gefitinib + Wortmannin; ', 'cell line: MCF7 breast cancer; treatment: U0126 + Wortmannin; ' GSE18539 Homo sapiens 143 Expression profiling by array GPL9006 Molecular characterization of Georgia cohort of primary breast cancer FFPE tissues on custom breast cancer DASL panel 2009-10-13 Analysis of 143 formalin-fixed, paraffin-embedded (FFPE) primary breast tumors using a Custom Breast Cancer Panel and Human Cancer Panel for the DASL platform. Molecular markers between the pathology defined subtypes of breast cancer were assessed to hypothesize potential therapeutic targets specific to the subtypes https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE18539 Differential activation of Wnt-β-catenin pathway in triple negative breast cancer increases MMP7 in a PTEN dependent manner. PloS one 2.776 https://doi.org/10.1371/journal.pone.0077425 {PloS one (2.776): 10.1371/journal.pone.0077425} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA121341 https://www.ebi.ac.uk/ena/browser/view/PRJNA121341 None [Overal design]Molecular Characterization of 143 primary breast carcinomas including 101 triple negative (TN: ER-, PR-, HER2-), 3 HER2-positive (HER2+: ER-, PR-, HER2+), and 39 hormone receptor-positive (HR+: ER+ and/or PR+); [Treatment]'None'; [Growth]'None'; [Extraction]'Specimen Type: FFPE tissues sections or cores; Required Reagents: Recoverall RNA Isolation Kit, Ambion, Inc., Austin, TX (Cat#: AM1975); Initial quality of RNA will be determined by spectrophotometry, using the NanoDrop. The absorbance is measured at 230, 260, and 280 nm, and the A260/A280 and A260/A230 ratios of 2 are ideal. In addition, expression of a ribosomal housekeeping gene, Rpl13a, will be measured to determine how many useful RNA molecules are present in the sample. Ideally, the Ct value should be less than 29. The samples that fail QC will not be further analyzed. Procedural Steps (general): 1. Assemble FFPE sections equivalent to up to 80 µm sections (5 – 20 µm sections). 2. Add 1 ml of 100% xylene; vortex briefly; heat at 50°C for 3 min. 3. Centrifuge for 2 min at max. speed; discard xylene. 4. Wash the pellet with 100% EtOH; vortex; centrifuge for 2 min at max. speed. 5. Repeat step 4. one more time. 6. Air dry for 10 – 15 min. 7. Add digestion buffer to each sample. 8. Add protease to each sample; swirl each tube to mix. 9. Incubate at 50°C for overnight [can store at -20°C at this point]. 10. DNA and RNA isolation procedures are identical from this point forward; add 480 µl Isolation Additive; vortex to mix. 11. Add 1.1 ml of 100% EtOH; mix by pipetting. 12. Pipet 700 µl of the sample/EtOH mixture onto the column and close the lid. 13. Centrifuge at 10,000 RPM for 30-60 sec; discard the flow-through. 14. Repeat steps 11 and 12 until all the mix has passed through the filter (3x). 15. Add 700 µl of Wash 1 to the filter cartridge. 16. Centrifuge for 30 sec at 10,000 RPM; discard flow-through. 17. Add 500 µl of Wash 2/3 . 18. Centrifuge for 30 sec at 10,000 RPM; discard flow-through. 19. Preheat the Elution solution or nuclease-free water to 95°C . 20. For RNA isolation (per sample): 6 µl 10 DNase Buffer. 4 µl DNase. 50 µl Nuclease-free water. a. Add 60 µl of the DNase mix to the center of each filter. b. Incubate at RT for 30 min. 21. Add 700 µl Wash 1 to the filter cartridge; Incubate at RT for 30-60 sec. 22. Centrifuge at 10,000 RPM for 30 sec; discard flow-through. 23. Add 500 µl Wash 2/3. 24. Centrifuge at 10,000 RPM for 30 sec; discard flow-through. 25. Repeat steps 22a and 23 one more time. 26. Centrifuge at 10,000 RPM for 1 min to dry. 27. Transfer filter cartridge to a fresh collection tube. 28. Add 30 µl of elution solution or water heated to 95°C to the center of the filter. 29. Incubate at RT for 1 min. 30. Centrifuge at full speed for 1 min. 31. Repeat steps 27 to 29 with an additional aliquot of water. 32. Store at -20°C or colder (if only a small amount of nucleic acid is collected, store in non-stick tubes)'; [Cell type]'Source: ''er: ER-; pr: PR-; her2: HER2-; ', 'er: ER-; pr: PR-; her2: HER2+; ', 'er: ER+; pr: PR-; her2: HER2-; ', 'er: ER+; pr: PR+; her2: HER2-; ', 'er: ER+; pr: PR+; her2: HER2+; ' GSE136671 Homo sapiens 8 Expression profiling by array GPL20569 Human Breast Cancer cells: Control vs Treated with Palbociclib 2019-08-30 Analysis miRNA profiling of breast cancer cells treated without or with palbociclib.Results provide insight into the molecular mechanisms involved in resistance to pabbociclib. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE136671 c-myc regulates the sensitivity of breast cancer cells to palbociclib via c-myc/miR-29b-3p/CDK6 axis. Cell death & disease 5.959 https://doi.org/10.1038/s41419-020-02980-2 {Cell death & disease (5.959): 10.1038/s41419-020-02980-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA563027 https://www.ebi.ac.uk/ena/browser/view/PRJNA563027 None [Overal design]Four breast cancer cell lines,MDA-MB-231, Hs578t, SK-BR-3 and MCF7 cells were treated with or without palbociclib.; [Treatment]'without treatment', 'treated with 4μM palbociclib for 48 hours'; [Growth]'MDA-MB-231 cells were grown in RPMI MDA-MB-231 cells1640 (Gibco, USA) supplemented with 10% fetal bovine serum (FBS) (Hyclone USA)', 'MDA-MB-231 cells were grown in RPMI 1640 (Gibco, USA) supplemented with 10% fetal bovine serum (FBS) (Hyclone USA)', 'Hs578t cells were grown in DMEM supplemented with 10% FBS', 'SK-BR-3 cells were grown in RPMI 1640 (Gibco, USA) supplemented with 10% fetal bovine serum (FBS) (Hyclone USA)', 'MCF7 cells were grown in RPMI 1640 (Gibco, USA) supplemented with 10% fetal bovine serum (FBS) (Hyclone USA)'; [Extraction]'Total RNA was isolated from the four cell lines using the Trizol Reagent (Invitrogen, Carlsbad, CA, USA). Small RNA was extracted by using a mirVana kit (Ambion, Austin, USA).'; [Cell type]'Source: ''cell line: MDA-MB-231; agent: none; ', 'cell line: MDA-MB-231; agent: palbociclib; ', 'cell line: Hs578t; agent: none; ', 'cell line: Hs578t; agent: palbociclib; ', 'cell line: SK-BR-3; agent: none; ', 'cell line: SK-BR-3 treated with palbociclib; agent: palbociclib; ', 'cell line: MCF7; agent: none; ', 'cell line: MCF7; agent: palbociclib; ' GSE139870 Homo sapiens 15 Expression profiling by array GPL16686 Comparison of MPA regulated gene expression profiles to those regulated by PROG, DHT, DEX 2019-11-04 Medroxyprogesterone acetate (MPA) is a progestin that can bind to and activate progesterone, androgen and glucocorticoid receptors. However, it is not known which receptor mediates MPA action in a cellular context where all three of these receptors are co-expressed and functional. This microarray experiment was performed to compare the transcriptomes induced by MPA and the cognate ligands for these receptors ie progesterone (PROG), 5a-dihydrotestosterone (DHT) and dexamethasone (DEX) in breast cancer cells to determine which was most similar to MPA. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE139870 Anti-proliferative transcriptional effects of medroxyprogesterone acetate in estrogen receptor positive breast cancer cells are predominantly mediated by the progesterone receptor. The Journal of steroid biochemistry and molecular biology 3.785 https://doi.org/10.1016/j.jsbmb.2019.105548 {The Journal of steroid biochemistry and molecular biology (3.785): 10.1016/j.jsbmb.2019.105548} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA587414 https://www.ebi.ac.uk/ena/browser/view/PRJNA587414 None [Overal design]Transcriptome analysis by microarray for ZR-75-1 breast cancer cells treated for 6 hours with 10 nM MPA, PROG, DHT, DEX or vehicle.; [Treatment]'ZR-75-1 cells were treated for 6h with either vehicle (0.1% ethanol) or 10nM MPA, PROG, DHT or DEX.'; [Growth]'ZR-75-1 cells were grown in regular growth media (RPMI-1640 + 10% FBS).'; [Extraction]'TRIzol reagent was used to extract RNA, which was then purified with the RNeasy Mini Kit and its integrity confirmed using the Experion Automated Electrophoresis System.'; [Cell type]'Source: ''cell line: ZR-75-1; treatment: vehicle (untreated); ', 'cell line: ZR-75-1; treatment: 10 nM MPA; ', 'cell line: ZR-75-1; treatment: 10 nM PROG; ', 'cell line: ZR-75-1; treatment: 10 nM DHT; ', 'cell line: ZR-75-1; treatment: 10 nM DEX; ' GSE77497 Mus musculus 6 Genome variation profiling by SNP array GPL13147 Affymetrix SNP array data for Trp53-null mammary tumors developed in a mouse model with a K8+ luminal cell origin 2016-02-02 Mammary epithelium is hierarchically organized, with multipotent basal mammary stem cells (MaSCs) producing both luminal and basal cells during development or upon transplantation. Recent studies suggested that most breast cancers, including Basal-Like breast cancer (BLBC), might originate from luminal cells, and oncogenic events, such as ectopic expression of PIK3CA(H1047R), could induce multipotency in committed luminal cells. p53 is the most commonly mutated gene in human breast cancer; in particular, its inactivating mutations are found in most BLBCs, raising a question as to whether p53-loss plays a key role in acquisition of multipotent MaSC-like properties by luminal cells. By in situ lineage-tracing, we found that induced loss of p53 in Keratin 8 (K8)+ luminal cells led to their clonal expansion, due to increased cell cycle activity and attenuated apoptosis control, but did not directly affect their luminal identity. All induced mice eventually developed either Claudin-Low mammary tumors with 9qA1 (Yap1) amplification or Basal-Like tumors with 6qA1-A2 (Met) amplification. These data suggest that although p53 does not directly control the luminal fate, its loss facilitates acquisition of MaSC-like properties by luminal cells and predisposes them to development of mammary tumors with loss of luminal identity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE77497 Induced p53 loss in mouse luminal cells causes clonal expansion and development of mammary tumours. Nature communications 11.878 https://doi.org/10.1038/ncomms14431 {Nature communications (11.878): 10.1038/ncomms14431} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA310636 https://www.ebi.ac.uk/ena/browser/view/PRJNA310636 None [Overal design]Genomic DNAs from mammary tumors developed in Trp53L/L females 6-7 months after intraductal injection of Ad-K8-Cre adenovirus or from mammary glands of a strain background-matched wild-type female were prepared and subjected to mouse diversity SNP array analysis.; [Treatment]'Trp53-null mammary tumors were obtained from Trp53L/L females 6-7 months after intraductal injection of Ad-K8-Cre adenovirus.'; [Growth]'Trp53-null mammary tumors were collected from Trp53L/L female mice after Ad-K8-Cre injection.'; [Extraction]'Total genomic DNAs from Trp53-null mammary tumors and from mammary glands of a genetic background-matched wild-type female were prepared by the AllPrep DNA/RNA Mini Kit (Qiagen, Valencia, CA).'; [Cell type]'Trp53-null mammary tumor', 'wild-type mammary glands''strain: Trp53L/L;Rosa26-Stop-YFP; gender: female; cell type: Trp53-null mammary tumor; ', 'strain: Trp53L/L;Rosa26-Stop-YFP; gender: female; cell type: wild-type mammary glands; ' GSE139125 Mus musculus 2 Expression profiling by high throughput sequencing GPL21103 Single Cell RNA sequencing of mouse CD11b+, Gr1+ cells from the spleen from FVB/n and PYMT mice 2019-10-20 Myeloid-derived suppressor cells (MDSCs) are innate immune cells that acquire the capacity to suppress adaptive immune responses during cancer. It remains elusive how MDSCs differ from their normal myeloid counterparts, which limits our ability to specifically detect and therapeutically target MDSCs during cancer. Here, we used single-cell RNAseq to compare MDSC-containing splenic myeloid cells from breast tumor-bearing mice to wildtype controls. Our computational analysis of 14,646 single-cell transcriptomes reveals that MDSCs emerge through a previously unrealized aberrant neutrophil maturation trajectory in the spleen giving rise to a unique chemokine-responsive, immunosuppressive cell state that strongly differs from normal myeloid cells. We establish the first MDSC-specific gene signature and identify novel surface markers for improved detection and enrichment of MDSCs in murine and human samples. Our study provides a single-cell transcriptional map defining the development of MDSCs, which will ultimately enable us to specifically target these cells in cancer patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE139125 Defining the emergence of myeloid-derived suppressor cells in breast cancer using single-cell transcriptomics. Science immunology 10.551 https://doi.org/10.1126/sciimmunol.aay6017 {Science immunology (10.551): 10.1126/sciimmunol.aay6017} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA578550 https://www.ebi.ac.uk/ena/browser/view/PRJNA578550 https://www.ncbi.nlm.nih.gov/sra?term=SRP226381 [Overal design]Droplet Based Single Cell RNA sequencing libraries were generated for 5 pooled FVB/n mouse spleens and 3 pooled PYMT mouse spleens using the 10x Genomics Chromium Platform and sequenced on the Illumina HighSeq 4000; [Treatment]'None'; [Growth]'None'; [Extraction]'The spleen was pushed through a 70-μm cell strainer and washed with RPMI to create a cell suspension of splenocytes. Cells were centrifuged at 500g at 4ºC for 5 min and then incubated for 5 min in 5 mL RBC lysis buffer at RT. Cells were quenched with 10 mL RPMI (Corning, 10-040-CV) with 5% FBS and centrifuged at 500g at 4ºC for 5 min. Cells were resuspended in 3 mL FACS buffer (1xPBS, 3% FBS), and total remaining live cells were counted by Countessä II and processed for FACS. Tissue samples were harvested from mice and mechanically dissociated to generate single cell suspensions as described above. Cells were blocked with anti-mouse FcγR (CD16/CD32) (BioLegend, 101301) on ice for at least 10 min. Cells were then centrifuged at 500g for 5 min at 4\uf0b0C and washed once with FACS buffer (1xPBS with 3%FBS). Cells were incubated for 30 min at 4ºC with pre-conjugated fluorescent labeled antibodies with the following combinations: CD45 (30-F11) (BioLegend, 103112 (APC) or 103115 (APC-cy7)), CD11b (M1/70) (BioLegend, 101206 (FITC) or 101212 (APC), Gr1 (Rb6-8C5) (BioLegend, 101206 (PE) or 108439 (BV605), CD84 (mCD84.7) (BioLegend, 122805 (PE)), and Jaml (4e10) (BioLegend, 128503 (PE)). Sytox Blue dye (Life Technologies, S34857) was added to stained cells to assay for viability. Cells sorted by BD FACSAria™ Fusion\nFACS-isolated CD11b+/Gr1+ cells from the spleens of control WT (5 mice pooled) and tumor-bearing PyMT mice (3 mice pooled) were washed once in PBS with 0.04% BSA, resuspended to a concentration of approximately 1,000 cell/µL and loaded onto the 10X Genomics Chromium platform for droplet-enabled scRNAseq according to the manufacturer’s instructions. Library generation was performed following the Chromium Single Cell 3ʹ Reagents Kits v2 User Guide: CG00052 Rev B. Each library was sequenced on the Illumina HiSeq 4000 platform to achieve an average of 48,488 reads per cell'; [Cell type]'Source: ''tissue: Spleen; strain: FVB/n; ', 'tissue: Spleen; strain: PYMT; ' GSE112194 Mus musculus 192 Genome binding/occupancy profiling by high throughput sequencing GPL21103 Joint single-cell chromatin and protein profiling reveals environmental regulation of epigenomic heterogeneity [4T1-Splenocyte] 2018-03-22 A novel scATAC-seq approach, Multi-Index single cell ATAC-seq (MI-ATAC), in which we not only index the accessible chromatin of individual cells, but also index their protein expression using index Fluorescence Activated Cell Sorting (FACS). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112194 Joint single-cell DNA accessibility and protein epitope profiling reveals environmental regulation of epigenomic heterogeneity. Nature communications 11.878 https://doi.org/10.1038/s41467-018-07115-y {Nature communications (11.878): 10.1038/s41467-018-07115-y} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA445230 https://www.ebi.ac.uk/ena/browser/view/PRJNA445230 https://www.ncbi.nlm.nih.gov/sra?term=SRP136231 [Overal design]Freshly isolated splenocytes were fixed, permeabilized and stained against CD45, then sorted into single wells of a 96 well plate for MI-ATAC; [Treatment]'None'; [Growth]'None'; [Extraction]'single cell MI-ATAC of 4T1 and splenocytes. Single cells were first fixed, then lysed, followed by staining for respective antibodies and transposition. The transposition reaction is the same as for standard ATAC-seq except with 0.05% Igepal CA-630 in the lysis buffer. After 30 min transposition, at 37 degrees, the reaction was quenched using 40 mM EDTA, then cells were centrifuged and supernatant was discarded. 20 µl of reverse crosslinking solution was added to the cell pellet (with final concentration of 5 ng/ml proteinase K). Reverse crosslinking was performed 65 degree overnight and inactivated by a 10 min incubation at 80 degrees the next day. The 25 µl PCR master mix (NEB, M0541S) and 5 µl of two unique primer combinations were directly added to the reverse crosslinking mixture and PCR was performed as previous described. The PCR product was purified with Qiagen MinElute purification kit and eluted in 20 µl Qiagen EB elution buffer'; [Cell type]'Source: ', 'mouse splenocytes''cell line: 4T1 mouse breast cancer cell; antibody: EpCam; ', 'cell line: mouse splenocytes; antibody: CD45; cell type: mouse splenocytes; ' GSE87588 Homo sapiens 9 Expression profiling by array GPL16686 Restoring miR-150-5p to an estrogen receptor positive breast cancer cell line [ZR-75-1] 2016-10-04 The objective of these experiments is to identify novel direct and indirect targets of miR-150-5p in breast cancer cell lines. The goal is that these will give direction as to what targets or pathways may be contributing to the reduced growth observed in these cell lines upon restoration of miR-150-5p. A therapy directed towards one or more critical subtype-specific targets could be developed as a therapeutic for breast cancer patients. Using has-miR-150-5p mirVana miRNA mimic (Ambion, 4464066), miR-150-5p was restored to an estrogen receptor positive breast cancer cell line, ZR-75-1. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE87588 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA345315 https://www.ebi.ac.uk/ena/browser/view/PRJNA345315 None [Overal design]Cells were transfected in triplicate for 48 hours with either mock, negative control, or mimic, and RNA isolated from each sample was hybridized onto Affymetrix GeneChip® Human Gene Array 2.0 ST ( probesets).; [Treatment]"Mature miR-150-5p (miRNA mimic) or non-specific negative control (NC) (Ambion, Austin, TX, USA) at a concentration of 50 nM were incubated with Lipofectamine RNAiMAX (Invitrogen, Carlsbad, CA, USA) in culture medium per the manufacturer's instructions before addition to cells. Mock transfection using just lipofectamine without added RNA was also used as a negative control. Cells were incubated at 37°C for 24 hrs before replacement of medium. Transfected cells were then harvested for RNA and protein at 48 hours."; [Growth]'ZR-75-1 cell were grown in RPMI-1640 supplemented with 10% FBS.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'breast cancer cell line''cell line: ZR-75-1; cell type: breast cancer cell line; transfected with: mock; time point: 48 hours post transfection; ', 'cell line: ZR-75-1; cell type: breast cancer cell line; transfected with: negative control; time point: 48 hours post transfection; ', 'cell line: ZR-75-1; cell type: breast cancer cell line; transfected with: miR-150-5p mimic; time point: 48 hours post transfection; ' GSE9764 Homo sapiens 11 Expression profiling by array GPL570 Carcinoma Associated Fibroblast Like Differentiation of Human Mesenchymal Stem Cells 2007-12-03 Carcinoma associated fibroblasts (CAFs) have recently been implicated in important aspects of epithelial solid tumor biology such as neoplastic progression, tumor growth, angiogenesis, and metastasis. However, neither the source of CAFs nor the differences between CAFs and fibroblasts from non-neoplastic tissue have been well defined. In this study we demonstrate that human bone marrow-derived mesenchymal stem cells (hMSCs) exposed to tumor-conditioned medium (TCM) over a prolonged period of time assume a CAF-like myofibroblastic phenotype. More importantly, these cells exhibit functional properties of CAFs including sustained expression of stromal derived factor 1 (SDF-1) and the ability to promote tumor cell growth both in vitro and in an in vivo co-implantation model and expression of myofibroblast markers including α-smooth muscle actin and fibroblast surface protein. hMSCs induced to differentiate to a myofibroblast-like phenotype using 5-azacytidine do not promote tumor cells growth as efficiently as hMSCs cultured in tumor-conditioned medium nor do they demonstrate increased SDF-1 expression. Furthermore, gene expression profiling revealed similarities between TCM exposed hMSCs and carcinoma associated fibroblasts. Taken together these data suggest that hMSCs are a source of carcinoma associated fibroblasts and can be used in the modeling of tumor-stroma interactions. To our knowledge this is the first report demonstrating that hMSCs become activated and resemble carcinoma associated myofibroblasts upon prolonged exposure to conditioned medium from MDAMB231 human breast cancer cells. Keywords: differentiation https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE9764 Carcinoma-associated fibroblast-like differentiation of human mesenchymal stem cells. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-08-0943 {Cancer research (8.378): 10.1158/0008-5472.CAN-08-0943} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA103695 https://www.ebi.ac.uk/ena/browser/view/PRJNA103695 None [Overal design]The experiment was done to test the differentiation of hMSCs upon exposure to tumor condition media or epigenetic modifiers.; [Treatment]'Cells were exposed to 100 % condition media collected overnight from MDAMB231 cells for 30 days. Condition media was changed every 3 days.', 'Cells were exposed to 5-Azacytidine and cultured for 21 days. Media was changed every 3 days.', 'Cells were grown in DMEM media for 30 days as a control. Media was changed every 3 days.', 'Cells were grown in alpha MEM media for 30 days as a control. Media was changed every 3 days.'; [Growth]'standard cell culture condition (95% air, 5% CO2, 37C)'; [Extraction]'Total RNA was extracted using RNeasy kit from Qiagen'; [Cell type]'Source: ''' GSE106638 Homo sapiens 4 Expression profiling by high throughput sequencing GPL20301 RNA-Seq analysis to identify novel genes associated with Neuropilin-1 expression in the BT-474 breast cancer cell model 2017-11-07 Background: Neuropilin-1 (NRP-1) is a non-tyrosine kinase glycoprotein receptor that elicits multiple functions depending on the ligand bound. It is known to promote cancer progression however; transcriptome-wide changes triggered by NRP-1 are not defined. In this study we aimed to identify novel molecules associated with NRP-1 expression using a global transcriptomic approach in a recombinant breast cancer cell model. Methods: NRP-1 was stably overexpressed in the BT-474 breast cancer cell line (BT-474 NRP-1) and subjected to next generation RNA sequencing using the Illumina HiSeq 4000 sequencing system. Two replicates each of the control BT-474 and BT474-NRP1 were utilized for sequencing. The count per million (CPM) method was utilized for filtering low counts/noise by NOISeq. The clean reads were mapped to reference genome using HISAT/ Bowtie2 tool. The Fragments Per Kilobase of transcript per Million mapped reads (FPKM) method was utilized to calculate the expression levels. False Detection Rate (FDR) ≤ 0.001, absolute value of Log2 ratio ≥ 2 and consistency between the two replicates were used as the default threshold to identify significant DEGs. Results: A total of 22,655,647 clean reads from 22,914,684 raw sequencing reads were generated upon sequencing. 22 upregulated and 61 downregulated genes were identified. Among the DEGs, 11 upregulated and 11 downregulated genes were shortlisted based on their known roles in cancer and/or EMT for confirmation with real-time qPCR. 2 upregulated genes TNC and TARP and 5 downregulated genes ACE, APOD, DDIT3, P2RX6 and ATF3 indicated consistently differential expression with qPCR. Conclusion: We report for the first time the global transcriptome-wide changes elicited by NRP-1 overexpression in a breast cancer cell model. Our study identified the novel association between several candidate molecules such as TNC, a known oncogene, and NRP-1 expression that may controbute to the tumourigenic role of NRP-1 in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE106638 Neuropilin-1 promotes the oncogenic Tenascin-C/integrin β3 pathway and modulates chemoresistance in breast cancer cells. BMC cancer 2.933 https://doi.org/10.1186/s12885-018-4446-y {BMC cancer (2.933): 10.1186/s12885-018-4446-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA417487 https://www.ebi.ac.uk/ena/browser/view/PRJNA417487 https://www.ncbi.nlm.nih.gov/sra?term=SRP124497 [Overal design]Transcriptome-wide profile changes were determined on Neuropilin-1 overexpression in the BT-474 breast cancer cell line using Illumina HiSeq4000-based RNA sequencing; [Treatment]'None'; [Growth]'Cells were grown in RPMI-1640 media supplemented with 10% FBS. Cells harbouring the NRP-1 overexpression vector were selected using Geneticin antibiotic. Cells were maintained at 37°C in 5% CO2.'; [Extraction]"RNA was extracted using the Trizol reagent and a QC was conducted using the Agilent Bioanalyzer. Total RNA was treated with Dnase I and mRNA was enriched using the oligo (dT) magnetic beads. mRNA was fragmented into short fragments and cDNA was synthesized using random hexamer primer. The double strand cDNA was purified with magentic beads. End reparation and 3'-end single nucleotide adenine addition was performed. Finally, sequencing adaptors were ligated to the fragments. The fragments were enriched by PCR amplification.\nRNA libraries were prepared for sequencing using standard Illumina protocols"; [Cell type]'Source: ''cell line: BT-474; cell line tissue source: Human breast cancer (luminal B-like); genotype/variation: wild-type; ', 'cell line: BT-474; cell line tissue source: Human breast cancer (luminal B-like); genotype/variation: NRP-1 overexpression; ' GSE56612 Mus musculus 6 Expression profiling by array GPL16570 Genetic deletion or pharmacologic blockade of the amino acid transporter Slc6a14 in mice suppresses breast cancer induced by Polyoma middle T oncogene 2014-04-08 Tumor cells have an increased need for amino acids. Mammalian cells cannot synthesize essential amino acids; they must obtain these amino acids via specific transporters. Glutamine, though a non-essential amino acid, is critical for tumor cells (glutamine addiction). Entry of amino acids into tumor cells is enhanced by upregulation of specific transporters. If the transporters that are specifically induced in tumor cells are identified, blockade of the induced transporters would constitute a logical strategy for cancer treatment. The transporter SLC6A14 is unique and transports all essential amino acids as well as glutamine and is expressed only at low levels in normal tissues, but induced in colon cancer and in ER+ breast cancer. We have now established the potential of this transporter as a drug target for breast cancer treatment using genetic and pharmacologic approaches. We then examined the progression of breast cancer in Polyoma middle T antigen (Py-MT) Tg mouse on Slc6a14+/+ and Slc6a14-/- background using microarray analysis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE56612 Deletion of the amino acid transporter Slc6a14 suppresses tumour growth in spontaneous mouse models of breast cancer. The Biochemical journal 4.331 https://doi.org/10.1042/BJ20150437 {The Biochemical journal (4.331): 10.1042/BJ20150437} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA244079 https://www.ebi.ac.uk/ena/browser/view/PRJNA244079 None [Overal design]We have used three Affy-chips for each tumor sample (Group 1: WT/PyMT; Group 2: Slc6a14-KO/PyMT). Three biological replicates were used for each group.; [Treatment]'Sample was collected from mammary tumor excised from WT/PyMT and Slc6a14-/-/PyMT mice for total RNA isolation.'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions (Invitrogen, Life Technologies, NY)."; [Cell type]'Source: ''strain/background: C57BL/6; genotype/variation: WT/PyMT; tissue: mammary tumor tissue; age: 16 weeks; ', 'strain/background: C57BL/6; genotype/variation: Slc6a14-KO/PyMT; tissue: mammary tumor tissue; age: 16 weeks; ' GSE87455 Homo sapiens 275 Expression profiling by array GPL10558 Assessment of tumor pathological and transcriptional biomarkers in pre- and on-treatment core biopsies predictive of response and outcome after neoadjuvant chemotherapy plus Bevacizumab in patients with HER2-negative breast cancer 2016-09-28 Assessment of tumor pathological and transcriptional biomarkers in pre- and on-treatment core biopsies predictive of response and outcome after neoadjuvant chemotherapy plus Bevacizumab in patients with HER2-negative breast cancer: Results from a multi-center, single-arm, phase 2 study (the PROMIX trial) Global gene expression profiling was performed on samples from 3 time points (baseline, after 2 cycles and surgery) from women with breast cancer receivcing neoadjuvant chemotherapy with bevacizumab in a phase 2 trial https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE87455 An HIF-1α/VEGF-A Axis in Cytotoxic T Cells Regulates Tumor Progression. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2017.10.003 {International journal of cancer (4.982) doi:10.1002/ijc.31070}; {Oncoimmunology (5.333) doi:10.1080/2162402X.2018.1466017}; {Cancer cell (23.916) doi:10.1016/j.ccell.2017.10.003}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA344794 https://www.ebi.ac.uk/ena/browser/view/PRJNA344794 None [Overal design]Multi-center, single-arm, phase 2 study of neoadjuvant anthracycline (epirubicin) plus taxane (docetaxel) with the addition of bevacizumab (avastin) for women with large operable and locally advanced HER2-negative breast cancer.; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen Allprep DNA/RNA mini kit, with a QIAcube'; [Cell type]'Source: ''treatment: Baseline (no treatment); tissue: Breast; ', 'treatment: Cycle 2 (chemo only); tissue: Breast; ', 'treatment: Surgery (chemo+bevacizumab); tissue: Breast; ' GSE103388 Homo sapiens 6 Expression profiling by array GPL16686 MiR-1287-5p has inhibitory effects on breast cancer growth mediated by interaction with phosphoinositide 3-kinase CB (miR-1287-5p overexpression study) 2017-09-01 Background: Non-coding RNAs and especially microRNAs have been discovered as master regulators of cancer initiation and progression. The aim of our study was to discover and characterize the function of yet uncharacterized microRNAs in human breast carcinogenesis. Methods: In an unbiased approach, we made use of a commonly used model system for breast cancer (BC) stem cells (“mammospheres”) to identify whole miRNome alterations with a special focus on previously uncharacterized miRNAs in BC. We further characterized the influence of microRNA-1287-5p, a yet uncharacterized microRNA in BC, in patient samples (n=1262) and on several hallmarks of cancer in vitro and in vivo with a special focus on triple negative BC. The molecular mode of action was further characterized using whole transcriptome analysis, in silico prediction tools, miRNA-interaction luciferase assays and pheno-copy assays. Results: We identified miR-1287-5p among many others as differentially expressed in mammospheres. Clinical validation indicated that miR-1287-5p is significantly downregulated in human BC and associated with poor prognosis. This clinical finding can be explained by miR-1287-5p mediated growth inhibitory effects, G1 cell cycle arrest, decreased anchorage-independent growth and tumor growth in vivo. Finally, we identified PIK3CB as a direct molecular interactor of miR-1287-5p and a pheno-copy factor for miR-1287-5p. Finally, targeting PI3K-signaling pathway with chemical inhibitors together with miR-1287-5p mimics increased the pharmacological growth inhibitory potential. Conclusion: In conclusion, our data identified for the first time an involvement of miR-1287-5p in human BC and suggest a potential for therapeutic interventions in hardly to treat triple negative BC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE103388 MiR-1287-5p inhibits triple negative breast cancer growth by interaction with phosphoinositide 3-kinase CB, thereby sensitizing cells for PI3Kinase inhibitors. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-019-1104-5 {Breast cancer research : BCR (5.676): 10.1186/s13058-019-1104-5} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA401682 https://www.ebi.ac.uk/ena/browser/view/PRJNA401682 None [Overal design]three biological replicates of stably transduced SUM159 miR-1287-5p overexpressing cells or empty vector transducted cells as control cells; [Treatment]'None'; [Growth]'SUM159 cells were grown in Ham`s F12 containing 1 mmol/L L-glutamine, 2 mmol/L HEPES buffer, 5µg/ml insulin actrapid, 1µg/ml hydrocortisone, 1% penicillin/streptomycin ( (50 units per ml of penicillin, 50μg/ml of streptomycin) and 5% FBS gold. Cells were incubated in a 5% CO2 humidified atmosphere at 37°C.'; [Extraction]'miRNeasy'; [Cell type]'Source: ''cell line: SUM159; genotype/variation: control; ', 'cell line: SUM159; genotype/variation: miR-1287-5p overexpression; ' GSE11223 Homo sapiens 202 Expression profiling by array GPL1708 Colon biopsies from UC patients and healthy controls 2008-04-21 Transcriptional profiling of colon epithelial biopsies from ulcerative colitis patients and healthy control donors. Study aims to survey and analyze variation from disease in different GI regions. Keywords: disease state analysis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE11223 Regional variation in gene expression in the healthy colon is dysregulated in ulcerative colitis. Gut 17.943 https://doi.org/10.1136/gut.2008.148395 {Gut (17.943): 10.1136/gut.2008.148395} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA106831 https://www.ebi.ac.uk/ena/browser/view/PRJNA106831 None [Overal design]Biopsies from a variety of anatomic locations, from patients of various treatment status or healthy controls.; [Treatment]'None'; [Growth]'None'; [Extraction]'micro total RNA isolation from animal tissues protocol (Qiagen, Valencia, CA)'; [Cell type]'Source: ''patient: 101; current medication: Paracetamol; birth date: 10/5/63; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/2/04; indictation for procedure: Weight loss, altered bowel habbit.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'sample type: total RNA from 10 human cell lines; ', 'patient: 102; current medication: Movicol 1 sachet daily; birth date: 9/5/62; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/2/04; indictation for procedure: RIF pain, persistent anaemia.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 103; current medication: None; birth date: 6/30/65; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/9/04; indictation for procedure: Diarrhoea, now settled, Mum has UC; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 105; current medication: None; birth date: 7/29/84; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/15/04; indictation for procedure: IBS type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 106; current medication: None; birth date: 5/29/87; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/18/04; indictation for procedure: Abdominal pain, upper GI symptoms.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 108; current medication: Asacol 400mg BD; birth date: 8/30/33; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/25/04; indictation for procedure: Altered bowel habbit, ? UC 1974, never on Bx.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 104; current medication: None; birth date: 1/2/72; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/15/04; indictation for procedure: IBS type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 107; current medication: None; birth date: 07/28/1060; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/25/04; indictation for procedure: FH Colon Cancer; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 109; current medication: None; birth date: 10/10/57; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/2/04; indictation for procedure: FH of Colon Cancer; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 110; current medication: None; birth date: 3/13/54; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/2/04; indictation for procedure: Diarrhoea; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 111; current medication: Paracetamol; birth date: 9/5/82; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/3/04; indictation for procedure: FH of CD, Path Increased lymphiod in TI Bx.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 112; current medication: None; birth date: 7/5/81; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/7/04; indictation for procedure: Altered bowel habit; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 113; current medication: OCP; birth date: 8/17/81; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/14/04; indictation for procedure: Recurrant abcess, ?IBD; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 114; current medication: None; birth date: 6/27/36; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/14/04; indictation for procedure: Altered bowel habit, Alcohol excess; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 115; current medication: Frusemide, Codine Phosphate; birth date: 9/14/28; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/21/04; indictation for procedure: Diarrhoea, Also has Prostate Ca; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 116; current medication: Clomiprimine; birth date: 1/19/56; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/21/04; indictation for procedure: FH Colon cancer; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 117; current medication: Loperamide; birth date: 3/31/67; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/21/04; indictation for procedure: IBS type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 101; current medication: Paracetamol; birth date: 10/5/63; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/2/04; indictation for procedure: Weight loss, altered bowel habbit.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 6-2-01; anatomic_location: terminal ileum; inflammation_status: Uninflamed; ', 'patient: 104; current medication: None; birth date: 1/2/72; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/15/04; indictation for procedure: IBS type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 6-2-01; anatomic_location: terminal ileum; inflammation_status: Uninflamed; ', 'patient: 110; current medication: None; birth date: 3/13/54; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/2/04; indictation for procedure: Diarrhoea; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 6-2-01; anatomic_location: terminal ileum; inflammation_status: Uninflamed; ', 'patient: 101; current medication: Paracetamol; birth date: 10/5/63; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/2/04; indictation for procedure: Weight loss, altered bowel habbit.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 103; current medication: None; birth date: 6/30/65; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/9/04; indictation for procedure: Diarrhoea, now settled, Mum has UC; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 104; current medication: None; birth date: 1/2/72; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/15/04; indictation for procedure: IBS type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 105; current medication: None; birth date: 7/29/84; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/15/04; indictation for procedure: IBS type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 106; current medication: None; birth date: 5/29/87; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/18/04; indictation for procedure: Abdominal pain, upper GI symptoms.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 107; current medication: None; birth date: 07/28/1060; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/25/04; indictation for procedure: FH Colon Cancer; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 102; current medication: Movicol 1 sachet daily; birth date: 9/5/62; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/2/04; indictation for procedure: RIF pain, persistent anaemia.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 109; current medication: None; birth date: 10/10/57; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/2/04; indictation for procedure: FH of Colon Cancer; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 110; current medication: None; birth date: 3/13/54; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/2/04; indictation for procedure: Diarrhoea; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 111; current medication: Paracetamol; birth date: 9/5/82; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/3/04; indictation for procedure: FH of CD, Path Increased lymphiod in TI Bx.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 112; current medication: None; birth date: 7/5/81; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/7/04; indictation for procedure: Altered bowel habit; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 114; current medication: None; birth date: 6/27/36; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/14/04; indictation for procedure: Altered bowel habit, Alcohol excess; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 115; current medication: Frusemide, Codine Phosphate; birth date: 9/14/28; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/21/04; indictation for procedure: Diarrhoea, Also has Prostate Ca; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 116; current medication: Clomiprimine; birth date: 1/19/56; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/21/04; indictation for procedure: FH Colon cancer; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 117; current medication: Loperamide; birth date: 3/31/67; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/21/04; indictation for procedure: IBS type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 103; current medication: None; birth date: 6/30/65; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/9/04; indictation for procedure: Diarrhoea, now settled, Mum has UC; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 104; current medication: None; birth date: 1/2/72; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/15/04; indictation for procedure: IBS type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 105; current medication: None; birth date: 7/29/84; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/15/04; indictation for procedure: IBS type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 107; current medication: None; birth date: 07/28/1060; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/25/04; indictation for procedure: FH Colon Cancer; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 109; current medication: None; birth date: 10/10/57; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/2/04; indictation for procedure: FH of Colon Cancer; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 110; current medication: None; birth date: 3/13/54; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/2/04; indictation for procedure: Diarrhoea; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 111; current medication: Paracetamol; birth date: 9/5/82; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/3/04; indictation for procedure: FH of CD, Path Increased lymphiod in TI Bx.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 112; current medication: None; birth date: 7/5/81; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/7/04; indictation for procedure: Altered bowel habit; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 114; current medication: None; birth date: 6/27/36; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/14/04; indictation for procedure: Altered bowel habit, Alcohol excess; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 115; current medication: Frusemide, Codine Phosphate; birth date: 9/14/28; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/21/04; indictation for procedure: Diarrhoea, Also has Prostate Ca; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 117; current medication: Loperamide; birth date: 3/31/67; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/21/04; indictation for procedure: IBS type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 119; current medication: Salubtamol, Bricanyl; birth date: 9/30/70; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/27/05; indictation for procedure: FH Colon Ca; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 120; current medication: Minicycline; birth date: 5/6/54; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/18/05; indictation for procedure: Altered bowel habit; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 120; current medication: Minicycline; birth date: 5/6/54; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/18/05; indictation for procedure: Altered bowel habit; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 121; current medication: Cp-tenedone, Enalapril, Loperamide.; birth date: 4/8/59; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/1/05; indictation for procedure: Diarrhoea, Blastocytitis on stool cultures.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: terminal ileum; inflammation_status: Uninflamed; ', 'patient: 121; current medication: Cp-tenedone, Enalapril, Loperamide.; birth date: 4/8/59; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/1/05; indictation for procedure: Diarrhoea, Blastocytitis on stool cultures.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 121; current medication: Cp-tenedone, Enalapril, Loperamide.; birth date: 4/8/59; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/1/05; indictation for procedure: Diarrhoea, Blastocytitis on stool cultures.; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 122; current medication: Venlafaxine; birth date: 7/10/61; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/10/05; indictation for procedure: FH Colon Ca; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 122; current medication: Venlafaxine; birth date: 7/10/61; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/10/05; indictation for procedure: FH Colon Ca; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 122; current medication: Venlafaxine; birth date: 7/10/61; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/10/05; indictation for procedure: FH Colon Ca; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 124; current medication: OCP; birth date: 6/25/77; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/1/05; indictation for procedure: IBS Type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 124; current medication: OCP; birth date: 6/25/77; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/1/05; indictation for procedure: IBS Type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 124; current medication: OCP; birth date: 6/25/77; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/1/05; indictation for procedure: IBS Type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 125; current medication: OCP; birth date: 3/17/78; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/1/05; indictation for procedure: Diarrhoea predominant IBS; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: terminal ileum; inflammation_status: Uninflamed; ', 'patient: 125; current medication: OCP; birth date: 3/17/78; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/1/05; indictation for procedure: Diarrhoea predominant IBS; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', "patient: 126; current medication: None; birth date: 4/4/87; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/1/05; indictation for procedure: FH of Crohn's disease, Symtom free at procedure; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ", 'patient: 127; current medication: Prednisolone 10mg Heparin Questran Gabapentin FA; birth date: 9/9/36; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/29/05; indictation for procedure: Pseudomembranous Colitis; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 128; current medication: Pentaza; birth date: 3/19/81; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 4/1/05; indictation for procedure: IBS Type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: terminal ileum; inflammation_status: Uninflamed; ', 'patient: 128; current medication: Pentaza; birth date: 3/19/81; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 4/1/05; indictation for procedure: IBS Type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', "patient: 126; current medication: None; birth date: 4/4/87; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/1/05; indictation for procedure: FH of Crohn's disease, Symtom free at procedure; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ", 'patient: 128; current medication: Pentaza; birth date: 3/19/81; ethnicity: JEWISH; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 4/1/05; indictation for procedure: IBS Type symptoms; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 134; current medication: None; birth date: 12/21/50; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 7/12/05; indictation for procedure: Abdominal pain; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 135; current medication: none; birth date: 8/14/59; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 7/28/05; indictation for procedure: bloody diahorrea; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 11-15-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 135; current medication: none; birth date: 8/14/59; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 7/28/05; indictation for procedure: bloody diahorrea; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: TRUE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 11-15-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 136; current medication: metranidazole 400mg TDS Prednisolone; birth date: 5/21/51; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 7/20/05; indictation for procedure: Diarrhoea PR bleeding; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 11-15-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 136; current medication: metranidazole 400mg TDS Prednisolone; birth date: 5/21/51; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 7/20/05; indictation for procedure: Diarrhoea PR bleeding; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 133; current medication: Omeprazole 20mg; birth date: 4/23/65; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: ; aza tolerant: FALSE; aza at present: FALSE; procedure date: 5/13/05; indictation for procedure: FH Colon Cancer; ucss: 0; calprotectin: ; esr: ; crp: ; hb: ; wcc: ; neutrophils: ; albumin: ; blood obtained: FALSE; ibd affected relatives: ; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: ; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: ; category: 0; smoking status: ; smoking start date: ; smoking stop date: ; smoking amount: ; other illnesses: ; disease: Normal; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 205; current medication: Pentaza 3g/d; birth date: 6/8/79; ethnicity: CAUCASIAN; symptoms onset date: 10/1/03; diagnosis date: 8/30/04; joint problems: FALSE; uc flare up: TRUE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/8/04; indictation for procedure: ; ucss: 4; calprotectin: 0; esr: 15; crp: 19; hb: 110; wcc: 5; neutrophils: 3; albumin: 43; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 10/8/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: NEW; smoking status: ex; smoking start date: 1/1/85; smoking stop date: 3/1/03; smoking amount: 15-24; other illnesses: None; disease: UC; run_date: 1-25-01; anatomic_location: terminal ileum; inflammation_status: Inflamed; ', 'patient: 229; current medication: Naproxen; birth date: 11/27/61; ethnicity: CAUCASIAN; symptoms onset date: 1/14/05; diagnosis date: 1/18/05; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/18/05; indictation for procedure: ; ucss: 6; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 3/26/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 7/7/05; category: NEW; smoking status: unknown; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 6-2-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 205; current medication: Pentaza 3g/d; birth date: 6/8/79; ethnicity: CAUCASIAN; symptoms onset date: 10/1/03; diagnosis date: 8/30/04; joint problems: FALSE; uc flare up: TRUE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/8/04; indictation for procedure: ; ucss: 4; calprotectin: 0; esr: 15; crp: 19; hb: 110; wcc: 5; neutrophils: 3; albumin: 43; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 10/8/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: NEW; smoking status: ex; smoking start date: 1/1/85; smoking stop date: 3/1/03; smoking amount: 15-24; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 205; current medication: Pentaza 3g/d; birth date: 6/8/79; ethnicity: CAUCASIAN; symptoms onset date: 10/1/03; diagnosis date: 8/30/04; joint problems: FALSE; uc flare up: TRUE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/8/04; indictation for procedure: ; ucss: 4; calprotectin: 0; esr: 15; crp: 19; hb: 110; wcc: 5; neutrophils: 3; albumin: 43; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 10/8/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: NEW; smoking status: ex; smoking start date: 1/1/85; smoking stop date: 3/1/03; smoking amount: 15-24; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 238; current medication: Enalapril Zantac; birth date: 9/27/38; ethnicity: CAUCASIAN; symptoms onset date: 9/25/03; diagnosis date: 1/14/05; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/6/05; indictation for procedure: ; ucss: 4; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/6/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: NEW; smoking status: ex; smoking start date: ; smoking stop date: 1/1/03; smoking amount: 5-14; other illnesses: Hypertension Diverticular disease; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 238; current medication: Enalapril Zantac; birth date: 9/27/38; ethnicity: CAUCASIAN; symptoms onset date: 9/25/03; diagnosis date: 1/14/05; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/6/05; indictation for procedure: ; ucss: 4; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/6/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: NEW; smoking status: ex; smoking start date: ; smoking stop date: 1/1/03; smoking amount: 5-14; other illnesses: Hypertension Diverticular disease; disease: UC; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 243; current medication: Atenolol Pravastatin Asprin Adalat BFZ Balsalizide; birth date: 2/17/25; ethnicity: CAUCASIAN; symptoms onset date: 8/1/04; diagnosis date: 3/29/05; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/29/05; indictation for procedure: ; ucss: 5; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 3/29/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 6/1/05; category: NEW; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: IHD Deaf; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 245; current medication: Pentaza 1g BD; birth date: 11/4/67; ethnicity: CAUCASIAN; symptoms onset date: 11/4/04; diagnosis date: 3/16/05; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/16/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 3/16/05; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 6/3/05; category: NEW; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Asthma; disease: UC; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 251; current medication: Bumetanide Asprin Lisinopril Colifoam; birth date: 5/22/21; ethnicity: CAUCASIAN; symptoms onset date: 1/1/05; diagnosis date: 6/6/05; joint problems: FALSE; uc flare up: TRUE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/6/05; indictation for procedure: ; ucss: 9; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/6/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 7/7/05; category: NEW; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Vaginal Prolapse-Angina; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 256; current medication: None; birth date: 10/16/44; ethnicity: CAUCASIAN; symptoms onset date: 4/1/05; diagnosis date: 6/2/05; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/2/05; indictation for procedure: ; ucss: 10; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: unknown; last followup date: 6/2/05; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 9/14/05; category: NEW; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 270; current medication: Becotide inhaler; birth date: 4/30/52; ethnicity: CAUCASIAN; symptoms onset date: 1/1/99; diagnosis date: 8/24/05; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 8/24/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 8/24/05; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 9/14/05; category: NEW; smoking status: current; smoking start date: ; smoking stop date: ; smoking amount: 5-14; other illnesses: Asthma; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 201; current medication: None; birth date: 4/12/56; ethnicity: CAUCASIAN; symptoms onset date: 6/19/03; diagnosis date: 7/4/03; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 9/30/04; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 9/30/04; followup rectum: BOTH; followup recto sigmoid: HISTOLOGICAL; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/7/04; category: FAILURE OF THERAPY; smoking status: ex; smoking start date: 1/1/70; smoking stop date: 1/1/99; smoking amount: 25+; other illnesses: None; disease: UC; run_date: 1-25-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 201; current medication: None; birth date: 4/12/56; ethnicity: CAUCASIAN; symptoms onset date: 6/19/03; diagnosis date: 7/4/03; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 9/30/04; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 9/30/04; followup rectum: BOTH; followup recto sigmoid: HISTOLOGICAL; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/7/04; category: FAILURE OF THERAPY; smoking status: ex; smoking start date: 1/1/70; smoking stop date: 1/1/99; smoking amount: 25+; other illnesses: None; disease: UC; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 202; current medication: Sulphasalazine 3g/d, Folic Acid 5mg/d, HRT, DF118; birth date: 10/3/50; ethnicity: CAUCASIAN; symptoms onset date: 1/1/68; diagnosis date: 1/1/69; joint problems: TRUE; uc flare up: TRUE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: FALSE; procedure date: 9/30/04; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 9/30/04; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Polymyalgia rheumatica; disease: UC; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 203; current medication: Asacol 800mg BD, Simvastatin; birth date: 1/10/35; ethnicity: CAUCASIAN; symptoms onset date: 11/1/92; diagnosis date: 3/23/93; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/1/04; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 14; crp: 0; hb: 147; wcc: 6; neutrophils: 4; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: HISTOLOGICAL; diagnosis recto sigmoid: HISTOLOGICAL; diagnosis splen flex: HISTOLOGICAL; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 10/1/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: 1/1/50; smoking stop date: 1/1/57; smoking amount: 25+; other illnesses: None; disease: UC; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 206; current medication: Asacol 800mg BD; birth date: 9/10/59; ethnicity: CAUCASIAN; symptoms onset date: 1/1/79; diagnosis date: 1/1/80; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/8/04; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 2; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 10/8/04; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/94; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 207; current medication: Asacol 800mg BD, Colifoam Enemas Daily; birth date: 4/29/47; ethnicity: CAUCASIAN; symptoms onset date: 3/1/88; diagnosis date: 8/18/88; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/14/04; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 10/14/04; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: BOTH; followup hep flex: BOTH; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: 1/10/62; smoking stop date: 3/15/75; smoking amount: 25 +; other illnesses: None; disease: UC; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 208; current medication: Prednisolone 25mg/d, Pentaza 1g BD, Fosomax weekly; birth date: 8/16/85; ethnicity: CAUCASIAN; symptoms onset date: 6/1/04; diagnosis date: 6/25/04; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/14/04; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 17; crp: 3; hb: 121; wcc: 8; neutrophils: 5; albumin: 39; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/14/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 210; current medication: Mesalazine 800mg B, Prednisolone Supps; birth date: 6/28/56; ethnicity: CAUCASIAN; symptoms onset date: 1/1/73; diagnosis date: 1/10/74; joint problems: FALSE; uc flare up: TRUE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/19/04; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 10/14/04; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Scarlet Fever 1964; disease: UC; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 211; current medication: Predfoam Adcal D3 Alendronate; birth date: 11/10/44; ethnicity: CAUCASIAN; symptoms onset date: 1/1/77; diagnosis date: 6/7/79; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/5/04; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/5/04; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 5/31/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Coeliac disease 1991; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 213; current medication: PRED 7MG, ATENOLOL 100MG, ASPRIN 75MG, SIMVASTATI; birth date: 11/1/43; ethnicity: CAUCASIAN; symptoms onset date: 3/1/82; diagnosis date: 2/2/83; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/12/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/12/04; followup rectum: COLONOSCOPIC; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/74; smoking amount: unknown; other illnesses: ISCHEAMIC HEART DISEASE; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 216; current medication: NONE; birth date: 5/10/36; ethnicity: CAUCASIAN; symptoms onset date: 2/19/66; diagnosis date: 8/20/66; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/18/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 11; igr2198: 11; igr2230: 11; octn1: 11; octn2: 11; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 12; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/18/04; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: NONE; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 217; current medication: Asacol 1.2g daily; birth date: 2/9/57; ethnicity: CAUCASIAN; symptoms onset date: 1/1/79; diagnosis date: 1/10/79; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/26/04; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 11; octn2: 11; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/26/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 3/4/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 218; current medication: Sulphasalazine Asprin Metoprolol Atorvastatin; birth date: 9/27/24; ethnicity: CAUCASIAN; symptoms onset date: 1/1/58; diagnosis date: 1/1/58; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/3/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 12/3/04; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/4/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Breast cancer; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 219; current medication: Sulphasalazine 1.2g Colifoam; birth date: 1/5/43; ethnicity: CAUCASIAN; symptoms onset date: 1/1/81; diagnosis date: 1/1/81; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/7/04; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 12/7/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 220; current medication: Asacol 800mg BFZ 2.5mg Metformin Simvastatin; birth date: 6/28/48; ethnicity: CAUCASIAN; symptoms onset date: 1/10/95; diagnosis date: 3/25/95; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/10/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 12/10/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 3/7/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/90; smoking amount: 5-14; other illnesses: Type 2 DM.; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 223; current medication: Prednisolone 20mg Asacol 2.4g; birth date: 1/18/44; ethnicity: CAUCASIAN; symptoms onset date: 3/1/04; diagnosis date: 3/15/04; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/16/04; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 12/16/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 5/31/05; category: DISEASE IN REMISSION; smoking status: unknown; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', "patient: 224; current medication: Salazopyrin BFZ Losartan Thyroxine Doxazosin; birth date: 2/21/38; ethnicity: CAUCASIAN; symptoms onset date: 1/1/77; diagnosis date: 1/1/77; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/6/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 12; octn2: 12; nod 702: 11; nod 908: 12; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/6/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/4/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Hypertension Hashimoto's Thyroditis; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ", 'patient: 225; current medication: Asacol; birth date: 5/30/76; ethnicity: CAUCASIAN; symptoms onset date: 1/1/03; diagnosis date: 6/2/03; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/6/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/6/05; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/99; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 206; current medication: Asacol 800mg BD; birth date: 9/10/59; ethnicity: CAUCASIAN; symptoms onset date: 1/1/79; diagnosis date: 1/1/80; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/8/04; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 2; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 10/8/04; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/94; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 6-2-01; anatomic_location: terminal ileum; inflammation_status: Uninflamed; ', 'patient: 210; current medication: Mesalazine 800mg B, Prednisolone Supps; birth date: 6/28/56; ethnicity: CAUCASIAN; symptoms onset date: 1/1/73; diagnosis date: 1/10/74; joint problems: FALSE; uc flare up: TRUE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/19/04; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 10/14/04; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Scarlet Fever 1964; disease: UC; run_date: 6-2-01; anatomic_location: terminal ileum; inflammation_status: Uninflamed; ', 'patient: 228; current medication: None; birth date: 11/22/48; ethnicity: CAUCASIAN; symptoms onset date: 1/1/80; diagnosis date: 1/1/82; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: TRUE; aza at present: FALSE; procedure date: 1/14/05; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 12; octn2: 12; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/6/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/4/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Migraines; disease: UC; run_date: 6-2-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 233; current medication: Asacol 1.2g Asprin 75mg Amilodipine 10mg; birth date: 2/2/29; ethnicity: CAUCASIAN; symptoms onset date: 1/1/92; diagnosis date: 1/1/92; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/1/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 2/1/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/86; smoking amount: 15-24; other illnesses: MI 1986, Prostate cancer 1994; disease: UC; run_date: 6-2-01; anatomic_location: terminal ileum; inflammation_status: Uninflamed; ', 'patient: 233; current medication: Asacol 1.2g Asprin 75mg Amilodipine 10mg; birth date: 2/2/29; ethnicity: CAUCASIAN; symptoms onset date: 1/1/92; diagnosis date: 1/1/92; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/1/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 2/1/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/86; smoking amount: 15-24; other illnesses: MI 1986, Prostate cancer 1994; disease: UC; run_date: 6-2-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 202; current medication: Sulphasalazine 3g/d, Folic Acid 5mg/d, HRT, DF118; birth date: 10/3/50; ethnicity: CAUCASIAN; symptoms onset date: 1/1/68; diagnosis date: 1/1/69; joint problems: TRUE; uc flare up: TRUE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: FALSE; procedure date: 9/30/04; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 9/30/04; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Polymyalgia rheumatica; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 203; current medication: Asacol 800mg BD, Simvastatin; birth date: 1/10/35; ethnicity: CAUCASIAN; symptoms onset date: 11/1/92; diagnosis date: 3/23/93; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/1/04; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 14; crp: 0; hb: 147; wcc: 6; neutrophils: 4; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: HISTOLOGICAL; diagnosis recto sigmoid: HISTOLOGICAL; diagnosis splen flex: HISTOLOGICAL; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 10/1/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: 1/1/50; smoking stop date: 1/1/57; smoking amount: 25+; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 204; current medication: AZA 200mg, Insulin, Asprin, Atenolol, Simvastatin; birth date: 8/15/43; ethnicity: CAUCASIAN; symptoms onset date: 7/1/02; diagnosis date: 8/1/02; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: TRUE; procedure date: 11/1/04; indictation for procedure: ; ucss: 5; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 11; igr2198: 12; igr2230: 12; octn1: 12; octn2: 0; nod 702: 0; nod 908: 0; dlg5 133a: 0; nod 1007 fs: 0; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/1/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 12/16/04; category: FAILURE OF THERAPY; smoking status: ex; smoking start date: 1/1/58; smoking stop date: 1/1/01; smoking amount: 25+; other illnesses: Type 2 DM 02/2004.-Gout.; disease: UC; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 209; current medication: AZA 150mg/d, Mesalazine 800mg TDS; birth date: 3/27/80; ethnicity: CAUCASIAN; symptoms onset date: 1/1/89; diagnosis date: 1/1/89; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: TRUE; procedure date: 10/15/04; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 11; igr2198: 12; igr2230: 12; octn1: 12; octn2: 12; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/15/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 12/16/04; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 1-25-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 212; current medication: Pred 10mg, AZA150mg, ADCAL D3; birth date: 8/3/76; ethnicity: CAUCASIAN; symptoms onset date: 1/1/97; diagnosis date: 9/1/01; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: TRUE; procedure date: 11/9/04; indictation for procedure: ; ucss: 7; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: 0; igr2198: 11; igr2230: 12; octn1: 11; octn2: 12; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/9/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/16/04; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 214; current medication: NONE; birth date: 1/10/37; ethnicity: CAUCASIAN; symptoms onset date: 1/1/59; diagnosis date: 1/10/61; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/12/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 1; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 11/12/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 12/9/04; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: CENTRAL RETINAL VEIN OCCLUSION 01/04; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 215; current medication: Prednisolone 5ng Balsalazide Lansoperazole; birth date: 5/6/60; ethnicity: CAUCASIAN; symptoms onset date: 5/1/02; diagnosis date: 8/16/02; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/16/04; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: unknown; last followup date: 11/16/04; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 5/31/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: 1/1/03; smoking stop date: 1/1/04; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 221; current medication: Prednisolone 7mg Asacol Adcal Seretide Fe SO4; birth date: 1/29/86; ethnicity: CAUCASIAN; symptoms onset date: 12/10/01; diagnosis date: 12/10/01; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/14/04; indictation for procedure: ; ucss: 4; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 12/14/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 3/7/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Asthma Eczema; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 222; current medication: Prednisolone 20mg Balsalazide; birth date: 4/13/52; ethnicity: CAUCASIAN; symptoms onset date: 9/1/85; diagnosis date: 6/20/86; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: TRUE; aza at present: FALSE; procedure date: 12/16/04; indictation for procedure: ; ucss: 9; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 12/16/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 5-25-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 215; current medication: Prednisolone 5ng Balsalazide Lansoperazole; birth date: 5/6/60; ethnicity: CAUCASIAN; symptoms onset date: 5/1/02; diagnosis date: 8/16/02; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/16/04; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: unknown; last followup date: 11/16/04; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 5/31/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: 1/1/03; smoking stop date: 1/1/04; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 6-2-01; anatomic_location: terminal ileum; inflammation_status: Uninflamed; ', 'patient: 226; current medication: Azathioprine 150mg Asacol 1.6g Ca Vit D B12; birth date: 6/15/74; ethnicity: CAUCASIAN; symptoms onset date: 1/1/89; diagnosis date: 1/1/89; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: TRUE; procedure date: 1/11/05; indictation for procedure: ; ucss: 8; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/11/05; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: FAILURE OF THERAPY; smoking status: current; smoking start date: ; smoking stop date: ; smoking amount: 15-24; other illnesses: None; disease: UC; run_date: 6-2-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', "patient: 227; current medication: Asacol Prednisolone 5 Omeprazole Warfarin Cal VitD; birth date: 4/17/28; ethnicity: CAUCASIAN; symptoms onset date: 1/1/90; diagnosis date: 1/1/90; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/14/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 1/14/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 3/7/05; category: FAILURE OF THERAPY; smoking status: ex; smoking start date: ; smoking stop date: 1/1/72; smoking amount: 5-14; other illnesses: Prostate cancer 1985, Previous DVT's on warfarin; disease: UC; run_date: 6-2-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ", 'patient: 231; current medication: prednisolone 40mg heparin clarithromycin; birth date: 10/29/77; ethnicity: CAUCASIAN; symptoms onset date: 10/1/00; diagnosis date: 11/19/02; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/28/05; indictation for procedure: ; ucss: 7; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 9/14/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 9/14/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 6-2-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 232; current medication: Pentaza 2g BD; birth date: 1/9/63; ethnicity: CAUCASIAN; symptoms onset date: 1/1/95; diagnosis date: 1/1/95; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/31/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 1/31/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 3/7/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 6-2-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 204; current medication: AZA 200mg, Insulin, Asprin, Atenolol, Simvastatin; birth date: 8/15/43; ethnicity: CAUCASIAN; symptoms onset date: 7/1/02; diagnosis date: 8/1/02; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: TRUE; procedure date: 11/1/04; indictation for procedure: ; ucss: 5; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 11; igr2198: 12; igr2230: 12; octn1: 12; octn2: 0; nod 702: 0; nod 908: 0; dlg5 133a: 0; nod 1007 fs: 0; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/1/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 12/16/04; category: FAILURE OF THERAPY; smoking status: ex; smoking start date: 1/1/58; smoking stop date: 1/1/01; smoking amount: 25+; other illnesses: Type 2 DM 02/2004.-Gout.; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 215; current medication: Prednisolone 5ng Balsalazide Lansoperazole; birth date: 5/6/60; ethnicity: CAUCASIAN; symptoms onset date: 5/1/02; diagnosis date: 8/16/02; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/16/04; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: unknown; last followup date: 11/16/04; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 5/31/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: 1/1/03; smoking stop date: 1/1/04; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 226; current medication: Azathioprine 150mg Asacol 1.6g Ca Vit D B12; birth date: 6/15/74; ethnicity: CAUCASIAN; symptoms onset date: 1/1/89; diagnosis date: 1/1/89; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: TRUE; procedure date: 1/11/05; indictation for procedure: ; ucss: 8; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/11/05; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: FAILURE OF THERAPY; smoking status: current; smoking start date: ; smoking stop date: ; smoking amount: 15-24; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 232; current medication: Pentaza 2g BD; birth date: 1/9/63; ethnicity: CAUCASIAN; symptoms onset date: 1/1/95; diagnosis date: 1/1/95; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/31/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 1/31/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 3/7/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 214; current medication: NONE; birth date: 1/10/37; ethnicity: CAUCASIAN; symptoms onset date: 1/1/59; diagnosis date: 1/10/61; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/12/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 1; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 11/12/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 12/9/04; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: CENTRAL RETINAL VEIN OCCLUSION 01/04; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Inflamed; ', 'patient: 215; current medication: Prednisolone 5ng Balsalazide Lansoperazole; birth date: 5/6/60; ethnicity: CAUCASIAN; symptoms onset date: 5/1/02; diagnosis date: 8/16/02; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/16/04; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: unknown; last followup date: 11/16/04; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 5/31/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: 1/1/03; smoking stop date: 1/1/04; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 221; current medication: Prednisolone 7mg Asacol Adcal Seretide Fe SO4; birth date: 1/29/86; ethnicity: CAUCASIAN; symptoms onset date: 12/10/01; diagnosis date: 12/10/01; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/14/04; indictation for procedure: ; ucss: 4; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 12/14/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 3/7/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Asthma Eczema; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Inflamed; ', 'patient: 226; current medication: Azathioprine 150mg Asacol 1.6g Ca Vit D B12; birth date: 6/15/74; ethnicity: CAUCASIAN; symptoms onset date: 1/1/89; diagnosis date: 1/1/89; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: TRUE; procedure date: 1/11/05; indictation for procedure: ; ucss: 8; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/11/05; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: FAILURE OF THERAPY; smoking status: current; smoking start date: ; smoking stop date: ; smoking amount: 15-24; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', "patient: 227; current medication: Asacol Prednisolone 5 Omeprazole Warfarin Cal VitD; birth date: 4/17/28; ethnicity: CAUCASIAN; symptoms onset date: 1/1/90; diagnosis date: 1/1/90; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/14/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 1/14/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 3/7/05; category: FAILURE OF THERAPY; smoking status: ex; smoking start date: ; smoking stop date: 1/1/72; smoking amount: 5-14; other illnesses: Prostate cancer 1985, Previous DVT's on warfarin; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Inflamed; ", 'patient: 231; current medication: prednisolone 40mg heparin clarithromycin; birth date: 10/29/77; ethnicity: CAUCASIAN; symptoms onset date: 10/1/00; diagnosis date: 11/19/02; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/28/05; indictation for procedure: ; ucss: 7; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 9/14/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 9/14/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 232; current medication: Pentaza 2g BD; birth date: 1/9/63; ethnicity: CAUCASIAN; symptoms onset date: 1/1/95; diagnosis date: 1/1/95; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/31/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 1/31/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 3/7/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Inflamed; ', 'patient: 216; current medication: NONE; birth date: 5/10/36; ethnicity: CAUCASIAN; symptoms onset date: 2/19/66; diagnosis date: 8/20/66; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/18/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophil s: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 11; igr2198: 11; igr2230: 11; octn1: 11; octn2: 11; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 12; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/18/04; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: NONE; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 217; current medication: Asacol 1.2g daily; birth date: 2/9/57; ethnicity: CAUCASIAN; symptoms onset date: 1/1/79; diagnosis date: 1/10/79; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/26/04; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 11; octn2: 11; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/26/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 3/4/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 218; current medication: Sulphasalazine Asprin Metoprolol Atorvastatin; birth date: 9/27/24; ethnicity: CAUCASIAN; symptoms onset date: 1/1/58; diagnosis date: 1/1/58; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/3/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 12/3/04; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/4/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Breast cancer; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 219; current medication: Sulphasalazine 1.2g Colifoam; birth date: 1/5/43; ethnicity: CAUCASIAN; symptoms onset date: 1/1/81; diagnosis date: 1/1/81; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/7/04; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 12/7/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 220; current medication: Asacol 800mg BFZ 2.5mg Metformin Simvastatin; birth date: 6/28/48; ethnicity: CAUCASIAN; symptoms onset date: 1/10/95; diagnosis date: 3/25/95; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/10/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 12/10/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 3/7/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/90; smoking amount: 5-14; other illnesses: Type 2 DM.; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 225; current medication: Asacol; birth date: 5/30/76; ethnicity: CAUCASIAN; symptoms onset date: 1/1/03; diagnosis date: 6/2/03; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/6/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/6/05; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/99; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', "patient: 224; current medication: Salazopyrin BFZ Losartan Thyroxine Doxazosin; birth date: 2/21/38; ethnicity: CAUCASIAN; symptoms onset date: 1/1/77; diagnosis date: 1/1/77; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/6/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 12; octn2: 12; nod 702: 11; nod 908: 12; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/6/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/4/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Hypertension Hashimoto's Thyroditis; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ", 'patient: 228; current medication: None; birth date: 11/22/48; ethnicity: CAUCASIAN; symptoms onset date: 1/1/80; diagnosis date: 1/1/82; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: TRUE; aza at present: FALSE; procedure date: 1/14/05; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 12; octn2: 12; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/6/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/4/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Migraines; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 230; current medication: Asacol 1.6g/ day; birth date: 12/27/57; ethnicity: CAUCASIAN; symptoms onset date: 3/12/02; diagnosis date: 12/3/03; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/25/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/25/05; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: ? MS never proven; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 235; current medication: Asacol Predfoam Lanzoprazole; birth date: 1/9/47; ethnicity: CAUCASIAN; symptoms onset date: 6/24/97; diagnosis date: 8/26/97; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/11/05; indictation for procedure: ; ucss: 5; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 2/11/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/31/05; category: FAILURE OF THERAPY; smoking status: ex; smoking start date: ; smoking stop date: 1/1/97; smoking amount: 15-24; other illnesses: TURP; disease: UC; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 241; current medication: Asacol 800mg bd Azathioprine 100mg; birth date: 6/25/62; ethnicity: CAUCASIAN; symptoms onset date: 11/1/90; diagnosis date: 11/11/91; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/10/05; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 22; igr2198: 22; igr2230: 22; octn1: 22; octn2: 22; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 3/10/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/30/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Inflamed; ', 'patient: 241; current medication: Asacol 800mg bd Azathioprine 100mg; birth date: 6/25/62; ethnicity: CAUCASIAN; symptoms onset date: 11/1/90; diagnosis date: 11/11/91; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/10/05; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 22; igr2198: 22; igr2230: 22; octn1: 22; octn2: 22; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 3/10/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/30/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 241; current medication: Asacol 800mg bd Azathioprine 100mg; birth date: 6/25/62; ethnicity: CAUCASIAN; symptoms onset date: 11/1/90; diagnosis date: 11/11/91; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/10/05; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 22; igr2198: 22; igr2230: 22; octn1: 22; octn2: 22; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 3/10/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/30/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 201; current medication: None; birth date: 4/12/56; ethnicity: CAUCASIAN; symptoms onset date: 6/19/03; diagnosis date: 7/4/03; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 9/30/04; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 9/30/04; followup rectum: BOTH; followup recto sigmoid: HISTOLOGICAL; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/7/04; category: FAILURE OF THERAPY; smoking status: ex; smoking start date: 1/1/70; smoking stop date: 1/1/99; smoking amount: 25+; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 206; current medication: Asacol 800mg BD; birth date: 9/10/59; ethnicity: CAUCASIAN; symptoms onset date: 1/1/79; diagnosis date: 1/1/80; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/8/04; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 2; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 10/8/04; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/94; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 210; current medication: Mesalazine 800mg B, Prednisolone Supps; birth date: 6/28/56; ethnicity: CAUCASIAN; symptoms onset date: 1/1/73; diagnosis date: 1/10/74; joint problems: FALSE; uc flare up: TRUE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 10/19/04; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 10/14/04; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Scarlet Fever 1964; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 213; current medication: PRED 7MG, ATENOLOL 100MG, ASPRIN 75MG, SIMVASTATI; birth date: 11/1/43; ethnicity: CAUCASIAN; symptoms onset date: 3/1/82; diagnosis date: 2/2/83; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/12/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/12/04; followup rectum: COLONOSCOPIC; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/74; smoking amount: unknown; other illnesses: ISCHEAMIC HEART DISEASE; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 216; current medication: NONE; birth date: 5/10/36; ethnicity: CAUCASIAN; symptoms onset date: 2/19/66; diagnosis date: 8/20/66; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/18/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 11; igr2198: 11; igr2230: 11; octn1: 11; octn2: 11; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 12; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/18/04; followup rectum: unknown; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 12/9/04; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: NONE; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 217; current medication: Asacol 1.2g daily; birth date: 2/9/57; ethnicity: CAUCASIAN; symptoms onset date: 1/1/79; diagnosis date: 1/10/79; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 11/26/04; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 11; octn2: 11; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 11/26/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 3/4/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 218; current medication: Sulphasalazine Asprin Metoprolol Atorvastatin; birth date: 9/27/24; ethnicity: CAUCASIAN; symptoms onset date: 1/1/58; diagnosis date: 1/1/58; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/3/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 12/3/04; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/4/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Breast cancer; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 220; current medication: Asacol 800mg BFZ 2.5mg Metformin Simvastatin; birth date: 6/28/48; ethnicity: CAUCASIAN; symptoms onset date: 1/10/95; diagnosis date: 3/25/95; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/10/04; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 12/10/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 3/7/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/90; smoking amount: 5-14; other illnesses: Type 2 DM.; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 223; current medication: Prednisolone 20mg Asacol 2.4g; birth date: 1/18/44; ethnicity: CAUCASIAN; symptoms onset date: 3/1/04; diagnosis date: 3/15/04; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 12/16/04; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 12/16/04; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 5/31/05; category: DISEASE IN REMISSION; smoking status: unknown; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', "patient: 224; current medication: Salazopyrin BFZ Losartan Thyroxine Doxazosin; birth date: 2/21/38; ethnicity: CAUCASIAN; symptoms onset date: 1/1/77; diagnosis date: 1/1/77; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/6/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 12; octn2: 12; nod 702: 11; nod 908: 12; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/6/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/4/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: Hypertension Hashimoto's Thyroditis; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ", 'patient: 225; current medication: Asacol; birth date: 5/30/76; ethnicity: CAUCASIAN; symptoms onset date: 1/1/03; diagnosis date: 6/2/03; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 1/6/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 1/6/05; followup rectum: BOTH; followup recto sigmoid: unknown; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/99; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 233; current medication: Asacol 1.2g Asprin 75mg Amilodipine 10mg; birth date: 2/2/29; ethnicity: CAUCASIAN; symptoms onset date: 1/1/92; diagnosis date: 1/1/92; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/1/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 2/1/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 3/7/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/86; smoking amount: 15-24; other illnesses: MI 1986, Prostate cancer 1994; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 234; current medication: Aza 150mg Atenolol Atorvastatin BFZ Clopidogril; birth date: 9/29/46; ethnicity: CAUCASIAN; symptoms onset date: 2/1/88; diagnosis date: 9/29/95; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: TRUE; aza at present: FALSE; procedure date: 2/3/05; indictation for procedure: ; ucss: 4; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 2/3/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/31/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: IHD Angina; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Inflamed; ', 'patient: 234; current medication: Aza 150mg Atenolol Atorvastatin BFZ Clopidogril; birth date: 9/29/46; ethnicity: CAUCASIAN; symptoms onset date: 2/1/88; diagnosis date: 9/29/95; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: TRUE; aza at present: FALSE; procedure date: 2/3/05; indictation for procedure: ; ucss: 4; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 2/3/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/31/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: IHD Angina; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 234; current medication: Aza 150mg Atenolol Atorvastatin BFZ Clopidogril; birth date: 9/29/46; ethnicity: CAUCASIAN; symptoms onset date: 2/1/88; diagnosis date: 9/29/95; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: TRUE; aza at present: FALSE; procedure date: 2/3/05; indictation for procedure: ; ucss: 4; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 2/3/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/31/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: IHD Angina; disease: UC; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 236; current medication: None; birth date: 11/20/53; ethnicity: CAUCASIAN; symptoms onset date: 5/1/05; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/18/05; indictation for procedure: ; ucss: 15; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 2/18/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: current; smoking start date: 1/1/71; smoking stop date: ; smoking amount: 15-24; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: terminal ileum; inflammation_status: Uninflamed; ', 'patient: 237; current medication: Omep 20mg Losartan 50mg Bisoprolol 5mg Prav 40mg; birth date: 11/12/28; ethnicity: CAUCASIAN; symptoms onset date: 10/1/95; diagnosis date: 11/13/95; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 2/18/05; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 12; octn2: 12; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/5/03; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 5/30/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: 1/1/50; smoking stop date: 1/1/52; smoking amount: 0-4; other illnesses: Hypercholesteremia Prev CABG; disease: UC; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 239; current medication: Asacol Fybogel Amitriptiline; birth date: 4/10/41; ethnicity: CAUCASIAN; symptoms onset date: 12/1/63; diagnosis date: 12/12/64; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/3/05; indictation for procedure: ; ucss: 6; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 1; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 3/3/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 6/1/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 240; current medication: Asacol 800mg BD; birth date: 1/10/59; ethnicity: ASIAN; symptoms onset date: 8/2/04; diagnosis date: 12/14/04; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/3/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 3/3/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/31/05; category: DISEASE IN REMISSION; smoking status: current; smoking start date: ; smoking stop date: ; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 240; current medication: Asacol 800mg BD; birth date: 1/10/59; ethnicity: ASIAN; symptoms onset date: 8/2/04; diagnosis date: 12/14/04; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/3/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 3/3/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/31/05; category: DISEASE IN REMISSION; smoking status: current; smoking start date: ; smoking stop date: ; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 242; current medication: Salazopyrin Folic acid; birth date: 10/18/39; ethnicity: CAUCASIAN; symptoms onset date: 1/1/75; diagnosis date: 1/1/75; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/22/05; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 3/22/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 7/7/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/95; smoking amount: 0-4; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 242; current medication: Salazopyrin Folic acid; birth date: 10/18/39; ethnicity: CAUCASIAN; symptoms onset date: 1/1/75; diagnosis date: 1/1/75; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/22/05; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 3/22/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 7/7/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/95; smoking amount: 0-4; other illnesses: None; disease: UC; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 244; current medication: Seratide Bricanyl BFZ; birth date: 1/29/55; ethnicity: CAUCASIAN; symptoms onset date: 1/1/03; diagnosis date: 6/16/03; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/29/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 3/29/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 6/1/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/94; smoking amount: 15-24; other illnesses: Asthma Hypertension; disease: UC; run_date: 8-9-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 244; current medication: Seratide Bricanyl BFZ; birth date: 1/29/55; ethnicity: CAUCASIAN; symptoms onset date: 1/1/03; diagnosis date: 6/16/03; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/29/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 3/29/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 6/1/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/94; smoking amount: 15-24; other illnesses: Asthma Hypertension; disease: UC; run_date: 8-9-01; anatomic_location: descending colon; inflammation_status: Uninflamed; ', 'patient: 244; current medication: Seratide Bricanyl BFZ; birth date: 1/29/55; ethnicity: CAUCASIAN; symptoms onset date: 1/1/03; diagnosis date: 6/16/03; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 3/29/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 3/29/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 6/1/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/94; smoking amount: 15-24; other illnesses: Asthma Hypertension; disease: UC; run_date: 8-9-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 250; current medication: Asacol 2.4g/d; birth date: 1/27/58; ethnicity: ASIAN; symptoms onset date: 1/1/94; diagnosis date: 5/30/94; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 4/29/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 11; igr2198: 11; igr2230: 11; octn1: 11; octn2: 11; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 4/29/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/30/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/95; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 250; current medication: Asacol 2.4g/d; birth date: 1/27/58; ethnicity: ASIAN; symptoms onset date: 1/1/94; diagnosis date: 5/30/94; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 4/29/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 11; igr2198: 11; igr2230: 11; octn1: 11; octn2: 11; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 4/29/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/30/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/95; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 253; current medication: Asacol 800mg BD; birth date: 3/14/58; ethnicity: CAUCASIAN; symptoms onset date: 8/24/97; diagnosis date: 9/4/97; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 5/24/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 12; octn2: 12; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 12; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 5/24/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/3/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: ascending colon; inflammation_status: Inflamed; ', 'patient: 253; current medication: Asacol 800mg BD; birth date: 3/14/58; ethnicity: CAUCASIAN; symptoms onset date: 8/24/97; diagnosis date: 9/4/97; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 5/24/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 12; octn2: 12; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 12; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 5/24/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/3/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 253; current medication: Asacol 800mg BD; birth date: 3/14/58; ethnicity: CAUCASIAN; symptoms onset date: 8/24/97; diagnosis date: 9/4/97; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 5/24/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 12; octn2: 12; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 12; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 5/24/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/3/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 254; current medication: Asacol 800mg TDS, Predfoam; birth date: 7/25/59; ethnicity: ASIAN; symptoms onset date: 1/1/00; diagnosis date: 11/1/00; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 5/31/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 5/31/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 255; current medication: Asacol 800mg BD; birth date: 3/14/77; ethnicity: CAUCASIAN; symptoms onset date: 1/1/93; diagnosis date: 1/1/93; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 5/31/05; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 5/31/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/01; smoking amount: 0-4; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: ascending colon; inflammation_status: Inflamed; ', 'patient: 255; current medication: Asacol 800mg BD; birth date: 3/14/77; ethnicity: CAUCASIAN; symptoms onset date: 1/1/93; diagnosis date: 1/1/93; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 5/31/05; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 5/31/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/01; smoking amount: 0-4; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 255; current medication: Asacol 800mg BD; birth date: 3/14/77; ethnicity: CAUCASIAN; symptoms onset date: 1/1/93; diagnosis date: 1/1/93; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 5/31/05; indictation for procedure: ; ucss: 0; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 5/31/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/01; smoking amount: 0-4; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 257; current medication: 6MP 50mg; birth date: 5/16/64; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/2/05; indictation for procedure: ; ucss: 7; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/2/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 9/14/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 2/1/05; smoking amount: 0-4; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 257; current medication: 6MP 50mg; birth date: 5/16/64; ethnicity: CAUCASIAN; symptoms onset date: ; diagnosis date: ; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: unknown; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/2/05; indictation for procedure: ; ucss: 7; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: unknown; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/2/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 9/14/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 2/1/05; smoking amount: 0-4; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 258; current medication: Azathioprine 200mg Pentaza 1g TDS; birth date: 10/26/64; ethnicity: CAUCASIAN; symptoms onset date: 6/1/87; diagnosis date: 6/1/88; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/7/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/7/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 259; current medication: pentaza 2g D; birth date: 9/20/78; ethnicity: CAUCASIAN; symptoms onset date: 8/1/03; diagnosis date: 1/13/04; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/7/05; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/7/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/03; smoking amount: 5-14; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 259; current medication: pentaza 2g D; birth date: 9/20/78; ethnicity: CAUCASIAN; symptoms onset date: 8/1/03; diagnosis date: 1/13/04; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/7/05; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/7/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 1/1/03; smoking amount: 5-14; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 261; current medication: Asacol 800mg BD; birth date: 1/7/57; ethnicity: CAUCASIAN; symptoms onset date: 1/1/98; diagnosis date: 1/1/98; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/14/05; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 2; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/14/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: ascending colon; inflammation_status: Inflamed; ', 'patient: 261; current medication: Asacol 800mg BD; birth date: 1/7/57; ethnicity: CAUCASIAN; symptoms onset date: 1/1/98; diagnosis date: 1/1/98; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/14/05; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 2; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/14/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 261; current medication: Asacol 800mg BD; birth date: 1/7/57; ethnicity: CAUCASIAN; symptoms onset date: 1/1/98; diagnosis date: 1/1/98; joint problems: FALSE; uc flare up: FALSE; family history: TRUE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/14/05; indictation for procedure: ; ucss: 2; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 2; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/14/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 263; current medication: Azathioprine 75mg Fosomax 70mg; birth date: 11/9/58; ethnicity: CAUCASIAN; symptoms onset date: 3/1/00; diagnosis date: 6/1/00; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: TRUE; procedure date: 7/8/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 7/8/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 263; current medication: Azathioprine 75mg Fosomax 70mg; birth date: 11/9/58; ethnicity: CAUCASIAN; symptoms onset date: 3/1/00; diagnosis date: 6/1/00; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: TRUE; procedure date: 7/8/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 7/8/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Uninflamed; ', 'patient: 265; current medication: Pentaza 500mg TDS; birth date: 8/17/71; ethnicity: CAUCASIAN; symptoms onset date: 2/5/04; diagnosis date: 3/22/04; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 7/19/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 7/19/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: current; smoking start date: ; smoking stop date: ; smoking amount: 0-4; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: ascending colon; inflammation_status: Inflamed; ', 'patient: 265; current medication: Pentaza 500mg TDS; birth date: 8/17/71; ethnicity: CAUCASIAN; symptoms onset date: 2/5/04; diagnosis date: 3/22/04; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 7/19/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 7/19/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: current; smoking start date: ; smoking stop date: ; smoking amount: 0-4; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 265; current medication: Pentaza 500mg TDS; birth date: 8/17/71; ethnicity: CAUCASIAN; symptoms onset date: 2/5/04; diagnosis date: 3/22/04; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 7/19/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 7/19/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: current; smoking start date: ; smoking stop date: ; smoking amount: 0-4; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 267; current medication: Mesalazine 800mg TDS; birth date: 8/16/74; ethnicity: CAUCASIAN; symptoms onset date: 5/1/05; diagnosis date: 5/10/05; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 8/15/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 9/20/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 9/30/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 5/1/03; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: ascending colon; inflammation_status: Inflamed; ', 'patient: 267; current medication: Mesalazine 800mg TDS; birth date: 8/16/74; ethnicity: CAUCASIAN; symptoms onset date: 5/1/05; diagnosis date: 5/10/05; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 8/15/05; indictation for procedure: ; ucss: 1; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 9/20/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 9/30/05; category: DISEASE IN REMISSION; smoking status: ex; smoking start date: ; smoking stop date: 5/1/03; smoking amount: 5-14; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 249; current medication: Azathioprine 150mg Salazopyrine; birth date: 1/12/60; ethnicity: CAUCASIAN; symptoms onset date: 3/1/90; diagnosis date: 3/24/90; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: FALSE; procedure date: 4/8/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 12; octn2: 12; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 12; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 4/8/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/30/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 249; current medication: Azathioprine 150mg Salazopyrine; birth date: 1/12/60; ethnicity: CAUCASIAN; symptoms onset date: 3/1/90; diagnosis date: 3/24/90; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: FALSE; aza at present: FALSE; procedure date: 4/8/05; indictation for procedure: ; ucss: 3; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 12; igr2198: 12; igr2230: 12; octn1: 12; octn2: 12; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 12; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 4/8/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 5/30/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: None; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 260; current medication: asacol 800mg TDS Asprin coproxamol; birth date: 1/1/54; ethnicity: CAUCASIAN; symptoms onset date: 1/1/79; diagnosis date: 1/1/79; joint problems: FALSE; uc flare up: TRUE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/9/05; indictation for procedure: ; ucss: 12; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/9/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: current; smoking start date: ; smoking stop date: ; smoking amount: 5-14; other illnesses: Arthritis Depression Alcohol excess; disease: UC; run_date: 11-15-01; anatomic_location: ascending colon; inflammation_status: Uninflamed; ', 'patient: 260; current medication: asacol 800mg TDS Asprin coproxamol; birth date: 1/1/54; ethnicity: CAUCASIAN; symptoms onset date: 1/1/79; diagnosis date: 1/1/79; joint problems: FALSE; uc flare up: TRUE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/9/05; indictation for procedure: ; ucss: 12; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/9/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: current; smoking start date: ; smoking stop date: ; smoking amount: 5-14; other illnesses: Arthritis Depression Alcohol excess; disease: UC; run_date: 11-15-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 260; current medication: asacol 800mg TDS Asprin coproxamol; birth date: 1/1/54; ethnicity: CAUCASIAN; symptoms onset date: 1/1/79; diagnosis date: 1/1/79; joint problems: FALSE; uc flare up: TRUE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 6/9/05; indictation for procedure: ; ucss: 12; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: TRUE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: unknown; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 6/9/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: unknown; followup total: unknown; casenote review date: 8/15/05; category: DISEASE IN REMISSION; smoking status: current; smoking start date: ; smoking stop date: ; smoking amount: 5-14; other illnesses: Arthritis Depression Alcohol excess; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 262; current medication: Asacol 2.4g co-codamol; birth date: 7/17/43; ethnicity: CAUCASIAN; symptoms onset date: 1/1/87; diagnosis date: 1/1/87; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: TRUE; aza at present: FALSE; procedure date: 7/5/05; indictation for procedure: ; ucss: 6; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 7/5/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 8/15/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: descending colon; inflammation_status: Inflamed; ', 'patient: 262; current medication: Asacol 2.4g co-codamol; birth date: 7/17/43; ethnicity: CAUCASIAN; symptoms onset date: 1/1/87; diagnosis date: 1/1/87; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: YES; aza tolerant: TRUE; aza at present: FALSE; procedure date: 7/5/05; indictation for procedure: ; ucss: 6; calprotectin: 0; esr: 0; crp: 0; hb: 0; wcc: 0; neutrophils: 0; albumin: 0; blood obtained: FALSE; ibd affected relatives: 0; igr2096: ; igr2198: ; igr2230: ; octn1: ; octn2: ; nod 702: ; nod 908: ; dlg5 133a: ; nod 1007 fs: ; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: unknown; diagnosis hep flex: unknown; diagnosis total: unknown; last followup date: 7/5/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: unknown; followup hep flex: unknown; followup total: unknown; casenote review date: 8/15/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: none; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ', 'patient: 266; current medication: Prednisolone ciproxin mesalazine fosomax Fe SO4; birth date: 8/12/40; ethnicity: CAUCASIAN; symptoms onset date: 1/1/93; diagnosis date: 1/1/93; joint problems: FALSE; uc flare up: FALSE; family history: FALSE; aza treated: NO; aza tolerant: FALSE; aza at present: FALSE; procedure date: 7/22/05; indictation for procedure: ; ucss: 6; calprotectin: 700; esr: 0; crp: 20; hb: 93; wcc: 17; neutrophils: 16; albumin: 23; blood obtained: FALSE; ibd affected relatives: 0; igr2096: 0; igr2198: 11; igr2230: 11; octn1: 11; octn2: 11; nod 702: 11; nod 908: 11; dlg5 133a: 11; nod 1007 fs: 11; diagnosis rectum: BOTH; diagnosis recto sigmoid: BOTH; diagnosis splen flex: BOTH; diagnosis hep flex: BOTH; diagnosis total: BOTH; last followup date: 7/22/05; followup rectum: BOTH; followup recto sigmoid: BOTH; followup splen flex: BOTH; followup hep flex: BOTH; followup total: BOTH; casenote review date: 8/15/05; category: FAILURE OF THERAPY; smoking status: never; smoking start date: ; smoking stop date: ; smoking amount: unknown; other illnesses: COPD-Previous severe pneumonia; disease: UC; run_date: 11-15-01; anatomic_location: sigmoid colon; inflammation_status: Inflamed; ' GSE64722 Homo sapiens 100 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL18224 Post-zygotic structural variants in histologically normal breast tissue may predispose to sporadic breast cancer [SET 4] 2015-01-07 Sporadic breast cancer (SBC) is a common and heterogeneous disease. There is no reliable way of early prediction of risk for SBC in the general population. We studied 282 females with SBC concentrating on copy number aberrations in tumor-free breast tissue (uninvolved margin, UM) outside the area of primary tumor (PT). Totally 1162 UMs (1-14 per breast) were studied. PT and blood/skin as control was also analyzed. Comparative analysis between genetic profiles for UM(s), PT(s) and blood/skin from the same patient is the core of study design. We identified 108 patients with at least one aberrant UM specimen, representing 38.3% of all cases. Gains were the dominating mutations in microscopically normal breast cells and gain of ERBB2, with overexpression of HER2 protein, was the most common aberration in normal cells. Five additional receptor genes (EGFR, FGFR1, IGF1R, LIFR and NGFR) also showed gains, and these were occasionally present in combination with the gain of ERBB2. Up to 67.6% of patients showed gain of one or more of these genes in normal cells. The aberrations found in normal cells from UMs were previously described in cancer literature, which suggest their causative, driving role in this disease. We demonstrate that analysis of normal cells from cancer-bearing patients leads to identification of genetic signatures that may predispose to SBC. Early detection of signals suggesting a predisposition towards development of SBC, long before detectable tumors are formed, is a key to the anticipated shift into a preventive paradigm of personalized medicine of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64722 Signatures of post-zygotic structural genetic aberrations in the cells of histologically normal breast tissue that can predispose to sporadic breast cancer. Genome research 9.944 https://doi.org/10.1101/gr.187823.114 {Genome research (9.944): 10.1101/gr.187823.114} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA271758 https://www.ebi.ac.uk/ena/browser/view/PRJNA271758 None [Overal design]We studied 282 female breast cancer patients that were assessed as affected by sporadic disease at the time of diagnosis and all underwent mastectomy. In total, 1162 UMs (uninvolved margin tissues), ranging from 1 to 14 UMs per patient, taken outside the location of clinically characterized index primary tumor, were analyzed on Illumina arrays. For each subject, DNA from at least one control tissue was also analyzed, which was predominantly blood DNA, alternatively skin-derived DNA. We also studied primary tumor (PT), or up to 3 primary tumor foci from patients with diagnosis of multifocal disease. This GEO project contains the genotyping profiles (processed and normalized data including Log R Ratio and B allele frequency) for these 1162 UMs used in the study. Information on phenotypes (age at diagnosis, tumor focality, tumor grade, tumor molecular phenotype) is also provided, whenever available. The 201-300 samples out of 811 experiments runned on platform GPL18224 (Infinium HumanOmniExpressExome); [Treatment]'None'; [Growth]'None'; [Extraction]'The tissues were stored at -70 degrees C prior to DNA extraction. The solid tissues were homogenized with a Tissuerupter (Qiagen). Proteinase K and Sarcosine was then added and the sample was incubated at 50oC over-night. The samples were transferred to PhaseLock Gel tubes and the DNA was purified with phenol/chloroform extraction. Due to very rich content of fat in UMs, phenol/chloroform extraction was repeated 6 times for all UMs, and 3 times for PTs and control samples from skin. The purified DNA was precipitated with sodium acetate, pH 5.4 and 95% ethanol. The DNA precipitate was dried before dissolving in water. Control samples of blood were extracted with QIAmp DNA Blood Maxi Kit (Qiagen).'; [Cell type]'Source: ''subject_code: 075JS; gender: female; age at cancer diagnosis (yrs): 65; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; ', 'subject_code: 078AW; gender: female; age at cancer diagnosis (yrs): 63; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ', 'subject_code: 082HM; gender: female; age at cancer diagnosis (yrs): 53; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: 089SD; gender: female; age at cancer diagnosis (yrs): 60; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: 098WC; gender: female; age at cancer diagnosis (yrs): 69; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 099OLZ; gender: female; age at cancer diagnosis (yrs): 63; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: 123HS; gender: female; age at cancer diagnosis (yrs): 66; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 124AA; gender: female; age at cancer diagnosis (yrs): 56; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: multifocal; ', 'subject_code: 125KL; gender: female; age at cancer diagnosis (yrs): 67; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 126AS; gender: female; age at cancer diagnosis (yrs): 85; tumor grade: 2; molecular_phenotype: HER2+; tumor focality: unifocal; ', 'subject_code: 127ZR; gender: female; age at cancer diagnosis (yrs): 54; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: unifocal; ', 'subject_code: 128WS; gender: female; age at cancer diagnosis (yrs): 62; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ', 'subject_code: 129EB; gender: female; age at cancer diagnosis (yrs): 69; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; ', 'subject_code: 130JT; gender: female; age at cancer diagnosis (yrs): 50; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ', 'subject_code: 131SD; gender: female; age at cancer diagnosis (yrs): 82; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: 132EM; gender: female; age at cancer diagnosis (yrs): 47; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 133ML; gender: female; age at cancer diagnosis (yrs): 34; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 134GJ; gender: female; age at cancer diagnosis (yrs): 75; tumor grade: 3; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: 135LS; gender: female; age at cancer diagnosis (yrs): 74; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ', 'subject_code: 136BS; gender: female; age at cancer diagnosis (yrs): 77; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: 137WK; gender: female; age at cancer diagnosis (yrs): 87; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ' GSE115302 Homo sapiens 6 Expression profiling by high throughput sequencing GPL11154 Next Generation Sequencing Facilitates Quantitative Analysis of ALDH+ E-BCSC, CD24-CD44+ M-BCSC and Bulk tumor cell Transcriptomes from MC1 and Vari068 PDX models of TNBC 2018-06-04 We report the application of single-molecule-based sequencing technology for high-throughput profiling of genes in E-, M-BCSCs and bulk tumor cells in two PDX models of triple negative breast cancer . https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115302 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA474498 https://www.ebi.ac.uk/ena/browser/view/PRJNA474498 https://www.ncbi.nlm.nih.gov/sra?term=SRP149709 [Overal design]Examination of global gene expression in E and M-BCSCs and Bulk tumor cells in 2 PDXs. Total RNA was extracted from E- (H2Kd-ALDH+), M- (H2Kd-CD44+/CD24-) BCSC-enriched and bulk (H2Kd-ALDH-CD44-/CD24+) cell populations freshly sorted from dissociated tumor cells of Vari068 and MC1 PDXs. Total RNA was extracted with RNeasy Mini Kit (Qiagen) according to manufacturer's instructions, and 500 ng was then taken out from each of them and subjected to mRNA isolation using NEBNext Poly (A) mRNA Magnetic Isolation Module (NEB, Ipswich, MA, USA). The mRNA library was constructed using NEBNext UltraTM RNA Library Prep Kit for Illumina (NEB, Ipswich, MA) according to the instruction manual, which includes sequential RNA fragmentation, reverse transcription using random primers, second strand cDNA synthesis, end repair, dA-tailing, adapter ligation, U excision, and PCR enrichment. mRNA libraries were sequenced on an Illumina HiSeq X Ten platform with 150bp pair-end reads. All reads passed filter were trimmed to remove low-quality bases and adaptor sequences. Reads were then aligned to the mm10 reference genome using tophat2 (v2.0.13), and FPKMs were calculated.; [Treatment]'None'; [Growth]'None'; [Extraction]'FACS sorted cells were pelleted and flash frozen in 50ul PBS. Total RNA from the frozen cell pellets were extracted using Norgen Single Cell RNA Purification Kit (catalog number 51800) as per manufacturer protocol. Quality of RNA was determined using Agilent BioAnalyzer with the Eukaryote total RNA Pico assay kit. RNA libraries were prepared with 10ng total RNA as input using the Nugen Ovation RNASeq V2 library kit (cat# 7102-08) along with Kapa LTP library kit cat# KK8230).\nRNA libraries were prepared as per standard manufacturer protocol'; [Cell type]'Source: ''rna integrity number: 8.5; tissue: PDX; ', 'rna integrity number: 9.3; tissue: PDX; ', 'rna integrity number: 8.8; tissue: PDX; ', 'rna integrity number: 7.8; tissue: PDX; ', 'rna integrity number: 8; tissue: PDX; ' GSE49349 Homo sapiens 20 Expression profiling by array GPL570 CHIP knockdown effect on breast cancer cell line 2013-07-30 Analysis of MCF-7 cell clones lacking the E3 ubiquitin liganse CHIP. We used microarrays to detail the global gene expression profiles effected by CHIP in human brest cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE49349 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA213708 https://www.ebi.ac.uk/ena/browser/view/PRJNA213708 None [Overal design]Total RNA was extracted from CHIP or LacZ knockdown MCF7 and hybridized on Affymetrix microarrays.; [Treatment]'MCF-7 cells were incubated with the shCHIP- or shLacZ-containing retroviral supernatant in the presence of 8 μg/ml polybrene. Twenty-four hours after infection, the viral supernatant was replaced with fresh DMEM containing 10% FBS. The infected cells were selected with 1 mg/ml G418. Clones were isolated from shLacZ or shCHIP cells.'; [Growth]'MCF-7 cells were maintained in Dulbecco’s modified Eagle’s medium supplemented with 10% fetal bovine serum (FBS).'; [Extraction]"Total RNA was extracted using Fast pure RNA kit (TAKARA) according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MCF7; treatment: CHIP knockdown; ', 'cell line: MCF7; treatment: LacZ knockdown; ' GSE132513 Homo sapiens 18 Methylation profiling by genome tiling array GPL21145 Epigenetic remodelling of enhancers in response to estrogen deprivation and re-stimulation [methylArray] 2019-06-11 Estrogen hormones are implicated in a majority of breast cancers and estrogen receptor alpha (ER) orchestrates a complex molecular circuitry that is not yet fully elucidated. Here we investigated genome-wide DNA methylation, histone acetylation and transcription after estradiol (E2) deprivation and re-stimulation to better characterise the ability of ER to coordinate gene regulation. We found that E2 deprivation mostly resulted in DNA hypermethylation and histone deacetylation in enhancers. Transcriptome analysis revealed that E2 deprivation leads to a global down-regulation in gene expression. Enrichment analysis of transcription factor (TF) binding and motif occurrence in the proximity of E2 deprivation-mediated differentially methylated and acetylated sites reinforces the importance of AP-1 and FOX proteins, Finally, most deprivation-dependent epigenetic changes were reversed following E2 re-stimulation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132513 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA548421 https://www.ebi.ac.uk/ena/browser/view/PRJNA548421 None [Overal design]Control MCF-7 HTB-22 breast cancer cells (CTR) were cultured continuously for 14 days in E2-containing medium, while E2-deprived cells (E2D) were cultured in the same conditions as CTR only lacking E2. The re-stimulated cells (ReSt) were E2-deprived for 4 days and re-stimulated for the 10 following. Each treatment (CTR, E2D and ReSt) and time point (d0, d4, d14) is available in triplicates. See publication for schematic design; [Treatment]'10nM 17β-estradiol in 0.1% DMSO (CTR and ReSt) or only 0.1% DMSO (E2D)'; [Growth]'For maintainance, cells were cultured in DMEM/F-12 supplemented with 10% (v/v) charcoal-stripped fetal bovine serum, 1% nonessential amino acids, sodium pyruvate and penicillin/streptomycin and with a daily addition of 10nM E2 in 0.1% DMSO'; [Extraction]'AllPrep DNA/RNA Mini kit (Qiagen)'; [Cell type]'Source: ''cell line: MCF-7 HTB22 (ATCC); treatment: CTR; time point: d0; ', 'cell line: MCF-7 HTB22 (ATCC); treatment: E2D; time point: d4; ', 'cell line: MCF-7 HTB22 (ATCC); treatment: ReSt; time point: d14; ', 'cell line: MCF-7 HTB22 (ATCC); treatment: CTR; time point: d4; ', 'cell line: MCF-7 HTB22 (ATCC); treatment: CTR; time point: d14; ', 'cell line: MCF-7 HTB22 (ATCC); treatment: E2D; time point: d14; ' GSE20737 Homo sapiens 12 Genome binding/occupancy profiling by genome tiling array GPL6325; GPL6326 Long non-coding RNA HOTAIR reprograms chromatin state to promote breast cancer metastasis 2010-03-10 Large intervening noncoding RNAs (lincRNAs) are pervasively transcribed in the genome yet their potential involvement in human disease is not well understood4,5. Recent studies of dosage compensation, imprinting, and homeotic gene expression suggest that individual lincRNAs can function as the interface between DNA and specific chromatin remodeling activities. Here we show that lincRNAs in the HOX loci become systematically dysregulated during breast cancer progression. The lincRNA termed HOTAIR is increased in expression in primary breast tumors and metastases, and HOTAIR expression level in primary tumors is a powerful predictor of eventual metastasis and death. Enforced expression of HOTAIR in epithelial cancer cells induced genome-wide re-targeting of Polycomb Repressive Complex 2 (PRC2) to an occupancy pattern more resembling embryonic fibroblasts, leading to altered histone H3 lysine 27 methylation, gene expression, and increased cancer invasiveness and metastasis in a manner dependent on PRC2. Conversely, loss of HOTAIR can inhibit cancer invasiveness, particularly in cells that possess excessive PRC2 activity. These findings suggest that lincRNAs play active roles in modulating the cancer epigenome and may be important targets for cancer diagnosis and therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE20737 Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. Nature 43.070 https://doi.org/10.1038/nature08975 {Nature (43.070): 10.1038/nature08975} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA124975 https://www.ebi.ac.uk/ena/browser/view/PRJNA124975 None [Overal design]Comparision of MDA-MB-231 Breast Cancer Cells expressing vector or HOTAIR. Each cell line was subjected to ChIP-chip with anti-H3K27, SUZ12, and EZH2 and interrogated on whole genome promoter arrays; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was isolated from MDA-MB-231 Vector or HOTAIR cells and amplifed using the Sigma Whole Genome Amplification Kit'; [Cell type]'Source: ''cell line: MDA-MB-231; ab: anti-SUZ12; ', 'cell line: MDA-MB-231; ab: none; ', 'cell line: MDA-MB-231; ab: anti-EZH2; ', 'cell line: MDA-MB-231; ab: anti-H3K27; ' GSE162272 Mus musculus 12 Expression profiling by high throughput sequencing GPL19057 Co-dependency for MET and FGFR1 in basal triple negative breast cancers 2020-11-27 Triple-negative breast cancer (TNBC) is a heterogeneous disease that lacks both effective patient stratification strategies and therapeutic targets. In the present study, we assay tumour-initiating cells (TICs) properties, using established Met-dependent transgenic mouse models of TNBC, breast cancer cell lines and, patient-derived xenografts, to directly investigate the role of Met in tumour initiation and identify FGFR1 signaling as a key convergent pathway with Met for the maintenance of TICs. To understand the events that occur in TICs upon inhibition of Met and FGFR1, we performed gene expression profiling by RNA-Sequencing of RNA prepared from tumoursphere from 3 independent MMTV-Metmt;Trp53fl/+;Cre derived spindloid tumour cell lines (A1005, A1129, A1471) following treatment with Met or FGFR inhibitor alone (Crizotinib or PD173074, respectively), or in combination for 24h. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE162272 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA681227 https://www.ebi.ac.uk/ena/browser/view/PRJNA681227 https://www.ncbi.nlm.nih.gov/sra?term=SRP294504 [Overal design]Differential gene expression profile following drugs treatment of tumoursphere from 3 independent MMTV-Metmt;Trp53fl/+;Cre derived spindloid tumour cell lines (A1005, A1129, A1471) following treatment with Met or FGFR inhibitor alone (Crizotinib or PD173074, respectively), or in combination for 24h, by RNA-Sequencing using a NextSeq500 sequencer (Illumina).; [Treatment]'None'; [Growth]'None'; [Extraction]'A1005, A1129, and A1471 tumourspheres treated with inhibitors (DMSO, Crizotinib, PD173074, or drug combination for 24h) were collected and total RNA was extracted using the AllPrep DNA/RNA Mini Kit (Qiagen) according to the manufacturer’s instructions. High RNA quality was verified using the Bioanalyzer RNA 6000 Nano assay (Agilent).\nThe samples were sequenced using a NextSeq500 sequencer (Illumina) by the Genomics Core Facility of the Institute of for Research in Immunology and Cancer, Université de Montréal.'; [Cell type]'Source: ''tissue: breast tumour; genotype: MMTV-Metmt;Trp53fl/+;Cre-A1005; treatment: Crizotinib; ', 'tissue: breast tumour; genotype: MMTV-Metmt;Trp53fl/+;Cre-A1005; treatment: DMSO; ', 'tissue: breast tumour; genotype: MMTV-Metmt;Trp53fl/+;Cre-A1005; treatment: PD173074; ', 'tissue: breast tumour; genotype: MMTV-Metmt;Trp53fl/+;Cre-A1005; treatment: Combo; ', 'tissue: breast tumour; genotype: MMTV-Metmt;Trp53fl/+;Cre-A1129; treatment: Crizotinib; ', 'tissue: breast tumour; genotype: MMTV-Metmt;Trp53fl/+;Cre-A1129; treatment: DMSO; ', 'tissue: breast tumour; genotype: MMTV-Metmt;Trp53fl/+;Cre-A1129; treatment: PD173074; ', 'tissue: breast tumour; genotype: MMTV-Metmt;Trp53fl/+;Cre-A1129; treatment: Combo; ', 'tissue: breast tumour; genotype: MMTV-Metmt;Trp53fl/+;Cre-A1471; treatment: Crizotinib; ', 'tissue: breast tumour; genotype: MMTV-Metmt;Trp53fl/+;Cre-A1471; treatment: DMSO; ', 'tissue: breast tumour; genotype: MMTV-Metmt;Trp53fl/+;Cre-A1471; treatment: PD173074; ', 'tissue: breast tumour; genotype: MMTV-Metmt;Trp53fl/+;Cre-A1471; treatment: Combo; ' GSE133608 Homo sapiens 8 Expression profiling by array GPL10558 Genome-wide analysis of gene expression in MDA-MB-231 breast cancer cells in response to conditional miRNA mediated OPN knockdown 2019-07-01 Our goal was to identify the genes, which are modulated following conditional OPN knockdown for 3 and 6 days. Thus, to elucidate the OPN relevance and to broaden the knowledge on the affected signalling pathways. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE133608 Conditional Knockdown of Osteopontin Inhibits Breast Cancer Skeletal Metastasis. International journal of molecular sciences 4.183 https://doi.org/10.3390/ijms20194918 {International journal of molecular sciences (4.183): 10.3390/ijms20194918} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA552038 https://www.ebi.ac.uk/ena/browser/view/PRJNA552038 None [Overal design]Cell pellets were collected after 3 and 6 days of cultivating the cells in media with or without doxycycline. There were duplicated total RNA samples for each time interval and each condition.The mRNA expression of the in vitro miRNA treated cells was compared to the respective +dox control.; [Treatment]'None'; [Growth]'The established cell clone was cultivated in appropriate media with or without doxycycline for 3 or 6 days.'; [Extraction]'The RNA was isolated by RNeasy mini-kit (Qiagen) in accordance with the prescribed protocol provided with the kit. The quality control of the total RNA was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''cell line: MDA-MB-231; genotype: control; time (mirna expression): 3 days off; ', 'cell line: MDA-MB-231; genotype: miRNA mediated OPN knockdown; time (mirna expression): 3 days on; ', 'cell line: MDA-MB-231; genotype: control; time (mirna expression): 6 days off; ', 'cell line: MDA-MB-231; genotype: miRNA mediated OPN knockdown; time (mirna expression): 6 days on; ' GSE45256 Mus musculus 16 Expression profiling by array GPL6885 Genome-wide analysis of gene expression in murine breast fibroblasts from normal tissue, hyperplasia, adenoma and carcinoma (MMTV-PyMT model) 2013-03-18 Analysis of differences at gene expression level of hpvE6 immortalized fibroblasts isolated from normal mammary glands and from hyperplasia, adenoma and carcinoma stages using the MMTV-PyMT model (FVB/N background). Analysis demonstrated the activation of specific transcriptional programs in fibroblasts from later stages. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE45256 Mechanotransduction and YAP-dependent matrix remodelling is required for the generation and maintenance of cancer-associated fibroblasts. Nature cell biology 17.728 https://doi.org/10.1038/ncb2756 {Nature cell biology (17.728): 10.1038/ncb2756} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA193324 https://www.ebi.ac.uk/ena/browser/view/PRJNA193324 None [Overal design]Total RNA obtained from isolated hpvE6 immortalized fibroblasts from normal mammary gland (NF) and from different stages of tumour development using the MMTV-PyMT murine breast cancer model. Stages were hyperplasia (HpAF), adenoma (AdAF) and carcinoma (CAF). Fibroblasts were seeded in a deformable Matrigel:collagen I matrix and total RNA isolated 72h later.; [Treatment]'No treatment'; [Growth]'Cells were isolated from the defined tissues, immortalized using hpvE6 and seeded on a Matrigel:Collagen I deformable matrix and cultured for 72h on 10%FBS DMEM'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''background strain: FVB/N; tumour stage: Normal; ', 'background strain: FVB/N; tumour stage: Hyperplasia; ', 'background strain: FVB/N; tumour stage: Adenoma; ', 'background strain: FVB/N; tumour stage: Carcinoma; ' GSE107109 Homo sapiens 6 Expression profiling by array GPL887; GPL1390; GPL5325 Asparagine availability governs metastasis in a model of breast cancer 2017-11-17 Single - cell profiling of patient tumours and of mouse models is revealing that many cancers are constituted of communities of genetically and phenotypically distinct clonal lineages 1 - 12. A functional model of breast cancer heterogeneity revealed that clonal sub - populations proficient at generating circulating tumour cells were not equally capable of forming metastases at secondary sites 13. A combination of differential expression and focused in vitro and in vivo RNAi screens revealed candidate drivers of metastasis discriminating these clones, which were then evaluated in gene expression datasets from breast cancer patients. Among these, Asparagine Synthetase (Asns) expression in a patient's primary tumour was most strongly correlated with later metastatic relapse. Silencing of Asns reduced both metastatic potential in vivo and invasive potential in vitro. Conversely, increasing the availability of extracellular asparagine increased the invasive potential of mouse and human breast cancer cells, and enforced Asns expression promoted metastasis. Decreasing asparagine availability in mice by treatment with L-asparaginase or even by dietary restriction strongly reduced metastasis from orthotopic tumours. Asparagine availability varies betwe en tissues, potentially explaining selective effects on particular steps of tumor progression. Asparagine limitation reduced the production of proteins that promote the epithelial to mesenchymal transition, providing one potential mechanism for how the availability of a single amino acid could regulate metastatic progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE107109 Asparagine bioavailability governs metastasis in a model of breast cancer. Nature 43.070 https://doi.org/10.1038/nature25465 {Nature (43.070): 10.1038/nature25465} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA419005 https://www.ebi.ac.uk/ena/browser/view/PRJNA419005 None [Overal design]Microarrays were used to analyze primary breast tumors and distant metastases in order to identify biological features associated with distant metastases.; [Treatment]'None', 'N/A'; [Growth]'None', 'samples were taken from patients at autopsy'; [Extraction]'Total RNA isolated by Stratagene.', 'Qiagen Rneasy Kit', 'Total RNA isolated by stratagene', 'Total RNA isolated by Stratagene', 'Total RNA using Qiagen Rneasy Kit'; [Cell type]'Source: ''reference: Stratagene Human Universal Reference that contained 1/10 added MCF7 and ME16C RNAs; ', 'age: --; er (1=positive; 0=negative): --; pgr (1=positive; 0=negative): --; her2 clinical status ihc/fish (1=positive; 0=negative): 0; node status (1=positive=1 or more nodes+; 0=negative): --; grade: --; size (1= <=2cm; 2= >2cm to <=5cm; 3=>5cm; 4=any size with direct extension to chest wall or skin): --; rfs event (0=no relapse, 1=relapsed at any site or died of disease): --; rfs months: --; overall survival event (0=alive, 1=dod or doc): --; overall suvival months: --; pam50 predictions plus claudin-low classification (cell line predictor): Basal; dscores unc337: -0.17335459; ', '', 'reference: Human Reference B; ', 'tumor: breast tumor; ', 'tumor: lung metastasis; ', 'sample type: Reference; ', 'tissue: breast tumor; tissue_type: flash frozen tissue; ' GSE30871 Homo sapiens 14 Expression profiling by array GPL9052; GPL10558 Genome-Wide Progesterone Receptor Binding: Cell Type-Specific and Shared Mechanisms in Uterine Fibroids and Breast Cancer 2011-07-22 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE30871 Genome-wide progesterone receptor binding: cell type-specific and shared mechanisms in T47D breast cancer cells and primary leiomyoma cells. PloS one 2.776 https://doi.org/10.1371/journal.pone.0029021 {PloS one (2.776): 10.1371/journal.pone.0029021} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA146143 https://www.ebi.ac.uk/ena/browser/view/PRJNA146143 None [Overal design]Refer to individual Series; [Treatment]'T47D cells were hormone starved 2 days in RPMI 1640 with 5% charcol stripped FBS before treated with vehicle (ethanol) or RU486 (10-6 M). Uterine leiomyoma smooth muscle cells were hormone starved for 1 day in DMEM/F12 containing 1% charcol stripped FBS before treated with vehicle (ethanol) or RU486 (10-6 M).', 'T47D or leiomyoma cells treated with RU486 for 1 hour were fixed with 1% formaldehyde for 15 min and quenched with 0.125 M glycine. Chromatin was isolated by adding lysis buffer, followed by disruption with a Dounce homogenizer. Lysates were sonicated and the DNA sheared to an average length of 300-500 bp. Genomic DNA was prepared by treating aliquots of chromatin with RNase, proteinase K and heat for de-crosslinking, followed by ethanol precipitation. Pellets were resuspended and the resulting DNA was quantified on a NanoDrop spectrophotometer. Extrapolation to the original chromatin volume allowed quantitation of the total chromatin yield.'; [Growth]'T47D cells were cultured in RPMI 1640 with 10 % FBS. Human uterine leiomyoma smooth muscle cells were cultured in DEME/F12 with 10% FBS.', 'T47D cells were cultured in RPMI 1640 with 10 % FBS. Human uterine leiomyoma smooth muscle cells were cultured in DEME/F12 with 10% FBS. T47D cells were hormone starved 2 days in RPMI 1640 with 5% charcol stripped FBS before treated with vehicle (ethanol) or RU486 (10-6 M). Uterine leiomyoma smooth muscle cells were hormone starved for 1 day in DMEM/F12 containing 1% charcol stripped FBS before treated with vehicle (ethanol) or RU486 (10-6 M).'; [Extraction]'Total RNA from T47D and leiomyoma cells was extracted using Tri-reagent (Sigma-Aldrich). Complementary DNA was prepared with Superscript III first-Strand Synthesis System (Invitrogen)', 'An aliquot of chromatin (30 µg) was precleared with protein G agarose beads (Invitrogen). Genomic DNA regions of interest were isolated using 4 µg antibody against PR (sc-7208, Santa Cruz Biotechnology). Complexes were washed, eluted from the beads with SDS buffer, and subjected to RNase and proteinase K treatment. Crosslinks were reversed by incubation overnight at 65° C, and ChIP DNA was purified by phenol-chloroform extraction and ethanol precipitation.'; [Cell type]'Source: ', 'Leiomyoma cells''tissue: breast; Sex: female; source: pleural efusion of an infiltrating ductal carcinoma of the breast; cell line: T47D; ', 'tissue: uterine; Sex: female; source: uterine leiomyoma; cell line: --; ', 'cell type: Leiomyoma cells; treatment: RU486; chip antibody: PR; chip antibody manufacturer: Santa Cruz; chip antibody catalog #: sc-7208; ', 'cell line: T47D; treatment: RU486; chip antibody: PR; chip antibody manufacturer: Santa Cruz; chip antibody catalog #: sc-7208; ' GSE87440 Homo sapiens 8 Expression profiling by array GPL15207 Expression data from human breast cancer cell MCF-7 and human gastric cancer cell SGC-7901 2016-09-28 Piper longum L. is a well-known traditional antihyperlipidemic medicine,and it has ability to inhibit proliferation of cancer cells,potassium piperate (GBK) maybe have the same effect. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated and down-regulated genes during this process. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE87440 The synthetic antihyperlipidemic drug potassium piperate selectively kills breast cancer cells through inhibiting G1-S-phase transition and inducing apoptosis. Oncotarget None https://doi.org/10.18632/oncotarget.16872 {Oncotarget (None): 10.18632/oncotarget.16872} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA344773 https://www.ebi.ac.uk/ena/browser/view/PRJNA344773 None [Overal design]treat and untreat with GBK on MCF-7 and SGC-7901 for RNA extraction and hybridization on Affymetrix microarrays. And then analysis the result to compare the express level between two cells that treat or untreat with GBK.; [Treatment]'treat with GBK and cultured for 48h'; [Growth]'37℃,5% CO2 cultured for 48h'; [Extraction]'standard Affymetrix protocol'; [Cell type]'Source: ''cell line: MCF-7; treatment: GBK; ', 'cell line: MCF-7; treatment: untreated; ', 'cell line: SGC-7901; treatment: GBK; ', 'cell line: SGC-7901; treatment: untreated; ' GSE66108 Homo sapiens 36 Expression profiling by array GPL6696; GPL9257 CCL171, T47D, MDA-MB231 cell lines: stimulation with BMP7 and antagonists 2015-02-19 Methods: We used an ex vivo culture model and measured gene expression changes in human lung fibroblasts after stimulation with BMPs and their antagonists using HEEBO microarrays. The in vitro data were correlated with in vivo observations in published expression datasets of human lung adenocarcinomas. Results: We have systematically analyzed the response to BMP2, BMP4, BMP7 and their antagonists, gremlin and noggin, to define common and specific gene expression patterns. A BMP2 induced gene expression signature was defined, which is specific for stromal fibroblasts. Gene expression profiles from lung adenocarcinoma biopsies were analyzed to determine the prognostic significance of the Fibroblast specific BMP2 induced gene list. This gene list successfully segregated patients with different prognostic outcome in 3 datasets. In a small dataset (Garber et al.) there was a strong trend for a worse prognosis of patients with adenocarcinomas of all stages over-expressing the Fibroblast specific BMP2 induced gene list. In two larger datasets with stage I adenocarcinomas we observed a significantly worse disease-free (p=0.002, Lee et al. and p=0.002, Bhattacharjee et al.) and overall survival (p=0.0002). Conclusions: The effects of BMPs and their antagonists are heterogeneous in different cell types. The gene expression pattern induced by BMP2 in primary lung fibroblasts may predict outcomes of patients with lung adenocarcinomas. A stimulus or stress experiment design type is where that tests response of an organism(s) to stress/stimulus. e.g. osmotic stress, behavioral treatment https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE66108 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA275959 https://www.ebi.ac.uk/ena/browser/view/PRJNA275959 None [Overal design]stimulus_or_stress_design; [Treatment]'None', 'BMP stimulation experiments: For the experiment, 30?000 cells/cm2 were seeded in 3 ml of 5% FBS D-MEM and incubated for 6 h to allow attachment. The cells were washed extensively with phosphate-buffered saline and starved for 48 h in fresh low-serum D-MEM supplemented with 0.2% FBS. The cells were starved to reduce the effects of any stimulation from the regular cell culture medium. The medium was subsequently replaced with fresh low-serum D-MEM with or without 200 ng/ml BMP2 (human recombinant in Escherichia coli; Sigma Aldrich, St. Louis, MO, USA), 24 ng/ml BMP4, 200 ng/ml BMP7, 240 ng/ml Noggin or 1 ug/ml Gremlin. The cells were stimulated for 24 h, and the RNA was harvested to test the effects of BMP and their antagonists on mRNA expression patterns.'; [Growth]'None', "Primary human fibroblasts (CCL-171) and the human breast cancer cell lines MDA-MB-231 and T47D were obtained from the American Type Culture Collection (ATTC, Atlanta, Georgia, USA) on the 15. November 2005. After resuscitation the cells were propagated in Dulbecco's modified Eagle's medium (D-MEM, Invitrogen, Carlsbad, USA) supplemented with 10% heat-inactivated FBS (Invitrogen, Carlsbad, CA, USA), 4.5 g/l glucose, 4 mM L-glutamine, 100 U/ml penicillin and 100 ug/ml streptomycin (Gibco, Carlsbad, CA, USA). The cells were maintained by regular passages when confluence was reached and used for the experiments within 3-4 months. The study was approved by the Ethikkommission beider Basel, Switzerland (approval No. 271/05)."; [Extraction]'not provided', "RNA extraction and amplification: After aspirating the culture medium, the cell monolayer was washed once with phosphate-buffered saline. The cells were lysed in a buffer containing guanidine isothiocyanate (RLT buffer, QIAGEN, CA, USA). The total RNA was extracted with an RNeasy kit (QIAGEN, Valencia, CA, USA) according to the manufacturer?s instructions. The RNA concentration was measured with a NanoDrop system spectrophotometer (ND-1000 Spectrophotometer Technologies, Wilmington, NC, USA). The integrity of extracted RNA was assessed by electrophoresis in a 1% agarose gel in MOPS buffer. For mRNA amplification, an Amino Allyl MasageAmp II aRNA Amplification Kit was used (Ambion, Austin, TX, USA). The amplification of mRNA from 500 ng total RNA, purification of the cDNA, in vitro transcription and purification of aRNA were performed according to the manufacturer's instructions. The integrity and quantity of the amplified RNA were verified as described above."; [Cell type]'Source: ''reference: stratagene universal reference; ', 'cell line: MDA-MB-231; ', 'cell line: T47D; ', 'cell line: CCL171; ' GSE83934 Homo sapiens 69 Non-coding RNA profiling by array GPL20712 Profiling of microRNAs in tumor interstitial fluid of breast cancer patients - a novel resource to identify biomarkers for prognostic classification and detection of cancer 2016-06-30 The purpose of this study was to identify biomarkers and to elucidate the crosstalk between stromal cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE83934 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA327438 https://www.ebi.ac.uk/ena/browser/view/PRJNA327438 None [Overal design]Compare the level of microRNA in tumor interstitial fluid (TIF) and breast tumor tissue of breast cancer patients.; [Treatment]'Fresh-frozen tumor tissue.'; [Growth]'None'; [Extraction]'Total RNA was extracted using Trizol for tumor samples and Exiqon RNA isolation for biofluids (TIF).'; [Cell type]'Source: ''disease state: control; ', 'disease state: breast cancer; tissue: tumor interstitial fluid; ', 'disease state: breast cancer; tissue: breast tumor; ' GSE67295 Homo sapiens 56 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL11154 Inflammatory cytokines activate unliganded estrogen receptor and alter the sensitivity of breast cancer cells to tamoxifen 2015-03-25 Genome-wide analyses of the transcriptomes and transcription factor recruitment in estrogen receptor breast cancer cells in response to estradiol, IL1b, or TNFa treatments. Also, the role of inflammatory cytokines on affecting tamoxifen sensitivity is analyzed on a genome-wide scale. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE67295 Structural and Molecular Mechanisms of Cytokine-Mediated Endocrine Resistance in Human Breast Cancer Cells. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2017.02.008 {Molecular cell (14.548): 10.1016/j.molcel.2017.02.008} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA279424 https://www.ebi.ac.uk/ena/browser/view/PRJNA279424 https://www.ncbi.nlm.nih.gov/sra?term=SRP056552 [Overal design]Transcription factor binding (ERa, p65) and transcriptome analyses were performed in estradiol- and pro-inflammatory cytokine-treated MCF7 cells.; [Treatment]'See above'; [Growth]'None'; [Extraction]"ChIP-Seq: Sequencing libraries were prepared from collected DNA by blunting, A-tailing, adapter ligation as previously described (Heinz, S. et al. Molecular Cell 38, 576-589 (2010)) using barcoded adapters (NextFlex, Bioo Scientific). Libraries were PCR-amplified for 12-15 cycles, size selected by gel extraction and sequenced on a HiSeq 2000 (Illumina) for 51 cycles.\nRNA-Seq: Enriched mRNA was hydrolyzed with Fragmentation Buffer (Ambion) for 10 min at 70°C and re-buffered to 10 mM Tris pH 7.4 using P-30 size exclusion columns (Bio-Rad). RNA was then de-capped for 2 h at 37°C with 0.5 µl (10 U/µl) TAP (Epicentre) in 20 µl TAP buffer containing 1 U/µl SUPERase-IN. Samples were 3’ dephosphorylated for 50’ at 37°C with 1 µl PNK (Enzymatics), 0.5 µl 10x TAP buffer, 1.5 µl water, 0.5 ul 0.25 M MgCl2 (3 mM free Mg2+ final), 0.5 µl 10 mM ATP (0.2 µM final to protect PNK). Subsequently, RNA was 5’-phosphorylated for 60 min at 37°C by adding 2 µl (10 U/µl) PNK, 10 ul 10x T4 DNA ligase buffer and 63 µl water. RNA was extracted with Trizol LS, precipitated in the presence of Glycoblue (Ambion), and dissolved in 4.5 µl water. 0.5 µl 9 µM of a 5’-adenylated sRNA3'MPX adapter /5Phos/AG ATC GGA AGA GCA CAC GTC TGA /3AmMO/ (IDT, desalted; adenylated with Mth ligase (NEB) according to the manufacturer’s instructions, phenol-chloroform/chloroform-extracted, ethanol-precipitated with glycogen and dissolved in water at 9 µM) were heat-denatured together with the RNA for 2 minutes at 70°C, and ligated with 100 U truncated T4RNA ligase 2 K227Q (NEB) in 10 µl 1x T4 RNA ligase buffer without ATP, containing 10 U SUPERase-In and 15% PEG8000 for 2 hours at 16°C. To reduce adapter dimer formation, 0.5 µl 10 µM MPX_ RT primer 5’-GTG ACT GGA GTT CAG ACG TGT GCT CTT CCG ATC T-3’ (IDT, desalted) was added and annealed to the ligation product by incubating at 75°C for 2 minutes, then 37°C for 30 minutes, then 25°C for 15 minutes. Finally, 0.5 µl 5 µM hybrid DNA/RNA sRNA5'h adapter 5’-GTT CAG AGT TCT ACA rGrUrC rCrGrA rCrGrA rUrC-3’ (IDT) were ligated to previously capped RNA 5’ ends by adding 2 µl T4 RNA ligase buffer, 6 µl 50% PEG8000 (15% final), 1 µl 10 mM ATP, 9.5 µl water and 0.5 µl (5 U) T4 RNA ligase 1 for 90 minutes at 20°C. To 15 µl ligation reaction, an additional 0.5 µl 10 µM MPX_ RT primer were added, reactions were denatured at to 70°C for 1 minute, then placed on ice. RNA was reverse-transcribed by adding 3 µl 10x first strand buffer, 4.5 µl water, 1.5 µl 10 mM dNTP, 3 µl 0.1 M DTT, 1.5 µl RNaseOUT and 1 µl Superscript III reverse transcriptase (Invitrogen), and incubating for 30 minutes at at 50°C. Complementary DNA was isolated by adding 35 µl AMPure XL beads (Beckman), binding and washing according to manufacturer’s instructions and dissolved in 40 µl TET. Libraries were PCR-amplified for 13 cycles with 0.75 µM primers oNTI201 (5'-AAT GAT ACG GCG ACC ACC GAC AGG TTC AGA GTT CTA CAG TCC GAC G-3' and TruSeq-compatible indexed primers (e.g. 5’-CAA GCA GAA GAC GGC ATA CGA GAT iii iii GTG ACT GGA GTT CAG ACG TGT GCT CTT-3’ (desalted, IDT, i signifies index nucleotides) using Phusion Hot Start II (Thermo Scientific) in HF buffer containing 0.5 M betaine (98°C, 30s/12x(98°C, 10s/57°C, 25s/72°C, 20s)/ 72°C, 1min/4°C, ?), 175-225 bp fragments were size-selected on 10% PAGE gels and sequenced for 51 cycles on a HiSeq 2000 sequencer (Illumina) with small RNA sequencing primer 5’-CGA CAG GTT CAG AGT TCT ACA GTC CGA CGA TC-3’ and TruSeq Index sequencing primer (Illumina).\nGro-Seq: Nuclei were extracted from 8-12 million cells grown on 10 cm plates and nuclear run-on reactions were performed for 5 minutes at 30°C in the presence of Sarkosyl and BrUTP. RNA was extracted with Trizol, DNase-treated, base-hydrolyzed and dephosphorylated with PNK. BrUTP-labeled run-on RNA was immunopurified with anti-BrdUTP-coated agarose beads and precipitated overnight. Poly(A)-tailing was followed by cDNA synthesis using complementary poly(T)-primers. Excess oligo was removed by Exonuclease I and cDNA fragments were purified on a denaturing 10% polyacrylamide TBE-urea gel. The recovered cDNA was circularized, linearized, amplified for 10-16 cycles. The final product was run on 10% TBE gel, gel purified and cleaned-up using ChIP DNA clean & Concentrator Kit. The final libraries were sequenced using an Illumina HiSeq 2000."; [Cell type]'breast cancer cell line''cell line: MCF7; cell type: breast cancer cell line; treatment: vehicle; chip antibody: ERa (Vendor: Santa Cruz, cat# sc-543, lot# C2114); ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: E2 for 45m; chip antibody: ERa (Vendor: Santa Cruz, cat# sc-543, lot# C2114); ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: IL1b for 45m; chip antibody: ERa (Vendor: Santa Cruz, cat# sc-543, lot# C2114); ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: TNFa for 45m; chip antibody: ERa (Vendor: Santa Cruz, cat# sc-543, lot# C2114); ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: IKK7; chip antibody: ERa (Vendor: Santa Cruz, cat# sc-543, lot# C2114); ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: IL1b+IKK7; chip antibody: ERa (Vendor: Santa Cruz, cat# sc-543, lot# C2114); ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: vehicle; chip antibody: p65 (Vendor: Santa Cruz, cat# sc-372, lot# D0604); ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: E2 for 45m; chip antibody: p65 (Vendor: Santa Cruz, cat# sc-372, lot# D0604); ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: IL1b for 45m; chip antibody: p65 (Vendor: Santa Cruz, cat# sc-372, lot# D0604); ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: TNFa for 45m; chip antibody: p65 (Vendor: Santa Cruz, cat# sc-372, lot# D0604); ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: vehicle; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: E2 for 3h; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: E2+ICI for 3h; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: IL1b for 3h; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: IL1b+ICI for 3h; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: TNFa for 3h; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: TNFa+ICI for 3h; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: E2; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: E2+TOT; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: E2+TOT+IL1b; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: E2+TOT+TNFa; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: E2 for 30m; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: IL1b for 30m; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: TNFa for 30m; ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: E2+ICI; chip antibody: ERa (Vendor: Santa Cruz, cat# sc-543, lot# C2114); ', 'cell line: MCF7; cell type: breast cancer cell line; treatment: IL1b+ICI; chip antibody: ERa (Vendor: Santa Cruz, cat# sc-543, lot# C2114); ' GSE8565 Homo sapiens 17 Expression profiling by array GPL570 Argyrin A is a p27 stabilizing drug with potent antiproliferative activity in vivo 2007-07-23 Reduction in the cellular levels of the cyclin kinase inhibitor p27kip1 are frequently found in many human cancers and correlate directly with patient prognosis. Specifically ubiquitin dependent proteasomal turnover has been shown to cause reduced p27 expression in many human cancers. We recently demonstated that expression of a stabilized version of p27kip1 (p27kip1T187A) in a genetically modified mouse significantly reduced the number of intestinal adenomatous polyps which progressed to invasive carcinomas. Based on this work we set out to identify compounds which lead to a re-expression of p27 in cancer tissues. In this work we identify Argyrin A a compound derived from myxobacterium archangium gephyra as a potent inducer of p27kip1 expression. Argyrin A induces apoptosis in human colon cancer xenografts and tumor vasculature in vivo leading to a profound reduction in tumor size at well tolerated levels. Argyrin A functions are strictly dependent on the expression of p27kip1 as neither tumor cells nor endothelial cells which do not express p27kip1 respond to this compound. Surprisingly the molecular mechanism by which Argyrin A exerts its p27 dependent biological function is through a potent inhibition of the 20S proteasome. Keywords: protasome inhibitor, time course, MCF7 cells, genome wide gene expression response, siRNA https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE8565 Argyrin a reveals a critical role for the tumor suppressor protein p27(kip1) in mediating antitumor activities in response to proteasome inhibition. Cancer cell 23.916 https://doi.org/10.1016/j.ccr.2008.05.016 {Cancer cell (23.916): 10.1016/j.ccr.2008.05.016} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA101709 https://www.ebi.ac.uk/ena/browser/view/PRJNA101709 None [Overal design]MCF7 cells were incubated with proteasome inhibitors bortezomib or Argyrin A or proteasome activity was reduced by treatment with siRNA against proteasomal subunits and gene expression profiles were determined at different timepoints thereafter.; [Treatment]'no', 'Velcade, Proteasom inhibitor'; [Growth]'DMEM, FCS Pen/Strep, 37° , 5% CO2'; [Extraction]'RNAeasy'; [Cell type]'Source: ''genetic modification: ; tissue: breast adenocarcinoma; ' GSE136287 Homo sapiens 18 Expression profiling by array GPL6244 Transcriptomic characterisation of ALDH+ cells in therapy resistant breast cancer patient samples 2019-08-23 This study is part of a larger multidisciplinary study entitled A dormant sub-population expressing interleukin-1 receptor characterises anti-estrogen resistant ALDH+ breast cancer stem cells. In particular these data were generated to gain understanding of the development of resistance to AE therapies in ER+ breast cancer patients by comparing the gene expression pattern between ALDH+ and ALDH- cells in 9 metastatic ER+ patient samples. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE136287 Increased Expression of Interleukin-1 Receptor Characterizes Anti-estrogen-Resistant ALDH+ Breast Cancer Stem Cells. Stem cell reports 5.499 https://doi.org/10.1016/j.stemcr.2020.06.020 {Stem cell reports (5.499): 10.1016/j.stemcr.2020.06.020} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA561838 https://www.ebi.ac.uk/ena/browser/view/PRJNA561838 None [Overal design]18 tissue samples of 9 patients were analysed separating tissue cells into ALDH+ and ALDH- populations and using the RNA for microarray analysis.; [Treatment]'Ascites or pleural effusions were spun for 10min at 1000g and pellets were resuspended in PBS. Red and white blood cells were excluded from the epithelial tumour cells using the density gradient Lymphoprep (Stemcell Technologies) following manufacturer’s protocol.'; [Growth]'Metastatic fluid samples were collected at the Christie NHS Foundation Trusts. All patients provided written informed consent before samples were taken, in agreement with local research ethics committee guidelines.'; [Extraction]'The Aldefluor reagent system (StemCell Technologies) was used to isolate the cancer stem-like population on the basis of their aldehyde dehydrogenase (ALDH) activity. The protocol was carried out following the manufacturer’s guidelines. Briefly, 5x10e5 cells were resuspended in 0.5 ml of Aldefluor buffer per eppendorf. 10 µl of the internal control Diethylaminobenzaldehyde (DEAB) was added to one of the eppendorfs for each treatment which was used to correct for background staining and to define the ALDH-positive region in the flow cytometer. 2.5 µl of the fluorescent activated aldefluor reagent Bodipy-aminoacetaldehyde (BAAA) was added to all eppendorfs and samples were incubated in the dark at 37ºC for 45 min shaking. Samples were washed with Aldefluor buffer and centrifuged at 400g for 3 min. Samples were resuspended in 300 µl of aldefluor buffer and 3 µl of the cell viability stain 7-aminoactinomycin (7-AAD) was added to each eppendorf for cell death exclusion. ALDH-bright cells were detected in the green fluorescence channel (520-540 nm) by the FACS aria II sorter (BD Bioscience).Unstained cells were always used to ensure accurate gating. Cell debris and doublets were also gated out based on cell size and complexity. Data was analysed using the FlowJo software package. Once the Aldefluor assay was performed, 10,000 cells were sorted with Hank’s Buffered Saline Solution (HBSS) as sheath fluid. ALDH positive and ALDH negative populations were sorted into 100 µl of RLT lysis buffer (Qiagen) for direct lysis. Total RNA extraction from PDS was carried out using the RNase Plus Micro Kit (Qiagen) according to manufacturer’s instructions. The 2100 Bioanalyzer (Agilent 2100 Bioanalyzer system, Agilent Technologies) was used for quantitation and quality control of the RNA from sorted cells.'; [Cell type]'Source: ''diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Negative; patient: BB3RC68; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Positive; patient: BB3RC68; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Negative; patient: BB3RC69; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Positive; patient: BB3RC69; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Negative; patient: BB3RC71; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Positive; patient: BB3RC71; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Negative; patient: BB3RC89; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Positive; patient: BB3RC89; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Negative; patient: BB3RC90; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Positive; patient: BB3RC90; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Negative; patient: BB3RC90A; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Positive; patient: BB3RC90A; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Negative; patient: BB3RC91; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Positive; patient: BB3RC91; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Negative; patient: BB3RC91A; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Positive; patient: BB3RC91A; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Negative; patient: BB3RC94; ', 'diagnosis: Breast cancer; er status: ER+; Stage: Metastasis; tissue: Metastatic fluid; aldh population: Positive; patient: BB3RC94; ' GSE76116 Homo sapiens 2 Genome binding/occupancy profiling by high throughput sequencing GPL18573 ChIP-seq analysis of MBD3 in human breast cancer cells 2015-12-17 Chromatin immunoprecipitation followed by massively parallel sequencing (ChIP-seq) is a powerful approach to identify the genome-wide localization of protein of interest. However, to perform ChIP-seq experiments for large protein complex, such as Mi-2/NuRD complex, is still challenging. Here, we present high-quality MBD3 ChIP-seq data in human breast cancer cells, MDA-MB-231. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76116 High-quality ChIP-seq analysis of MBD3 in human breast cancer cells. Genomics data 0.527 https://doi.org/10.1016/j.gdata.2015.12.029 {Genomics data (0.527): 10.1016/j.gdata.2015.12.029} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA306261 https://www.ebi.ac.uk/ena/browser/view/PRJNA306261 https://www.ncbi.nlm.nih.gov/sra?term=SRP067510 [Overal design]MBD3 ChIP-seq experiment was perform using human breast cancer cells, MDA-MB-231. Two bilogical replicates were prepared.; [Treatment]'none'; [Growth]'Cells were grown on 15 cm plates in DMEM medium with 10% FBS'; [Extraction]'Tagmentation and PCR amplification were performed using Nextera XT kit (Illumina).'; [Cell type]'Source: ''tissue: Breast; chip antibody: MBD3; cell line: MDA-MB-231; ' GSE5327 Homo sapiens 58 Expression profiling by array GPL96 Breast cancer relapse free survival and lung metastasis free survival 2006-07-17 Validation of lung metastasis signature (LMS) and its association with risk of developing lung metastasis and with primary tumor size. Keywords: Disease state analysis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE5327 Lung metastasis genes couple breast tumor size and metastatic spread. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.0701138104 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.0701138104} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA96341 https://www.ebi.ac.uk/ena/browser/view/PRJNA96341 None [Overal design]58 tumor samples; [Treatment]'None'; [Growth]'None'; [Extraction]"RNAzol B extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''ID: 76; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 11.3388; lung met free survival (yr): 11.3388; lms status: 1; ', 'ID: 123; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 7.360655833; lung met free survival (yr): 7.360655833; lms status: 1; ', 'ID: 401; cohort: Erasmus; metastasis: 1; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 1.019125833; lung met free survival (yr): 1.019125833; lms status: 0; ', 'ID: 120; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 7.9972675; lung met free survival (yr): 7.9972675; lms status: 1; ', 'ID: 131; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 8.10929; lung met free survival (yr): 8.10929; lms status: 0; ', 'ID: 243; cohort: Erasmus; metastasis: 1; lung met first event: 1; lung met all: 1; metastasis free survival (yr): 0.84153; lung met free survival (yr): 0.84153; lms status: 1; ', 'ID: 245; cohort: Erasmus; metastasis: 1; lung met first event: 1; lung met all: 1; metastasis free survival (yr): 1.874316667; lung met free survival (yr): 1.874316667; lms status: 1; ', 'ID: 632; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 5.090164167; lung met free survival (yr): 5.090164167; lms status: 1; ', 'ID: 746; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 10.22130833; lung met free survival (yr): 10.22130833; lms status: 1; ', 'ID: 755; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 8.756833333; lung met free survival (yr): 8.756833333; lms status: 0; ', 'ID: 812; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 9.704916667; lung met free survival (yr): 9.704916667; lms status: 1; ', 'ID: 838; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 7.213115; lung met free survival (yr): 7.213115; lms status: 0; ', 'ID: 872; cohort: Erasmus; metastasis: 1; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 5.729508333; lung met free survival (yr): 5.729508333; lms status: 0; ', 'ID: 248; cohort: Erasmus; metastasis: 1; lung met first event: 0; lung met all: 1; metastasis free survival (yr): 2.412568333; lung met free survival (yr): 3.662568333; lms status: 1; ', 'ID: 282; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 6.931694167; lung met free survival (yr): 6.931694167; lms status: 0; ', 'ID: 929; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 13.04098333; lung met free survival (yr): 13.04098333; lms status: 0; ', 'ID: 941; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 7.2896175; lung met free survival (yr): 7.2896175; lms status: 0; ', 'ID: 1060; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 5.939890833; lung met free survival (yr): 5.939890833; lms status: 0; ', 'ID: 1222; cohort: Erasmus; metastasis: 1; lung met first event: 1; lung met all: 1; metastasis free survival (yr): 0.598360667; lung met free survival (yr): 0.598360667; lms status: 0; ', 'ID: 1582; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 8.019125833; lung met free survival (yr): 8.019125833; lms status: 0; ', 'ID: 1487; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 5.879781667; lung met free survival (yr): 5.879781667; lms status: 0; ', 'ID: 1069; cohort: Erasmus; metastasis: 1; lung met first event: 0; lung met all: 1; metastasis free survival (yr): 1.969945; lung met free survival (yr): 2.219945; lms status: 1; ', 'ID: 1412; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 10.64480833; lung met free survival (yr): 10.64480833; lms status: 1; ', 'ID: 1455; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 5.357923333; lung met free survival (yr): 5.357923333; lms status: 0; ', 'ID: 1482; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 7.193989167; lung met free survival (yr): 7.193989167; lms status: 1; ', 'ID: 1497; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 9.95355; lung met free survival (yr): 9.95355; lms status: 1; ', 'ID: 1501; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 6.142076667; lung met free survival (yr): 6.142076667; lms status: 0; ', 'ID: 1524; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 5.696721667; lung met free survival (yr): 5.696721667; lms status: 0; ', 'ID: 1416; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 8.86885; lung met free survival (yr): 8.86885; lms status: 0; ', 'ID: 1535; cohort: Erasmus; metastasis: 1; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 3.469945; lung met free survival (yr): 3.469945; lms status: 1; ', 'ID: 1563; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 8.606558333; lung met free survival (yr): 8.606558333; lms status: 1; ', 'ID: 1568; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 9.587433333; lung met free survival (yr): 9.587433333; lms status: 0; ', 'ID: 1571; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 6.360655833; lung met free survival (yr): 6.360655833; lms status: 1; ', 'ID: 1593; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 10.57104167; lung met free survival (yr): 10.57104167; lms status: 1; ', 'ID: 1622; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 10.92895833; lung met free survival (yr): 10.92895833; lms status: 0; ', 'ID: 1650; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 7.327869167; lung met free survival (yr): 7.327869167; lms status: 0; ', 'ID: 1661; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 6.737705; lung met free survival (yr): 6.737705; lms status: 0; ', 'ID: 1555; cohort: Erasmus; metastasis: 1; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 0.765027333; lung met free survival (yr): 0.765027333; lms status: 1; ', 'ID: 1589; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 10.84153333; lung met free survival (yr): 10.84153333; lms status: 1; ', 'ID: 854; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 5; lung met free survival (yr): 5; lms status: 1; ', 'ID: 1821; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 7.3196725; lung met free survival (yr): 7.3196725; lms status: 0; ', 'ID: 1828; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 8.565575; lung met free survival (yr): 8.565575; lms status: 0; ', 'ID: 1858; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 7.385245833; lung met free survival (yr): 7.385245833; lms status: 1; ', 'ID: 1853; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 5.218579167; lung met free survival (yr): 5.218579167; lms status: 0; ', 'ID: 1871; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 7.177595833; lung met free survival (yr): 7.177595833; lms status: 0; ', 'ID: 1938; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 7.489070833; lung met free survival (yr): 7.489070833; lms status: 1; ', 'ID: 1939; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 12.62568333; lung met free survival (yr): 12.62568333; lms status: 1; ', 'ID: 1949; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 9.286883333; lung met free survival (yr): 9.286883333; lms status: 0; ', 'ID: 1966; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 5.122950833; lung met free survival (yr): 5.122950833; lms status: 1; ', 'ID: 1967; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 6.644808333; lung met free survival (yr): 6.644808333; lms status: 0; ', 'ID: 1976; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 6.060109167; lung met free survival (yr): 6.060109167; lms status: 1; ', 'ID: 1978; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 5.748634167; lung met free survival (yr): 5.748634167; lms status: 0; ', 'ID: 2001; cohort: Erasmus; metastasis: 1; lung met first event: 1; lung met all: 1; metastasis free survival (yr): 0.363388; lung met free survival (yr): 0.363388; lms status: 1; ', 'ID: 2007; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 7.6010925; lung met free survival (yr): 7.6010925; lms status: 1; ', 'ID: 2021; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 7.595628333; lung met free survival (yr): 7.595628333; lms status: 0; ', 'ID: 2025; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 6.909835833; lung met free survival (yr): 6.909835833; lms status: 1; ', 'ID: 2038; cohort: Erasmus; metastasis: 0; lung met first event: 0; lung met all: 0; metastasis free survival (yr): 8.513658333; lung met free survival (yr): 8.513658333; lms status: 1; ', 'ID: 2024; cohort: Erasmus; metastasis: 1; lung met first event: 1; lung met all: 1; metastasis free survival (yr): 1.800546667; lung met free survival (yr): 1.800546667; lms status: 0; ' GSE130703 Homo sapiens 12 Genome binding/occupancy profiling by high throughput sequencing GPL18573 GATA3 mutation disrupts functional network governed by Estrogen receptor, FOXA1 and GATA3 2019-05-03 Estrogen Receptor (ER) is a steroid hormone receptor that regulates epithelial genes in breast cancer. ER forms a regulatory network with the other transcription factors, FOXA1 and GATA3. GATA3 is known to be capable of specifying chromatin localization of FOXA1 and ER. GATA3 has been identified as one of the most frequently mutated genes in breast cancer. However, how GATA3 mutations impact this transcriptional network is unknown. Here we investigate the function of one of the recurrent patient-derived GATA3 mutations (R330fs) for this regulatory network. Genomic analysis indicates that the R330fs mutant can disrupt the cooperative action of ER, FOXA1, and GATA3, and induce chromatin relocalization of these factors. Relocalizations of ER and FOXA1 are associated with altered chromatin architectures leading to differential gene expression in the GATA3 mutant cells. These results suggest the active role of GATA3 mutants in ER positive breast tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130703 Cancer-specific mutation of GATA3 disrupts the transcriptional regulatory network governed by Estrogen Receptor alpha, FOXA1 and GATA3. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkaa179 {Nucleic acids research (11.147): 10.1093/nar/gkaa179} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA541008 https://www.ebi.ac.uk/ena/browser/view/PRJNA541008 https://www.ncbi.nlm.nih.gov/sra?term=SRP194971 [Overal design]Genome-wide mapping of chromatin architectures in GATA3 mutant T47D cells; [Treatment]'None'; [Growth]'Cells were grown on 15 cm plats in high glucose DMEM medium with 10% FBS'; [Extraction]'Cells were treated with a hypotonic buffer, and lysed with Tris-HCl pH 8.0 based buffer with appropriate concentration of SDS. Chromatin fragmentation was performed by sonication with Covaris. DNA was precipitated with antibody against each target protein.\nLibraries were prepared according to BIOO SCIENTIFIC instruction.'; [Cell type]'Source: ''cell line: T47D; genotype/variation: T47D Flp control cells; passages: <10; antibody: anti-H3K4me1 (abcam, ab8895); ', 'cell line: T47D; genotype/variation: T47D wt/R330fsl cells; passages: <10; antibody: anti-H3K4me1 (abcam, ab8895); ', 'cell line: T47D; genotype/variation: T47D Flp control cells; passages: <10; antibody: anti-H3K27me3 (abcam, ab192985); ', 'cell line: T47D; genotype/variation: T47D wt/R330fsl cells; passages: <10; antibody: anti-H3K27me3 (abcam, ab192985); ', 'cell line: T47D; genotype/variation: T47D Flp control cells; passages: <10; antibody: anti-H3K27ac (abcam, ab4729); ', 'cell line: T47D; genotype/variation: T47D wt/R330fsl cells; passages: <10; antibody: anti-H3K27ac (abcam, ab4729); ' GSE28544 Homo sapiens 56 Expression profiling by array; Non-coding RNA profiling by array GPL6244; GPL10850 Expression Profiling of Inflammatory Breast Cancer Cells Treated with the Novel Histone Deacetylase Inhibitor, CG-1521 2011-04-12 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28544 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA139055 https://www.ebi.ac.uk/ena/browser/view/PRJNA139055 None [Overal design]Refer to individual Series; [Treatment]'SUM149PT cells were plated at 1.5 x 10^6 cells per 150 x 25mm dish with 25mL of growth media, and allowed to adhere for 48h prior to treatment. The media in each plate was replaced with 25mL fresh media containing the drug treatment.', 'SUM190PT cells were plated at 1.5 x 10^6 cells per 150 x 25mm dish with 25mL of growth media containing 2%FBS and allowed to adhere for 24h. The media in each plate was then replaced with 25mL fresh media without FBS. After another 24h, each treatment was prepared at 6x concentration, so that 5mL of treatment solution was added to the 25mL growth media.'; [Growth]"SUM149PT cells were grown in Ham's F-12 media with 5% fetal bovine serume supplemented with 5 µg/mL insulin, 1 µg/mL hydrocortisone, 10 mM HEPES and Antimycotic/Antibiotic at 37°C with 5%CO2 and 85% humidity.", "SUM190PT cells were grown in Ham's F-12 media supplemented with 5 µg/mL insulin, 1 µg/mL hydrocortisone, 10 mM HEPES, 5mM Ethanolamine, 5µg/mL Transferrin, 10nM Triiodo Thyronine, 50nM Sodium Selenite, 1g/L Bovine Serum Albumin and Antibiotic/Antimycotic at 37° with 5% CO2 and 85% Humidity."; [Extraction]'Total RNA was extracted using the RNeasy Mini kit (Qiagen Inc., Valencia, CA, USA). RNA quality and concentration was determined by analysis with an Agilent 2100 bioanalyzer at the Center for Functional Genomics at State University of New York at Albany (Rensselaer, NY, USA)', 'Total RNA was extracted using the miRNeasy Mini kit (Qiagen Inc., Valencia, CA, USA). RNA quality and concentration was determined by analysis with an Agilent 2100 bioanalyzer at the Center for Functional Genomics at State University of New York at Albany (Rensselaer, NY, USA)'; [Cell type]'Source: ''cell line: SUM149PT; er: ER(-); p53: mut (M237I); ', 'cell line: SUM190PT; er: ER(-); p53: mut (Q317X); ' GSE26083 Homo sapiens 4 Genome binding/occupancy profiling by high throughput sequencing GPL9052 Genome-wide maps of Tamoxifen resistance MCF7 cell line 2010-12-15 We report the ER alpha regulatory network of Tamoxifen resistance MCF7 cell line using the Chromatin immunoprecipitated high-throughput sequencing technology (ChIP-seq). By Integrating the gene expression data (previously reported) with the ChIP-seq data, we generated ER alpha regulatory network and pathways. For ER alpha regulatory network, hub TFs with enriched motifs were identified from ER alpha peak together with PolII peaks. We then scan the position weight matrix (PWM) of ER alpha peak region of certain gene to find out the regulatory relationship between hub TF and normal TF. For regulatory pathway, genes were grouped base on their expression value at 4 different time point. Then the hub TF that plays important role in each time point of each group was identified. This study provides a framework for the application of ChIP-seq and gene expression data for the construction of ER alpha regulatory network. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26083 Inference of hierarchical regulatory network of estrogen-dependent breast cancer through ChIP-based data. BMC systems biology 2.048 https://doi.org/10.1186/1752-0509-4-170 {BMC systems biology (2.048): 10.1186/1752-0509-4-170} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA135221 https://www.ebi.ac.uk/ena/browser/view/PRJNA135221 https://www.ncbi.nlm.nih.gov/sra?term=SRP004916 [Overal design]4 different ChIP-seq dataset in Tamoxifen resistance MCF7 cell line; [Treatment]'MCF7-T cells were treated with E2 (108 mol/L) for 3 hours'; [Growth]'MCF7-T cells were maintained in a hormone-free medium (phenol red–free MEM with 2 mmol/L L-glutamine, 0.1 mmol/L nonessential amino acids, 50 units/mL penicillin, 50 Ag/mL streptomycin, 6 ng/mL insulin, and 10% charcoal-stripped FBS) supplemented with 10-7 mol/L 4-hydroxytamoxifen for 1 week to deplete any residual OHT, and then MCF7-T cells were cultured in hormone-free basal medium (phenol-red free MEM with 2 mM L-glutamine, 0.1 mM non-essential amino acids, 50 units/ml penicillin, 50 μg/ml streptomycin, and 3% charcoal-dextran stripped FBS) for three days.'; [Extraction]'cells were crosslinked with 1% formaldehyde for 10 min, at which point 0.125 M glycine was used to stop the crosslinking. In brief, after crosslinking, cells were treated by lysis buffers and sonicated to fragment the chromatin to a size range of 200bp-1kb.'; [Cell type]'Breast cancer cell''cell type: Breast cancer cell; cell line: MCF7, tamoxifen resistance; agent: untreated; chip antibody: PolII; vendor: Santa Cruz Biotechnology; catalog number: sc-899; ', 'cell type: Breast cancer cell; cell line: MCF7, tamoxifen resistance; agent: E2 treated; chip antibody: PolII; vendor: Santa Cruz Biotechnology; catalog number: sc-899; ', 'cell type: Breast cancer cell; cell line: MCF7, tamoxifen resistance; agent: untreated; chip antibody: ER; vendor: Santa Cruz Biotechnology; catalog number: sc-8005; ', 'cell type: Breast cancer cell; cell line: MCF7, tamoxifen resistance; agent: E2 treated; chip antibody: ER; vendor: Santa Cruz Biotechnology; catalog number: sc-8005; ' GSE101927 Homo sapiens 42 Expression profiling by high throughput sequencing GPL10999 Ancestry as a potential modifier of gene expression in breast tumors from Colombian women 2017-07-26 Background: Differences in breast cancer outcomes according to race/ethnicity have been reported. Hispanic/Latino (H/L) populations are a genetically admixed and heterogeneous group, with variable fractions of European, Indigenous American and African ancestries. Some studies suggest that breast cancer-specific mortality is higher in U.S. Hispanic/Latinas compared to non-Hispanic Whites (NHW) even after adjustment for socioeconomic status and education. The molecular profile of breast cancer has been widely described in NHWs but equivalent knowledge is lacking in Hispanic/Latinas. We have previously reported that the most prevalent breast cancer intrinsic subtype in Colombian H/L women was Luminal B as defined by surrogate St. Gallen 2013 criteria. In this study we explored ancestry-associated differences in molecular profiles of Luminal B tumors among these highly admixed women. Methods: We performed whole-transcriptome RNA-seq analysis in 42 Luminal tumors (21 Luminal A and 21 Luminal B) from Colombian women. Genetic ancestry was estimated from a panel of 80 ancestry-informative markers (AIM). We categorized patients according to Luminal subtype and to the proportion of European and Indigenous American ancestry and performed differential expression analysis comparing Luminal B against Luminal A tumors according to the assigned ancestry groups. Results: We found 5 genes potentially modulated by genetic ancestry: ERBB2 (Fold Change = 2.367, padj < 0.01), GRB7 (Fold Change = 2.327, padj < 0.01), GSDMB (Fold Change = 1.723, padj < 0.01, MIEN1 (Fold Change = 2.195, padj < 0.01 and ONECUT2 (Fold Change = 2.204, padj < 0.01). In the replication set we found a statistical significant association between European ancestry fraction and the expression levels of ERBB2 (p = 0.02, B = 2.49) and ONECUT2 (p = 0.04, B = -4.87). We also observed statistical significant associations for ERBB2 expression with Indigenous American ancestry (p < 0.001, B = 3.82). This association was not biased by the distribution of HER2+ tumors among the groups analyzed. Conclusions: Our results suggest that genetic ancestry in Hispanic/Latina women might modify ERBB2 gene expression in Luminal tumors. Further analyses are needed to confirm these findings and explore their prognostic value. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE101927 Ancestry as a potential modifier of gene expression in breast tumors from Colombian women. PloS one 2.776 https://doi.org/10.1371/journal.pone.0183179 {PloS one (2.776): 10.1371/journal.pone.0183179} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA395937 https://www.ebi.ac.uk/ena/browser/view/PRJNA395937 https://www.ncbi.nlm.nih.gov/sra?term=SRP113639 [Overal design]RNA profile of 42 luminal breast cancer tumors (21 luminal A and 21 luminal B) from Colombian patients; [Treatment]'None'; [Growth]'None'; [Extraction]'Hematoxylin and eosin-stained slides were evaluated by a pathologist to estimate the percentage of tumor present in the paraffin block selected. For cases with more than 60% of tumor content, five 10µm sections were used for RNA extraction. For cases with less than 60% of tumor content, areas that contained tumor were marked to obtain 5 tumor cores using a 1-mm punch needle. RNA extraction was done using the RecoverAll™ Total Nucleic Acid Isolation Kit (Life Technologies®) following the manufacturer’s recommendations.\nLibrary preparation was performed from 1µg of total RNA using the TruSeq® Stranded RNA Sample Preparation kit (Illumina Inc., San Diego, CA). Briefly, isolated RNA was depleted of ribosomal RNA using the rRNA Removal Mix provided by the kit. Random hexamers were used for cDNA synthesis. Subsequently, cDNA was subjected to end repair, adapter ligation and size selection using AMPure XP beads (Beckman Coulter Inc., Brea, CA). Fragmentation step was omitted due to the sample quality, as recommended by the protocol. Libraries were quantified by Qubit dsDNA HS Assay Kit (Life Technologies, Carlsbad, CA) and the validation of the library size was performed in an Agilent Bioanalyzer using a DNA 1000 kit (© Agilent Technologies) to verify the presence of a 260 base pair fragment'; [Cell type]'Source: ''tissue: breast tumor; intrinsic subtype: Luminal A; ', 'tissue: breast tumor; intrinsic subtype: Luminal B; ' GSE82172 Homo sapiens 152 Expression profiling by array GPL13158 Expression data from primary breast tumors, M0 patients 2016-06-02 Expression data were used to predict the activity status of diverse pathways, which were compared to Tamoxifen response 152 samples from 135 unique breast cancer patients were used to establish the activity of transcriptomic pathways. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE82172 ER and PI3K Pathway Activity in Primary ER Positive Breast Cancer Is Associated with Progression-Free Survival of Metastatic Patients under First-Line Tamoxifen. Cancers 6.162 https://doi.org/10.3390/cancers12040802 {Scientific reports (4.011) doi:10.1038/s41598-017-02296-w}; {Cancers (6.162) doi:10.3390/cancers12040802}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA324253 https://www.ebi.ac.uk/ena/browser/view/PRJNA324253 None [Overal design]Comparison of response to Tamoxifen; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted with RNABee (Campro, Veenendaal, the Netherlands) according to the manufacturer procedure'; [Cell type]'Source: ''response: CR; ', 'response: PR; ', 'response: SD; ', 'response: PD; ' GSE15412 Saccharomyces cerevisiae 4 Expression profiling by array GPL4069 Yeast response to the DNA damaging beta-lapachone 2009-03-26 β-lapachone (b-lap) is an anticancer agent that selectively induces cell death in human cancer cells. A mechanism for b-lap cytotoxicity was shown to be mediated by the NQO1 NAD(P)H dehydrogenase and radical oxygen species (ROS) generation in several tumour cells. To further characterise the molecular effects of b-lap action, we compared the gene expression profile of yeast cells treated or not with b-lap using cDNA microarrays. Genes involved in tolerance to oxidative stress were enriched in the set of differentially expressed genes. Accordingly, b-lap treatment generated reactive oxygen species (ROS), which were efficiently blocked by dicoumarol, and inhibitor of NADH dehydrogenases (NADH-DH). In addition, a mutant defective in the mitocondrial NADH dehydrogenase Nde2p was found to be resistant to b-lap treatment, thus resembling tumour cell responses to b-lap exposure. However, b-lap treatment elicited similar ROS production in WT and nde2 cells, and dicoumarol did not affect cell viability in b-lap treated yeasts. Most interestingly, DNA damage responses triggered by b-lap were abolished in the nde2 mutant. Furthermore, the nde2 mutant was sensitive to DNA damaging agents other than b-lap. These data indicated that ROS production did not mediate b-lap cytotoxicity and highlighted a role of Nde2p in DNA damage checkpoints. Amino acid biosynthesis genes were also differentially expressed in b-lap treated cells, suggesting that b-lap exposure somehow triggered the General Control of Nutrients (GCN) pathway. Supporting this, b-lap treatment increased phosphorylation of eIF2 alpha in a Gcn2p-dependent manner. eIF2alpha phosphorylation required Gcn1p and Gcn20p and surprisingly Nde2p. Gcn2p was also shown to be required for the G1 checkpoint triggered by b-lap and for cell survival. Remarkably, b-lap treatment also increased phosphorylation of eIF2 alpha in breast tumour cells, which was partially dependent on the Nde2p orthologue AMID. These findings i) suggest that Gcn2p and Nde2p are key determinants of b-lap toxicity in yeast and human cells, ii) uncover a new functional connection between Nde2p, Gcn2p and DNA damage checkpoints conserved throughout evolution and iii) suggest that pharmacological modulation of Gcn2p could provide an effective strategy for antitumour drug discovery. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15412 eIF2 kinases mediate β-lapachone toxicity in yeast and human cancer cells. Cell cycle (Georgetown, Tex.) 3.259 https://doi.org/10.4161/15384101.2014.994904 {Cell cycle (Georgetown, Tex.) (3.259): 10.4161/15384101.2014.994904} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA117087 https://www.ebi.ac.uk/ena/browser/view/PRJNA117087 None [Overal design]Direct comparison between wt samples and b-lapachone treated-wt samples. Four biological replicates. Dye was swapped in two of them; [Treatment]'Cells were grown at 28ºC in YPD rich medium until Ab660=0.6. 50 ml of yeast culture was treated with vehicle (1% DMSO) for 1 hour. Cells were then harvested by centrifugation and washed with cold water. Dried cell pellet was kept at-80 until RNA purification', 'Cells were grown at 28ºC in YPD rich medium until Ab660=0.6. 50 ml of yeast culture was treated with 10 ug/ml b-lapachone in DMSO for 1 hour. Cells were then harvested by centrifugation and washed with cold water. Dried cell pellet was kept at-80 until RNA purification'; [Growth]'None'; [Extraction]'standard protocol (acid-phenol extraction).'; [Cell type]'Source: ''strain: by4741; genotype: : MATa, his3Δ1, leu2Δ0, LYS2, met15Δ0, ura3Δ0; ' GSE85351 Mus musculus; Homo sapiens 2 Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing GPL16791; GPL17021 DNA methylation repels binding of hypoxia-inducible transcription factors to maintain tumour immunotolerance [ChIPBS] 2016-08-09 Background: Hypoxia is pervasive in cancer and other diseases. Cells sense and adapt to hypoxia by activating hypoxia-inducible transcription factors (HIFs), but it is still an outstanding question why cell types differ in their transcriptional response to hypoxia. Results: Here, we report that HIFs fail to bind CpG dinucleotides that are methylated in their consensus binding sequence, both in in vitro biochemical binding assays and in vivo studies of differentially methylated isogenic cell lines. Based on in silico structural modelling, we show that 5-methylcytosine indeed causes steric hindrance in the HIF binding pocket. A model wherein cell-type-specific methylation landscapes, as laid-down by the differential expression and binding of other transcription factors under normoxia control cell-type-specific hypoxia responses is observed. We also discover ectopic HIF binding sites in repeat regions which are normally methylated. Genetic and pharmacological DNA demethylation, but also cancer-associated DNA hypomethylation, expose these binding sites, inducing HIF-dependent expression of cryptic transcripts. In line with such cryptic transcripts being more prone to cause double-stranded RNA and viral mimicry, we observe low DNA methylation and high cryptic transcript expression in tumours with high immune checkpoint expression, but not in tumours with low immune checkpoint expression, where they would compromise tumour immunotolerance. In a low-immunogenic tumour model, DNA demethylation upregulates cryptic transcript expression in a HIF-dependent manner, causing immune activation and reducing tumour growth. Conclusions: Our data elucidate the mechanism underlying cell-type specific responses to hypoxia, and suggest DNA methylation and hypoxia to underlie tumour immunotolerance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE85351 DNA methylation repels binding of hypoxia-inducible transcription factors to maintain tumor immunotolerance. Genome biology 14.028 https://doi.org/10.1186/s13059-020-02087-z {Genome biology (14.028): 10.1186/s13059-020-02087-z} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA338261 https://www.ebi.ac.uk/ena/browser/view/PRJNA338261 https://www.ncbi.nlm.nih.gov/sra?term=SRP081129 [Overal design]Examination of the methylation level of the DNA fragment immunoprecipitate by HIF1b antibody in one human breast cancer cell line (MCF7) and mES Tet-TKO cell line, upon exposure to hypoxia; [Treatment]'None'; [Growth]'cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.', 'cultured feeder-free in fibroblast-conditioned medium'; [Extraction]"Cells were incubated in hypoxic conditions for 16 hours. Cultured cells were subsequently immediately fixed by adding 1% Formaldehyde (16% Formaldehyde (w/v), Methanol-free, Thermo Scientific) directly in the medium and incubating for 8 minutes. Fixed cells were incubated with 150 µM of glycine for 5 min to revert the cross-links, washed twice with ice-cold PBS 0.5% Triton-X100, scraped and collected by centrifugation (1000 ×G 5min at 4°C). The pellet was resuspended in 1400 µL of RIPA buffer (50 mM Tris-HCl pH 8, 150 mM NaCl, 2 mM EDTA pH 8, 1% Triton-X100, 0.5% Sodium deoxycholate, 1% SDS, 1% protease inhibitors) and transferred in a new eppendorf tube. The chromatin was sonicated for 3 min by using a Branson 250 Digital Sonifier with 0.7 s 'On' and 1.3 s 'Off' pulses at 40% power amplitude, yielding a size of 100 to 500 bp. The sample was kept ice-cold at all times during the sonication. The samples were centrifuged (10 min at 16000 ×G at 4°C) and the supernatant were transferred in a new eppendorf tube. The protein concentration was assessed using a BCA assay. Fifty µL of shared chromatin was used as “input” and 1.4 µg of primary ARNT/HIF-1β monoclonal antibody (NB100-124, Novus) per 1 mg of protein was added to the remainder of the chromatin, and incubated overnight at 4°C in a rotator. Pierce Protein A/G Magnetic Beads (Life Technologies) were added to the samples in a volume that is 4X the volume of the primary Ab and incubated at 4°C for at least 5 hours. A/G Magnetic Beads were collected and the samples were washed 5 times with the washing buffer (50 mM Tris-HCl, 200 mM LiCl, 2 mM EDTA, pH 8, 1% Triton, 0.5% Sodium deoxycholate, 0.1% SDS, 1% protease inhibitors), and twice with TE buffer. The A/G magnetic beads were resuspended in 50 µL of TE buffer, and 1.5 µL of RNAse A (200 units, NEB, Ipswich, MA, USA) were added to the A/G beads samples and to the input, incubated for 10 minutes at 37°C. After addition of 1.5 µL of proteinase K (200 units) and overnight incubation at 65°C, the DNA was purified using 1.8´ volume of Agencourt AMPure XP (Beckman Coulter) according to the manufactory instructions\nDNA libraries were prepared using methylated adapters and the NEBNext DNA library prep master mix set following manufacturer recommendations. DNA libraries were bisulfite converted using the EZ DNA Methylation-Lightning™ kit (Zymo) prior to library amplification using HiFi Uracil+ (KAPA)."; [Cell type]'Beast cancer cell line', 'Embryonic Stem Cells''cell line: MCF7; cell type: Beast cancer cell line; treatment: 0.5% O2 16h; type of sample: ChIP-BS; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); ', 'cell type: Embryonic Stem Cells; treatment: 0.5% O2 16h; type of sample: ChIP-BS; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); ' GSE13225 Mus musculus 6 Expression profiling by array GPL1261 (AKR/J x FVB/NJ)F1 versus (DBA/2J x FVB)F1 spleen expression data 2008-10-16 F1 hybrids from (AKR/J x FVB/NJ) and (DBA/2J x FVB/NJ) outcrosses display a 20-fold difference in mammary tumor metastatic capacity, due to differences in inherited polymorphisms. Expression studies were performed to determine whether polymorphism-driven gene expression signatures predictive of outcome could be generated from normal tissues Keywords: Basal transcription profiles https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE13225 The origins of breast cancer prognostic gene expression profiles. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-08-3520 {Cancer research (8.378): 10.1158/0008-5472.CAN-08-3520} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA114047 https://www.ebi.ac.uk/ena/browser/view/PRJNA114047 None [Overal design]Spleen from adult F1 animals from (AKR/J x FVB/NJ) and (DBA/2J x FVB/NJ) outcrosses was collected and arrayed on Affymetrics chip to identify basal differences in gene expression between the different genotypes; [Treatment]'animals were euthanized by cervical dislocation under Avertin anesthesia. Tissue was snap frozen in LN2 prior to RNA extraction'; [Growth]'None'; [Extraction]'RNA was extracted by Trizol following the manufacturers suggested protocol.'; [Cell type]'Source: ''' GSE9354 Mus musculus 8 Expression profiling by array GPL339 ETV6-NTRK3 fusion oncoprotein transduces NIH 3T3 cells 2007-10-17 We report a mouse model that recapitulates expression of the ETV6-NTRK3 (EN) fusion oncoprotein, the product of the t(12;15)(p13;q25) translocation characteristic of human secretory breast carcinoma. Activation of EN expression in mammary tissues by Whey acidic protein (Wap) promoter-driven Cre leads to fully penetrant, multifocal malignant breast cancer with short latency. We provide genetic evidence that committed bipotent or CD61+ luminal alveolar progenitors, are targets of tumorigenesis. Furthermore, EN transforms these otherwise transient progenitors through activation of the AP1 complex. To study the initial effects of ETV6-NTRK3 (EN) mediated transformation, we retrovirally transduced NIH 3T3 cells and generated microarray expression profiling data of EN transduced 3T3 cells as well as control 3T3 cells. Using gene set enrichment analysis (GSEA), we identified a signature involving the AP1 transcriptional complex in EN transduced 3T3 cells. Keywords: genetic modification, cell type comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE9354 ETV6-NTRK3 fusion oncogene initiates breast cancer from committed mammary progenitors via activation of AP1 complex. Cancer cell 23.916 https://doi.org/10.1016/j.ccr.2007.11.012 {Cancer cell (23.916): 10.1016/j.ccr.2007.11.012} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA103047 https://www.ebi.ac.uk/ena/browser/view/PRJNA103047 None [Overal design]We retrovirally transduced NIH 3T3 cells with either EN, or controls (either the empty vector or a kinase-dead version of EN with a mutation at the kinase domain of NTRK3). We then prepared total RNAs from these cells and collected microarray expression profiling data from them using Affymetrix mouse MOE430A chips.; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNAs were extracted by using Trizol following the manufacturar's instruction."; [Cell type]'Source: ''' GSE147929 Mus musculus 8 Expression profiling by high throughput sequencing GPL13112 Myocardial Infarction accelerates breast cancer progression via innate immune reprogramming (RNA-seq: sham vs LAD ligation) 2020-04-01 Breast cancer patients have increased risk of myocardial infarction (MI), but whether these events impact cancer pathogenesis is not known. In mouse models of breast cancer, MI increased circulating Ly6Chigh monocytes and their recruitment to tumors, accelerating cancer progression and metastasis. Analysis of the bone marrow reservoir revealed that MI epigenetically reprogrammed Ly6Chigh monocytes to an immunosuppressive phenotype that was maintained in monocytes in the circulation and tumor at the transcriptional level. Depletion of Ly6Chigh monocytes abrogated MI-induced cancer progression and increased activated cytotoxic T cells in the tumor. In early-stage breast cancer patients, post-diagnosis incident cardiovascular events, such as MI, increased the risk of recurrence and cancer-specific mortality, highlighting the clinical relevance of our findings. Collectively, our results indicate that MI induces cross-disease communication that accelerates breast cancer progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE147929 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA622560 https://www.ebi.ac.uk/ena/browser/view/PRJNA622560 https://www.ncbi.nlm.nih.gov/sra?term=SRP254927 [Overal design]Bulk RNA sequencing of five sham samples and 3 LAD ligation samples. Bone marrow monocytes were isloated from mice 9 days following LAD ligation or sham surgery.; [Treatment]'Bone marrow monocytes were isloated from mice 9 days following LAD ligation or sham surgery.'; [Growth]'None'; [Extraction]'Cells were MACS sorted and RNA was harvested with trizol LS. RNA library preparation with polyA selection was used with 50-350 ng of total RNA for the construction of sequencing libraries.\nRNA library preparation with polyA selection'; [Cell type]'Source: ''strain: C57BL/6; age: 10-12 weeks; tissue: Bone marrow monocytes; treatment: LAD ligation; ', 'strain: C57BL/6; age: 10-12 weeks; tissue: Bone marrow monocytes; treatment: SHAM surgery; ' GSE25710 Homo sapiens 53 Genome binding/occupancy profiling by high throughput sequencing GPL9115; GPL10999 [E-MTAB-223] ChIP-seq for FOXA1, ER and CTCF in breast cancer cell lines 2010-11-30 Growth cells and map of ER, FoxA1 and CTCF binding at whole genome level. ArrayExpress Release Date: 2010-10-29 Person Roles: submitter Person Last Name: Hurtado Person First Name: Antoni Person Email: toni.hurtado@cancer.org.uk Person Affiliation: Uppsala University https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE25710 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA133829 https://www.ebi.ac.uk/ena/browser/view/PRJNA133829 https://www.ncbi.nlm.nih.gov/sra?term=ERP000380 [Overal design]Experimental Design: high_throughput_sequencing_design Experimental Design: binding_site_identification_design Experimental Factor Name: IMMUNOPRECIPITATE Experimental Factor Name: CELL_LINE Experimental Factor Type: immunoprecipitate Experimental Factor Type: cell_line; [Treatment]'None', 'Drug treatments were performed with Dox (Clontech) at 0.1 ug/ml, R5020 (Du Pont) at 10 nM or 17beta-estradiol (Sigma) at 10 mM. Dox-containing medium was changed every 24 hours to ensure optimum Dox activity. Adherent cells on tissue culture plates were incubated in fresh, warm, serum-free medium supplemented with 1% formaldehyde, at 37 C for 10 minutes. Cells were washed 2 times with cold PBS and scraped into 600 ul PBS with protease inhibitors (P8340, Sigma). Fixed cells were spun for 2 minutes at 6,000xg, washed as before and snap frozen in liquid nitrogen.'; [Growth]'grow | RPMI 1640 medium por DMEM supplemented with 10% inactivated FBS, l-glutamine and PEST at 37C with 5% CO2.'; [Extraction]'immunoprecipitate | Antibodies were from Santa Cruz Biotechnology (sc-543), abcam (ab5089 and ab23738) and Millipore (07-729) and ChIP was performed using 10e7-10e8 cells per reaction. Briefly, crosslinking of protein and DNA was done in room temperature for 10 minutes with serum free media containing 0,37 % formaldehyde. Cells were scraped and washed in PBS before treatment of cell lysis buffer with protease inhibitors on ice. Pelleted nuclei were resuspeded in RIPA buffer and a BioRuptor (Diagenode) was used to sonicate DNA. ChIP was performed with 10 micrograms of antibody. ChIP DNA was gel fractionated and amplified to create two size libraries corresponding to insert sizes of 200-300 bp. For DNase I hypersensitivity was performed as previously described (Eeckhoute et al., 2006). Digested DNA was run on a gel and the digested material (between 200bp and 500bp in size). For all ChIPs washing was done six times with RIPA buffer and once with TE-buffer and DNA-protein complexes were eluted from beads twice with 200 microlitres of 0.1 M NaHCO3 and 1 % SDS and treated with RNAseA at 65C for 6 hours and Proteinase K at 45C over night. Chromatin was amplified with Solexa protocol chromatin amplification.\nsequencing | Sequencing was carried out by the genomic service of Cambridge Research Institute-CRUK using the Illumina genome analyzer II'; [Cell type]'Source: ''material type: cell_line; cellline: MCF-7; Sex: female; diseasestate: breast cancer; chip antibody: ER; ', 'material type: cell_line; cellline: TAM_R; Sex: female; diseasestate: breast cancer; chip antibody: ER; ', 'material type: cell_line; cellline: MCF-7; Sex: female; diseasestate: breast cancer; chip antibody: FoxA1; ', 'material type: cell_line; cellline: ZR75-1; Sex: female; diseasestate: breast cancer; chip antibody: FoxA1; ', 'material type: cell_line; cellline: T-47D; Sex: female; diseasestate: breast cancer; chip antibody: FoxA1; ', 'material type: cell_line; cellline: TAM_R; Sex: female; diseasestate: breast cancer; chip antibody: FoxA1; ', 'material type: cell_line; cellline: MCF-7; Sex: female; diseasestate: breast cancer; chip antibody: CTCF; ', 'material type: cell_line; cellline: ZR75-1; Sex: female; diseasestate: breast cancer; chip antibody: ER; ', 'material type: cell_line; cellline: T74-D; Sex: female; diseasestate: breast cancer; chip antibody: ER; ', 'material type: cell_line; cellline: MCF-7; Sex: female; diseasestate: breast cancer; chip antibody: input_DNA; ', 'material type: cell_line; cellline: ZR75-1; Sex: female; diseasestate: breast cancer; chip antibody: input_DNA; ', 'material type: cell_line; cell line: T-47D; treatment: doxycycline; timepoint: 24h; Sex: female; disease state: breast cancer; chip antibody: input_DNA; ', 'material type: cell_line; cell line: T-47D; treatment: doxycycline; timepoint: 48h; Sex: female; disease state: breast cancer; chip antibody: input_DNA; ', 'material type: cell_line; cellline: TAM_R; Sex: female; diseasestate: breast cancer; chip antibody: input_DNA; ', 'material type: cell_line; cellline: MCF-7; Sex: female; diseasestate: breast cancer; chip antibody: not applicable; ' GSE119937 Homo sapiens 131 Expression profiling by high throughput sequencing GPL11154 Molecular Determinants of Post-Mastectomy Breast Cancer Recurrence 2018-09-13 Breast cancer (BC) adjuvant therapy after mastectomy in the setting of 1-3 positive lymph nodes has been controversial. This retrospective Translational Breast Cancer Research Consortium study evaluated molecular aberrations in primary cancers associated with locoregional recurrence (LRR) or distant metastasis (DM) compared to non-recurrent controls. We identified 115 HER2 negative, therapy naïve, T 1-3 and N 0-1 BC patients treated with mastectomy but no post-mastectomy radiotherapy. This included 32 LRR, 34 DM and 49 controls. RNAseq was performed on primary tumors in 110 patients; with no difference in RNA profiles between patients with LRR, DM or controls. DNA analysis on 57 primary tumors (17 LRR, 15 DM and 25 controls) identified significantly more NF1 mutations and mitogen activated protein kinase (MAPK) pathway gene mutations in patients with LRR (24%, 47%) and DM (27%, 40%) compared to controls (0%, 0%; p<0.0001 and p=0.0070, respectively). Three patients had matched primary vs LRR samples, one patient had a gain of a NF1 mutation in the LRR. There was no significant difference between the groups for PTEN loss or cleaved caspase 3 expression. The mean percentage Ki 67 labeling index was higher in patients with LRR (29.2%) and DM (26%) versus controls (14%,p= 0.0045). In summary, mutations in the MAPK pathway, specifically NF1, were associated with both LRR and DM, suggesting that alterations in MAPK signaling are associated with a more aggressive tumor phenotype. Validation of these associations in tissues from randomized trials may support targeted therapy to reduce breast cancer recurrence. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE119937 Molecular determinants of post-mastectomy breast cancer recurrence. NPJ breast cancer 32.43 https://doi.org/10.1038/s41523-018-0089-z {NPJ breast cancer (32.43): 10.1038/s41523-018-0089-z} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA490741 https://www.ebi.ac.uk/ena/browser/view/PRJNA490741 https://www.ncbi.nlm.nih.gov/sra?term=SRP161704 [Overal design]This is a multicenter retrospective study of patients who underwent mastectomy at a participating Translational Breast Cancer Research Consortium (TBCRC) institution. Study centers included Memorial Sloan Kettering Cancer Center, University of Pittsburgh, Duke University, Dana Farber Cancer Institute, University of North Carolina at Chapel Hill, Georgetown University, University of Michigan at Ann Arbor, Vanderbilt University, University of Alabama at Birmingham and MD Anderson Cancer Center. Eligible patients included those patients who underwent mastectomy without radiation for T stage 1-3 and N stage 0-1 breast cancer, and for whom archived tissues and outcome data were available. Patients with any recurrence, loco-regional (LRR) or with distant metastasis (DM), were treated from 1997 to present time as this was felt to represent an era when treatment recommendations would be the most uniform and consistent. Patients with LRR could have a subsequent DM as long as this DM was diagnosed at least 3 months after the LRR. Patients who developed LRR after developing distant metastases were placed in the DM group. Control patients were treated from 1997 to 2007 to allow at least five years follow-up with a disease-free interval. Controls were matched to cases for age, ER/PR status, chemotherapy and endocrine therapy regimens and year of diagnosis. All patients were treated with an upfront mastectomy followed by systemic therapy if indicated, which included chemotherapy, endocrine therapy or both. Patients were ineligible if they received post-mastectomy radiation therapy, neoadjuvant chemotherapy, had a T4 primary tumor, N2 nodal disease, were HER2 positive, had positive margins after mastectomy, had fewer than 10 lymph nodes retrieved at axillary lymph node dissection, or had inadequate follow-up (<5 years) if a control patient. If specimens were available from the recurrent tumors, these were also collected for exploratory analysis.; [Treatment]'None'; [Growth]'None'; [Extraction]'After isolation, RNA was quantified by Picogreen (Invitrogen) and quality was assessed using the 2200 Tapestation (Agilent). RNA from each sample (10-100 ng) was converted in double stranded cDNA using Ovation RNA-Seq System V2 kit from Nugen. cDNA was sheared by sonication with the following conditions: Peak Incident Power 175, Duty Cycle 20%, Intensity 5, Cycles per Burst 200, and 120 seconds using Covaris E220 instrument (Covaris).\nThe sheared DNA proceeded to library prep using KAPA library prep hyper kit (KAPA) following the “with beads” manufacturer protocol. At the end of the library prep, samples were analyzed on TapeStation to verify correct fragment size and to ensure the absence of extra bands. Samples were quantified using KAPA qPCR quantification kit. DNA was pooled for capture (2-6 samples per pool).\nWe used whole exome biotin labeled probes from Roche Nimblegen (V3) and followed manufacture’s protocol for the capture step. The quality of each captured sample was analyzed on TapeStation using the DNA High Sensitivity kit and the enrichment was accessed by qPCR using specific primers designed by Roche Nimblegen. The cutoff for the enrichment was 50 fold minimum.'; [Cell type]'Source: ''sample type: Primary; primary_id: IPCT-LRR-PT262-101381-B-TU-F01; recurrence_id: IPCT-LRR-PT262-101382-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 49; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Adenocarcinoma NOS; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Recurrent; primary_id: IPCT-LRR-PT262-101381-B-TU-F01; recurrence_id: IPCT-LRR-PT262-101382-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 49; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Adenocarcinoma NOS; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: FALSE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT262-101383-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 50; t stage: T3; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 4; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT267-101384-B-TU-F01; recurrence_id: IPCT-LRR-PT267-101385-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 57; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Recurrent; primary_id: IPCT-LRR-PT267-101384-B-TU-F01; recurrence_id: IPCT-LRR-PT267-101385-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 57; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: FALSE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT267-101386-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 54; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT272-101387-B-TU-F01; recurrence_id: IPCT-LRR-PT272-101388-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 56; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Recurrent; primary_id: IPCT-LRR-PT272-101387-B-TU-F01; recurrence_id: IPCT-LRR-PT272-101388-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 56; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: FALSE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT272-101389-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 53; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT277-101390-B-TU-F01; recurrence_id: IPCT-LRR-PT277-101391-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 55; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Recurrent; primary_id: IPCT-LRR-PT277-101390-B-TU-F01; recurrence_id: IPCT-LRR-PT277-101391-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 55; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: FALSE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT277-101392-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 59; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT282-101393-B-TU-F01; recurrence_id: IPCT-LRR-PT282-101394-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 56; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Recurrent; primary_id: IPCT-LRR-PT282-101393-B-TU-F01; recurrence_id: IPCT-LRR-PT282-101394-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 56; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: FALSE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT282-101395-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 51; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 1; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT287-101396-B-TU-F01; recurrence_id: IPCT-LRR-PT287-101397-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 42; t stage: T1b; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Recurrent; primary_id: IPCT-LRR-PT287-101396-B-TU-F01; recurrence_id: IPCT-LRR-PT287-101397-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 42; t stage: T1b; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: FALSE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT287-101398-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 46; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Mixed ductal/lobular; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT292-101399-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 64; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT296-101401-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 67; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT298-101402-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 43; t stage: T2a; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT298-101403-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 41; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT302-101404-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 61; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT304-101405-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 58; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT306-101406-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 41; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT308-101407-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 83; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT308-101408-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 86; t stage: T1b; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT312-101409-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 69; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRR-PT312-101410-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 72; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 1; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRDF-8396-200345-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 42; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRDF-8397-200346-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 47; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive lobular carcinoma; grade: 1; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRDF-8398-200347-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 47; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRDF-8399-200348-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 48; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRDF-8401-200350-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 61; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRDF-8402-200351-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 88; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive lobular carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRDF-8403-200352-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 82; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRDF-8404-200353-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 60; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive lobular carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRDF-8405-200354-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 62; t stage: T1b; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52286-207734-B-TU-F01; recurrence_id: IPCT-LRRM2016-52286-207735-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 53; t stage: T1c; n stage: N1a; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: yes; progesterone receptor positive?: yes; was hormonal therapy given?: yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Recurrent; primary_id: IPCT-LRRM2016-52286-207734-B-TU-F01; recurrence_id: IPCT-LRRM2016-52286-207735-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 53; t stage: T1c; n stage: N1a; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: yes; progesterone receptor positive?: yes; was hormonal therapy given?: yes; primary: FALSE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52287-207736-B-TU-F01; recurrence_id: IPCT-LRRM2016-52287-207737-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 68; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52287-207736-B-TU-F01; recurrence_id: IPCT-LRRM2016-52287-207737-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 68; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: FALSE; with_dna: FALSE; ', 'sample type: Recurrent; primary_id: IPCT-LRRM2016-52288-207738-B-TU-F01; recurrence_id: IPCT-LRRM2016-52288-207739-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 63; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Recurrent; primary_id: IPCT-LRRM2016-52288-207738-B-TU-F01; recurrence_id: IPCT-LRRM2016-52288-207739-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 63; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: FALSE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52289-207740-B-TU-F01; recurrence_id: IPCT-LRRM2016-52289-207741-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 56; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Recurrent; primary_id: IPCT-LRRM2016-52289-207740-B-TU-F01; recurrence_id: IPCT-LRRM2016-52289-207741-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 56; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: FALSE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52290-207742-B-TU-F01; dm_id: IPCT-LRRM2016-52290-207743-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 58; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52290-207742-B-TU-F01; dm_id: IPCT-LRRM2016-52290-207743-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 58; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: FALSE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52291-207744-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 44; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52292-207745-B-TU-F01; dm_id: IPCT-LRRM2016-52292-207746-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 42; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52292-207745-B-TU-F01; dm_id: IPCT-LRRM2016-52292-207746-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 42; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: FALSE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52296-207395-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 38; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52297-207681-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 83; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive lobular carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52298-207682-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 58; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52299-207683-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 55; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52300-207684-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 67; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive lobular carcinoma; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52301-207685-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 58; t stage: T1b; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52302-207686-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 25; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52303-207687-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 62; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52304-207688-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 32; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52305-207689-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 37; t stage: T1; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52306-207690-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 83; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Mixed ductal/lobular; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52307-207691-B-TU-F01; recurrence_id: IPCT-LRRM2016-52307-207692-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 30; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Recurrent; primary_id: IPCT-LRRM2016-52307-207691-B-TU-F01; recurrence_id: IPCT-LRRM2016-52307-207692-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 30; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: FALSE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52308-207693-B-TU-F01; recurrence_id: IPCT-LRRM2016-52308-207694-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 58; t stage: T3; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Recurrent; primary_id: IPCT-LRRM2016-52308-207693-B-TU-F01; recurrence_id: IPCT-LRRM2016-52308-207694-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 58; t stage: T3; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: FALSE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52309-207695-B-TU-F01; recurrence_id: IPCT-LRRM2016-52309-207696-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 71; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Recurrent; primary_id: IPCT-LRRM2016-52309-207695-B-TU-F01; recurrence_id: IPCT-LRRM2016-52309-207696-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 71; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: FALSE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52310-207697-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 41; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Unknown; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52311-207698-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 52; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52312-207699-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 48; n stage: N0; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: Unknown; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52313-207700-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 39; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52314-207701-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 49; t stage: T1a; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52315-207702-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 73; t stage: T1b; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52316-207703-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 42; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52317-207704-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 42; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52318-207705-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 78; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; estrogen receptor positive: Yes; was hormonal therapy given?: Unknown; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52319-207706-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 41; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52320-207707-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 42; t stage: T1c; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52321-207708-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 65; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52322-207709-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 33; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52323-207396-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 41; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52324-207397-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 39; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52325-207385-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 33; t stage: T1b; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52326-207386-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 45; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive lobular carcinoma; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Unknown; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52327-207387-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 43; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52328-207388-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 48; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 1; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52329-207389-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 74; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52330-207390-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 49; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52331-207391-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 48; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52332-207392-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 44; t stage: T3; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 4; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52333-207393-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 45; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52334-207394-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 49; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive lobular carcinoma; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52343-207710-B-TU-F01; recurrence_id: IPCT-LRRM2016-52343-207711-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 66; t stage: T1; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: N; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Recurrent; primary_id: IPCT-LRRM2016-52343-207710-B-TU-F01; recurrence_id: IPCT-LRRM2016-52343-207711-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 66; t stage: T1; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: N; was hormonal therapy given?: Yes; primary: FALSE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52344-207712-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 43; t stage: T1; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 1; histology of invasive disease: Invasive ductal carcinoma; grade: 2; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRM2016-52345-207713-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 56; t stage: T2; n stage: N0; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: N; was hormonal therapy given?: No; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT595-102365-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 40; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Unknown; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT599-102367-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 65; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT601-102368-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 64; t stage: T2; n sta ge: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT603-102369-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 78; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT605-102370-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 77; n stage: N1; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT607-102371-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: DM; age group (<= 50=1, >50=2): 2; age at diagnosis: 78; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT609-102372-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 79; t stage: T1c; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive lobular carcinoma; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT611-102373-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 44; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: FALSE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT613-102374-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 44; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT615-102375-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 33; t stage: T1b; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT617-102376-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 35; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT619-102377-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 35; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT621-102378-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 34; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT623-102379-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 37; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT625-102380-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 35; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT627-102381-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 40; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT629-102382-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 38; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: No; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT631-102383-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 70; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT635-102385-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 56; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT637-102386-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 56; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT639-102387-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 41; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT641-102388-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 42; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT643-102389-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 45; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT647-102391-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 58; t stage: T2; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 3; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT649-102392-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 54; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT651-102393-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 2; age at diagnosis: 53; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT653-102394-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 53; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT655-102395-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 40; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT657-102396-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 39; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT659-102397-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: LRR; age group (<= 50=1, >50=2): 1; age at diagnosis: 40; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT661-102398-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 2; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 37; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: No; progesterone receptor positive?: No; was hormonal therapy given?: No; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT665-102400-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 2; age at diagnosis: 70; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive lobular carcinoma; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT667-102401-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: DM; age group (<= 50=1, >50=2): 1; age at diagnosis: 50; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ', 'sample type: Primary; primary_id: IPCT-LRRMSKCC-PT669-102402-B-TU-F01; eligible (0=no,1=yes,2=not perfect match): 1; group: CTL; age group (<= 50=1, >50=2): 1; age at diagnosis: 50; t stage: T1a; n stage: N1; group stage (i=1; iia=2; iib=3; iiia=4): 2; histology of invasive disease: Invasive ductal carcinoma; grade: 3; estrogen receptor positive: Yes; progesterone receptor positive?: Yes; was hormonal therapy given?: Yes; primary: TRUE; with_dna: TRUE; ' GSE136673 Homo sapiens 36 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing GPL11154 Regulation of DNA Methylation at Enhancers by TET2 Finetunes Gene Transcription in ERα-Positive Breast Cancer Cells 2019-08-30 Background: Aberrant DNA methylation is an epigenetic hallmark of most malignant tumors including breast cancer. However, the exact role of TET2-mediated DNA demethylation in ERα-positive luminal breast cancer is not well understood. Results: Here we showed by TCGA analyses that lower TET2 mRNA expression level is associated with worse clinical outcomes (i.e., overall survival) in ERα-positive but not ERα-negative breast cancer. Moreover, depletion of TET2 by CRISPR/Cas9 results in increased tumorigenesis capability of MCF7 cells in vitro. Whole genome bisulfite sequencing (WGBS) analysis revealed that DNA hypermethylation (gain-of-5mC) occurs within a subgroup of enhancers including estrogen responsive element (EREs) in MCF7 cells upon TET2 depletion. ChIP-seq and RNA-seq analysis showed that TET2 depletion impairs E2-induced ERα binding to these ‘gain-of-5mC’ EREs and gene transcription. Conclusions: Our data suggest that TET2-mediated enhancer DNA demethylation fine-tunes ERα-dependent and independent gene transcription in ERα-positive breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE136673 None None None None None 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA563038 https://www.ebi.ac.uk/ena/browser/view/PRJNA563038 https://www.ncbi.nlm.nih.gov/sra?term=SRP219798 [Overal design]We used WGBS-seq, ChIP-seq and RNA-seq to study the regulation role of TET2 on the relationship among DNA methylation, histone modification and gene transcription in ERα positive MCF7 cell line.; [Treatment]'None'; [Growth]'MCF-7 cells were cultured in Dulbecco’s Modified Eagle’s Medium (DMEM, Hyclone) supplemented with 10% fetal bovine serum (FBS, Gibco) and 100 U/ml penicillin/streptomycin (Invitrogen).For estrogen stimulation, MCF-7 cells were cultured in phenol red-free RPMI 1640 medium (HyClone) plus 10% charcoal-depleted FBS (Biological Industries) for 5 days and followed by EtOH or E2 (1nM) treatment for 24 hours.'; [Extraction]'Lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody.\nLibrary preparation and sequencing procedures were carried out as described previously according to Illumina protocols with minor modifications (Illumina, San Diego).', 'RNA samples were prepared by RNeasy minikit (Qiagen). Depletion of rRNA was carried out using ribo-zero kit (Epicentre).\nBarcoded RNA-seq libraries were constructed using NEBNext ultra directional RNA library prep kit for Illumina according to the manufacturer’s instructions (New England Biolabs).', 'DNA (1 mg) with 0.5% non-methylated DNA spike-in was sheared by Covaris M220 instrument to an average size of 350 bp in length.\nDNA was then end-repaired, dA-tailed, and ligated with methylated adaptors. Bisulfite conversion was carried out using an EpiTect fast bisulfite conversion kit (Qiagen) according to the manufacturer’s instructions. Twenty minutes were used in both conversion steps. Bisulfite-converted DNA was then amplified with five PCR cycles to obtain the final library.'; [Cell type]'Source: ''genotype: wild type; chip antibody: anti-ERα, Cell Signaling Technology, 8644S; ', 'genotype: wild type; chip antibody: none; ', 'genotype: TET2 knockout; chip antibody: anti-ERα, Cell Signaling Technology, 8644S; ', 'genotype: TET2 knockout; chip antibody: none; ', 'genotype: wild type; chip antibody: anti-H3K27Ac, Active Motif, 39133; ', 'genotype: wild type; chip antibody: anti-H3K4me1, Active Motif, 39297; ', 'genotype: TET2 knockout; chip antibody: anti-H3K27Ac, Active Motif, 39133; ', 'genotype: TET2 knockout; chip antibody: anti-H3K4me1, Active Motif, 39297; ', 'genotype: wild type; ', 'genotype: TET2 knockout; ' GSE19940 Homo sapiens 30 Expression profiling by array GPL5175; GPL5188 Human Negative Elongation Factor Activates Transcription and Regulates Alternative Transcription Initiation 2010-01-19 The human Negative Elongation Factor (NELF) is a four-subunit protein complex that inhibits the movement of RNA polymerase II (RNAPII) at an early elongation stage in vitro. NELF-mediated stalling of RNAPII also attenuates transcription of a number of inducible genes in human cells. To obtain a genome-wide understanding of human NELF-mediated transcriptional regulation in vivo, we carried out an exon-array study in T47D breast cancer cells with transient siRNA knockdown of individual NELF subunits. Upon depletion of NELF-A, -C, or -E, the vast majority of NELF-regulated genes were down-regulated. Many of the down-regulated genes encode proteins that play key roles in cell cycle progression. Consequently, NELF knockdown resulted in significant reduction in DNA synthesis and cell proliferation. Chromatin immunoprecipitation showed that NELF knockdown led to dissociation of RNAPII from the promoter-proximal region of the cell cycle-regulating genes. This was accompanied by decreased histone modifications associated with active transcription initiation (H3K9Ac) and elongation (H3K36Me3), as well as reduced recruitment of the general transcription factor TFIIB and increased overall histone occupancy at a subset of the down-regulated promoters. Lastly, our study indicates that NELF regulates alternative transcription initiation of Basigin gene (BSG) by differentially influencing RNAPII density at the two neighboring exons at the 5’ end of the gene. Taken together, our data suggest a diverse transcriptional consequence of NELF-mediated RNAPII pausing in the human genome. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE19940 Human negative elongation factor activates transcription and regulates alternative transcription initiation. The Journal of biological chemistry 4.106 https://doi.org/10.1074/jbc.M109.084285 {The Journal of biological chemistry (4.106): 10.1074/jbc.M109.084285} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA122633 https://www.ebi.ac.uk/ena/browser/view/PRJNA122633 None [Overal design]Gene expression analysis of RNA samples from NELF-depleted T47D breast cancer cell line. We analyzed gene expression of T47D cells transfected with siRNAs for control and each of the four NELF subunits by exon array. Each knockdown condition contains three technical repeats. Differentially expressed genes and exons between knockdown of the individual NELF subunits and the control are analyzed by the Arrayassist software from Stratagene. The commonly affected genes and exons among all four NELF subunits knockdown samples are chosen for further studies.; [Treatment]'Transfection of the siRNA duplex into T47D cells was carried out by using RNAiMAX reagent (Invitrogen, Carlsbad, CA) according to manufacturer’s instructions. Briefly, 1.5 x 10^6 cells in a 10 cm culture dish were transfected with 10 nM of siRNA duplex with 15 ul of RNAiMAX reagent. Growth medium was replenished 48 hours after transfection, and cells were allowed to grow for additional 48 hours before harvest.'; [Growth]'siRNA transfected T47D cells are grown in DMEM with 10% FBS.'; [Extraction]"Total RNA is extracted with Trizol reagent (Invitrogen) following manufacturer's protocol."; [Cell type]'breast cancer''cell line: T47D; cell type: breast cancer; sirna: siControl against luciferase; ', 'cell line: T47D; cell type: breast cancer; sirna: siNELF-A; ', 'cell line: T47D; cell type: breast cancer; sirna: siNELF-B; ', 'cell line: T47D; cell type: breast cancer; sirna: siNELF-C; ', 'cell line: T47D; cell type: breast cancer; sirna: siNELF-E; ' GSE110770 Mus musculus 2 Expression profiling by high throughput sequencing GPL13112 Profiling of differential RNAs in LY500307-treated 4T1 cells and control cells 2018-02-18 In this study, we examined the differential RNA profile of LY500307-treated 4T1 cells compared with control-treated 4T1 cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE110770 Pharmacological activation of estrogen receptor beta augments innate immunity to suppress cancer metastasis. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1803291115 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1803291115} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA434514 https://www.ebi.ac.uk/ena/browser/view/PRJNA434514 https://www.ncbi.nlm.nih.gov/sra?term=SRP133037 [Overal design]We used RNA sequencing to compare the differential RNAs of LY500307-treated 4T1 cells compared with control-treated 4T1 cells; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA extracted using Trizol by following manufacturer’s instruction (Invitrogen).\nRNA libraries were constructed by using rRNA-depleted RNAs with TruSeq Stranded Total RNA Library Prep Kit (Illumina, San Diego, CA,\xa0 USA) according to the manufacturer’s instructions. Libraries were controlled for quality and quantified using\xa0 the BioAnalyzer 2100 system (Agilent Technologies, Inc., USA).'; [Cell type]'Source: ''treatment: control-treated 4T1 group; ', 'treatment: LY500307-treated 4T1 group; ' GSE50226 Homo sapiens 6 Expression profiling by array GPL6244 Gene expression data from 1833 cells and 1833 cells depleted of BACH1 mRNA expression 2013-08-27 The transcription factor BACH1 is a master regulator of human breast cancer metastasis. Here we use gene expression array analysis to identify and compare the genes regulated by BACH1 depletion in a metastatic human breast cancer cell line. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50226 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA217320 https://www.ebi.ac.uk/ena/browser/view/PRJNA217320 None [Overal design]Total RNAs were extracted from vector control 1833 cells or 1833 cells with shBACH mRNA BACH1 depletion. Affymetrix GeneChip Human Gene 1.0 ST Arrays were performed to detail the gene expression and identify the genes regulated by BACH1in metastatic human breast cancer cells.; [Treatment]'BACH1 depletion(shBACH1) and control were generated by transducing the cells with BACH1 shRNA or scrambled control in a pLKO.1 lentiviral vector (Open Biosystems). After transduction, cells were selected and maintained in 0.5 μg/mL puromycin.'; [Growth]'Stablely transfected 1833 cell lines were cultured in a complete medium consisting of DMEM supplemented with 10% (vol/vol) FBS, 50 U/mL penicillin, and 50 μg/mL streptomycin.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'metastatic triple-negative breast cancer cell line', 'metastatic triple-negative breast cancer cell line depleted of BACH1''cell type: metastatic triple-negative breast cancer cell line; ', 'cell type: metastatic triple-negative breast cancer cell line depleted of BACH1; ' GSE150458 Homo sapiens 10 Expression profiling by array GPL27956 Akt inhibition with MK-2206 is associated with favorable immune profile changes within the tumor microenvironment of hormone receptor positive, HER2 negative breast cancer [IO360 panel] 2020-05-13 Gene expression was assessed with Nanostring in the surgical specimens obtained from a Window of Opportunity trial with MK-2206 in early stage breast cancer. Tumor biopsies and surgical specimens were compared for patients who received MK-2206 along with a prospective untreated control group of patients. Greater expression of interferon related genes was seen in surgical specimens following MK-2206 and compared to untreated controls. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE150458 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA632489 https://www.ebi.ac.uk/ena/browser/view/PRJNA632489 None [Overal design]In the study/data presented here, patients with early stage breast cancer were treated with MK-2206 for two doses in a Window of Opportunity trial. Patients had corrollary studies performed on their pretreatment and post-treatment (surgical excision) specimens to assess the effect of MK-2206 on both known direct targets of the PI3KCA/Akt pathway as well as tumor immune microenvironment. Enclosed here is the nanostring data from the IO360 panel analysis of the surgical specimens from patients treated with MK-2206 as well as surgical specimens from an untreated prospective control cohort.; [Treatment]'None'; [Growth]'None'; [Extraction]'mRNA was manually extracted from macrodissected tumor rich areas of surgical specimens of patients treated with MK-2206 (e.g. MK-2206 Patient 1) as well as prospectively enrolled untreated control patients (e.g. Untreated Control 1) and stored at -80C.'; [Cell type]'Source: ''tissue: primary breast cancer; histology: IDC; age: 44; Sex: Female; grade: 2; treatment: MK-2206; ', 'tissue: primary breast cancer; histology: IDC; age: 69; Sex: Female; grade: 2; treatment: MK-2206; ', 'tissue: primary breast cancer; histology: IDC; age: 50; Sex: Female; grade: 2; treatment: MK-2206; ', 'tissue: primary breast cancer; histology: IDC; age: 61; Sex: Female; grade: 2; treatment: MK-2206; ', 'tissue: primary breast cancer; histology: IDC; age: 37; Sex: Female; grade: 2; treatment: MK-2206; ', 'tissue: primary breast cancer; histology: IDC; age: 59; Sex: Female; grade: 1; treatment: Untreated; ', 'tissue: primary breast cancer; histology: ILC; age: 45; Sex: Female; grade: 3; treatment: Untreated; ', 'tissue: primary breast cancer; histology: ILC; age: 53; Sex: Female; grade: 2; treatment: Untreated; ', 'tissue: primary breast cancer; histology: IDC; age: 48; Sex: Female; grade: 3; treatment: Untreated; ', 'tissue: primary breast cancer; histology: IDC; age: 75; Sex: Female; grade: 2; treatment: Untreated; ' GSE69951 Homo sapiens 32 Non-coding RNA profiling by array GPL16770 Hsa-miR-375 in early breast cancer 2015-06-17 Purpose of the current study was to identify miRs that can differentiate between patients with and without local relapse after breast conserving therapy in early stage breast cancer, which is especially important in the context of individualized treatment selection. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE69951 Hsa-miR-375 is a predictor of local control in early stage breast cancer. Clinical epigenetics 5.496 https://doi.org/10.1186/s13148-016-0198-1 {Clinical epigenetics (5.496) doi:10.1186/s13148-016-0198-1}; {Genes (3.331) doi:10.3390/genes11121404}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA287261 https://www.ebi.ac.uk/ena/browser/view/PRJNA287261 None [Overal design]The study was conducted in a pilot and a validation phase. First, 32 patients were screened for the most de-regulated miRs in a panel of 1250 miRs by microarray technology. Second, the candidate miRs were analyzed in an independent cohort of 115 patients using reverse transcription quantitative polymerase chain reaction (RT-qPCR).; [Treatment]'breast cancer tissue from surgical procedure'; [Growth]'None'; [Extraction]'slices from FFPE samples were sent to the comprehensive biomarker center (cbc™) in Heidelberg, RNA was extracted according to cbc standard procedures'; [Cell type]'Source: ''patient id: Patient 1; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 2; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 3; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 4; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 5; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 6; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 7; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 8; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 9; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 10; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 11; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 12; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 13; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 14; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 15; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 16; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 17; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 18; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 19; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 20; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 21; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 22; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 23; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 24; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 25; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 26; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 27; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 28; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 29; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 30; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 31; gender: female; tissue type: primary tumor; sample type: FFPE material; ', 'patient id: Patient 32; gender: female; tissue type: primary tumor; sample type: FFPE material; ' GSE171364 Homo sapiens 45 Expression profiling by high throughput sequencing GPL24676 Mediator of DNA damage checkpoint 1 (MDC1) is a novel estrogen receptor co-regulator in invasive lobular carcinoma of the breast 2021-04-01 We identified MDC1 as a putative novel transcriptional co-regulator of estrogen receptor alpha (ER) in models of invasive lobular carcinoma. In this study, our goal was to define the contribution of MDC1 to regulation of the ER transcriptome in ILC cell lines versus invasive ductal carcinoma cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE171364 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA719219 https://www.ebi.ac.uk/ena/browser/view/PRJNA719219 https://www.ncbi.nlm.nih.gov/sra?term=SRP313175 [Overal design]RNAseq was used to examine estrogen-driven changes in gene expression, with or without knockdown of MDC1, ER, or FOXA1. We compared gene expression in invasive lobular carcinoma cell lines (MM134/MDA MB 134VI, MM330/MDA MB 330) to invasive ductal carcinoma cell line HCC1428.; [Treatment]'After 3d hormone-deprivation, cells were transfected with the indicated siRNA (siNT = non-targeting control). 24hrs post-siRNA transfection, cells were treated with vehicle (0.01% EtOH) or 100pM estradiol. 24hrs after vehicle or E2 treatment, cells were collected for RNA extraction, processing, and sequencing.'; [Growth]'Cells were hormone-deprived via maintenance in medium supplemented with charcoal-stripped serum for 3 days prior to further treatment.'; [Extraction]'RNA extractions were performed using the RNeasy Mini kit (Qiagen).\nIllumina Stranded mRNA Prep, for sequencing on NovaSEQ6000 with 2x150 paired-end reads.'; [Cell type]'Source: ''cell line: HCC1428; treatment: E2; sirna: ER; ', 'cell line: HCC1428; treatment: E2; sirna: FOXA1; ', 'cell line: HCC1428; treatment: E2; sirna: MDC1; ', 'cell line: HCC1428; treatment: Untreated; sirna: NT; ', 'cell line: HCC1428; treatment: E2; sirna: NT; ', 'cell line: MM134; treatment: E2; sirna: ER; ', 'cell line: MM134; treatment: E2; sirna: FOXA1; ', 'cell line: MM134; treatment: E2; sirna: MDC1; ', 'cell line: MM134; treatment: E2; sirna: NT; ', 'cell line: MM134; treatment: Untreated; sirna: NT; ', 'cell line: MM330; treatment: E2; sirna: ER; ', 'cell line: MM330; treatment: E2; sirna: FOXA1; ', 'cell line: MM330; treatment: E2; sirna: MDC1; ', 'cell line: MM330; treatment: Untreated; sirna: NT; ', 'cell line: MM330; treatment: E2; sirna: NT; ' GSE43766 synthetic construct 10 Non-coding RNA profiling by array GPL16384 identification of miRNA differential expression patterns in a new model of acquired letrozole resistance 2013-01-25 Since differential miRNA expression patterns associated with acquired AI resistance have been poorly investigated, the aim of this study was to delineate the deregulation of miRNA expression associated with aromatase inhibitor (AI) response failure in new cellular models of AI resistance. For this purpose, we generated and characterized novel cellular models of acquired resistance to letrozole (Res-Let cells) and to anastrozole (Res-Ana cells) and performed microarray experiments to identify miRNAs whose expression was either deregulated between control (MCF-7aro) and resistant cells (Res-Let or Res-Ana). With the aim to select relevant miRNAs, two independent cell culture replicates were performed for each experimental condition. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43766 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA187554 https://www.ebi.ac.uk/ena/browser/view/PRJNA187554 None [Overal design]MCF-7aro and Res-Let cells were grown in the presence of androstenedione (AD) combined or not with letrozole. Two independent cell culture replicates for each experimental condition were used to generate total RNA. Total RNA was extracted from cell culture using a Qiagen RNA extraction kit and RNA quality was assessed using the BioAnalyzer 2100? (Agilent Technologies). Complex probes were produced from these RNA, then hybridized to GeneChip® miRNA 3.0 array according to the manufacturer's recommendations (Affymetrix). Res-Ana cells were grown in the presence of androstenedione (AD). Two independent cell culture replicates for each experimental condition were used to generate total RNA. Total RNA was extracted from cell culture using a Qiagen RNA extraction kit and RNA quality was assessed using the BioAnalyzer 2100 (Agilent Technologies). Complex probes were produced from these RNA, then hybridized to GeneChip® miRNA 3.0 array according to the manufacturer's recommendations (Affymetrix).; [Treatment]'Prior to experiment, cells were purged in Dulbecco’s Modified Eagle Medium without phenol red, supplemented with 3% steroid-depleted, dextran-coated and charcoal-treated fetal calf serum (DCC medium) for 4 days. MCF-7aro and Res-Let cells were then grown for 4 days in the presence of 25 nM of androstenedione combined or not with 10-6 M of letrozole. Media and treatment were changed every 2 days.', 'Prior to experiment, cells were purged in Dulbecco’s Modified Eagle Medium without phenol red, supplemented with 3% steroid-depleted, dextran-coated and charcoal-treated fetal calf serum (DCC medium) for 4 days. Cells were then grown for 4 days in the presence of 25 nM of androstenedione. Media and treatment were changed every 2 days.'; [Growth]'Cells were grown in DMEM medium supplemented with 10% fetal bovine serum'; [Extraction]'Total RNA from cell culture was prepared using the miRNeasy Mini Kit (Qiagen, Hilden, Germany) according to the manufacturer’s recommendations and subsequently quantified on a Nanodrop ND1000 spectrophotometer (Nanodrop Technologies, Wilmington, DE, USA). RNA integrity was checked using the BioAnalyzer 2100 (Agilent Technologies, Palo Alto, CA, USA).'; [Cell type]'Source: ', 'Breast cancer''cell line: MCF-7; ', 'cell type: Breast cancer; cell line: MCF-7; ' GSE9887 Homo sapiens 4 Genome variation profiling by array GPL2826 Understanding Vitamin D resistance using array comparative genomic hybridization 2007-12-14 Vitamin D is the strongest known natural anti-proliferative. A large number of studies in a wide spectrum of cancers, including epidemiological, in vitro and animal models, demonstrate that the active form of Vitamin D has anti-cancer benefits, affecting both progression and metastasis. Alike the role in calcium Vitamin D regulation, its anti-proliferative effect is thought to function through the Vitamin D receptor (VDR), although convincing evidence is lacking. Notwithstanding, separation of the calcemic and the anti-proliferative activity of Vitamin D analogues has been a major obstacle in developing new drugs for the treatment of cancer. The work presented attempts to unveil the molecular mechanism behind the anti-proliferative action of Vitamin D using genomic tools. For that purpose four independently developed Vitamin D sensitive/resistant MCF7 cell line pairs were collected. These unique biological replicates enabled us, both to increase the power of our study and to omit the use of Vitamin D. We deem this omission crucial since in the presence of Vitamin D only downstream genes involved in proliferation and cell cycle would be identified rather than causal resistance genes. The use of a variety of genomic techniques including expression, NMD and oligo CGH arrays reveal in the resistant cell lines the 11q13-14 as a region of DNA copy number loss and an altered expression of EGFR signaling pathway genes. Surprisingly, no genes known from calcium Vitamin D regulation were identified, nor did the VDR silencing by RNAi induce resistance to the sensitive cell lines. Keywords: comparative genomic hybridization, cell type comparision https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE9887 Anti-proliferative action of vitamin D in MCF7 is still active after siRNA-VDR knock-down. BMC genomics 3.501 https://doi.org/10.1186/1471-2164-10-499 {BMC genomics (3.501): 10.1186/1471-2164-10-499} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA103881 https://www.ebi.ac.uk/ena/browser/view/PRJNA103881 None [Overal design]Several MCF7 breast tumor cell lines independently derived from the human breast cancer cell line, both resistant and sensitive to Vitamin D, were used. The pairs of cell lines (parental-resistant) were developed in different laboratories and using different methodologies; while some cell lines acquired resistance by long exposure to the physiological concentration of Vitamin D (100nM), others were induced to resistant by being exposed to increasing amounts of Vitamin D. A total of 4 microarray expression experiments were carried out. In all microarray experiments DNA from the Vitamin D resistant cell line was hybrizided agains DNA from the respsective sensitive/parental cell line.; [Treatment]'None'; [Growth]'None'; [Extraction]'Cells (70-80% confluent) cultured in 75 cm2 flasks were harvested using 1 ml/10 cm2 of TRIzol reagent (Invitrogen) and stored at -80ºC until use. RNA and DNA were extracted using TRIzol reagent and according to the manufacturers protocols. Nucleic acids were quantified using a NanoDrop ND-1000 (NanoDrop Technologies, Wilmington, USA) and quality was visually confirmed by gel electrophoresis.'; [Cell type]'Source: ''' GSE113684 Homo sapiens 40 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [ChIP-Seq] 2018-04-25 Purpose:Assess the reprogramming of H3K4me1, H3K4me3, H3K27ac and H3K27me3 in paclitaxel-resistant triple-negative breast cancer cells relative to paclitaxel-sensitive cells Methods: ChIP-seq was performed on paclitaxel-treated MDA-MB-436 cells that are resistant to Paclitaxel (R20A, R20B, R20C) and in control-treated (DMSO) parental MDA-MB-436 cells that are sensitive to Paclitaxel (DMSO) Results: Using we mapped about 20 million sequence reads per sample to the human genome (hg19) and identified significant peaks in each cell lines using MACS.2.0 tool. Conclusions: Our study identified major reprogramming of H3K27me3 in the taxol-resistant TNBC cells relative to parental (TNBC cells), with loss of discrete H3K27me3 peaks in the resistant cells concomittent to acquisition of clusters of H3K27me3. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113684 Epigenetic Switch-Induced Viral Mimicry Evasion in Chemotherapy-Resistant Breast Cancer. Cancer discovery 26.370 https://doi.org/10.1158/2159-8290.CD-19-1493 {Cancer discovery (26.370): 10.1158/2159-8290.CD-19-1493} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA453603 https://www.ebi.ac.uk/ena/browser/view/PRJNA453603 https://www.ncbi.nlm.nih.gov/sra?term=SRP142635 [Overal design]ChIP-seq was performed on paclitaxel-treated MDA-MB-436 cells that are resistant to Paclitaxel (R20A, R20B, R20C) and in control-treated (DMSO) parental MDA-MB-436 cells that are sensitive to Paclitaxel (DMSO); [Treatment]'Taxol-resistant cells were grown in presence of 20nM of Paclitaxel at all time. Parental cells (MDA-MB-436 and Hs 578T) were grown in DMEM with 1:1000 DMSO at all time.'; [Growth]'MDA-MB-436 and HS 578T cells were grown in DMSO supplemented with 10%FBS and Penicilin/Streptomycin (100 U/mL Penicilium and 100 μg/mL. Streptomycin). Taxane-resistant cells were generated upon long-term exposure to increasing concentrations of paclitaxel at a starting concentration 0.05 nM with increments (dose and time adjusted to the growth and survival of adapting cells), until the cytotoxic concentration of 10 to 20 nM was reached with the resistant cells growing at a similar rate than the parental cells (>6 months).'; [Extraction]"Lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody.\nLibraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit (Part# 0801-0303). Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation DNA was PCR amplified with Illumina primers for 15 cycles and library fragments of ~250 bp (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the Genome Analyzer following the manufacturer's protocols."; [Cell type]'TNBC''cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_31; antibody: none; agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_32; antibody: H3K4me1 (Abcam Ab8895); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_33; antibody: H3K4me3 (Millipore 05-1339); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_34; antibody: H3K27ac (Abcam Ab4729); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_35; antibody: H3K27me3 (Diagenode C15410069); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_43; antibody: none; agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_44; antibody: H3K4me1 (Abcam Ab8895); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_45; antibody: H3K4me3 (Millipore 05-1339); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_46; antibody: H3K27ac (Abcam Ab4729); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_47; antibody: H3K27me3 (Diagenode C15410069); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_49; antibody: none; agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_50; antibody: H3K4me1 (Abcam Ab8895); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_51; antibody: H3K4me3 (Millipore 05-1339); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_52; antibody: H3K27ac (Abcam Ab4729); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_53; antibody: H3K27me3 (Diagenode C15410069); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_55; antibody: none; agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_56; antibody: H3K4me1 (Abcam Ab8895); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_57; antibody: H3K4me3 (Millipore 05-1339); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_58; antibody: H3K27ac (Abcam Ab4729); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_59; antibody: H3K27me3 (Diagenode C15410069); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_1; antibody: none; agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_2; antibody: H3K4me1 (Abcam Ab8895); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_3; antibody: H3K4me3 (Millipore 05-1339); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_4; antibody: H3K27ac (Abcam Ab4729); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_5; antibody: H3K27me3 (Diagenode C15410069); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_13; antibody: none; agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_14; antibody: H3K4me1 (Abcam Ab8895); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_15; antibody: H3K4me3 (Millipore 05-1339); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_16; antibody: H3K27ac (Abcam Ab4729); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_17; antibody: H3K27me3 (Diagenode C15410069); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_19; antibody: none; agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_20; antibody: H3K4me1 (Abcam Ab8895); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_21; antibody: H3K4me3 (Millipore 05-1339); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_22; antibody: H3K27ac (Abcam Ab4729); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_23; antibody: H3K27me3 (Diagenode C15410069); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_25; antibody: none; agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_26; antibody: H3K4me1 (Abcam Ab8895); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_27; antibody: H3K4me3 (Millipore 05-1339); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_28; antibody: H3K27ac (Abcam Ab4729); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_29; antibody: H3K27me3 (Diagenode C15410069); agent: paclitaxel; cell line: MDA-MB-436; ' GSE86181 Homo sapiens 6 Expression profiling by array GPL16686 Evidence of two distinct functionally specialized fibroblast lineages in breast stroma 2016-08-29 Background: The terminal duct lobular unit (TDLU) is the most dynamic structure in the human breast and the putative site of origin of human breast cancer. Although stromal cells contribute to a specialized microenvironment in many organs, this component remains largely understudied in the human breast. We here demonstrate the impact on epithelium of two lineages of breast stromal fibroblasts, one of which accumulates in the TDLU while the other resides outside the TDLU in the interlobular stroma. Methods: The two lineages are prospectively isolated by FACS based on different expression levels of CD105 and CD26. The characteristics of the two fibroblast lineages are assessed by immunocytochemical staining and gene expression analysis. The differentiation capacity of the two fibroblast populations is determined by exposure to specific differentiating conditions followed by analysis of adipogenic and osteogenic differentiation. To test whether the two fibroblast lineages are functionally imprinted by their site of origin, single cell sorted CD271low/MUC1high normal breast luminal epithelial cells are plated on fibroblast feeders for the observation of morphological development. Epithelial structure formation and polarization is shown by immunofluorescence and digitalized quantification of immunoperoxidase stained cultures. Results: Lobular fibroblasts are CD105high/CD26low while interlobular fibroblasts are CD105low/CD26high. Once isolated the two lineages remain phenotypically stable and functionally distinct in culture. Lobular fibroblasts have properties in common with bone marrow derived mesenchymal stem cells and they specifically convey growth and branching morphogenesis of epithelial progenitors. Conclusions: Two distinct functionally specialized fibroblast lineages exist in the normal human breast, of which the lobular fibroblasts have properties in common with mesenchymal stem cells and support epithelial growth and morphogenesis. We propose that lobular fibroblasts constitute a specialized microenvironment for human breast luminal epithelial progenitors, i.e. the putative precursors of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE86181 Evidence of two distinct functionally specialized fibroblast lineages in breast stroma. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-016-0769-2 {Breast cancer research : BCR (5.676): 10.1186/s13058-016-0769-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA340468 https://www.ebi.ac.uk/ena/browser/view/PRJNA340468 None [Overal design]CD105high and CD26high fibroblasts in technical triplicates were analyzed.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA isolated using GenElute Mammalian Total RNA Miniprep Kit (Sigma-Aldrich) according to manufacturers instructions'; [Cell type]'mammary fibroblast''cell type: mammary fibroblast; lineage mark: CD105; ', 'cell type: mammary fibroblast; lineage mark: CD26; ' GSE74417 Homo sapiens 3 Expression profiling by high throughput sequencing GPL16791 RNA-seq of normal breast epithelial cells 2015-10-27 RNA-seq was performed on primary normal breast epithelial cells that were grown briefly in culture https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74417 Transcriptional Selectivity of Epigenetic Therapy in Cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-16-0834 {Cancer research (8.378): 10.1158/0008-5472.CAN-16-0834} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA300315 https://www.ebi.ac.uk/ena/browser/view/PRJNA300315 https://www.ncbi.nlm.nih.gov/sra?term=SRP065359 [Overal design]Biological triplicates were performed for a total of 3 samples.; [Treatment]'none'; [Growth]'Normal breast epithelial cells were grown in 1:1 DMEM/F12 medium with 2.4 g/L sodium bicarbonate, 5% chelated horse serum, 20 ng/ml EGF (BD Biosciences), 100 ng/ml cholera toxin (Sigma-Aldrich), 10 mg/L insulin (Sigma-Aldrich), 0.5 mg/L hydrocortisone (Sigma-Aldrich), and 0.04 mM calcium chloride (Sigma-Aldrich)'; [Extraction]'RNA was isolated using Rneasy Mini Kit (Qiagen)\nStrand-specific RNA libraries were generated from 1μg of RNA using TruSeq stranded total RNA with Ribo-Zero Gold (Illumina)'; [Cell type]'Source: ''tissue: adjacent normal tissue from patient with lobular carcinoma in situ; Sex: female; age: 69 year old; ' GSE77096 Mus musculus 12 Methylation profiling by high throughput sequencing GPL13112 Genome wide DNA methylation analysis of C3(1) SV40TAg mouse model of breast cancer 2016-01-21 Genome-wide screen for aberrant DNA methylation in mammary gland tumors of the C3(1) Sv40Tag mouse model of breast cancer in comparison with wildtype mammary glands. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE77096 Genome-wide screen for differentially methylated long noncoding RNAs identifies Esrp2 and lncRNA Esrp2-as regulated by enhancer DNA methylation with prognostic relevance for human breast cancer. Oncogene 6.634 https://doi.org/10.1038/onc.2017.246 {Oncogene (6.634): 10.1038/onc.2017.246} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA309428 https://www.ebi.ac.uk/ena/browser/view/PRJNA309428 https://www.ncbi.nlm.nih.gov/sra?term=SRP068729 [Overal design]MCIp (methyl CpG immunoprecipitation)-seq on mammary gland tumors of C3(1) SV40TAg and wildtype mammary glands of 2 age groups. Three biological replicates for each group were analyzed.; [Treatment]'None'; [Growth]'None'; [Extraction]"genomic DNA was isolated with AllPrep DNA&RNA kit (Qiagen, Germany) and fragmented to ≈ 150bp with Covaris S2 sonicator. Enrichment for highly methylated fragments was performed with Methyl CpG immunoprecipitation (MCIp) according to Sonnet et al, (Methods Mol Biol, 2013) with 5µg of genomic DNA as input and 60µg of MBD2 fusion protein\n10ng MCIP-enriched DNA was used as input for library preparation according to the manufacturer's protocol for the Illumina ChIP Sample Prep Kit with minor modifications."; [Cell type]'Source: ''strain background: FVB/N; age: 20 weeks; genotype/variation: C3(1)SV40Tag; tissue: mammary gland tumor; ', 'strain background: FVB/N; age: 24 weeks; genotype/variation: C3(1)SV40Tag; tissue: mammary gland tumor; ', 'strain background: FVB/N; age: 20 weeks; genotype/variation: wild type; tissue: mammary gland; ', 'strain background: FVB/N; age: 24 weeks; genotype/variation: wild type; tissue: mammary gland; ' GSE21832 Homo sapiens 9 Expression profiling by array GPL570 Identification of the receptor tyrosine kinase AXL in triple negative breast cancer as a novel target for the human miR-34a microRNA (gene expression) 2010-05-14 Triple negative breast cancer (TNBC) is histologically characterized by the absence of the hormone receptors estrogen and progesterone, in addition to having a negative immunostain for HER-2. The aggressiveness of this disease and lack of targeted therapeutic options for treatment is of high clinical importance. MicroRNAs are short 21- to 23 nucleotide endogenous non-coding RNAs that regulate gene expression by binding to mRNA transcripts, resulting in either decreased protein translation or mRNA degradation. Dysregulated expression of miRNAs is now a hallmark of many human cancers. In order to identify a miRNA/mRNA interaction that is biologically relevant to the triple negative breast cancer genotype/phenotype, we initially conducted a miRNA profiling experiment to detect differentially expressed miRNAs in cell line models representing the triple negative (MDA-MB-231), ER+ (MCF7), and HER-2 overexpressed (SK-BR-3) histotypes. We identified human miR-34a expression as being >3-fold down (from its median expression value across all cell lines) in MDA-MB-231 cells, and identified AXL as a putative mRNA target using multiple miRNA/target prediction algorithms. The miR-34a/AXL interaction was functionally characterized through ectopic overexpression experiments with a miR-34a mimic. In reporter assays, miR-34a binds to the putative target site within the AXL 3’UTR to affect luciferase expression. We also observed degradation of AXL mRNA and decreased AXL protein levels, as well as cell signaling effects on AKT phosphorylation and phenotypic effects on cell migration. Finally, we present an inverse correlative trend in miR-34a and AXL expression for both cell line and patient tumor samples. Comparison of the changes in gene expression as a result of transfections with miR-34a mimic molecules (representing two different vendors; Qiagen and Dharmacon) in MDA-MB-231 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE21832 Identification of the receptor tyrosine kinase AXL in breast cancer as a target for the human miR-34a microRNA. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-011-1690-0 {Breast cancer research and treatment (3.471): 10.1007/s10549-011-1690-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA129329 https://www.ebi.ac.uk/ena/browser/view/PRJNA129329 None [Overal design]MDA-MB-231 cells were transfected in 6-well dishes (600,000 cells) with either AllStar negative control, Qmimic, or Dmimic at 10 nM final concentration using Lipofectamine™ 2000 (Invitrogen; Carlsbad, CA). All transfections were performed in triplicate. Forty-eight hours post-transfection, total RNA was isolated from each sample using Qiagen’s miRNeasy extraction kit (Qiagen; Germantown, MD). Total RNA samples were sent to the Laboratory of Molecular Technology (National Cancer Institute at Frederick; Frederick, MD), for processing on Affymetrix GeneChip Human Genome U133 Plus 2.0 microarrays (Affymetrix; Santa Clara, CA). Expression values were normalized using Robust Multichip Averaging (RMA). Only gene probes (AllStar vs. Mimic) that passed a log2 1.5-fold change, p < 0.05 threshold using an Empirical Bayes moderated t statistics with a Benjamini-Hochberg correction for the false discovery rate were reported. All analyses were performed with Bioconductor packages AFFYGUI and LIMMA on a R environment.; [Treatment]'MDA-MB-231 cells (600,000 cells/well) were reverse transfected in 6 well dishes with either AllStar negative control, Qmimic, or Dmimic at 10 nM final concentration using Lipofectamine 2000 (10.5 ul/well),'; [Growth]'MDA-MB-231 cells were grown in T75 flasks containing RPMI 1640 basal medium + 10% Fetal Bovine Serum at 37C with 5% CO2. Cells at 80-90% confluency were used in transfections.'; [Extraction]"At 48 hrs post-transfection, total RNA was extracted from each well using Qiagen's miRNeasy extraction kit according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MDA-MB-231; ' GSE20076 Homo sapiens 8 Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing GPL6884; GPL9115 BRD7 is a candidate tumour suppressor gene required for p53 function 2010-01-28 Oncogene-induced senescence (OIS) is a p53-dependent defence mechanism against uncontrolled proliferation. Consequently, many human tumours harbour p53 mutations while others show a dysfunctional p53 pathway, frequently by unknown mechanisms. We identified BRD7, a bromodomain-containing protein whose inhibition allows full neoplastic transformation in the presence of wild-type p53. Intriguingly, in human breast tumours harbouring wild-type, but not mutant p53, the BRD7 gene locus was frequently deleted and low BRD7 expression was found in a subgroup of tumours. Functionally, BRD7 is required for efficient p53-mediated transcription of a subset of target genes. BRD7 interacts with p53 and p300, and is recruited to target gene promoters, affecting histone acetylation, p53 acetylation, and promoter activity. Thus, BRD7 suppresses tumourigenicity by serving as a p53 cofactor required for efficient induction of p53-dependent OIS. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE20076 BRD7 is a candidate tumour suppressor gene required for p53 function. Nature cell biology 17.728 https://doi.org/10.1038/ncb2038 {Nature cell biology (17.728): 10.1038/ncb2038} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA124195 https://www.ebi.ac.uk/ena/browser/view/PRJNA124195 https://www.ncbi.nlm.nih.gov/sra?term=SRP002101 [Overal design]We recorded mRNA expression profiles of BJ primary fibroblasts expressing the oncogene RasV12 and either control vector, one of two BRD7 knockdown vectors, or p53 knockdown vector. In addition, we profiled genome-wide protein DNA interactions for p53 and BRD7 using ChIP-Seq. p53- and BRD7-binding sites were recorded in RasV12-expressing BJ cells; as a control we used knockdown of the gene of interest (BRD7 or p53).; [Treatment]'BJ/ET/RASV12ER cells containing control vector were cultured in the presence (+RASV12) of 4OHT for 10 days. mRNA levels were determined by microarray.', 'BJ/ET/RASV12ER cells containing p53 knockdown vector were cultured in the presence (+RASV12) of 4OHT for 10 days. mRNA levels were determined by microarray.', 'BJ/ET/RASV12ER cells containing BRD7#1 knockdown vector were cultured in the presence (+RASV12) of 4OHT for 10 days. mRNA levels were determined by microarray.', 'BJ/ET/RASV12ER cells containing BRD7#4 knockdown vector were cultured in the presence (+RASV12) of 4OHT for 10 days. mRNA levels were determined by microarray.', 'The antibody used for the p53 IPs was DO-1 (Santa Cruz Biotechnology), and the one for the BRD7 IPs was produced in-house.'; [Growth]'None', 'BJ/ET/RASV12ER cells expressing vector, BRD7KD, or p53KD were cultured in the presence of 4OHT.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions.", "Libraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit."; [Cell type]'foreskin fibroblasts''cell line: BJ; cell type: foreskin fibroblasts; oncogene expression: RasV12; vector: empty pRS; ', 'cell line: BJ; cell type: foreskin fibroblasts; oncogene expression: RasV12; vector: pRS-p53; ', 'cell line: BJ; cell type: foreskin fibroblasts; oncogene expression: RasV12; vector: pRS-BRD7#1; ', 'cell line: BJ; cell type: foreskin fibroblasts; oncogene expression: RasV12; vector: pRS-BRD7#4; ', 'cell line: BJ; cell type: foreskin fibroblasts; oncogene expression: RasV12; vector: empty; antibody: anti-BRD7; sample type: experiment; ', 'cell line: BJ; cell type: foreskin fibroblasts; oncogene expression: RasV12; vector: BRD7 knockdown; antibody: anti-BRD7; sample type: control; ', 'cell line: BJ; cell type: foreskin fibroblasts; oncogene expression: RasV12; vector: empty; antibody: anti-p53; sample type: experiment; ', 'cell line: BJ; cell type: foreskin fibroblasts; oncogene expression: RasV12; vector: p53 knockdown; antibody: anti-p53; sample type: control; ' GSE137528 Homo sapiens 10 Expression profiling by high throughput sequencing GPL20301 ECM mediated FGF-induced estrogen receptor activity and therapy response 2019-09-16 We wanted to investigate the effects of stromal signaling on ER+ breast cancer cells as recent work implicates the tumor microenvironment in the acquisition of resistance to endocrine therapy. We desired to examine the effects of both coculture with fibroblasts, and 2.5D monoculture of breast cancer cells on decellularized, fibroblast-derived extracellular matrix scaffolds. We cultured MCF7 cells alone (Unc_#_Mono) or in coculture (Co_#) with BJ fibroblasts to examine stromal signalling on ER+ breast cancer. Cocultured MCF7 were isolated by magnetically activated cell sorting. We also cultured MCF7 cells in decellularized ECM scaffolds generated by BJ fibroblasts (ECM1_#) or IMR90 fibroblasts (ECM2_#) or on an uncoated, plastic cell culture dish (Unc_#). Total RNA was extracted from cells using TRIzol (Invitrogen) and purified using Direct-zol RNA mini kit (Zymo Research) with DNase I treatment. After RNA purification, samples were confirmed to have a RIN value > 9.0 when measured on an Agilent Bioanalyzer. Libraries for RNA-Seq were prepared with KAPA Stranded RNA-Seq Kit. The workflow consisted of mRNA enrichment, cDNA generation, end repair to generate blunt ends, A-tailing, adaptor ligation and 14 cycles of PCR amplification. Unique adaptors were used for each sample in order to multiplex samples into several lanes. Sequencing was performed on Illumina Hiseq 4000 with a 150bp pair-end run. A data quality check was done on Illumina SAV. Demultiplexing was performed with Illumina Bcl2fastq2 v 2.17 program. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE137528 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA565784 https://www.ebi.ac.uk/ena/browser/view/PRJNA565784 https://www.ncbi.nlm.nih.gov/sra?term=SRP221801 [Overal design]Replicate coculture sets were generated by culturing MCF7 cells alone or in coculture with BJ fibroblasts prior to magnetic separation. Replicate ECM sets were generated by culturing MCF7 cells on ECM generated by IMR90 or BJ fibroblasts or on uncoated surfaces.; [Treatment]'We cultured MCF7 cells alone or in coculture with BJ fibroblasts to examine stromal signalling on ER+ breast cancer. Cocultured MCF7 were isolated by magnetically activated cell sorting. We also cultured MCF7 cells in decellularized ECM scaffolds generated by BJ fibroblasts or IMR90 fibroblasts or on an uncoated, plastic cell culture dish.'; [Growth]'MCF7 cells and fibroblasts were obtained from ATCC and cultured as recommended.'; [Extraction]'Total RNA was extracted from cells using TRIzol (Invitrogen) and purified using Direct-zol RNA mini kit (Zymo Research) with DNase I treatment.\nLibraries for RNA-Seq were prepared with KAPA Stranded RNA-Seq Kit. The workflow consisted of mRNA enrichment, cDNA generation, end repair to generate blunt ends, A-tailing, adaptor ligation and 14 cycles of PCR amplification. Unique adaptors were used for each sample in order to multiplex samples into several lanes. Sequencing was performed on Illumina Hiseq 4000 with a 150bp pair-end run. A data quality check was done on Illumina SAV. Demultiplexing was performed with Illumina Bcl2fastq2 v 2.17 program.'; [Cell type]'Source: ''cell line: MCF7; culture method: Monoculture control; ', 'cell line: MCF7; culture method: Cocultured with BJ fibroblasts then magnetically separated; ', 'cell line: MCF7; culture method: Uncoated control; ', 'cell line: MCF7; culture method: ECM from BJ fibroblasts; ', 'cell line: MCF7; culture method: ECM from IMR90 fibroblasts; ' GSE37828 Mus musculus 6 Expression profiling by array GPL4134 Silencing of Irf7 pathways in breast cancer cells promotes bone metastasis through immune escape mechanisms 2012-05-07 Breast cancer metastasis to bone is a critical determinant of long-term survival after treatment of primary tumors. We used a mouse model of spontaneous bone metastasis to determine new molecular mechanisms. Differential transcriptome comparisons of primary and metastatic tumor cells revealed that a substantial set of genes suppressed in bone metastases were highly enriched for promoter elements for the type I interferon (IFN) regulatory factor, Irf7, itself suppressed in mouse and human metastases. The critical function of the Irf7 pathway was demonstrated by restoration of exogenous Irf7 or systemic interferon administration, which significantly reduced bone metastases and prolonged metastasis free survival. Using mice deficient in the type I receptor (Ifnar1-/-) or mature B, T and NK cell responses (NOD Scid IL-2rγ-/- mice) we demonstrated that Irf7-driven suppression of metastasis was reliant on IFN signaling to host immune cells. Metastasis suppression correlated with decreased accumulation of myeloid-derived suppressor cells and increased CD4++, CD8 T cells and NK cells in the peripheral blood and was reversed by depletion of CD8+ cells and NK cells. Clinical importance of our findings was demonstrated as increased primary tumor Irf7 expression predicted prolonged bone and lung metastasis-free survival. Thus we report for the first time, a novel innate immune pathway, intrinsic to breast cancer cells, whose suppression in turn restricts systemic immunosurveillance to enable metastasis. This pathway may constitute a novel therapeutic target for restricting breast cancer metastases. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37828 Silencing of Irf7 pathways in breast cancer cells promotes bone metastasis through immune escape. Nature medicine 30.641 https://doi.org/10.1038/nm.2830 {Nature medicine (30.641): 10.1038/nm.2830} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA163619 https://www.ebi.ac.uk/ena/browser/view/PRJNA163619 None [Overal design]Comparison of basal gene expression in breast cancer 4T1.2 cell line stably transfected using the pMSCV retroviral expression vector system with IRF7 or the base vector. Three independent experiments were performed comparing the IRF7 expressing cells to the base vector cells; [Treatment]'None'; [Growth]'The pMSCV retroviral expression vector (Clonetech, Palo Alto, CA, USA) was utilized enforce the expression of Irf7 or empty plasmid in 4T1.2 cell line. These constructs were transfected into HEK-293 packaging cells using lipofectamine (Invitrogen, Carlsbad, CA, USA). Conditioned media was filtered and incubated with target 4T1.2 cells. 4T1.2 cells were then selected using puromycin, single cell cloned and multiple clones pooled. Stably transfected cells were cultured in α-MEM supplemented with 5% FCS and grown at 37 ºC in a humidified incubator with 5% CO2.'; [Extraction]'Total RNA was extracted using Qiagen RNeasy mini columns according to the manufacturers instructions. The protocol includes an on-column DNAse digestion step. RNA was quantified using a NanoDrop-1000 spectrophotometer and quality was monitored with the Agilent 2100 Bioanalyzer'; [Cell type]'Source: ''strain background: BALB/c; cell line: 4T1.2; stably transfected with: pMSCV retroviral expression vector system the base vector (BV); expressing: base vector (BV); tissue: Mammary Tumour; ', 'strain background: BALB/c; cell line: 4T1.2; stably transfected with: pMSCV retroviral expression vector system with IRF7; expressing: IRF7; tissue: Mammary Tumour; ' GSE61368 Homo sapiens 36 Expression profiling by array GPL6884 Combinatorial effects of estrogen with progestogens or androgen in the breast cancer cell line ZR-75-1 2014-09-12 Cells were cotreated with dihydrotestosterone, progesterone or medroxyprogesterone acetate and estrdiol to assess the combinatorial effects of hormone exposure in breast cancer cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE61368 The unique transcriptional response produced by concurrent estrogen and progesterone treatment in breast cancer cells results in upregulation of growth factor pathways and switching from a Luminal A to a Basal-like subtype. BMC cancer 2.933 https://doi.org/10.1186/s12885-015-1819-3 {BMC cancer (2.933): 10.1186/s12885-015-1819-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA260887 https://www.ebi.ac.uk/ena/browser/view/PRJNA260887 None [Overal design]Cells were plated in hormone stripped media for 56h, followed by treatment for 16h with 10nM of the nominated hormone(s); [Treatment]'Cells were plated at 500,000 cells per well in 6 well plates in phenol red free RPMI 1640 (Life Technologies) supplemented with 10% dextran charcoal stripped FBS (Sigma-Aldrich), and treated with 10nM E2 where indicated (E2L). Cells were subsequently treated for 16h with the nominated hormone(s).'; [Growth]'Cells were sourced from ATCC and used at passage 16. Cells were grown in RPMI 1640 (Life Technologies) supplemented with 10% FBS (Sigma-Aldrich)'; [Extraction]"Total RNA was isolated using a Qiagen Rneasy RNA extraction kit, incorporating Dnase on-column digestion according to manufacturer's instructions"; [Cell type]'breast cancer cells''cell line: ZR-75-1; cell type: breast cancer cells; treatment group: 16h 10nM estradiol cotreated with 16h 10nM medroxyprogesterone acetate; ', 'cell line: ZR-75-1; cell type: breast cancer cells; treatment group: 16h 10nM estradiol cotreated with 16h 10nM dihydrotestosterone; ', 'cell line: ZR-75-1; cell type: breast cancer cells; treatment group: 16h 10nM estradiol cotreated with 16h 10nM progesterone; ', 'cell line: ZR-75-1; cell type: breast cancer cells; treatment group: 16h eqivalent vehicle (ethanol; 2 parts per million); ', 'cell line: ZR-75-1; cell type: breast cancer cells; treatment group: 16h 10nM progesterone; ', 'cell line: ZR-75-1; cell type: breast cancer cells; treatment group: 16h 10nM medroxyprogesterone acetate; ', 'cell line: ZR-75-1; cell type: breast cancer cells; treatment group: 72h 10nM estradiol cotreated with 10nM progesterone for final 16h; ', 'cell line: ZR-75-1; cell type: breast cancer cells; treatment group: 16h 10nM estradiol; ', 'cell line: ZR-75-1; cell type: breast cancer cells; treatment group: 16h 10nM dihydrotestosterone; ' GSE155467 synthetic construct 6 Non-coding RNA profiling by array GPL21572 DK2, a newly synthesized chalcone, induced apoptosis and differential expression profiles of miRNA and mRNA on breast cancer MCF-7 cell line 2020-07-30 In this study, the cytotoxic effect of DK2, a newly synthesized chalcone and its underlying mechanism against breast cancer cell line, MCF-7 were investigated. MCF-7 was treated with 8.2 μM of DK2 at several time points. The apoptotic analysis was carried out using MTT assay, morphology observation (using inverted microscope and fluorescent microscope) and flow cytometry analysis (using Annexin V/7ADD apoptosis analysis and cell cycle analysis). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE155467 Induction of Apoptosis and Regulation of MicroRNA Expression by (2E,6E)-2,6-bis-(4-hydroxy-3-methoxybenzylidene)-cyclohexanone (BHMC) Treatment on MCF-7 Breast Cancer Cells. Molecules (Basel, Switzerland) 3.060 https://doi.org/10.3390/molecules26051277 {Molecules (Basel, Switzerland) (3.060): 10.3390/molecules26051277} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA649811 https://www.ebi.ac.uk/ena/browser/view/PRJNA649811 None [Overal design]Triplicate of DK2-treated MCF-7 cell and control untreated MCF-7 were subjected to miRNA and mRNA microarray profiling (Affymetrix, USA).; [Treatment]'MCF-7 was treated with 8.2 μM of DK2 at several time points.'; [Growth]'The control and DK2-treated MCF-7 cells were cultured in tissue culture-treated flasks. Both are maintained in 5% CO2 humidified incubator.'; [Extraction]"Total RNA with retention of small RNAs from the cells were extracted using miRNeasy kit according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MCF-7; culture type: Monolayer; treatment: Control; ', 'cell line: MCF-7; culture type: Monolayer; treatment: DK2; ' GSE45584 Homo sapiens 90 Expression profiling by array; Genome variation profiling by array GPL6480; GPL16895 Expression Analysis and Genomic Analysis of Microdissected Inflammatory Breast Cancer 2013-03-28 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE45584 Genomic and expression analysis of microdissected inflammatory breast cancer. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-013-2501-6 {Breast cancer research and treatment (3.471): 10.1007/s10549-013-2501-6} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA194617 https://www.ebi.ac.uk/ena/browser/view/PRJNA194617 None [Overal design]Refer to individual Series; [Treatment]'For tumor samples, 5–20 frozen sections of biopsy (16 μm thick) were manually microdissected. Under the guidance of a pathologist, normal tissue was removed leaving tumor cells comprising greater than 90% of the specimen. For normal breast samples, 40–60 frozen sections of surgical specimen (16 μm thick) were subjected for microdissection manually.'; [Growth]'None'; [Extraction]'Total RNA was extracted using the RNeasy micro kit (Qiagen; Valencia, CA, USA), and quality was characterized with BioAnalyzer (Agilent Technologies; Waldbronn, Germany).', 'Genomic DNA was extracted using the Quick Gene SP-kit DNA tissue (Fujifilm; Tokyo, Japan), and quality was characterized with Agarose gel electrophoresis. Human Female Genomic DNA (Novagen; Madison, WI, USA) was used for normal reference DNA.'; [Cell type]'Source: ''sample type: non-IBC; her2: 3+; er: 5; ', 'sample type: non-IBC; her2: 0; er: 5; ', 'sample type: non-IBC; her2: 2+; er: 5; ', 'sample type: non-IBC; her2: 1+; er: 4; ', 'sample type: non-IBC; her2: 3+; er: 0; ', 'sample type: non-IBC; her2: 1+; er: 0; ', 'sample type: non-IBC; her2: 1+; er: 5; ', 'sample type: non-IBC; her2: 3+; er: 4; ', 'sample type: non-IBC; her2: 0; er: 0; ', 'sample type: non-IBC; her2: 0; er: 4; ', 'sample type: non-IBC; her2: 0; er: 2; ', 'sample type: IBC; her2: 3+; er: 4; ', 'sample type: IBC; her2: 2+ (FISH-); er: 5; ', 'sample type: IBC; her2: 1+; er: 5; ', 'sample type: IBC; her2: 0; er: 0; ', 'sample type: IBC; her2: 0; er: 1; ', 'sample type: IBC; her2: 0; er: 5; ', 'sample type: IBC; her2: 0; er: 4; ', 'sample type: IBC; her2: 3+; er: 5; ', 'sample type: IBC; her2: 1+; er: 0; ', 'sample type: IBC; her2: 3+; er: 0; ', 'sample type: IBC; her2: 2+ (FISH+); er: 4; ', 'sample type: IBC; her2: 1+; er: 4; ', 'sample type: IBC; her2: 0; er: 3; ', 'sample type: Normal; her2: -; er: -; ', 'tag: Novagen Catalogue Number: 70605; ' GSE45255 Homo sapiens 139 Expression profiling by array GPL96 Expression Profiles of Breast Tumors from Singapore and Europe 2013-03-18 To facilitate a better understanding of the molecular heterogeneity of breast cancer and to uncover gene-survival associations that segregate with distinct molecular subtypes, we recently compiled a meta-analytical database of over 2,000 human breast tumor expression profiles variously annotated for clinical and pathological variables and derived from various institutions worldwide. This database was utilized for the breast tumor study cited below: Nagalla, et. al., Genome Biology, 2013. While the majority of the tumor expression profiles included in this database derived from publicly accessible microarray repositories, a number of the samples had not been previously published. Here, we describe the origin of these samples and provide their associated clinical and pathological annotations with the hope that other investigators will be able to utilize these data in their own research. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE45255 Interactions between immunity, proliferation and molecular subtype in breast cancer prognosis. Genome biology 14.028 https://doi.org/10.1186/gb-2013-14-4-r34 {Genome biology (14.028): 10.1186/gb-2013-14-4-r34} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA193335 https://www.ebi.ac.uk/ena/browser/view/PRJNA193335 None [Overal design]Breast tumor samples derived from the Institut Jules Bordet (IJB; Belgium), John Radcliffe Hospital (JRH; Oxford) and the National University Hospital (NUH, Singapore) were profiled on the Affymetrix U133A platform. The number of tumors profiled (n) and the corresponding dates of tumor diagnosis are as follows. IJB: n=41, 1994-2001; JRH: n=8, 1990-1993; and NUH: n=100, 2000-2002.; [Treatment]'None'; [Growth]'None'; [Extraction]'Tumor specimens from the IJB and JRH we processed and profiled at the IJB (Christos Sotiriou). Specimens from the NUH were processed and profiled at the Genome Institute of Singapore. Total RNA was extracted from fozen tumor specimens by the Trizol method, cleaned on Qiagen RNeasy columns and analyzed for integrity on the Agilent Bioanalyzer.'; [Cell type]'Source: ''ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 20; patient age: 41; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+ACx4 cycles; dfs time: 6.17; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 6.17; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.17; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G2; size (mm): 30; patient age: 62; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 1.13; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 1.13; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 1.13; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 30; patient age: 69; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 4.29; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.29; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.29; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 35; patient age: 69; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 5.88; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.88; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.04; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G2; size (mm): 25; patient age: 40; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+CMFx6 cycles; dfs time: 2.63; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 2.63; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 2.63; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He+; histological grade: G2; size (mm): 25; patient age: 69; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 6.25; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 6.25; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.25; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G2; size (mm): 60; patient age: 54; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 2.00; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 2.00; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 2.25; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G2; size (mm): 20; patient age: 48; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): NA; characteristics: endocrine? (0=no, 1=yes): NA; chemo? (0=no, 1=yes): NA; treatment type: NA; dfs time: 5.63; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.63; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.63; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G2; size (mm): 15; patient age: 46; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 0; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 0; treatment type: none; dfs time: 4.04; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.04; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.08; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He-; histological grade: G2; size (mm): 18; patient age: 53; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 6.00; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 6.00; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.00; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 18; patient age: 52; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CMF; dfs time: 5.79; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.79; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.79; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 25; patient age: 50; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CAF; dfs time: 5.83; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.83; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.83; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 22; patient age: 53; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CMF; dfs time: 5.75; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.75; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.92; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He+; histological grade: G2; size (mm): 35; patient age: 77; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 5.58; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.58; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.58; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 20; patient age: 60; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+CMFx6 cycles; dfs time: 6.33; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 6.33; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.33; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR-; her2 status: He+; histological grade: G2; size (mm): 25; patient age: 51; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+ACx8;taxol; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: NA; dmfs event (defined as distant metastasis or death from breast cancer): NA; DSS time: NA; dss event (defined as death from breast cancer): NA; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 25; patient age: 69; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CAF; dfs time: 5.00; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.00; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.00; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G2; size (mm): 23; patient age: 49; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+CAFx6 cycles; dfs time: 5.25; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.25; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.25; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He-; histological grade: G2; size (mm): 15; patient age: 48; histology: invasive lobular carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: anastrozole;taxol; dfs time: 0.04; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 0.04; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 3.08; dss event (defined as death from breast cancer): 1; ', 'ln status: LN+; er status: ER-; pgr status: PgR+; her2 status: He+; histological grade: G2; size (mm): 40; patient age: 75; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 0.92; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 0.67; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.42; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G2; size (mm): 25; patient age: 67; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 0; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 0; treatment type: none; dfs time: 2.83; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 2.83; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 2.83; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 15; patient age: 55; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 0; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 0; treatment type: none; dfs time: 1.25; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 0.67; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.58; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 40; patient age: 35; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+ACx4 cycles; dfs time: 4.67; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.67; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.67; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G2; size (mm): 30; patient age: 46; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CAF; dfs time: 5.67; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.67; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.67; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 35; patient age: 44; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CMF; dfs time: 4.67; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.67; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.67; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 23; patient age: 40; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CAF; dfs time: 5.17; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.17; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.17; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G2; size (mm): 21; patient age: 57; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 4.75; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.75; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.75; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 19; patient age: 55; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 4.92; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.92; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.92; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G2; size (mm): 24; patient age: 44; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 0; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 0; treatment type: none; dfs time: 0.42; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 0.42; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 0.42; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR-; her2 status: He+; histological grade: G2; size (mm): 60; patient age: 46; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+CAFx2 cycles; dfs time: 1.67; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 1.67; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 1.75; dss event (defined as death from breast cancer): 1; ', 'ln status: LN+; er status: ER+; pgr status: PgR-; her2 status: He-; histological grade: G2; size (mm): 30; patient age: 42; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): NA; characteristics: endocrine? (0=no, 1=yes): NA; chemo? (0=no, 1=yes): NA; treatment type: NA; dfs time: 4.50; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.50; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.50; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 15; patient age: 46; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+CMFx6 cycles; dfs time: 4.88; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.88; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.88; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 20; patient age: 73; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 4.83; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.83; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.92; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 40; patient age: 46; histology: invasive ductal and lobular carcinoma; adjuvant treated? (0=no, 1=yes): NA; characteristics: endocrine? (0=no, 1=yes): NA; chemo? (0=no, 1=yes): NA; treatment type: NA; dfs time: 4.00; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.00; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.50; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G2; size (mm): 17; patient age: 66; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): NA; characteristics: endocrine? (0=no, 1=yes): NA; chemo? (0=no, 1=yes): NA; treatment type: NA; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: NA; dmfs event (defined as distant metastasis or death from breast cancer): NA; DSS time: 0.08; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 12; patient age: 64; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 5.58; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.58; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.58; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 15; patient age: 49; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 5.33; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.33; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.33; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 35; patient age: 47; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 5.00; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.00; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.00; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 40; patient age: 34; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 1.54; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 1.54; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.46; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G1; size (mm): 15; patient age: 45; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen;goserelin; dfs time: 5.46; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.46; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.46; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 20; patient age: 55; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 4.46; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.46; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.46; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G3; size (mm): 32; patient age: 47; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CAF; dfs time: 4.88; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.88; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.88; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G1; size (mm): 38; patient age: 66; histology: mucinous carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 0.13; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 0.13; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 60; patient age: 55; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 1.00; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 1.00; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.00; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 35; patient age: 52; histology: invasive lobular carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 4.00; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.00; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.33; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 30; patient age: 74; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 2.04; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 2.04; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 2.25; dss event (defined as death from breast cancer): 1; ', 'ln status: LN+; er status: ER-; pgr status: PgR-; her2 status: NA; histological grade: G3; size (mm): 50; patient age: 44; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 4.00; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.00; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.00; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 20; patient age: 54; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 3.96; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 3.96; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 4.63; dss event (defined as death from breast cancer): 1; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 25; patient age: 45; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: AC; dfs time: 5.25; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.25; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.29; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 30; patient age: 58; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CAF; dfs time: 1.96; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 1.96; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 1.96; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 25; patient age: 62; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Arimidex+CMFx2 cycles; dfs time: 0.00; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 0.00; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 2.08; dss event (defined as death from breast cancer): 1; ', 'ln status: LN+; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 35; patient age: 62; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 0; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 0; treatment type: none; dfs time: 0.88; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 0.88; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 1.00; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 30; patient age: 64; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 5.08; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.08; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.08; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 20; patient age: 45; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CAF; dfs time: 4.83; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.83; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.83; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G3; size (mm): 40; patient age: 80; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 1.96; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 1.96; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 1.96; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 40; patient age: 41; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 5.54; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.54; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.54; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 22; patient age: 46; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): NA; characteristics: endocrine? (0=no, 1=yes): NA; chemo? (0=no, 1=yes): NA; treatment type: NA; dfs time: 0.13; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 0.13; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 0.38; dss event (defined as death from breast cancer): 1; ', 'ln status: LN+; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 35; patient age: 54; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CAF; dfs time: 1.29; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 1.29; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 1.38; dss event (defined as death from breast cancer): 1; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G1; size (mm): 21; patient age: 86; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 3.13; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 3.13; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.38; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G1; size (mm): 80; patient age: 29; histology: invasive lobular carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CAFx6 cycles; dfs time: 2.21; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 2.21; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 3.04; dss event (defined as death from breast cancer): 1; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 35; patient age: 34; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx8 cycles; taxol; dfs time: 4.38; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.38; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.38; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 30; patient age: 48; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 5.08; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.08; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.08; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 22; patient age: 42; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: AC; dfs time: 4.17; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.17; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.25; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 35; patient age: 48; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 0.75; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 0.75; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 0.75; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 45; patient age: 52; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+ACx4 cycles; dfs time: 6.29; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 6.29; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.29; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G1; size (mm): 15; patient age: 60; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+CMFx6 cycles; dfs time: 5.58; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.58; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.79; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 30; patient age: 51; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 0.79; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 0.79; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 1.46; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 36; patient age: 38; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+ACx4 cycles; dfs time: 2.29; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 2.29; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 2.88; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 23; patient age: 42; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): NA; characteristics: endocrine? (0=no, 1=yes): NA; chemo? (0=no, 1=yes): NA; treatment type: NA; dfs time: 4.00; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.00; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.00; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G1; size (mm): 40; patient age: 81; histology: papillary carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: NA; dmfs event (defined as distant metastasis or death from breast cancer): NA; DSS time: NA; dss event (defined as death from breast cancer): NA; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G1; size (mm): 40; patient age: 77; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 3.50; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 3.50; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.33; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 20; patient age: 42; histology: medullary carcinoma; adjuvant treated? (0=no, 1=yes): 0; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 0; treatment type: none; dfs time: 1.17; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 1.17; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.50; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 25; patient age: 61; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CMF; dfs time: 5.88; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.88; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.88; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 32; patient age: 48; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 5.71; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.71; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.71; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 15; patient age: 61; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CAFx6 cycles; dfs time: 5.83; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.83; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.83; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G3; size (mm): 25; patient age: 36; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+CMFx6 cycles; dfs time: 6.17; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 6.17; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.17; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 27; patient age: 51; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 1.92; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 1.33; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.58; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 25; patient age: 46; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 5.83; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.83; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.83; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 35; patient age: 48; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 5.83; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.83; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.83; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 18; patient age: 51; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+CMFx6 cycles; dfs time: 5.79; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.79; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.79; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 21; patient age: 47; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4 cycles; dfs time: 5.88; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.88; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.88; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 51; patient age: 58; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+ACx4 cycles; dfs time: 5.92; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.92; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.92; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 38; patient age: 38; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+ACx4 cycles; dfs time: 5.58; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.58; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.58; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G3; size (mm): 30; patient age: 47; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CAF; dfs time: 4.54; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.54; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.54; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 50; patient age: 64; histology: medullary carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 5.21; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.21; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.21; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER-; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 16; patient age: 50; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+ACx4 cycles; dfs time: 3.83; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 3.83; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 5.75; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G1; size (mm): 20; patient age: 52; histology: invasive lobular carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 5.17; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 5.17; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.17; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 25; patient age: 67; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 4.92; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.92; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.92; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 40; patient age: 38; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+AC; dfs time: 2.00; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 2.00; dmfs even t (defined as distant metastasis or death from breast cancer): 1; DSS time: 2.00; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G3; size (mm): 28; patient age: 84; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 0.83; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 0.83; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 0.83; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: NA; pgr status: NA; her2 status: NA; histological grade: G1; size (mm): 25; patient age: 55; histology: invasive ductal carcinoma and papillary carcinoma; adjuvant treated? (0=no, 1=yes): 0; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 0; treatment type: none; dfs time: 4.67; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.67; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.67; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G1; size (mm): 24; patient age: 43; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+ACx4 cycles; dfs time: 2.67; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 2.67; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 2.67; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G3; size (mm): 20; patient age: 62; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: tamoxifen; dfs time: 4.38; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.38; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.38; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G1; size (mm): 60; patient age: 59; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): NA; characteristics: endocrine? (0=no, 1=yes): NA; chemo? (0=no, 1=yes): NA; treatment type: NA; dfs time: 4.83; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.83; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.83; dss event (defined as death from breast cancer): 0; ', 'ln status: LN+; er status: ER+; pgr status: PgR+; her2 status: NA; histological grade: G3; size (mm): 35; patient age: 53; histology: invasive ductal carcinoma; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tam+CMFx6 cycles; dfs time: 4.33; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 4.33; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.33; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: NA; her2 status: He+; histological grade: G2; size (mm): 30; patient age: 63; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 3.05; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 3.44931506849315; dss event (defined as death from breast cancer): 1; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 28; patient age: 47; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: CMFx6; Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 1.39; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 2.12602739726027; dss event (defined as death from breast cancer): 1; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 25; patient age: 59; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 0.65; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 3.07945205479452; dss event (defined as death from breast cancer): 1; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 21; patient age: 66; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 4.18; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 4.19452054794521; dss event (defined as death from breast cancer): 1; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G3; size (mm): 17; patient age: 68; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 4.51; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 6.17260273972603; dss event (defined as death from breast cancer): 1; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: NA; size (mm): 85; patient age: 57; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 0.25; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 5.03561643835616; dss event (defined as death from breast cancer): 1; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 32; patient age: 38; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: ECx4; Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 1.35; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 2.75342465753425; dss event (defined as death from breast cancer): 1; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G3; size (mm): 46; patient age: 63; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 2.21; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 4.92876712328767; dss event (defined as death from breast cancer): 1; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 34; patient age: 73; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx3/CMFx1; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 3.80; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 4.62191780821918; dss event (defined as death from breast cancer): 1; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 35; patient age: 70; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 0.76; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 0.991780821917808; dss event (defined as death from breast cancer): 1; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He-; histological grade: G1; size (mm): 10; patient age: 46; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tamoxifen+Zoledronic acid; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 2.18; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 2.18904109589041; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G2; size (mm): 13; patient age: 36; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tamoxifen+Zoledronic acid; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 2.42; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 7.07945205479452; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He-; histological grade: G1; size (mm): 55; patient age: 54; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 6.15; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 8.02191780821918; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G3; size (mm): 40; patient age: 60; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: CMFx2; Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 3.65; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 6.75068493150685; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 37; patient age: 72; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Arimidex/Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 3.30; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: 5.16438356164384; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G2; size (mm): 10; patient age: 54; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 7.82; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 7.82191780821918; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: NA; her2 status: He+; histological grade: G2; size (mm): 12; patient age: 48; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: Tamoxifen+Zoledronic acid; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 7.85; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 7.85479452054795; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G3; size (mm): 18; patient age: 55; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 7.31; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 7.30684931506849; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He+; histological grade: G2; size (mm): 20; patient age: 81; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 7.57; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 7.57260273972603; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G2; size (mm): 20; patient age: 52; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: ACx4; Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 6.02; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.01917808219178; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G2; size (mm): 15; patient age: 77; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 6.18; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.17534246575342; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He+; histological grade: G2; size (mm): 35; patient age: 70; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 6.65; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.65205479452055; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 40; patient age: 67; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: ACx6; Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 6.61; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.61369863013699; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G3; size (mm): 27; patient age: 62; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 6.13; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.12876712328767; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G1; size (mm): 27; patient age: 66; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 5.94; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.93698630136986; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He+; histological grade: G1; size (mm): 20; patient age: 57; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 3.12; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 3.11506849315069; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: NA; pgr status: NA; her2 status: NA; histological grade: G3; size (mm): 32; patient age: 46; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: CMFx6; Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 2.57; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 2.57260273972603; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: NA; size (mm): 38; patient age: 73; histology: NA; adjuvant treated? (0=no, 1=yes): NA; characteristics: endocrine? (0=no, 1=yes): NA; chemo? (0=no, 1=yes): NA; treatment type: NA; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 6.19; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.18630136986301; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 14; patient age: 42; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CMFx6; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 6.69; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.69315068493151; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G3; size (mm): 19; patient age: 53; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 5.52; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.52328767123288; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G3; size (mm): 20; patient age: 60; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: ACx4; Arimidex/Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 5.11; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.10958904109589; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 14; patient age: 61; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: CMFx6; Arimidex/Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 5.57; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.56712328767123; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: NA; histological grade: G3; size (mm): 45; patient age: 59; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: ACx4; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 6.26; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 6.25753424657534; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He-; histological grade: G2; size (mm): 20; patient age: 70; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 5.13; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.13424657534247; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He-; histological grade: G2; size (mm): 20; patient age: 45; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CMFx6; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 4.64; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.64383561643836; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He+; histological grade: G3; size (mm): 60; patient age: 48; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CMFx6; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 5.01; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 5.00821917808219; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G2; size (mm): 30; patient age: 45; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 4.56; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.56164383561644; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 27; patient age: 46; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 1; treatment type: CMFx6; Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 4.96; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.95890410958904; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR+; her2 status: He+; histological grade: G1; size (mm): 30; patient age: 56; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 3.93; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 3.92602739726027; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER+; pgr status: PgR-; her2 status: He-; histological grade: G2; size (mm): 20; patient age: 72; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 1; chemo? (0=no, 1=yes): 0; treatment type: Tamoxifen; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 4.51; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 4.50958904109589; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: PgR-; her2 status: He-; histological grade: G3; size (mm): 29; patient age: 50; histology: NA; adjuvant treated? (0=no, 1=yes): 1; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 1; treatment type: CMFx6; dfs time: NA; dfs event (defined as any type of recurrence or death from breast cancer): NA; dmfs time: 1.66; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: 1.66027397260274; dss event (defined as death from breast cancer): 0; ', 'ln status: LN-; er status: ER-; pgr status: NA; her2 status: NA; histological grade: NA; size (mm): 10; patient age: 67; histology: NA; adjuvant treated? (0=no, 1=yes): 0; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 0; treatment type: none; dfs time: 7.15; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 7.151; dmfs event (defined as distant metastasis or death from breast cancer): 1; DSS time: NA; dss event (defined as death from breast cancer): NA; ', 'ln status: LN-; er status: ER-; pgr status: NA; her2 status: NA; histological grade: G2; size (mm): 23; patient age: 37; histology: NA; adjuvant treated? (0=no, 1=yes): 0; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 0; treatment type: none; dfs time: 10.61; dfs event (defined as any type of recurrence or death from breast cancer): 1; dmfs time: 10.614; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: NA; dss event (defined as death from breast cancer): NA; ', 'ln status: LN-; er status: ER+; pgr status: NA; her2 status: NA; histological grade: G1; size (mm): 21; patient age: 43; histology: NA; adjuvant treated? (0=no, 1=yes): 0; characteristics: endocrine? (0=no, 1=yes): 0; chemo? (0=no, 1=yes): 0; treatment type: none; dfs time: 9.42; dfs event (defined as any type of recurrence or death from breast cancer): 0; dmfs time: 9.419; dmfs event (defined as distant metastasis or death from breast cancer): 0; DSS time: NA; dss event (defined as death from breast cancer): NA; ' GSE37915 Mus musculus 19 Expression profiling by array GPL4134 Predicting drug responsiveness in humans cancers using genetically engineered mice 2012-05-10 Anti-cancer drug testing is challenging, but genetically engineered mouse models (GEMMs) and orthotopic, syngeneic transplants (OSTs) may offer advantages for pre-clinical testing including an intact microenvironment. We examined the efficacy of six chemotherapeutic or targeted anti-cancer drugs, alone and in combination, using over 500 GEMMs/OSTs representing three distinct breast cancer subtypes: Basal-like (C3(1)-T-antigen GEMM), Luminal B (MMTV-Neu GEMM), and Claudin-low (T11/TP53-/- OST). While a few single agents offered exceptional efficacy like lapatinib in the Neu/ERBB2 driven model, combination therapies tended to be more active and life prolonging. Using expression profiling of chemotherapy treated murine tumors, we identified an expression signature that was able to predict pathological complete response to neoadjuvant anthracycline-taxane treated human breast cancer patients, even after accounting for the common clinical variables and other genomic signatures. These results show that credentialed murine models can predict the efficacy of would-be anti-cancer compounds in humans, and that GEMMs can be used to develop new biomarkers of therapeutic responsiveness in humans. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37915 Predicting drug responsiveness in human cancers using genetically engineered mice. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-13-0522 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-13-0522} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA166913 https://www.ebi.ac.uk/ena/browser/view/PRJNA166913 None [Overal design]control X treatment; [Treatment]'described in He et al., 2004. BioTechniques, Vol. 37:464–468', 'described in Hu et al., 2005, BioTechniques, 38:121-124'; [Growth]'described in He et al., 2004. BioTechniques, Vol. 37:464–468', 'described in Hu et al., 2005, BioTechniques, 38:121-124'; [Extraction]'Qiagen Rneasy Kit', 'total RNA', 'Total RNA'; [Cell type]'Source: ''reference: Whole Mouse Reference; ', 'strain: FVB; tissue: mammary adenocarcinoma; promoter: C3(1) rat; transgene: Simian virus 40 T antigen; origin: Jeff Green NIH; availability: Jackson Laboratories strain #013591; ' GSE85317 Homo sapiens 7 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Analysis of genome-wide occupancy of menin, MLL1 and MLL2 in MCF-7 cells 2016-08-08 We performed ChIP-seq using antibodies directed at menin, MLL1 and MLL2 in MCF-7 cells in order to assess the genome-wide presence of these proteins in MCF-7 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE85317 Enhancer-Mediated Oncogenic Function of the Menin Tumor Suppressor in Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2017.02.025 {Cell reports (7.815): 10.1016/j.celrep.2017.02.025} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA338168 https://www.ebi.ac.uk/ena/browser/view/PRJNA338168 https://www.ncbi.nlm.nih.gov/sra?term=SRP081098 [Overal design]MCF-7 cells were synchronized in phenol red-free medium containing 10% charcoal dextran-treated fetal bovine serum (CDT medium). Cells were treated with 10 nM estradiol (E2) or vehicle for 45 minutes. Menin, MLL1 and MLL2 ChIP-seq was performed after vehicle treatment. In addition, the menin cistrome was defined 45 min after treatment with E2.; [Treatment]'MCF-7 cells were synchronized for 72 hrs in phenol red-free medium (DMEM) containing 10% charcoal dextran-treated fetal bovine serum (CDT medium). Cells were treated with 10 nM estradiol or vehicle for 45 min.'; [Growth]'Cells were maintained at 37oC and 5% CO2 in DMEM + 10% FBS and Pen-Strep.'; [Extraction]'Cells were crosslinked, lysed in a buffer containing sarkosyl and sonicated.\nThruPLEX-FD Prep kit, Rubicon Genomics'; [Cell type]'Source: ''chip antibody: anti-Menin(MEN1) (A300-115A,Bethyl); cell line: MCF7; treatment: vehicle; ', 'chip antibody: none; cell line: MCF7; treatment: vehicle; ', 'chip antibody: anti-Menin(MEN1) (A300-115A,Bethyl); cell line: MCF7; treatment: 10 nM estradiol (E2); ', 'chip antibody: none; cell line: MCF7; treatment: 10 nM estradiol (E2); ', 'chip antibody: anti-MLL1 (A300-086A, Bethyl); cell line: MCF7; treatment: vehicle; ', 'chip antibody: anti-MLL2/TRX2 (A300-113A, Bethyl); cell line: MCF7; treatment: vehicle; ', 'chip antibody: none; cell line: MCF7; ' GSE28949 Mus musculus 16 Expression profiling by array GPL6885 miR-135b exerts metastatic activity in the ErbB2 driven mammary carcinogenesis 2011-04-28 In view of the roles played by miRNAs in cancer progression, we performed a microarray analysis aimed at identifying miR-135b target genes in breast cancer cells. Detection of transcripts affected by silencing of mir-135b was done using a time course at 24, 48 and 72 h both transfecting cell with mir-135b specific miRIDIAN microRNA Hairpin Inhibitor or miRIDIAN microRNA Hairpin Inhibitor negative control. Each experimental condition was repeated three times and analysed on on MOUSEREF-8 V2 Illumina bead chips. Genome studio was used to generate raw intensity signal without normalization. Data log2 transformation and loess normalization was performed with oneChannelGUI. Data were filtered using an IQR filter (i.e. only genes characterized by an IQR > 0.25, were retained for further analysis). Detection of differentially expressed transcripts was also performed with oneChannelGUI, using masigpro package with default parameters. Data were visualized by hierarchical clustering, as log2 ratio between anti-miR135b and the negative control using TMEV software. The subset of transcripts characterized by an increase in expression as consequence of a reduction of expression of miR135b were selected. MicroRNA target data for mir135b were retrieved from miranda database (microRNAsmiranda.mouse_predictions_S_C_aug2010.txt, http://www.microrna.org/microrna/home.do). Miranda data and transcripts increasing their expression upon silencing of miR135b were intersected to find the genes in common. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28949 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA140431 https://www.ebi.ac.uk/ena/browser/view/PRJNA140431 None [Overal design]Detection of transcripts affected by silencing of mir-135b was done using a time course at 24, 48 and 72 h both transfecting cell with mir-135b specific miRIDIAN microRNA Hairpin Inhibitor or miRIDIAN microRNA Hairpin Inhibitor negative control.; [Treatment]'To obtain BALB-neuT cells silenced or overexpressing miR-135a and miR-135b, cells were plated in 6-well plates at 90% confluency and transfected 24h later using using LipofectamineTM2000 (Invitrogen Life Technologies, Carlsbad, CA) reagent, according to manufacturer’s instruction, with 200 nM of specific miRIDIAN microRNA Hairpin Inhibitor (anti-miR-135b) or Mimics (miR-135b-over)(Thermo Scientific Dharmacon). For each experiments cells were also transfected with miRIDIAN microRNA Hairpin Inhibitor or Mimics negative control (control).'; [Growth]'BALB-neuT mammary cell lines were cultured in DMEM with Glutamax 1 (DMEM, Life Technologies) supplemented with 20% heat-inactivated fetal bovine serum (Invitrogen)'; [Extraction]'mirVana miRNA isolation kit (Applied Biosystems, Milano, Italy)'; [Cell type]'Source: ''cell line: TUBO; knockdown: scrambled; time: 48h; ', 'cell line: TUBO; knockdown: anti-mir135b; time: 48h; ', 'cell line: TUBO; knockdown: scrambled; time: 24h; ', 'cell line: TUBO; knockdown: scrambled; time: 72h; ', 'cell line: TUBO; knockdown: anti-mir135b; time: 72h; ', 'cell line: TUBO; knockdown: anti-mir135b; time: 24h; ' GSE10450 Mus musculus 52 Expression profiling by array GPL2872; GPL4134 Met induces mammary tumors with diverse histologies and is associated with poor outcome and human basal breast cancer 2008-02-08 Elevated Met receptor tyrosine kinase (RTK) expression correlates with poor outcome in breast cancer, yet a causal role for Met in the development of breast cancer has not been directly established. To examine this question, we generated a transgenic mouse model that targets expression of an oncogenic Met receptor (MetMut) to the mammary epithelium. We show that MetMut induces mammary tumors with a variety of histopathologies that exhibit gene expression profiles sharing similarities with human basal and luminal breast tumor subtypes. Among all breast cancers, we further demonstrate that the Met receptor is primarily overexpressed in human basal and HER2 positive breast cancers, and that a Met associated gene expression signature identifies patients with poor prognosis. Keywords: Met, mammary, poor outcome, EMT, basal breast cancer https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE10450 Met induces mammary tumors with diverse histologies and is associated with poor outcome and human basal breast cancer. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.0810402106 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.0810402106} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA108003 https://www.ebi.ac.uk/ena/browser/view/PRJNA108003 None [Overal design]Common reference design. 26 samples (including 20 normal tissue and 32 tumor tissue samples) replicated twice as dye swaps, generating a total of 52 arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'Phenol-chloroform extraction', 'No extraction'; [Cell type]'Source: ''Sample identifier: 562T; Diagnosis: MIN with solid, nodular intra lobular polyps; Sex: Female; Strain: FVB/N; ', '', 'Sample identifier: 4164N; Diagnosis: Normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 5156T; Diagnosis: erbb2-type carcinoma; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 4691T; Diagnosis: erbb2-type carcinoma; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 5156N; Diagnosis: normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 5033N; Diagnosis: normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 4691N; Diagnosis: Normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 5154N; Diagnosis: Normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 5154T; Diagnosis: adenosquamous carcinoma with cellular stroma; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 3229N; Diagnosis: Normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 3229T; Diagnosis: adenosquamous carcinoma; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 5033T; Diagnosis: erbb2-type carcinoma; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 4164T; Diagnosis: erbb2-type carcinoma; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 562N; Diagnosis: normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 559N; Diagnosis: normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 559T; Diagnosis: solid nodular, erbb2-type carcinoma; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 6696N; Diagnosis: normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 6696T; Diagnosis: erbb2-type carcinoma; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 4164N; Diagnosis: normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 4691N; Diagnosis: normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 5154N; Diagnosis: normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 3229N; Diagnosis: normal; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 5612T; Diagnosis: adenocarcinoma; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 4425T; Diagnosis: adenocarcinoma; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 4695T; Diagnosis: scirrhous adenocarcinoma; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 5033T4; Diagnosis: papillary carcinoma; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 5482T; Diagnosis: type A microacinar carcinoma with squamous metaplasia; Sex: Female; Strain: FVB/N; ', 'Sample identifier: 567T; Diagnosis: adenocarcinoma with sclerosis; Sex: Female; Strain: FVB/N; ' GSE132434 Homo sapiens 2 Other GPL20795 Genome-wide maps of chromatin accessibility before and after NR2F2 knock down using ATAC-seq. 2019-06-10 FOXA1 and GATA3 can remodel chromatin accessibility, we further explored what effect of NR2F2 would have on chromatin properties. ATAC-seq (Assay for Transposase Accessible Chromatin with high-throughput sequencing) is widely used to map chromatin accessibility genome-wide. Thus, We perform ATAC-seq without oestrogen stimulation before and after NR2F2 depletion.Covalent modifications are a main chromatin property.To test whether NR2F2 favoured histone modification deposition on chromatin, we profiled ChIP-Seq of H3K4me1, H3K4me3, and H3K27ac following NR2F2 depletion in oestrogen-starved MCF-7 cells to gain comprehensive histone medication landscape. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132434 Cooperativity of co-factor NR2F2 with Pioneer Factors GATA3, FOXA1 in promoting ERα function. Theranostics 8.063 https://doi.org/10.7150/thno.34874 {Theranostics (8.063): 10.7150/thno.34874} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA548081 https://www.ebi.ac.uk/ena/browser/view/PRJNA548081 https://www.ncbi.nlm.nih.gov/sra?term=SRP200961 [Overal design]Study of chromatin accessibility in WT and NR2F2 KO MCF-7 cells by deep sequencing using Illumina xten.; [Treatment]'DNA of MCF-7 cells with WT and NR2F2 KO were extracted using standard Illumina protocals.'; [Growth]'The MCF-7 cells were maintained in DMEM supplemented with 10% fetal bovinw serum at 37℃ incubator'; [Extraction]'50,000 sorted cells were washed with cold PBS and suspended in lysis buffer for 10-15 min on ice. DNA was purified using MinElute PCR Purification Kit (Qiagen). Transposed DNA was amplified using NEB Next High-Fidelity 2X PCR Master Mix and libraries were sequenced on HiSeq 4000\nDNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'breast cancer cell line''cell line: MCF7; cell type: breast cancer cell line; genotype/variation: shCTRL; ', 'cell line: MCF7; cell type: breast cancer cell line; genotype/variation: shNR2F2; ' GSE157060 Homo sapiens 6 Expression profiling by array GPL10558 lncRNA Mitochondrial oxygen responsive transcript 1 (MTORT1) downstream gene microarray 2020-08-28 Long non-coding RNAs (lncRNAs) have been regarded to participate in multiple genetic pathways in cancer. Also, mitochondria-associated lncRNAs have been discovered to module mitochondrial function and metabolism. Previously, our lab identified oxygen responsive lncRNAs in breast cancer MCF-7 cells under normoxic, hypoxic and re-oxygenated conditions by using next generation sequencing technology. Among them, a novel mitochondrial lncRNA Mitochondrial Oxygen Responsive Transcript 1 (MTORT1) was chosen for further investigation. Therefore, the purpose of this study was to investigate the characterizations, function roles, and mechanisms of MTORT1 in breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE157060 Regulatory Mechanisms and Functional Roles of Hypoxia-Induced Long Non-Coding RNA MTORT1 in Breast Cancer Cells. Frontiers in oncology 4.137 https://doi.org/10.3389/fonc.2021.663114 {Frontiers in oncology (4.137): 10.3389/fonc.2021.663114} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA659997 https://www.ebi.ac.uk/ena/browser/view/PRJNA659997 None [Overal design]Total RNA obtained from MCF-7 cells transfected with siRNA against MTORT1 for 48 hours compared to MCF-7 cells transfected with control siRNA; [Treatment]'MCF-7 cells were transfected with 100 nM siRNA against MTORT1 for 48 hours.'; [Growth]'None'; [Extraction]'Total RNA was extracted using NucleoZOL reagent (Machery-Nagel, Düren, Germany) according to the manufacturer’s protocol.'; [Cell type]'Source: ''cell line: MCF-7; transfection: Negative control siRNA; ', 'cell line: MCF-7; transfection: siRNA against MTORT1; ' GSE103093 Homo sapiens 171 Non-coding RNA profiling by array GPL21439 Profiling of microRNA expression in canine mammary cancer 2017-08-25 MicroRNAs may act as oncogenes or tumour suppressor genes, which make these small molecules potential diagnostic/prognostic factors and targets for anticancer therapies. On account of this, we performed large-scale profiling of microRNA expression in canine mammary cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE103093 MicroRNA expression patterns in canine mammary cancer show significant differences between metastatic and non-metastatic tumours. BMC cancer 2.933 https://doi.org/10.1186/s12885-017-3751-1 {BMC cancer (2.933): 10.1186/s12885-017-3751-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA400178 https://www.ebi.ac.uk/ena/browser/view/PRJNA400178 None [Overal design]Expression profiles of 317 microRNAs in 146 canine mammary tumours of different histological type, malignancy grade and clinical history (presence/absence of metastases) and in 25 control samples were evaluated.; [Treatment]'None'; [Growth]'None'; [Extraction]"RNA was isolated from tumour pieces with a diameter of 1 cm. Each piece was washed with RNase Away Reagent (Ambion) and disrupted in Tissue Lyser LT (QIAGEN) at 50 Hz for 30 min. After disruption, total RNA was isolated from samples using miRNeasy Mini Kit (QIAGEN) according to the manufacturer's protocol."; [Cell type]'Source: ''tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Bobtail; age [years]: 10; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Cocker Spaniel-mix; age [years]: 12; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Rottweiler; age [years]: 10; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Dalmatian; age [years]: 10; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Irish Setter; age [years]: 7; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Cocker Spaniel; age [years]: 11; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Staffordshire Terrier; age [years]: 10; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: West Highland White Terrier; age [years]: 10; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Soft Coated Wheaton Terrier; age [years]: 12; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Crossbreed; age [years]: 11; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Bavarian Mountain Hound; age [years]: 13; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Terrier-mix; age [years]: 11; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Staffordshire Terrier; age [years]: 11; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: German Shorthaired Pointer; age [years]: 12; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Poodle; age [years]: 11; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Golden Retriever; age [years]: 11; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Kromfohrlander; age [years]: 11; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Kerry Blue Terrier; age [years]: 10; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Shepherd-mix; age [years]: 11; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: West Highland White Terrier; age [years]: 12; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Yorkshire Terrier; age [years]: 12; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Yorkshire Terrier; age [years]: 11; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Shepherd-mix; age [years]: 9; ', 'tissue: normal mammary gland; control/tumour type: Control; grade of malignancy: Not applicable; metastasis: Not applicable; histological type: Not applicable; breed: Dachshund; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Tubulopapillary carcinoma; breed: Shih-Tzu; age [years]: 8; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Noninfiltrating carcinoma; breed: Staffordshire Terrier; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Benign mesenchymal tumour (chondroma); breed: West Highland White Terrier; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: No; histological type: Tubulopapillary carcinoma; breed: Terrier-mix; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Complex carcinoma; breed: Staffordshire Terrier; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Noninfiltrating carcinoma; breed: Kerry Blue Terrier; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Atypical complex adenoma; breed: Yorkshire Terrier; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Benign mesenchymal tumour (chondroma and osteoma); breed: Shepherd-mix; age [years]: 9; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Dachshund; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Complex carcinoma; breed: Cocker Spaniel; age [years]: 7; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: No; histological type: Complex carcinoma; breed: Great Dane; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Tubulopapillary carcinoma + Solid carcinoma; breed: Shepherd-mix; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: No; histological type: Complex carcinoma; breed: Shepherd-mix; age [years]: 14; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Tubulopapillary carcinoma; breed: Unknown; age [years]: Unknown; ', 'tissue: mammary tumour; control/tumour type: Malignant + Hyperplasia; grade of malignancy: I; metastasis: No; histological type: Complex carcinoma + Mammary ductal ectasia; breed: Labrador; age [years]: 5; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Complex carcinoma; breed: Miniature Poodle; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Atypical papilloma; breed: Dalmatian; age [years]: 9; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Complex carcinoma; breed: Cairn-Terrier; age [years]: 14; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Solid carcinoma / Lipid-rich carcinoma; breed: Dachshund; age [years]: 13; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Complex carcinoma; breed: Munsterlander; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Irish Setter; age [years]: 9; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Basaloid adenoma; breed: Kleiner Munsterlander; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: No; histological type: Simple carcinoma; breed: Poodle; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Solid carcinoma; breed: Shepherd-mix; age [years]: 8; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Yes; histological type: Comedocarcinoma; breed: West Highland White Terrier; age [years]: 13; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Labrador-mix; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Simple adenoma + Complex adenoma; breed: Spitz-mix; age [years]: 7; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Weimaranian; age [years]: 7; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Simple adenoma; breed: Doberman; age [years]: 7; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Comedocarcinoma; breed: Yorkshire Terrier; age [years]: 14; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Atypical papilloma; breed: Sharpei; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Yes; histological type: Squamous cell carcinoma; breed: French Bulldog; age [years]: 15; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: Spitz-mix; age [years]: 16; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: Beagle; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Yes; histological type: Comedocarcinoma; breed: Crossbreed; age [years]: 9; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Noninfiltrating carcinoma; breed: Crossbreed; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: American Cocker Spaniel; age [years]: 6; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Tubulopapillary carcinoma / Noninfiltrating carcinoma; breed: Terrier-mix; age [years]: 9; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Lipid-rich carcinoma; breed: Labrador-mix; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Complex carcinoma; breed: Collie-mix; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Unknown; age [years]: Unknown; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; breed: Crossbreed; age [years]: Unknown; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: Pointer; age [years]: 14; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Comedocarcinoma; breed: Crossbreed; age [years]: Unknown; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Bolognese; age [years]: 7; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Atypical simple adenoma; breed: Crossbreed; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Fox Terrier; age [years]: 9; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Anaplastic carcinoma; breed: Crossbreed; age [years]: Unknown; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; breed: German Shepherd; age [years]: 14; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: Dachshund; age [years]: 14; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Labrador-mix; age [years]: 8; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: No; histological type: Squamous cell carcinoma; breed: Crossbreed; age [years]: Unknown; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Complex carcinoma; breed: Crossbreed; age [years]: 13; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Comedocarcinoma; breed: Crossbreed; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Complex carcinoma; breed: Cavalier King Charles Spaniel; age [years]: 8; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Simple adenoma; breed: Shepherd-mix; age [years]: 8; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Crossbreed; age [years]: 13; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Comedocarcinoma; breed: Crossbreed; age [years]: 7; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Complex carcinoma; breed: Dachshund; age [years]: 15; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Poodle; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Crossbreed; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Basaloid carcinoma; breed: Golden Retriever; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Benign mixed tumour; breed: Pekingese; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant + Benign; grade of malignancy: III; metastasis: No; histological type: Tubulopapillary carcinoma + Noninfiltrating carcinoma + Benign mixed tumour; breed: Dachshund; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Tubulopapillary carcinoma; breed: Crossbreed; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Solid carcinoma; breed: Scent Hound; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: German Shepherd; age [years]: 9; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Unknown; histological type: Tubulopapillary carcinoma; breed: Crossbreed; age [years]: ~ 7; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: Unknown; metastasis: No; histological type: Tubulopapillary carcinoma; breed: Crossbreed; age [years]: 16; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Simple adenoma; breed: Crossbreed; age [years]: 5; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Complex carcinoma; breed: Crossbreed; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: Unknown; metastasis: Unknown; histological type: Complex carcinoma; breed: Dachshund; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Tubulopapillary carcinoma; breed: Dachshund; age [years]: 13; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Complex carcinoma; breed: Welsh Terrier; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: No; histological type: Tubulopapillary carcinoma; breed: German Shepherd; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: Unknown; metastasis: No; histological type: Tubulopapillary carcinoma; breed: Boxer; age [years]: 7; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: No; histological type: Tubulopapillary carcinoma; breed: Unknown; age [years]: Unknown; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Unknown; histological type: Tubulopapillary carcinoma; breed: Crossbreed; age [years]: 13; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Atypical papilloma; breed: Crossbreed; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: No; histological type: Complex carcinoma; breed: Braque; age [years]: 6; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Irish Terrier; age [years]: 7; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Mucinous carcinoma + Tubulopapillary carcinoma; breed: Dachshund; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: No; histological type: Mucinous carcinoma; breed: Crossbreed; age [years]: 6; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Unknown; histological type: Scirrhous carcinoma; breed: Crossbreed; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Complex carcinoma; breed: German Shepherd; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: No; histological type: Tubulopapillary carcinoma; breed: Crossbreed; age [years]: 9; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Atypical adenoma; breed: French Bulldog; age [years]: 5; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Fox Terrier; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Unknown; histological type: Solid carcinoma; breed: Akita; age [years]: 5; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Solid carcinoma; breed: German Shepherd; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Solid carcinoma; breed: Bavarian Mountain Hound; age [years]: 6; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Unknown; histological type: Tubulopapillary carcinoma; breed: German Shepherd; age [years]: 9; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: No; histological type: Tubulopapillary carcinoma; breed: Braque; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: No; histological type: Solid carcinoma; breed: German Shepherd; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Unknown; histological type: Comedocarcinoma; breed: Dachshund; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: No; histological type: Carcinoma; breed: York; age [years]: 13; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Solid carcinoma; breed: Unknown; age [years]: Unknown; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: No; histological type: Solid carcinoma; breed: German Shepherd; age [years]: 13; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: Unknown; metastasis: Unknown; histological type: Carcinosarcoma; breed: Unknown; age [years]: Unknown; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Unknown; histological type: Tubulopapillary carcinoma; breed: Stafford Shire Bulterier; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: Bobtail; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Yes; histological type: Tubulopapillary carcinoma + Solid carcinoma; breed: Rottweiler; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: Dachshund; age [years]: 13; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Anaplastic carcinoma; breed: Bavarian Mountain Hound; age [years]: 13; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Yes; histological type: Solid carcinoma; breed: Golden Retriever; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Yes; histological type: Solid carcinoma; breed: West Highland White Terrier; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Yes; histological type: Special type of carcinoma; breed: Poodle; age [years]: 16; ', 'tissue: mammary tumour; control/tumour type: Benign; grade of malignancy: Not applicable; metastasis: No; histological type: Complex adenoma; breed: Afghan Hound; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: West Highland White Terrier; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: Unknown; metastasis: Yes; breed: Unknown; age [years]: Unknown; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Yes; histological type: Comedocarcinoma; breed: Crossbreed; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: German Shepherd; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: Rottweiler-mix; age [years]: 6; ', 'tissue: mammary tumour; control/tumour type: Malignant + Benign; grade of malignancy: I; metastasis: Yes; histological type: Tubulopapillary carcinoma + Complex adenoma; breed: Shih-Tzu; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Solid carcinoma; breed: Crossbreed; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Comedocarcinoma; breed: Poodle; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Comedocarcinoma; breed: German Shorthaired Pointer; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Anaplastic carcinoma; breed: Airedale Terrier; age [years]: 9; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: Dachshund; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Solid carcinoma; breed: Dunker Hound; age [years]: 14; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Solid carcinoma; breed: Dachshund; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Comedocarcinoma; breed: Lhasa Apso; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Solid carcinoma; breed: Cocker Spaniel; age [years]: 8; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Solid carcinoma; breed: Dachshund; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; histological type: Squamous cell carcinoma; breed: Boxer; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; histological type: Scirrhous carcinoma; breed: Elkhound; age [years]: 11; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Yes; histological type: Solid carcinoma; breed: Poodle; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Comedocarcinoma; breed: Border Collie; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: Shetland Sheepdog; age [years]: 8; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Comedocarcinoma; breed: German Shepherd; age [years]: 8; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; histological type: Comedocarcinoma; breed: Elkhound; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: Borzoi; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; histological type: Scirrhous carcinoma; breed: German Shepherd; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Yes; histological type: Tubulopapillary carcinoma + Bi-phasic carcinoma; breed: Samoyed; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Solid carcinoma; breed: Pointer; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; histological type: Solid carcinoma; breed: German Shepherd; age [years]: 10; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: III; metastasis: Yes; histological type: Lipid-rich carcinoma; breed: Drever; age [years]: 8; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: I; metastasis: Yes; histological type: Tubulopapillary carcinoma; breed: Shih-Tzu; age [years]: 12; ', 'tissue: mammary tumour; control/tumour type: Malignant; grade of malignancy: II; metastasis: Yes; histological type: Solid carcinoma; breed: Labrador; age [years]: 11; ' GSE77138 Homo sapiens 13 Genome variation profiling by SNP array; Genome binding/occupancy profiling by genome tiling array GPL16131; GPL17586 Large genomic alteration of 7q in two patients with multiple primary cancers, including triple negative breast cancer, and family history of malignant neoplasms 2016-01-22 A great percentage of patients with multiple primary cancers (MPCs) and family history of cancer are suspected to have a hereditary cancer predisposition syndrome. However, only a small proportion of these cases are explained by mutations in high-penetrance genes, suggesting the involvement of undiscovered genes in cancer predisposition. In this study, we report the molecular and clinical characterization of two unrelated patients with MPCs, a positive family history of cancer, no germline pathogenic mutations in BRCA1, BRCA2 and TP53 genes and large genomic rearrangements mapped on chromosome 7q. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE77138 Germline large genomic alterations on 7q in patients with multiple primary cancers. Scientific reports 4.011 https://doi.org/10.1038/srep41677 {Scientific reports (4.011): 10.1038/srep41677} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA309532 https://www.ebi.ac.uk/ena/browser/view/PRJNA309532 None [Overal design]Genomic rearrangements were assessed with Affymetrix CytoScan HD Array platform in two unrelated patients (Patient 1 and Patient 2) with multiple primary cancers. The mother of Patient 2 and five children (two of Patient 1 and three of Patient 2) were also evaluated. In addition, we performed the transcriptome analysis of the triple negative BC from Patient 2 using the Affymetrix HTA 2.0 platform.; [Treatment]'Not applicable'; [Growth]'Not applicable'; [Extraction]'Genomic DNA was extracted from peripheral blood of patients, mother of Patient 2 and four children and from breast tumor tissue (Patient 2) using the standard protocol of Gentra Puregene Blood Kit (Qiagen, Valencia, Ca, USA)', 'Total RNA was isolated from the BC tissue of Patient 2 using the RNeasy Mini Kit (Qiagen, Valencia, Ca, USA), according to the manufacturer’s instructions. The Human Universal Reference RNA (Stratagene, Santa Clara, USA) was used as a reference sample for comparison with the tumor tissue.'; [Cell type]'Source: ''gender: female; ', 'gender: male; ', 'gender: female; tissue: Breast cancer tissue; ', 'tissue: Pool of 10 cell lines; ' GSE21994 Mus musculus 24 Expression profiling by array GPL6096; GPL6193 Exon-level transcriptome profiling in murine breast cancer reveals splicing changes specific to tumors with different metastatic abilities 2010-05-25 BACKGROUND: Breast cancer is the second most frequent type of cancer affecting women. We are increasingly aware that changes in mRNA splicing are associated with various characteristics of cancer. The most deadly aspect of cancer is metastasis, the process by which cancer spreads from the primary tumor to distant organs. However, little is known specifically about the involvement of alternative splicing in the formation of macroscopic metastases. Our study investigates transcript isoform changes that characterize tumors of different abilities to form growing metastases. METHODS AND FINDINGS: To identify alternative splicing events (ASEs) that are associated with the fully metastatic phenotype in breast cancer, we used Affymetrix Exon Microarrays to profile mRNA isoform variations genome-wide in weakly metastatic (168FARN and 4T07) and highly metastatic (4T1) mammary carcinomas. Statistical analysis identified significant expression changes in 7606 out of 155,994 (4%) exons and in 1725 out of 189,460 (1%) intronic regions, which affect 2623 out of 16,654 (16%) genes. These changes correspond to putative alternative isoforms-several of which are novel-that are differentially expressed between tumors of varying metastatic phenotypes. Gene pathway analysis showed that 1224 of genes expressing alternative isoforms were involved in cell growth, cell interactions, cell proliferation, cell migration and cell death and have been previously linked to cancers and genetic disorders. We chose ten predicted splice variants for RT-PCR validation, eight of which were successfully confirmed (MED24, MFI2, SRRT, CD44, CLK1 and HNRNPH1). These include three novel intron retentions in CD44, a gene in which isoform variations have been previously associated with the metastasis of several cancers. CONCLUSION: Our findings reveal that various genes are differently spliced and/or expressed in association with the metastatic phenotype of tumor cells. Identification of metastasis-specific isoforms may contribute to the development of improved breast cancer stage identification and targeted therapies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE21994 Exon-level transcriptome profiling in murine breast cancer reveals splicing changes specific to tumors with different metastatic abilities. PloS one 2.776 https://doi.org/10.1371/journal.pone.0011981 {PloS one (2.776): 10.1371/journal.pone.0011981} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA127213 https://www.ebi.ac.uk/ena/browser/view/PRJNA127213 None [Overal design]We used RNA tumor tissues derived from three murine mammary carcinoma cell lines (168FARN, 4T07 and 4T1); four biological replicates of 168FARN, four biological replicates of 4T07, and four biological replicates of 4T1 were hybridized independently at McGill university site.; [Treatment]'Four mice were injected (1×10^-5 cells) with 168FARN, five mice with 4T07 and four mice with 4T01. Tumor volumes were calculated using the following formula: (?LW^2)/6, where L is the length and W is the width of the tumor. Tumors were surgically removed, using a cautery unit, once they reached a volume between 100 and 125 mm^3.'; [Growth]'All cell lines were grown in DMEM supplemented with 10% fetal bovine serum, 10 mmol/L HEPES, 1 mmol/L sodium pyruvate, 1.5 g/L sodium bicarbonate, penicillin/streptomycin, and fungizone.'; [Extraction]'Total RNA was purified using RNeasy Mini Kit Columns following the manufacturers instructions. We assessed The RNA quality using RNA 6000 NanoChips with the Agilent 2100 Bioanalyzer (Agilent, Palo Alto, USA). Tumors were hybridized independently at the functional genomics facility of McGill University and Genome Quebec Innovation Centre (Montreal, Quebec, Canada).'; [Cell type]'Source: ''cell line: 168FARN; ', 'cell line: 4T07; ', 'cell line: 4T1; ' GSE58990 Homo sapiens 28 Expression profiling by array GPL5175 Activation of IFN/STAT1 signaling is a hallmark of response to chemotherapy in patient-derived xenografts of triple-negative breast cancer 2014-07-01 By using patient-derived xenografts (PDXs) as living surrogate of the clinical practice, we identify here induction of genes related to the IFN pathway as an early and specific predictor of tumor response to treatment. Gene expression profile of tumor cells after laser-capture microdissection of residual tumor foci to characterize the molecular changes occurring in residual tumor cells surviving chemotherapy https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58990 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA254062 https://www.ebi.ac.uk/ena/browser/view/PRJNA254062 None [Overal design]RNA was extracted from microdissected areas using the RNeasy Mini kit (Qiagen, Valencia, CA). This approach allowed isolating foci of human tumor cells from the murine stroma. Gene expression analysis was performed with Affymetrix Exon 1.0 ST microarrays. Hybridization, data normalization and statistical analysis were outsourced to GenoSplice Technology (Paris, France).; [Treatment]'Female Swiss nude mice, 10-week old, were purchased from Charles River (Les Arbresles, France). PDXs with tumors in a range between 60 and 200 mm3 received one dose of adriamycin (DOX, Doxorubicin, Teva Pharmaceuticals, Paris, France) and cyclophosphamide (Endoxan, Baxter, Maurepas, France) at the doses of 2 mg/kg, 6 mg/kg and 100 mg/kg'; [Growth]'None'; [Extraction]'RNA was extracted from microdissected areas using the RNeasy Mini kit (Qiagen, Valencia, CA). This approach allowed isolating foci of human tumor cells from the murine stroma. Gene expression analysis was performed with Affymetrix Exon 1.0 ST microarrays. Hybridization, data normalization and statistical analysis were outsourced to GenoSplice Technology (Paris, France).'; [Cell type]'Source: ''tissue: human breast cancer xenograft; sample type: control tumor; ', 'tissue: human breast cancer xenograft; sample type: residual nodules post-treatment; ' GSE63351 Homo sapiens 16 Expression profiling by array GPL10904 Combination of epigenetic, differentiation and DNA damaging agents induce tumor cell death and stem cell depletion in breast cancer 2014-11-17 Gene expression profiles were performed on MDA-MB-231 TNBC cell line treated with entinostast, all-trans retinoic acid (ATRA), and doxorubicin as single, double, and triple combinations using Illumina. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE63351 Combined Treatment with Epigenetic, Differentiating, and Chemotherapeutic Agents Cooperatively Targets Tumor-Initiating Cells in Triple-Negative Breast Cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-15-1619 {Cancer research (8.378) doi:10.1158/0008-5472.CAN-15-1619}; {Breast cancer research : BCR (None) doi:10.1186/s13058-018-1068-x}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA267553 https://www.ebi.ac.uk/ena/browser/view/PRJNA267553 None [Overal design]Treatment signatures were made from each drug treatment and integrated to find a comprehensive view of changes associated with the epigenetic, differentiation and chemotherapy combination; [Treatment]'MDA-MB-231 cells treated with entinostat (2.5 µM), ATRA (1 µM) and doxorubicin (0.2 µM), single and combinations treatments for 48h'; [Growth]'MDA-MB-231 cells grown in DMEM 10% FBS'; [Extraction]'RNA was extracted using RNeasy Mini Kit (Qiagen)'; [Cell type]'Source: ''cell line: MDA-MB-231; treatment: DMSO; replicate: 1; ', 'cell line: MDA-MB-231; treatment: Entinostat; replicate: 1; ', 'cell line: MDA-MB-231; treatment: ATRA; replicate: 1; ', 'cell line: MDA-MB-231; treatment: Doxorubicin; replicate: 1; ', 'cell line: MDA-MB-231; treatment: Entinostat and ATRA; replicate: 1; ', 'cell line: MDA-MB-231; treatment: Entinostat and Doxorubicin; replicate: 1; ', 'cell line: MDA-MB-231; treatment: ATRA and Doxorubicin; replicate: 1; ', 'cell line: MDA-MB-231; treatment: Entinostat and ATRA and Doxorubicin; replicate: 1; ', 'cell line: MDA-MB-231; treatment: DMSO; replicate: 2; ', 'cell line: MDA-MB-231; treatment: Entinostat; replicate: 2; ', 'cell line: MDA-MB-231; treatment: ATRA; replicate: 2; ', 'cell line: MDA-MB-231; treatment: Doxorubicin; replicate: 2; ', 'cell line: MDA-MB-231; treatment: Entinostat and ATRA; replicate: 2; ', 'cell line: MDA-MB-231; treatment: Entinostat and Doxorubicin; replicate: 2; ', 'cell line: MDA-MB-231; treatment: ATRA and Doxorubicin; replicate: 2; ', 'cell line: MDA-MB-231; treatment: Entinostat and ATRA and Doxorubicin; replicate: 2; ' GSE144463 Homo sapiens 50 Non-coding RNA profiling by array GPL15468 MicroRNA profiling in different types,grades and stages of breast cancer 2020-01-29 MicroRNA profiling was done using Taqman Low Density Arrays (TLDA) platform consisting of 667 microRNAs covering Sanger miRBase version10 cross 50 samples along with their adjacent normals consisting of different types (ER+ and ER-ve), grades (grade 2 and grade 3) with their different stages (I to III). The above isolated RNA which displayed good RIN value and linearity (R2>0.96), were used for reverse transcription (RT) reactions with the help of TaqMan MicroRNA Reverse Transcription Kit followed by real time PCR Reactions (ABI 7900 HT) as per manufacturer's instructions.A pre -amplification step of cDNA with pre-amp megaplex pool primers was carried out to significantly enhance the ability to detect highly down regulated miRNAs. The TaqMan human microRNA arrays consists of two plates, pool A and pool B. RNU 46 and RNU 48 were used as endogenous controls for data normalization. Another control not related to human was also included as a negative control. Each TaqMan Assay was run in quadruplicate. RNU 46 and RNU 48 expression was consistent in all the samples and displayed good range of CT values (22–24 ) where as in ‘No Template’ Control (NTC) CT value was above 38. The average CT values of total profiled miRNAs in all samples were normalized with RNU 46 & RNU 48 using spotfire (statminer) software and fold changes were represented in terms of 2 - Δ Δ CT (RQ ) and log10RQ. Only valid and significant miRNAs were picked up for further analysis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144463 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA603741 https://www.ebi.ac.uk/ena/browser/view/PRJNA603741 None [Overal design]Taqman Low Density Arrays (TLDA) were performed across 50 samples along with their adjacent normals consisting of different typs (ER+/ER-ve), grades (grade 2 and grade 3) and stages (stages I,II,III) of breast cancer samples. Another control not related to human is also included as a negative control.; [Treatment]'None'; [Growth]'None'; [Extraction]'A portion of the samples stored in RNA later was used for RNA isolation. Total RNAs were isolated by miRvana kit from homogenized samples using automated tissue homogenizer. The quantity of these RNAs were checked using nanodrop, whereas quality were assessed by agarose gel electrophoresis.RNA integrity number (RIN) was determined in Agilent Bioanalyzer (2100) to provide more robust measurement of RNA. The RIN values are algorithm which ranges between 1-10 where 10 indicates total intactness of RNA quality.Those samples >7 was taken for further analysis.'; [Cell type]'Source: ''disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 65 years; Stage: Stage I; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 52 years; Stage: Stage I; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 39 years; Stage: Stage I; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 42 years; Stage: Stage I; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 60 years; Stage: Stage I; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 60 years; Stage: Stage II; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 54 years; Stage: Stage II; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 57 years; Stage: Stage II; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 36 years; Stage: Stage II; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 50 years; Stage: Stage II; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 45 years; Stage: Stage II; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 67 years; Stage: Stage II; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 55 years; Stage: Stage III; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 66 years; Stage: Stage III; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 45 years; Stage: Stage III; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 60 years; Stage: Stage III; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 56 years; Stage: Stage III; grade: Grade 2; ', 'disease state: Breast cancer; tissue: Breast Normal tissue; gender: Female; age: 34 years; Stage: --; grade: --; ', 'disease state: Breast cancer; tissue: Breast Normal tissue; gender: Female; age: 67 years; Stage: --; grade: --; ', 'disease state: Breast cancer; tissue: Breast Normal tissue; gender: Female; age: 60 years; Stage: --; grade: --; ', 'disease state: Breast cancer; tissue: Breast Normal tissue; gender: Female; age: 36 years; Stage: --; grade: --; ', 'disease state: Breast cancer; tissue: Breast Normal tissue; gender: Female; age: 50 years; Stage: --; grade: --; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 35 years; Stage: Stage I; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 70 years; Stage: Stage I; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 40 years; Stage: Stage I; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 47 years; Stage: Stage I; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 51 years; Stage: Stage I; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 41 years; Stage: Stage I; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 65 years; Stage: Stage I; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 53 years; Stage: Stage II; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 57 years; Stage: Stage II; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 48 years; Stage: Stage II; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 35 years; Stage: Stage II; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 33 years; Stage: Stage II; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 39 years; Stage: Stage II; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 61 years; Stage: Stage II; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 57 years; Stage: Stage III; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 42 years; Stage: Stage III; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 53 years; Stage: Stage III; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 46 years; Stage: Stage III; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 55 years; Stage: Stage III; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 59 years; Stage: Stage III; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast tumor tissue; gender: Female; age: 48 years; Stage: Stage III; grade: Grade 3; ', 'disease state: Breast cancer; tissue: Breast Normal tissue; gender: Female; age: 41 years; Stage: --; grade: --; ', 'disease state: Breast cancer; tissue: Breast Normal tissue; gender: Female; age: 39 years; Stage: --; grade: --; ', 'disease state: Breast cancer; tissue: Breast Normal tissue; gender: Female; age: 64 years; Stage: --; grade: --; ', 'disease state: Breast cancer; tissue: Breast Normal tissue; gender: Female; age: 48 years; Stage: --; grade: --; ', 'disease state: Breast cancer; tissue: Breast Normal tissue; gender: Female; age: 49 years; Stage: --; grade: --; ' GSE138434 Homo sapiens 8 Expression profiling by high throughput sequencing GPL18573 CDH2 and Cx43 knockdown CSCs compaired with scramble (control) in breast cancer 2019-10-04 We report the gene expression changes in CDH2 and Cx43 knockdown CSCs as compaired to scramble (control) in MDA-MB-231 https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE138434 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA575855 https://www.ebi.ac.uk/ena/browser/view/PRJNA575855 None [Overal design]RNA sequencing on CDH2 and Cx43 knockdown CSCs to find difference in expression from control; [Treatment]'The CSCs from MDA-MB-231 with CDH2, Cx43 and Scramble knockdown were sorted using Flow cytometry. Cells were then incubated overnight at 37C / 5% CO2'; [Growth]'The CSCs from MDA-MB-231 with CDH2, Cx43 and Scramble knockdown cultured in DMEM supplemented with 10% FBS, L-glutamine and penicillin and streptomycin'; [Extraction]'Total RNA extraction was performed according to manufacturer’s protocols with the RNeasy Mini Kit (Qiagen). Ribosomal RNA was depleted with Ribo-Zero gold from Illumina (San Diego, CA)\nLibraries were prepared using the NEB Ultra II Library Preparation Kit and NEBNext® Multiplex Oligos for Illumina (Dual Index Primers Set 1) (New England BioLabs) following the manufacturer’s protocol.'; [Cell type]'Source: ''cell line: MDA-MB-231; knocked down: CDH2; ', 'cell line: MDA-MB-231; knocked down: CX43; ', 'cell line: MDA-MB-231; knocked down: scramble negative control; ' GSE63608 Homo sapiens 6 Expression profiling by high throughput sequencing GPL11154 Effect of REST on cancer invasiveness in MCF-7 and MDA-MB-231 cells using RNA-sequencing (RNA-seq) analysis . 2014-11-25 We report a negative correlation of invasiveness with REST expression. In addition, one alternatively spliced product (ASP) of REST, REST-003, shows a positive correlation with invasiveness. REST has a well-established role in regulating transcription of genes important for neuronal development. Its role in cancer, though significant, is less well understood. We would like to investigate the effect of REST on invasive phenotype. In order to do so, we downregulate REST by siRNA treatment in weakly invasive MCF-7 breast cancer cells in which REST is expressed highly: 1) si-GAPDH (control), two si-RESTs (2)si-REST_1 and 3) si-REST_2). Conversely, we overexpress REST by transfection of wt-REST cDNA in highly invasive MDA-MB-231 cells in which REST is expressed at the low level: 4) EGFP (control), 5) mt-REST (another control) and 6) wt-REST. REST (repressor element-1 (RE-1) silencing transcription factor) contains a DNA-binding domain that is localized within eight zinc fingers and two repressor domains located at the N-terminal and C-terminal, respectively. REST suppresses expression of neural-specific genes. mt-REST lacks two repressor domains, so it can be used as a control for wt-REST. In contrast, REST-003 is one of alternatively spliced products (ASPs) of REST. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE63608 Non-coding RNAs derived from an alternatively spliced REST transcript (REST-003) regulate breast cancer invasiveness. Scientific reports 4.011 https://doi.org/10.1038/srep11207 {Scientific reports (4.011): 10.1038/srep11207} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA268448 https://www.ebi.ac.uk/ena/browser/view/PRJNA268448 https://www.ncbi.nlm.nih.gov/sra?term=SRP050245 [Overal design]Downregulation of REST using two siRNAs in MCF-7 cells or overexpression of REST with wt- or mt-REST cDNA in MDA-MB-231 cells REST_ISOFORM_FIG1.pdf was provided to explain *rawRestIsoformCnts.txt files described in the README1.txt file.; [Treatment]'Lipofectamine 2000 (Invitrogen) was used for mt- or wt-REST cDNA plasmid transfection experiments. For siRNA transfection, we used DharmaFect (Thermo Scientific) or RNAiMax (Invitrogen) according to the manufacturer’s instructions.'; [Growth]'MDA-MB-231 and MCF-7 cancer cell lines were maintained in a modified complete medium (RPMI, 10% FBS, 10mM HEPES, 2 mM L-glutamine, 1mM sodium-pyruvate, 0.05mM 2-mercaptoethanol, 11 mM D-glucose).'; [Extraction]'Total RNAs were isolated from cell lines using Trizol (Invitrogen) and digested with Turbo DNase (Ambion) to remove genomic DNA, according to the manufacturer’s instructions.\nLibraries from rRNA-depleted samples were prepared using a TruSeq RNA Sample Preparation kit v2 (Illumina) following the recommended protocol starting from the RNA fragmentation stage. Purification of polyadenylated RNA was omitted. Libraries were pooled (4 samples per pool), clustered on cBOT (Illumina), and sequenced on HiSeq2000, each pool in one lane. We performed single-end 100 bp reads. Reads were mapped using TopHat followed by data analysis using Cufflinks and Cuffdiff software, as well as our own pipeline.'; [Cell type]'weakly invasive', 'highly invasive''cell line: MCF-7; cell type: weakly invasive; transfected with: si-GAPDH (control); genotype/variation: control; ', 'cell line: MCF-7; cell type: weakly invasive; transfected with: si-REST; genotype/variation: Downregulation of REST; ', 'cell line: MDA-MB-231; cell type: highly invasive; transfected with: EGFP (control); genotype/variation: EGFP control; ', 'cell line: MDA-MB-231; cell type: highly invasive; transfected with: mt-REST; genotype/variation: overexpression of mutant REST; ', 'cell line: MDA-MB-231; cell type: highly invasive; transfected with: wt-REST; genotype/variation: overexpression of wild type REST; ' GSE22600 Homo sapiens 15 Expression profiling by array GPL570 Tissue Specific Pathways for Estrogen Regulation of Ovarian Cancer Growth and Metastasis 2010-06-28 Menopausal estrogen (E2) replacement therapy increases the risk of estrogen receptor (ER)-positive epithelial ovarian cancers (EOC). Whether E2 is tumorigenic or promotes expansion of undiagnosed pre-existing disease is unknown. To determine E2 effects on tumor promotion, we developed an intraperitoneal mouse xenograft model using ZsGreen fluorescent ER- 2008 and ER+ PEO4 human EOC cells. Tumor growth was quantified by in vivo fluorescent imaging. In ER+ tumors, E2 significantly increased size, induced progesterone receptors, and promoted lymph node metastasis, confirming that ER are functional and foster aggressiveness. Laser captured human EOC cells from ER- and ER+ xenografted tumors were profiled for expression of E2-regulated genes. Three classes of E-regulated EOC genes were defined, but less than 10% were shared with E-regulated breast cancer genes. Since breast cancer selective ER modulators (SERM) are therapeutically ineffective in EOC, we suggest that our EOC-specific E-regulated genes can assist pharmacologic discovery of ovarian targeted SERM. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22600 Tissue-specific pathways for estrogen regulation of ovarian cancer growth and metastasis. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-10-1238 {Cancer research (8.378): 10.1158/0008-5472.CAN-10-1238} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA128381 https://www.ebi.ac.uk/ena/browser/view/PRJNA128381 None [Overal design]15 samples were included in this experiment with a 2x2 factorial design with 2 different cell lines (2008 and PEO4) and 2 different hormone treatments (E for Estrogen and C for Placebo Control) and 4 replicates per treatment. 1 sample was excluded (a replicate of PEO4 with C treatment) because of poor quality.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was isolated from the laser captured human cells using the Picopure RNA Isolation kit (Molecular Devices)'; [Cell type]'PEO4 (ER+) ovarian cancer cells', '2008 (ER-) ovarian cancer cells''cell type: PEO4 (ER+) ovarian cancer cells; protocol: human ovarian cancer cells xenografted into female ovariectomized athymic nude mice; agent: Estrogen; ', 'cell type: 2008 (ER-) ovarian cancer cells; protocol: human ovarian cancer cells xenografted into female ovariectomized athymic nude mice; agent: Placebo; ', 'cell type: 2008 (ER-) ovarian cancer cells; protocol: human ovarian cancer cells xenografted into female ovariectomized athymic nude mice; agent: Estrogen; ', 'cell type: PEO4 (ER+) ovarian cancer cells; protocol: human ovarian cancer cells xenografted into female ovariectomized athymic nude mice; agent: Placebo; ' GSE144495 Homo sapiens 195 Expression profiling by high throughput sequencing GPL11154 Deregulation of ribosomal protein expression and translation promotes breast cancer metastasis [rna-Seq CTCs 2] 2020-01-29 We conducted an in vivo genome-wide CRISPR activation screen to identify genes that accelerate distal metastasis by breast cancer patient-derived circulating tumor cells (CTCs) following direct intravascular inoculation in mice. Regulators of translation and ribosomal proteins were prominent among these, and expression of RPL15, a component of the large ribosome subunit, was sufficient to increase metastatic growth in multiple organs. RPL15 overexpression selectively increases translation of other ribosomal proteins and cell cycle regulators. Unsupervised analysis of single-cell RNA sequencing of freshly-isolated CTCs from breast cancer patients identifies a subset with strong ribosomal and protein translation signatures, correlated with increased proliferative markers, epithelial markers and poor clinical outcome. Thus, ribosome protein expression identifies an aggressive subset of CTCs, whose therapeutic targeting may suppress metastatic progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144495 Deregulation of ribosomal protein expression and translation promotes breast cancer metastasis. Science (New York, N.Y.) 41.037 https://doi.org/10.1126/science.aay0939 {Science (New York, N.Y.) (41.037): 10.1126/science.aay0939} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA603789 https://www.ebi.ac.uk/ena/browser/view/PRJNA603789 https://www.ncbi.nlm.nih.gov/sra?term=SRP245907 [Overal design]The CTC-iChip microfluidic device [PMID: 23552373 ] enables isolation of rare viable circulating tumor cells (CTCs) directly from whole blood specimens of patients with cancer, with RNA quality compatible with single-cell RNA sequencing (RNA-seq). We generated RNA-seq profiles of 195 freshly isolated single candidate CTCs or CTC-clusters from 41 women with metastatic breast cancer. Fifty-four candidate CTCs had fewer than 100,000 uniquely mapped reads and therefore were dropped from further consideration. Of the remaining candidate CTCs, 32 expressed PTPRC at a level higher than 10 reads-per-million, so were deemed potential white blood cells and therefore dropped from further consideration. This resulted in profiles of 109 CTCs or CTC-clusters from 33 patients.; [Treatment]'None'; [Growth]'None'; [Extraction]'Single CTCs were isolated from fresh whole blood following leukocyte depletion using the microfluidic CTC-iChip as described in PMID 23552373. Single cells were individually micromanipulated using a 10 μm transfer tip on an Eppendorf TransferMan NK 2 micromanipulator, transferred into PCR tubes containing RNA protective lysis buffer, and flash frozen in liquid nitrogen.\nClontech SMARTer Ultra Low Input Kit for RNA v3 for cDNA synthesis and the Nextera XT kit for library construction'; [Cell type]'Source: ''patient: BRx-102; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-10; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-110; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-110; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-129; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-129; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-129; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-139; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-139; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-152; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-170; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-171; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-172; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-172; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-18; clinical her2: HER2+; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-18; clinical her2: HER2+; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-42; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-42; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-82; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-82; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-82; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-97; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-97; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-122; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-122; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-129; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-131; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-132; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-136; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-146; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-16; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-16; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-172; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-18; clinical her2: HER2+; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-183; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-189; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-189; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-189; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-193; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-194; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-42; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-47; clinical hormone receptor: HR+; clinical her2: HER2+; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-47; clinical hormone receptor: HR+; clinical her2: HER2+; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-55; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-55; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-65; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-96; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-110; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-110; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-111; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-131; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-132; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-156; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-156; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-16; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-164; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-180; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-180; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-188; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-193; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-194; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-206; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-212; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-212; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-213; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-213; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-221; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-233; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-233; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-233; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-239; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-239; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-245; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-245; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-267; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-267; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-267; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-278; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-278; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-47; clinical hormone receptor: HR+; clinical her2: HER2+; number uniquely mapped reads: pass; ptprc expression: fail; ' GSE138435 Homo sapiens 6 Expression profiling by high throughput sequencing GPL18573 Naïve and Primed MSC derived exosomes 2019-10-04 Here we report the change in gene expression in naïve and primed MSC exosomes https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE138435 Mesenchymal Stem Cell-Secreted Extracellular Vesicles Instruct Stepwise Dedifferentiation of Breast Cancer Cells into Dormancy at the Bone Marrow Perivascular Region. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-20-2434 {Cancer research (8.378): 10.1158/0008-5472.CAN-20-2434} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA575856 https://www.ebi.ac.uk/ena/browser/view/PRJNA575856 None [Overal design]RNA sequencing on naïve and primed (i.e. co-cultured with breast cancer cells) MSC derived exosomes to find differentially expressed genes; [Treatment]'Primed MSC were co-cultured with BCCs for 24 hrs. in a transwell co culture system with 0.4 μm membrane (BD Falcon, ThermoFisher). Cells were plated at 1:1 ratio of 5e4. After 24 hrs insert containing BCCs were removed and media was replaced with DMEM supplemented with 2% exosome depleted FCS for 48 hrs.'; [Growth]'MSC were co-cultured with/without breast cancer cells (BCCs) for 24 hrs. in DMEM supplemented with 10% FCS and glutamine'; [Extraction]'Exosomes were isolated by ultracentrifugation. Total RNA was extracted from purifed exosomes according to manufacturer’s protocols with the RNeasy Mini Kit (Qiagen).\nLibraries were prepared using the NEB Ultra II Library Preparation Kit and NEBNext® Multiplex Oligos for Illumina (Dual Index Primers Set 1) (New England BioLabs) following the manufacturer’s protocol.'; [Cell type]'MSC''cell type: MSC; cellular component: exosome; tissue source: bone marrow; passage: 4; replicate: 1; co-culture: none; ', 'cell type: MSC; cellular component: exosome; tissue source: bone marrow; passage: 4; replicate: 2; co-culture: none; ', 'cell type: MSC; cellular component: exosome; tissue source: bone marrow; passage: 4; replicate: 1; co-culture: with breast cancer cells; ', 'cell type: MSC; cellular component: exosome; tissue source: bone marrow; passage: 4; replicate: 2; co-culture: with breast cancer cells; ', 'cell type: MSC; cellular component: exosome; tissue source: bone marrow; passage: 4; replicate: 3; co-culture: with breast cancer cells; ', 'cell type: MSC; cellular component: exosome; tissue source: bone marrow; passage: 4; replicate: 3; co-culture: none; ' GSE74663 Homo sapiens 67 Expression profiling by array GPL10558 High FGFR2 expression is associated with reduced breast cancer risk and represses the estrogen response 2015-11-04 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74663 FGFR2 risk SNPs confer breast cancer risk by augmenting oestrogen responsiveness. Carcinogenesis 4.004 https://doi.org/10.1093/carcin/bgw065 {Carcinogenesis (4.004): 10.1093/carcin/bgw065} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA301107 https://www.ebi.ac.uk/ena/browser/view/PRJNA301107 None [Overal design]Refer to individual Series; [Treatment]'Estrogen-deprived cells were stimulated with 1 nM estradiol (Sigma); 100ng/mL FGF10 (Invitrogen) for a period of 6 h.', 'Estrogen deprived cells that had been transfected with siRNA directed againsy FGFR2 or a non-targeting control siRNA were stimulated with 1 nM estradiol (Sigma); 100ng/mL FGF10 (Invitrogen) for a period of 6 h.', 'Estrogen deprived cells were stimulated with 1 nM estradiol (Sigma); 100ng/mL FGF10 (Invitrogen) for a period of 6 h.'; [Growth]'MCF-7 human breast cancer cells were cultured in DMEM (Invitrogen) supplemented with 10% FBS and antibiotics. ZR751 and T47D human breast cancer cells were cultured in RPMI (Invitrogen) supplemented with 10% FBS and antibiotics. All cells were maintained at 37°C, 5% CO2. Cell synchronisation via estrogen deprivation was carried out for three consecutive days in phenol red-free media supplemented with 5% charcoal dextran-treated FBS and antibiotics, with media changed every 24 h.', 'MCF-7 human breast cancer cells were cultured in DMEM (Invitrogen) supplemented with 10% FBS and antibiotics. All cells were maintained at 37°C, 5% CO2. Cells were transfected with either ON-TARGETplus SMARTpool siRNA directed against FGFR2 (Dharmacon), or a non-targeting control siRNA (Dharmacon) and left for 24 h. Cell synchronisation via estrogen deprivation was carried out for three consecutive days in the transfected cells in phenol red-free media supplemented with 5% charcoal dextran-treated FBS and antibiotics, with media changed every 24 h.', 'MCF-7 human breast cancer cells were cultured in DMEM (Invitrogen) supplemented with 10% FBS and antibiotics. ZR751, T47D and BT474 human breast cancer cells were cultured in RPMI (Invitrogen) supplemented with 10% FBS and antibiotics. SUM52PE human breast cancer cells were cultured in Ham/F-12 (Invitrogen) supplemented with 10% FBS, 5 μg/ml insulin, 1 μg/ml hydrocortisone and antibiotics. All cells were maintained at 37°C, 5% CO2. Cell synchronisation via estrogen deprivation was carried out for three consecutive days in phenol red-free media supplemented with 5% charcoal dextran-treated FBS and antibiotics, with media changed every 24 h.'; [Extraction]'RNA was extracted using the miRNeasy spin column kit (QIAGEN) and quality checked using an RNA 6000 Nano chip on a 2100 Bioanalyser (Agilent). 250ng RNA (RIN>7) was used for cRNA amplification and labelling using the Illumina TotalPrep-96 kit (Ambion 4397949).'; [Cell type]'estrogen receptor-positive breast cancer cell line', 'breast cancer''cell line: T47D; cell type: estrogen receptor-positive breast cancer cell line; treatment: estrogen and FGF10; tme point: 6 h; ', 'cell line: ZR751; cell type: estrogen receptor-positive breast cancer cell line; treatment: vehicle; tme point: 6 h; ', 'cell line: T47D; cell type: estrogen receptor-positive breast cancer cell line; treatment: estrogen; tme point: 6 h; ', 'cell line: T47D; cell type: estrogen receptor-positive breast cancer cell line; treatment: vehicle; tme point: 6 h; ', 'cell line: MCF-7; cell type: estrogen receptor-positive breast cancer cell line; treatment: estrogen; tme point: 6 h; ', 'cell line: MCF-7; cell type: estrogen receptor-positive breast cancer cell line; treatment: estrogen and FGF10; tme point: 6 h; ', 'cell line: MCF-7; cell type: estrogen receptor-positive breast cancer cell line; treatment: vehicle; tme point: 6 h; ', 'cell line: ZR751; cell type: estrogen receptor-positive breast cancer cell line; treatment: estrogen; tme point: 6 h; ', 'cell line: ZR751; cell type: estrogen receptor-positive breast cancer cell line; treatment: estrogen and FGF10; tme point: 6 h; ', 'cell line: MCF-7; cell type: breast cancer; ', 'cell line: BT474; cell type: breast cancer; ', 'cell line: SUM52PE; cell type: breast cancer; ' GSE32488 Homo sapiens 48 Expression profiling by array GPL13938 Expression profiling of formalin-fixed, paraffin-embedded (FFPE) breast cancer metastases of the lymph node and autopsy tissues [DASL HT-12 samples] 2011-09-29 We performed an expression profiling study of 168 primary breast tumors, lymph node metastases, and autopsy samples of primary breast tumours and metastases to liver, chest wall, lymph node, lung, and spleen, as well as positive and negative RNA controls, with technical replicates, to assess quality control methodology and probe-level reproducibility of the Illumina DASL microarray assay. The experiment included both Illumina DASL HumanRef-v3 and DASL HT-12; this series includes only the 48 HT12 samples . https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32488 Expression profiling of archival tumors for long-term health studies. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-12-1915 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-12-1915} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA154441 https://www.ebi.ac.uk/ena/browser/view/PRJNA154441 None [Overal design]This series includes 48 samples in total: 9 positive controls, 4 negative controls, and 35 primary breast tumors and metastatic lymph nodes.; [Treatment]'None'; [Growth]'None'; [Extraction]'Using formalin-fixed, paraffin-embedded HCC tissues, total RNA was extracted using Roche High Pure FFPE Kit.'; [Cell type]'Source: ''sample_name: positive (10A); expt_name: Dec Trial; run_date: Dec-10; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: i4; expt_name: Dec Trial; run_date: Dec-10; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: Negative; expt_name: Dec Trial; run_date: Dec-10; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: ML14; expt_name: Dec Trial; run_date: Dec-10; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: i5; expt_name: Dec Trial; run_date: Dec-10; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: ML37LN; expt_name: Dec Trial; run_date: Dec-10; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: WL11LN; expt_name: Dec Trial; run_date: Dec-10; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: i6; expt_name: Dec Trial; run_date: Dec-10; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: ML60; expt_name: Dec Trial; run_date: Dec-10; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: i7; expt_name: Dec Trial; run_date: Dec-10; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: MCF7; expt_name: Dec Trial; run_date: Dec-10; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: WL93LN; expt_name: Dec Trial; run_date: Dec-10; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: Negative; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: MCF7 intact; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: WL11LN; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: BR POOL HEAT; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: yes; ct_mean: --; ', 'sample_name: PR POOL; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: BR POOL; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: WL113LN; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: WL93LN; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: MCF7 heat; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: yes; ct_mean: --; ', 'sample_name: PR POOL HEAT; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: yes; ct_mean: --; ', 'sample_name: MCF7 FFPE; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: ML37LN; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: --; ', 'sample_name: BR POOL; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: 19.7; ', 'sample_name: MCF7 intact; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: 19.3; ', 'sample_name: Negative; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: 35; ', 'sample_name: WL113LN; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: 40; ', 'sample_name: PR POOL; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: 19.5; ', 'sample_name: MCF7 FFPE; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: 27.9; ', 'sample_name: BR POOL HEAT; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: yes; ct_mean: 21.8; ', 'sample_name: WL93LN; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: 35.1; ', 'sample_name: ML37LN; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: 32; ', 'sample_name: MCF7 heat; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: yes; ct_mean: 23; ', 'sample_name: PR POOL HEAT; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: yes; ct_mean: 22.5; ', 'sample_name: WL11LN; expt_name: Feb Trial; run_date: Feb-11; tissue_type: FFPE tissue sample; heat_treated: no; ct_mean: 33.2; ' GSE85997 Homo sapiens 3 Expression profiling by array GPL15207 Differential Gene Expression in a Patient-Derived Xenograft from transduction of cells with shRNA targeting CDK19 and CDK8 2016-08-24 When CDK19 was initially discovered, it was assumed that CDK19 played a redundant role to CDK8 because they share 84% amino acid sequence similarity. However, biological clues such as CDK19s different chromosomal location and its more limited tissue distribution suggested a role distinct from CDK8 To investigate whether CDK19 and CDK8 had distinct biological functions in Triple-Negative breast cancer, we knocked down CDK19 and CDK8 in a patient-derived xenograft (PDX-C69) and examined differences in the resulting gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE85997 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA339961 https://www.ebi.ac.uk/ena/browser/view/PRJNA339961 None [Overal design]EpCAM enriched PDX-C69 cells were infected with shRNA targeting CDK19, shRNA targeting CDK8, 'empty vector' control shRNA and grown in organoid culture conditions for 72 hours; [Treatment]'None'; [Growth]'EpCAM enriched PDX-C69 cells were infected with shRNA targeting CDK19, shRNA targeting CDK8, control shRNA or not infected and grown in organoid culture conditions for 72 hours'; [Extraction]'Total RNA was extracted from these cells by RNeasy plus micro kit (Qiagen) according to manufacturer’s instructions'; [Cell type]'Source: ''tissue: breast cancer; subtype: Triple-Negative; host: mouse; ' GSE121946 Mus musculus 15 Expression profiling by array GPL1261 Transcriptomic profiling of fibroblasts at different stages of lung colonization by MDA-MB-231 or MDA-MB-231-LM2 cells 2018-10-29 Cancer-associated fibroblasts promote the development of many primary malignancies, but their function in metastatic progression is poorly understood. Here, we demonstrate that colonization of the lungs by metastatic breast cancer cells induces an inflammatory phenotype in lung fibroblasts. CXCL9 and CXCL10 are induced in an NFκB-dependent manner in metastasis-associated fibroblasts in response IL-1α and IL-1β secreted by disseminated breast cancer cells. We find that the chemokine receptor CXCR3, that binds CXCL9/10, is expressed in a small subset of breast cancer cells that exhibits greater tumor-initiating ability when co-transplanted with fibroblasts. CXCR3-expressing cancer cells maintain JNK signaling that drives IL-1A/B expression, and thus rendering this subpopulation efficient in both inducing CXCL9/10 in lung fibroblasts and responding to the chemokines. Importantly, disruption of the CXCL9/10-CXCR3 axis significantly reduces metastatic colonization in xenograft and syngeneic mouse models suggesting an essential role of this paracrine crosstalk in metastatic progression and a potential therapeutic vulnerability for the treatment of metastatic breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE121946 Metastasis-initiating cells induce and exploit a fibroblast niche to fuel malignant colonization of the lungs. Nature communications 11.878 https://doi.org/10.1038/s41467-020-15188-x {Nature communications (11.878): 10.1038/s41467-020-15188-x} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA499117 https://www.ebi.ac.uk/ena/browser/view/PRJNA499117 None [Overal design]For profiling of fibroblasts at different metastatic stages, NSG mice (6-8 weeks of age) were injected with MDA-MB-231 (MDA) or highly metastatic MDA-MB-231-LM2 (MDA-LM2) breast cancer cells via the tail vein. At week 1 and 3 post cancer cell injection (representing micro- and macrometastatic stages, respectively), lungs from mice with similar metastatic burden were harvested. Lungs from age-matched healthy mice were used as control group. Fibroblasts were isolated from whole lungs by fluorescence-activated cell sorting (FACS) using a panel of negative selection markers and CD140a/b as positive fibroblast markers. For each time point and metastasis group, 3 biological replicates were analyzed, and each biological replicate encompasses 1-3 mice.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA extraction was performed using the Arcturus PicoPure Extraction Kit (ThermoFisher Scientific) according to the manufacturer’s protocol.'; [Cell type]'Source: ''metastatic stage: Healthy; ', 'metastatic stage: Micrometastasis; ', 'metastatic stage: Macrometastasis; ' GSE63452 Homo sapiens 25 Expression profiling by high throughput sequencing GPL11154 Knock-in of PIK3CA-H1047R into MCF-10A 2014-11-19 We have compared the proteome, transcriptome and metabolome of two isogenic cell lines: MCF-10A, derived from human breast epithelium, and the mutant MCF-10A-H1047R. These cell lines differ by a single amino acid substitution (H1047R) caused by single nucleotide change in one allele of the PIK3CA gene which encodes the catalytic subunit p110α of phosphatidylinositol 3-kinase (PI3K). The H1047R mutation of PIK3CA is one of the most frequently encountered somatic cancer-specific mutations. In MCF-10A, this mutation induces an extensive cellular reorganization that far exceeds the known signaling activities of PI3K. The changes are highly diverse; with examples in structural protein levels, the DNA repair machinery and sterol synthesis. Gene set enrichment analysis reveals a highly significant concordance of the genes differentially expressed in MCF-10A-H1047R cells and the established protein and RNA signatures of basal breast cancer. No such concordance was found with the specific gene signatures of other histological types of breast cancer. Our data document the power of a single base mutation, inducing an extensive remodeling of the cell toward the phenotype of a specific cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE63452 The butterfly effect in cancer: a single base mutation can remodel the cell. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1424012112 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1424012112} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA267827 https://www.ebi.ac.uk/ena/browser/view/PRJNA267827 https://www.ncbi.nlm.nih.gov/sra?term=SRP050036 [Overal design]2 cell lines (H1047R and WT), 4 time points (0, 6, 12, 24 hours), 3 replicates; [Treatment]'No drug treatments'; [Growth]'500k Cells were seeded in 10cm petri dishes in DMEM/F12 growth medium. After 24 hours, medium was changed to MCDB-170 serum free media. Cells were allowed to grow an additional 24 hours. Medium was changed once more and cells harvested at 0, 6, 12, 24 hours post medium exchange.'; [Extraction]'Total RNA was extracted using Trizol following standard protocol. 1mL Trizol was added directly to cells, RNA was separated from protein and DNA using 200uL chloroform. Aqueous layer was removed and total RNA was precipitated using 500uL isopropanol precipitation. This precipitate was redissolved and precipitated with 250uL DEPC treated water folled by 750uL anhydrous ethanol. Pellet was redissolved in 200uL DEPC treated water. Residual DNA was eliminated using Ambion Dneasy kits.\nNugen Ovation protocol'; [Cell type]'Source: ''cell line: MCF-10A-H1047R; time: 12hr; ', 'cell line: MCF-10A-H1047R; time: 24hr; ', 'cell line: MCF-10A-H1047R; time: 6hr; ', 'cell line: MCF-10A; time: 6hr; ', 'cell line: MCF-10A-H1047R; time: 0hr; ', 'cell line: MCF-10A; time: 0hr; ', 'cell line: MCF-10A; time: 12hr; ', 'cell line: MCF-10A; time: 24hr; ' GSE7659 Canis lupus familiaris 15 Expression profiling by array GPL5117 cDNA microarray profiles of canine mammary tumour cell lines reveal deregulated pathways pertaining to their phenotype 2007-04-27 Mammary cancer is the most common type of cancer in female dogs with a lifetime risk of over 24% when dogs are not spayed. The elucidation of the complete canine genome opens new areas for development of cancer therapies. These should be tested first by in vitro models such as cell lines. However, to date, no canine mammary cell lines have been characterized by expression profiling. In this study, canine mammary tumour cell lines with histologically distinct primary tumours of origin were characterized using a newly developed canine cDNA microarray. Comparisons of gene expression profiles showed enrichment for distinct biological pathways and were related to biological properties of the cell lines such as growth rate and in vitro tumourigenicity. Additionally, gene expression profiles of cell lines also showed correspondence to their tumour of origin. Major differences were found in Wnt, cell cycle, cytokine/Rho-GTPase, alternative complement and integrin signalling pathways. Because these pathways show an overlap at the molecular level with those found in human breast cancer, the expression profiling of spontaneous canine mammary cancer may also function as a biological sieve to identify conserved gene expression or pathway profiles of evolutionary significance that are involved in tumourigenesis. These results are the basis for further characterization of canine mammary carcinomas and development of new therapies directed towards specific pathways. In addition these cell lines can be used to further investigate identified deregulated pathways and characterize until now unannotated genes. Keywords: cell line type comparision https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7659 cDNA microarray profiles of canine mammary tumour cell lines reveal deregulated pathways pertaining to their phenotype. Animal genetics 2.244 https://doi.org/10.1111/j.1365-2052.2008.01733.x {Animal genetics (2.244): 10.1111/j.1365-2052.2008.01733.x} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA99757 https://www.ebi.ac.uk/ena/browser/view/PRJNA99757 None [Overal design]Three canine mammary tumor cell lines (CMT) originating from benign mixed tumor (CMT-U229), primary mammary osteosarcoma (CMT-U335) and primary mammary anaplastic carcinoma (P114) were compared directly to each other in this study. Total RNA was isolated from cells grown to near confluence. In vitro transcription followed by labeling and hybridization to cDNA microarray was carried out. In a loop design of hybridization, labeled cRNA from cell lines were hybridized against each other. Statistical analysis of the log transformed normalized data was done using SAM (significance analysis of microarray) and differentially expressed genes from each experimental subset (comparison of two cell lines) were identified. Dye swaps and at least one biological replicates were included under each experimental subset (each comparision).; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was isolated using Qiagen RNA isolation (mini) kit and DNAse treatment kit'; [Cell type]'Source: ''' GSE69986 Homo sapiens 255 Expression profiling by high throughput sequencing GPL16311 Expression profiling of invasive breast carcinoma samples from Institut Curie 2015-06-18 Genomic hallmarks of homologous recombination deficiency in invasive breast carcinomas to appear in Internationa Journal of Cancer Transcriptome analysis of 243 (plus 12 duplicates) primary breast invasive carcinoma samples of various molecular subtypes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE69986 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA287349 https://www.ebi.ac.uk/ena/browser/view/PRJNA287349 None [Overal design]This dataset contains 255 arrays for 243 primary breast tumor samples obtained from 243 patient; 12 duplicated cases. Data production involved different array batches and hybridation series.; [Treatment]'No'; [Growth]'Tumor samples were obtained from patients treated at the hospital of Institut Curie (Biological Resource Center, Paris, France). Healthy samples were obtained from mammary plastic surgery. Cell lines were grown from the American Type Culture Collection (ATCC),'; [Extraction]'Total RNA was extracted and purified from frozen tumor samples using the RNeasy Mini Kit (Qiagen) followed by the RNA clean up kit (Macherey Nagel), according to manufacturer instructions.'; [Cell type]'Source: ''gender: female; tissue: invasive breast carcinoma sample; molecular subtype: luminal; ', 'gender: female; tissue: invasive breast carcinoma sample; molecular subtype: HER2+; ', 'gender: female; tissue: invasive breast carcinoma sample; molecular subtype: TNBC; ' GSE59515 Homo sapiens 75 Expression profiling by array GPL10558 Accurate prediction and validation of response to endocrine therapy in breast cancer 2014-07-17 Purpose Aromatase inhibitors (AIs) have an established role in breast cancer treatment. Response rates are only 50-70% in the neoadjuvant setting and lower in advanced disease. Accurate biomarkers are urgently needed to predict response in these settings and to determine which individuals will benefit from adjuvant AI therapy. Participants and Methods Pre- and on-treatment (after 2 weeks and 3 months) biopsies were obtained from 89 post-menopausal women with ER+ breast cancer receiving neoadjuvant letrozole for transcript profiling. Dynamic clinical response was assessed by three-dimensional ultrasound measurements. Results The molecular response to letrozole was characterised and a four gene classifier of clinical response was established (accuracy of 96%) based upon the level of two genes prior to treatment (one associated with immune signalling, IL6ST and the other with apoptosis, NGFRAP1) and two proliferation genes (ASPM, MCM4) at 2 weeks of therapy. The four gene signature was found to be 91% accurate in a blinded, completely independent validation dataset of patients treated with anastrozole. Matched 2 week on-treatment biopsies improved predictive power over pre-treatment biopsies alone. This signature also significantly predicted recurrence free survival (p=0.029) and breast cancer specific survival (p=0.009). We demonstrate that the test can also be performed using quantitative PCR or immunohistochemistry. Conclusion A four gene predictive model of clinical response to AIs by two weeks has been generated and validated. Deregulated immune and apoptotic responses before treatment and a failure to reduce proliferation by 2 weeks are functional characteristics of breast tumours that do not respond to AIs. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59515 Accurate Prediction and Validation of Response to Endocrine Therapy in Breast Cancer. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 28.245 https://doi.org/10.1200/JCO.2014.57.8963 {Journal of clinical oncology : official journal of the American Society of Clinical Oncology (28.245): 10.1200/JCO.2014.57.8963} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA255496 https://www.ebi.ac.uk/ena/browser/view/PRJNA255496 None [Overal design]25 Pre treatment, 25 two week and 25 three month on-treatment primary breast tumour samples from the same patients. Data was analysed with two previously generated datasets, GSE55374 which was also processed on Illumina HT-12v4 BeadChips (GPL10558) and GSE20181 on Affymetrix U133A GeneChips (GPL96); [Treatment]'Patients were treated within a neoadjuvant protocol in which letrozole (Femara, 2.5mg; Novartis Pharma AG, Basel, Switzerland) was given daily'; [Growth]'Tumour biopsies were taken with a 14-guage needle before and approximately 2 weeks and 3 months following commencement of continuous letrozole treatment. Samples were snap-frozen in liquid nitrogen and frozen sections taken, stained with haematoxylin and eosin (H&E) and the cellularity and percentage presence of cancerous tissue within each specimen was assessed by a pathologist.'; [Extraction]'Biopsies were homogenised and RNA was extracted using the RNeasy Mini Kit with RNAse-free DNAse treatment (Qiagen). RNA quantity and quality was verified on a Bioanalyser 2100 with RNA 6000 Nano Kit (Agilent) and Nanodrop 2000c (Thermo Scientific).'; [Cell type]'Source: ''patient id: 150; gender: Female; clinical response: Non-responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 150; gender: Female; clinical response: Non-responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 150; gender: Female; clinical response: Non-responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 171; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 171; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 171; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 172; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 172; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 172; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 179; gender: Female; clinical response: Non-responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 179; gender: Female; clinical response: Non-responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 179; gender: Female; clinical response: Non-responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 203; gender: Female; clinical response: Non-responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 203; gender: Female; clinical response: Non-responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 203; gender: Female; clinical response: Non-responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 214; gender: Female; clinical response: Non-responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 214; gender: Female; clinical response: Non-responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 214; gender: Female; clinical response: Non-responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 215; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 215; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 215; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 226; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 226; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 226; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 269; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 269; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 269; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 300; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 300; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 300; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 311; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 311; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 311; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 328; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 328; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 328; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 329; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 329; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 329; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 331; gender: Female; clinical response: Non-responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 331; gender: Female; clinical response: Non-responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 331; gender: Female; clinical response: Non-responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 332; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 332; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 332; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 340; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 340; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 340; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 341; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 341; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 341; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 346; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 346; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 346; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 355; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 355; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 355; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 357; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 357; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 357; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 363; gender: Female; clinical response: Non-responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 363; gender: Female; clinical response: Non-responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 363; gender: Female; clinical response: Non-responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 364; gender: Female; clinical response: Non-responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 364; gender: Female; clinical response: Non-responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 364; gender: Female; clinical response: Non-responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 367; gender: Female; clinical response: Non-responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 367; gender: Female; clinical response: Non-responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 367; gender: Female; clinical response: Non-responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 369; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 369; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 369; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 373R; gender: Female; clinical response: Responder; time point: pre-treatment; tissue: tumour biopsies; ', 'patient id: 373R; gender: Female; clinical response: Responder; time point: 2 wks of letrozole treatment; tissue: tumour biopsies; ', 'patient id: 373R; gender: Female; clinical response: Responder; time point: 3 months of letrozole treatment; tissue: tumour biopsies; ' GSE33723 Homo sapiens 38 Expression profiling by array GPL4133; GPL6848 Molecular events in endometrial carcinosarcomas and the role of high mobility group AT-hook 2 in endometrial carcinogenesis. 2011-11-15 The molecular events implicated in the development of endometrial carcinosarcoma remain poorly understood. Using complementary DNA microarrays, we analyzed a group of 15 endometrial carcinosarcomas and compared their gene expression profiles with those obtained from a group of 23 endometrioid endometrial carcinomas. We demonstrated changes in the expression of genes modulating processes such as the epithelial to mesenchymal transition, muscle differentiation, the expression of cancer/testis antigens, and immune response in endometrial carcinosarcomas. The high mobility group AT-hook 2 gene is an embryonic nuclear factor that mediates epithelial to mesenchymal transition in various tumor models, and it was among the genes overexpressed in endometrial carcinosarcomas. High mobility group AT-hook 2 overexpression was confirmed in 54% of endometrial carcinosarcomas by quantitative real time-polymerase chain reaction and immunohistochemistry. Moreover, we found a significant inverse correlation between the expression of high mobility group AT-hook 2 and let-7b, a member of the let-7 family of microRNAs that represses high mobility group AT-hook 2 expression. These changes were also associated with overexpression of Lin28B, a suppressor of microRNA biogenesis that is implicated in cancer progression and metastasis. Finally, high mobility group AT-hook 2 overexpression, which was detected in less than 3% of endometrioid endometrial carcinomas, was observed in many nonendometrioid carcinomas (46% of 28 samples). This pattern of expression, restricted to nonendometrioid carcinomas and endometrial carcinosarcomas, reflects a role for high mobility group AT-hook 2 in endometrial carcinogenesis that is associated with aggressive phenotypes and points to its potential use as a marker to distinguish between endometrioid and nonendometrioid tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE33723 Molecular events in endometrial carcinosarcomas and the role of high mobility group AT-hook 2 in endometrial carcinogenesis. Human pathology 2.740 https://doi.org/10.1016/j.humpath.2012.05.013 {Human pathology (2.740): 10.1016/j.humpath.2012.05.013} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA148455 https://www.ebi.ac.uk/ena/browser/view/PRJNA148455 None [Overal design]15 endometrial carcinosarcomas and 23 endometrioid endometrial carcinoma; [Treatment]'None'; [Growth]'None'; [Extraction]'1mg of total RNA from each independent tumours were labelled with Cy5-dUTP and as control a pooled RNA obtained from equal concentration of each RNA tumor sample labelled with Cy3-dUTP was used. The amplification and labelling of mRNA were performed using Low RNA Linear Amplification Kit (Agilent technologies), following manufacturer’s protocol'; [Cell type]'Source: ''disease state: endometrial carcinosarcomas; gender: Female; ', 'gender: Female; ', 'disease state: endometrioid endometrial carcinomas; gender: Female; ' GSE74036 Homo sapiens 30 Expression profiling by high throughput sequencing GPL16791 RNA-seq of MCF7 cells treated with epigenetic therapy 2015-10-14 RNA-seq was performed after MCF7 cells were treated with S2101, UNC0638, GSK343, depsipeptide alone or in combination with decitabine https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74036 Transcriptional Selectivity of Epigenetic Therapy in Cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-16-0834 {Cancer research (8.378): 10.1158/0008-5472.CAN-16-0834} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA298835 https://www.ebi.ac.uk/ena/browser/view/PRJNA298835 https://www.ncbi.nlm.nih.gov/sra?term=SRP064832 [Overal design]Biological triplicates were performed for a total of 30 samples. Fold change of each gene was calculated by comparing change in expression after inhibitor treatment to expression in the control samples; [Treatment]'Cells were treated daily with 100nM decitabine (5-aza-CdR, Sigma), 10uM S2101 (Millipore), 1uM UNC0638 (Sigma), and 1uM GSK343 (Sigma) for 96 hours, or 20nM depsipeptide (Romidepsin, Sigma) was added for 24 hours'; [Growth]'MCF7 cell line was cultured in DMEM medium with 10% fetal bovine serum'; [Extraction]'RNA was isolated using Rneasy Mini Kit (Qiagen)\nStrand-specific RNA libraries were generated from 1μg of RNA using TruSeq stranded total RNA with Ribo-Zero Gold (Illumina)'; [Cell type]'Source: ''tissue: mammary gland, breast; cell line: breast cancer cell line MCF7; er status: positive; treatment: Cntrl; gender: female; ', 'tissue: mammary gland, breast; cell line: breast cancer cell line MCF7; er status: positive; treatment: DAC; gender: female; ', 'tissue: mammary gland, breast; cell line: breast cancer cell line MCF7; er status: positive; treatment: S2101; gender: female; ', 'tissue: mammary gland, breast; cell line: breast cancer cell line MCF7; er status: positive; treatment: DAC+S2101; gender: female; ', 'tissue: mammary gland, breast; cell line: breast cancer cell line MCF7; er status: positive; treatment: UNC0638; gender: female; ', 'tissue: mammary gland, breast; cell line: breast cancer cell line MCF7; er status: positive; treatment: DAC+UNC0638; gender: female; ', 'tissue: mammary gland, breast; cell line: breast cancer cell line MCF7; er status: positive; treatment: GSK343; gender: female; ', 'tissue: mammary gland, breast; cell line: breast cancer cell line MCF7; er status: positive; treatment: DAC+GSK343; gender: female; ', 'tissue: mammary gland, breast; cell line: breast cancer cell line MCF7; er status: positive; treatment: Depsi; gender: female; ', 'tissue: mammary gland, breast; cell line: breast cancer cell line MCF7; er status: positive; treatment: DAC+Depsi; gender: female; ' GSE81380 Mus musculus 16 Expression profiling by high throughput sequencing GPL17021 HDAC inhibitor panobinostat engages host immune defenses to promote the tumoricidal effects of trastuzumab in HER2+ tumors 2016-05-12 Characterisation of the tumor extrinsic (immune-mediated) mechanisms by which panobinostat and trastuzumab can collaboratively promote tumor-associated NK cell infiltration to eradicate trastuzumab-refractory HER2+ tumors https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE81380 HDAC Inhibitor Panobinostat Engages Host Innate Immune Defenses to Promote the Tumoricidal Effects of Trastuzumab in HER2+ Tumors. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-16-2247 {Cancer research (8.378): 10.1158/0008-5472.CAN-16-2247} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA321407 https://www.ebi.ac.uk/ena/browser/view/PRJNA321407 https://www.ncbi.nlm.nih.gov/sra?term=SRP074892 [Overal design]RNA sequencing was performed on established whole AU565(pv) HER2+ human breast tumors, harvested from SCID mice 2-days post treatment initiation with vehicle (PBS/D5W), panobinostat (15mg/kg/day), trastuzumab (10mg/kg day 1) or both drugs in combination. Each treatment group comprised of 4 mice.; [Treatment]'Vehicle and Drug treatments were administered intraperitoneally. Treatment Groups: Vehicle (D5W days 0,1; PBS days 0), Trastuzumab (D5W days 0,1; Trastuzumab 10mg/kg days 0), Panobinostat (Panobinostat 15mg/kg days 0,1; PBS days 0), Panobinostat + Trastuzumab (Panobinostat 15mg/kg days 0,1; Trastuzumab 10mg/kg days 0)'; [Growth]'1.5x1E6 AU565(pv) tumor cells were injected into the mammary fat pad of SCID mice. Established tumours (20-25mm2) were treated as outlined below.'; [Extraction]'Whole tumors were mashed and lysed in QIAzol (Qiagen). Total RNA was extracted using a Qiagen miRNeasy Mini Kit and cleaned and concentrated using a Qiagen RNeasy MinElute Cleanup Kit. Illumina TruSeq RNA Sample Prep Kit (Cat#FC-122-1001) was used with 1 ug of total RNA for the construction of sequencing libraries.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Whole AU565(pv) tumor: human tumour cells, mouse stroma, epithelial cells and immune cells''cell type: Whole AU565(pv) tumor: human tumour cells, mouse stroma, epithelial cells and immune cells; origin: Mammary fat pad AU565(pv) xenograft, harvest 2-days post initiation of drug treatment; strain: SCID mice; ' GSE163025 Homo sapiens 4 Expression profiling by high throughput sequencing GPL24676 Splicing factor SRSF1 promotes breast cancer progression via regulating alternative splicing 2020-12-10 Purpose:Intensive evidence have highlighted the effect of aberrant alternative splicing (AS) events triggered by dysregulation of SR protein family on cancer progression. Nonetheless, the underlying mechanism in breast cancer (BRCA) remains elusive. Here we sought to explore the molecular function of SRSF1 and identify the key AS events regulated by SRSF1 in BRCA. Methods:We conducted comprehensive analysis for the expression and the clinical correlation of SRSF1 in BRCA based on TCGA, Metabric database, clinical tissue samples and BRCA cell lines. Functional analysis of SRSF1 in BRCA was conducted in vitro and in vivo. SRSF1-mediated AS events and its binding motif were identified by RNA-seq, RNA immunoprecipitation-PCR (RIP-PCR) and in vivo crosslinking followed by immunoprecipitation (CLIP), which was further validated by the minigene reporter assay. Finally, the expression and their clinical significance were validated in clinical samples and TCGA database. Results:SRSF1 was upregulated in BRCA samples, associated positively with tumor grade and Ki-67 index, and correlated with poor prognosis in hormone receptor positive (HR+) cohort, which facilitated tumor progression in vitro and in vivo. We identified SRSF1-mediated AS events and discovered the SRSF1 binding motif in the regulation of PTPMT1. Furthermore, PTPMT1 splice switching regulated by SRSF1 partially mediated the oncogenic role of SRSF1 via the AKT/C-MYC axis. Additionally, PTPMT1 splice switching was validated in tissue samples of BRCA patients. Conclusions:Collectively, SRSF1 exerts the oncogenic roles in BRCA partially through regulating AS of PTPMT1, which could be a candidate prognostic factor and therapeutic target in HR+ BRCA cohort. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE163025 Splicing factor SRSF1 promotes breast cancer progression via oncogenic splice switching of PTPMT1. Journal of experimental & clinical cancer research : CR 5.646 https://doi.org/10.1186/s13046-021-01978-8 {Journal of experimental & clinical cancer research : CR (5.646): 10.1186/s13046-021-01978-8} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA684349 https://www.ebi.ac.uk/ena/browser/view/PRJNA684349 https://www.ncbi.nlm.nih.gov/sra?term=SRP297599 [Overal design]mRNA alternative splicing profiles of MCF7 NC and MCF7 sh SRSF1 cells; [Treatment]'MCF7 cells were transfected with NC/shSRNSF1 lentiviruses and filtered with puromycin'; [Growth]'DMEM (Gibco) containing 10% FBS (Gibco) was used to culture MCF7 cell lines in a humidified incubator at 37℃ with 5% CO2'; [Extraction]'Cells were extracted, flash frozen on dry ice, and RNA was harvested using Trizol reagent. Illumina TruSeq RNA Sample Prep Kit (Cat#FC-122-1001) was used with 1 ug of total RNA for the construction of sequencing libraries.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''cell line: MCF7; knockdown: control; ', 'cell line: MCF7; knockdown: SRSF1; ' GSE114168 Homo sapiens 53 Expression profiling by array GPL570 Medullary breast carcinoma, a triple-negative breast cancer subtype associated with BCLG overexpression. 2018-05-08 Gene expression was compared between medullary breast carcinoma (MBC) and non medullary basal-like breast carcinoma (non-MBC BLC). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE114168 Medullary Breast Carcinoma, a Triple-Negative Breast Cancer Associated with BCLG Overexpression. The American journal of pathology 3.762 https://doi.org/10.1016/j.ajpath.2018.06.021 {The American journal of pathology (3.762): 10.1016/j.ajpath.2018.06.021} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA466799 https://www.ebi.ac.uk/ena/browser/view/PRJNA466799 None [Overal design]The transcriptome of 19 MBC and 34 non-MBC BLC were analyzed using Affymetrix U133plus2 Arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions. A cleanup with RNAII Nucleospin was conducted according Macherey Nagel recommendations"; [Cell type]'Source: ''disease state: medullary breast carcinoma; ', 'disease state: non medullary basal-like breast carcinoma; ' GSE58644 Homo sapiens 321 Expression profiling by array GPL6244 The prognostic ease and difficulty of invasive breast carcinoma 2014-06-18 Breast carcinoma (BC) have been extensively profiled by high-throughput technologies for over a decade, and broadly speaking, these studies can be grouped into those that seek to identify patient subtypes (studies of heterogeneity) or those that seek to identify gene signatures with prognostic or predictive capacity. The shear number of reported signatures has led to speculation that everything is prognostic in BC. Here we show that this ubiquity is an apparition caused by a poor understanding of the inter- relatedness between subtype and the molecular determinants of prognosis. Our approach constructively shows how to avoid confounding due to a patient's subtype, clinicopathological or treatment profile. The approach identifies patients who are predicted to have good outcome at time of diagnosis by all available clinical and molecular markers, but who experience a distant metastasis within five years. These inherently difficult patients (~7% of BC) are prioritized for investigations of intra-tumoral heterogeneity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58644 The prognostic ease and difficulty of invasive breast carcinoma. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2014.08.073 {Cell reports (7.815): 10.1016/j.celrep.2014.08.073} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA253066 https://www.ebi.ac.uk/ena/browser/view/PRJNA253066 None [Overal design]321 samples from breast cancer patients.; [Treatment]'None'; [Growth]'None'; [Extraction]"Samples were collected from patients undergoing breast surgeries at the McGill University Health Centre (MUHC) between 1999 and 2012 who provided written, informed consent. All tissues were snap-frozen in O.C.T. Tissue-Tek Compound within 30 minutes of removal. Information regarding clinical variables was obtained through review of Medical Records at the MUHC. 5 microM sections were prepared for each sample and subjected to routine haematoxylin and eosin (H&E) staining. Subsequently, each section was evaluated by an attending clinical pathologist with expertise in breast tissue (A.O.) and scored for presence and relative proportions of invasive, in situ and normal components. Samples with less than 70% normal tissue were selected for further processing. Additional frozen sections (n = 3 to 40, depending on sample area) were cut on a cryostat at 20 microM thickness. RNA was then extracted from these sections using the AllPrep Mini kit (Qiagen), following the manufacturer's instructions. Following extraction, RNA quality was assessed using an Agilent Bioanalyzer; results were subjected to visual inspection, and samples exhibiting distinct 28S and 18S rRNA peaks of similar sizes were selected for microarray-based profiling at the McGill Genome-Quebec Innovation Centre. Amounts submitted for profiling ranged between 220 and 450 ng. Total RNA was quantified using a NanoDrop Spectrophotometer ND-1000 (NanoDrop Technologies, Inc.) and its integrity was assessed using a 2100 Bioanalyzer (Agilent Technologies)."; [Cell type]'Source: ''time: 44; event: 1; er: 1; her2: 0; grade: 2; Stage: NA; lymph: NA; chemo: 0; tamoxifen: NA; herceptin: 0; age: 45; size: 1.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 143; event: 0; er: NA; her2: NA; grade: 1; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 0; herceptin: 0; age: 66; size: 0.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 138; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 58; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 139; event: 0; er: 1; her2: 1; grade: 3; Stage: 1; lymph: NA; chemo: 0; tamoxifen: 0; herceptin: 0; age: 53; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 86; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 70; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 93; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 49; size: 2.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 94; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 59; size: 2.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 36; event: 1; er: 1; her2: 0; grade: 3; Stage: NA; lymph: NA; chemo: 0; tamoxifen: 1; herceptin: 0; age: 77; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 91; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 72; size: 2.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 60; event: 1; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: 0; age: 65; size: 1.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 95; event: 0; er: 1; her2: 1; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 1; age: 46; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 86; event: 0; er: 0; her2: 1; grade: 3; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: 0; age: 74; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 92; event: 0; er: 0; her2: 1; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 0; herceptin: 0; age: 59; size: 3.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 88; event: 0; er: 1; her2: 1; grade: 3; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 1; age: 49; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 90; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: 0; age: 55; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 24; event: 1; er: 1; her2: 0; grade: 3; Stage: 3; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 66; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 73; event: 0; er: 0; her2: 1; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 0; herceptin: 1; age: 55; size: 3.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 118; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 64; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 41; event: 1; er: 1; her2: 0; grade: 3; Stage: 3; lymph: 1; chemo: 1; tamoxifen: 0; herceptin: 0; age: 39; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 5; event: 1; er: 1; her2: 0; grade: 3; Stage: 4; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 77; size: 5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 43; event: 0; er: 1; her2: 1; grade: 1; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 33; size: 2.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 61; event: 1; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 65; size: 3.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 125; event: 1; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 44; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 135; event: 1; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 44; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 133; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: NA; chemo: 1; tamoxifen: 0; herceptin: 0; age: 66; size: 1.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 3; event: 0; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 0; chemo: 0; tamoxifen: 0; herceptin: 0; age: 46; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 127; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 58; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 133; event: 0; er: 0; her2: 1; grade: 2; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: 0; age: 64; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 15; event: 1; er: 1; her2: 1; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 51; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 95; event: 0; er: 1; her2: 1; grade: 3; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 49; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 54; event: 0; er: 0; her2: 1; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 71; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 87; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: 0; age: 56; size: 2.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 73; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: 0; age: 37; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 125; event: 0; er: 1; her2: 1; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 0; herceptin: 0; age: 51; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 66; event: 1; er: 1; her2: 0; grade: 3; Stage: 3; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 48; size: 9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 76; event: 0; er: 1; her2: 0; grade: 2; Stage: 3; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 69; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 56; event: 1; er: 1; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 53; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 139; event: 0; er: 1; her2: 0; grade: 1; Stage: 1; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 53; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 1; er: 1; her2: 1; grade: 3; Stage: 3; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 77; size: 4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 17; event: 1; er: 1; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: NA; tamoxifen: 1; herceptin: 0; age: 66; size: 0.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 126; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 56; size: 2.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 105; event: 0; er: 0; her2: 0; grade: 3; Stage: 2; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: NA; age: 35; size: 3.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 107; event: 0; er: 0; her2: 1; grade: 3; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: 1; age: 45; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 12; event: 1; er: 0; her2: 0; grade: 3; Stage: 3; lymph: 1; chemo: 1; tamoxifen: 0; herceptin: 0; age: 55; size: 2.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 70; event: 0; er: 0; her2: 0; grade: 2; Stage: 2; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: 0; age: 81; size: 9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 75; event: 0; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 67; size: 1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 0; event: 0; er: 1; her2: 0; grade: 1; Stage: NA; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: 0; age: 72; size: 1.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 124; event: 0; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 70; size: 1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 65; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: NA; herceptin: 0; age: 50; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 1; er: 0; her2: 1; grade: 3; Stage: 3; lymph: 1; chemo: 1; tamoxifen: 0; herceptin: 0; age: 58; size: 7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 118; event: 0; er: 1; her2: 0; grade: 1; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 52; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 121; event: 0; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 0; chemo: NA; tamoxifen: 1; herceptin: 0; age: 62; size: 1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 77; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: NA; chemo: 0; tamoxifen: 1; herceptin: 0; age: 80; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 115; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 50; size: 1.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 119; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 61; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 28; event: 0; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 87; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 15; event: 1; er: 0; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: 0; age: 43; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 119; event: 0; er: 1; her2: 0; grade: 1; Stage: 1; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 65; size: 0.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 50; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: 0; age: 75; size: 2.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 86; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 61; size: 1.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 80; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 50; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 77; event: 0; er: 1; her2: 1; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 1; age: 70; size: 5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 111; event: 0; er: 1; her2: 1; grade: 3; Stage: 1; lymph: 0; chemo: 0; tamoxifen: 0; herceptin: 0; age: 66; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 1; er: 1; her2: 1; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 1; age: 51; size: 2.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 46; size: 2.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 62; event: 0; er: 1; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: 0; age: 31; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 25; event: 1; er: 1; her2: 1; grade: 3; Stage: 1; lymph: 0; chemo: NA; tamoxifen: 1; herceptin: 0; age: 77; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 83; event: 0; er: 1; her2: 0; grade: 1; Stage: 1; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 48; size: 1.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 116; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 45; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 103; event: 0; er: 1; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 60; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 18; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 69; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 80; event: 0; er: 1; her2: 0; grade: 1; Stage: 2; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 79; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 51; event: 0; er: 0; her2: 1; grade: 3; Stage: NA; lymph: NA; chemo: 1; tamoxifen: 0; herceptin: 1; age: 49; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 18; event: 1; er: 0; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 0; herceptin: 0; age: 55; size: 3.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 43; event: 1; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 65; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 66; event: 1; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: 1; herceptin: 0; age: 74; size: 2.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 96; event: 1; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 75; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 69; event: 1; er: 1; her2: 0; grade: 2; Stage: 3; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 48; size: 1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 105; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 0; herceptin: 0; age: 38; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 101; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 52; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 17; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 46; size: 3.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 106; event: 0; er: 1; her2: 1; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 1; age: 58; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 104; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 67; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 7; event: 1; er: 1; her2: 0; grade: 3; Stage: 3; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 83; size: 3.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 64; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 0; chemo: NA; tamoxifen: 1; herceptin: 0; age: 57; size: 4.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 100; event: 0; er: 0; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 40; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 105; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 62; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 108; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: NA; age: 57; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 23; event: 1; er: 0; her2: 0; grade: 3; Stage: 3; lymph: 1; chemo: 1; tamoxifen: 0; herceptin: NA; age: 57; size: 3.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 78; event: 0; er: 1; her2: 1; grade: 3; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 1; age: 43; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 52; event: 1; er: 1; her2: 0; grade: 2; Stage: NA; lymph: NA; chemo: 0; tamoxifen: 1; herceptin: NA; age: 83; size: 3.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 101; event: 0; er: 0; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: NA; age: 64; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 103; event: 0; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: NA; age: 64; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 101; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: NA; chemo: 0; tamoxifen: 1; herceptin: NA; age: 83; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 101; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: NA; age: 61; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 91; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 61; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 1; event: 1; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 85; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 94; event: 0; er: 1; her2: 0; grade: 1; Stage: 1; lymph: 0; chemo: 0; tamoxifen: 0; herceptin: 0; age: 46; size: 0.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 88; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 50; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 89; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 46; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 80; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 72; size: 1.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 1; event: 1; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 47; size: 2.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 96; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 38; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 46; event: 1; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 44; size: 1.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 103; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 73; size: 2.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 1; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: NA; chemo: 0; tamoxifen: 0; herceptin: 0; age: 93; size: 4.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 105; event: 0; er: 0; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 56; size: 1.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 6; event: 1; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: NA; herceptin: 0; age: 72; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 67; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 0; herceptin: NA; age: 41; size: 3.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 55; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: NA; chemo: 1; tamoxifen: 0; herceptin: NA; age: 80; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 53; event: 0; er: 0; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 55; size: 1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 54; event: 0; er: 0; her2: 0; grade: 3; Stage: 2; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 47; size: 2.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 55; event: 1; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 56; size: 3.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 2; event: 1; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 45; size: 7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 77; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 44; size: 3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 27; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 76; size: 1.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 70; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: NA; age: 56; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 82; event: 0; er: 0; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 43; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 74; event: 0; er: 0; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: 0; age: 57; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 63; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 55; size: 2.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 94; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 49; size: 3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 4; event: 1; er: 1; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: NA; tamoxifen: 1; herceptin: 0; age: 52; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 46; event: 0; er: 0; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 48; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 40; event: 0; er: 0; her2: 1; grade: 3; Stage: 1; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 56; size: 3.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 37; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 41; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 18; event: 1; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 62; size: 2.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 38; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 64; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 24; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 55; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 40; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 44; size: 6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 9; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 81; size: 1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 41; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 46; size: 2.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 39; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: NA; tamoxifen: 1; herceptin: 0; age: 48; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 24; event: 1; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 75; size: 2.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 13; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: NA; chemo: 0; tamoxifen: 0; herceptin: 0; age: 90; size: 3.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 1; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 60; size: 1.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 19; event: 1; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 63; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 2; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: NA; age: 48; size: 4.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 17; event: 1; er: 0; her2: 0; grade: 3; Stage: 1; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: 0; age: 64; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 19; event: 1; er: 0; her2: 0; grade: 3; Stage: NA; lymph: NA; chemo: 1; tamoxifen: 0; herceptin: 0; age: 74; size: 1.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 0; event: 0; er: 0; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 54; size: 2.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 6; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 38; size: 6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 27; event: 1; er: 1; her2: 1; grade: 3; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 51; size: 2.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 21; event: 1; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 66; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 80; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 67; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 79; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 62; size: 2.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 69; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 58; size: 3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 73; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 29; size: 2.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 62; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: NA; age: 46; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 52; event: 0; er: 1; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: NA; age: 49; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 34; event: 0; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 74; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 11; event: 1; er: 0; her2: 1; grade: 3; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 79; size: 2.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 23; event: 0; er: 0; her2: 1; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 48; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 17; event: 0; er: 0; her2: 1; grade: 3; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 38; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 38; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 39; size: 1.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 41; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 59; size: 2.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 30; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: NA; age: 89; size: 2.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 37; event: 0; er: 1; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 64; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 27; event: 0; er: 1; her2: 1; grade: 2; Stage: 2; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 31; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 34; event: 0; er: 1; her2: 1; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 51; size: 3.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 83; event: 0; er: 1; her2: NA; grade: 2; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 44; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 75; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 66; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 10; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 78; size: 3.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 36; event: 0; er: 1; her2: 1; grade: 3; Stage: 1; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 59; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 38; event: 0; er: 1; her2: 0; grade: 1; Stage: 2; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 63; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 14; event: 0; er: 0; her2: 1; grade: 3; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 76; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 17; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 73; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 64; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 59; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 27; event: 1; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 72; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 36; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: NA; age: 85; size: 6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 43; event: 0; er: 0; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 34; size: 1.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 33; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 60; size: 3.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 21; event: 1; er: 1; her2: 0; grade: 3; Stage: 3; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 74; size: 3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 14; event: 1; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 47; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 96; event: 0; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 50; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 12; event: 1; er: 1; her2: 1; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 0; herceptin: 0; age: 39; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 1; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 81; size: 2.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 52; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 74; size: 2.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 103; event: 0; er: 1; her2: 0; grade: 3; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: NA; age: 47; size: 4.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 86; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: NA; chemo: 0; tamoxifen: 1; herceptin: 0; age: 44; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 82; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 60; size: 2.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 39; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 57; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 74; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 39; size: 2.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 75; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 70; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 1; er: 0; her2: 0; grade: 3; Stage: 3; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 34; size: 3.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 13; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 60; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 14; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 54; size: 1.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 43; event: 0; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 79; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 51; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 64; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 37; event: 0; er: 1; her2: 0; grade: 1; Stage: 1; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 39; size: 1.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 48; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 50; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 141; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 73; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 50; event: 0; er: 1; her2: NA; grade: 3; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 58; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 70; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 46; size: 2.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 92; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 55; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 115; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: NA; age: 89; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 13; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 50; size: 1.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 64; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 69; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 110; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 37; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 47; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 52; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 29; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: NA; age: 63; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 39; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 62; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 15; event: 1; er: 1; her2: 1; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 52; size: 4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 40; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 52; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 35; event: 1; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 44; size: 2.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 34; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 75; size: 1.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 38; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 58; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 34; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 48; size: 3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 10; event: 1; er: 1; her2: 1; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 50; size: 3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 33; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 41; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 35; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 65; size: 2.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 36; event: 0; er: 1; her2: NA; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 60; size: 6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 69; event: 0; er: 1; her2: 0; grade: 1; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 72; size: 3.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 92; event: 1; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 40; size: 4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 35; event: 0; er: 0; her2: 0; grade: 1; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 0; herceptin: 0; age: 68; size: 1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 9; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: 0; age: 56; size: 2.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 37; event: 0; er: 1; her2: 1; grade: 2; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 51; size: 15; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 14; event: 1; er: 1; her2: 0; grade: 1; Stage: NA; lymph: NA; chemo: 0; tamoxifen: 1; herceptin: 0; age: 81; size: 1.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 35; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 43; size: 4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 29; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 50; size: 1.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 31; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 60; size: 3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 31; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 73; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 33; event: 0; er: 0; her2: 1; grade: 3; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 0; herceptin: 0; age: 65; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 27; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 75; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 29; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 66; size: 2.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 19; event: 0; er: 1; her2: 0; grade: 1; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 0; herceptin: 0; age: 66; size: 2.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 123; event: 0; er: 0; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 58; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 36; event: 1; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 47; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 94; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 63; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 29; event: 0; er: 1; her2: 0; grade: 1; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 49; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 2; event: NA; er: 1; her2: 0; grade: 1; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 47; size: 1.3; suderman.et.al: 0; paquet.et.al: 1; ', 'time: 26; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 57; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 28; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: 0; age: 62; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: 0; age: 73; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 33; event: 0; er: 1; her2: NA; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: 0; age: 64; size: 3.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 27; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 53; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 27; event: 0; er: 1; her2: NA; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 48; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 25; event: 0; er: 1; her2: 0; grade: 1; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: 0; age: 47; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 28; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: 0; age: 42; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: 0; age: 57; size: 2.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 24; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: 0; age: 63; size: 3.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 0; er: 1; her2: 0; grade: 1; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: 0; age: 50; size: 1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 33; event: NA; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: 0; age: 51; size: 2; suderman.et.al: 0; paquet.et.al: 1; ', 'time: 81; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 61; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 0; event: NA; er: 1; her2: 1; grade: 2; Stage: NA; lymph: NA; chemo: 0; tamoxifen: 1; herceptin: 0; age: 80; size: 4; suderman.et.al: 0; paquet.et.al: 1; ', 'time: 11; event: 1; er: 1; her2: 0; grade: 1; Stage: NA; lymph: NA; chemo: 0; tamoxifen: 1; herceptin: 0; age: 81; size: 1.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 30; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 0; herceptin: 0; age: 52; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 97; event: 0; er: 1; her2: 1; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: 1; age: 71; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 23; event: 0; er: 1; her2: 1; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: 0; age: 77; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 97; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: 0; age: 69; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 89; event: 0; er: 0; her2: 1; grade: 3; Stage: NA; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: 0; age: 46; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 84; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: 0; age: 83; size: 3.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 60; event: NA; er: 1; her2: 1; grade: 2; Stage: NA; lymph: NA; chemo: 0; tamoxifen: NA; herceptin: 0; age: 56; size: 2.5; suderman.et.al: 0; paquet.et.al: 1; ', 'time: 27; event: 1; er: 1; her2: 1; grade: 2; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 51; size: 2.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 24; event: 0; er: 1; her2: 0; grade: 1; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 64; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 24; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 75; size: 4.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 22; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 52; size: 1.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 78; event: 0; er: 1; her2: 1; grade: 2; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 79; size: 1.6; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 41; event: 0; er: 1; her2: 0; grade: 1; Stage: 1; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: NA; age: 81; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 38; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 57; size: 5.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 11; event: 1; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 69; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 19; event: 1; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 34; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 0; er: 1; her2: 1; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 35; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 116; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 63; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 121; event: 0; er: 1; her2: 0; grade: 3; Stage: 1; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 64; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 116; event: 0; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 71; size: 1.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 109; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: NA; age: 82; size: 1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 23; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 75; size: 2.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 21; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: NA; tamoxifen: NA; herceptin: NA; age: 74; size: 3.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 20; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: NA; tamoxifen: NA; herceptin: NA; age: 69; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 6; event: 1; er: 1; her2: 1; grade: 3; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: 1; age: 35; size: 3.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 100; event: 0; er: 1; her2: 1; grade: 3; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 63; size: 3.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 75; event: 0; er: 0; her2: 1; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: 0; age: 64; size: 2.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 25; event: 0; er: 1; her2: 0; grade: 1; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 56; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 23; event: 0; er: 1; her2: NA; grade: 3; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 73; size: 1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 22; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 47; size: 4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 140; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 60; size: 3.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 142; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: 0; age: 49; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 138; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 48; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 120; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 49; size: 1.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 119; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 57; size: 0.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 104; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 54; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 90; event: 1; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 59; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 132; event: 0; er: 0; her2: 1; grade: 3; Stage: NA; lymph: NA; chemo: 0; tamoxifen: NA; herceptin: 0; age: 34; size: 0.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 41; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 60; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 64; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 85; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 117; event: 0; er: 1; her2: 0; grade: 1; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 51; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 105; event: 1; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 41; size: 2.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 14; event: NA; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 56; size: 2; suderman.et.al: 0; paquet.et.al: 1; ', 'time: 45; event: NA; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: 0; age: 83; size: 1.6; suderman.et.al: 0; paquet.et.al: 1; ', 'time: 72; event: NA; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: 0; age: 39; size: 2.7; suderman.et.al: 0; paquet.et.al: 1; ', 'time: 16; event: 1; er: 0; her2: 1; grade: 3; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: 0; age: 65; size: 1.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 102; event: 1; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 0; tamoxifen: 1; herceptin: 0; age: 79; size: 3.5; suderman.et.al: 1; paquet.et.al: 1; ', 'ti me: 102; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 45; size: 2.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 0; er: 1; her2: 0; grade: 1; Stage: NA; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: 0; age: 80; size: 1.3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 42; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: 0; age: 51; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 26; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: NA; age: 58; size: 1.8; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 23; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: NA; age: 57; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 23; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: NA; age: 53; size: 3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 23; event: 0; er: 1; her2: 1; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: NA; age: 57; size: 2.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 24; event: 0; er: 1; her2: 0; grade: 3; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: NA; age: 61; size: 1.4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 20; event: 0; er: 1; her2: 0; grade: 2; Stage: NA; lymph: NA; chemo: 0; tamoxifen: NA; herceptin: NA; age: 81; size: 4; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 28; event: 1; er: 1; her2: 0; grade: 2; Stage: NA; lymph: 1; chemo: 0; tamoxifen: NA; herceptin: NA; age: 50; size: 3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 25; event: 0; er: 1; her2: 1; grade: 2; Stage: NA; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: NA; age: 66; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 24; event: 0; er: 1; her2: 1; grade: 3; Stage: NA; lymph: 0; chemo: 0; tamoxifen: NA; herceptin: NA; age: 50; size: 1.7; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 135; event: 1; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: NA; age: 64; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 86; event: 1; er: 1; her2: 1; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: NA; age: 54; size: 2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 144; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: NA; age: 54; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 141; event: 0; er: 0; her2: 1; grade: 3; Stage: 2; lymph: 0; chemo: 1; tamoxifen: NA; herceptin: NA; age: 58; size: 2.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 73; event: 0; er: 1; her2: 0; grade: 2; Stage: 1; lymph: 0; chemo: 1; tamoxifen: 1; herceptin: NA; age: 42; size: 1.9; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 131; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: NA; age: 60; size: 1.1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 131; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: NA; age: 55; size: 3; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 112; event: 0; er: 0; her2: 1; grade: 2; Stage: NA; lymph: NA; chemo: 0; tamoxifen: NA; herceptin: NA; age: 73; size: 2.2; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 49; event: 0; er: 1; her2: 0; grade: 2; Stage: 2; lymph: 1; chemo: 1; tamoxifen: 1; herceptin: NA; age: 56; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 66; event: 0; er: 1; her2: 1; grade: 3; Stage: 2; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: NA; age: 55; size: 3.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 104; event: 0; er: 1; her2: 0; grade: NA; Stage: NA; lymph: NA; chemo: 0; tamoxifen: NA; herceptin: NA; age: 77; size: 1.5; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 129; event: 0; er: 1; her2: 1; grade: 1; Stage: 1; lymph: 0; chemo: 0; tamoxifen: 1; herceptin: NA; age: 65; size: 1; suderman.et.al: 1; paquet.et.al: 1; ', 'time: 104; event: 0; er: 0; her2: 0; grade: 3; Stage: NA; lymph: NA; chemo: 0; tamoxifen: NA; herceptin: NA; age: 58; size: 0.6; suderman.et.al: 1; paquet.et.al: 1; ' GSE159052 Homo sapiens 12 Expression profiling by high throughput sequencing GPL16791 Hyperactive CDK2 Activity in Basal-like Breast Cancer Imposes a Genome Integrity Liability that can be Exploited by Targeting DNA Polymerase Epsilon 2020-10-05 RNAseq data for MDA-MB-231, CAMA-1, and MCF7 cells expressing shPOLE and either a vector control or cDNA POLE rescue https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE159052 Hyperactive CDK2 Activity in Basal-like Breast Cancer Imposes a Genome Integrity Liability that Can Be Exploited by Targeting DNA Polymerase ε. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2020.10.016 {Molecular cell (14.548): 10.1016/j.molcel.2020.10.016} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA667486 https://www.ebi.ac.uk/ena/browser/view/PRJNA667486 https://www.ncbi.nlm.nih.gov/sra?term=SRP286423 [Overal design]Cell Lines express an shRNA targeting DNA Polymerase epsilon (POLE) and either a POLE cDNA or vector control.; [Treatment]'shRNA infection of cell lines with stable expression of POLE or control, 5 days prior to extraction'; [Growth]'RPMI-10'; [Extraction]'RNeasy Plus Mini Kit\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''cell line: MDA-MB-231; replicate: 1; treatment: Vector Control; ', 'cell line: MDA-MB-231; replicate: 2; treatment: Vector Control; ', 'cell line: MDA-MB-231; replicate: 1; treatment: shRNA targeting DNA Polymerase epsilon (POLE); ', 'cell line: MDA-MB-231; replicate: 2; treatment: shRNA targeting DNA Polymerase epsilon (POLE); ', 'cell line: CAMA-1; replicate: 1; treatment: Vector Control; ', 'cell line: CAMA-1; replicate: 2; treatment: Vector Control; ', 'cell line: CAMA-1; replicate: 1; treatment: shRNA targeting DNA Polymerase epsilon (POLE); ', 'cell line: CAMA-1; replicate: 2; treatment: shRNA targeting DNA Polymerase epsilon (POLE); ', 'cell line: MCF7; replicate: 1; treatment: Vector Control; ', 'cell line: MCF7; replicate: 2; treatment: Vector Control; ', 'cell line: MCF7; replicate: 1; treatment: shRNA targeting DNA Polymerase epsilon (POLE); ', 'cell line: MCF7; replicate: 2; treatment: shRNA targeting DNA Polymerase epsilon (POLE); ' GSE119671 Homo sapiens 2 Expression profiling by array GPL17077 Expression data from knockdown of HSD3B1 in MDA-MD-231 breast cancer cell line 2018-09-07 HSD3B1 (3beta-hydroxysteroid dehydrogenase type 1) plays a vital role in steroidogenesis. Transcription profiling analysis was performed in MDA-MD-231 breast cancer cells transfected with negative control siRNA or siRNAs against HSD3B1. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE119671 Inhibition of 3β-Hydroxysteroid Dehydrogenase Type 1 Suppresses Interleukin-6 in Breast Cancer. The Journal of surgical research 1.872 https://doi.org/10.1016/j.jss.2019.03.024 {The Journal of surgical research (1.872): 10.1016/j.jss.2019.03.024} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA489894 https://www.ebi.ac.uk/ena/browser/view/PRJNA489894 None [Overal design]HSD3B1 expression was stably knocked-down in MDA-MB-231 cells. RNA was extracted from cells transfected with negative control siRNA or siRNAs against HSD3B1 and submitted to microarray analysis.; [Treatment]'MDA-MB-231 cells were transfected with negative control siRNA or siRNAs against HSD3B1.'; [Growth]'None'; [Extraction]'RNA was prepared and quantified using a NanoDrop-1000 spectrophotometer. Quality was monitored with the Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA).'; [Cell type]'Source: ''cell line: MDA-MB-231; genotype/variation: siRNA control; ', 'cell line: MDA-MB-231; genotype/variation: siRNA HSD3B1; ' GSE31645 Homo sapiens 26 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL8882; GPL13314 Landscape of somatic allelic imbalances and copy number alterations in HER2-amplified breast cancer 2011-08-24 A survey of the somatic allelic imbalances and copy number alterations in HER2-amplified breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE31645 Landscape of somatic allelic imbalances and copy number alterations in HER2-amplified breast cancer. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr3075 {Breast cancer research : BCR (5.676): 10.1186/bcr3075} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA145413 https://www.ebi.ac.uk/ena/browser/view/PRJNA145413 None [Overal design]Genomic profiling of 26 breast tumors with amplification of HER2 using 1M and 2.5M Illumina SNP beadchips. Sample identifiers correspond to GSE21259 where sample annotations may be extracted.; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA from fresh frozen breast tumor tissue was extracted using overnight digestion with proteinase K at 55C, followed by repeated phenol-chloroform purification steps.'; [Cell type]'Source: ''disease state: Breast cancer (HER2+); er: er_pos; osbin: 0; os: 13.75342466; age: 46.61465; ln: 0; size_mm: 27; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 16.47945205; age: 48; ln: 1; size_mm: 40; primary: 1; grade: 3; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 1.567123288; age: 74.5024; ln: 1; size_mm: 38; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 1; os: 2.912328767; age: 30.6037; ln: 0; size_mm: 30; primary: 1; grade: 2; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 13.30410959; age: 42.94593; ln: 1; size_mm: 25; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 3.632876712; age: 57.61533; ln: 0; size_mm: 22; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 1; os: 13.91232877; age: 57.9603; ln: 1; size_mm: 22; primary: 1; grade: 2; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 1.416438356; age: 44; ln: 0; size_mm: 23; primary: 1; grade: 3; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 15.0630137; age: 52.3039; ln: 1; size_mm: 32; primary: 1; grade: 3; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 0.15890411; age: 70.02601; ln: 1; size_mm: 50; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 14.82191781; age: 49; ln: 0; size_mm: 30; primary: 1; grade: 2; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 0; os: 12.45205479; age: 40; ln: 0; size_mm: 18; primary: 1; grade: 3; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 5.515068493; age: 72.75291; ln: 1; size_mm: 18; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 9.410958904; age: 65; ln: 1; size_mm: 25; primary: 1; grade: 3; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 1; os: 3.608219178; age: 42; ln: 0; size_mm: 5; primary: 1; grade: 3; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 0; os: 12.59726027; age: 45; ln: 0; size_mm: 10; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 12.16986301; age: 62.03696; ln: 0; size_mm: 25; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 12.0630137; age: 61.40726; ln: 0; size_mm: 35; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 11.98356164; age: 37; ln: 0; size_mm: 2; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 11.30684932; age: 63; ln: 0; size_mm: 18; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 10.64383562; age: 65.17454; ln: 0; size_mm: 26; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 1.824657534; age: 44; ln: 1; size_mm: 30; primary: NA; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 12.09589041; age: 59.36756; ln: 0; size_mm: 22; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 0.564383562; age: 69.24298; ln: 1; size_mm: 25; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 1.435616438; age: 75.56468; ln: 1; size_mm: 35; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 1; os: 1.583561644; age: 75.17043; ln: 1; size_mm: 22; primary: 1; grade: 3; ' GSE128600 Homo sapiens 24 Expression profiling by array GPL17077 Late recurrence-associated long non-coding RNA NR2F1 antisense 1 (NR2F1-AS1) 2019-03-20 Long non-coding RNA NR2F1 antisense RNA1 (lncRNA NR2F1-AS1) was identified as the main candidate associated to late recurrence in ER-positive breast cancer clinical samples. Gain-of-function of NR2F1-AS1 induced the expression of dormancy-inducers BMP4 and DEC2, and upregulated pluripotency markers NANOG and OCT4. Representative pathways entailed to metastatic events such as HER2/Neu, hypoxia, EMT and inflammatory-response were also found enriched. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE128600 Long non-coding NR2F1-AS1 is associated with tumor recurrence in estrogen receptor-positive breast cancers. Molecular oncology 5.962 https://doi.org/10.1002/1878-0261.12704 {Molecular oncology (5.962): 10.1002/1878-0261.12704} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA528281 https://www.ebi.ac.uk/ena/browser/view/PRJNA528281 None [Overal design]Applied microarray-based analysis to 24 ER-positive breast cancer clinical specimens. The clinical specimens were selected from ER-positive breast cancer patients who did not receive any treatment previously to the needle-biopsy and developed distant metastases 10 years after the initial diagnosis. Same criteria were applied for ER-positive breast cancer specimens from patients with no signs of distant metastases after 10 years. We successfully identified the lncRNA NR2F1 antisense RNA1 (NR2F1-AS1) as a main lncRNA linked to recurrence. Clinical samples were gifted from the National Cancer Center Hospital of Japan (Tsukiji, Tokyo, Japan).; [Treatment]'Isolation of total RNA from ER-positive breast primary tumor tissues.'; [Growth]'None'; [Extraction]'Total RNA was extracted using QIAzol and the RNeasy Mini Kit (Qiagen, Hilden, Germany) according to manufacturer’s protocols. RNA was quantified using a NanoDrop-1000 spectrophotometer and a Agilent 2100 bioanalyzer (Agilent Technologies, Palo Alto, Calif.).'; [Cell type]'Source: ''cell: breast invasive ductal carcinoma; recurrence status: non-recurrence; subtype: Luminal A; ', 'cell: breast invasive ductal carcinoma; recurrence status: non-recurrence; subtype: Luminal B; ', 'cell: breast invasive ductal carcinoma; recurrence status: recurrence; subtype: Luminal A; ', 'cell: breast invasive ductal carcinoma; recurrence status: recurrence; subtype: Luminal B; ', 'cell: breast invasive lobular carcinoma; recurrence status: recurrence; subtype: Luminal B; ' GSE7161 Homo sapiens 12 Expression profiling by array GPL570 Non-Classical Functions of Human Topoisomerase I: Genome-wide and Pharmacological Analyses 2007-02-28 The biological functions of nuclear topoisomerase I (Top1) have been difficult to study because knocking out TOP1 is lethal in metazoans. To reveal the functions of human Top1, we have generated stable Top1siRNA cell lines from colon and breast carcinomas (HCT116-siTop1 and MCF-7-siTop1, respectively). In those cells, Top2 compensates for Top1 deficiency. A prominent feature of the siTop1 cells is genomic instability, with chromosomal aberrations and histone gamma-H2AX foci associated with replication. siTop1 cells also show rDNA and nucleolar alterations, and increased nuclear volume. Genome-wide transcription profiling revealed 55 genes with consistent changes in siTop1 cells. Among them, asparagine synthetase (ASNS) was reduced in siTop1 cells, as it also was in cells with transient Top1 downregulation. Conversely, Top1 complementation increased ASNS, indicating a causal link between Top1 and ASNS expression. Correspondingly, pharmacological profiling showed l-asparaginase hypersensitivity in the siTop1 cells. Resistance to camptothecin, aphidicolin, hydroxyurea and staurosporine, and hypersensitivity to etoposide and actinomycin D demonstrated that Top1, in addition to being the target of camptothecins, also regulates DNA replication, rDNA stability and apoptosis. Overall, our studies demonstrate the pleiotropic nature of human Top1 activities. In addition to its classical DNA nicking-closing functions, Top1 plays critical non-classical roles in genomic stability, gene-specific transcription, and response to various anticancer agents. Keywords: genetic modification design https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7161 Nonclassic functions of human topoisomerase I: genome-wide and pharmacologic analyses. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-06-4554 {Cancer research (8.378): 10.1158/0008-5472.CAN-06-4554} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA98165 https://www.ebi.ac.uk/ena/browser/view/PRJNA98165 None [Overal design]We are using Affymetrix whole genome array U133 Plus 2, which is a single color microarray platform. For colon experiments, we analyzed 2 different samples as 4 replicates. For breast experiments, we analyzed 2 samples as replicates.; [Treatment]'Treatment type: small molecule\nIn-vivo treatment: To generate Top1-knockdown cell lines, the plasmid pBS/U6 was cleaved with ApaI and EcoRI. Synthetic DNA oligonucleotides were then ligated into pBS/U6. For Top1-siRNA, the core sequence of the inserted DNA oligonucleotides corresponds to a sequence from exon 17 of the TOP1 gene. The siRNA-expressing cassette was removed with BamHI, and inserted into the BamHI site of the plasmid vector pRep4 (X+S). The resulting vector corresponds to a human U6 promoter-driven DNA construct stably expressing an siRNA hairpin (shRNA) targeting human Top1 mRNA. The siTop1 constructs were transfected into HCT116 and MCF-7 cells, using the Lipofectamine™ 2000 Transfection Reagent. Hygromycin B-resistant clones were selected with 600 or 400 µg/ml hygromycin B for HCT116 or MCF-7 cells, respectively. The resulting cell lines were designated as HCT116-siTop1, MCF-7-siTop1, HCT116-sictrl and MCF-7-sictrl.', 'Treatment type: small molecule\nIn-vivo treatment: To generate si Control cell lines, the plasmid pBS/U6 was cleaved with ApaI and EcoRI. Synthetic DNA oligonucleotides were then ligated into pBS/U6. A random nonsense sequence was used to produce the control siRNA (siCtrl). The siRNA-expressing cassette was removed with BamHI, and inserted into the BamHI site of the plasmid vector pRep4 (X+S). The siCtrl constructs were transfected into HCT116 and MCF-7 cells, using the Lipofectamine™ 2000 Transfection Reagent. Hygromycin B-resistant clones were selected with 600 or 400 µg/ml hygromycin B for HCT116 or MCF-7 cells, respectively. The resulting cell lines were designated as HCT116-siTop1, MCF-7-siTop1, HCT116-sictrl and MCF-7-sictrl.'; [Growth]'None'; [Extraction]'RNeasy Qiagen Extraction Protocol\nOther: Total RNA was extracted using the RNeasy® Midi Kit and kept at -80°C. A260/280 ratios ranged from 1.8-2.0.'; [Cell type]'Source: ''', 'Tissue: colon; Cell line: Colon Cancer Cell Line HCT116; Cell type: epithelial cells; Disease state: Colorectal carcinoma; ', 'Tissue: breast; Cell line: Breast Cancer Cell Line MCF7; Cell type: epithelial cells; Disease state: Adenocarcinoma; ' GSE1902 Homo sapiens 88 Expression profiling by SAGE GPL1485 Cancer Genome Anatomy Project (CGAP) Human LongSAGE 2004-10-28 This series represents the Cancer Genome Anatomy Project SAGE library collection. Libraries contained herein were either produced through CGAP funding, or donated to CGAP. The Cancer Genome Anatomy Project (CGAP: http://cgap.nci.nih.gov) is an interdisciplinary program established and administered by the National Cancer Institute (NCI: http://www.nci.nih.gov) to generate the information and technological tools needed to decipher the molecular anatomy of the cancer cell. SAGE libraries are named according to the following convention: * SAGE_Organ_histology_code_unique identifier, e.g., SAGE_Colon_adenocarcinoma_CL_Caco2 * Codes: B = bulk; CL = cell line; CS = short-term cell culture; MD = micro-dissected; AP = antibody purified. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE1902 An anatomy of normal and malignant gene expression. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.152324199 {Human molecular genetics (4.544) doi:10.1093/hmg/10.7.663}; {Proceedings of the National Academy of Sciences of the United States of America (9.580) doi:10.1073/pnas.152324199}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA85561 https://www.ebi.ac.uk/ena/browser/view/PRJNA85561 None [Overal design]88 libraries; [Treatment]'None'; [Growth]'None'; [Extraction]'N/A'; [Cell type]'Stem Proginitor Cells, CD34+, CD38+', 'Acute myelogenous leukemia', 'Source: ', 'Medulloblastoma cell line', 'Medulloblastoma', 'ER+, PR+, HER2-, grade II', 'Grade II, ER+, PR+, Her2- tumor', 'Grade I, ER+, PR+, Her2- invasive ductal carcinoma', 'ductal carcinoma in situ, extensive, gradeIII, Her2+', 'invasive breast cancer ER+, PR+, Her2-, grade II', 'primary ductal in situ breast carcinoma, intermediate grade', 'primary grade III. ductal invasive breast carcinoma', 'invasive breast cancer, ER+, PR+, Her-, grade II', 'Invasive ductal carcinoma, ER+,PR+,HER2-', 'Invasive ductal carcinoma, high-grade, ER+,PR+,HER2-', 'Pleural effusion, HER2-, recurrence of ER+ tumor', 'Ascites, mixed lobular/ductal carcinoma, HER2-, recurrence of ER+ tumor', 'invasive ductal carcinoma ER+,PR+,HER2-', 'MUC1 bead purified cells from MCF10DCIS xenografts', 'extensive LCIS', 'ITGB6 bead purified cells from MCF10DCIS xenografts', 'juvenile fibroadenoma', 'Normal breast tissue reduction', 'normal breast tissue from a breast cancer patient (corresponding to IDC7)', 'spontenously immortalized mammary myoepithelial cell line from Li-Fraumeni patient', 'recurrent phyllodes tumor, malignant, high grade, poorly differentiated', 'cell line derived from colorectal carcinoma', 'adenocarcinoma', 'high grade dysplasia', 'low grade dysplasia', 'Adenocarcinoma', 'Adenocarcinoma, tubular, poorly differentiated', 'Adenocarcinoma, tubular', 'ventral body wall', 'poorly differentiated adenocarcinoma', 'Large B cell Lymphoma, Malignant, high grade, involving the serosa of the appendix', 'rhabdomyosarcoma', 'central retina', 'Bilateral retinoblastoma, poorly differentiated, left orbit', 'synovial fibroblasts from rheumatoid arthritis', 'Embyronal Carcinoma, Mixed germ cell tumor consisting primarily of embryonal carcinoma with foci of yolk sac tumor and teratoma seen. Size: 4.5 x 3.8 x 2.8 cm. Non-neoplastic tissue: Marked hypospermatogenesis with Leydig cell hyperplasia and chronic inflammation.', 'normal liver', 'invasive breast cancer, ER+, PR+, Her2-', 'lung macrophage', 'monocyte-depleted mononuclear cells', 'monocyte', 'plaque macrophage''organ/tissue: bone marrow; tissue preparation: flow-sorted; sex: unknown; cell type: Stem Proginitor Cells, CD34+, CD38+; ', 'organ/tissue: bone marrow; tissue preparation: flow-sorted; sex: unknown; cell type: Acute myelogenous leukemia; ', 'organ/tissue: brain; tissue preparation: bulk; age: Spontaneously aborted male/female Caucasian fetuses, ages 20-33 weeks; sex: unknown; ', 'organ/tissue: brain; tissue preparation: cell line; age: unknown; sex: unknown; mutations: unknown; ', 'organ/tissue: brain; tissue preparation: cell line; age: 5; sex: male; cell type: Medulloblastoma cell line; ', 'organ/tissue: brain; tissue preparation: cell line; age: 5; sex: male; other information: Medulloblastoma cell line treated with Otx2 siRNA; ', 'organ/tissue: brain; tissue preparation: cell line; age: 9; sex: female; cell type: Medulloblastoma; ', 'organ/tissue: brain; tissue preparation: bulk; sex: unknown; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 47; sex: female; cell type: ER+, PR+, HER2-, grade II; other information: CD10 positive purified myofibroblasts from invasive breast carcinoma. Library name in Cancer Cell, 2004, 6(1):17-32 "I-MYOFIB-7 myofibroblasts"; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; sex: female; cell type: Grade II, ER+, PR+, Her2- tumor; other information: CD10+ purified myofibroblasts from invasive breast cancer. Library name in Cancer Cell, 2004, 6(1):17-32 "I-MYOFIB-8 myofibroblasts"; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; sex: female; cell type: Grade I, ER+, PR+, Her2- invasive ductal carcinoma; other information: CD10+ purified myofibroblasts from invasive breast cancer Library name in Cancer Cell, 2004, 6(1):17-32 "I-MYOFIB-9-myofibroblasts"; ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 28; sex: female; cell type: ductal carcinoma in situ, extensive, gradeIII, Her2+; other information: Library name in Cancer Cell, 2004, 6(1):17-32 "D-STR-6-fibroblast"; ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 47; sex: female; cell type: invasive breast cancer ER+, PR+, Her2-, grade II; other information: Library name in Cancer Cell, 2004, 6(1):17-32 "I-STR-7-fibroblast"; ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 44 yrs; sex: female; cell type: primary ductal in situ breast carcinoma, intermediate grade; other information: Estrogen and progesteron receptor positive, erbB2 negative, 0/25 lymph nodes (no lymph node metastasis); ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 71 yrs; sex: female; cell type: primary grade III. ductal invasive breast carcinoma; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 47; sex: female; cell type: invasive breast cancer, ER+, PR+, Her-, grade II; other information: BerEP4 purified epithelial cells. Library name in Cancer Cell, 2004, 6(1):17-32 "I-EPI-7 epithelial cells"; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; sex: female; cell type: Grade II, ER+, PR+, Her2- tumor; other information: BerEP4 purified epithelial cells from invasive breast cancer. Library name in Cancer Cell, 2004, 6(1):17-32 "I-EPI-8 epithelial cells"; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; sex: female; cell type: Grade I, ER+, PR+, Her2- invasive ductal carcinoma; other information: BerEP4 purified epithelial cells from invasive breast cancer. Library name in Cancer Cell, 2004, 6(1):17-32 "I-EPI-9 epithelial cells"; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 32; sex: female; cell type: Invasive ductal carcinoma, ER+,PR+,HER2-; other information: cells purified using CD24 antibody, these cells are CD24+ more differentiated breast cancer cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 50; sex: female; cell type: Invasive ductal carcinoma, high-grade, ER+,PR+,HER2-; other information: cells purified using CD24 antibody, these cells are CD24+ more differentiated breast cancer cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: unknown; sex: female; cell type: Pleural effusion, HER2-, recurrence of ER+ tumor; other information: cells purified using CD24 antibody, these cells are CD24+ more differentiated breast cancer cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: unknown; sex: female; cell type: Ascites, mixed lobular/ductal carcinoma, HER2-, recurrence of ER+ tumor; other information: cells purified using CD44 antibody, these cells are CD44+ breast "cancer stem" cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: unknowm; sex: female; cell type: Pleural effusion, HER2-, recurrence of ER+ tumor; other information: cells purified using CD44 antibody, these cells are CD44+ breast "cancer stem" cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 50; sex: female; cell type: Invasive ductal carcinoma, high-grade, ER+,PR+,HER2-; other information: cells purified using PROCR antibody, these cells are CD44+ breast "cancer stem" cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 55; sex: female; cell type: invasive ductal carcinoma ER+,PR+,HER2-; other information: cells purified using PROCR antibody, these cells are CD44+ breast "cancer stem" cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; sex: female; cell type: MUC1 bead purified cells from MCF10DCIS xenografts; mutations: 8q gain, CDKN1A and LRP1B homozygous deletions; ', 'organ/tissue: mammary gland; tissue preparation: microscope dissected; age: 34; sex: female; cell type: extensive LCIS; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; sex: female; cell type: ITGB6 bead purified cells from MCF10DCIS xenografts; mutations: 8q gain, CDKN1A and LRP1B homozygous deletions; ', 'organ/tissue: mammary gland; tissue preparation: microscope dissected; age: 11; sex: female; cell type: juvenile fibroadenoma; other information: Library name in Cancer Cell, 2004, 6(1):17-32 "FA"; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 22; sex: female; cell type: Normal breast tissue reduction; other information: cells purified using CD24 antibody, these cells are CD24+ mammary epithelial cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 22; sex: female; cell type: Normal breast tissue reduction; other information: cells purified using CD24 antibody, these cells are CD24+ differentiated luminal epithelial cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 58; sex: female; cell type: Normal breast tissue reduction; other information: cells purified using CD24 antibody, these cells are CD24+ mammary epithelial cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 22; sex: female; cell type: Normal breast tissue reduction; other information: cells purified using CD44 antibody, these cells are CD44+ mammary epithelial stem cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 58; sex: female; cell type: Normal breast tissue reduction; other information: cells purified using CD44 antibody, these cells are CD44+ mammary epithelial stem cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 22; sex: female; cell type: Normal breast tissue reduction; other information: cells purified using MUC1 antibody, these cells are MUC1+ mammary epithelial cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 58; sex: female; cell type: Normal breast tissue reduction; other information: cells purified using MUC1 antibody, these cells are MUC1+ mammary epithelial cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 47; sex: female; cell type: normal breast tissue from a breast cancer patient (corresponding to IDC7); other information: CD10 positive purified myoepithelial cells. Library name in Cancer Cell, 2004, 6(1):17-32 "N-MYO-I7"; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 22; sex: female; cell type: Normal breast tissue reduction; other information: cells purified using CD10 antibody, these cells are CD10+ mammary myoepithelial cells; ', 'organ/tissue: mammary gland; tissue preparation: antibody purified; age: 58; sex: female; cell type: Normal breast tissue reduction; other information: cells purified using CD10 antibody, these cells are CD10+ mammary myoepithelial cells; ', 'organ/tissue: mammary gland; tissue preparation: cell line; sex: female; cell type: spontenously immortalized mammary myoepithelial cell line from Li-Fraumeni patient; mutations: Li-Fraumeni patient (heterozygous TP53 mutation); ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 44; sex: female; ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 52; sex: female; cell type: recurrent phyllodes tumor, malignant, high grade, poorly differentiated; other information: Library name in Cancer Cell, 2004, 6(1):17-32 "PHY"; ', 'organ/tissue: colon; tissue preparation: cell line; sex: unknown; ', 'organ/tissue: colon; tissue preparation: cell line; sex: unknown; cell type: cell line derived from colorectal carcinoma; ', 'organ/tissue: stem cell; tissue preparation: cell line; age: Passage 20 after derivation; sex: male; ', 'organ/tissue: stem cell; tissue preparation: cell line; age: p31; sex: male; ', 'organ/tissue: stem cell; tissue preparation: cell line; age: p54; sex: male; ', 'organ/tissue: stem cell; tissue preparation: cell line; age: p22; sex: male; ', 'organ/tissue: stem cell; tissue preparation: cell line; age: passage 22; sex: male; ', 'organ/tissue: stem cell; tissue preparation: cell line; age: passage 33; sex: female; ', 'organ/tissue: stem cell; tissue preparation: cell line; age: passage 38; sex: female; ', 'organ/tissue: stem cell; tissue preparation: cell line; age: passage 16; sex: female; ', 'organ/tissue: stem cell; tissue preparation: cell line; age: p36; sex: male; ', 'organ/tissue: stem cell; tissue preparation: cell line; age: passage 50; sex: female; ', 'organ/tissue: other; tissue preparation: bulk; age: 69; sex: male; cell type: adenocarcinoma; ', 'organ/tissue: other; tissue preparation: bulk; age: 69; sex: male; cell type: high grade dysplasia; ', 'organ/tissue: other; tissue preparation: bulk; age: 69; sex: male; cell type: low grade dysplasia; ', 'organ/tissue: other; tissue preparation: bulk; age: 69; sex: male; ', 'organ/tissue: other; tissue preparation: bulk; age: 60; sex: male; cell type: Adenocarcinoma; ', 'organ/tissue: other; tissue preparation: bulk; age: 53; sex: female; cell type: Adenocarcinoma, tubular, poorly differentiated; ', 'organ/tissue: other; tissue preparation: bulk; age: 43; sex: female; cell type: Adenocarcinoma, tubular; ', 'organ/tissue: other; tissue preparation: bulk; age: 67; sex: female; cell type: ventral body wall; ', 'organ/tissue: kidney; tissue preparation: bulk; age: 72; sex: male; other information: Glomeruli are from the unaffected pole of a kidney that was surgically removed for renal cell carcinoma. Glomeruli were isolated by sieving to >95% purity. Linker Sequences have been removed from the library.; ', 'organ/tissue: lung; tissue preparation: bulk; sex: male; cell type: poorly differentiated adenocarcinoma; other information: Stage IV lung cancer. Cells isolated from pleural effusions.; ', 'organ/tissue: lymph node; tissue preparation: bulk; age: 52; sex: male; cell type: Large B cell Lymphoma, Malignant, high grade, involving the serosa of the appendix; ', 'organ/tissue: muscle; tissue preparation: bulk; age: 5; sex: male; cell type: rhabdomyosarcoma; ', 'organ/tissue: pancreas; tissue preparation: bulk; age: 25-59 yrs; sex: unknown; ', 'organ/tissue: retina; tissue preparation: bulk; age: 41-66 year old pool of 7 donors; sex: male and female; cell type: central retina; other information: The library was constructed using RNA isolated from pooled 4 mm punches of human macula and central peripheral retina from 7 morphologically normal donor eyes.; ', 'organ/tissue: retina; tissue preparation: bulk; age: 3; sex: female; cell type: Bilateral retinoblastoma, poorly differentiated, left orbit; ', 'organ/tissue: other; tissue preparation: short term culture; sex: unknown; cell type: synovial fibroblasts from rheumatoid arthritis; ', 'organ/tissue: testis; tissue preparation: bulk; age: 32; sex: male; cell type: Embyronal Carcinoma, Mixed germ cell tumor consisting primarily of embryonal carcinoma with foci of yolk sac tumor and teratoma seen. Size: 4.5 x 3.8 x 2.8 cm. Non-neoplastic tissue: Marked hypospermatogenesis with Leydig cell hyperplasia and chronic inflammation.; ', 'organ/tissue: vascular; tissue preparation: antibody purified; age: 39; sex: unknown; cell type: normal liver; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; age: 47; sex: female; cell type: invasive breast cancer, ER+, PR+, Her2-; other information: CD45+ purified tumor infiltrating leukocytes. Library name in Cancer Cell, 2004, 6(1):17-32 "I-LEU-7-leukocytes"; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; age: 53; sex: male; cell type: lung macrophage; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; age: 45; sex: male; cell type: monocyte-depleted mononuclear cells; mutations: none; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; age: 71; sex: male; cell type: monocyte-depleted mononuclear cells; mutations: none; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; age: 45; sex: male; cell type: monocyte; mutations: none; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; age: 71; sex: male; cell type: monocyte; mutations: none; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; age: 39; sex: male; cell type: monocyte; mutations: none; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; age: 68; sex: female; cell type: monocyte; mutations: none; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; age: 72; sex: female; cell type: monocyte; mutations: none; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; age: 71; sex: male; cell type: plaque macrophage; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; age: 72; sex: female; cell type: plaque macrophage; ' GSE14803 Homo sapiens 15 Genome variation profiling by genome tiling array GPL5114 Positioning of Necrotic Lobular Intraepithelial Neoplasias within the sequence of breast carcinoma progression 2009-02-12 Lobular intraepithelial neoplasia grade 3 (LIN) is a recently recognized variant of intraepithelial lobular neoplasia of the breast composed of either uniform, generally small, cells (classic) with massive lobular distension, pleomorphic cells, signet-ring cells, or any cell type with necrosis. In contrast to classic forms of LIN, there is no consensus on therapeutic strategies for LIN3. In part this is due to the paucity of molecular data that could assist in defining the relationship of LIN3 to classic LIN and carcinomas. In this study we have employed array CGH to determine the patterns of chromosomal aberrations in 9 LIN3 lesions. By comparison to array CGH data of 13 classic LIN lesions, we demonstrate that LIN and LIN3 share several recurrent changes, in particular gains of 1q and losses of 16q. Both aberrations are known to appear early in tumorigenesis and to be associated with good prognosis. However, apart from this overlap, there were a number of karyotypic features that were observed exclusively in LIN3. Clearly, this lesion was characterized by a significantly higher number of DNA copy number changes (9 vs. 31 on average), a considerable complexity of chromosomal rearrangements with up to 16 breakpoints in one chromosome and overlapping high copy amplifications. The amplicons encompassed a number of known oncogenes such as ERBB2, CyclinD1 and FGF3 that have already been reported to be overexpressed in breast carcinomas. Our data suggest that, at the genetic level, LIN3 represents a highly advanced lesion with considerable resemblance to carcinomas and, therefore, reflects a lesion on the verge of invasion, and might represent the transition state from an intraepithelial neoplasm to breast carcinoma. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE14803 Positioning of necrotic lobular intraepithelial neoplasias (LIN, grade 3) within the sequence of breast carcinoma progression. Genes, chromosomes & cancer 2.940 https://doi.org/10.1002/gcc.20756 {Genes, chromosomes & cancer (2.940): 10.1002/gcc.20756} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA111975 https://www.ebi.ac.uk/ena/browser/view/PRJNA111975 None [Overal design]In this study, nine cases of pleomorphic/necrotic LIN lesions as well as one classic LIN and the concurrent invasive lobular carcinoma (ILC) were analyzed by array CGH. Sections of formalin-fixed paraffin-embedded (FFPE) specimens cut at 7-8µm were mounted on special foil-coated slides (Molecular Devices, San Diego, USA). The sections were then deparaffinized with Xylene, processed in decreasing concentrations of ethanol and stained with haematoxylin. Lasercapture microdissection for both lesions was performed at multiple sites using Veritas Arcturus. For reference-DNA, female mammary tissue without histomorphological changes obtained from reduction mammoplasty specimens was procecessed and laser-microdissected as explained above. Cells were digested in 10µl TE, pH 9, and 0.5µl proteinase K (20mg/ml) for 48h at 55°C. After inactivation of proteinase K at 99°C for 10min, the digest was stored at -20°C. Without any further purification, the complete digest was used for whole genome amplification by means of the WGA (Whole Genome Amplification) kit from Sigma following the manufacturer’s recommendations. Array CGH was performed as described previously. In brief, two µg of amplified tumor and reference DNA were labelled by random priming (BioPrime® Total Genomic Labeling System, Invitrogen, Carlsbad, CA) with Alexa Fluor® 3 and Alexa Fluor® 5, respectively, and hybridized onto a tiling path BAC array, consisting of the human 32k BAC Re-Array Set (BACPAC Resources Center; http://bacpac.chori.org/pHumanMinSet.htm; DNA kindly provided by Pieter de Jong) and a 1Mb Resolution BAC set (clones kindly provided by Nigel Carter, Wellcome Trust Sanger Centre). All protocols are provided in detail on our website (http://www.molgen.mpg.de/~abt_rop/molecular_cytogenetics/) and more information concerning this platform have been submitted to the Gene Expression Omnibus (GEO; http://www.ncbi.nlm.nih.gov/geo/; GLP: 5114). For the analysis and visualization of array CGH data, our software-package CGH-PRO was employed. No background subtraction was applied. Raw data were normalized by “Subgrid LOWESS”. For the assessment of copy number gains and losses, we used circular binary segmentation in combination with log2 ratio thresholds of 0.15 and -0.15, respectively. High copy amplifications were defined by focal appearance and a log2 ratio exceeding 0.45. In order to statistically investigate the similarity of aberration profiles we applied Pearson's product-moment correlation to cbs ratios of each of the corresponding arrays.; [Treatment]'Whole genome amplification by GenomePlex (Sigma).'; [Growth]'None'; [Extraction]'Sections of formalin-fixed paraffin-embedded (FFPE) specimens cut at 7-8um were mounted on special foil-coated slides (Molecular Devices, San Diego, USA). The sections were then deparaffinized with Xylene, processed in decreasing concentrations of ethanol and stained with haematoxylin. Lasercapture microdissection for both lesions was performed at multiple sites using Veritas Arcturus. Cells were digested in 10ul TE, pH 9, and 0.5ul proteinase K (20mg/ml) for 48h at 55degC . After inactivation of proteinase K at 99degC for 10min, the digest was stored at -20°C. Without any further purification, the complete digest was used for whole genome amplification by means of the WGA (Whole Genome Amplification) kit from Sigma.', 'Sections of formalin-fixed paraffin-embedded (FFPE) specimens cut at 7-8um were mounted on special foil-coated slides (Molecular Devices, San Diego, USA). The sections were then deparaffinized with Xylene, processed in decreasing concentrations of ethanol and stained with haematoxylin. Lasercapture microdissection for both lesions was performed at multiple sites using Veritas Arcturus. Cells were digested in 10ul TE, pH 9, and 0.5ul proteinase K (20mg/ml) for 48h at 55degC . After inactivation of proteinase K at 99degC for 10min, the digest was stored at -20degC . Without any further purification, the complete digest was used for whole genome amplification by means of the WGA (Whole Genome Amplification) kit from Sigma.', 'Sections of formalin-fixed paraffin-embedded (FFPE) specimens cut at 7-8µm were mounted on special foil-coated slides (Molecular Devices, San Diego, USA). The sections were then deparaffinized with Xylene, processed in decreasing concentrations of ethanol and stained with haematoxylin. Lasercapture microdissection for both lesions was performed at multiple sites using Veritas Arcturus. Cells were digested in 10µl TE, pH 9, and 0.5µl proteinase K (20mg/ml) for 48h at 55°C. After inactivation of proteinase K at 99°C for 10min, the digest was stored at -20°C. Without any further purification, the complete digest was used for whole genome amplification by means of the WGA (Whole Genome Amplification) kit from Sigma.', 'Sections of formalin-fixed paraffin-embedded (FFPE) specimens cut at 7-8?m were mounted on special foil-coated slides (Molecular Devices, San Diego, USA). The sections were then deparaffinized with Xylene, processed in decreasing concentrations of ethanol and stained with haematoxylin. Lasercapture microdissection for both lesions was performed at multiple sites using Veritas Arcturus. Cells were digested in 10?l TE, pH 9, and 0.5?l proteinase K (20mg/ml) for 48h at 55?C. After inactivation of proteinase K at 99?C for 10min, the digest was stored at -20?C. Without any further purification, the complete digest was used for whole genome amplification by means of the WGA (Whole Genome Amplification) kit from Sigma.'; [Cell type]'Source: ''gender: female; tissue: lobular intraepithelial neoplasia grade 3 (LIN3); ', 'gender: female; tissue: mammary tissue without histomorphological changes obtained from reduction mammoplasty specimens; ', 'gender: female; tissue: classic lobular intraepithelial neoplasia (LIN); ', 'gender: female; tissue: lobular intraepithelial neoplasia; ', '', 'gender: female; tissue: intraepithelial lobular carcinoma (ILC); ' GSE83756 Homo sapiens 60 Genome variation profiling by genome tiling array GPL21986 A map of mobile DNA insertions in the NCI-60 human cancer cell panel 2016-06-27 The National Cancer Institute-60 (NCI-60) cell lines are among the most widely used models of human cancer. They provide a platform to integrate DNA sequence information, epigenetic data, RNA and protein expression, and pharmacologic susceptibilities in studies of cancer cell biology. Genome-wide studies of the NCI-60 have included exome sequencing, karyotyping, and copy number analyses but have not targeted repetitive sequences. Interspersed repeats are a significant source of heritable genetic variation, and insertions of active elements can occur somatically in malignancy. To approach a functional understanding of these sequences in transformed cells, we used transposon insertion profiling (TIP) to map Long INterspersed Element-1 (LINE-1, L1) and Alu Short INterspersed Element (SINE) insertions in cancer genes in NCI-60 cells. As expected, this identified known insertions, polymorphisms shared in unrelated tumor cell lines, as well as unique, potentially tumor-specific insertions. Here, we report a map of these insertion sites and conduct association analyses relating individual insertions to a variety of cellular phenotypes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE83756 A map of mobile DNA insertions in the NCI-60 human cancer cell panel. Mobile DNA 3.630 https://doi.org/10.1186/s13100-016-0078-4 {Mobile DNA (3.630): 10.1186/s13100-016-0078-4} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA326942 https://www.ebi.ac.uk/ena/browser/view/PRJNA326942 None [Overal design]60 cell lines representing nine different types of neoplasias were mapped for LINE-1 and Alu transposable elements using a TIP-CHIP microarray tiling known cancer genes Please note that a technique called TIP-Chip was used to discover transposable elements (TE) in the NCI-60 cancer cell lines. The process uses labeled unique 3' DNA amplicons adjacent to these elements to map the TEs in the genome. These 3' amplicons are hybridized to the array and serve as a marker to identify a genomic coordinate. When the array scanner generate .gff output files as raw data output files on which clean-up algorithms and subsequent analysis were performed (resulting in peak files in text format).; [Treatment]'None'; [Growth]'DNA obtained directly from NCI. Cells grown in RPMI 1640 with 5% FBS (Bio Whittaker, not heat inactivated) and 1% L-glutamine. Cells not grown past 80% confluencey for attached cells, or 0,5 x 10-6 cells for suspended. Trypsinize (for attached cells) cells with 5 ml trypsin-EDTA per T162, for 15 min., at 370C.'; [Extraction]'isolated gDNA for each cell line was obtained from the NCI who used the Qiagen Maxi Kit Spin Protocol to extract DNA according to the manufacturers instructions'; [Cell type]'Source: ''mapped te_cell line info: L1_Leukemia1_CCRF_CEM; cell line: CCRFCEM; cell line source: Leukemia; tissue/cell info.: ALL; ', 'mapped te_cell line info: Alu_Leukemia1_CCRF_CEM; cell line: CCRFCEM; cell line source: Leukemia; tissue/cell info.: ALL; ', 'mapped te_cell line info: L1_Leukemia2_HL_60; cell line: HL60; cell line source: Leukemia; tissue/cell info.: Pro myelocytic leukemia; ', 'mapped te_cell line info: Alu_Leukemia2_HL_60; cell line: HL60; cell line source: Leukemia; tissue/cell info.: Pro myelocytic leukemia; ', 'mapped te_cell line info: L1_Leukemia3_K_562; cell line: K562; cell line source: Leukemia; tissue/cell info.: CML; ', 'mapped te_cell line info: Alu_Leukemia3_K_562; cell line: K562; cell line source: Leukemia; tissue/cell info.: CML; ', 'mapped te_cell line info: L1_Leukemia4_MOLT_4; cell line: MOLT4; cell line source: Leukemia; tissue/cell info.: ALL (cells were taken when patient was in relapse); ', 'mapped te_cell line info: Alu_Leukemia4_MOLT_4; cell line: MOLT4; cell line source: Leukemia; tissue/cell info.: ALL (cells were taken when patient was in relapse); ', 'mapped te_cell line info: L1_Leukemia5_RPMI_8226; cell line: RPMI8226; cell line source: Leukemia; tissue/cell info.: Myeloma; ', 'mapped te_cell line info: Alu_Leukemia5_RPMI_8226; cell line: RPMI8226; cell line source: Leukemia; tissue/cell info.: Myeloma; ', 'mapped te_cell line info: L1_Leukemia6_SR; cell line: SR; cell line source: Leukemia; tissue/cell info.: Lymphoma; ', 'mapped te_cell line info: Alu_Leukemia6_SR; cell line: SR; cell line source: Leukemia; tissue/cell info.: Lymphoma; ', 'mapped te_cell line info: L1_Lung1_A549ATCC; cell line: A549ATCC; cell line source: Lung; tissue/cell info.: Adenocarcinoma-p/md; ', 'mapped te_cell line info: Alu_Lung1_A549ATCC; cell line: A549ATCC; cell line source: Lung; tissue/cell info.: Adenocarcinoma-p/md; ', 'mapped te_cell line info: L1_Lung2_EKVX; cell line: EKVX; cell line source: Lung; tissue/cell info.: Adenocarcinoma-md; ', 'mapped te_cell line info: Alu_Lung2_EKVX; cell line: EKVX; cell line source: Lung; tissue/cell info.: Adenocarcinoma-md; ', 'mapped te_cell line info: L1_Lung3_HOP_62; cell line: HOP62; cell line source: Lung; tissue/cell info.: adenocarcinoma-ud; ', 'mapped te_cell line info: Alu_Lung3_HOP_62; cell line: HOP62; cell line source: Lung; tissue/cell info.: adenocarcinoma-ud; ', 'mapped te_cell line info: L1_Lung4_HOP_92; cell line: HOP92; cell line source: Lung; tissue/cell info.: Large cell-ud; ', 'mapped te_cell line info: Alu_Lung4_HOP_92; cell line: HOP92; cell line source: Lung; tissue/cell info.: Large cell-ud; ', 'mapped te_cell line info: L1_Lung5_NCI_H226; cell line: NCIH226; cell line source: Lung; tissue/cell info.: Squamous cell carcinoma-vpd; ', 'mapped te_cell line info: Alu_Lung5_NCI_H226; cell line: NCIH226; cell line source: Lung; tissue/cell info.: Squamous cell carcinoma-vpd; ', 'mapped te_cell line info: L1_Lung6_NCI_H23; cell line: NCIH23; cell line source: Lung; tissue/cell info.: Adenocarcinoma-ud; ', 'mapped te_cell line info: Alu_Lung6_NCI_H23; cell line: NCIH23; cell line source: Lung; tissue/cell info.: Adenocarcinoma-ud; ', 'mapped te_cell line info: L1_Lung7_NCI_H322M; cell line: NCIH322M; cell line source: Lung; tissue/cell info.: Small cell Bronchioalveolar Carcinoma; ', 'mapped te_cell line info: Alu_Lung7_NCI_H322M; cell line: NCIH322M; cell line source: Lung; tissue/cell info.: Small cell Bronchioalveolar Carcinoma; ', 'mapped te_cell line info: L1_Lung8_NCI_H460; cell line: NCIH460; cell line source: Lung; tissue/cell info.: Large Cell Carcinoma-ud; ', 'mapped te_cell line info: Alu_Lung8_NCI_H460; cell line: NCIH460; cell line source: Lung; tissue/cell info.: Large Cell Carcinoma-ud; ', 'mapped te_cell line info: L1_Lung9_NCI_H522; cell line: NCIH522; cell line source: Lung; tissue/cell info.: Adenocarcinoma-vpd; ', 'mapped te_cell line info: Alu_Lung9_NCI_H522; cell line: NCIH522; cell line source: Lung; tissue/cell info.: Adenocarcinoma-vpd; ', 'mapped te_cell line info: L1_Colon1_COLO205; cell line: COLO205; cell line source: Colon; tissue/cell info.: Adenocarcinoma; ', 'mapped te_cell line info: Alu_Colon1_COLO205; cell line: COLO205; cell line source: Colon; tissue/cell info.: Adenocarcinoma; ', 'mapped te_cell line info: L1_Colon2_HCC_2998; cell line: HCC2998; cell line source: Colon; tissue/cell info.: carcinoma; ', 'mapped te_cell line info: Alu_Colon2_HCC_2998; cell line: HCC2998; cell line source: Colon; tissue/cell info.: carcinoma; ', 'mapped te_cell line info: L1_Colon3_HCT_116; cell line: HCT116; cell line source: Colon; tissue/cell info.: carcinoma-vpd; ', 'mapped te_cell line info: Alu_Colon3_HCT_116; cell line: HCT116; cell line source: Colon; tissue/cell info.: carcinoma-vpd; ', 'mapped te_cell line info: L1_Colon4_HCT_15; cell line: HCT15; cell line source: Colon; tissue/cell info.: Adenocarcinoma p/md; ', 'mapped te_cell line info: Alu_Colon4_HCT_15; cell line: HCT15; cell line source: Colon; tissue/cell info.: Adenocarcinoma p/md; ', 'mapped te_cell line info: L1_Colon5_HT29; cell line: HT29; cell line source: Colon; tissue/cell info.: Adenocarcinoma-md; ', 'mapped te_cell line info: Alu_Colon5_HT29; cell line: HT29; cell line source: Colon; tissue/cell info.: Adenocarcinoma-md; ', 'mapped te_cell line info: L1_Colon6_KM12; cell line: KM12; cell line source: Colon; tissue/cell info.: Adenocarcinome-pd; ', 'mapped te_cell line info: Alu_Colon6_KM12; cell line: KM12; cell line source: Colon; tissue/cell info.: Adenocarcinome-pd; ', 'mapped te_cell line info: L1_Colon7_SW_620; cell line: SW620; cell line source: Colon; tissue/cell info.: Carcinoma-ud; ', 'mapped te_cell line info: Alu_Colon7_SW_620; cell line: SW620; cell line source: Colon; tissue/cell info.: Carcinoma-ud; ', 'mapped te_cell line info: L1_CNS1_SF_268; cell line: SF268; cell line source: CNS; tissue/cell info.: Glioblastoma, ud; ', 'mapped te_cell line info: Alu_CNS1_SF_268; cell line: SF268; cell line source: CNS; tissue/cell info.: Glioblastoma, ud; ', 'mapped te_cell line info: L1_CNS2_SF_295; cell line: SF295; cell line source: CNS; tissue/cell info.: Glioblastoma, ud; ', 'mapped te_cell line info: Alu_CNS2_SF_295; cell line: SF295; cell line source: CNS; tissue/cell info.: Glioblastoma, ud; ', 'mapped te_cell line info: L1_CNS3_SF_539; cell line: SF539; cell line source: CNS; tissue/cell info.: Glial cell neoplasm; ', 'mapped te_cell line info: Alu_CNS3_SF_539; cell line: SF539; cell line source: CNS; tissue/cell info.: Glial cell neoplasm; ', 'mapped te_cell line info: L1_CNS4_SNB_19; cell line: SNB19; cell line source: CNS; tissue/cell info.: Glioblastoma, ud; ', 'mapped te_cell line info: Alu_CNS4_SNB_19; cell line: SNB19; cell line source: CNS; tissue/cell info.: Glioblastoma, ud; ', 'mapped te_cell line info: L1_CNS5_SNB_75; cell line: SNB75; cell line source: CNS; tissue/cell info.: Astrocytoma; ', 'mapped te_cell line info: Alu_CNS5_SNB_75; cell line: SNB75; cell line source: CNS; tissue/cell info.: Astrocytoma; ', 'mapped te_cell line info: L1_CNS6_U251; cell line: U251; cell line source: CNS; tissue/cell info.: Glioblastoma,ud; ', 'mapped te_cell line info: Alu_CNS6_U251; cell line: U251; cell line source: CNS; tissue/cell info.: Glioblastoma,ud; ', 'mapped te_cell line info: L1_Melanoma1_LOXIMVI; cell line: LOXIMVI; cell line source: Melanoma; tissue/cell info.: Malignant amelanotic melanoma; ', 'mapped te_cell line info: Alu_Melanoma1_LOXIMVI; cell line: LOXIMVI; cell line source: Melanoma; tissue/cell info.: Malignant amelanotic melanoma; ', 'mapped te_cell line info: L1_Melanoma2_M14; cell line: M14; cell line source: Melanoma; tissue/cell info.: Melanotic melanoma; ', 'mapped te_cell line info: Alu_Melanoma2_M14; cell line: M14; cell line source: Melanoma; tissue/cell info.: Melanotic melanoma; ', 'mapped te_cell line info: L1_Melanoma3_MALME_3M; cell line: MALME3M; cell line source: Melanoma; tissue/cell info.: Malignant melanotic melanoma; ', 'mapped te_cell line info: Alu_Melanoma3_MALME_3M; cell line: MALME3M; cell line source: Melanoma; tissue/cell info.: Malignant melanotic melanoma; ', 'mapped te_cell line info: L1_Melanoma4_MDA_MB_435; cell line: MDAMB435; cell line source: Melanoma; tissue/cell info.: Ductal carcinoma- mammary gland; breast; duct; metastatic site: pleural effusion;; ', 'mapped te_cell line info: Alu_Melanoma4_MDA_MB_435; cell line: MDAMB435; cell line source: Melanoma; tissue/cell info.: Ductal carcinoma- mammary gland; breast; duct; metastatic site: pleural effusion;; ', 'mapped te_cell line info: L1_Melanoma5_SK_MEL_2; cell line: SKMEL2; cell line source: Melanoma; tissue/cell info.: Malignant melanotic melanoma; ', 'mapped te_cell line info: Alu_Melanoma5_SK_MEL_2; cell line: SKMEL2; cell line source: Melanoma; tissue/cell info.: Malignant melanotic melanoma; ', 'mapped te_cell line info: L1_Melanoma6_SK_MEL_28; cell line: SKMEL28; cell line source: Melanoma; tissue/cell info.: Malignant melanotic melanoma; ', 'mapped te_cell line info: Alu_Melanoma6_SK_MEL_28; cell line: SKMEL28; cell line source: Melanoma; tissue/cell info.: Malignant melanotic melanoma; ', 'mapped te_cell line info: L1_Melanoma7_SK_MEL_5; cell line: SKMEL5; cell line source: Melanoma; tissue/cell info.: Malignant melanotic melanoma; ', 'mapped te_cell line info: Alu_Melanoma7_SK_MEL_5; cell line: SKMEL5; cell line source: Melanoma; tissue/cell info.: Malignant melanotic melanoma; ', 'mapped te_cell line info: L1_Melanoma8_UACC_257; cell line: UACC257; cell line source: Melanoma; tissue/cell info.: Melanotic melanoma; ', 'mapped te_cell line info: Alu_Melanoma8_UACC_257; cell line: UACC257; cell line source: Melanoma; tissue/cell info.: Melanotic melanoma; ', 'mapped te_cell line info: L1_Melanoma9_UACC_62; cell line: UACC62; cell line source: Melanoma; tissue/cell info.: Melanotic melanoma; ', 'mapped te_cell line info: Alu_Melanoma9_UACC_62; cell line: UACC62; cell line source: Melanoma; tissue/cell info.: Melanotic melanoma; ', 'mapped te_cell line info: L1_Ovarian1_IGROV1; cell line: IGROV1; cell line source: Ovarian; tissue/cell info.: Cystoadenocarcinoma-pd; ', 'mapped te_cell line info: Alu_Ovarian1_IGROV1; cell line: IGROV1; cell line source: Ovarian; tissue/cell info.: Cystoadenocarcinoma-pd; ', 'mapped te_cell line info: L1_Ovarian2_NCI_ADR_RES; cell line: NCIADRRES; cell line source: Ovarian; tissue/cell info.: Adenocarinoma; ', 'mapped te_cell line info: Alu_Ovarian2_NCI_ADR_RES; cell line: NCIADRRES; cell line source: Ovarian; tissue/cell info.: Adenocarinoma; ', 'mapped te_cell line info: L1_Ovarian3_OVCAR_3; cell line: OVCAR3; cell line source: Ovarian; tissue/cell info.: Adenocarcinoma-md; ', 'mapped te_cell line info: Alu_Ovarian3_OVCAR_3; cell line: OVCAR3; cell line source: Ovarian; tissue/cell info.: Adenocarcinoma-md; ', 'mapped te_cell line info: L1_Ovarian4_OVCAR_4; cell line: OVCAR4; cell line source: Ovarian; tissue/cell info.: Adenocarcinoma-md; ', 'mapped te_cell line info: Alu_Ovarian4_OVCAR_4; cell line: OVCAR4; cell line source: Ovarian; tissue/cell info.: Adenocarcinoma-md; ', 'mapped te_cell line info: L1_Ovarian5_OVCAR_5; cell line: OVCAR5; cell line source: Ovarian; tissue/cell info.: Adenocarcinoma-wd; ', 'mapped te_cell line info: Alu_Ovarian5_OVCAR_5; cell line: OVCAR5; cell line source: Ovarian; tissue/cell info.: Adenocarcinoma-wd; ', 'mapped te_cell line info: L1_Ovarian6_OVCAR_8; cell line: OVCAR8; cell line source: Ovarian; tissue/cell info.: Carcinoma-ud; ', 'mapped te_cell line info: Alu_Ovarian6_OVCAR_8; cell line: OVCAR8; cell line source: Ovarian; tissue/cell info.: Carcinoma-ud; ', 'mapped te_cell line info: L1_Ovarian7_SK_OV_3; cell line: SKOV3; cell line source: Ovarian; tissue/cell info.: Adenocarcinoma-vpd; ', 'mapped te_cell line info: Alu_Ovarian7_SK_OV_3; cell line: SKOV3; cell line source: Ovarian; tissue/cell info.: Adenocarcinoma-vpd; ', 'mapped te_cell line info: L1_Renal1_786_0; cell line: 7860; cell line source: Renal; tissue/cell info.: Adenocarcinoma; ', 'mapped te_cell line info: Alu_Renal1_786_0; cell line: 7860; cell line source: Renal; tissue/cell info.: Adenocarcinoma; ', 'mapped te_cell line info: L1_Renal2_A498; cell line: A498; cell line source: Renal; tissue/cell info.: Adenocarcinoma; ', 'mapped te_cell line info: Alu_Renal2_A498; cell line: A498; cell line source: Renal; tissue/cell info.: Adenocarcinoma; ', 'mapped te_cell line info: L1_Renal3_ACHN; cell line: ACHN; cell line source: Renal; tissue/cell info.: Renal cell carcinoma-p/md; ', 'mapped te_cell line info: Alu_Renal3_ACHN; cell line: ACHN; cell line source: Renal; tissue/cell info.: Renal cell carcinoma-p/md; ', 'mapped te_cell line info: L1_Renal4_CAKI_1; cell line: CAKI1; cell line source: Renal; tissue/cell info.: Clear cell carcinoma; ', 'mapped te_cell line info: Alu_Renal4_CAKI_1; cell line: CAKI1; cell line source: Renal; tissue/cell info.: Clear cell carcinoma; ', 'mapped te_cell line info: L1_Renal5_RXF_393; cell line: RXF393; cell line source: Renal; tissue/cell info.: hypernephroma-pd; ', 'mapped te_cell line info: Alu_Renal5_RXF_393; cell line: RXF393; cell line source: Renal; tissue/cell info.: hypernephroma-pd; ', 'mapped te_cell line info: L1_Renal6_SN12C; cell line: SN12C; cell line source: Renal; tissue/cell info.: Renal cell carcinoma-pd; ', 'mapped te_cell line info: Alu_Renal6_SN12C; cell line: SN12C; cell line source: Renal; tissue/cell info.: Renal cell carcinoma-pd; ', 'mapped te_cell line info: L1_Renal7_TK_10; cell line: TK10; cell line source: Renal; tissue/cell info.: Renal Spindle cell carcinoma; ', 'mapped te_cell line info: Alu_Renal7_TK_10; cell line: TK10; cell line source: Renal; tissue/cell info.: Renal Spindle cell carcinoma; ', 'mapped te_cell line info: L1_Renal8_UO_31; cell line: UO31; cell line source: Renal; tissue/cell info.: Renal cell carcinoma-vpd; ', 'mapped te_cell line info: Alu_Renal8_UO_31; cell line: UO31; cell line source: Renal; tissue/cell info.: Renal cell carcinoma-vpd; ', 'mapped te_cell line info: L1_Prostate1_DU_145; cell line: DU145; cell line source: Prostate; tissue/cell info.: prostate; metastatic site: brain; carcinoma (patient with metastatic carcinoma of the prostate and a 3 year history of lymphocytic leukemia.); ', 'mapped te_cell line info: Alu_Prostate1_DU_145; cell line: DU145; cell line source: Prostate; tissue/cell info.: prostate; metastatic site: brain; carcinoma (patient with metastatic carcinoma of the prostate and a 3 year history of lymphocytic leukemia.); ', 'mapped te_cell line info: L1_Prostate2_PC_3; cell line: PC3; cell line source: Prostate; tissue/cell info.: Adenocarcinoma- prostate; metastatic site: bone;; ', 'mapped te_cell line info: Alu_Prostate2_PC_3; cell line: PC3; cell line source: Prostate; tissue/cell info.: Adenocarcinoma- prostate; metastatic site: bone;; ', 'mapped te_cell line info: L1_Breast1_BT_549; cell line: BT549; cell line source: Breast; tissue/cell info.: Papillary infiltrating ductal carcinoma-mammary gland; breast; ', 'mapped te_cell line info: Alu_Breast1_BT_549; cell line: BT549; cell line source: Breast; tissue/cell info.: Papillary infiltrating ductal carcinoma-mammary gland; breast; ', 'mapped te_cell line info: L1_Breast2_HS578T; cell line: HS578T; cell line source: Breast; tissue/cell info.: Carcinosarcoma-mammary gland; breast; ', 'mapped te_cell line info: Alu_Breast2_HS578T; cell line: HS578T; cell line source: Breast; tissue/cell info.: Carcinosarcoma-mammary gland; breast; ', 'mapped te_cell line info: L1_Breast3_MCF7; cell line: MCF7; cell line source: Breast; tissue/cell info.: Adenocarcinoma- mammary gland; breast; metastatic site: pleural effusion;; ', 'mapped te_cell line info: Alu_Breast3_MCF7; cell line: MCF7; cell line source: Breast; tissue/cell info.: Adenocarcinoma- mammary gland; breast; metastatic site: pleural effusion;; ', 'mapped te_cell line info: L1_Breast4_MDA_MB_231; cell line: MDAMB231; cell line source: Breast; tissue/cell info.: Adenocarcinoma-mammary gland; breast; epithelial; metastatic site: pleural effusion;; ', 'mapped te_cell line info: Alu_Breast4_MDA_MB_231; cell line: MDAMB231; cell line source: Breast; tissue/cell info.: Adenocarcinoma-mammary gland; breast; epithelial; metastatic site: pleural effusion;; ', 'mapped te_cell line info: L1_Breast5_T47D; cell line: T47D; cell line source: Breast; tissue/cell info.: infiltrating ductal carcinoma; ', 'mapped te_cell line info: Alu_Breast5_T47D; cell line: T47D; cell line source: Breast; tissue/cell info.: infiltrating ductal carcinoma; ', 'mapped te_cell line info: L1_Breast6_MDA_468; cell line: MDAN; cell line source: Breast; tissue/cell info.: Ductal carcinoma- mammary gland; breast; duct; metastatic site: pleural effusion;; ', 'mapped te_cell line info: Alu_Breast6_MDA_468; cell line: MDAN; cell line source: Breast; tissue/cell info.: Ductal carcinoma- mammary gland; breast; duct; metastatic site: pleural effusion;; ' GSE121642 Homo sapiens 6 Genome binding/occupancy profiling by high throughput sequencing GPL20795 Histone demethylase KDM4B promotes DNA damage by activating long interspersed nuclear element-1 2018-10-23 We assess whole-genome H3K9me3 distribution in cancer cells and find that H3K9me3 is largely enriched in long interspersed nuclear element-1 (LINE-1). A significant proportion of KDM4B-dependent H3K9me3 was located in evolutionarily young LINE-1 elements, which likely retain retrotransposition activity. Ectopic expression of KDM4B promoted LINE-1 expression, while depletion of KDM4B reduced it. Furthermore, KDM4B overexpression enhanced LINE-1 retrotransposition efficacy, copy number, and associated DNA damage, presumably via the histone demethylase activity of KDM4B. Breast cancer cell lines expressing high levels of KDM4B also exhibited increased LINE-1 expression and copy number compared with other cell lines. Pharmacological inhibition of KDM4B significantly reduced LINE-1 expression and DNA damage in breast cancer cells with excessive KDM4B. Our study not only identifies KDM4B as a novel regulator of LINE-1, but it also suggests an unexpected oncogenic role for KDM4B overexpression in tumorigenesis, providing clues for the development of new cancer prevention strategies and therapies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE121642 Histone Demethylase KDM4B Promotes DNA Damage by Activating Long Interspersed Nuclear Element-1. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-18-1310 {Cancer research (8.378): 10.1158/0008-5472.CAN-18-1310} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA497996 https://www.ebi.ac.uk/ena/browser/view/PRJNA497996 https://www.ncbi.nlm.nih.gov/sra?term=SRP166420 [Overal design]We performed H3K9me3 ChIP-seq with wild-type (WT), shKDM4B and KDM4B in MCF7 cell lines; [Treatment]'None'; [Growth]'MCF7 cells were cultured in Eagle’s minimum essential medium (EMEM; Genom, 11700) with 10% FBS, 0.01 mg/mL human recombinant insulin (Sigma, I9278), and nonessential amino acids (Invitrogen, 11140050)'; [Extraction]"Lysates were clarified from enzyme digested nuclei and histone-DNA complexes were isolated with antibody.\nLibraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit (Part# 0801-0303). Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation DNA was PCR amplified with Illumina primers for 15 cycles and library fragments of ~250 bp (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the Genome Analyzer following the manufacturer's protocols."; [Cell type]'Source: ''gender: female; cell line: MCF7; tissue: Human breast adenocarcinoma; passage: 12-15; chip antibody: H3K9me3 (ABclonal, A2360); ', 'gender: female; cell line: MCF7; tissue: Human breast adenocarcinoma; passage: 12-15; chip antibody: none; ' GSE26677 Homo sapiens 2 Expression profiling by array GPL6884 Development of gene expression signatures for breast cancer stem cells (SP cells) 2011-01-18 To further compare gene expression profile between breast cancer stem cells (SP cells) and non-SP cells, we have employed illumina GEX microarray as a discovery platform to identify gene differential expression between SP with non-SP cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26677 Global profiling of signaling networks: study of breast cancer stem cells and potential regulation. The oncologist 5.252 https://doi.org/10.1634/theoncologist.2010-0230 {The oncologist (5.252): 10.1634/theoncologist.2010-0230} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA136577 https://www.ebi.ac.uk/ena/browser/view/PRJNA136577 None [Overal design]SP analysis and sorting were done using a FACSVantage SE.The breast cancer cells were sorted into SP and non-SP cells.Total RNA was isolated from the FACS-sorted SP or non-SP cells, and gene expression signiture was detected by microarray.; [Treatment]'MCF-7 cells were detached by trypsinization and washed with ice-cold PBS.Cells (1×106) were labeled in the growth medium with 5.0 µg/mL Hoechst33342 dye, either alone or in combination with 50 µg/mL verapamil at 37°C for 90 minutes. Then, the cells were incubated with 2 μg/mL PI to exclude dead cells. SP analysis and sorting were done using a FACSVantage SE.The breast cancer cells were sorted into SP and non-SP cells.Total RNA was isolated from the FACS-sorted SP or non-SP cells.'; [Growth]'None'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''cell line: MCF-7; facs-sorted type: breast cancer stem cells (SP cells); ', 'cell line: MCF-7; facs-sorted type: non-SP cells; ' GSE155855 Homo sapiens 1536 Other GPL24676 Quantitative and multiplexed chemical-genetic phenotyping in mammalian cells using QMAP-Seq 2020-08-07 Here, we develop Quantitative and Multiplexed Analysis of Phenotype by Sequencing (QMAP-Seq), which leverages next-generation sequencing for pooled high-throughput chemical-genetic profiling. We apply QMAP-Seq to investigate how cellular stress response factors affect therapeutic response in cancer. Using minimal automation, we treat pools of 60 cell types—comprising 12 genetic perturbations in five cell lines—with 1,440 compound-dose combinations, generating 86,400 chemical-genetic measurements. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE155855 Quantitative and multiplexed chemical-genetic phenotyping in mammalian cells with QMAP-Seq. Nature communications 11.878 https://doi.org/10.1038/s41467-020-19553-8 {Nature communications (11.878): 10.1038/s41467-020-19553-8} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA655843 https://www.ebi.ac.uk/ena/browser/view/PRJNA655843 https://www.ncbi.nlm.nih.gov/sra?term=SRP276634 [Overal design]Targeted sequencing of sgRNAs and cell line barcodes from samples consisting of 5 cell lines x 12 sgRNAs + cell spike-in standards. Sequencing run was composed of 1,536 samples, each representing a unique compound-dose-replicate combination. 96 samples were DMSO-treated (control), and 1,440 samples were compound-treated.; [Treatment]'Cell line pools were treated with compound or DMSO over a four-point concentration range (10-fold dilutions) in duplicate using either a standard dose range (10 nM to 10 μM) or a low dose range (1 nM to 1 μM). Dose1=lowest dose. Dose4=highest dose. Cells were treated for 72 hours.'; [Growth]'Cell line pools were cultured in RPMI-1640, 10% Tet System Approved FBS, 1% Penicillin/Streptomycin, 100 ng/mL doxycycline for 7 days prior to compound treatment.'; [Extraction]'Cell line pools were lysed with lysis buffer (10% 10x Taq DNA Polymerase Buffer, 0.45% IGEPAL CA-630, 0.45% TWEEN 20, 10% Proteinase K, 79.1% Nuclease-Free Water) containing cell spike-in standards. Cells were incubated at 60°C for 1 hour. Proteinase K from lysis buffer was inactivated at 95°C for 15 minutes.\nBarcoded region was PCR amplified with a unique set of indexed primers for each sample. PCR products were pooled and purified twice. Sequencing library was diluted, combined with PhiX, denatured, and sequenced on a NovaSeq 6000 (Illumina).'; [Cell type]'Source: ''cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bendamustine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tacrolimus_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dexamethasone_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Temozolomide_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Thalidomide_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PHA793887_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cediranib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RITA_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cimetidine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mitoxantrone_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Regorafenib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nelarabine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Exemestane_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NVPAUY922_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Alisertib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Blebbistatin_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Anastrozole_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Abiraterone_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate1WellC3_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erlotinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dabrafenib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate1WellF3_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Parthenolide_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK0752_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fulvestrant_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cabozantinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Niclosamide_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gefitinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fluvastatin_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ki8751_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CHIR99021_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linsitinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Clofarabine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PLX4720_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fingolimod_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Valdecoxib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sorafenib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PIK93_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: VER155008_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lenvatinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dacarbazine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Decitabine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate1WellC6_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tigecycline_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bexarotene_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate1WellF6_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Zebularine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SR1001_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cisplatin_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ruxolitinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nilotinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sitagliptin_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Doxorubicin_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KX2391_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trametinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PD318088_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mebendazole_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Letrozole_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etoposide_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FiveFluorouracil_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Simvastatin_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WP1130_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF31_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cyclophosphamide_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Carfilzomib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trifluoperazine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Crizotinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Vincristine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RacRotigotine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BardoxoloneMethyl_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivantinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Selumetinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lapatinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DimethylFumarate_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate1WellC10_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nitroxoline_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Paclitaxel_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate1WellF10_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU55933_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RG108_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lovastatin_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gemcitabine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ciclopirox_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Chlorambucil_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ornidazole_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Rigosertib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PYR41_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Saracatinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Topotecan_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Pazopanib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Everolimus_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sildenafil_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dasatinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Brivanib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivozanib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BrefeldinA_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bendamustine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tacrolimus_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dexamethasone_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Temozolomide_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Thalidomide_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PHA793887_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cediranib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RITA_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cimetidine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mitoxantrone_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Regorafenib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nelarabine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Exemestane_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NVPAUY922_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Alisertib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Blebbistatin_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Anastrozole_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Abiraterone_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate2WellC3_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erlotinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dabrafenib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate2WellF3_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Parthenolide_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK0752_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fulvestrant_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cabozantinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Niclosamide_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gefitinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fluvastatin_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ki8751_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CHIR99021_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linsitinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Clofarabine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PLX4720_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fingolimod_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Valdecoxib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sorafenib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PIK93_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: VER155008_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lenvatinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dacarbazine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Decitabine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate2WellC6_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tigecycline_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bexarotene_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate2WellF6_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Zebularine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SR1001_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cisplatin_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ruxolitinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nilotinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sitagliptin_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Doxorubicin_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KX2391_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trametinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PD318088_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mebendazole_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Letrozole_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etoposide_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FiveFluorouracil_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Simvastatin_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WP1130_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF31_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cyclophosphamide_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Carfilzomib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trifluoperazine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Crizotinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Vincristine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RacRotigotine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BardoxoloneMethyl_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivantinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Selumetinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lapatinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DimethylFumarate_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate2WellC10_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nitroxoline_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Paclitaxel_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate2WellF10_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU55933_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RG108_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lovastatin_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gemcitabine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ciclopirox_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Chlorambucil_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ornidazole_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Rigosertib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PYR41_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Saracatinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Topotecan_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Pazopanib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Everolimus_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sildenafil_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dasatinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Brivanib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivozanib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BrefeldinA_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bendamustine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tacrolimus_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dexamethasone_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Temozolomide_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Thalidomide_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PHA793887_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cediranib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RITA_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cimetidine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mitoxantrone_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Regorafenib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nelarabine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Exemestane_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NVPAUY922_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Alisertib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Blebbistatin_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Anastrozole_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Abiraterone_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate3WellC3_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erlotinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dabrafenib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate3WellF3_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Parthenolide_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK0752_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fulvestrant_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cabozantinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Niclosamide_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gefitinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fluvastatin_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ki8751_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CHIR99021_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linsitinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Clofarabine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PLX4720_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fingolimod_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Valdecoxib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sorafenib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PIK93_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: VER155008_Dose2_Rep1; ', 'cell lines: ZR-75 -1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lenvatinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dacarbazine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Decitabine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate3WellC6_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tigecycline_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bexarotene_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate3WellF6_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Zebularine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SR1001_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cisplatin_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ruxolitinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nilotinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sitagliptin_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Doxorubicin_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KX2391_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trametinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PD318088_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mebendazole_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Letrozole_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etoposide_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FiveFluorouracil_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Simvastatin_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WP1130_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF31_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cyclophosphamide_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Carfilzomib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trifluoperazine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Crizotinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Vincristine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RacRotigotine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BardoxoloneMethyl_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivantinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Selumetinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lapatinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DimethylFumarate_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate3WellC10_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nitroxoline_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Paclitaxel_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate3WellF10_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU55933_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RG108_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lovastatin_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gemcitabine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ciclopirox_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Chlorambucil_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ornidazole_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Rigosertib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PYR41_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Saracatinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Topotecan_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Pazopanib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Everolimus_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sildenafil_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dasatinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Brivanib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivozanib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BrefeldinA_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bendamustine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tacrolimus_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dexamethasone_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Temozolomide_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Thalidomide_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PHA793887_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cediranib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RITA_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cimetidine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mitoxantrone_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Regorafenib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nelarabine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Exemestane_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NVPAUY922_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Alisertib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Blebbistatin_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Anastrozole_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Abiraterone_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate4WellC3_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erlotinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dabrafenib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate4WellF3_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Parthenolide_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK0752_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fulvestrant_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cabozantinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Niclosamide_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gefitinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fluvastatin_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ki8751_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CHIR99021_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linsitinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Clofarabine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PLX4720_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fingolimod_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Valdecoxib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sorafenib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PIK93_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: VER155008_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lenvatinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dacarbazine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Decitabine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate4WellC6_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tigecycline_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bexarotene_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate4WellF6_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Zebularine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SR1001_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cisplatin_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ruxolitinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nilotinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sitagliptin_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Doxorubicin_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KX2391_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trametinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PD318088_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mebendazole_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Letrozole_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etoposide_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FiveFluorouracil_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Simvastatin_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WP1130_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF31_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cyclophosphamide_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Carfilzomib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trifluoperazine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Crizotinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Vincristine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RacRotigotine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BardoxoloneMethyl_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivantinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Selumetinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lapatinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DimethylFumarate_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate4WellC10_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nitroxoline_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Paclitaxel_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate4WellF10_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU55933_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RG108_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lovastatin_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gemcitabine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ciclopirox_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Chlorambucil_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ornidazole_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Rigosertib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PYR41_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Saracatinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Topotecan_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Pazopanib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Everolimus_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sildenafil_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dasatinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Brivanib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivozanib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BrefeldinA_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bendamustine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tacrolimus_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dexamethasone_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Temozolomide_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Thalidomide_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PHA793887_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cediranib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RITA_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cimetidine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mitoxantrone_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Regorafenib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nelarabine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Exemestane_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NVPAUY922_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Alisertib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Blebbistatin_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Anastrozole_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Abiraterone_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate5WellC3_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erlotinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dabrafenib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate5WellF3_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Parthenolide_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK0752_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fulvestrant_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cabozantinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Niclosamide_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gefitinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fluvastatin_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ki8751_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CHIR99021_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linsitinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Clofarabine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PLX4720_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fingolimod_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Valdecoxib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sorafenib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PIK93_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: VER155008_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lenvatinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dacarbazine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Decitabine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate5WellC6_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tigecycline_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bexarotene_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate5WellF6_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Zebularine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SR1001_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cisplatin_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ruxolitinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nilotinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sitagliptin_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Doxorubicin_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KX2391_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trametinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PD318088_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mebendazole_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Letrozole_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etoposide_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FiveFluorouracil_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Simvastatin_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WP1130_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF31_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cyclophosphamide_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Carfilzomib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trifluoperazine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Crizotinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Vincristine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RacRotigotine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BardoxoloneMethyl_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivantinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Selumetinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lapatinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DimethylFumarate_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate5WellC10_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nitroxoline_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Paclitaxel_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate5WellF10_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU55933_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RG108_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lovastatin_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gemcitabine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ciclopirox_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Chlorambucil_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ornidazole_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Rigosertib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PYR41_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Saracatinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Topotecan_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Pazopanib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Everolimus_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sildenafil_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dasatinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Brivanib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivozanib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BrefeldinA_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bendamustine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tacrolimus_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dexamethasone_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Temozolomide_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Thalidomide_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PHA793887_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cediranib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RITA_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cimetidine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mitoxantrone_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Regorafenib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nelarabine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Exemestane_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NVPAUY922_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Alisertib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Blebbistatin_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Anastrozole_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Abiraterone_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate6WellC3_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erlotinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dabrafenib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate6WellF3_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Parthenolide_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK0752_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fulvestrant_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cabozantinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Niclosamide_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gefitinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fluvastatin_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ki8751_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CHIR99021_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linsitinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Clofarabine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PLX4720_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fingolimod_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Valdecoxib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sorafenib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PIK93_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: VER155008_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lenvatinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dacarbazine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Decitabine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate6WellC6_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tigecycline_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bexarotene_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate6WellF6_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Zebularine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SR1001_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cisplatin_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ruxolitinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nilotinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sitagliptin_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Doxorubicin_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KX2391_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trametinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PD318088_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mebendazole_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Letrozole_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etoposide_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FiveFluorouracil_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Simvastatin_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WP1130_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF31_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cyclophosphamide_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Carfilzomib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trifluoperazine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Crizotinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Vincristine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RacRotigotine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BardoxoloneMethyl_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivantinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Selumetinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lapatinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DimethylFumarate_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate6WellC10_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nitroxoline_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Paclitaxel_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate6WellF10_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU55933_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RG108_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lovastatin_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gemcitabine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ciclopirox_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Chlorambucil_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ornidazole_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Rigosertib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PYR41_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Saracatinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Topotecan_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Pazopanib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Everolimus_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sildenafil_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dasatinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Brivanib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivozanib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BrefeldinA_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bendamustine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tacrolimus_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dexamethasone_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Temozolomide_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Thalidomide_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PHA793887_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cediranib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RITA_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cimetidine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mitoxantrone_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Regorafenib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nelarabine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Exemestane_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NVPAUY922_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Alisertib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Blebbistatin_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Anastrozole_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Abiraterone_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate7WellC3_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erlotinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dabrafenib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate7WellF3_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Parthenolide_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK0752_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fulvestrant_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cabozantinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Niclosamide_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gefitinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fluvastatin_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ki8751_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CHIR99021_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linsitinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Clofarabine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PLX4720_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fingolimod_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Valdecoxib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sorafenib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PIK93_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: VER155008_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lenvatinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dacarbazine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Decitabine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate7WellC6_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tigecycline_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bexarotene_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate7WellF6_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Zebularine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SR1001_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cisplatin_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ruxolitinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nilotinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sitagliptin_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Doxorubicin_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KX2391_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trametinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PD318088_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mebendazole_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Letrozole_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etoposide_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FiveFluorouracil_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Simvastatin_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WP1130_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF31_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cyclophosphamide_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Carfilzomib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trifluoperazine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Crizotinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Vincristine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RacRotigotine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BardoxoloneMethyl_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivantinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Selumetinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lapatinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DimethylFumarate_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate7WellC10_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nitroxoline_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Paclitaxel_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate7WellF10_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU55933_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RG108_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lovastatin_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gemcitabine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ciclopirox_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Chlorambucil_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ornidazole_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Rigosertib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PYR41_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Saracatinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Topotecan_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Pazopanib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Everolimus_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sildenafil_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dasatinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Brivanib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivozanib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BrefeldinA_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bendamustine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tacrolimus_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dexamethasone_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Temozolomide_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Thalidomide_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PHA793887_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cediranib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RITA_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cimetidine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mitoxantrone_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Regorafenib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nelarabine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Exemestane_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NVPAUY922_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Alisertib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Blebbistatin_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Anastrozole_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Abiraterone_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate8WellC3_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erlotinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dabrafenib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate8WellF3_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Parthenolide_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK0752_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fulvestrant_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cabozantinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Niclosamide_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gefitinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fluvastatin_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ki8751_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CHIR99021_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linsitinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Clofarabine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PLX4720_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2 , sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Fingolimod_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Valdecoxib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sorafenib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PIK93_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: VER155008_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lenvatinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dacarbazine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Decitabine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate8WellC6_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tigecycline_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bexarotene_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate8WellF6_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Zebularine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SR1001_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cisplatin_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ruxolitinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nilotinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sitagliptin_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Doxorubicin_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KX2391_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trametinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PD318088_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mebendazole_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Letrozole_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etoposide_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FiveFluorouracil_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Simvastatin_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WP1130_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF31_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Cyclophosphamide_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Carfilzomib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Trifluoperazine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Crizotinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Vincristine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RacRotigotine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BardoxoloneMethyl_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivantinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Selumetinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lapatinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DimethylFumarate_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate8WellC10_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Nitroxoline_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Paclitaxel_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate8WellF10_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU55933_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RG108_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lovastatin_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gemcitabine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ciclopirox_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Chlorambucil_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ornidazole_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Rigosertib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PYR41_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Saracatinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Topotecan_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Pazopanib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Everolimus_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Sildenafil_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Dasatinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Brivanib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Tivozanib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BrefeldinA_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Veliparib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF573228_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT199_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD8186_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Phloretin_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entrectinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RO4929097_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IC87114_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: APY29_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0879_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DBeQ_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT737_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AT7867_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ifosfamide_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gossypol_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PI103_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: LRRK2IN1_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TPCA1_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate9WellC3_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ETP46464_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Curcumin_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate9WellF3_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: JQ1_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK2636771_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PAC1_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS536924_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SixMercaptopurine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SJ172550_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SU11274_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Necrostatin1_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TG101348_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etomoxir_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Methotrexate_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Canertinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS345541_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PifithrinAlpha_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Purmorphamine_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erastin_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SN38_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU0063794_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WAY362450_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MG132_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate9WellC6_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SNS032_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD7545_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate9WellF6_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SB743921_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Neratinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS754807_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF083010_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Spautin1_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IBET151_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Isoliquiritigenin_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Masitinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FourHydroxytamoxifen_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entinostat_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK461364_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BGJ398_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MLN2238_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mdivi1_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK1775_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Navitoclax_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bortezomib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PX12_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD4547_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BetulinicAcid_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0941_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Teniposide_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Belinostat_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK1059615_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Olaparib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD5363_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NSC74859_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: EX527_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate9WellC10_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TubastatinA_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KW2449_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate9WellF10_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lomeguatrib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU60019_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Afatinib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF3758309_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Semagacestat_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Palbociclib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linifanib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BIX01294_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Triptolide_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: OSI027_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Istradefylline_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ZSTK474_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSKJ4_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: StemRegenin1_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CAL101_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK4112_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: YM155_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ganetespib_Dose1_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Veliparib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF573228_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT199_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD8186_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Phloretin_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entrectinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RO4929097_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IC87114_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: APY29_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0879_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DBeQ_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT737_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AT7867_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ifosfamide_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gossypol_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PI103_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: LRRK2IN1_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TPCA1_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate10WellC3_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ETP46464_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Curcumin_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate10WellF3_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: JQ1_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK2636771_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PAC1_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS536924_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SixMercaptopurine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SJ172550_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SU11274_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Necrostatin1_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TG101348_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etomoxir_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Methotrexate_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Canertinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS345541_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PifithrinAlpha_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Purmorphamine_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erastin_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SN38_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU0063794_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WAY362450_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MG132_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate10WellC6_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SNS032_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD7545_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate10WellF6_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SB743921_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Neratinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS754807_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF083010_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Spautin1_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IBET151_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Isoliquiritigenin_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Masitinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FourHydroxytamoxifen_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entinostat_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK461364_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BGJ398_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MLN2238_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mdivi1_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK1775_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Navitoclax_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bortezomib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PX12_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD4547_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BetulinicAcid_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0941_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Teniposide_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Belinostat_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK1059615_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Olaparib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD5363_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NSC74859_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: EX527_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate10WellC10_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TubastatinA_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KW2449_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate10WellF10_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lomeguatrib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU60019_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Afatinib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF3758309_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Semagacestat_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Palbociclib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linifanib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BIX01294_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Triptolide_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: OSI027_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Istradefylline_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ZSTK474_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSKJ4_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: StemRegenin1_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CAL101_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK4112_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: YM155_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ganetespib_Dose1_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Veliparib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF573228_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT199_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD8186_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Phloretin_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entrectinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RO4929097_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IC87114_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: APY29_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0879_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DBeQ_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT737_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AT7867_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ifosfamide_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gossypol_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PI103_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: LRRK2IN1_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TPCA1_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate11WellC3_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ETP46464_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Curcumin_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate11WellF3_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: JQ1_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK2636771_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PAC1_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS536924_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SixMercaptopurine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SJ172550_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SU11274_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Necrostatin1_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TG101348_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etomoxir_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Methotrexate_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Canertinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS345541_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PifithrinAlpha_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Purmorphamine_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erastin_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SN38_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU0063794_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WAY362450_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MG132_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate11WellC6_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SNS032_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD7545_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate11WellF6_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SB743921_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Neratinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS754807_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF083010_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Spautin1_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IBET151_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Isoliquiritigenin_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Masitinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FourHydroxytamoxifen_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entinostat_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK461364_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BGJ398_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MLN2238_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mdivi1_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK1775_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Navitoclax_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bortezomib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PX12_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD4547_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BetulinicAcid_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0941_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Teniposide_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Belinostat_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK1059615_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Olaparib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD5363_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NSC74859_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: EX527_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate11WellC10_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TubastatinA_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KW2449_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate11WellF10_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lomeguatrib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU60019_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Afatinib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF3758309_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Semagacestat_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Palbociclib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linifanib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BIX01294_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Triptolide_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: OSI027_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Istradefylline_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ZSTK474_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSKJ4_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: StemRegenin1_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CAL101_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK4112_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: YM155_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ganetespib_Dose2_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Veliparib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF573228_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT199_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD8186_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Phloretin_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entrectinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RO4929097_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IC87114_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: APY29_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0879_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DBeQ_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT737_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AT7867_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ifosfamide_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gossypol_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PI103_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: LRRK2IN1_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TPCA1_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate12WellC3_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ETP46464_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Curcumin_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate12WellF3_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: JQ1_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK2636771_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PAC1_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS536924_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SixMercaptopurine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SJ172550_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SU11274_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Necrostatin1_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TG101348_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etomoxir_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Methotrexate_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Canertinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS345541_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PifithrinAlpha_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Purmorphamine_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erastin_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SN38_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU0063794_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WAY362450_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MG132_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate12WellC6_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SNS032_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD7545_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate12WellF6_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SB743921_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Neratinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS754807_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF083010_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Spautin1_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IBET151_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Isoliquiritigenin_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Masitinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FourHydroxytamoxifen_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entinostat_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK461364_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BGJ398_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MLN2238_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mdivi1_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK1775_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Navitoclax_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bortezomib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PX12_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD4547_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BetulinicAcid_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0941_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Teniposide_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Belinostat_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK1059615_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Olaparib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD5363_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NSC74859_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: EX527_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate12WellC10_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TubastatinA_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KW2449_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate12WellF10_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lomeguatrib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU60019_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Afatinib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF3758309_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Semagacestat_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Palbociclib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linifanib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BIX01294_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Triptolide_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: OSI027_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Istradefylline_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ZSTK474_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSKJ4_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: StemRegenin1_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CAL101_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK4112_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: YM155_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ganetespib_Dose2_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Veliparib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF573228_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT199_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD8186_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Phloretin_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entrectinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RO4929097_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IC87114_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: APY29_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0879_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DBeQ_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT737_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AT7867_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ifosfamide_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gossypol_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PI103_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: LRRK2IN1_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TPCA1_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate13WellC3_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ETP46464_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Curcumin_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate13WellF3_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: JQ1_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK2636771_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PAC1_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS536924_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SixMercaptopurine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SJ172550_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SU11274_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Necrostatin1_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TG101348_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etomoxir_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgAT F6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Methotrexate_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Canertinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS345541_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PifithrinAlpha_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Purmorphamine_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erastin_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SN38_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU0063794_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WAY362450_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MG132_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate13WellC6_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SNS032_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD7545_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate13WellF6_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SB743921_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Neratinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS754807_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF083010_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Spautin1_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IBET151_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Isoliquiritigenin_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Masitinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FourHydroxytamoxifen_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entinostat_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK461364_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BGJ398_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MLN2238_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mdivi1_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK1775_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Navitoclax_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bortezomib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PX12_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD4547_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BetulinicAcid_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0941_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Teniposide_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Belinostat_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK1059615_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Olaparib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD5363_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NSC74859_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: EX527_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate13WellC10_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TubastatinA_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KW2449_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate13WellF10_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lomeguatrib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU60019_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Afatinib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF3758309_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Semagacestat_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Palbociclib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linifanib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BIX01294_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Triptolide_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: OSI027_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Istradefylline_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ZSTK474_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSKJ4_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: StemRegenin1_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CAL101_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK4112_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: YM155_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ganetespib_Dose3_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Veliparib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF573228_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT199_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD8186_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Phloretin_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entrectinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RO4929097_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IC87114_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: APY29_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0879_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DBeQ_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT737_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AT7867_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ifosfamide_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gossypol_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PI103_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: LRRK2IN1_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TPCA1_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate14WellC3_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ETP46464_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Curcumin_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate14WellF3_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: JQ1_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK2636771_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PAC1_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS536924_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SixMercaptopurine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SJ172550_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SU11274_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Necrostatin1_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TG101348_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etomoxir_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Methotrexate_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Canertinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS345541_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PifithrinAlpha_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Purmorphamine_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erastin_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SN38_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU0063794_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WAY362450_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MG132_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate14WellC6_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SNS032_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD7545_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate14WellF6_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SB743921_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Neratinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS754807_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF083010_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Spautin1_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IBET151_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Isoliquiritigenin_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Masitinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FourHydroxytamoxifen_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entinostat_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK461364_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BGJ398_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MLN2238_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mdivi1_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK1775_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Navitoclax_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bortezomib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PX12_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD4547_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BetulinicAcid_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0941_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Teniposide_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Belinostat_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK1059615_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Olaparib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD5363_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NSC74859_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: EX527_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate14WellC10_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TubastatinA_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KW2449_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate14WellF10_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lomeguatrib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU60019_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Afatinib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF3758309_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Semagacestat_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Palbociclib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linifanib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BIX01294_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Triptolide_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: OSI027_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Istradefylline_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ZSTK474_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSKJ4_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: StemRegenin1_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CAL101_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK4112_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: YM155_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ganetespib_Dose3_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Veliparib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF573228_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT199_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD8186_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Phloretin_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entrectinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RO4929097_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IC87114_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: APY29_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0879_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DBeQ_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT737_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AT7867_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ifosfamide_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gossypol_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PI103_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: LRRK2IN1_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TPCA1_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate15WellC3_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ETP46464_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Curcumin_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate15WellF3_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: JQ1_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK2636771_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PAC1_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS536924_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SixMercaptopurine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SJ172550_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SU11274_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Necrostatin1_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TG101348_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etomoxir_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Methotrexate_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Canertinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS345541_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PifithrinAlpha_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Purmorphamine_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erastin_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SN38_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU0063794_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WAY362450_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MG132_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate15WellC6_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SNS032_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD7545_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate15WellF6_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SB743921_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Neratinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS754807_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF083010_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Spautin1_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IBET151_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Isoliquiritigenin_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Masitinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FourHydroxytamoxifen_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entinostat_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK461364_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BGJ398_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MLN2238_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mdivi1_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK1775_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Navitoclax_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bortezomib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PX12_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD4547_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BetulinicAcid_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0941_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Teniposide_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Belinostat_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK1059615_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Olaparib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD5363_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NSC74859_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: EX527_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate15WellC10_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TubastatinA_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KW2449_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate15WellF10_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lomeguatrib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEA P1, sgATG7, sgSLC35F2; compound treatment: KU60019_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Afatinib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF3758309_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Semagacestat_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Palbociclib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linifanib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BIX01294_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Triptolide_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: OSI027_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Istradefylline_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ZSTK474_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSKJ4_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: StemRegenin1_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CAL101_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK4112_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: YM155_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ganetespib_Dose4_Rep1; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Veliparib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF573228_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT199_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD8186_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Phloretin_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entrectinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: RO4929097_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IC87114_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: APY29_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0879_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DBeQ_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ABT737_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AT7867_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ifosfamide_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Gossypol_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PI103_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: LRRK2IN1_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TPCA1_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate16WellC3_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ETP46464_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Curcumin_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate16WellF3_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: JQ1_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK2636771_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PAC1_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS536924_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SixMercaptopurine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SJ172550_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SU11274_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Necrostatin1_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TG101348_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Etomoxir_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Methotrexate_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Canertinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS345541_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PifithrinAlpha_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Purmorphamine_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Erastin_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SN38_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU0063794_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: WAY362450_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MG132_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate16WellC6_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SNS032_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD7545_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate16WellF6_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: SB743921_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Neratinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BMS754807_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: STF083010_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Spautin1_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: IBET151_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Isoliquiritigenin_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Masitinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: FourHydroxytamoxifen_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Entinostat_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK461364_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BGJ398_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MLN2238_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Mdivi1_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: MK1775_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Navitoclax_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Bortezomib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PX12_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD4547_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BetulinicAcid_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GDC0941_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Teniposide_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Belinostat_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK1059615_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Olaparib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: AZD5363_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: NSC74859_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: EX527_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate16WellC10_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: TubastatinA_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KW2449_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: DMSOPlate16WellF10_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Lomeguatrib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: KU60019_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Afatinib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: PF3758309_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Semagacestat_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Palbociclib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Linifanib_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: BIX01294_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Triptolide_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: OSI027_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Istradefylline_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: ZSTK474_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSKJ4_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: StemRegenin1_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: CAL101_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: GSK4112_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: YM155_Dose4_Rep2; ', 'cell lines: ZR-75-1, SKBR3, HCC-38, MDA-MB-231, BT-20; sgrnas: sgNT, sgHSF1, sgHSF2, sgERN1, sgXBP1, sgATF3, sgATF4, sgATF6, sgNFE2L2, sgKEAP1, sgATG7, sgSLC35F2; compound treatment: Ganetespib_Dose4_Rep2; ' GSE24473 Homo sapiens 6 Expression profiling by array GPL570 Ras-Association Domain Family 1C Protein Promotes Breast Cancer Cell Migration 2010-09-30 RASSF1C, unlike RASSF1A, is not a tumor suppressor, but instead may play a role in stimulating metastasis and survival in breast cancer cells RASSF1C over-expression enhances T47D cell invasion/migration in vitro https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24473 Ras-association domain family 1C protein promotes breast cancer cell migration and attenuates apoptosis. BMC cancer 2.933 https://doi.org/10.1186/1471-2407-10-562 {BMC cancer (2.933): 10.1186/1471-2407-10-562} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA132775 https://www.ebi.ac.uk/ena/browser/view/PRJNA132775 None [Overal design]Three RASSF1C over-expression samples vs three controls; [Treatment]'over-expression techniques were used to modulate RASSF1C expression in human breast cancer cells'; [Growth]'Cell culture was grown as recommended by the supplier'; [Extraction]'Total RNA from human cell lines was isolated from confluent cultures using the Absolutely RNA Microprep Kit'; [Cell type]'Source: ''cell line: T47D cell; genotype/variation: over-expression RASSF1C; ', 'cell line: T47D cell; genotype/variation: control; ' GSE107000 Homo sapiens 17 Expression profiling by high throughput sequencing GPL16791 RNAseq analysis of ruxolitinib treated breast cancers 2017-11-16 We performed RNA sequencing analysis on fresh-frozen biopsies of metastatic triple-negative breast cancer prior to undergoing therapy with ruxolitinib, or after 2 cycles of therapy in a subset of patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE107000 Phase II study of ruxolitinib, a selective JAK1/2 inhibitor, in patients with metastatic triple-negative breast cancer. NPJ breast cancer 32.43 https://doi.org/10.1038/s41523-018-0060-z {NPJ breast cancer (32.43): 10.1038/s41523-018-0060-z} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA418761 https://www.ebi.ac.uk/ena/browser/view/PRJNA418761 https://www.ncbi.nlm.nih.gov/sra?term=SRP125109 [Overal design]Seventeen samples were successfully sequenced, including two pairs of baseline and cycle 2, two unmatched cycle 2 samples, and eleven unmatched baseline samples.; [Treatment]'None'; [Growth]'None'; [Extraction]"10um slides were macrodissected to enrich for tumor regions, followed by RNA isolation using the Promega Maxwell simplyRNA kit according to manufacturer's recommended protocol\nIllumina RNAaccess"; [Cell type]'Source: ''patient #: 3; treatment: Baseline; tissue site: Neck lymph node; ', 'patient #: 9; treatment: Cycle 2; tissue site: Contralateral Breast; ', 'patient #: 19; treatment: Baseline; tissue site: Ipsilateral breast; ', 'patient #: 23; treatment: Baseline; tissue site: Pleural effusion; ', 'patient #: 9; treatment: Baseline; tissue site: Contralateral Breast; ', 'patient #: 1; treatment: Baseline; tissue site: Soft tissue; ', 'patient #: 2; treatment: Baseline; tissue site: Liver; ', 'patient #: 6; treatment: Baseline; tissue site: Inguingal node; ', 'patient #: 6; treatment: Cycle 2; tissue site: Inguingal node; ', 'patient #: 7; treatment: Baseline; tissue site: Liver; ', 'patient #: 13; treatment: Cycle 2; tissue site: Skin; ', 'patient #: 15; treatment: Baseline; tissue site: Liver; ', 'patient #: 14; treatment: Cycle 2; tissue site: Skin; ', 'patient #: 18; treatment: Baseline; tissue site: Lymph node; ', 'patient #: 17; treatment: Baseline; tissue site: Liver; ', 'patient #: 23; treatment: Baseline; tissue site: Liver; ', 'patient #: 16; treatment: Baseline; tissue site: Ipsilateral breast; ' GSE111587 Mus musculus 2 Expression profiling by array; Non-coding RNA profiling by array GPL22782 Adam12 and lnc015192 act as ceRNAs in breast cancer by regulating miR-34a 2018-03-08 Long non-coding RNAs (lncRNAs) are involved in the pathology of various tumors. However, the role of lncRNA in breast cancer remains unclear. We performed microarrays to identify the differentially expressed mRNAs and lncRNAs in breast tissues with or without miR-34a knockout. In vitro and in vivo assays were preformed to explore the biological effects of the differentially expressed mRNA and lncRNA in breast cancer cells. We found that Adam12 and lnc015192 were significantly upregulated in miR-34a knockout breast tissues. Knockdown of Adam12 and lnc015192 inhibited breast cancer cells migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and in vivo. Further study indicated that lnc015192 acted as a competing endogenous RNA (ceRNA) for miR-34a to regulate Adam12 expression. Taken together, our findings demonstrate how Adam12 and lnc015192 induce breast cancer metastasis and offer novel therapeutic targets for breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE111587 Adam12 and lnc015192 act as ceRNAs in breast cancer by regulating miR-34a. Oncogene 6.634 https://doi.org/10.1038/s41388-018-0410-1 {Oncogene (6.634): 10.1038/s41388-018-0410-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA437473 https://www.ebi.ac.uk/ena/browser/view/PRJNA437473 None [Overal design]We performed microarrays to identify the differentially expressed mRNAs and lncRNAs in female mice breast tissues with or without miR-34a knockout.; [Treatment]'Mammary glands from miR-34a -/- (KO) and miR-34a fl/fl (NC) mice were harvested and RNA were extracted.'; [Growth]'The miR-34a floxed mice (miR-34a fl/fl) and the mammary gland specific Cre expressing mice were purchased from The Jackson Laboratory (Stock Numbers 018545 and 003553, Maine, USA). And the miR-34a fl/fl mice were crossed to Cre mice to obtain mammary gland specific miR-34a knock out mice (miR-34a -/-). Female miR-34a -/- mice (KO) were used for all experiments and miR-34a fl/fl mice (NC) were used as control.'; [Extraction]"RNA was prepared using the TRIzol reagent following the manufacturer's recommendations. RNA was quantified using a NanoDrop-1000 spectrophotometer."; [Cell type]'Source: ''genotype/variation: miR-34a fl/fl (control); tissue: breast; gender: female; ', 'genotype/variation: miR-34a -/- (KO); tissue: breast; gender: female; ' GSE39694 Homo sapiens 8 Expression profiling by array GPL13667; GPL15207 Expression data from orthotopic tumors and the MCF7 and HCC1937 breast cancer cell lines 2012-07-27 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39694 Stem cell-like transcriptional reprogramming mediates metastatic resistance to mTOR inhibition. Oncogene 6.634 https://doi.org/10.1038/onc.2016.427 {Oncogene (6.634): 10.1038/onc.2016.427} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA171488 https://www.ebi.ac.uk/ena/browser/view/PRJNA171488 None [Overal design]Refer to individual Series; [Treatment]'A daily oral treatment with sirolimus (Rapamune) or control solution (DMSO) was applied (60 days).', 'A daily oral treatment with sirolimus (Rapamune) or control solution (DMSO) was applied (30 days).', 'MCF7 cells were treated with everolimus (100 nM) and HCC1937 cells were treated with everolimus (150 nM) or vehicle (DMSO) for 120 days.'; [Growth]'Primary triple-negative breast tumor (from a BRCA1 mutation carrier) orthotopically engrafted in immunocompromised mice was monitored 2 to 3 times per week.', 'Primary breast tumor (from a BRCA mutation carrier) orthotopically implanted in immunocompromised mice was monitored 2 to 3 times per week.', 'MCF7 and HCC1937 cells were cultured and maintained in RPMI medium containing 10% FBS and 2 mM glutamine.'; [Extraction]"Trizol extraction of total RNA was performed according to manufacturer's instructions.", "Trizol extraction of total RNA was performed according to manufacturer's instructions"; [Cell type]'Source: ''agent: DMSO; tissue: Breast cancer; ', 'agent: Sirolimus; tissue: Breast cancer; ', 'cell line: MCF7; cell line orgin: Breast cancer; agent: vehicle (DMSO); ', 'cell line: MCF7; cell line orgin: Breast cancer; agent: Everolimus (100 nM); ', 'cell line: HCC1937; cell line orgin: Breast cancer; agent: vehicle (DMSO); ', 'cell line: HCC1937; cell line orgin: Breast cancer; agent: Everolimus (150 nM); ' GSE167473 Homo sapiens 68 Expression profiling by high throughput sequencing GPL24676 Cancer of Unknown Primary stem-like cells model multi-organ metastasis and unveil liability to MEK inhibition 2021-02-24 Cancers of Unknown Primary (CUPs), featuring metastatic dissemination in the absence of a primary tumor, are a biological enigma and a fatal disease. We propose that CUPs are a distinct, yet unrecognized, pathological entity originating from stem-like cells endowed with distinguished properties. These cells can be isolated in vitro (agnospheres) and propagated in vivo by serial transplantation, displaying a high tumor-initiating cell frequency. After subcutaneous engraftment, agnospheres recapitulated the CUP phenotype, by spontaneously and quickly disseminating, and forming widespread established metastases. Regardless of different genetic backgrounds, agnospheres invariably displayed cell-autonomous proliferation and self-renewal, mostly relying on unrestrained activation of the MAP kinase/MYC axis, which confers sensitivity to MEK inhibitors in vitro and in vivo. Such sensitivity is associated with a transcriptomic signature predicting that more than 70% of CUP patients could be eligible to MEK inhibition. These data shed light on CUP biology and unveil an opportunity for therapeutic intervention. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE167473 Cancer of unknown primary stem-like cells model multi-organ metastasis and unveil liability to MEK inhibition. Nature communications 11.878 https://doi.org/10.1038/s41467-021-22643-w {Nature communications (11.878): 10.1038/s41467-021-22643-w} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA704700 https://www.ebi.ac.uk/ena/browser/view/PRJNA704700 https://www.ncbi.nlm.nih.gov/sra?term=SRP308023 [Overal design]Transcriptional characterization of CUP stem-like cells and CUP tissues; [Treatment]'none'; [Growth]'CUP stem-like cells were isolated and grown in ultra-low attachment flasks in DMEM/F12 supplemented with N2 (Gibco), BSA 0.5%, L-Glutamine 2mM, Pen/strep'; [Extraction]"Cell pellets of growing spheres were lysed in Triazol and RNA was extracted with RNeasy Micro Kit (Qiagen); FFPE tissue slices were extracted with Maxwell® RSC RNA FFPE Kit (promega)\nTotal RNA (100 ng) from each sample was prepared using QuantSeq 3'mRNA-Seq Library prep kit (Lexogen, Vienna, Austria) according to manufacturer's instructions\nThe amplified fragmented cDNA of 300 bp in size were sequenced in single-end mode using the Illumina NovaSeq 6000 with a read length of 100 bp"; [Cell type]'Metastatic Colorectal Cancer Primary cells', 'Cancers of Unknown Primary cells', 'Metastatic Melanoma Primary cells', 'Cancer of Unknown Primary FFPE Tissue', 'Early Metastatic Merkeloma FFPE Tissue', 'Early Metastatic Melanoma FFPE Tissue', 'Melanoma FFPE Tissue', 'Early Metastatic Skin Carcinoma FFPE Tissue', 'Early Metastatic Breast Cancer FFPE Tissue', 'Early Metastatic Head and Neck Cancer FFPE Tissue''cell type: Metastatic Colorectal Cancer Primary cells; patient: mCRC729; type: Cell; ', 'cell type: Cancers of Unknown Primary cells; patient: AS901; type: Cell; ', 'cell type: Cancers of Unknown Primary cells; patient: AS906; type: Cell; ', 'cell type: Cancers of Unknown Primary cells; patient: AS43; type: Cell; ', 'cell type: Cancers of Unknown Primary cells; patient: N-AS47; type: Cell; ', 'cell type: Metastatic Melanoma Primary cells; patient: mMS321; type: Cell; ', 'cell type: Cancers of Unknown Primary cells; patient: AS914; type: Cell; ', 'cell type: Metastatic Colorectal Cancer Primary cells; patient: mCRC0155; type: Cell; ', 'cell type: Cancers of Unknown Primary cells; patient: AS67; type: Cell; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN901; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN906; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN43; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN47; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN909; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN912; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN918; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN913; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN57; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN58; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN60; type: tissue; ', 'cell type: Early Metastatic Merkeloma FFPE Tissue; patient: mMERK44; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN325; type: tissue; ', 'cell type: Early Metastatic Melanoma FFPE Tissue; patient: mMEL321; type: tissue; ', 'cell type: Melanoma FFPE Tissue; patient: MEL2; type: tissue; ', 'cell type: Melanoma FFPE Tissue; patient: MEL4; type: tissue; ', 'cell type: Early Metastatic Skin Carcinoma FFPE Tissue; patient: mSKI61; type: tissue; ', 'cell type: Early Metastatic Breast Cancer FFPE Tissue; patient: mBRE35; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN327; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN331; type: tissue; ', 'cell type: Early Metastatic Breast Cancer FFPE Tissue; patient: mBRE40; type: tissue; ', 'cell type: Early Metastatic Breast Cancer FFPE Tissue; patient: mBRE45; type: tissue; ', 'cell type: Early Metastatic Skin Carcinoma FFPE Tissue; patient: mSKIN49; type: tissue; ', 'cell type: Early Metastatic Head and Neck Cancer FFPE Tissue; patient: mH&N50; type: tissue; ', 'cell type: Early Metastatic Head and Neck Cancer FFPE Tissue; patient: mH&N54; type: tissue; ', 'cell type: Early Metastatic Breast Cancer FFPE Tissue; patient: mBRE56; type: tissue; ', 'cell type: Early Metastatic Breast Cancer FFPE Tissue; patient: mBRE923; type: tissue; ', 'cell type: Cancer of Unknown Primary FFPE Tissue; patient: AGN322; type: tissue; ' GSE56871 Homo sapiens 4 Expression profiling by array GPL15207 Massive LINE1 retrotransposon Invasion in Tuberous Sclerosis Astrocytomas 2014-04-17 Somatic retrotranspositions of various mobile genetic elements take place in tumors, and L1 retroelements physiologically transpose in neural progenitor cells during neurogenesis. We sequenced whole genomes of the neural progenitor cell-derived subependymal giant cell astrocytomas that typically affect patients suffering from the neurodevelopmental disease Tuberous Sclerosis. Here we show an unprecedented increased L1 retrotransposition in these tumors, with tens of thousands new genomic insertions, that preferentially invade genes involved in neural activity, synaptic transmission and cancer. The prevalent insertions are short, nested in preexisting L1 repeats in the same orientation, trimmed in both the 5’ and 3’ ends, representing unorthodox retrotransposition”. Most somatic L1 inserts in the genomically stable astrocytomas are nested in preexisting L1 elements. This preferred nested integration may act as a “lightning rod” mechanism dampening the effects of massive retrotransposition. In contrast, the enhanced transposition found in genomically unstable breast tumors includes regions of high-density clustered insertion, transposminos. These clustered insertions are expected to be more detrimental, as many of them are non-nested and frequently invade genic and exonic sequences. Exaggerated L1 retrotransposition may be a common stochastic damaging pathway in neurological disorders and cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE56871 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA244833 https://www.ebi.ac.uk/ena/browser/view/PRJNA244833 None [Overal design]four subependymal giant cell astrocytomas (SEGAs). Three out of four showed a massive number of Mobile Element Insertions (MEI), mainly L1 retrotranspositions(Hil1 samples ) , those are compared to the fourth without this high MEI element number (Lol1 sample ); [Treatment]'None'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''individual: Tuberous Sclerosis patient; tissue: SEGA with high MEI (Hil1); ', 'individual: Tuberous Sclerosis patient; tissue: SEGA with normal MEI number (LoL1); ', 'individual: Patient with no Tuberous Sclerosis; tissue: SEGA with high MEI (Hil1); ' GSE71400 Homo sapiens 28 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Tumor hypoxia causes DNA hypermethylation by reducing TET activity (DIP-Seq) 2015-07-27 Hypermethylation of tumor suppressor gene (TSG) promoters confers growth advantages to cancer cells, but how these changes arise is poorly understood. Here, we report that tumor hypoxia reduces the activity of oxygen-dependent TET enzymes, which catalyze DNA de-methylation through 5-methylcytosine oxidation. This occurs independently of hypoxia-associated alterations in TET gene expression, basal metabolism, HIF activity or nuclear reactive oxygen species, but directly depends on oxygen shortage. Hypoxia-induced loss of TET activity increases hypermethylation at gene promoters in vitro, while also in patients, gene promoters are markedly more methylated in hypoxic than normoxic tumors. Affected genes are frequently involved in DNA repair, cell cycle regulation, angiogenesis and metastasis, indicating cellular selection of hypermethylation events. Overall, up to 50% of the tumor-associated hypermethylation is ascribable to hypoxia across various cancer types. Accordingly, spontaneous murine breast tumors become hypermethylated when rendered hypoxic through vessel pruning, whereas vessel normalisation rescues this effect. Tumor hypoxia thus acts as a novel regulator underlying DNA methylation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE71400 Tumour hypoxia causes DNA hypermethylation by reducing TET activity. Nature 43.070 https://doi.org/10.1038/nature19081 {Nature (43.070): 10.1038/nature19081} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA291094 https://www.ebi.ac.uk/ena/browser/view/PRJNA291094 https://www.ncbi.nlm.nih.gov/sra?term=SRP061650 [Overal design]mDIPseq and hmDIPseq of MCF7 cells grown under hypoxic and normoxic conditions. Submission includes data on 4 independent DIPseq experiments, each containing 2 biological replicates grown under hypoxic conditions (0.5% oxygen), and 2 biological replicates grown under normoxic conditions.; [Treatment]'cells were grown for 24 hours at normoxic or hypoxic oxygen tensions'; [Growth]'MCF7cells were cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM'; [Extraction]'Nucleic acids were subsequently extracted using the Wizard Genomic DNA Purification (Promega, Leiden, The Netherlands) kit according to instructions, with all buffers supplemented with DFO (200 µM), dissolved in 80 µL PBS-DFO with RNAse A (200 units, NEB, Ipswich, MA, USA), incubated for 10 minutes at 37°C. After proteinase K addition (200 units) and incubation for 30 minutes at 56°C, DNA was purified using the QIAQuick blood and tissue kit (all buffers supplemented with DFO), eluted in 100 µL of a 10 mM Tris, 1mM EDTA solution (pH 8) and stored at -80°C until further processing.\nLibrary preparations and DNA immunoprecipitations were as described by Taiwo and colleagues (Nat Protoc 2012), using established antibodies targeting 5mC and 5hmC.\nDIP-seq', 'Nucleic acids were subsequently extracted using the Wizard Genomic DNA Purification (Promega, Leiden, The Netherlands) kit according to instructions, with all buffers supplemented with DFO (200 µM), dissolved in 80 µL PBS-DFO with RNAse A (200 units, NEB, Ipswich, MA, USA), incubated for 10 minutes at 37°C. After proteinase K addition (200 units) and incubation for 30 minutes at 56°C, DNA was purified using the QIAQuick blood and tissue kit (all buffers supplemented with DFO), eluted in 100 µL of a 10 mM Tris, 1mM EDTA solution (pH 8) and stored at -80°C until further processing.\nLibrary preparations and DNA immunoprecipitations were as described by Taiwo and colleagues (Nat Protoc 2012), using established antibodies targeting 5mC and 5hmC.'; [Cell type]'Source: ''oxygen concentration: 0.5% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 1; replicate: A; cell line: MCF7; ', 'oxygen concentration: 0.5% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 1; replicate: B; cell line: MCF7; ', 'oxygen concentration: 0.5% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 2; replicate: A; cell line: MCF7; ', 'oxygen concentration: 0.5% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 2; replicate: B; cell line: MCF7; ', 'oxygen concentration: 0.5% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 3; replicate: A; cell line: MCF7; ', 'oxygen concentration: 0.5% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 3; replicate: B; cell line: MCF7; ', 'oxygen concentration: 0.5% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 4; replicate: A; cell line: MCF7; ', 'oxygen concentration: 0.5% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 4; replicate: B; cell line: MCF7; ', 'oxygen concentration: 21% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 1; replicate: A; cell line: MCF7; ', 'oxygen concentration: 21% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 1; replicate: B; cell line: MCF7; ', 'oxygen concentration: 21% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 2; replicate: A; cell line: MCF7; ', 'oxygen concentration: 21% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 2; replicate: B; cell line: MCF7; ', 'oxygen concentration: 21% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 3; replicate: A; cell line: MCF7; ', 'oxygen concentration: 21% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 3; replicate: B; cell line: MCF7; ', 'oxygen concentration: 21% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 4; replicate: A; cell line: MCF7; ', 'oxygen concentration: 21% oxygen; dip antibody: anti 5mC (clone 33D3, Eurogentec); experiment: 4; replicate: B; cell line: MCF7; ', 'oxygen concentration: 0.5% oxygen; dip antibody: anti 5hmC (Active Motif cat 39791); experiment: 1; replicate: A; ', 'oxygen concentration: 0.5% oxygen; dip antibody: anti 5hmC (Active Motif cat 39791); experiment: 2; replicate: A; ', 'oxygen concentration: 0.5% oxygen; dip antibody: anti 5hmC (Active Motif cat 39791); experiment: 3; replicate: A; ', 'oxygen concentration: 21% oxygen; dip antibody: anti 5hmC (Active Motif cat 39791); experiment: 1; replicate: A; ', 'oxygen concentration: 21% oxygen; dip antibody: anti 5hmC (Active Motif cat 39791); experiment: 2; replicate: A; ', 'oxygen concentration: 21% oxygen; dip antibody: anti 5hmC (Active Motif cat 39791); experiment: 3; replicate: A; ', 'oxygen concentration: 0.5% oxygen; dip antibody: NA; experiment: 1; replicate: A; ', 'oxygen concentration: 0.5% oxygen; dip antibody: NA; experiment: 2; replicate: A; ', 'oxygen concentration: 0.5% oxygen; dip antibody: NA; experiment: 3; replicate: A; ', 'oxygen concentration: 21% oxygen; dip antibody: NA; experiment: 1; replicate: A; ', 'oxygen concentration: 21% oxygen; dip antibody: NA; experiment: 2; replicate: A; ', 'oxygen concentration: 21% oxygen; dip antibody: NA; experiment: 3; replicate: A; ' GSE49334 Homo sapiens 9 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Mapping of somatic linker histone H1 variants in T47D-MTVL cells 2013-07-29 At least six histone H1 variants exist in mammalian somatic cells that bind to the linker DNA and stabilize the nucleosome particle contributing to higher order chromatin compaction. In addition, H1 seems to be involved in the active regulation of gene expression. It is not well known whether the different variants have specific roles, are distributed differentially along the genome, or regulate specific promoters. By taking advantage of specific antibodies to H1 variants and HA-tagged recombinant H1 variants expressed in a breast cancer-derived cell line, we have investigated the distribution of the different somatic H1 variants (H1.2 to H1.5, H1.0 and H1X) in particular promoters and genome-wide. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE49334 Mapping of six somatic linker histone H1 variants in human breast cancer cells uncovers specific features of H1.2. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gku079 {Nucleic acids research (11.147) doi:10.1093/nar/gku079}; {The Journal of biological chemistry (None) doi:10.1074/jbc.M114.617324}; 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA213643 https://www.ebi.ac.uk/ena/browser/view/PRJNA213643 https://www.ncbi.nlm.nih.gov/sra?term=SRP028307 [Overal design]Genome-wide analysis of H1.0, H1.2, H1.4, H1X and H3; [Treatment]'no treatment'; [Growth]'RPMI 1640 medium + 10%FBS, 1%glutamine, 1%penicillin/streptomycin'; [Extraction]'T47D-MTVL cells were fixed using 1% formaldehyde, harvested and sonicated using a Diagenode Bioruptor to generate chromatin fragments between 200 and 500 bp. To perform the chromatin immunoprecipitation, 30 µg of chromatin was immunoprecipitated overnight using the indicated antibody. Rabbit IgG (Santa Cruz Biothechnology) was used as a control for nonspecific interaction of DNA. Input was prepared with 10% of the chromatin material used for an immunoprecipitation. Immunocomplexes were recovered using Protein A magnetic beads from Millipore. Beads with bound antibody/protein/DNA complexes were washed, decross-linked at 65ºC overnight and immunoprecipitated DNA was recovered using the IPure Kit from Diagenode.\nDNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-HA (Abcam 9110); ', 'gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H1.2 (Abcam 4086); ', 'gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H1X (Abcam 31972); ', 'gender: female; tissue: breast cancer ductal carcinoma; antibody: H1.4-HA histone protein immunoprecipitated DNA; ', 'gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H3 (Abcam 1791); ' GSE130903 Homo sapiens 12 Expression profiling by high throughput sequencing GPL11154 Short and long-term effects of CDK4/6 inhibition on early stage breast cancer 2019-05-08 CDK4/6 inhibitors are used in the treatment of advanced estrogen receptor (ER)(+) breast cancer (BC). Their efficacy in ER(-) and early stage BC is currently under investigation. Here, we show that palbociclib, a CDK4/6 inhibitor, can inhibit both progression of ductal carcinoma in situ (DCIS) and growth of invasive disease in both an ER(-) basal BC model (MCFDCIS) and an ER(+) luminal model (MCF7 intraductal injection). In MCFDCIS cells palbociclib repressed cell cycle gene expression, inhibited proliferation, induced senescence and normalized tumorspheres formed in Matrigel whilst the formation of acini by normal mammary epithelial cells (MCF10A) was not affected. Palbociclib treatment of mice with MCFDCIS tumors inhibited their malignant progression and reduced proliferation of invasive lesions. Transcriptomic analysis of the tumor and stromal cell compartments showed that cell cycle and senescence genes, and MUC16, an ovarian cancer biomarker gene, were repressed during treatment. Knockdown of MUC16 in MCFDCIS cells inhibited proliferation of invasive lesions but not progression of DCIS. After cessation of palbociclib treatment genes associated with differentiation, e.g. p63, inflammation, IFNγ response and antigen processing and presentation remained suppressed in the tumor and surrounding stroma. We conclude that palbociclib can prevent progression of DCIS and is anti-proliferative in ER(-) invasive disease mediated in part via MUC16. Lasting effects of CDK4/6 inhibition after drug withdrawal on differentiation and the immune response could impact the approach to treatment of early stage ER(-) breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130903 Short- and Long-Term Effects of CDK4/6 Inhibition on Early-Stage Breast Cancer. Molecular cancer therapeutics 4.856 https://doi.org/10.1158/1535-7163.MCT-19-0231 {Molecular cancer therapeutics (4.856): 10.1158/1535-7163.MCT-19-0231} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA541931 https://www.ebi.ac.uk/ena/browser/view/PRJNA541931 https://www.ncbi.nlm.nih.gov/sra?term=SRP197105 [Overal design]3 Tumor Replicates/group. 4 Groups - 2wk Palbociclib, 2wk Vehicle, 2wk Palbociclib + Recovery and 2wk Vehicle + Recovery. Vehicle treated tumors were used as baseline for comparisons and interrogation of drug effects.; [Treatment]'Animals were treated daily with 50mg/kg Palbociclib by oral gavage'; [Growth]'1 Million MCFDCIS cells were injected subcutaneously into Athymic Nude Mice and given 2 weeks to establish DCIS tumors in the animals prior to treatment initiation'; [Extraction]'Qiagen RNeasy extraction following tumor homogenization using the Roche MagNA Lyser\nTruSeq RNA Library Prep'; [Cell type]'Source: ''cell line: MCFDCIS; treatment: Palbo; Stage: initial; ', 'cell line: MCFDCIS; treatment: Palbo; Stage: recovery; ', 'cell line: MCFDCIS; treatment: Vehicle; Stage: initial; ', 'cell line: MCFDCIS; treatment: Vehicle; Stage: recovery; ' GSE22210 Homo sapiens 193 Methylation profiling by array GPL9183 Molecular subtypes of breast cancer are associated with characteristic DNA methylation patterns 2010-06-08 Introduction: Five different molecular subtypes of breast cancer have been identified through gene expression profiling. Each subtype has a characteristic expression pattern suggested to partly depend on cellular origin. We aimed to investigate whether the molecular subtypes also display distinct methylation profiles. Methods: We analysed methylation status of 807 cancer-related genes in 189 fresh frozen primary breast tumours and four normal breast tissue samples using an array-based methylation assay. Results: Unsupervised analysis revealed three groups of breast cancer with characteristic methylation patterns. The three groups were associated with the luminal A, luminal B and basal-like molecular subtypes of breast cancer, respectively, whereas cancers of the HER2-enriched and normal-like subtypes were distributed among the three groups. The methylation frequencies were significantly different between subtypes, with luminal B and basal-like tumours being most and least frequently methylated, respectively. Moreover, targets of the polycomb repressor complex in breast cancer and embryonic stem cells were more methylated in luminal B tumours than in other tumours. BRCA2-mutated tumours had a particularly high degree of methylation. Finally, by utilizing gene expression data, we observed that a large fraction of genes reported as having subtype-specific expression patterns might be regulated through methylation. Conclusions: We have found that breast cancers of the basal-like, luminal A and luminal B molecular subtypes harbour specific methylation profiles. Our results suggest that methylation may play an important role in the development of breast cancers. DNA methylation profiling of breast cancer samples and normal breast tissue samples. The Illumina GoldenGate Methylation Cancer Panel I was used to obtain DNA methylation profiles across approximately 1500 CpGs. Samples included 189 breast cancer samples and 4 normal breast tissue samples. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22210 Molecular subtypes of breast cancer are associated with characteristic DNA methylation patterns. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr2590 {Breast cancer research : BCR (5.676): 10.1186/bcr2590} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA128879 https://www.ebi.ac.uk/ena/browser/view/PRJNA128879 None [Overal design]Bisulphite converted DNA from the samples were hybridised to the Illumina GoldenGate Methylation Cancer Panel I; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was isolated from fresh frozen primary breast tumours in a three-step procedure. Tumour cells were pre-treated with Proteinase K (20 mg/ml) at 55C over-night, DNA was further purified using the Promega Wizard Genomic DNA Purification kit (Promega Corporation, Madison, Wisconsin) and finally DNA was purified by phenol/chloroform treatment in phase-lock tubes.'; [Cell type]'Source: ''tissue: breast tumor; family status: brca1; er: er_neg; pgr: pgr_neg; overall survival time: 486; overall survival event: 1; hu subtype: Basal; spfpercent: 5; nodestatus: NA; grade: 3; hc_cluster: 3; fga: 0.63; ezh2_gain: Gain; sizemm: NA; sizestatus: NA; ageyear: 44; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 4378; overall survival event: 1; hu subtype: Basal; spfpercent: 9; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.51; ezh2_gain: Gain; sizemm: 30; sizestatus: 2; ageyear: 81; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 5076; overall survival event: 0; hu subtype: Basal; spfpercent: NA; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.51; ezh2_gain: NoGain; sizemm: 30; sizestatus: 2; ageyear: 49; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: NA; overall survival event: NA; hu subtype: Basal; spfpercent: 11; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: NA; ezh2_gain: NA; sizemm: 37; sizestatus: 2; ageyear: 39; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 4811; overall survival event: 0; hu subtype: Basal; spfpercent: NA; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.39; ezh2_gain: Gain; sizemm: 22; sizestatus: 2; ageyear: 49; agestatus: 1; ', 'tissue: breast tumor; family status: brca1; er: er_neg; pgr: pgr_neg; overall survival time: 969; overall survival event: 1; hu subtype: Basal; spfpercent: 15; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.67; ezh2_gain: Gain; sizemm: 40; sizestatus: 2; ageyear: 51; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 4580; overall survival event: 0; hu subtype: Basal; spfpercent: 16; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.73; ezh2_gain: Gain; sizemm: 15; sizestatus: 1; ageyear: 41; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 4514; overall survival event: 0; hu subtype: Basal; spfpercent: 20; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.5; ezh2_gain: NoGain; sizemm: 12; sizestatus: 1; ageyear: 42; agestatus: 1; ', 'tissue: breast tumor; family status: brca1; er: er_neg; pgr: pgr_neg; overall survival time: 4444; overall survival event: 0; hu subtype: Basal; spfpercent: 13; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.51; ezh2_gain: Gain; sizemm: 25; sizestatus: 2; ageyear: 38; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: NA; overall survival event: NA; hu subtype: Basal; spfpercent: 21; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: NA; ezh2_gain: NA; sizemm: 21; sizestatus: 2; ageyear: 47; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 4367; overall survival event: 0; hu subtype: Basal; spfpercent: 14; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.51; ezh2_gain: NoGain; sizemm: 19; sizestatus: 1; ageyear: 44; agestatus: 1; ', 'tissue: breast tumor; family status: brca1; er: er_neg; pgr: pgr_neg; overall survival time: 2725; overall survival event: 1; hu subtype: Basal; spfpercent: 26; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.64; ezh2_gain: Gain; sizemm: 25; sizestatus: 2; ageyear: 38; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_neg; pgr: pgr_neg; overall survival time: 4223; overall survival event: 0; hu subtype: Basal; spfpercent: 16; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.56; ezh2_gain: NoGain; sizemm: 26; sizestatus: 2; ageyear: 36; agestatus: 1; ', 'tissue: breast tumor; family status: brca1; er: er_neg; pgr: pgr_neg; overall survival time: 1051; overall survival event: 1; hu subtype: Basal; spfpercent: NA; nodestatus: node_pos; grade: 3; hc_cluster: 3; fga: 0.74; ezh2_gain: NoGain; sizemm: 25; sizestatus: 2; ageyear: 61; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_neg; pgr: pgr_neg; overall survival time: 3957; overall survival event: 0; hu subtype: Basal; spfpercent: 18; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.63; ezh2_gain: NoGain; sizemm: 25; sizestatus: 2; ageyear: 65; agestatus: 2; ', 'tissue: breast tumor; family status: brca1; er: er_neg; pgr: pgr_neg; overall survival time: 713; overall survival event: 1; hu subtype: Basal; spfpercent: 12; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.61; ezh2_gain: Gain; sizemm: 18; sizestatus: 1; ageyear: 62; agestatus: 2; ', 'tissue: breast tumor; family status: brca1; er: er_neg; pgr: pgr_neg; overall survival time: 3584; overall survival event: 0; hu subtype: Basal; spfpercent: 18; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.36; ezh2_gain: Gain; sizemm: 23; sizestatus: 2; ageyear: 47; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 3345; overall survival event: 0; hu subtype: Basal; spfpercent: 18; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.39; ezh2_gain: NoGain; sizemm: 26; sizestatus: 2; ageyear: 49; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_neg; pgr: pgr_neg; overall survival time: 954; overall survival event: 1; hu subtype: Basal; spfpercent: 23; nodestatus: node_pos; grade: 3; hc_cluster: 3; fga: 0.44; ezh2_gain: Gain; sizemm: 27; sizestatus: 2; ageyear: 41; agestatus: 1; ', 'tissue: breast tumor; family status: brca1; er: er_neg; pgr: pgr_neg; overall survival time: 2828; overall survival event: 0; hu subtype: Basal; spfpercent: 13; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.68; ezh2_gain: Gain; sizemm: 40; sizestatus: 2; ageyear: 73; agestatus: 2; ', 'tissue: breast tumor; family status: brca2; er: er_neg; pgr: pgr_neg; overall survival time: 2821; overall survival event: 0; hu subtype: Basal; spfpercent: NA; nodestatus: node_pos; grade: 3; hc_cluster: 3; fga: 0.56; ezh2_gain: NoGain; sizemm: 14; sizestatus: 1; ageyear: 60; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: NA; pgr: NA; overall survival time: 2079; overall survival event: 0; hu subtype: Basal; spfpercent: 25; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.66; ezh2_gain: Gain; sizemm: 30; sizestatus: 2; ageyear: 35; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: NA; pgr: NA; overall survival time: NA; overall survival event: NA; hu subtype: Basal; spfpercent: NA; nodestatus: node_pos; grade: 3; hc_cluster: 3; fga: NA; ezh2_gain: NA; sizemm: 32; sizestatus: 2; ageyear: 66; agestatus: 2; ', 'tissue: breast tumor; family status: brca1; er: NA; pgr: NA; overall survival time: NA; overall survival event: NA; hu subtype: Basal; spfpercent: 24; nodestatus: NA; grade: 3; hc_cluster: 3; fga: NA; ezh2_gain: NA; sizemm: NA; sizestatus: NA; ageyear: 36; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_neg; pgr: pgr_neg; overall survival time: 210; overall survival event: 1; hu subtype: Basal; spfpercent: NA; nodestatus: node_pos; grade: 3; hc_cluster: 3; fga: 0.5; ezh2_gain: NoGain; sizemm: 20; sizestatus: 1; ageyear: 86; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 995; overall survival event: 1; hu subtype: Basal; spfpercent: 20; nodestatus: node_pos; grade: 3; hc_cluster: 3; fga: 0.61; ezh2_gain: NoGain; sizemm: 18; sizestatus: 1; ageyear: 48; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 805; overall survival event: 1; hu subtype: Basal; spfpercent: 11; nodestatus: node_pos; grade: 3; hc_cluster: 3; fga: 0.46; ezh2_gain: Gain; sizemm: 38; sizestatus: 2; ageyear: 46; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 290; overall survival event: 1; hu subtype: Basal; spfpercent: 23; nodestatus: node_neg; grade: NA; hc_cluster: 1; fga: 0.5; ezh2_gain: NoGain; sizemm: 18; sizestatus: 1; ageyear: 56; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 6678; overall survival event: 0; hu subtype: Basal; spfpercent: 13; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.58; ezh2_gain: Gain; sizemm: 27; sizestatus: 2; ageyear: 37; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 732; overall survival event: 1; hu subtype: Basal; spfpercent: 17; nodestatus: node_pos; grade: 3; hc_cluster: 3; fga: 0.45; ezh2_gain: NoGain; sizemm: 30; sizestatus: 2; ageyear: 41; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 6505; overall survival event: 0; hu subtype: Basal; spfpercent: NA; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.38; ezh2_gain: NoGain; sizemm: 21; sizestatus: 2; ageyear: 53; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 917; overall survival event: 1; hu subtype: Basal; spfpercent: 19; nodestatus: node_pos; grade: 3; hc_cluster: 3; fga: 0.59; ezh2_gain: NoGain; sizemm: 25; sizestatus: 2; ageyear: 41; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 1171; overall survival event: 1; hu subtype: Basal; spfpercent: 18; nodestatus: node_pos; grade: 3; hc_cluster: 2; fga: 0.15; ezh2_gain: NoGain; sizemm: 23; sizestatus: 2; ageyear: 33; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 6175; overall survival event: 0; hu subtype: Basal; spfpercent: 16; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.51; ezh2_gain: NoGain; sizemm: 30; sizestatus: 2; ageyear: 44; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 6131; overall survival event: 0; hu subtype: Basal; spfpercent: NA; nodestatus: node_pos; grade: 3; hc_cluster: 2; fga: 0.66; ezh2_gain: NoGain; sizemm: 20; sizestatus: 1; ageyear: 48; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 5629; overall survival event: 0; hu subtype: Basal; spfpercent: 21; nodestatus: node_neg; grade: NA; hc_cluster: 3; fga: 0.52; ezh2_gain: NoGain; sizemm: 20; sizestatus: 1; ageyear: 42; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 5525; overall survival event: 0; hu subtype: Basal; spfpercent: 13; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.52; ezh2_gain: NoGain; sizemm: 17; sizestatus: 1; ageyear: 44; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 1716; overall survival event: 1; hu subtype: Basal; spfpercent: 22; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.27; ezh2_gain: NoGain; sizemm: 17; sizestatus: 1; ageyear: 49; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 1190; overall survival event: 1; hu subtype: Basal; spfpercent: 5; nodestatus: node_neg; grade: 2; hc_cluster: 3; fga: 0.83; ezh2_gain: NoGain; sizemm: 17; sizestatus: 1; ageyear: 42; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 722; overall survival event: 1; hu subtype: Basal; spfpercent: 15; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.21; ezh2_gain: NoGain; sizemm: 23; sizestatus: 2; ageyear: 44; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 5287; overall survival event: 0; hu subtype: Basal; spfpercent: 18; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.48; ezh2_gain: Gain; sizemm: 20; sizestatus: 1; ageyear: 46; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5287; overall survival event: 0; hu subtype: Basal; spfpercent: 8; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.55; ezh2_gain: NoGain; sizemm: 26; sizestatus: 2; ageyear: 46; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_neg; pgr: pgr_neg; overall survival time: 1115; overall survival event: 1; hu subtype: Basal; spfpercent: 4; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.3; ezh2_gain: Gain; sizemm: 40; sizestatus: 2; ageyear: 78; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5231; overall survival event: 0; hu subtype: LumB; spfpercent: 5; nodestatus: node_neg; grade: 1; hc_cluster: 1; fga: 0.23; ezh2_gain: NoGain; sizemm: 18; sizestatus: 1; ageyear: 49; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5186; overall survival event: 0; hu subtype: LumA; spfpercent: 6; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.24; ezh2_gain: NoGain; sizemm: 19; sizestatus: 1; ageyear: 43; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_neg; overall survival time: 4255; overall survival event: 1; hu subtype: LumA; spfpercent: 1; nodestatus: node_neg; grade: NA; hc_cluster: 1; fga: 0.13; ezh2_gain: NoGain; sizemm: 12; sizestatus: 1; ageyear: 63; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5131; overall survival event: 0; hu subtype: LumA; spfpercent: 1; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: 0.07; ezh2_gain: NoGain; sizemm: 8; sizestatus: 1; ageyear: 48; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 2374; overall survival event: 1; hu subtype: LumA; spfpercent: 4; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.38; ezh2_gain: NoGain; sizemm: 17; sizestatus: 1; ageyear: 48; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5042; overall survival event: 0; hu subtype: LumB; spfpercent: 7; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.3; ezh2_gain: NoGain; sizemm: 15; sizestatus: 1; ageyear: 60; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5042; overall survival event: 0; hu subtype: LumA; spfpercent: 2; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.06; ezh2_gain: NoGain; sizemm: 8; sizestatus: 1; ageyear: 64; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5043; overall survival event: 0; hu subtype: LumA; spfpercent: 4; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.13; ezh2_gain: NoGain; sizemm: 26; sizestatus: 2; ageyear: 52; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 4978; overall survival event: 0; hu subtype: LumA; spfpercent: 2; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.05; ezh2_gain: NoGain; sizemm: 11; sizestatus: 1; ageyear: 67; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 4930; overall survival event: 0; hu subtype: LumA; spfpercent: 8; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.26; ezh2_gain: Gain; sizemm: 19; sizestatus: 1; ageyear: 50; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 4860; overall survival event: 0; hu subtype: LumA; spfpercent: NA; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.22; ezh2_gain: NoGain; sizemm: 20; sizestatus: 1; ageyear: 43; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 4699; overall survival event: 0; hu subtype: LumA; spfpercent: 7; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: 0.17; ezh2_gain: NoGain; sizemm: 25; sizestatus: 2; ageyear: 45; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 3876; overall survival event: 1; hu subtype: LumA; spfpercent: 5; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.34; ezh2_gain: Gain; sizemm: 23; sizestatus: 2; ageyear: 46; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 4656; overall survival event: 0; hu subtype: LumA; spfpercent: 5; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.2; ezh2_gain: NoGain; sizemm: 12; sizestatus: 1; ageyear: 50; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 4284; overall survival event: 0; hu subtype: LumA; spfpercent: 7; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.15; ezh2_gain: NoGain; sizemm: 22; sizestatus: 2; ageyear: 40; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 3192; overall survival event: 0; hu subtype: LumA; spfpercent: 4; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.22; ezh2_gain: NoGain; sizemm: 25; sizestatus: 2; ageyear: 74; agestatus: 2; ', 'tissue: breast tumor; family status: brca2; er: er_pos; pgr: pgr_pos; overall survival time: 2194; overall survival event: 1; hu subtype: LumA; spfpercent: 8; nodestatus: node_pos; grade: 2; hc_cluster: 2; fga: 0.41; ezh2_gain: NoGain; sizemm: 21; sizestatus: 2; ageyear: 57; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 3059; overall survival event: 0; hu subtype: LumA; spfpercent: NA; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.09; ezh2_gain: NoGain; sizemm: 15; sizestatus: 1; ageyear: 67; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 2842; overall survival event: 0; hu subtype: LumA; spfpercent: 4; nodestatus: node_pos; grade: 2; hc_cluster: 2; fga: 0.06; ezh2_gain: Gain; sizemm: 10; sizestatus: 1; ageyear: 57; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 2507; overall survival event: 0; hu subtype: LumA; spfpercent: 3; nodestatus: node_pos; grade: 3; hc_cluster: 2; fga: 0.22; ezh2_gain: NoGain; sizemm: 17; sizestatus: 1; ageyear: 34; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: NA; overall survival event: 0; hu subtype: LumA; spfpercent: 5; nodestatus: NA; grade: 2; hc_cluster: 1; fga: 0.19; ezh2_gain: Gain; sizemm: NA; sizestatus: NA; ageyear: 55; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 2320; overall survival event: 0; hu subtype: LumA; spfpercent: 4; nodestatus: node_pos; grade: 2; hc_cluster: 1; fga: 0.2; ezh2_gain: NoGain; sizemm: 20; sizestatus: 1; ageyear: 42; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: NA; pgr: NA; overall survival time: 1689; overall survival event: 0; hu subtype: Normal; spfpercent: 4; nodestatus: node_pos; grade: 1; hc_cluster: 3; fga: 0.3; ezh2_gain: NoGain; sizemm: 11; sizestatus: 1; ageyear: 59; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 6950; overall survival event: 0; hu subtype: LumA; spfpercent: 3; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.3; ezh2_gain: Gain; sizemm: 20; sizestatus: 1; ageyear: 49; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 2693; overall survival event: 1; hu subtype: LumA; spfpercent: 5; nodestatus: node_pos; grade: 2; hc_cluster: 1; fga: 0.19; ezh2_gain: Gain; sizemm: 30; sizestatus: 2; ageyear: 39; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 6510; overall survival event: 0; hu subtype: LumA; spfpercent: 5; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: 0.17; ezh2_gain: NoGain; sizemm: 16; sizestatus: 1; ageyear: 45; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 802; overall survival event: 1; hu subtype: LumA; spfpercent: 4; nodestatus: node_pos; grade: 2; hc_cluster: 2; fga: 0.17; ezh2_gain: NoGain; sizemm: 22; sizestatus: 2; ageyear: 46; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 6133; overall survival event: 0; hu subtype: LumB; spfpercent: NA; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.47; ezh2_gain: NoGain; sizemm: 45; sizestatus: 2; ageyear: 45; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 6111; overall survival event: 0; hu subtype: LumA; spfpercent: NA; nodestatus: node_pos; grade: 2; hc_cluster: 2; fga: 0.11; ezh2_gain: NoGain; sizemm: 22; sizestatus: 2; ageyear: 43; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 6069; overall survival event: 0; hu subtype: LumA; spfpercent: NA; nodestatus: node_neg; grade: NA; hc_cluster: 1; fga: 0.31; ezh2_gain: NoGain; sizemm: 30; sizestatus: 2; ageyear: 44; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_neg; overall survival time: 5979; overall survival event: 0; hu subtype: Normal; spfpercent: NA; nodestatus: node_pos; grade: 2; hc_cluster: 2; fga: 0.05; ezh2_gain: NoGain; sizemm: 26; sizestatus: 2; ageyear: 49; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5816; overall survival event: 0; hu subtype: LumA; spfpercent: NA; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.25; ezh2_gain: Gain; sizemm: 24; sizestatus: 2; ageyear: 47; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 2082; overall survival event: 1; hu subtype: LumA; spfpercent: NA; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.17; ezh2_gain: NoGain; sizemm: 35; sizestatus: 2; ageyear: 44; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5641; overall survival event: 0; hu subtype: LumA; spfpercent: 4; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.41; ezh2_gain: NoGain; sizemm: 10; sizestatus: 1; ageyear: 67; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5609; overall survival event: 0; hu subtype: LumA; spfpercent: 3; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.05; ezh2_gain: NoGain; sizemm: 10; sizestatus: 1; ageyear: 67; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5608; overall survival event: 0; hu subtype: LumA; spfpercent: 2; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.07; ezh2_gain: NoGain; sizemm: 15; sizestatus: 1; ageyear: 66; agestatus: 2; ', 'tissue: breast tumor; family status: brca1; er: er_pos; pgr: pgr_pos; overall survival time: 5520; overall survival event: 1; hu subtype: LumA; spfpercent: 6; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.63; ezh2_gain: NoGain; sizemm: 14; sizestatus: 1; ageyear: 56; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 5518; overall survival event: 0; hu subtype: LumA; spfpercent: 6; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: 0.16; ezh2_gain: NoGain; sizemm: 22; sizestatus: 2; ageyear: 43; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: NA; overall survival event: NA; hu subtype: LumA; spfpercent: 4; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: NA; ezh2_gain: NA; sizemm: 18; sizestatus: 1; ageyear: 47; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5480; overall survival event: 0; hu subtype: LumA; spfpercent: NA; nodestatus: node_neg; grade: NA; hc_cluster: 1; fga: 0.11; ezh2_gain: NoGain; sizemm: 17; sizestatus: 1; ageyear: 68; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5438; overall survival event: 0; hu subtype: LumB; spfpercent: 2; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.41; ezh2_gain: Gain; sizemm: 15; sizestatus: 1; ageyear: 44; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5392; overall survival event: 0; hu subtype: LumA; spfpercent: 5; nodestatus: node_neg; grade: NA; hc_cluster: 1; fga: 0.22; ezh2_gain: NoGain; sizemm: 15; sizestatus: 1; ageyear: 66; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 2387; overall survival event: 1; hu subtype: LumA; spfpercent: 5; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: 0.26; ezh2_gain: Gain; sizemm: 15; sizestatus: 1; ageyear: 48; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_pos; overall survival time: 5374; overall survival event: 0; hu subtype: LumA; spfpercent: 3; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: 0.08; ezh2_gain: NoGain; sizemm: 10; sizestatus: 1; ageyear: 51; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 5364; overall survival event: 0; hu subtype: LumA; spfpercent: 3; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.25; ezh2_gain: NoGain; sizemm: 17; sizestatus: 1; ageyear: 56; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5362; overall survival event: 0; hu subtype: LumA; spfpercent: 3; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.2; ezh2_gain: NoGain; sizemm: 30; sizestatus: 2; ageyear: 53; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_neg; overall survival time: 5350; overall survival event: 0; hu subtype: LumA; spfpercent: 8; nodestatus: node_neg; grade: 1; hc_cluster: 1; fga: 0.3; ezh2_gain: NoGain; sizemm: 20; sizestatus: 1; ageyear: 48; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 3813; overall survival event: 1; hu subtype: LumA; spfpercent: 9; nodestatus: node_neg; grade: NA; hc_cluster: 1; fga: 0.36; ezh2_gain: NoGain; sizemm: 13; sizestatus: 1; ageyear: 50; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5287; overall survival event: 0; hu subtype: LumA; spfpercent: 2; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.09; ezh2_gain: NoGain; sizemm: 10; sizestatus: 1; ageyear: 65; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: NA; overall survival event: NA; hu subtype: LumA; spfpercent: 2; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: NA; ezh2_gain: NA; sizemm: 10; sizestatus: 1; ageyear: 50; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 4969; overall survival event: 1; hu subtype: LumA; spfpercent: 4; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.24; ezh2_gain: NoGain; sizemm: 18; sizestatus: 1; ageyear: 47; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 1899; overall survival event: 1; hu subtype: LumB; spfpercent: 2; nodestatus: node_neg; grade: 1; hc_cluster: 1; fga: 0.4; ezh2_gain: NoGain; sizemm: 16; sizestatus: 1; ageyear: 43; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: NA; overall survival event: NA; hu subtype: LumB; spfpercent: 2; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: NA; ezh2_gain: NA; sizemm: 40; sizestatus: 2; ageyear: 47; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 1731; overall survival event: 1; hu subtype: LumB; spfpercent: 13; nodestatus: NA; grade: 2; hc_cluster: 1; fga: 0.31; ezh2_gain: Gain; sizemm: NA; sizestatus: NA; ageyear: 38; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 1325; overall survival event: 1; hu subtype: LumB; spfpercent: 20; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.55; ezh2_gain: NoGain; sizemm: 17; sizestatus: 1; ageyear: 49; agestatus: 1; ', 'tissue: breast tumor; family status: brca2; er: er_pos; pgr: pgr_neg; overall survival time: 2126; overall survival event: 1; hu subtype: LumB; spfpercent: 9; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.64; ezh2_gain: NoGain; sizemm: 34; sizestatus: 2; ageyear: 58; agestatus: 2; ', 'tissue: breast tumor; family status: brca2; er: er_pos; pgr: pgr_pos; overall survival time: 1943; overall survival event: 1; hu subtype: LumB; spfpercent: 14; nodestatus: NA; grade: 3; hc_cluster: 1; fga: 0.6; ezh2_gain: Gain; sizemm: NA; sizestatus: NA; ageyear: 76; agestatus: 2; ', 'tissue: breast tumor; family status: brca2; er: er_neg; pgr: pgr_pos; overall survival time: 4403; overall survival event: 0; hu subtype: LumB; spfpercent: 15; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.52; ezh2_gain: NoGain; sizemm: 30; sizestatus: 2; ageyear: 27; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 985; overall survival event: 1; hu subtype: LumB; spfpercent: 14; nodestatus: NA; grade: 2; hc_cluster: 1; fga: 0.2; ezh2_gain: NoGain; sizemm: NA; sizestatus: NA; ageyear: 46; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_neg; overall survival time: 933; overall survival event: 1; hu subtype: LumB; spfpercent: NA; nodestatus: node_pos; grade: 2; hc_cluster: 1; fga: 0.23; ezh2_gain: NoGain; sizemm: 20; sizestatus: 1; ageyear: 58; agestatus: 2; ', 'tissue: breast tumor; family status: brca1; er: er_pos; pgr: pgr_neg; overall survival time: 2951; overall survival event: 1; hu subtype: LumB; spfpercent: NA; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.62; ezh2_gain: Gain; sizemm: 18; sizestatus: 1; ageyear: 52; agestatus: 2; ', 'tissue: breast tumor; family status: brca2; er: er_pos; pgr: pgr_pos; overall survival time: 1041; overall survival event: 1; hu subtype: LumB; spfpercent: 6; nodestatus: NA; grade: 3; hc_cluster: 1; fga: 0.61; ezh2_gain: NoGain; sizemm: NA; sizestatus: NA; ageyear: 85; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 3138; overall survival event: 0; hu subtype: LumB; spfpercent: 13; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.38; ezh2_gain: NoGain; sizemm: 17; sizestatus: 1; ageyear: 48; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 3135; overall survival event: 0; hu subtype: LumB; spfpercent: 5; nodestatus: NA; grade: 1; hc_cluster: 1; fga: 0.28; ezh2_gain: Gain; sizemm: NA; sizestatus: NA; ageyear: 40; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 2976; overall survival event: 0; hu subtype: LumB; spfpercent: NA; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.78; ezh2_gain: NoGain; sizemm: 28; sizestatus: 2; ageyear: 68; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 664; overall survival event: 1; hu subtype: LumB; spfpercent: 6; nodestatus: node_pos; grade: 3; hc_cluster: 2; fga: 0.3; ezh2_gain: NoGain; sizemm: 55; sizestatus: 2; ageyear: 48; agestatus: 1; ', 'tissue: breast tumor; family status: brca2; er: er_pos; pgr: pgr_pos; overall survival time: 2040; overall survival event: 1; hu subtype: LumB; spfpercent: 6; nodestatus: node_neg; grade: 3; hc_cluster: 2; fga: 0.4; ezh2_gain: NoGain; sizemm: 20; sizestatus: 1; ageyear: 34; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 2402; overall survival event: 0; hu subtype: LumB; spfpercent: NA; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.12; ezh2_gain: NoGain; sizemm: 14; sizestatus: 1; ageyear: 77; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 2233; overall survival event: 0; hu subtype: LumB; spfpercent: 6; nodestatus: node_pos; grade: 2; hc_cluster: 1; fga: 0.33; ezh2_gain: NoGain; sizemm: 24; sizestatus: 2; ageyear: 49; agestatus: 1; ', 'tissue: breast tumor; family status: brca2; er: NA; pgr: NA; overall survival time: 1656; overall survival event: 0; hu subtype: LumB; spfpercent: 8; nodestatus: NA; grade: 2; hc_cluster: 1; fga: 0.26; ezh2_gain: Gain; sizemm: NA; sizestatus: NA; ageyear: 48; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: NA; overall survival event: NA; hu subtype: LumB; spfpercent: 7; nodestatus: node_pos; grade: NA; hc_cluster: 2; fga: NA; ezh2_gain: NA; sizemm: 25; sizestatus: 2; ageyear: 26; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 6868; overall survival event: 0; hu subtype: LumB; spfpercent: 9; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.33; ezh2_gain: NoGain; sizemm: 35; sizestatus: 2; ageyear: 50; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 2754; overall survival event: 1; hu subtype: LumB; spfpercent: 4; nodestatus: node_pos; grade: 2; hc_cluster: 1; fga: 0.53; ezh2_gain: NoGain; sizemm: 21; sizestatus: 2; ageyear: 64; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_neg; overall survival time: 1009; overall survival event: 1; hu subtype: LumB; spfpercent: NA; nodestatus: NA; grade: 3; hc_cluster: 1; fga: 0.44; ezh2_gain: NoGain; sizemm: NA; sizestatus: NA; ageyear: 45; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 6316; overall survival event: 0; hu subtype: LumB; spfpercent: NA; nodestatus: node_pos; grade: NA; hc_cluster: 2; fga: 0.39; ezh2_gain: NoGain; sizemm: 30; sizestatus: 2; ageyear: 55; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 3685; overall survival event: 1; hu subtype: LumB; spfpercent: NA; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.39; ezh2_gain: NoGain; sizemm: 23; sizestatus: 2; ageyear: 51; agestatus: 2; ', 'tissue: breast tumor; family status: brca2; er: er_neg; pgr: pgr_neg; overall survival time: 733; overall survival event: 1; hu subtype: LumB; spfpercent: 11; nodestatus: node_pos; grade: 3; hc_cluster: 2; fga: 0.41; ezh2_gain: NoGain; sizemm: 35; sizestatus: 2; ageyear: 28; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: NA; overall survival event: NA; hu subtype: LumB; spfpercent: 10; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: NA; ezh2_gain: NA; sizemm: 9; sizestatus: 1; ageyear: 72; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5550; overall survival event: 0; hu subtype: LumB; spfpercent: 4; nodestatus: node_neg; grade: NA; hc_cluster: 1; fga: 0.13; ezh2_gain: NoGain; sizemm: 10; sizestatus: 1; ageyear: 42; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_neg; overall survival time: 5544; overall survival event: 0; hu subtype: LumB; spfpercent: 6; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.32; ezh2_gain: NoGain; sizemm: 15; sizestatus: 1; ageyear: 36; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5280; overall survival event: 0; hu subtype: LumB; spfpercent: 2; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.6; ezh2_gain: NoGain; sizemm: 35; sizestatus: 2; ageyear: 34; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 2059; overall survival event: 1; hu subtype: Her2; spfpercent: 3; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.32; ezh2_gain: NoGain; sizemm: 13; sizestatus: 1; ageyear: 36; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 4927; overall survival event: 0; hu subtype: Her2; spfpercent: 6; nodestatus: node_neg; grade: NA; hc_cluster: 1; fga: 0.12; ezh2_gain: NoGain; sizemm: 18; sizestatus: 1; ageyear: 63; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_pos; overall survival time: 4888; overall survival event: 0; hu subtype: LumB; spfpercent: 18; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.54; ezh2_gain: Gain; sizemm: 36; sizestatus: 2; ageyear: 46; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_neg; pgr: pgr_neg; overall survival time: 808; overall survival event: 1; hu subtype: Her2; spfpercent: 10; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.51; ezh2_gain: NoGain; sizemm: 50; sizestatus: 2; ageyear: 74; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 1842; overall survival event: 1; hu subtype: Her2; spfpercent: 11; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.09; ezh2_gain: NoGain; sizemm: 5; sizestatus: 1; ageyear: 42; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_neg; pgr: pgr_neg; overall survival time: 4816; overall survival event: 0; hu subtype: Her2; spfpercent: 9; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.36; ezh2_gain: NoGain; sizemm: 19; sizestatus: 1; ageyear: 61; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 4793; overall survival event: 0; hu subtype: Her2; spfpercent: 15; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.52; ezh2_gain: NoGain; sizemm: 15; sizestatus: 1; ageyear: 47; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 4725; overall survival event: 0; hu subtype: Her2; spfpercent: 15; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.46; ezh2_gain: NoGain; sizemm: 15; sizestatus: 1; ageyear: 46; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 4609; overall survival event: 0; hu subtype: Her2; spfpercent: 6; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.17; ezh2_gain: NoGain; sizemm: 31; sizestatus: 2; ageyear: 42; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_neg; pgr: pgr_neg; overall survival time: 1359; overall survival event: 1; hu subtype: Her2; spfpercent: 14; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.29; ezh2_gain: Gain; sizemm: 15; sizestatus: 1; ageyear: 61; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_pos; overall survival time: 4660; overall survival event: 1; hu subtype: LumA; spfpercent: 8; nodestatus: node_pos; grade: NA; hc_cluster: 1; fga: 0.38; ezh2_gain: NoGain; sizemm: 35; sizestatus: 2; ageyear: 48; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 6722; overall survival event: 0; hu subtype: Normal; spfpercent: 10; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.2; ezh2_gain: NoGain; sizemm: 30; sizestatus: 2; ageyear: 49; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 6237; overall survival event: 0; hu subtype: Her2; spfpercent: 19; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.34; ezh2_gain: NoGain; sizemm: 35; sizestatus: 2; ageyear: 31; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 5830; overall survival event: 0; hu subtype: Her2; spfpercent: 23; nodestatus: NA; grade: NA; hc_cluster: 2; fga: 0.39; ezh2_gain: NoGain; sizemm: NA; sizestatus: NA; ageyear: 50; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_neg; overall survival time: 1837; overall survival event: 1; hu subtype: Normal; spfpercent: 5; nodestatus: node_pos; grade: 2; hc_cluster: 1; fga: 0.16; ezh2_gain: NoGain; sizemm: 24; sizestatus: 2; ageyear: 35; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5586; overall survival event: 0; hu subtype: Her2; spfpercent: 5; nodestatus: node_neg; grade: NA; hc_cluster: 1; fga: 0.1; ezh2_gain: NoGain; sizemm: 10; sizestatus: 1; ageyear: 45; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5511; overall survival event: 0; hu subtype: Her2; spfpercent: 5; nodestatus: node_neg; grade: 3; hc_cluster: 3; fga: 0.17; ezh2_gain: NoGain; sizemm: 18; sizestatus: 1; ageyear: 40; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5266; overall survival event: 0; hu subtype: Her2; spfpercent: 4; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.26; ezh2_gain: NoGain; sizemm: 1; sizestatus: 1; ageyear: 44; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_neg; overall survival time: 2391; overall survival event: 1; hu subtype: non-classified; spfpercent: 1; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.07; ezh2_gain: NoGain; sizemm: 17; sizestatus: 1; ageyear: 62; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: NA; overall survival event: NA; hu subtype: non-classified; spfpercent: NA; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: NA; ezh2_gain: NA; sizemm: 15; sizestatus: 1; ageyear: 51; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 4916; overall survival event: 0; hu subtype: non-classified; spfpercent: NA; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.4; ezh2_gain: NoGain; sizemm: 19; sizestatus: 1; ageyear: 52; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 4913; overall survival event: 0; hu subtype: non-classified; spfpercent: 4; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: 0.26; ezh2_gain: NoGain; sizemm: 12; sizestatus: 1; ageyear: 38; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 4613; overall survival event: 1; hu subtype: non-classified; spfpercent: 16; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.34; ezh2_gain: NoGain; sizemm: 15; sizestatus: 1; ageyear: 42; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_pos; overall survival time: 4648; overall survival event: 0; hu subtype: non-classified; spfpercent: 6; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: 0.13; ezh2_gain: NoGain; sizemm: 15; sizestatus: 1; ageyear: 49; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_pos; overall survival time: 1684; overall survival event: 1; hu subtype: non-classified; spfpercent: 18; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.27; ezh2_gain: NoGain; sizemm: 13; sizestatus: 1; ageyear: 32; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 4615; overall survival event: 0; hu subtype: non-classified; spfpercent: 5; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: 0.48; ezh2_gain: NoGain; sizemm: 20; sizestatus: 1; ageyear: 51; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_neg; overall survival time: 4585; overall survival event: 0; hu subtype: non-classified; spfpercent: 6; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.31; ezh2_gain: NoGain; sizemm: 13; sizestatus: 1; ageyear: 50; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 2407; overall survival event: 1; hu subtype: non-classified; spfpercent: 10; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.58; ezh2_gain: NoGain; sizemm: 18; sizestatus: 1; ageyear: 48; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_neg; overall survival time: 3745; overall survival event: 0; hu subtype: non-classified; spfpercent: 4; nodestatus: node_neg; grade: 1; hc_cluster: 2; fga: 0.15; ezh2_gain: NoGain; sizemm: 19; sizestatus: 1; ageyear: 43; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 1567; overall survival event: 1; hu subtype: non-classified; spfpercent: NA; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.35; ezh2_gain: NoGain; sizemm: 28; sizestatus: 2; ageyear: 62; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: NA; overall survival event: NA; hu subtype: non-classified; spfpercent: NA; nodestatus: NA; grade: 3; hc_cluster: 1; fga: NA; ezh2_gain: NA; sizemm: NA; sizestatus: NA; ageyear: 71; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_neg; pgr: pgr_pos; overall survival time: 2241; overall survival event: 0; hu subtype: non-classified; spfpercent: 4; nodestatus: node_pos; grade: 2; hc_cluster: 2; fga: 0.13; ezh2_gain: NoGain; sizemm: 25; sizestatus: 2; ageyear: 35; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_neg; pgr: pgr_pos; overall survival time: 1694; overall survival event: 1; hu subtype: non-classified; spfpercent: 13; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.26; ezh2_gain: NoGain; sizemm: 90; sizestatus: 2; ageyear: 35; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5086; overall survival event: 1; hu subtype: non-classified; spfpercent: 14; nodestatus: node_pos; grade: 3; hc_cluster: 2; fga: 0.38; ezh2_gain: NoGain; sizemm: 27; sizestatus: 2; ageyear: 34; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 1097; overall survival event: 1; hu subtype: non-classified; spfpercent: 7; nodestatus: node_pos; grade: 3; hc_cluster: 3; fga: 0.33; ezh2_gain: NoGain; sizemm: 25; sizestatus: 2; ageyear: 46; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 6260; overall survival event: 0; hu subtype: non-classified; spfpercent: 18; nodestatus: node_pos; grade: 3; hc_cluster: 2; fga: 0.29; ezh2_gain: NoGain; sizemm: 29; sizestatus: 2; ageyear: 42; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 3551; overall survival event: 1; hu subtype: non-classified; spfpercent: 3; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.2; ezh2_gain: NoGain; sizemm: 10; sizestatus: 1; ageyear: 54; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5446; overall survival event: 0; hu subtype: non-classified; spfpercent: 4; nodestatus: node_neg; grade: 2; hc_cluster: 1; fga: 0.26; ezh2_gain: Gain; sizemm: 22; sizestatus: 2; ageyear: 52; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5448; overall survival event: 0; hu subtype: non-classified; spfpercent: 19; nodestatus: node_neg; grade: 3; hc_cluster: 2; fga: 0.38; ezh2_gain: NoGain; sizemm: 30; sizestatus: 2; ageyear: 46; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_neg; overall survival time: 5341; overall survival event: 0; hu subtype: non-classified; spfpercent: 11; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.12; ezh2_gain: NoGain; sizemm: 16; sizestatus: 1; ageyear: 50; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 2685; overall survival event: 1; hu subtype: non-classified; spfpercent: 9; nodestatus: node_neg; grade: 3; hc_cluster: 2; fga: 0.12; ezh2_gain: NoGain; sizemm: 30; sizestatus: 2; ageyear: 37; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5275; overall survival event: 0; hu subtype: non-classified; spfpercent: 5; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.34; ezh2_gain: NoGain; sizemm: 10; sizestatus: 1; ageyear: 56; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; ove rall survival time: 5123; overall survival event: 0; hu subtype: Normal; spfpercent: 2; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.15; ezh2_gain: NoGain; sizemm: 20; sizestatus: 1; ageyear: 52; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_pos; overall survival time: 2745; overall survival event: 1; hu subtype: Normal; spfpercent: 6; nodestatus: node_pos; grade: 3; hc_cluster: 1; fga: 0.34; ezh2_gain: NoGain; sizemm: 50; sizestatus: 2; ageyear: 49; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 4656; overall survival event: 0; hu subtype: Normal; spfpercent: 6; nodestatus: node_neg; grade: 2; hc_cluster: 2; fga: 0.14; ezh2_gain: NoGain; sizemm: 20; sizestatus: 1; ageyear: 47; agestatus: 1; ', 'tissue: breast tumor; family status: familial; er: er_neg; pgr: pgr_pos; overall survival time: 985; overall survival event: 1; hu subtype: Normal; spfpercent: 8; nodestatus: NA; grade: 2; hc_cluster: 1; fga: 0.25; ezh2_gain: Gain; sizemm: NA; sizestatus: NA; ageyear: 46; agestatus: 1; ', 'tissue: breast tumor; family status: brca1; er: er_neg; pgr: pgr_neg; overall survival time: 3465; overall survival event: 0; hu subtype: Normal; spfpercent: 13; nodestatus: node_pos; grade: 3; hc_cluster: 3; fga: 0.48; ezh2_gain: NoGain; sizemm: 45; sizestatus: 2; ageyear: 58; agestatus: 2; ', 'tissue: breast tumor; family status: familial; er: er_pos; pgr: pgr_neg; overall survival time: 2242; overall survival event: 0; hu subtype: Normal; spfpercent: NA; nodestatus: node_pos; grade: 2; hc_cluster: 2; fga: 0.06; ezh2_gain: NoGain; sizemm: 25; sizestatus: 2; ageyear: 64; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_neg; overall survival time: 584; overall survival event: 1; hu subtype: Normal; spfpercent: 5; nodestatus: node_neg; grade: 3; hc_cluster: 2; fga: 0.02; ezh2_gain: NoGain; sizemm: 45; sizestatus: 2; ageyear: 46; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 6014; overall survival event: 0; hu subtype: Normal; spfpercent: NA; nodestatus: node_pos; grade: 2; hc_cluster: 1; fga: 0.32; ezh2_gain: Gain; sizemm: 18; sizestatus: 1; ageyear: 34; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: NA; pgr: NA; overall survival time: 5753; overall survival event: 0; hu subtype: Normal; spfpercent: 6; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.06; ezh2_gain: NoGain; sizemm: 10; sizestatus: 1; ageyear: 67; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_neg; pgr: pgr_pos; overall survival time: 2327; overall survival event: 1; hu subtype: Normal; spfpercent: 7; nodestatus: node_neg; grade: 3; hc_cluster: 1; fga: 0.21; ezh2_gain: NoGain; sizemm: 15; sizestatus: 1; ageyear: 43; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_neg; overall survival time: 2549; overall survival event: 1; hu subtype: Normal; spfpercent: 4; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.13; ezh2_gain: NoGain; sizemm: 12; sizestatus: 1; ageyear: 62; agestatus: 2; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5336; overall survival event: 0; hu subtype: Normal; spfpercent: 5; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.08; ezh2_gain: NoGain; sizemm: 20; sizestatus: 1; ageyear: 48; agestatus: 1; ', 'tissue: breast tumor; family status: sporadic; er: er_pos; pgr: pgr_pos; overall survival time: 5284; overall survival event: 0; hu subtype: Normal; spfpercent: 3; nodestatus: node_neg; grade: NA; hc_cluster: 2; fga: 0.19; ezh2_gain: NoGain; sizemm: 15; sizestatus: 1; ageyear: 54; agestatus: 2; ', 'tissue: breast tumor; family status: brca2; er: er_pos; pgr: pgr_pos; overall survival time: NA; overall survival event: NA; hu subtype: non-GEX; spfpercent: 6; nodestatus: NA; grade: NA; hc_cluster: 1; fga: NA; ezh2_gain: NA; sizemm: NA; sizestatus: NA; ageyear: NA; agestatus: NA; ', 'tissue: breast tumor; family status: NA; er: NA; pgr: NA; overall survival time: NA; overall survival event: NA; hu subtype: non-GEX; spfpercent: NA; nodestatus: NA; grade: NA; hc_cluster: 2; fga: NA; ezh2_gain: NA; sizemm: NA; sizestatus: NA; ageyear: NA; agestatus: NA; ', 'tissue: breast tumor; family status: NA; er: NA; pgr: NA; overall survival time: NA; overall survival event: NA; hu subtype: non-GEX; spfpercent: 1; nodestatus: NA; grade: NA; hc_cluster: 3; fga: NA; ezh2_gain: NA; sizemm: NA; sizestatus: NA; ageyear: NA; agestatus: NA; ', 'tissue: breast tumor; family status: NA; er: NA; pgr: NA; overall survival time: NA; overall survival event: NA; hu subtype: non-GEX; spfpercent: NA; nodestatus: NA; grade: NA; hc_cluster: 1; fga: NA; ezh2_gain: NA; sizemm: NA; sizestatus: NA; ageyear: NA; agestatus: NA; ', 'tissue: breast tumor; family status: brca1; er: NA; pgr: NA; overall survival time: NA; overall survival event: NA; hu subtype: non-GEX; spfpercent: 8; nodestatus: NA; grade: NA; hc_cluster: 3; fga: NA; ezh2_gain: NA; sizemm: NA; sizestatus: NA; ageyear: NA; agestatus: NA; ', 'tissue: breast tumor; family status: brca2; er: NA; pgr: NA; overall survival time: NA; overall survival event: NA; hu subtype: non-GEX; spfpercent: 8; nodestatus: NA; grade: NA; hc_cluster: 1; fga: NA; ezh2_gain: NA; sizemm: NA; sizestatus: NA; ageyear: NA; agestatus: NA; ', 'tissue: breast tumor; family status: brca2; er: NA; pgr: NA; overall survival time: NA; overall survival event: NA; hu subtype: non-GEX; spfpercent: 9; nodestatus: NA; grade: NA; hc_cluster: 1; fga: NA; ezh2_gain: NA; sizemm: NA; sizestatus: NA; ageyear: NA; agestatus: NA; ', 'tissue: breast tumor; family status: brca2; er: NA; pgr: NA; overall survival time: NA; overall survival event: NA; hu subtype: non-GEX; spfpercent: 23; nodestatus: NA; grade: NA; hc_cluster: 1; fga: NA; ezh2_gain: NA; sizemm: NA; sizestatus: NA; ageyear: NA; agestatus: NA; ', 'tissue: breast tumor; family status: brca1; er: NA; pgr: NA; overall survival time: NA; overall survival event: NA; hu subtype: non-GEX; spfpercent: NA; nodestatus: NA; grade: NA; hc_cluster: 3; fga: NA; ezh2_gain: NA; sizemm: NA; sizestatus: NA; ageyear: NA; agestatus: NA; ', 'tissue: normal breast tissue; family status: NA; er: NA; pgr: NA; overall survival time: NA; overall survival event: NA; hu subtype: NA; spfpercent: NA; nodestatus: NA; grade: NA; hc_cluster: NA; fga: NA; ezh2_gain: NA; sizemm: NA; sizestatus: NA; ageyear: NA; agestatus: NA; ' GSE15043 Homo sapiens 10 Expression profiling by array GPL570 Gene expression profiles of Herceptin-resistant breast cancer cells 2009-02-27 Herceptin (trastuzumab) is a humanized monoclonal antibody targeted to the Her2 receptor tyrosine kinase. Despite a robust response rate to Herceptin-based therapies in Her2-positive patients, resistance frequently arises within one year of the initial response. To address the mechanism of Herceptin resistance, we selected clonal variants of Her2-positive BT474 human breast cancer cells (BT/HerR) that are highly resistant to the anti-proliferative effects of Herceptin in the presence of 0.2 uM or 1.0 uM Herceptin. Our original report on these cell lines demonstrated sustained PI3K/Akt signaling and sensitivity to PI3K inhibitors in BT/HerR cells in the presence of Herceptin, suggesting dysregulation of that pathway as an essential component of Herceptin-resistant proliferation. To address the mechanism by which BT/HerR cells and their PI3K/Akt signaling pathway became resistant to Herceptin, we analyzed gene expression profiles of two clones (BT/HerR1.0C and BT/HerR 1.0E) that were selected in 1.0 uM Herceptin and two clones (BT/HerR0.2D and BT/HerR 0.2J) that were selected in 0.2 uM Herceptin, in comparison to the Herceptin sensitive BT474 parent cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15043 Darpp-32 and its truncated variant t-Darpp have antagonistic effects on breast cancer cell growth and herceptin resistance. PloS one 2.776 https://doi.org/10.1371/journal.pone.0006220 {PloS one (2.776) doi:10.1371/journal.pone.0006220}; {Clinical cancer research : an official journal of the American Association for Cancer Research (None) doi:10.1158/1078-0432.CCR-09-0585}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA114809 https://www.ebi.ac.uk/ena/browser/view/PRJNA114809 None [Overal design]Total cellular RNAs were extracted from BT474 (control) and four BT/HerR subclones, two that were originally selected in 1.0 uM Herceptin and two that were originally selected in 0.2 uM Herceptin. Two RNA samples independently prepared from each clone were analyzed.; [Treatment]'None'; [Growth]'Cells were maintained in DMEM with 10% FBS and 1% penicillin/streptomycin in 5% CO2.'; [Extraction]'Total RNA was purified using the RNeasy kit purchased from Qiagen (Valencia, CA).'; [Cell type]'Wildtype BT474 cells', 'Herceptin-resistant clone BT/HerR1.0C', 'Herceptin-resistant clone BT/HerR1.0E', 'Herceptin-resistant clone BT/HerR0.2D', 'Herceptin-resistant clone BT/HerR0.2J''cell type: Wildtype BT474 cells; ', 'cell type: Herceptin-resistant clone BT/HerR1.0C; ', 'cell type: Herceptin-resistant clone BT/HerR1.0E; ', 'cell type: Herceptin-resistant clone BT/HerR0.2D; ', 'cell type: Herceptin-resistant clone BT/HerR0.2J; ' GSE32578 Homo sapiens 94 Genome variation profiling by genome tiling array GPL4723; GPL7247 Characterization of amplification patterns and target genes at chromosome 11q13 in CCND1-amplified sporadic and familial breast tumors 2011-10-03 Amplification of chromosomal region 11q13, containing the cell cycle regulatory gene CCND1, is frequently found in breast cancer and other malignancies. It is associated with the favourable oestrogen receptor (ER) positive breast tumour phenotype, but also with poor prognosis and treatment failure. 11q13 spans almost 14 Mb and contains more than 200 genes and is affected by various patterns of copy number gains, suggesting complex mechanisms and selective pressure during tumour progression. In the present study we used 32k tiling BAC array CGH to analyse 94 CCND1-amplified breast tumours from sporadic, hereditary and familial breast cancers to fine map chromosome 11q13. A set containing 281 CCND1-non-amplified breast tumours was used for comparisons. We used gene expression data to further validate the functional effect of gene amplification. We identified six core regions covering 11q13.1-q14.1 that were amplified in different combinations. The major core contained CCND1, whereas two cores were found proximal of CCND1 and three distal. The majority of the CCND1-amplified tumours were ER-positive and classified as luminal B. Furthermore, we found that CCND1 amplification is associated with a more aggressive phenotype within histological grade 2 tumours and luminal A subtype tumours. Amplification was equally prevalent in familial and sporadic tumours, but strikingly rare in BRCA1- and BRCA2- mutated tumours. We conclude that 11q13 includes many potential target genes in addition to CCND1. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32578 Characterisation of amplification patterns and target genes at chromosome 11q13 in CCND1-amplified sporadic and familial breast tumours. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-011-1817-3 {Breast cancer research and treatment (3.471): 10.1007/s10549-011-1817-3} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA147099 https://www.ebi.ac.uk/ena/browser/view/PRJNA147099 None [Overal design]Genomic profiling of 94 CCND1-amplified breast tumors using tiling BAC aCGH. A number of cases were hybridized as replicates or replicate as dye-swaps.; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA from fresh frozen breast tumor tissue was extracted using overnight digestion with proteinase K at 55C, followed by repeated phenol-chloroform purification steps. Genomic DNA from FFPE tissue was extracted according to protocol from http://cancer.ucsf.edu/array/protocols/index.php. DNA concentrations were measured using a Nanodrop.', 'Genomic DNA from fresh frozen breast tumor tissue was extracted using overnight digestion with proteinase K at 55C, followed by repeated phenol-chloroform purification steps. DNA concentrations were measured using a Nanodrop.'; [Cell type]'Source: ''disease state: Breast cancer (HER2+); er: er_pos; osbin: 1; os: 4.534246575; age: 59.0527; ln: 1; size_mm: 20; primary: 1; grade: 2; ', 'reference: Promega male reference DNA; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 0; os: 10.22739726; age: 73.44559; ln: 1; size_mm: 20; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 0; os: 10.68493151; age: 42; ln: 0; size_mm: 31; primary: NA; grade: 3; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 0; os: 11.73972603; age: 39; ln: 0; size_mm: 15; primary: 1; grade: 2; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 4.082191781; age: 45; ln: 0; size_mm: 30; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 1; os: 5.273972603; age: 39; ln: 1; size_mm: 30; primary: 1; grade: 2; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 1; os: 1.153424658; age: 44; ln: 1; size_mm: 34; primary: 1; grade: 3; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 1; os: 1.065753425; age: 64; ln: 0; size_mm: 25; primary: 1; grade: 2; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 0; os: 8.443835616; age: 68; ln: NA; size_mm: 22; primary: 1; grade: 3; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 11.23287671; age: 46; ln: 0; size_mm: 36; primary: 1; grade: 3; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 1.824657534; age: 44; ln: 1; size_mm: 30; primary: NA; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 1; os: 2.328767123; age: 38; ln: 1; size_mm: 17; primary: 1; grade: NA; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 1.161643836; age: 69; ln: 1; size_mm: 120; primary: 1; grade: 2; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 0.271232877; age: 68; ln: 1; size_mm: 80; primary: 1; grade: 2; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 1; os: 6.052054795; age: 71; ln: 1; size_mm: 48; primary: 1; grade: 2; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 0; os: 13.35890411; age: 41; ln: 0; size_mm: 15; primary: 1; grade: 3; ', 'disease state: Breast cancer (HER2+); er: er_pos; osbin: 1; os: 3.052054795; age: 62; ln: 1; size_mm: 28; primary: 1; grade: 3; ', 'disease state: Breast cancer (HER2+); er: er_neg; osbin: 1; os: 1.145205479; age: 46; ln: 0; size_mm: 45; primary: 1; grade: 3; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: sporadic; er: er_pos; osbin: 0; os: 13.07671233; pgr: pgr_pos; grade: 2; genomic subtype: amplifier; ', 'reference: promega male reference; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: sporadic; er: er_pos; osbin: 1; os: 3.630136986; pgr: pgr_pos; grade: 3; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 0; os: 8.597260274; pgr: pgr_pos; grade: 3; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: nonClassified; familial status: sporadic; er: er_pos; osbin: 1; os: 12.63835616; pgr: pgr_pos; grade: 3; genomic subtype: Basal-complex; ', 'tissue: Breast tumor; hu subtype: LumA; familial status: sporadic; er: er_pos; osbin: 1; os: 6.504109589; pgr: pgr_pos; grade: 2; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: sporadic; er: er_pos; osbin: 1; os: 2.734246575; pgr: pgr_neg; grade: NA; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: Basal; familial status: brca1; er: er_neg; osbin: 1; os: 7.465753425; pgr: pgr_neg; grade: 3; genomic subtype: Basal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 1; os: 2.698630137; pgr: pgr_pos; grade: 2; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: Normal; familial status: familial; er: er_neg; osbin: 1; os: 2.698630137; pgr: pgr_pos; grade: 2; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: sporadic; er: er_pos; osbin: 0; os: 18.81643836; pgr: pgr_pos; grade: NA; genomic subtype: amplifier; ', 'tissue: Breast tumor; hu subtype: LumA; familial status: familial; er: er_pos; osbin: 1; os: 3.723287671; pgr: pgr_neg; grade: 3; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 1; os: 1.819178082; pgr: pgr_pos; grade: 3; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: sporadic; er: er_pos; osbin: 1; os: 3.980821918; pgr: pgr_pos; grade: NA; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 0; os: 6.117808219; pgr: pgr_pos; grade: 2; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: sporadic; er: er_pos; osbin: 0; os: 15.1890411; pgr: pgr_neg; grade: 3; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 1; os: 3.591780822; pgr: pgr_pos; grade: 3; genomic subtype: amplifier; ', 'tissue: Breast tumor; hu subtype: Basal; familial status: brca1; er: er_neg; osbin: 1; os: 1.498630137; pgr: pgr_neg; grade: NA; genomic subtype: Basal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 1; os: 4.545205479; pgr: pgr_pos; grade: 2; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: nonClassified; familial status: sporadic; er: er_pos; osbin: 1; os: 3.005479452; pgr: pgr_pos; grade: NA; genomic subtype: mixed; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 1; os: 5.454794521; pgr: pgr_pos; grade: 1; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumA; familial status: sporadic; er: er_pos; osbin: 0; os: 15.04109589; pgr: pgr_pos; grade: NA; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 1; os: 2.764383562; pgr: pgr_neg; grade: 3; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: Basal; familial status: sporadic; er: er_neg; osbin: 0; os: 18.29589041; pgr: pgr_neg; grade: NA; genomic subtype: Basal-complex; ', 'tissue: Breast tumor; hu subtype: nonClassified; familial status: sporadic; er: er_pos; osbin: 0; os: 13.73150685; pgr: pgr_pos; grade: 2; genomic subtype: amplifier; ', 'tissue: Breast tumor; hu subtype: nonClassified; familial status: familial; er: er_neg; osbin: 1; os: 5.197260274; pgr: pgr_neg; grade: 2; genomic subtype: amplifier; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 1; os: 2.556164384; pgr: pgr_neg; grade: 2; genomic subtype: amplifier; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: sporadic; er: er_pos; osbin: 1; os: 5.202739726; pgr: pgr_pos; grade: 1; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumA; familial status: familial; er: er_pos; osbin: 0; os: 5.509589041; pgr: pgr_pos; grade: 1; genomic subtype: amplifier; ', 'tissue: Breast tumor; hu subtype: LumA; familial status: familial; er: er_pos; osbin: 1; os: 14.71506849; pgr: pgr_pos; grade: NA; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumA; familial status: sporadic; er: er_pos; osbin: 1; os: 5.704109589; pgr: pgr_pos; grade: NA; genomic subtype: mixed; ', 'tissue: Breast tumor; hu subtype: Basal; familial status: sporadic; er: er_neg; osbin: 0; os: 10.06849315; pgr: pgr_neg; grade: 3; genomic subtype: Basal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: sporadic; er: er_pos; osbin: 1; os: 7.887671233; pgr: pgr_neg; grade: 3; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: nonClassified; familial status: familial; er: er_neg; osbin: 1; os: 4.64109589; pgr: pgr_pos; grade: 3; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: Basal; familial status: sporadic; er: er_neg; osbin: 0; os: 13.47123288; pgr: pgr_neg; grade: 3; genomic subtype: Basal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 0; os: 5.465753425; pgr: pgr_pos; grade: 2; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumA; familial status: sporadic; er: er_pos; osbin: 0; os: 15.01369863; pgr: pgr_pos; grade: NA; genomic subtype: mixed; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: sporadic; er: er_pos; osbin: 1; os: 4.043835616; pgr: pgr_neg; grade: NA; genomic subtype: amplifier; ', 'tissue: Breast tumor; hu subtype: Basal; familial status: sporadic; er: er_neg; osbin: 1; os: 5.123287671; pgr: pgr_neg; grade: 2; genomic subtype: amplifier; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: sporadic; er: er_pos; osbin: 0; os: 5.235616438; pgr: pgr_pos; grade: 3; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: Basal; familial status: familial; er: er_neg; osbin: 1; os: 10.69863014; pgr: pgr_neg; grade: 3; genomic subtype: amplifier; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: sporadic; er: er_pos; osbin: 0; os: 5.964383562; pgr: pgr_pos; grade: 3; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 1; os: 9; pgr: pgr_neg; grade: 2; genomic subtype: amplifier; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 1; os: 7.150684932; pgr: pgr_neg; grade: 2; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumB; familial status: familial; er: er_pos; osbin: 0; os: 12.52328767; pgr: pgr_neg; grade: NA; genomic subtype: amplifier; ', 'tissue: Breast tumor; hu subtype: LumA; familial status: familial; er: er_pos; osbin: 1; os: 7.876712329; pgr: pgr_pos; grade: 2; genomic subtype: Luminal-complex; ', 'tissue: Breast tumor; hu subtype: LumA; familial status: familial; er: er_pos; osbin: 1; os: 5.016438356; pgr: pgr_neg; grade: 3; genomic subtype: Luminal-simple; ', 'tissue: Breast tumor; hu subtype: LumA; familial status: familial; er: er_neg; osbin: 1; os: 7.57260274; pgr: pgr_neg; grade: 2; genomic subtype: Luminal-simple; ', 'tissue: Breast tumor; hu subtype: LumA; familial status: familial; er: er_pos; osbin: 0; os: 11.89041096; pgr: pgr_pos; grade: 2; genomic subtype: amplifier; ', 'tissue: Breast tumor; hu subtype: Normal; familial status: familial; er: er_pos; osbin: 0; os: 10.84109589; pgr: pgr_neg; grade: NA; genomic subtype: amplifier; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: brca1; er: er neg; pr: pr neg; age: NA; size (mm): NA; lymph node status: NA; histologic grade: 3; s-phase fraction: 11; ', 'sample type: promega male reference; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: sporadic; er: er neg; pr: pr pos; age: 40; size (mm): 16; lymph node status: node neg; histologic grade: 2; s-phase fraction: 15; ', 'tissue: breast tumor; molecular subtype: LumB; genomic subtype: NA; family status: NA; er: er pos; pr: pr neg; age: NA; size (mm): NA; lymph node status: NA; histologic grade: NA; s-phase fraction: 12; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: familial; er: NA; pr: NA; age: NA; size (mm): NA; lymph node status: NA; histologic grade: NA; s-phase fraction: NA; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: sporadic; er: er pos; pr: pr pos; age: 37; size (mm): 12; lymph node status: NA; histologic grade: 3; s-phase fraction: 7.9; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: brca1; er: er neg; pr: pr neg; age: NA; size (mm): NA; lymph node status: NA; histologic grade: NA; s-phase fraction: 20; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: familial; er: NA; pr: NA; age: NA; size (mm): NA; lymph node status: NA; histologic grade: NA; s-phase fraction: 7.3; ', 'tissue: breast tumor; molecular subtype: Basal; genomic subtype: NA; family status: NA; er: er neg; pr: pr neg; age: NA; size (mm): NA; lymph node status: NA; histologic grade: NA; s-phase fraction: 7.9; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: sporadic; er: er pos; pr: pr pos; age: NA; size (mm): NA; lymph node status: node pos; histologic grade: 2; s-phase fraction: 3; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: familial; er: NA; pr: NA; age: NA; size (mm): NA; lymph node status: NA; histologic grade: 3; s-phase fraction: NA; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: sporadic; er: er pos; pr: pr pos; age: NA; size (mm): NA; lymph node status: node neg; histologic grade: 3; s-phase fraction: 2.2; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: familial; er: er pos; pr: pr pos; age: NA; size (mm): NA; lymph node status: NA; histologic grade: 2; s-phase fraction: 4.6; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: sporadic; er: er neg; pr: pr pos; age: 47; size (mm): 16; lymph node status: NA; histologic grade: 3; s-phase fraction: 15; ', 'tissue: breast tumor; molecular subtype: Her2; genomic subtype: NA; family status: NA; er: er neg; pr: pr neg; age: NA; size (mm): NA; lymph node status: NA; histologic grade: NA; s-phase fraction: 16; ', 'tissue: breast tumor; molecular subtype: LumA; genomic subtype: NA; family status: NA; er: er pos; pr: pr pos; age: NA; size (mm): NA; lymph node status: NA; histologic grade: NA; s-phase fraction: 13; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: sporadic; er: er pos; pr: pr pos; age: 44; size (mm): 14; lymph node status: NA; histologic grade: 2; s-phase fraction: 6.2; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: familial; er: er pos; pr: pr pos; age: NA; size (mm): NA; lymph node status: node pos; histologic grade: 2; s-phase fraction: NA; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: familial; er: er pos; pr: pr pos; age: NA; size (mm): NA; lymph node status: NA; histologic grade: 2; s-phase fraction: NA; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: familial; er: er pos; pr: pr neg; age: NA; size (mm): NA; lymph node status: node neg; histologic grade: 2; s-phase fraction: NA; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: familial; er: er pos; pr: pr pos; age: NA; size (mm): NA; lymph node status: node pos; histologic grade: 3; s-phase fraction: NA; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: sporadic; er: er pos; pr: pr pos; age: NA; size (mm): NA; lymph node status: NA; histologic grade: 2; s-phase fraction: NA; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: familial; er: er pos; pr: pr pos; age: NA; size (mm): NA; lymph node status: node neg; histologic grade: 2; s-phase fraction: NA; ', 'tissue: breast tumor; molecular subtype: NA; genomic subtype: NA; family status: familial; er: NA; pr: NA; age: NA; size (mm): NA; lymph node status: NA; histologic grade: 1; s-phase fraction: NA; ', 'tissue: breast tumor; molecular subtype: LumB; genomic subtype: NA; family status: sporadic; er: er pos; pr: pr pos; age: NA; size (mm): NA; lymph node status: node neg; histologic grade: 2; s-phase fraction: 10; ' GSE7263 Homo sapiens 11 Expression profiling by array GPL3372; GPL4989 Effect of heterotypic interaction between breast cancer cell line MDA-MB231 and CCL-171 fibroblast 2007-03-14 These 12 arrays are the basis for Figure 1 of the "An interferon-response induced by tumor-stroma interaction in a subset of human breast cancers" manuscript. Figure 1: Effect of heterotypic interaction between breast cancer cell line MDA-MB231 and CCL-171 fibroblast. Biologically independent replicates of the mono-cultured fibroblast CCL-171, the breast cancer cell line MDA-MB231 and the mixed co-culture of CCL-171 and MDA-MB231 were grown for 48h at low serum conditions and characterized by DNA microarray hybridization. Hierarchical clustering of a total of 4333 elements that display a greater than 3-fold variance in expression in more than 3 different experimental samples. Data from individual elements or genes are represented as single rows, and different experiments are shown as columns. Red and green denote expression levels of the samples. The intensity of the color reflects the magnitude of the deviation from baseline. Unsupervised hierarchical clustering of the experiments grouped the biological replicates together. Gene expression varied considerably between fibroblast and MDA-MB231 as expected for cells of mesenchymal or epithelial origin respectively. The co-culture profile showed mainly intermediate expression levels. However, the vertical black bar marks a cluster of genes induced in all co-cultures compared to both mono-cultures indicating that they are induced by heterotypic interaction Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7263 Characterization of heterotypic interaction effects in vitro to deconvolute global gene expression profiles in cancer. Genome biology 14.028 https://doi.org/10.1186/gb-2007-8-9-r191 {Genome biology (14.028): 10.1186/gb-2007-8-9-r191} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA104075 https://www.ebi.ac.uk/ena/browser/view/PRJNA104075 None [Overal design]Computed; [Treatment]'None'; [Growth]'None', 'Co-culture conditions; Human mammary epithelial cells (HMEC) (Cambrex Bio Science Walkersville, Inc) were expanded in mammary epithelial basal medium supplemented with bovine pituitary extract, human EGF, insulin and antibiotics (Clonetics, Cambrex Bio Science Walkersville, Inc). MCF-7, T47D, MDA-MB231, MDA-MB436, SKBR-3, Hs578T, BT549, CCL-171, HTB-125 (ATTC) and HDF (Cambrex Bio Science Walkersville, Inc) were propagated in DMEM supplemented with 10% FBS (HyClone, Logan UT), glutamine, 100U/ml penicillin and 100 μg/ml streptomycin (GIBCO, Grand Island, N.Y.). For co-culture experiments the cells were cultivated for 48 hours at 50,000 cells/cm2 in endothelial basal media (CAMBREX Bio Science Rockland, Inc Rockland, Maine) with 0.2% FBS, which was a good universal media for all cells involved. Separated co-cultures were kept in Transwell? chambers 0.4μm pore size (Costar, Corning Inc. Corning, NY). Cells negatively tested for mycoplasma infection using MycoAlert Tm (CAMBREX Bio Science Rocland, Inc Rockland, Maine) and VenorGem? (SIGMA, Saint Louis, Missouri) mycoplasma detection kits according to the manufacturer?s instructions.; Protocol Type = Biological Sample; Performer: Martin,,Buess'; [Extraction]'not provided', "RNeasy; Total RNA was isolated using the RNeasy mini kit (QIAGEN), according to the manufacturer's instructions.; Protocol Type = Extract preparation; Performer: Martin,,Buess"; [Cell type]'Source: ''StratageneRef; RNA for the reference was pooled from 11 cell lines - obtained from Stratagene.; Protocol Type = Biological Sample; Performer: Martin,,Buess; ', '' GSE10193 Mus musculus 7 Expression profiling by array GPL1261 Conjugated linoleic acid suppresses FAS and promotes mammary tumorigenesis in PyV-MT mice 2008-01-16 Overexpression of fatty acid synthase (FAS) has been reported in both malignant and premalignant breast lesions, and has been associated with poor outcome. FAS has gained interest as a metabolic target for the treatment of breast cancer based on evidence that blockade with the antifungal antibiotic, cerulenin or synthetic inhibitor C75 inhibits proliferation of breast cancer cells and delays tumor development. Conjugated linoleic acid (CLA), a class of fatty acids found in beef and dairy products, has been shown to inhibit FAS in bovine mammary adipose. Based on previously well-documented anti-tumor activity of CLA, we hypothesized that one mechanism of CLA’s anti-tumorigenic activity may be metabolic blockade of FAS. We fed virgin PyV-MT transgenic mice a diet supplemented with either 1% CLA, as mixed isomers, or control chow for four weeks. Tissue histology was determined by H&E staining. cDNA microarray and real-time quantitative PCR were performed to determine relative expression of lipogenic genes. Western blots were used to examine relative protein expression of FAS. Differences in protein densitometry were analyzed using Students 2-sided T-test. Probability was determined using the binomial sign test. Level of significance for all tests was 0.05. H&E staining revealed a shift towards advanced mammary lesions in the CLA-fed mice compared to control animals (24/26 vs. 11/26) (p for trend < 0.001). Microarray analysis revealed a >2-fold decrease in FAS in the CLA-fed group compared to controls, and was confirmed by quantitative RT-PCR (p < 0.001) and Western blot. The decrease in FAS mRNA expression was unexpectedly associated with more advanced disease (p for trend < 0.01). Conclusions: Dietary CLA suppressed fatty acid synthase in the mammary glands of the PyV-MT mouse while promoting mammary tumor progression. Keywords: dietary intervention to compare mammary tumorigenesis between groups https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE10193 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA108305 https://www.ebi.ac.uk/ena/browser/view/PRJNA108305 None [Overal design]PyV-MT and wild type FVB mice were obtained from Jackson Laboratories (Bay Harbor, ME) and housed 2–4 per cage in micro insulator rooms. Mice were genotyped according to Jackson Laboratory protocols (http://jaxmice.jax.org/pub-cgi/protocols/protocols). PyV-MT positive females were randomly selected at four weeks of age to receive either a control AIN93G chow (n=5) or 1% CLA-supplemented chow (n=6). . Food disappearance and animal weights were recorded weekly. Animals were palpated three times a week, and tumor area (length x width) was measured by caliper. Only palpable masses with an area >/= 0.5 cm2 were considered established growths. Animals were euthanized by CO2 inhalation. Eight-week-old animals were selected for tissue histology and analysis of mRNA and protein expression. Mammary gland sections were collected and processed to obtain mRNA or protein lysate, paraffin embedded for histology, or stored in liquid nitrogen until further processing.; [Treatment]'PyV-MT expressing female mice were fed a diet supplemented with 1% conjugated linoleic acid or control chow for 4 weeks. Animals were euthanized at 8 weeks of age and mammary glands were collected for RNA processing.'; [Growth]'None'; [Extraction]'Mammary glands were collected according to standard necropsis procedures. Tissue was stored in RNAlater (Sigma, St. Louis, MO) until processing. RNA was obtained using Qiagen RNeasy (Valencia CA) and stored in -80 degrees Celsius.'; [Cell type]'Source: ''Strain: FVB/PyV-Mt; Age: 8 weeks; Sex: Female; Parity: No; Tissue: Mammary gland; ' GSE124593 Mus musculus 8 Expression profiling by array GPL8321 Expression profile of mouse primary and recurrent breast cancer cell lines 2019-01-03 The molecular basis of tumor recurrence remain poorly understood. Here, we performed RNA microarrays to study the genetic basis of the phenotypic differences between the primary and recurrent breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124593 RIPK3 upregulation confers robust proliferation and collateral cystine-dependence on breast cancer recurrence. Cell death and differentiation 8.086 https://doi.org/10.1038/s41418-020-0499-y {Cell death and differentiation (8.086): 10.1038/s41418-020-0499-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA512619 https://www.ebi.ac.uk/ena/browser/view/PRJNA512619 None [Overal design]Primary and recurrent tumor cells were isolated and expanded from Her2 driven murine model of MTB/TAN tumor before the oncogenic withdrawal (primary tumors) and after the recurrence (recurrent tumors). biological replicate: 54074-1, 54074-2 biological replicate: 99142-1, 99142-2 biological replicate: 42929-1, 42929-2 biological replicate: 48316-1, 48316-2; [Treatment]'Primary and recurrent cells were grown as adherent. Primary cells were supplemented with 10ng/ml mouse EGF, 5ug/ml bovine insulin, 2ug/ml doxycycline 1uM progesterone and 1ug/ml hydrocortisone.Recurrent cells were supplemented with 10ng/ml mouse EGF and 5ug/ml bovine insulin.'; [Growth]'Dox-inducible Her2 driven murine model of MTB/TAN cells were grow in DMEM media with 4.5g/L glucose and 4mM glutamine (11995-DMEM, ThermoFisher Scientific) and supplement with 10% heat-inactivated fetal bovine serum (Hyclone #SH30070.03HI) in humidified incubator, 37°C with 5% CO2'; [Extraction]"Total RNA was extracted using RNeasy Mini Kit (Qiagen, #74104) according to the manufacturer's instructions."; [Cell type]'Source: ''tissue: breast cancer cell; cell line: MTB/TAN; ' GSE112230 Mus musculus; Homo sapiens 29 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL16791; GPL17021; GPL19057 LSD1 ablation stimulates anti-tumor immunity and enables checkpoint blockade 2018-03-22 Chromatin regulators play a broad role in regulating gene expression, and when gone awry, can lead to cancer. Here we demonstrate that ablation of the histone demethylase LSD1 in cancer cells increases repetitive element expression, including ERVs, and decreases expression of RNA-induced silencing complex (RISC) components. Significantly, this leads to dsRNA stress and activation of type 1 interferon, which stimulates anti-tumor T cell immunity and restrains tumor growth. Furthermore, LSD1 depletion enhances tumor immunogenicity and T cell infiltration in poorly immunogenic tumors, and elicits significant responses of checkpoint blockade-refractory mouse melanoma to anti-PD-1 therapy. Consistently, TCGA data analysis shows an inverse correlation between LSD1 expression and CD8+ T cell infiltration in various human cancers. Our study identifies LSD1 as a potent inhibitor of anti-tumor immunity and responsiveness to immunotherapy, and suggests LSD1 inhibition combined with PD-(L)1 blockade as a novel cancer treatment strategy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112230 LSD1 Ablation Stimulates Anti-tumor Immunity and Enables Checkpoint Blockade. Cell 36.216 https://doi.org/10.1016/j.cell.2018.05.052 {Cell (36.216): 10.1016/j.cell.2018.05.052} 'genomic DNA', 'total RNA', 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA445303 https://www.ebi.ac.uk/ena/browser/view/PRJNA445303 https://www.ncbi.nlm.nih.gov/sra?term=SRP136272 [Overal design]Gene expression profiling of in vitro control and LSD1 KD MCF-7 cells (in biological replicates), as well as ex vivo scramble, LSD1 KO and LSD1/MDA5 DKO B16 tumor cells (in biological triplicates) was analyzed by RNA-seq. Genomic occupancy of LSD1, H3K4me1 and H3K4me2 in in vitro control and LSD1 KD MCF-7 cells, as well as ex vivo scramble and LSD1 KO B16 tumor cells was analyzed by ChIP-seq.; [Treatment]'MCF-7 cells were infected with lentiviral shRNA targeting scramble or LSD1, and selected for 6-8 days before sample collections. B16 tumors grew in mice for 14 days before being excised and digested with collagenase for single cell suspension. GFP+ B16 cells were sorted.'; [Growth]'MCF-7 cells were cultured in normal DMEM supplemented with 10% FBS and 1% penicillin/streptomycin in 5% CO2 incubator at 37 °C. GFP-labeled B16 cells were transplanted into WT C56BL/6 mice subcutaneously and tumor grew for 14 days.'; [Extraction]"For MCF-7 cells, cell nuclei were obtained by lysing whole cells in hypotonic buffer (10 mM HEPES pH 7.9, 10 mM KCl, 1.5 mM MgCl2, 0.34 M sucrose, 10% v/v glycerol, 1 mM DTT, and 0.1% v/v Triton X-100) supplemented with protease inhibitor. For GFP-labeled B16 cells isolated from tumor-bearing immunocompetent mice, intact cells were used for the following steps. After washing with PBS, nuclei/cells were fixed in 1% formaldehyde for 10 min at room temperature, followed by quenching in 125 mM glycine. Nuclei/cells were then washed twice with ice-cold PBS, lysed in ChIP sonication buffer (50 mM HEPES pH7.9, 140 mM NaCl, 1 mM EDTA, 1% Triton X-100, 0.1% sodium deoxycholate, 0.2% SDS) supplemented with protease inhibitor, and were subjected to sonication to obtain DNA fragments of 300-800 bp. Subsequent procedures were carried out by following the Epigenesys protocol (https://www.epigenesys.eu/en/). The following antibodies were used to ChIP: anti-LSD1 (Abcam, cat# ab17721), anti-H3K4me1 (Abcam, cat#ab8895), anti-H3K4me2 (EMDMillipore, cat#07-030), and mouse IgG (Santa Cruz Biotechnology, cat# sc-2025). || For RNA extraction, cells weredirectly lyzed in TRIzol and total RNA was extracted according to manufacture's instructions.\nChIP-seq libraries were prepared using NEBNext® Ultra™ DNA Library Prep Kit for Illumina® (New England Biolabs, cat#E7370L) and NEBNext® Multiplex Oligos for Illumina® (New England Biolabs, cat# E7335L) according to the manufacture’s instructions. Library concentrations were quantified by Qubit (Invitrogen) and mixed equally for sequencing at HiSeq 2500 (Illumina) to generate 50 bp reads from single-end. || Purified total RNA from MCF-7 cells or GFP-labeled B16 cells isolated from tumor-bearing immunocompetent mice was quantified by Qubit (Invitrogen) and analyzed by Agilent Bioanalyzer to assess RNA integrity. 1 μg RNA (RIN>9) was used to generate rRNA-depleted RNA with NEBNext® rRNA Depletion Kit (New England Biolabs, cat# E6310S) or poly(A)+ RNA with Magnetic mRNA Isolation Kit (New England Biolabs, cat# S1550S) according to the manufacturer’s instructions. The rRNA-depleted or poly(A)+ RNA was subjected to Agilent Bioanalyzer to ensure the complete removal of rRNA, and then used to generate directional RNA library with NEBNext® Ultra™ II Directional RNA Library Prep Kit for Illumina® (New England Biolabs, cat# E7760L) and NEBNext® Multiplex Oligos for Illumina® (New England Biolabs, cat# E7335L) according to the manufacturer’s instructions. Library concentrations were quantified by Qubit (Invitrogen) and mixed equally for sequencing at HiSeq 2500 or Nextseq 500 (Illumina) to generate 50 bp reads (MCF-7) or 75 bp (B16) from paired-ends."; [Cell type]'Source: ''tissue: MCF-7 breast cancer cell line; molecule: genomic DNA; antibody: n/a; ', 'tissue: MCF-7 breast cancer cell line; molecule: genomic DNA; antibody: LSD1 (Abcam, cat#17721); ', 'tissue: MCF-7 breast cancer cell line; molecule: genomic DNA; antibody: H3K4me1 (Abcam, cat#ab8895); ', 'tissue: MCF-7 breast cancer cell line; molecule: genomic DNA; antibody: H3K4me2 (EMDMIpplipore, cat#07-030); ', 'tissue: MCF-7 breast cancer cell line; molecule: Ribosome depleted RNA; ', 'tissue: B16 tumor transplanted in C56BL/6 mice; molecule: genomic DNA; antibody: n/a; ', 'tissue: B16 tumor transplanted in C56BL/6 mice; molecule: genomic DNA; antibody: LSD1 (Abcam, cat#17721); ', 'tissue: B16 tumor transplanted in C56BL/6 mice; molecule: genomic DNA; antibody: H3K4me1 (Abcam, cat#ab8895); ', 'tissue: B16 tumor transplanted in C56BL/6 mice; molecule: genomic DNA; antibody: H3K4me2 (EMDMIpplipore, cat#07-030); ', 'tissue: B16 tumor transplanted in C56BL/6 mice; molecule: Ribosome depleted RNA; ', 'tissue: B16 tumor transplanted in C56BL/6 mice; molecule: Poly-A enriched RNA; ' GSE134359 Homo sapiens 86 Expression profiling by array GPL17586 Long noncoding RNA landscape in breast cancer [Mexico] 2019-07-16 Breast cancer (BC) is the most commonly diagnosed neoplasm in women worldwide and a well-recognized heterogeneous pathology classified into four molecular subtypes: Luminal A, Luminal B, HER2-enriched and Basal-like, each one with different biological and clinical characteristics. It is well recognize that clinical and molecular heterogeneity of BC is driven in part by mRNA and lncRNAs. We profiled mRNAs and lncRNA in 75 adjuvant tumors using an Affymetrix microarray platform. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE134359 A lncRNA landscape in breast cancer reveals a potential role for AC009283.1 in proliferation and apoptosis in HER2-enriched subtype. Scientific reports 4.011 https://doi.org/10.1038/s41598-020-69905-z {Scientific reports (4.011): 10.1038/s41598-020-69905-z} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA554862 https://www.ebi.ac.uk/ena/browser/view/PRJNA554862 None [Overal design]Breast cancer tumors were collected from the archives of the Fundacion de Cancer de Mama (FUCAM) after a carefully histopathological review by two training pathologist, according to the following criteria: adjuvant therapy and collection of the surgical sample without any treatment. We obtain molecular subtype by PAM50 algorithm; [Treatment]'None'; [Growth]'None'; [Extraction]'We used AllPrep DNA/RNA Mini Kit'; [Cell type]'Source: ''population: Mexico hispanic; pam50 molecular subtype: NA; tissue: Tissue; ', 'population: Mexico hispanic; pam50 molecular subtype: NA; tissue: RNA from adjacent normal tissue; ', 'population: Mexico hispanic; pam50 molecular subtype: Luminal B; tissue: RNA from tumor tissue; ', 'population: Mexico hispanic; pam50 molecular subtype: Her2-enriched; tissue: RNA from tumor tissue; ', 'population: Mexico hispanic; pam50 molecular subtype: Luminal A; tissue: RNA from tumor tissue; ', 'population: Mexico hispanic; pam50 molecular subtype: Basal-like; tissue: RNA from tumor tissue; ' GSE60788 Homo sapiens 55 Expression profiling by high throughput sequencing GPL11154 The Sweden Canceromics Analysis Network - Breast (SCAN-B) Initiative: a large-scale multicenter infrastructure towards implementation of breast cancer genomic analyses in the clinical routine [RNA-Seq] 2014-08-26 Breast cancer exhibits significant molecular, pathological, and clinical heterogeneity. Current clinicopathological evaluation is imperfect for predicting outcome, which results in overtreatment for many patients, and for others, leads to death from recurrent disease. Therefore, additional criteria are needed to better personalize care and maximize treatment effectiveness and survival. To address these challenges, the Sweden Cancerome Analysis Network - Breast (SCAN-B) consortium was initiated in 2010 as a multicenter prospective study with longsighted aims to 1) analyze breast cancers with next-generation genomic technologies for translational research in a population-based manner and integrated with healthcare; 2) decipher fundamental tumor biology from these analyses; 3) utilize genomic data to develop and validate new clinically-actionable biomarker assays; and 4) build the infrastructure for real-time clinical implementation of molecular diagnostic, prognostic, and predictive tests. In the first phase, we focus on molecular profiling by next-generation RNA-sequencing on the Illumina platform. In the three years from August 30, 2010 through August 31, 2013, we have consented and enrolled 3,979 patients with primary breast cancer at the seven hospital sites in South Sweden, representing approximately 85% of eligible patients in the catchment area. Pre-operative blood samples have been collected for 3,942 (99%) patients and primary tumor specimens collected for 2,929 (74%) patients. Herein we describe the study infrastructure and present initial proof of concept results from prospective RNA-sequencing including tumor molecular subtyping and detection of driver gene mutations. We demonstrate that large-scale population-based collection and RNA-sequencing analysis of breast cancer is feasible. The SCAN-B Initiative should significantly reduce the time to discovery, validation, and clinical implementation of novel molecular diagnostic and predictive tests. We welcome the participation of additional comprehensive cancer treatment centers. Due to privacy concerns, submitters were not allowed to release the actual sequencing reads https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60788 The Sweden Cancerome Analysis Network - Breast (SCAN-B) Initiative: a large-scale multicenter infrastructure towards implementation of breast cancer genomic analyses in the clinical routine. Genome medicine 10.886 https://doi.org/10.1186/s13073-015-0131-9 {Genome medicine (10.886): 10.1186/s13073-015-0131-9} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA259546 https://www.ebi.ac.uk/ena/browser/view/PRJNA259546 https://www.ncbi.nlm.nih.gov/sra?term=SRP046928 [Overal design]55 RNA samples (49 tumors, 6 as technical replicates) were sequenced (paired-end Illumina) and in parallel analyzed on Human HT12 v4 BeadChip microarrays following the manufacturer’s standard protocol (Illumina). Intrinsic subtypes were determined for both platforms using the gene lists PAM50, Sorlie and Hu. Mutation calling was performed on the RNA-seq data of the 49 tumors.; [Treatment]'None'; [Growth]'None'; [Extraction]'QIAGEN AllPrep\nPoly(A) mRNA is isolated from the total RNA in up to 96-well microtiter plate format by two rounds of purification with Dynabeads Oligo (dT)25 (Invitrogen) using a KingFisher Flex magnetic particle processor (ThermoScientific). Zinc-mediated fragmentation (Ambion) is performed and the fragmented mRNA retrieved using column purification (Zymo-Spin I-96 plates; Zymo). The sequencing library generation protocol is a modification of the dUTP method, which importantly retains the directionality (stranded-ness) of the sequenced RNA molecules. First strand cDNA synthesis is performed using random hexamers and standard dNTP mix followed by cleanup using Sephadex gel filtration (Illustra AutoScreen-96A plates; GE Healthcare), and second strand cDNA synthesis is performed using dUTP in place of dTTP in the dNTP-mix and cleanup using Zymo-Spin I-96 plates. The cDNA is end-repaired and A-tailed, and diluted TruSeq adapters with barcodes are ligated using a modified protocol (Illumina). Adapter-ligated cDNA is then size-selected to remove short oligonucleotides using carboxylic acid (CA) paramagnetic beads (Invitrogen) and polyethylene glycol (PEG), similar to the previously described methods, and automated on the KingFisher Flex. The second cDNA strand is digested using uracil-DNA glycosylase and the product is enriched by 12 PCR cycles (Illumina). The PCR product undergoes two cycles of size selection using CA-beads and varying concentrations of PEG, first to exclude DNA fragments >700 bp and then to exclude fragments <200 bp. Quality control is performed on control libraries using Qubit fluorometric measurement (Life Technologies) and Caliper LabChip XT microcapillary gel electrophoresis. Typically, 10-24 barcoded libraries are included in a pool and each pool is sequenced in at least one lane across dual flowcells. Paired-end sequencing of 50 bp read-length is performed on an Illumina HiSeq 2000 instrument.'; [Cell type]'Source: ''tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: LumB; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumB; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 1; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: Normal; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: Normal; er status: Positive; pgr status: Negative; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; map3k1 mutations: NM_005921:exon5:c.G1064A:p.C355Y:0.0741; pik3ca mutations: NM_006218:exon10:c.G1633A:p.E545K:0.4286; smad4 mutations: NM_005359:exon2:c.C247T:p.Q83X:0.08; ', 'tissue: primary breast tumor; ht12 subtype pam50: Her2; ht12 subtype sorlie: Her2; ht12 subtype hu: LumA; rna-seq subtype pam50: Her2; rna-seq subtype sorlie: Her2; rna-seq subtype hu: LumA; er status: Positive; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; erbb2 mutations: NM_004448:exon19:c.T2264C:p.L755S:0.5794; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Her2; ht12 subtype hu: Basal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Her2; rna-seq subtype hu: Basal; er status: Negative; pgr status: Negative; erbb2 status: Negative; nottingham grade: NA; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 1; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 4; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumA; ht12 subtype hu: LumB; rna-seq subtype pam50: LumB; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumB; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; setd2 mutations: NM_014159:exon8:c.G4920T:p.W1640C:0.0714; tp53 mutations: NM_001126115:exon5:c.540delC:p.T180fs:0.375,NM_001126115:exon1:c.G142C:p.E48Q:0.0909; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumA; ht12 subtype hu: LumB; rna-seq subtype pam50: LumB; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumB; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; tp53 mutations: NM_001126115:exon4:c.G519T:p.K173N:0.0588; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Basal; ht12 subtype hu: Basal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Her2; rna-seq subtype hu: Basal; er status: Positive; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 3; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 2; chek2 mutations: NM_007194:exon4:c.G451A:p.G151S:0.3333; nf1 mutations: NM_000267:exon50:c.G7438T:p.E2480X:0.0909; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Basal; ht12 subtype hu: Basal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Her2; rna-seq subtype hu: Basal; er status: Positive; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 3; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 2; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 2; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 3; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumA; ht12 subtype hu: LumB; rna-seq subtype pam50: LumB; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumB; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Basal; ht12 subtype hu: Normal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Basal; rna-seq subtype hu: Normal; er status: Negative; pgr status: Negative; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; tp53 mutations: NM_001126115:exon3:c.327delC:p.S109fs:0.2308; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 1; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; tp53 mutations: NM_001126115:exon3:c.G337A:p.G113S:0.642; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Basal; ht12 subtype hu: Basal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Basal; rna-seq subtype hu: Basal; er status: Negative; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; pik3ca mutations: NM_006218:exon10:c.G1633A:p.E545K:0.25,NM_006218:exon14:c.G2176A:p.E726K:0.1724; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Basal; ht12 subtype hu: Basal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Basal; rna-seq subtype hu: Basal; er status: Negative; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; rb1 mutations: NM_000321:exon20:c.T1970C:p.L657P:0.08; tp53 mutations: NM_001126115:exon3:c.290_291del:p.97_97del:0.5; ', 'tissue: primary breast tumor; ht12 subtype pam50: Normal; ht12 subtype sorlie: Normal; ht12 subtype hu: Normal; rna-seq subtype pam50: Normal; rna-seq subtype sorlie: Normal; rna-seq subtype hu: Normal; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 1; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Basal; ht12 subtype hu: Basal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Basal; rna-seq subtype hu: Basal; er status: Negative; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 2; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 2; atm mutations: NM_000051:exon41:c.T6055A:p.Y2019N:0.08; tbl1xr1 mutations: NM_024665:exon5:c.G337A:p.A113T:0.0541; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumA; ht12 subtype hu: LumB; rna-seq subtype pam50: LumB; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumB; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; map3k1 mutations: NM_005921:exon3:c.817_818del:p.273_273del:0.5; pik3ca mutations: NM_006218:exon21:c.A3140G:p.H1047R:0.5; ', 'tissue: primary breast tumor; ht12 subtype pam50: Her2; ht12 subtype sorlie: Normal; ht12 subtype hu: LumB; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: Normal; rna-seq subtype hu: LumB; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 3; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 2; pik3ca mutations: NM_006218:exon21:c.A3140G:p.H1047R:0.8125; tp53 mutations: NM_001126115:exon4:c.G430C:p.A144P:0.8095; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 1; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; arid1a mutations: NM_006015:exon20:c.G5197T:p.E1733X:0.275; pik3ca mutations: NM_006218:exon21:c.A3140G:p.H1047R:0.25; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumB; ht12 subtype hu: LumB; rna-seq subtype pam50: LumB; rna-seq subtype sorlie: LumB; rna-seq subtype hu: Her2; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 3; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; pik3ca mutations: NM_006218:exon10:c.G1633A:p.E545K:0.25; runx1 mutations: NM_001001890:exon1:c.211delC:p.L71fs:0.1782; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumB; ht12 subtype hu: Her2; rna-seq subtype pam50: LumB; rna-seq subtype sorlie: LumB; rna-seq subtype hu: Her2; er status: Positive; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: Normal; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Basal; ht12 subtype hu: Basal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Basal; rna-seq subtype hu: Basal; er status: Negative; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; tp53 mutations: NM_001126115:exon2:c.G250T:p.V84L:0.7111; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumB; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; nf1 mutations: NM_000267:exon47:c.7118delT:p.L2373fs:0.0952; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumA; ht12 subtype hu: LumB; rna-seq subtype pam50: LumB; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumB; er status: Positive; pgr status: Negative; erbb2 status: Amplified; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; tp53 mutations: NM_001126115:exon1:c.A94G:p.K32E:0.875; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumA; ht12 subtype hu: LumB; rna-seq subtype pam50: Her2; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumB; er status: Positive; pgr status: Negative; erbb2 status: Amplified; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumB; ht12 subtype hu: Her2; rna-seq subtype pam50: LumB; rna-seq subtype sorlie: LumB; rna-seq subtype hu: Her2; er status: Positive; pgr status: Positive; erbb2 status: Amplified; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 2; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 3; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumB; ht12 subtype hu: Her2; rna-seq subtype pam50: LumB; rna-seq subtype sorlie: LumB; rna-seq subtype hu: Her2; er status: Positive; pgr status: Positive; erbb2 status: Amplified; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 2; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 3; kmt2c mutations: NM_170606:exon16:c.G2758T:p.V920L:0.2857; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Basal; ht12 subtype hu: Basal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Basal; rna-seq subtype hu: Basal; er status: Negative; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; kmt2c mutations: NM_170606:exon14:c.2447dupA:p.Y816_I817delinsX:0.1875; tp53 mutations: NM_001126118:exon3:c.206delG:p.G69fs:0.48; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: LumB; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumB; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; pik3ca mutations: NM_006218:exon10:c.G1633A:p.E545K:0.25; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: Her2; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; pik3ca mutations: NM_006218:exon21:c.A3140G:p.H1047R:0.3; ', 'tissue: primary breast tumor; ht12 subtype pam50: Her2; ht12 subtype sorlie: Her2; ht12 subtype hu: Her2; rna-seq subtype pam50: Her2; rna-seq subtype sorlie: LumB; rna-seq subtype hu: Her2; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 3; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 2; tp53 mutations: NM_001126115:exon5:c.C553T:p.Q185X:0.1515; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Basal; ht12 subtype hu: Basal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Basal; rna-seq subtype hu: Basal; er status: Negative; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; nf1 mutations: NM_000267:exon36:c.G4999T:p.E1667X:0.0645; tp53 mutations: NM_001126115:exon3:c.G347A:p.R116Q:0.3286; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; pik3ca mutations: NM_006218:exon21:c.C3139T:p.H1047Y:0.2308; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; kmt2c mutations: NM_170606:exon43:c.A10462T:p.I3488L:0.0571; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Basal; ht12 subtype hu: Basal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Basal; rna-seq subtype hu: Basal; er status: Positive; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 2; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 3; pik3ca mutations: NM_006218:exon10:c.G1633A:p.E545K:0.5333; tp53 mutations: NM_001126115:exon4:c.C437T:p.P146L:0.6324; ', 'tissue: primary breast tumor; ht12 subtype pam50: Her2; ht12 subtype sorlie: LumB; ht12 subtype hu: Basal; rna-seq subtype pam50: Her2; rna-seq subtype sorlie: LumB; rna-seq subtype hu: Basal; er status: Positive; pgr status: Positive; erbb2 status: Amplified; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 2; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 3; sf3b1 mutations: NM_012433:exon15:c.A2098G:p.K700E:0.0612; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; pik3ca mutations: NM_006218:exon21:c.A3140G:p.H1047R:0.3514; ', 'tissue: primary breast tumor; ht12 subtype pam50: Her2; ht12 subtype sorlie: LumB; ht12 subtype hu: Her2; rna-seq subtype pam50: Her2; rna-seq subtype sorlie: LumB; rna-seq subtype hu: Her2; er status: Negative; pgr status: Negative; erbb2 status: Amplified; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; tp53 mutations: NM_001126115:exon3:c.C346T:p.R116W:0.5269; ', 'tissue: primary breast tumor; ht12 subtype pam50: Her2; ht12 subtype sorlie: Her2; ht12 subtype hu: Her2; rna-seq subtype pam50: Her2; rna-seq subtype sorlie: Her2; rna-seq subtype hu: Her2; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; pik3ca mutations: NM_006218:exon10:c.G1633A:p.E545K:0.6; ', 'tissue: primary breast tumor; ht12 subtype pam50: Normal; ht12 subtype sorlie: Normal; ht12 subtype hu: Normal; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: Normal; rna-seq subtype hu: Normal; er status: Positive; pgr status: Negative; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; sf3b1 mutations: NM_012433:exon15:c.A2098G:p.K700E:0.1533; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; tp53 mutations: NM_001126115:exon2:c.C190T:p.R64X:0.1538; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumB; ht12 subtype hu: Normal; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumB; rna-seq subtype hu: Normal; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 2; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 3; apc mutations: NM_001127511:exon14:c.C4531T:p.Q1511X:0.1538; tp53 mutations: NM_001126115:exon4:c.G460A:p.E154K:0.6875; ', 'tissue: primary breast tumor; ht12 subtype pam50: Normal; ht12 subtype sorlie: Her2; ht12 subtype hu: Normal; rna-seq subtype pam50: Normal; rna-seq subtype sorlie: Her2; rna-seq subtype hu: Normal; er status: Negative; pgr status: Negative; erbb2 status: Negative; nottingham grade: NA; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 2; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 3; erbb2 mutations: NM_004448:exon20:c.G2329T:p.V777L:0.45; pik3ca mutations: NM_006218:exon21:c.A3140G:p.H1047R:0.3125; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: Her2; ht12 subtype hu: Normal; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: Her2; rna-seq subtype hu: Basal; er status: Positive; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 3; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 2; pik3ca mutations: NM_006218:exon5:c.T1035A:p.N345K:0.2857; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumB; ht12 subtype sorlie: Her2; ht12 subtype hu: Normal; rna-seq subtype pam50: LumB; rna-seq subtype sorlie: Her2; rna-seq subtype hu: Basal; er status: Positive; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 3; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 2; pik3ca mutations: NM_006218:exon21:c.A3140G:p.H1047R:0.3125; tp53 mutations: NM_001126115:exon1:c.T141A:p.H47Q:0.6056; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Basal; ht12 subtype hu: Basal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Basal; rna-seq subtype hu: Basal; er status: Negative; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 3; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 2; cdh1 mutations: NM_004360:exon13:c.G1942T:p.E648X:0.1176; map3k1 mutations: NM_005921:exon14:c.A3028G:p.I1010V:0.05; ', 'tissue: primary breast tumor; ht12 subtype pam50: Basal; ht12 subtype sorlie: Basal; ht12 subtype hu: Basal; rna-seq subtype pam50: Basal; rna-seq subtype sorlie: Basal; rna-seq subtype hu: Basal; er status: Negative; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 2; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 3; pik3ca mutations: NM_006218:exon10:c.G1633A:p.E545K:0.52; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 3; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; kmt2c mutations: NM_170606:exon38:c.C7825T:p.R2609X:0.4; pik3ca mutations: NM_006218:exon10:c.G1624A:p.E542K:0.2143; pten mutations: NM_000314:exon9:c.G1093A:p.V365I:0.0556; tp53 mutations: NM_001126118:exon3:c.211delC:p.R71fs:0.1; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 1; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; ', 'tissue: primary breast tumor; ht12 subtype pam50: Her2; ht12 subtype sorlie: Basal; ht12 subtype hu: Basal; rna-seq subtype pam50: Her2; rna-seq subtype sorlie: Basal; rna-seq subtype hu: Basal; er status: Negative; pgr status: Negative; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 3; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; ', 'tissue: primary breast tumor; ht12 subtype pam50: Normal; ht12 subtype sorlie: Normal; ht12 subtype hu: Normal; rna-seq subtype pam50: Normal; rna-seq subtype sorlie: Normal; rna-seq subtype hu: Normal; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 4; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; ', 'tissue: primary breast tumor; ht12 subtype pam50: LumA; ht12 subtype sorlie: LumA; ht12 subtype hu: LumA; rna-seq subtype pam50: LumA; rna-seq subtype sorlie: LumA; rna-seq subtype hu: LumA; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 2; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 3; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; ', 'tissue: primary breast tumor; ht12 subtype pam50: Her2; ht12 subtype sorlie: Her2; ht12 subtype hu: Basal; rna-seq subtype pam50: Her2; rna-seq subtype sorlie: Her2; rna-seq subtype hu: Basal; er status: Positive; pgr status: Positive; erbb2 status: Negative; nottingham grade: 3; tumor cell content (1: 0%-29%, 2: 30%-49%, 3:50%-69%, 4: 70%-100%): 3; lymphocyte content (1: 0%-29%, 2: 30%-49%, 3: 50%-69%, 4: 70%-100%): 1; ' GSE36986 Homo sapiens 14 Genome variation profiling by genome tiling array GPL10197 Ten percent of aberrant cells is sufficient for detection of DNA copy number alterations (part 2) 2012-04-02 Array Comparative Genomic Hybridization (aCGH) is a widely used technique to assess chromosomal copy number alterations. Chromosomal content, however, is often not uniform throughout cell populations. The aim of our present study is to evaluate to what extent aCGH can detect DNA copy number alterations in a heterogeneous cell population. Reported detection limits are a compound of analytical software and laboratory technique whilst systematic evaluation is lacking, despite the importance in diagnostics and research. Detection limits were explored with DNA isolated from a patient with intellectual disability (ID) and from tumor cell line BT474. Both were diluted with increasing amounts of normal DNA to simulate different levels of cellularity. Samples were hybridized on CGH arrays containing 180880 oligonucleotides evenly distributed over the genome (space ~17kb). The ID sample has a single copy number gain of 4Mb and a single copy number loss of 7.5Mb that could both be detected with 10% mosaicism. The tumor cell line BT474 has a dual copy number gain (6 copies in a background of 4 copies) of 46Mb. This corresponds to a single copy number gain in a diploid sample and could be detected with 15% tumor cells. The diagnostic validity of these findings was verified using two clinical mosaic samples with alterations in 20% (40Mb) and 14% (34Mb) of cells. Both alterations could be accurately detected using t-statistics. In conclusion, single copy number gains and losses, down to 4Mb in as little as 10% of a cell population, can be detected by aCGH. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36986 Detection limits of DNA copy number alterations in heterogeneous cell populations. Cellular oncology (Dordrecht) 5.020 https://doi.org/10.1007/s13402-012-0108-2 {Cellular oncology (Dordrecht) (5.020): 10.1007/s13402-012-0108-2} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA157473 https://www.ebi.ac.uk/ena/browser/view/PRJNA157473 None [Overal design]Dilution range of breast cancer cell line BT474.; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA isolation protocol available via www.vumc.nl/microarrays. Also described in Buffart et al., J Pathol. 2007 Jan;211(1):45-51 (PMID 17117405).'; [Cell type]'breast cancer cells', 'Source: ''cell line: BT474; cell type: breast cancer cells; percent bt474: 100; ', 'sample type: pool of 19 healthy individuals; ', 'cell line: BT474; cell type: breast cancer cells; percent bt474: 90; ', 'cell line: BT474; cell type: breast cancer cells; percent bt474: 85; ', 'cell line: BT474; cell type: breast cancer cells; percent bt474: 80; ', 'cell line: BT474; cell type: breast cancer cells; percent bt474: 75; ', 'cell line: BT474; cell type: breast cancer cells; percent bt474: 70; ', 'cell line: BT474; cell type: breast cancer cells; percent bt474: 60; ', 'cell line: BT474; cell type: breast cancer cells; percent bt474: 50; ', 'cell line: BT474; cell type: breast cancer cells; percent bt474: 25; ', 'cell line: BT474; cell type: breast cancer cells; percent bt474: 12.5; ', 'cell line: BT474; cell type: breast cancer cells; percent bt474: 6.25; ', 'cell line: BT474; cell type: breast cancer cells; percent bt474: 40; ', 'cell line: BT474; cell type: breast cancer cells; percent bt474: 30; ' GSE37946 Homo sapiens 50 Expression profiling by array GPL96 HER2-enriched tumor initiating cell (HTIC) genomic predictor of response following neoadjuvant trastuzumab-based chemotherapy in HER2+ breast cancer 2012-05-11 We identified a 17-gene Her2-enriched tumor initiating cell (HTIC) signature in MMTV-Her2/Neu mouse mammary TICs. Here, we show that patients with HTICS+ HER2+:ERα− tumors are more likely to achieve a pathologic complete response to trastuzumab-based neoadjuvant chemotherapy compared with HER2+:ER+ tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37946 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA165715 https://www.ebi.ac.uk/ena/browser/view/PRJNA165715 None [Overal design]Neoadjuvant study of 50 HER2-positive breast cancer cases treated with trastuzumab-based chemotherapy pre-operatively. Pre-treatment FNA from primary tumors were obtained and RNA extracted and hybridized to Affymetrix microarrays according to manufacturer protocol. Pathologic response was assessed at the end of neoadjuvant treatment.; [Treatment]'None'; [Growth]'None'; [Extraction]'total RNA was extracted from the specimens using Qiagen RNeasy kit following the manufacturer’s instructions (http://www.qiagen.com).'; [Cell type]'Source: ''age: 50; er: NEG; pr: NEG; her2: POS; clin_stage: IIA; path_stage: 0; path_response: pCR; ', 'age: 34; er: NEG; pr: NEG; her2: POS; clin_stage: IIA; path_stage: 0; path_response: pCR; ', 'age: 52; er: NEG; pr: NEG; her2: POS; clin_stage: IIIB; path_stage: 0; path_response: pCR; ', 'age: 30; er: NEG; pr: NEG; her2: POS; clin_stage: IIIA; path_stage: 0; path_response: pCR; ', 'age: 38; er: POS; pr: POS; her2: POS; clin_stage: IIA; path_stage: 0; path_response: pCR; ', 'age: 36; er: NEG; pr: NEG; her2: POS; clin_stage: I; path_stage: 0; path_response: pCR; ', 'age: 47; er: NEG; pr: NEG; her2: POS; clin_stage: IIA; path_stage: 0; path_response: pCR; ', 'age: 56; er: NEG; pr: POS; her2: POS; clin_stage: IIIA; path_stage: 0; path_response: pCR; ', 'age: 45; er: NEG; pr: NEG; her2: POS; clin_stage: IIIC; path_stage: 0; path_response: pCR; ', 'age: 51; er: NEG; pr: NEG; her2: POS; clin_stage: IIIC; path_stage: 0; path_response: pCR; ', 'age: 43; er: NEG; pr: NEG; her2: POS; clin_stage: IIIA; path_stage: 0; path_response: pCR; ', 'age: 38; er: POS; pr: NEG; her2: POS; clin_stage: I; path_stage: 0; path_response: pCR; ', 'age: 63; er: POS; pr: NEG; her2: POS; clin_stage: IIA; path_stage: 0; path_response: pCR; ', 'age: 50; er: POS; pr: NEG; her2: POS; clin_stage: IIIA; path_stage: 0; path_response: pCR; ', 'age: 41; er: NEG; pr: NEG; her2: POS; clin_stage: IIIC; path_stage: 0; path_response: pCR; ', 'age: 53; er: POS; pr: POS; her2: POS; clin_stage: IIIA; path_stage: 0; path_response: pCR; ', 'age: 51; er: NEG; pr: NEG; her2: POS; clin_stage: IIIB; path_stage: 0; path_response: pCR; ', 'age: 55; er: NEG; pr: NEG; her2: POS; clin_stage: IIA; path_stage: 0; path_response: pCR; ', 'age: 62; er: NEG; pr: NEG; her2: POS; clin_stage: IIIC; path_stage: 0; path_response: pCR; ', 'age: 53; er: NEG; pr: NEG; her2: POS; clin_stage: IIB; path_stage: 0; path_response: pCR; ', 'age: 56; er: POS; pr: POS; her2: POS; clin_stage: IIIA; path_stage: 0; path_response: pCR; ', 'age: 46; er: NEG; pr: NEG; her2: POS; clin_stage: IIIC; path_stage: 0; path_response: pCR; ', 'age: 56; er: NEG; pr: NEG; her2: POS; clin_stage: IIB; path_stage: 0; path_response: pCR; ', 'age: 52; er: POS; pr: POS; her2: POS; clin_stage: IIIB; path_stage: 0; path_response: pCR; ', 'age: 65; er: NEG; pr: NEG; her2: POS; clin_stage: IIB; path_stage: 0; path_response: pCR; ', 'age: 30; er: POS; pr: POS; her2: POS; path_stage: 0; path_response: pCR; ', 'age: 57; er: NEG; pr: NEG; her2: POS; clin_stage: IIA; path_stage: I; path_response: RD; ', 'age: 28; er: POS; pr: POS; her2: POS; clin_stage: IIIB; path_stage: I; path_response: RD; ', 'age: 49; er: POS; pr: POS; her2: POS; clin_stage: IIA; path_stage: I; path_response: RD; ', 'age: 41; er: NEG; pr: NEG; her2: POS; clin_stage: IIIC; path_stage: I; path_response: RD; ', 'age: 47; er: POS; pr: POS; her2: POS; clin_stage: IIIC; path_stage: I; path_response: RD; ', 'age: 73; er: NEG; pr: NEG; her2: POS; clin_stage: IIA; path_stage: I; path_response: RD; ', 'age: 56; er: POS; pr: NEG; her2: POS; clin_stage: IIIC; path_stage: IIA; path_response: RD; ', 'age: 69; er: NEG; pr: NEG; her2: POS; clin_stage: IIA; path_stage: IIA; path_response: RD; ', 'age: 52; er: NEG; pr: NEG; her2: POS; clin_stage: IIIA; path_stage: IIA; path_response: RD; ', 'age: 30; er: NEG; pr: NEG; her2: POS; clin_stage: IIIB; path_stage: IIA; path_response: RD; ', 'age: 61; er: POS; pr: NEG; her2: POS; clin_stage: IIB; path_stage: IIA; path_response: RD; ', 'age: 51; er: NEG; pr: NEG; her2: POS; clin_stage: IIB; path_stage: IIB; path_response: RD; ', 'age: 44; er: NEG; pr: NEG; her2: POS; clin_stage: IIA; path_stage: IIB; path_response: RD; ', 'age: 50; er: POS; pr: NEG; her2: POS; clin_stage: IIIA; path_stage: IIB; path_response: RD; ', 'age: 39; er: NEG; pr: NEG; her2: POS; clin_stage: IIIC; path_stage: IIIA; path_response: RD; ', 'age: 48; er: POS; pr: POS; her2: POS; clin_stage: IIIA; path_stage: IIIA; path_response: RD; ', 'age: 61; er: NEG; pr: NEG; her2: POS; clin_stage: IIIC; path_stage: IIIB; path_response: RD; ', 'age: 55; er: NEG; pr: NEG; her2: POS; clin_stage: IIIC; path_stage: IIIC; path_response: RD; ', 'age: 72; er: POS; pr: POS; her2: POS; clin_stage: IIB; path_stage: IIIC; path_response: RD; ', 'age: 54; er: NEG; pr: NEG; her2: POS; clin_stage: IIIC; path_stage: IIIC; path_response: RD; ', 'age: 24; er: POS; pr: POS; her2: POS; clin_stage: IIIC; path_stage: IIIC; path_response: RD; ', 'age: 62; er: POS; pr: POS; her2: POS; clin_stage: IIIC; path_stage: IIIC; path_response: RD; ', 'age: 49; er: NEG; pr: NEG; her2: POS; clin_stage: IV; path_stage: IV; path_response: RD; ' GSE44118 Mus musculus 6 Expression profiling by array GPL1261 Expression Data from Endothelial Cells as a Consequence of Ets2 Signaling in PyMT Tumor Associated Fibroblasts 2013-02-06 Tumor associated fibroblasts are known to play an important role in angiogenesis, however the specific signaling pathways playing an important role in this cross talk remain ill defined. Here, we studied how Ets2 transcrpiton factor signaling in tumor associated fibroblasts effected gene expression in surrounding endothelial cells in the MMTV-PyMT mammary tumor model. Inactivation of Ets2 specifically in fibroblasts using Fsp-cre significantly reduced tumor associated angiogenesis, and was indicated to effect ECM remodeling, cell adhesion and cell chemotaxis processes in neighboring endothelial cells. We have identified Ets2 in fibroblasts as a key signaling molecule to induce tumor associated angiogenesis. Additionally, this function does not rely on the presence of tumor cells, indicating a memory in fibroblasts to induce angiogenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE44118 Ets2 in tumor fibroblasts promotes angiogenesis in breast cancer. PloS one 2.776 https://doi.org/10.1371/journal.pone.0071533 {PloS one (2.776): 10.1371/journal.pone.0071533} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA188714 https://www.ebi.ac.uk/ena/browser/view/PRJNA188714 None [Overal design]Primary mammary endothelial cells were isolated from mice with or without fibroblast Ets2 in the presence of the PyMT oncogene through sorting with a CD31 antibody. RNA was extracted and samples were submitted for Affymetrix gene expression arrays; [Treatment]'Endothelial cells were placed in Trizol directly after sorting.'; [Growth]'Endothelial cells were isolated from mammary gland tissue after a short collagenase digestion and florescence activated cell sorting using a CD31 specific antibody.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Endothelial Cells''strain: FVB/N; age: 9 Weeks; tissue: Mammary Gland; cell type: Endothelial Cells; genotype: PyMT;Ets2db/loxP; ', 'strain: FVB/N; age: 9 Weeks; tissue: Mammary Gland; cell type: Endothelial Cells; genotype: PyMT;Fsp-cre;Ets2db/loxP; ' GSE37210 Homo sapiens 143 Expression profiling by array GPL6947 The application of nonsense-mediated mRNA decay inhibition to the identification of breast cancer susceptibility genes 2012-04-12 Identification of novel, highly penetrant, breast cancer susceptibility genes will require the application of additional strategies beyond that of traditional linkage and candidate gene approaches. Approximately one-third of inherited genetic diseases, including breast cancer susceptibility, are caused by frameshift or nonsense mutations that truncate the protein product [1]. Transcripts harbouring premature termination codons are selectively and rapidly degraded by the nonsense-mediated mRNA decay (NMD) pathway. Blocking the NMD pathway in any given cell will stabilise these mutant transcripts, which can then be detected using gene expression microarrays. This technique, known as gene identification by nonsense-mediated mRNA decay inhibition (GINI), has proved successful in identifying sporadic nonsense mutations involved in many different cancer types. However, the approach has not yet been applied to identify germline mutations involved in breast cancer. We therefore attempted to use GINI on lymphoblastoid cell lines (LCLs) from multiple-case, non-BRCA1/2 breast cancer families in order to identify additional high-risk breast cancer susceptibility genes. We applied GINI to a total of 24 LCLs,established from breast-cancer affected and unaffected women from three multiple-case non-BRCA1/2 breast cancer families. We then used Illumina gene expression microarrays to identify transcripts stabilised by the NMD inhibition. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37210 The application of nonsense-mediated mRNA decay inhibition to the identification of breast cancer susceptibility genes. BMC cancer 2.933 https://doi.org/10.1186/1471-2407-12-246 {BMC cancer (2.933): 10.1186/1471-2407-12-246} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA158973 https://www.ebi.ac.uk/ena/browser/view/PRJNA158973 None [Overal design]Total RNA obtained from the lymphoblastoid cell lines derived from 24 individuals.; [Treatment]'Fresh medium (RPMI-1640 + 10% fetal bovine serum) containing 10mM caffeine (Sigma-Aldrich) was added to one 25cm2 flask containing 3.5 x 10^6 LCLs, whilst fresh medium with no caffeine was added to the control flask containing the same number of LCLs. After four hours of incubation at 37°C in a humidified atmosphere containing 5% carbon dioxide, the medium from both flasks was removed and cells were washed twice with phosphate-buffered saline (PBS). Normal media was added to the untreated control flask and the other flask was further treated for another four hours with 10mM caffeine media. After which, all medium was removed from both flasks and cells were washed twice with PBS before being pelleted and stored at -80°C until RNA extraction.'; [Growth]'RPMI1640 plus 10% Serum Supreme (Gibco).'; [Extraction]'RNA was extracted with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''family: A; gender: Female; breast cancer: Affected; cell line: Lymphoblastoid cell line (LCL); agent: Caffeine; ', 'family: A; gender: Female; breast cancer: Affected; cell line: Lymphoblastoid cell line (LCL); agent: Untreated; ', 'family: A; gender: Female; breast cancer: Unaffected; cell line: Lymphoblastoid cell line (LCL); agent: Caffeine; ', 'family: A; gender: Female; breast cancer: Unaffected; cell line: Lymphoblastoid cell line (LCL); agent: Untreated; ', 'family: B; gender: Female; breast cancer: Affected; cell line: Lymphoblastoid cell line (LCL); agent: Caffeine; ', 'family: B; gender: Female; breast cancer: Affected; cell line: Lymphoblastoid cell line (LCL); agent: Untreated; ', 'family: B; gender: Female; breast cancer: Unaffected; cell line: Lymphoblastoid cell line (LCL); agent: Caffeine; ', 'family: B; gender: Female; breast cancer: Unaffected; cell line: Lymphoblastoid cell line (LCL); agent: Untreated; ', 'family: C; gender: Female; breast cancer: Affected; cell line: Lymphoblastoid cell line (LCL); agent: Caffeine; ', 'family: C; gender: Female; breast cancer: Affected; cell line: Lymphoblastoid cell line (LCL); agent: Untreated; ', 'family: C; gender: Female; breast cancer: Unaffected; cell line: Lymphoblastoid cell line (LCL); agent: Caffeine; ', 'family: C; gender: Female; breast cancer: Unaffected; cell line: Lymphoblastoid cell line (LCL); agent: Untreated; ' GSE58984 Homo sapiens 94 Expression profiling by array GPL570 Gene profiling of HER2 breast cancer patients treated with adjuvant trastuzumab 2014-07-01 The human epidermal growth factor receptor 2 (HER2) gene encodes a tyrosine kinase receptor that controls important signal transduction pathways in breast cancer. Amplification and overexpression of the HER2 gene occurs in approximately 20% of breast cancers and is associated with an aggressive clinical phenotype. Trastuzumab, a humanized monoclonal antibody that targets HER2 showed exceptional efficacy in the treatment of breast cancer. In the adjuvant treatment of breast cancer patients, five randomized trials showed significant benefit of trastuzumab, with a reduction in the rate of recurrence of approximately 50% and improvement in the rate of survival of approximately 30%. In the current study, positive early stage breast cancer samples treated with adjuvant trastuzumab provided by institute Jules Bordet (IJB) and KUL. Gene expression and clinical outcome data were available. to better understand the genetic regulations and effects of the trastuzumab, we profile the the genes expression of positive early stage breast cancer samples treated with adjuvant trastuzumab. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58984 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA254048 https://www.ebi.ac.uk/ena/browser/view/PRJNA254048 None [Overal design]The dataset (as part of the FP7 EU consortium) is composed of 94 HER2 positive early stage breast cancer samples treated with adjuvant trastuzumab provided by the Jules Bordet Institute (IJB) and the Katholieke Universiteit Leuven (KULeuven) for patients followed between 2002 and 2011. The average age of these patients is 52.9 and their median follow-up time is 4.96 years. After hybridization on the chips, the quality controls were performed following the recommandation posted on http://www.arrayanalysis.org/.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted using TRIzol (Life Technologies, Carlsbad, California) following the manufacturer’s instructions. RNA concentration was measured using the NanoDrop 1000 (Thermo Scientific, Waltham, Massachusetts), and RNA integrity (RIN: RNA Integrity Number) was assessed using an Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, California).'; [Cell type]'Source: ''tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 42; tumor size: 60; nodes positive: 3; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 3645; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 49; tumor size: 18; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 3729; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 1; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 43; tumor size: 11; nodes positive: 1; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 3517; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 69; tumor size: 15; nodes positive: 13; er status: 1; pgr status: 0; distant metastasis: 1; time to ddfs: 1062; intratumoral lymphocytic infiltration: 3; stromal lymphocytic infiltration: 25; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 68; tumor size: 30; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 3125; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 10; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 68; tumor size: NA; nodes positive: NA; er status: 1; pgr status: 1; distant metastasis: 1; time to ddfs: 880; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 37; tumor size: 10; nodes positive: 1; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2786; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 60; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 52; tumor size: 50; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 1; time to ddfs: 2117; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 20; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 50; tumor size: 45; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2562; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 20; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 33; tumor size: 35; nodes positive: 5; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 914; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 7; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 60; tumor size: 55; nodes positive: 3; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2544; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 1; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 54; tumor size: 30; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 2665; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 5; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 56; tumor size: 23; nodes positive: 2; er status: 0; pgr status: 1; distant metastasis: 1; time to ddfs: 1000; intratumoral lymphocytic infiltration: 5; stromal lymphocytic infiltration: 30; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 64; tumor size: 45; nodes positive: 0; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 2397; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 7; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 40; tumor size: 40; nodes positive: 8; er status: 0; pgr status: 0; distant metastasis: 1; time to ddfs: 279; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 10; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 45; tumor size: 55; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2252; intratumoral lymphocytic infiltration: 3; stromal lymphocytic infiltration: 17; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 52; tumor size: 17; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2315; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 15; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 36; tumor size: 26; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 2420; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 38; tumor size: 15; nodes positive: 1; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2155; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 5; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 49; tumor size: 50; nodes positive: 7; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2541; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 2; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 54; tumor size: 10; nodes positive: 1; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2223; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 25; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 49; tumor size: 25; nodes positive: 4; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 2495; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 7; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 48; tumor size: 73; nodes positive: 2; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 2170; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 5; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 35; tumor size: 20; nodes positive: 4; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2267; intratumoral lymphocytic infiltration: 5; stromal lymphocytic infiltration: 30; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 65; tumor size: 23; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 2218; intratumoral lymphocytic infiltration: 3; stromal lymphocytic infiltration: 51; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 73; tumor size: 70; nodes positive: 28; er status: 0; pgr status: 0; distant metastasis: 1; time to ddfs: 1124; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 7; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 69; tumor size: 22; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2272; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 7; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 43; tumor size: 19; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2161; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 30; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 68; tumor size: 32; nodes positive: 0; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 1689; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 70; tumor size: 35; nodes positive: 1; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 921; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 0; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 61; tumor size: 19; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2201; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 2; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 35; tumor size: 22; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2219; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 10; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 66; tumor size: 44; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 2216; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 45; tumor size: 37; nodes positive: 1; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 2180; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 10; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 56; tumor size: 55; nodes positive: 1; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 2304; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 1; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 49; tumor size: 55; nodes positive: 1; er status: 0; pgr status: 0; distant metastasis: 1; time to ddfs: 876; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 0; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 55; tumor size: 23; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1846; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 12; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 54; tumor size: 35; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 1; time to ddfs: 966; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 25; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 43; tumor size: 25; nodes positive: 0; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 1845; intratumoral lymphocytic infiltration: 5; stromal lymphocytic infiltration: 51; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 48; tumor size: 35; nodes positive: 2; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 1985; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 0; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 51; tumor size: 60; nodes positive: 2; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1774; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 67; tumor size: 20; nodes positive: 1; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1943; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 51; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 56; tumor size: 15; nodes positive: 4; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1896; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 15; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 62; tumor size: 25; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1139; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 5; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 55; tumor size: 32; nodes positive: 5; er status: 1; pgr status: 1; distant metastasis: 1; time to ddfs: 1297; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 7; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 68; tumor size: 13; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1993; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 50; tumor size: 31; nodes positive: 1; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 701; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 30; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 70; tumor size: 30; nodes positive: 16; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1748; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 53; tumor size: 20; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 903; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 2; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 54; tumor size: 30; nodes positive: 6; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 788; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 51; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 51; tumor size: 15; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1892; intratumoral lymphocytic infiltration: 10; stromal lymphocytic infiltration: 60; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 51; tumor size: 40; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1629; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 15; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 68; tumor size: 18; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1822; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 53; tumor size: 77; nodes positive: 1; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1810; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 5; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 52; tumor size: 28; nodes positive: 1; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1757; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 25; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 41; tumor size: 35; nodes positive: 1; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1668; intratumoral lymphocytic infiltration: 3; stromal lymphocytic infiltration: 45; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 53; tumor size: 33; nodes positive: 1; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1921; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 43; tumor size: 19; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1430; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 2; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 45; tumor size: 24; nodes positive: 1; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1666; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 2; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 77; tumor size: 45; nodes positive: 4; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1780; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 1; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 54; tumor size: 56; nodes positive: 2; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1637; intratumoral lymphocytic infiltration: 3; stromal lymphocytic infiltration: 10; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 64; tumor size: 22; nodes positive: 1; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1726; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 2; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 34; tumor size: 25; nodes positive: 2; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 1735; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 55; tumor size: 25; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1820; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 30; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 47; tumor size: 15; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1521; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 40; tumor size: 50; nodes positive: 0; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 1774; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 5; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 72; tumor size: 19; nodes positive: 1; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1421; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 5; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 53; tumor size: 49; nodes positive: 2; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1453; intratumoral lymphocytic infiltration: 3; stromal lymphocytic infiltration: 25; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 52; tumor size: 45; nodes positive: 0; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 1408; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 49; tumor size: 17; nodes positive: 0; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 1539; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 0; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 49; tumor size: 14; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1518; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 10; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 44; tumor size: 40; nodes positive: 6; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1492; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 10; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 79; tumor size: 18; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1498; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 52; tumor size: 25; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1457; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 57; tumor size: 25; nodes positive: 6; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1610; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 10; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 57; tumor size: 20; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1508; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 39; tumor size: 37; nodes positive: 0; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 1469; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 1; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 45; tumor size: 20; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1483; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 7; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 49; tumor size: 45; nodes positive: 12; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1388; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 45; tumor size: 24; nodes positive: 11; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1372; intratumoral lymphocytic infiltration: 5; stromal lymphocytic infiltration: 95; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 68; tumor size: 22; nodes positive: 1; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1312; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 10; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 49; tumor size: 45; nodes positive: 2; er status: 0; pgr status: 0; distant metastasis: 1; time to ddfs: 660; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 10; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 65; tumor size: 23; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1175; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 7; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 52; tumor size: 22; nodes positive: 8; er status: 0; pgr status: 0; distant metastasis: 1; time to ddfs: 201; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 2; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 42; tumor size: 13; nodes positive: 18; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 2621; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 38; tumor size: 28; nodes positive: 5; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 3077; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 57; tumor size: 55; nodes positive: 3; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1492; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 10; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 48; tumor size: 17; nodes positive: 1; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1012; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 2; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 61; tumor size: 20; nodes positive: 0; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 2000; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 2; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 41; tumor size: 30; nodes positive: 1; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1723; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 5; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 71; tumor size: 45; nodes positive: 0; er status: 0; pgr status: 0; distant metastasis: 0; time to ddfs: 1471; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 2; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 40; tumor size: 21; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 1459; intratumoral lymphocytic infiltration: 1; stromal lymphocytic infiltration: 5; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 49; tumor size: 52; nodes positive: 12; er status: 1; pgr status: 0; distant metastasis: 0; time to ddfs: 470; intratumoral lymphocytic infiltration: 15; stromal lymphocytic infiltration: 70; ', 'tissue: HER2 breast cancer tumor; treatment: trastuzumab; age: 49; tumor size: 16; nodes positive: 0; er status: 1; pgr status: 1; distant metastasis: 0; time to ddfs: 844; intratumoral lymphocytic infiltration: 0; stromal lymphocytic infiltration: 3; ' GSE69082 Homo sapiens 4 Expression profiling by array GPL10558 Gene expression signature after γklotho knockdown in HCC1395 triple negative breast cancer cells 2015-05-20 γKlotho is critical for the survival of triple negative breast cancer (TNBC) cells HCC1395, since its depletion leads to decreased cell viability, cell cycle arrest and apoptosis. Here, we compare γKlotho knockdown cells with control HCC1395 cells at gene expression level in order to get insight into the possible cellular mechanisms contributing to the sensitivity of TNBC cells to γKlotho depletion. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE69082 γKlotho is a novel marker and cell survival factor in a subset of triple negative breast cancers. Oncotarget None https://doi.org/10.18632/oncotarget.6006 {Oncotarget (None): 10.18632/oncotarget.6006} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA284497 https://www.ebi.ac.uk/ena/browser/view/PRJNA284497 None [Overal design]HCC1395 cells were transfected with control siRNA (siRevL1) or a pool of siRNAs targeting γKlotho and 48 h later RNA was extracted for microarray expression analysis. Two biolgical replicates for each siRNA-transfection were used.; [Treatment]'Cells were transfected with siRevL1 or siKLG-134. siRNA transfections were performed with Lipofectamine RNAiMAX according to the manufacture’s protocol.'; [Growth]'Human breast cancer cells HCC1395 were maintained in RPMI-1640 medium supplemented with 10% FBS. Cells were grown in a humidified incubator at 37°C with 5% CO2.'; [Extraction]'RNA was extracted using RNAStat60 (TelTest) according to the manufacturer’s directions.'; [Cell type]'Epithelial breast cancer cells''cell line: HCC1395; cell type: Epithelial breast cancer cells; disease model: Triple negative breast cancer; ' GSE54140 Homo sapiens 131 Genome variation profiling by genome tiling array GPL10152 Identification of a genomic signature in BRCA1-mutated triple negative breast cancer by Comparative Genomic Hybridization 2014-01-16 Determination of recurrent chromosomal aberrations in Luninal A, Luminal B, HER2-positve, and triple negative breast cancers https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54140 Identification by array comparative genomic hybridization of a new amplicon on chromosome 17q highly recurrent in BRCA1 mutated triple negative breast cancer. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-014-0466-y {Breast cancer research : BCR (5.676): 10.1186/s13058-014-0466-y} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA235298 https://www.ebi.ac.uk/ena/browser/view/PRJNA235298 None [Overal design]131 samples, Tumour DNA vs Normal DNA; [Treatment]'None'; [Growth]'None'; [Extraction]'Agilent Technologies, protocol #G4410-90020, version 3.3'; [Cell type]'Source: ''gender: Female; tissue: Breast cancer; tumour type: HER2-positive; ', 'reference: normal pooled gDNA 7 women; gender: Female; tissue: Lymphocyte; ', 'gender: Female; tissue: Breast cancer; tumour type: Luminal A; ', 'gender: Female; tissue: Breast cancer; tumour type: Luminal B; ', 'gender: Female; tissue: Breast cancer; tumour type: Non-triple-negative; ', 'gender: Female; tissue: Breast cancer; tumour type: BRCA1-mutated; ', 'gender: Female; tissue: Breast cancer; tumour type: BRCA1-non-mutated; ', 'gender: Female; tissue: Breast cancer; tumour type: BRCA1-unscreened; ' GSE98337 Homo sapiens 6 Expression profiling by array GPL15207 Expression data from breast cancer cells MDA-MB-231 2017-04-28 CCCTC-binding factor (CTCF) is an important epigenetic regulator that has been implicated in multiple cellular processes including growth, proliferation, differentiation, and apoptosis. Deletion or mutation of CTCF is associated with human breast carcinogenesis. However, the exact role that CTCF plays in breast cancer has not been fully elucidated. To investigate the biological functions of CTCF in breast cancer and the underlying mechanisms, we carried out microarray analysis comparing the gene expression of CTCF overexpressing and control MDA-MB-231 cells to screen the possible target genes and pathways that CTCF regulated. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98337 CCCTC-binding factor inhibits breast cancer cell proliferation and metastasis via inactivation of the nuclear factor-kappaB pathway. Oncotarget None https://doi.org/10.18632/oncotarget.18977 {Oncotarget (None): 10.18632/oncotarget.18977} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA384779 https://www.ebi.ac.uk/ena/browser/view/PRJNA384779 None [Overal design]Total RNA from MDA-MB-231 cell infected with NC-lentivirus (n=3) or CTCF-OE-lentivirus (n=3) was extracted using Trizol reagents. NanoDrop 2000 and Agilent Bioanalyzer 2100 were used for detecting the RNA quantity and quality. The GeneChip PrimeView Human Gene Expression Array (Affymetrix) was used for microarray processing to determine gene expression profile depending on the manufacturer’s instruction.; [Treatment]'MDA-MB-231 cells stably expressing CTCF and negative control were established using lentivector-based overexpression system.Then cells were washed 3 times with PBS and lysed with Trizol'; [Growth]'MDA-MB-231 cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM, GIBCO) and supplemented with 10% fetal bovine serum (Hyclone).'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MDA-MB-231; expression: negative control; ', 'cell line: MDA-MB-231; expression: stably expressing CTCF; ' GSE24433 Homo sapiens 6 Expression profiling by array GPL571 Mesenchymal stem cells in local fat depots stimulate breast cancer growth, invasion and desmoplasia 2010-09-29 Studies investigating the role of mesenchymal stem cells (MSCs) in mammary carcinogenesis have almost exclusively relied on isolates from bone marrow aspirates or non-breast fat sources often making the general assumption that all MSCs are alike. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24433 Mesenchymal stem cells in mammary adipose tissue stimulate progression of breast cancer resembling the basal-type. Cancer biology & therapy 2.879 https://doi.org/10.4161/cbt.20561 {Cancer biology & therapy (2.879): 10.4161/cbt.20561} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA132785 https://www.ebi.ac.uk/ena/browser/view/PRJNA132785 None [Overal design]Here we conduct the first extensive analysis of human breast adipose MSCs to define similarities and differences to MSCs isolated from non-breast sources (subcutaneous abdominal tissue) and bone marrow.; [Treatment]'Tissues were cut into 5 – 10mm cubes, washed with sterile PBS and then digested in 1% collagenase at 37°C. Collagenase was neutralized with 10% FBS and the stromal vascular fraction was pelleted by centrifugation for 10 minutes at 400xg at room temperature. Red blood cells from the cell pellet was lysed with 160mM NH4Cl. The resulting suspensions were serially filtered through 100μm and 40μm filters followed by centrifugation at 400xg for 10 minutes. The cells were cultured overnight in low glucose DMEM with 30% fetal bovine serum (FBS) and 2% penicillin/streptomycin to allow attachment to standard plastic tissue culture dishes.'; [Growth]'MSCs were isolated from residual adipose tissues from reduction mammoplasties, lipoaspirates, and residual bone marrow specimens'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'bone marrow-derived mesenchymal stem cells', 'breast-derived mesenchymal stem cells', 'abdomen-derived mesenchymal stem cells''gender: female; cell type: bone marrow-derived mesenchymal stem cells; ', 'gender: female; cell type: breast-derived mesenchymal stem cells; ', 'gender: female; cell type: abdomen-derived mesenchymal stem cells; ' GSE58306 Mus musculus 2 Expression profiling by array GPL7202 Gene expression changes in mouse pancreatic cancer xenograft induced by exposure to enriched environment 2014-06-09 Previous studies reported that mice living in an enriched environment (EE) showed reduced growth of melanoma, colon and breast tumors. Our study extended the potential anti-tumor effect of EE exposure to pancreatic cancer, and firstly provided evidence demonstrating that EE exposure significantly inhibits tumor growth in a syngeneic murine model of pancreatic cancer. To further investigate the mechanisms underlying the EE-induced pancreatic tumor inhibition, we analyzed the gene expression changes in pancreatic tumor xenograft using an integrative transcriptomic and proteomic approach. Our results found that EE largely decreased the expression of genes associated with mitochondrial function at transcriptional level in pancreatic tumor, suggesting mitochondrial dysfunction in tumor cells may play a critical role in EE-induced anti-tumor phenotype. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58306 Enriched environment inhibits mouse pancreatic cancer growth and down-regulates the expression of mitochondria-related genes in cancer cells. Scientific reports 4.011 https://doi.org/10.1038/srep07856 {Scientific reports (4.011): 10.1038/srep07856} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA251964 https://www.ebi.ac.uk/ena/browser/view/PRJNA251964 None [Overal design]Three-week-old C57BL/6 mice were randomized to live in either enriched environment or standard environment conditions. Mice from both groups were given subcutaneous injection of Panc02 murine pancreatic cancer cells (6 × 105 cells per mouse) and lived in their respective homes for 5 additional weeks. Pooled RNA samples extracted from Panc02 tumors (6 mice for each group) were then subjected to Agilent-014868 Whole Mouse Genome 4☓44k Microarray analyses.; [Treatment]'Three-week-old C57BL/6 mice were randomized to live in either enriched environment or standard environment conditions. Mice from both groups were given subcutaneous injection of Panc02 murine pancreatic cancer cells (6 × 105 cells per mouse) and lived in their respective homes for 5 additional weeks. At the end of the experiment, the Panc02 tumors were harvested and processed for following analysis.'; [Growth]'None'; [Extraction]'Total RNA from homogenized tumors was extracted using Trizol reagent (Invitrogen, Carlsbad, CA) according to the manufacturer’s instructions. The RNA samples pooled from 6 mice for each group were subjected to microarray analysis.'; [Cell type]'Source: ''strain: C57BL/6; environment: Standard; treatment: subcutaneous injection of Panc02 murine pancreatic cancer cells; tissue (rna source): Pancreatic cancer xenograft; ', 'strain: C57BL/6; environment: Enriched; treatment: subcutaneous injection of Panc02 murine pancreatic cancer cells; tissue (rna source): Pancreatic cancer xenograft; ' GSE117612 Mus musculus 17 Expression profiling by array GPL24242 A Chemical Toolbox for the Study of Bromodomains and Epigenetic Signaling 2018-07-24 Bromodomains (BRDs) are evolutionary conserved epigenetic protein interaction modules which recognize (“read”) acetyl-lysine, however their role(s) in regulating cellular states and their potential as targets for the development of targeted treatment strategies is poorly understood. Here we present a set of 25 chemical probes, selective tool small molecule inhibitors, covering 29 human bromodomain targets. We comprehensively evaluate the selectivity of this probe-set using BROMOscan® and demonstrate the utility of the set in studies of muscle cell differentiation and triple negative breast cancer (TNBC). We identified cross talk between histone acetylation and the glycolytic pathway resulting in a vulnerability of TNBC cell lines to inhibition of BRPF2/3 BRDs under conditions of glucose deprivation or GLUT1 inhibition. This chemical probe set will serve as a resource for future applications in the discovery of new physiological roles of bromodomain proteins in normal and disease states and as a toolset for bromodomain target validation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE117612 A chemical toolbox for the study of bromodomains and epigenetic signaling. Nature communications 11.878 https://doi.org/10.1038/s41467-019-09672-2 {Nature communications (11.878): 10.1038/s41467-019-09672-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA482645 https://www.ebi.ac.uk/ena/browser/view/PRJNA482645 None [Overal design]C2C12 mouse myoblast cells were grown in DMEM containing 20% FBS. For differentiation experiments in the presence and absence of mentioned drugs, 0.3x106 cells were seeded and allowed to grow for 36 hrs before switching to differentiation media (DMEM containing 2% horse serum, 10 µg/ml insulin and 10 µg/ml Transferrin). Indicated drugs were added at the time of differentiation at 0.5 μM (JQ1, LP99) or 2 μM (GSK2801, BAZ2ICR, BSP) for 12h before they were harvested for extraction of total RNA. Total RNA was extracted using PureLinkTM RNA kit as per the manufacturer’s protocol. Raw CEL data were processed in R (v.3.5.1) using Bioconductor (v.3.7) and the oligo package (v.1.44). Quality controls were carried out using the arrayQualityMetrics package (v.3.36.0) taking into account array intensity distributions, distance between arrays and variance mean-dependence. Principal component analysis was used to decide which arrays to process together. On this basis one of the three arrays treated with BSP was considered to be an outlier and was discarded (sample 'BSP_rep3', file 'BSP_rep3.CEL'), with the rest of the analysis performed without taking it into account. Background correction and normalization were carried out employing the Robust Multichip Array (RMA) method implemented in the oligo package. Data were filtered using the genefilter package (v.1.62.0) employing the nsFilter function and an interquartile range (IQR) cut-off of 0.28 (or >log(1.2), determined by the midpoint of the shortest interval containing half of the data. Probe sets that did not have an Entrez gene identifier were also removed. From the 29129 features available on the Clariom S Mouse HT chip, 14538 remained after filtering. A linear model was applied employing the limma package (v.3.36.2) followed by empirical Bayesian analysis to determine differential expression between not-treated and treated samples. Genes were considered differentially expressed if the adjusted P-value, calculated using the Benjamini–Hochberg method in order to minimize false discovery rate, was less than 0.05 and the mean level of expression was greater than 1.5-fold. Data were annotated using the clariomsmousehttranscriptcluster.db annotation data (https://www.bioconductor.org/packages/release/data/annotation/html/clariomsmousehttranscriptcluster.db.html).; [Treatment]'C2C12 cells were incubated with the indicated drugs at concentrations of 500 nM (JQ1 & LP99) or 2 µM (GSK2801, BAZ2ICR & BSP) for 12 h before they were harvested for extraction of total RNA'; [Growth]'C2C12 mouse myoblast cells were grown in DMEM containing 20% FBS. 0.3x106 cells were seeded and allowed to grow for 36 hrs before switching to differentiation media (DMEM containing 2% horse serum, 10 µg/ml insulin and 10 µg/ml Transferrin)'; [Extraction]'Total RNA was extracted using PureLinkTM RNA kit as per the manufacturer’s protocol.'; [Cell type]'Source: ''cell line: C2C12; agent: DMSO; replicate: 1; ', 'cell line: C2C12; agent: DMSO; replicate: 2; ', 'cell line: C2C12; agent: DMSO; replicate: 3; ', 'cell line: C2C12; agent: GSK2801; replicate: 1; ', 'cell line: C2C12; agent: GSK2801; replicate: 2; ', 'cell line: C2C12; agent: GSK2801; replicate: 3; ', 'cell line: C2C12; agent: BAZ2ICR; replicate: 1; ', 'cell line: C2C12; agent: BAZ2ICR; replicate: 2; ', 'cell line: C2C12; agent: BAZ2ICR; replicate: 3; ', 'cell line: C2C12; agent: LP99; replicate: 1; ', 'cell line: C2C12; agent: LP99; replicate: 2; ', 'cell line: C2C12; agent: LP99; replicate: 3; ', 'cell line: C2C12; agent: JQ1; replicate: 1; ', 'cell line: C2C12; agent: JQ1; replicate: 2; ', 'cell line: C2C12; agent: JQ1; replicate: 3; ', 'cell line: C2C12; agent: BSP; replicate: 1; ', 'cell line: C2C12; agent: BSP; replicate: 2; ' GSE118539 Homo sapiens 4 Expression profiling by array GPL20844 Differentially expressed genes in human brest cancer specimens 2018-08-14 To identify differentially expressed genes in human brest cancer specimens were subjected to Agilent whole genome microarrays. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE118539 RNA-sequence-based microRNA expression signature in breast cancer: tumor-suppressive miR-101-5p regulates molecular pathogenesis. Molecular oncology 5.962 https://doi.org/10.1002/1878-0261.12602 {Molecular oncology (5.962): 10.1002/1878-0261.12602} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA485978 https://www.ebi.ac.uk/ena/browser/view/PRJNA485978 None [Overal design]Human breast cancer specimens divided with the state of receptor tyrosine kinase and estrogen receptor.; [Treatment]'None'; [Growth]'Normal cell culture medium RPMI 1640 or DMEM.'; [Extraction]"Total RNA was extracted using Trizol following the manufacturer's instructions"; [Cell type]'Source: ''tissue: breast cancer; ' GSE48196 Homo sapiens 18 Genome binding/occupancy profiling by genome tiling array GPL5082 TRIM37 is a novel H2A ubiquitin ligase and a Breast Cancer Oncogene 2013-06-21 The TRIM37 gene is mutatedin Mulbery nanism, a rare autosomal recessive disorder, and is in the 17q23 chromosomal region that is amplified in up to ~40% of breast cancers. Trim37 contains a RING finger domain, a hallmark of E3 ubiquitin ligases, but the protein substrate(s) of Trim37 is unknown. Mono-ubiquitination of histone H2A is a chromatin modification associated with transcriptional repression and here we report that Trim37 is an H2A ubiquitin ligase. Genome-wide Chip-CHIP experiments indicate that in human breast cancer cells containing amplified 17q23, Trim37 is bound to the promoters of many tumor suppressor genes. RNA interference (RNAi)-mediated knockdown of Trim37 results in loss of ubiquitinated H2A, dissociation of PRC1 and PRC2, and transcriptional reactivation of silenced genes. Knockdown of Trim37 in human breast cancer cells containing amplified 17q23 substantially decreases tumor growth in mouse xenografts. Collectively, our results reveal Trim37 as a new H2A ubiquitin ligase that is overexpressed in a subset of breast cancers and redirects PRC2 to silence tumor suppressors and other genes resulting in oncogenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48196 TRIM37 is a new histone H2A ubiquitin ligase and breast cancer oncoprotein. Nature 43.070 https://doi.org/10.1038/nature13955 {Nature (43.070): 10.1038/nature13955} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA209139 https://www.ebi.ac.uk/ena/browser/view/PRJNA209139 None [Overal design]Identification of TRIM37 Binding targets in MCF7 cells from the two replicate experiments; [Treatment]'Cells were washed twice with PBS and then fixed with 1% Formaldehyde. The fixation was terminated with 2.5M glycine and'; [Growth]'MCF7 cells were cultured in DMEM media supplemented with 10% FBS at 37 degrees and 5% CO2.'; [Extraction]'1x10E8 cells were rinsed with PBS, scraped, and pelleted in a 50 mL conical tube. Cells were fixed in 1% formaldehyde for 10 minutes and 0.125M glycine was added to quench the cross-linking reaction. Cells were spun down and the pellet was re-suspended in Lysis buffer (50mM Hepes pH 8.0, 150mM NaCl, 1mM EDTA, 01% Na-Deoxycholate, 1% Triton X-100, 0.1% SDS, 1mM PMSF and protease inhibitors) and subjected to sonication by Bioruptor. Cell debris was removed by centrifugation at 1500g for 15 min and cleared superntant was used for Chromatin immunoprecipitation.'; [Cell type]'Source: ''cell line: MCF7; antibody: anti-IgG; ', 'cell line: MCF7; antibody: Anti-Ezh2; ', 'cell line: MCF7; antibody: Anti-H3K27me3; ', 'cell line: MCF7; antibody: Anti-H2Aub; ', 'cell line: MCF7; antibody: Anti-TRIM37; ' GSE100850 Homo sapiens 39 Methylation profiling by genome tiling array GPL21145 Epigenetic alterations detected in the genome of very young breast cancer patients: identification of new biomarkers 2017-07-06 Breast cancer in very young women (< 35 years BCVY) presents more aggressive and complex biological features than in their older counterparts. In this study we aimed to identify the key pathways that may cause cancer in this younger age group. EPIC and 450k Illumina methylation arrays were used to identify differences in DNA methylation in 74 breast cancer tumours, including 37 from very young women. Additionally, we analysed copy number variation (CNV) and DNAm age using methylation intensities from Illumina Infinium MethylationEPIC BeadChip. Although we are able to identify aberrant CNV patterns in breast cancer samples, they were not highly specific to BCVY. However, we identified 2 219 CpG sites that were differently methylated in BCVY vs. older women (false discovery rate < 0.05 beta-value difference ± 0.1), with the general hypomethylation profile affecting genes involved in neuronal-system pathways, cell communication, and extracellular matrix organisation, as confirmed by our experimental data. Additionally, a specific hypermethylation profile comprising 502 CpG sites located mainly in open-sea regions distinguished BCVY from older patients. Pathway enrichment analysis showed that regions implicated in the hypermethylation profile were involved in regulating genes related to Notch signalling pathways, the immune system, DNA repair, and vesicular trafficking. Moreover, BCVY presented age acceleration comparing with older women. The expression of genes regulated by differentially-methylated CpG sites was validated using both Cancer Genome Atlas genomic data and by qRT-PCR, the latter in an independent sample (n = 40). This validation highlighted that 186 genes were consistently deregulated, including consistent hypomethylation and higher expression of HOXD9, PCDH10, and HDAC5 genes when considering BCVY vs. BC. Thus, we propose HDAC5 hypomethylation as a possible early detection biomarker in BCVY, and moreover, HDAC5 inhibitors, such as LMK-235, may be useful in treating breast cancer tumours in young women https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE100850 Methylation deregulation of miRNA promoters identifies miR124-2 as a survival biomarker in Breast Cancer in very young women. Scientific reports 4.011 https://doi.org/10.1038/s41598-018-32393-3 {Scientific reports (4.011): 10.1038/s41598-018-32393-3} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA393265 https://www.ebi.ac.uk/ena/browser/view/PRJNA393265 None [Overal design]We extracted DNA from 26 samples from BCVY (< 35 years) and 15 samples from older women with breast cancer (BCO) (> 45 years). Normal tissue samples from very young women (NVY) (n = 2) and older women (NO) (n = 3) were also included in the methylation study. All DNA samples were hybridized to the Illumina Infinium MethylationEPIC BeadChip. This Series represents 21 samples from BCVY (< 35 years) and 13 samples from older women with breast cancer (BCO) (> 45 years). Normal tissue samples from very young women (NVY) (n = 2) and older women (NO) (n = 3) .; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA FFPE samples were extracted using a commercial kit QIAamp DNA FFPE Tissue Kit from Qiagen\nQIAamp DNA FFPE Tissue Kit from Qiagen'; [Cell type]'Source: ''tissue: Breast; gender: Female; age_group: Normal Old; er status: NA; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Old; subgroup: LUMINAL/HER2; er status: 1; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Young; subgroup: TRIPLE NEG; er status: 0; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Old; subgroup: LUMINAL A; er status: 1; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Young; subgroup: HER2; er status: 0; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Old; subgroup: TRIPLE NEG; er status: 0; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Normal Young; er status: NA; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Young; subgroup: LUMINAL B; er status: 1; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Young; subgroup: LUMINAL A; er status: 1; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Old; subgroup: LUMINAL B; er status: 1; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Old; subgroup: HER2; er status: 0; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Young; subgroup: LUMINAL/HER2; er status: 1; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Young; subgroup: LUMINAL A; er status: NA; sample type: FFPE sample; ', 'tissue: Breast; gender: Female; age_group: Old; subgroup: TRIPLE NEG; er status: 1; sample type: FFPE sample; ' GSE4922 Homo sapiens 578 Expression profiling by array GPL96; GPL97 Genetic Reclassification of Histologic Grade Delineates New Clinical Subtypes of Breast Cancer 2006-05-25 Histological grading of breast cancer defines morphological subtypes informative of metastatic potential, although not without considerable inter-observer disagreement and clinical heterogeneity particularly among the moderately differentiated grade II (G2) tumors. We posited that a gene expression signature capable of discerning tumors of grade I (G1) and grade III (G3) histology might provide a more objective measure of grade with prognostic benefit for patients with moderately differentiated disease. To this end, we studied the expression profiles of 347 primary invasive breast tumors analyzed on Affymetrix microarrays. Using class prediction algorithms, we identified 264 robust grade-associated markers, six of which could accurately classify G1 and G3 tumors, and separate G2 tumors into two highly discriminant classes (termed G2a and G2b genetic grades) with patient survival outcomes highly similar to those with G1 and G3 histology, respectively. Statistical analysis of conventional clinical variables further distinguished G2a and G2b subtypes from each other, but also from histologic G1 and G3 tumors. In multivariate analyses, genetic grade was consistently found to be an independent prognostic indicator of disease recurrence comparable to that of lymph node status and tumor size. When incorporated into the Nottingham Prognostic Index, genetic grade enhanced detection of patients with less harmful tumors, likely to benefit little from adjuvant therapy. Our findings show that a genetic grade signature can improve prognosis and therapeutic planning for breast cancer patients, and support the view that low and high grade disease, as defined genetically, reflect independent pathobiological entities rather than a continuum of cancer progression. Three separate breast cancer cohorts were analyzed: 1) Uppsala (n=249), 2) Stockholm (n=58), 3) Singapore (n=40). The Uppsala and Singapore data can be accessed here. The Stockholm cohort data can be accessed at GEO Series GSE1456. Keywords: Tumor sample comparisons https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE4922 Genetic reclassification of histologic grade delineates new clinical subtypes of breast cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-05-4414 {Cancer research (8.378): 10.1158/0008-5472.CAN-05-4414} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA95863 https://www.ebi.ac.uk/ena/browser/view/PRJNA95863 None [Overal design]All tumor specimens were assessed on U133 A and B arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen RNeasy Mini Kit'; [Cell type]'Source: ''', 'NUH-sample ID: NT00-71; grade: Grade2; Probability 1-like (by SWS classifier): 0.122; Probability 3-like (by SWS classifier): 0.878; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT00-2; grade: Grade2; Probability 1-like (by SWS classifier): 0.001; Probability 3-like (by SWS classifier): 0.999; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT00-22; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-99; grade: Grade2; Probability 1-like (by SWS classifier): 0.924; Probability 3-like (by SWS classifier): 0.076; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-62; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-64; grade: Grade2; Probability 1-like (by SWS classifier): 0.776; Probability 3-like (by SWS classifier): 0.224; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-178; grade: Grade2; Probability 1-like (by SWS classifier): 0.006; Probability 3-like (by SWS classifier): 0.994; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT00-221; grade: Grade2; Probability 1-like (by SWS classifier): 0.442; Probability 3-like (by SWS classifier): 0.558; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT01-41; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-75; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-91; grade: Grade2; Probability 1-like (by SWS classifier): 0.894; Probability 3-like (by SWS classifier): 0.106; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-113; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-121; grade: Grade2; Probability 1-like (by SWS classifier): 0.703; Probability 3-like (by SWS classifier): 0.297; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-1; grade: Grade2; Probability 1-like (by SWS classifier): 0.004; Probability 3-like (by SWS classifier): 0.996; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT00-21; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-167; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-128; grade: Grade2; Probability 1-like (by SWS classifier): 0.003; Probability 3-like (by SWS classifier): 0.997; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT00-222; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-219; grade: Grade2; Probability 1-like (by SWS classifier): 0.894; Probability 3-like (by SWS classifier): 0.106; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-226; grade: Grade2; Probability 1-like (by SWS classifier): 0.894; Probability 3-like (by SWS classifier): 0.106; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT00-200; grade: Grade2; Probability 1-like (by SWS classifier): 0.008; Probability 3-like (by SWS classifier): 0.992; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT00-210; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT01-92; grade: Grade2; Probability 1-like (by SWS classifier): 0.141; Probability 3-like (by SWS classifier): 0.859; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT01-91; grade: Grade2; Probability 1-like (by SWS classifier): 0.122; Probability 3-like (by SWS classifier): 0.878; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT01-76; grade: Grade2; Probability 1-like (by SWS classifier): 0.001; Probability 3-like (by SWS classifier): 0.999; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT01-69; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT01-68; grade: Grade2; Probability 1-like (by SWS classifier): 0.584; Probability 3-like (by SWS classifier): 0.416; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT01-45; grade: Grade2; Probability 1-like (by SWS classifier): 0.056; Probability 3-like (by SWS classifier): 0.944; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT01-65; grade: Grade2; Probability 1-like (by SWS classifier): 0.876; Probability 3-like (by SWS classifier): 0.124; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT01-27; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT01-53; grade: Grade2; Probability 1-like (by SWS classifier): 0.924; Probability 3-like (by SWS classifier): 0.076; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT01-31; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT02-11; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT01-10; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT01-03; grade: Grade2; Probability 1-like (by SWS classifier): 0.479; Probability 3-like (by SWS classifier): 0.521; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT02-23; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT02-22; grade: Grade2; Probability 1-like (by SWS classifier): 0.085; Probability 3-like (by SWS classifier): 0.915; Genetic grade signature status prediction (by SWS classifier): 2b; ', 'NUH-sample ID: NT00-165; grade: Grade2; Probability 1-like (by SWS classifier): 0.876; Probability 3-like (by SWS classifier): 0.124; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT01-16; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ', 'NUH-sample ID: NT01-08; grade: Grade2; Probability 1-like (by SWS classifier): 0.959; Probability 3-like (by SWS classifier): 0.041; Genetic grade signature status prediction (by SWS classifier): 2a; ' GSE151191 Homo sapiens 8 Expression profiling by array GPL21185 Gene expression of breast cancer stem cells. 2020-05-26 Metastatic progression remains the major cause of death in human breast cancer. Cancer cells with cancer stem cell (CSC) properties drive initiation and growth of metastases at distant sites. We have previously established the breast cancer patient-derived tumor xenograft (PDX) mouse model in which CSC marker CD44+ cancer cells formed spontaneous microscopic metastases in the liver. In this PDX mouse, the expression levels of S100A10 and its family proteins were much higher in the CD44+ cancer cells metastasized to the liver than those at the primary site. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE151191 Upregulation of S100A10 in metastasized breast cancer stem cells. Cancer science 4.751 https://doi.org/10.1111/cas.14659 {Cancer science (4.751): 10.1111/cas.14659} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA635100 https://www.ebi.ac.uk/ena/browser/view/PRJNA635100 None [Overal design]Duplicated analyses of gene expression of the cancer stem cell marker CD44-positive breast cancer patient-derived xenograft (PDX) cells collected separately from the two breast cancer PDX mice.; [Treatment]'Cancer stem cell marker CD44-positive PDX cells were collected from the PDX tumor at the primary site and the liver of PDX mice using a cell sorter.'; [Growth]'Human breast cancer patient-derived xenograft (PDX) mouse model was established by xenotransplantation of the breast cancer tissue into mammary fat pad regions of female immunodeficient NSG mice.'; [Extraction]"From the 2,000 sorted PDX cells, total RNA was extracted using RNesy mini kit (Qiagen) according to the manufacturer's instructions. Tehn, cDNA was synthesized and amplified from total RNA exploiting Ovation Pico WTA System V2 (NuGEN)."; [Cell type]'Source: ''marker: CD44+ cells; cell tyep: PDX cells; sample type: primamary tumor; ', 'marker: CD44+ cells; cell tyep: PDX cells; sample type: metastatic tumor; ' GSE132615 Homo sapiens 2 Methylation profiling by array GPL13534 ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway [methylation 450K] 2019-06-12 Genome wide DNA methylation profiling of tamoxifen-resistant(Tam-R) breast cancer cell line MCF-7. The Illumina Infinium Human Methylation 450k Bead chip was used to obtain DNA methylation profiles across approximately 450,000 CpGs. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132615 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA548633 https://www.ebi.ac.uk/ena/browser/view/PRJNA548633 None [Overal design]Genomic DNA obtained from MCF-7 where acquires tamoxifen-resistance.; [Treatment]'None'; [Growth]'None'; [Extraction]'genomic DNA was extracted and purified from MCF-7 and Tam-R MCF-7 using ZR Dyet DNA/RNA kit (Zymo research) according to standard instructions'; [Cell type]'breast epithelial''cell line: parental MCF-7; cell type: breast epithelial; gender: female; disease: adenocarcinoma; ', 'cell line: tamoxifen-resistanct MCF-7; cell type: breast epithelial; gender: female; disease: adenocarcinoma; ' GSE95598 Homo sapiens 6 Non-coding RNA profiling by high throughput sequencing GPL11154 Phenotypic and microRNA characterisation of the hidden CD24+ cell population in MCF-7 breast cancer 3D spheroid culture 2017-03-02 Introduction: In vitro 3-dimension spheroid culture has been widely used as model to enrich CD44+CD24dim/- cancer stem cells with high ALDH1 activity. However, present of the CD24+ population in the 3D spheroid also requests further attention as this side-population of cells may response differently to drug treatment comparing to the cancer stem cells. Methods: In this study, CD24+ population from the MCF-7 spheroid was sorted and subjected to spheroid formation test, stem cell markers immunofluorescence, invasion/migration test, and microRNA expression profiling. MCF-7 CD24+ cells sorted from primary spheroid reform 3D spheroid after longer period of time associated with dim expression of surface SOX-2, CD44, CD49f and Nanog comparing to the primary spheroid. Results: Remarkably, the MCF-7 CD24+ cells was found with high expression of ALDH1 protein, which subsequently contributed to higher resistant against doxorubicin and cisplatin. MicroRNA profiling has shown that absent of cancer stem cell phenotypes were contributed by the downregulation of major cancer stem cells related pathways including Hedgehog, Wnt and MAPK signalling pathways. Besides, resistance of CD24+ cells was correlated to dyregulation of cell death pathway. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95598 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA377615 https://www.ebi.ac.uk/ena/browser/view/PRJNA377615 https://www.ncbi.nlm.nih.gov/sra?term=SRP100970 [Overal design]miRNA profiles of MCF-7 CD24+ cells spheroids and monolayer cultures were generated in triplicates by deep sequencing using TruSeq small RNA illumina; [Treatment]'None'; [Growth]'The monolayer and sorted CD24+ spheroid cells were cultured in tissue culture-treated flasks and as suspension spheroid respectively. Both are maintained in 5% CO2 humidified incubator.'; [Extraction]'Total RNA with retention of small RNAs from the cells were extracted using miRNAeasy\nRNA libraries were prepared for sequencing using standard Illumina protocols\nIllumina Tru-seq small RNA'; [Cell type]'Source: ''cell source: Estrogen-dependent human breast adenocarcinoma; culture condition: Monolayer; culture dimension: 2D; cell line: MCF-7; ', 'cell source: Estrogen-dependent human breast adenocarcinoma; culture condition: Sorted CD24+ spheroid; culture dimension: 3D; cell line: MCF-7; ' GSE41692 Homo sapiens 26 Expression profiling by array GPL6884 5AZA-induced Gene Expression in Human Breast Cancer Cell Lines and Benign Primary Mammary Epithelial Cell Cultures 2012-10-18 The goal of this experiment was to identify genes that were expressed at higher levels in benign human mammary epithelial cells than in breast cancer cell lines and that were induced by 5AZA treatment in breast cancer cell lines. Six breast cancer cell lines were selected for demethylation studies based on known tumor suppressor gene expression regulation by promoter region hypermethylation: HCC1569 (CCND2), HCC1954 (SCGB3A1, APC, RASSF1A), MCF-7 (RAR-beta2), MDA-MB-231 (ESR1), UACC3199 (BRCA1), and BT-549 (hypermethylator phenotype). Other than MCF10A we specifically avoided immortalized benign human mammary epithelial cell lines for this experiment as these cells frequently show tumor suppressor gene methylation (e.g. p16) and gene expression profiles that are intermediate between normal breast epithelial cells and breast cancer. Instead, we opted to test six first-passage benign human mammary epithelial cell cultures (HME) generated in serum-free media from small fragments of normal breast tissue obtained from young women undergoing fibroadenoma excision. The 5AZA dose (0.5 microM) was selected based on evaluation of growth curves and induction of BNC1, SERPINB, and TKTL1 gene expression measured by RT-PCR in benign and malignant cells. The breast cancer cell lines, HME cultures, and MC10A cells were treated with 0.5 microM 5AZA (Sigma-Aldrich, St. Louis, MO) in DMSO or DMSO alone for six days after which the cells were harvested, and RNA prepared using the Illumina TotalPrep kit (AMIL1791, Life Technologies, Grand Island, NY). Whole genome expression was assessed using the Illumina HumanWG-6-v3 chip https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41692 Identification of breast cancer DNA methylation markers optimized for fine-needle aspiration samples. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 5.057 https://doi.org/10.1158/1055-9965.EPI-13-0208 {Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology (5.057): 10.1158/1055-9965.EPI-13-0208} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA177955 https://www.ebi.ac.uk/ena/browser/view/PRJNA177955 None [Overal design]Gene expression was evaluated in 6 breast cancer cell lines, 6 primary breast epithelial cell cultures, and MCF10A cells after 6 days in DMSO or DMSO plus 0.5 microM 5AZA.; [Treatment]'The breast cancer cell lines, HME cultures, and MC10A cells were treated with 0.5 microM 5AZA (Sigma-Aldrich, St. Louis, MO) in DMSO or DMSO alone for six days after which the cells were harvested.'; [Growth]'None'; [Extraction]'RNA prepared using the Illumina TotalPrep kit (AMIL1791, Life Technologies, Grand Island, NY).'; [Cell type]'primary culture', 'cell line''Sex: female; tissue: breast; disease status: benign; cell type: primary culture; ', 'Sex: female; tissue: breast; disease status: immortalized; cell type: cell line; ', 'Sex: female; tissue: breast; disease status: maligant; cell type: cell line; ' GSE33450 Homo sapiens 36 Methylation profiling by array; Expression profiling by array GPL14550; GPL14835 DNA hypermethylation and gene expression in breast cancer: breast cancer tissues vs. normal breast tissues 2011-11-03 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE33450 Screening of significantly hypermethylated genes in breast cancer using microarray-based methylated-CpG island recovery assay and identification of their expression levels. International journal of oncology 3.571 https://doi.org/10.3892/ijo.2012.1464 {International journal of oncology (3.571): 10.3892/ijo.2012.1464} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA148709 https://www.ebi.ac.uk/ena/browser/view/PRJNA148709 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA was isolated from fresh frozen tissues using standard phenol/chloroform method.', 'Total RNA from fresh breast tumor and non-tumor tissues was extracted using Dr.P Kit (Biochain, Hayward, CA, USA), according to the manufacturer’s instructions.'; [Cell type]'Source: ''tissue: breast cancer; patient: 1; age: 40 years; sample type: methylated; ', 'tissue: breast cancer; patient: 1; sample type: Input; ', 'tissue: breast cancer; patient: 2; age: 40 years; sample type: methylated; ', 'tissue: breast cancer; patient: 2; sample type: Input; ', 'tissue: breast cancer; patient: 3; age: 43 years; sample type: methylated; ', 'tissue: breast cancer; patient: 3; sample type: Input; ', 'tissue: breast cancer; patient: 4; age: 57 years; sample type: methylated; ', 'tissue: breast cancer; patient: 4; sample type: Input; ', 'tissue: normal breast; patient: 1; age: 29 years; sample type: methylated; ', 'tissue: normal breast; patient: 1; sample type: Input; ', 'tissue: normal breast; patient: 2; age: 37 years; sample type: methylated; ', 'tissue: normal breast; patient: 2; sample type: Input; ', 'tissue: normal breast; patient: 3; age: 33 years; sample type: methylated; ', 'tissue: normal breast; patient: 3; sample type: Input; ', 'tissue: normal breast; patient: 4; age: 27 years; sample type: methylated; ', 'tissue: normal breast; patient: 4; sample type: Input; ', 'tissue: breast cancer; patient: 5; age: 55 years; sample type: methylated; ', 'tissue: breast cancer; patient: 5; sample type: Input; ', 'tissue: breast cancer; patient: 6; age: 49 years; sample type: methylated; ', 'tissue: breast cancer; patient: 6; sample type: Input; ', 'tissue: breast cancer; patient: 7; age: 44 years; sample type: methylated; ', 'tissue: breast cancer; patient: 7; sample type: Input; ', 'tissue: breast cancer; patient: 8; age: 43 years; sample type: methylated; ', 'tissue: breast cancer; patient: 8; sample type: Input; ', 'tissue: breast cancer; patient: 9; age: 44 years; sample type: methylated; ', 'tissue: breast cancer; patient: 9; sample type: Input; ', 'tissue: breast cancer; patient: 10; age: 49 years; sample type: methylated; ', 'tissue: breast cancer; patient: 10; sample type: Input; ', 'tissue: normal breast; patient: 5; age: 51 years; sample type: methylated; ', 'tissue: normal breast; patient: 5; sample type: Input; ', 'tissue: normal breast; patient: 6; age: 39 years; sample type: methylated; ', 'tissue: normal breast; patient: 6; sample type: Input; ', 'tissue: normal breast; patient: 7; age: 35 years; sample type: methylated; ', 'tissue: normal breast; patient: 7; sample type: Input; ', 'tissue: normal breast; patient: 8; age: 30 years; sample type: methylated; ', 'tissue: normal breast; patient: 8; sample type: Input; ', 'tissue: normal breast; patient: 9; age: 26 years; sample type: methylated; ', 'tissue: normal breast; patient: 9; sample type: Input; ', 'tissue: normal breast; patient: 10; age: 33 years; sample type: methylated; ', 'tissue: normal breast; patient: 10; sample type: Input; ', 'tissue: breast cancer; gender: Female; age: 40 years; ', 'tissue: breast cancer; gender: Female; age: 43 years; ', 'tissue: breast cancer; gender: Female; age: 57 years; ', 'tissue: normal breast; gender: Female; age: 33 years; ', 'tissue: normal breast; gender: Female; age: 29 years; ', 'tissue: normal breast; gender: Female; age: NA; ', 'tissue: breast cancer; gender: Female; age: 55 years; ', 'tissue: breast cancer; gender: Female; age: 49 years; ', 'tissue: breast cancer; gender: Female; age: 44 years; ', 'tissue: normal breast; gender: Female; age: 51 years; ', 'tissue: normal breast; gender: Female; age: 39 years; ' GSE110912 Mus musculus 18 Expression profiling by high throughput sequencing GPL17021 Effect of TGFb1 treatment and WISP1 overexpression on 4T1 breast cancer cells 2018-02-21 This study set out to identify TGFb1 transcriptional targets in breast cancer cells. 4T1 breast cancer cells were treated with TGFb1 for 24h and transcripts that were significantly regulated were identified. Wisp1 was identified as one of the genes most highly upregulated by TGFb1. To identify the transcriptional targets of Wisp1, 4T1 cells were then virally transduced to increase Wisp1 expression. The gene expression profiles of Wisp1-overexpressing 4T1 cells were determined and revealed that Wisp1 overexpression does not result in major gene expression changes in 4T1 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE110912 The tumor cell-secreted matricellular protein WISP1 drives pro-metastatic collagen linearization. The EMBO journal 11.227 https://doi.org/10.15252/embj.2018101302 {The EMBO journal (11.227): 10.15252/embj.2018101302} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA434801 https://www.ebi.ac.uk/ena/browser/view/PRJNA434801 https://www.ncbi.nlm.nih.gov/sra?term=SRP133203 [Overal design]mRNA profiles from 4T1 breast cancer cells treated with TGFb1 or with Wisp1 overexpression were examined.; [Treatment]'Medium was changed to fresh RPMI and RNA was extracted after 24h', 'Medium was changed to fresh RPMI + 2 ng/mL recombinant human TGFb1 (R&D systems) and RNA was extracted after 24h', '4T1 cells were transduced with an empty lentiviral vector and selected with puromycin to establish a stable cell line. The stable cell line was grown in tissue culture-treated plastic dishes. RNA was collected from subconfluent cultures.', '4T1 cells were transduced with a lentiviral vector expressing Wisp1 and selected with puromycin to establish a stable cell line. The stable cell line was grown in tissue culture-treated plastic dishes. RNA was collected from subconfluent cultures.', '4T1 cells were transduced with an empty lentiviral vector and selected with puromycin to establish a stable cell line. The stable cell line was grown in Collagen type I-coated plastic dishes. RNA was collected from subconfluent cultures.', '4T1 cells were transduced with a lentiviral vector expressing Wisp1 and selected with puromycin to establish a stable cell line. The stable cell line was grown in Collagen type I-coated plastic dishes. RNA was collected from subconfluent cultures.'; [Growth]'4T1 breast cancer cells were cultivated in RPMI 10% FCS, 1% Penicillin/Streptomycin.'; [Extraction]'RNA was isolated from total cell lysates with the Rneasy Plus Mini kit (Qiagen).\nTotal RNA was polyA enriched and prepared for RNA sequencing with TruSeq stranded mRNA library prep kit (Illumina).'; [Cell type]'Source: ''tissue: 4T1 breast cancer cells; treatment class: 4T1; ', 'tissue: 4T1 breast cancer cells; treatment class: 4T1+TGFb; ', 'tissue: 4T1 breast cancer cells; treatment class: 4T1-EV; ', 'tissue: 4T1 breast cancer cells; treatment class: 4T1-Wisp1; ', 'tissue: 4T1 breast cancer cells; treatment class: Col I-4T1-EV; ', 'tissue: 4T1 breast cancer cells; treatment class: Col I-4T1-Wisp1; ' GSE142011 Homo sapiens 63 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Chromatin state and Transcriptional regulation in MCF-7 breast cancer cells treated with proteasome inhibitor MG132 2019-12-13 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE142011 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA595560 https://www.ebi.ac.uk/ena/browser/view/PRJNA595560 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'MCF-7 cells were grown in a humidified incubator at 37°C with 5% CO2 in MEM, supplemented with 10% fetal bovine serum 100 μg/mL penicillin/streptomycin, 2 mM glutamine and 10 mM HEPES. For MG132 treatment, cells were seeded overnight in phenol red-free MEM supplemented with 5% charcoal-stripped calf serum and 2 mM glutamate. Next day, cells were treated with, vehicle (DMSO) or 1uM MG132 for 4 or 24 hours.'; [Extraction]'MNase digested ChIP DNA was collected from MCF7 cells cultured in phenol red free MEM, supplemented with charcoal stripped serum and containing 0.1% DMSO or 1 uM MG132 for 4 or 24H. Cells were incubated for 4 or 24 hours at 37 ºC in a humidified incubator with 5% CO2.\nNEXTFlex Rapid DNA-Seq Kit BIOO Scientific Cat#5144-02', 'ChIP DNA was collected from MCF7 cells cultured in phenol red free MEM, supplemented with charcoal stripped serum and containing 0.1% DMSO or 1 uM MG132 for 4 or 24H. Cells were incubated for 4 or 24 hours at 37 ºC in a humidified incubator with 5% CO2.\nNEXTFlex Rapid DNA-Seq Kit BIOO Scientific Cat#5144-02'; [Cell type]'breast cancer cells''cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: H3K4me3; chip antibody info.: Active Motif Cat#39159; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: H3K36me3; chip antibody info.: Abcam Ab9050; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: H3K27ac; chip antibody info.: Abcam Ab4729; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: H3K122ac; chip antibody info.: Abcam Ab33309; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: H3K914ac; chip antibody info.: Cell Signaling Technology CST#9677; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: H3; chip antibody info.: Abcam Ab1791; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: none (input); ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: H3K4me3; chip antibody info.: Active Motif Cat#39159; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: H3K36me3; chip antibody info.: Abcam Ab9050; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: H3K27ac; chip antibody info.: Abcam Ab4729; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: H3K122ac; chip antibody info.: Abcam Ab33309; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: H3K914ac; chip antibody info.: Cell Signaling Technology CST#9677; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: H3; chip antibody info.: Abcam Ab1791; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: none (input); ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: H3K4me3; chip antibody info.: Active Motif Cat#39159; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: H3K36me3; chip antibody info.: Abcam Ab9050; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: H3K27ac; chip antibody info.: Abcam Ab4729; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: H3K122ac; chip antibody info.: Abcam Ab33309; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: H3K914ac; chip antibody info.: Cell Signaling Technology CST#9677; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: allreps; chip antibody info.: Abcam Ab1791; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: allreps; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: PolIISer2; chip antibody info.: Abcam Ab5095; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: PolIISer5; chip antibody info.: Abcam Ab5131; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: PolII8WG16; chip antibody info.: Santa Cruz Biotechnology Sc-56767; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: PolIISer2; chip antibody info.: Abcam Ab5095; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: PolIISer5; chip antibody info.: Abcam Ab5131; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: PolII8WG16; chip antibody info.: Santa Cruz Biotechnology Sc-56767; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: PolIISer2; chip antibody info.: Abcam Ab5095; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: PolIISer5; chip antibody info.: Abcam Ab5131; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: PolII8WG16; chip antibody info.: Santa Cruz Biotechnology Sc-56767; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: none (input); ' GSE164955 Mus musculus 24 Expression profiling by array GPL13912 Tumor-Derived Thymic Stromal Lymphopoietin Expands Bone Marrow B-cell Precursors in Circulation to Support Metastasis 2021-01-16 Immature B cells in the bone marrow emigrate into the spleen during adult lymphopoiesis. Here, we report that emigration is shifted to earlier B-cell stages in mice with orthotopic breast cancer, spontaneous ovarian cancer, and possibly in human breast carcinoma. Using mouse and human bone marrow aspirates and mouse models challenged with highly metastatic 4T1 breast cancer cells, we demonstrated that this was the result of secretion of thymic stromal lymphopoietin (TSLP) by cancer cells. First, TSLP downregulated surface expression of bone marrow (BM) retention receptors CXCR4 and VLA4 in B-cell precursors, increasing their motility and, presumably, emigration. Then, TSLP supported peripheral survival and proliferation of BM B-cell precursors such as pre-B–like cells. 4T1 cancer cells used the increased pool of circulating pre-B–like cells to generate metastasis-supporting regulatory B cells. As such, the loss of TSLP expression in cancer cells alone or TSLPR deficiency in B cells blocked both accumulation of pre-B–like cells in circulation and cancer metastasis, implying that the pre-B cell–TSLP axis can be an attractive therapeutic target. Significance: Cancer cells induce premature emigration of B-cell precursors from the bone marrow to generate regulatory B cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE164955 Tumor-Derived Thymic Stromal Lymphopoietin Expands Bone Marrow B-cell Precursors in Circulation to Support Metastasis. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-19-1058 {Cancer research (8.378): 10.1158/0008-5472.CAN-19-1058} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA692612 https://www.ebi.ac.uk/ena/browser/view/PRJNA692612 None [Overal design]CD19+ B cells were FACS sorted from spleens of control naive or 4T1 cancer-bearing mice (female, BALB/c mice, N=3 per experimental group). CD19+ B cells of tumor-baring mice were further sorted into CD23+ (follicular B cells) or CD23-, CD25- (pro-B cell) or CD23-, CD25+ (pre-B cell) populations. CD19+ B cells from naïve mice were in vitro stimulated with 4T1 or 4T1-PE cancer cell conditioned media for 2 days, as described in Olkhanud et al., Cancer Research, 2011, to generate TU4T1 and TU4T1_PE cells, respectively. In addition, CD19+ B cells from naïve mice were in vitro stimulated with BAFF/Blys or with 4T1-P; [Treatment]'None'; [Growth]"Animal protocols were approved by the Institutional Animal Care and Use Committee review board and performed under the Guide for the Care and Use of Laboratory Animals (NIH Publication No. 86-23, 1985). Mice (5–20 weeks of age, females) were housed in a pathogen-free environment at the National Institute on Aging (NIA, Baltimore, MD). BALB/cj mice were purchased from The Jackson Laboratory, and murine breast cancer 4T1 from ATCC. Flow cytometry Antibodies were purchased from BioLegend, eBioscience, BD Biosciences, and R&D Systems.For FACS or magnetic sorting, murine B cells were predepleted of lineage-positive (Linþ) cells (Gr1/CD11b/CD3e/CD8a/TER119/ CD49b) with biotin-labeled antibody and EasySep Mouse Streptavidin RapidSpheres Isolation Kit (StemCell Technologies) or PE-labeled antibody and anti-PE microbeads (Miltenyi Biotec) following the manufacturer's instructions. B cells were positively sorted with anti-CD19-PE using AutoMACS Pro (Miltenyi Biotec) and then further enriched using relevant antibody in MoFlo XDP (Beckman Coulter, Inc.)."; [Extraction]"RNA was isolated with RNeasy Plus Micro Kit (QIAGEN) according to the manufacturer's instructions. RNA concentration and quality was assayed on an RNA6000 Bioanalyzer chip (Agilent)."; [Cell type]'Source: ''tissue: Naive spleen; Sex: Female; age: 5-20 weeks; treatment: control; strain: BALB/cj; ', 'tissue: Tumor-bearing spleen; Sex: Female; age: 5-20 weeks; treatment: 4T1; strain: BALB/cj; ', 'tissue: tBreg; Sex: Female; age: 5-20 weeks; treatment: control; strain: BALB/cj; ', 'tissue: tBreg; Sex: Female; age: 5-20 weeks; treatment: 4T1; strain: BALB/cj; ', 'tissue: tBreg; Sex: Female; age: 5-20 weeks; treatment: 4T1_PE; strain: BALB/cj; ', 'tissue: tBreg; Sex: Female; age: 5-20 weeks; treatment: 4T1_PE_LPS; strain: BALB/cj; ' GSE74981 Homo sapiens 30 Expression profiling by high throughput sequencing GPL18573 Next generation sequencing to elucidate the novel function of RORC (RORgamma) in breast cancer 2015-11-13 Exploring the novel role of RORC (RORgamma) in breast cancer, utilizing NEXTseq with genetic gain and loss of function and pharmacological treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74981 The Nuclear Receptor, RORγ, Regulates Pathways Necessary for Breast Cancer Metastasis. EBioMedicine 6.680 https://doi.org/10.1016/j.ebiom.2016.02.028 {EBioMedicine (6.680): 10.1016/j.ebiom.2016.02.028} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA302118 https://www.ebi.ac.uk/ena/browser/view/PRJNA302118 https://www.ncbi.nlm.nih.gov/sra?term=SRP066204 [Overal design]For loss of function, control-siRNA or RORC-siRNA was transfected for 48h in three cell lines (MCF-7, T-47D and MDA-MB-231). For gain of function, CMV-empty or CMV-RORC was transfected for 48h in MDA-MB-231 cells. Furthermore, the selective RORC antagonist, SR2211 was utilized. MCF-7 cells were treated either DMSO or SR2211 (5uM) for 24h. Total RNA was extracted with the RNeasy kit. NEXTseq was performed for transcriptome analysis.; [Treatment]'To obtain RORC knockdown, Control-siRNA or RORC-siRNA was transfected for 48h as described. For over-expression, CMV-empty or CMV-RORC was transfected for 48h. For antagonization of RORC protein, selective inhibitor (SR2211) was treated for 24h in MCF-7 and data was compared to DMSO treated cells.'; [Growth]'Cell lines were maintained in complete media as described.'; [Extraction]'RNA was harvested using Trizol reagent. Illumina TruSeq RNA Sample Prep Kit (Cat. no. RS-122-2101 and RS-122-2102) was used for the construction of sequencing libraries.\nRNA libraries were prepared for sequencing using standard Illumina protocols (Part oo. 15031047 Rev. E October 2013).'; [Cell type]'Source: ''cell line: breast cancer cell line MCF-7; breast cancer subtype: Luminal type; er status: ER+ve; treatment: control-siRNA; ', 'cell line: breast cancer cell line MCF-7; breast cancer subtype: Luminal type; er status: ER+ve; treatment: RORC-siRNA; ', 'cell line: breast cancer cell line T-47D; breast cancer subtype: Luminal type; er status: ER+ve; treatment: control-siRNA; ', 'cell line: breast cancer cell line T-47D; breast cancer subtype: Luminal type; er status: ER+ve; treatment: RORC-siRNA; ', 'cell line: breast cancer cell line MDA-MB-231; breast cancer subtype: Basal type; er status: ER-ve; treatment: control-siRNA; ', 'cell line: breast cancer cell line MDA-MB-231; breast cancer subtype: Basal type; er status: ER-ve; treatment: RORC-siRNA; ', 'cell line: breast cancer cell line MDA-MB-231; breast cancer subtype: Basal type; er status: ER-ve; treatment: CMV-empty; ', 'cell line: breast cancer cell line MDA-MB-231; breast cancer subtype: Basal type; er status: ER-ve; treatment: CMV-RORC; ', 'cell line: breast cancer cell line MCF-7; breast cancer subtype: Luminal type; er status: ER+ve; treatment: DMSO; ', 'cell line: breast cancer cell line MCF-7; breast cancer subtype: Luminal type; er status: ER+ve; treatment: SR2211; ' GSE148673 Homo sapiens 13 Expression profiling by high throughput sequencing GPL24676 Delineating copy number and clonal substructure in human tumors from single-cell transcriptomes 2020-04-14 Single-cell transcriptomic analysis is widely used to study human tumors. However it remains challenging to distinguish normal cell types in the tumor microenvironment from malignant cells and to resolve clonal substructure within the tumor. To address these challenges, we developed an integrative Bayesian segmentation approach called CopyKAT (Copynumber Karyotyping of Aneuploid Tumors) to estimate genomic copy number profiles at an average genomic resolution of 5Mb from read depth in high-throughput scRNA-seq data. We applied CopyKAT to analyze 46,501 single cells from 21 tumors, including triple-negative breast cancer, pancreatic ductal adenocarcinomas, anaplastic thyroid cancer, invasive ductal carcinoma and glioblastoma to accurately (98%) distinguish cancer cells from normal cell types. In three breast tumors, CopyKAT resolved clonal subpopulations that differed in the expression of cancer genes such as KRAS and signatures including EMT, DNA repair, apoptosis and hypoxia. These data show that CopyKAT can aid the analysis of scRNA-seq data in a variety of solid human tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148673 Delineating copy number and clonal substructure in human tumors from single-cell transcriptomes. Nature biotechnology 31.864 https://doi.org/10.1038/s41587-020-00795-2 {Nature biotechnology (31.864): 10.1038/s41587-020-00795-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA625321 https://www.ebi.ac.uk/ena/browser/view/PRJNA625321 https://www.ncbi.nlm.nih.gov/sra?term=SRP256378 [Overal design]We calculated single cell copy number profiles and inferred clonal structures of tumor cells from scRNAseq data using COPYKAT.; [Treatment]'samples are collected before treatment'; [Growth]'Single cell suspensions are made from fresh tumors'; [Extraction]"RNAs are extracted from single cell suspensions\nSingle cell capture, barcoding and library preparation was performed by following the 10X Genomics Single Cell Chromium 3’ protocol (PN-1000075)\nsingle cell 3' RNAseq", 'RNAs are extracted from single cell suspensions\nSingle cell capture, barcoding and library preparation was performed by following the 10X Genomics Single Cell Chromium 3’ protocol (PN-1000075)'; [Cell type]'Source: ''tissue: fresh tumor; sample type: biopsy; ', 'tissue: fresh tumor; sample type: surgical sample; ' GSE41198 Homo sapiens 22 Expression profiling by array GPL1352 Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 4 stroma) 2012-09-27 We used gene expression profiling of human DCIS and IBC to discover uniquely expressed genes that may also regulate progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41198 Differentially expressed genes regulating the progression of ductal carcinoma in situ to invasive breast cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-12-0636 {Cancer research (8.378): 10.1158/0008-5472.CAN-12-0636} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA176238 https://www.ebi.ac.uk/ena/browser/view/PRJNA176238 None [Overal design]RNA from human samples were extracted, purified, amplified, and evaluated for gene expression using Affymetrix U133-X3P gene expression arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'laser capture microdissection of target cells (Stromal) to estimated >95% total cells using Ambion RNA extraction kit'; [Cell type]'stromal''tissue: Breast; cell type: stromal; disease state: ductal carcinoma in situ; ', 'tissue: Breast; cell type: stromal; disease state: invasive breast cancer; ' GSE165273 Mus musculus 24 Expression profiling by high throughput sequencing GPL17021 Creatine mediated crosstalk between adipocytes and cancer cells regulates obesity-driven breast cancer 2021-01-21 Obesity is a major risk factor for adverse outcomes in breast cancer. Maguire, Ackerman et al. reveal Gatm and Acsbg1 as molecular regulators of obesity-driven breast cancer progression. They further show that in obesity creatine is a key metabolite in the crosstalk between adipocytes and breast tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE165273 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA693853 https://www.ebi.ac.uk/ena/browser/view/PRJNA693853 https://www.ncbi.nlm.nih.gov/sra?term=SRP302740 [Overal design]Examining 4th mammary subcutaneous adiose tissue in lean and obese mice, near and far from the breast tumor; [Treatment]'None'; [Growth]'None'; [Extraction]'flash frozen adipose, total RNA was exracted, DNAse protocol was used\nRNA libraries were prepared for sequencing using standard Illumina protocols, rRNA depletion'; [Cell type]'Source: ''strain: C57BL/6; diet: Chow; sample type: contralateral; ', 'strain: C57BL/6; diet: Chow; sample type: peritumoral; ', 'strain: C57BL/6; diet: HFD; sample type: contralateral; ', 'strain: C57BL/6; diet: HFD; sample type: peritumoral; ', 'strain: C57BL/6; diet: Chow; sample type: no tumor; ', 'strain: C57BL/6; diet: HFD; sample type: no tumor; ' GSE22840 Homo sapiens 42 Expression profiling by array; Genome variation profiling by SNP array GPL570; GPL3720 Integration of transcript expression, copy number and LOH analysis of infiltrating ductal carcinoma of the breast 2010-07-08 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22840 Integration of transcript expression, copy number and LOH analysis of infiltrating ductal carcinoma of the breast. BMC cancer 2.933 https://doi.org/10.1186/1471-2407-10-460 {BMC cancer (2.933): 10.1186/1471-2407-10-460} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA128043 https://www.ebi.ac.uk/ena/browser/view/PRJNA128043 None [Overal design]Refer to individual Series; [Treatment]'N/A.'; [Growth]'N/A.'; [Extraction]'Tissues microdissected for 80% tumor, total RNA extracted with TRIzol, quality assessed on Bioanalyzer.', 'Qiagen DNA extraction.'; [Cell type]'Source: ''tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 1; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 2; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 4; ', 'tissue: breast; tissue type: normal; patient: 4; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 5; ', 'tissue: breast cancer; tissue type: node metastasis; patient: 6; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 7; ', 'tissue: breast; tissue type: normal; patient: 28; ', 'tissue: breast; tissue type: normal; patient: 29; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 14; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 15; ', 'tissue: breast; tissue type: normal; patient: 15; ', 'tissue: breast cancer; tissue type: node metastasis; patient: 18; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 20; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 22; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 24; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 25; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 26; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 27; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 3; ', 'tissue: breast cancer; tissue type: nodal metastasis; patient: 6; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 8; ', 'tissue: breast cancer; tissue type: nodal metastasis; patient: 9; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 9; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 10; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 16; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 17; ', 'tissue: breast cancer; tissue type: nodal metastasis; patient: 18; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 19; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 21; ', 'tissue: breast cancer; tissue type: infiltrating ductal carcinoma (IDC); patient: 23; ' GSE9662 Homo sapiens 24 Expression profiling by array GPL96 Gene expression analysis of pre-defined sets of neoplastic tissues 2007-11-21 To identify a group of genes, characteristic of a single neoplasia and determinant for the risk to relapse, we have performed gene expression analysis of ductal breast carcinoma samples using Affymetrix oligonucletide microarray (HU133A). Biopses from 60 patients, 30 good prognosis (desease free from six to ten years after surgical treatment) and 30 poor prognosis, have been analyzed. From each group we have created six homogeneous pools to show, during the analysis, only genes expressed in a greatly different way. A reduced number of cases has been used to avoid dilution of genes expressed only in few samples. Analysis have identified 77 candidate genes with a specific ontological distribution that contained some genes that were linked to breast cancer by previous studies. Microarray results validation has been performed by real-time PCR analysis on 127 single cases of breast cancer. Gene function study and literature data allow to define our candidate genes as potential markers of prognosis. Keywords: Breast cancer gene expression analysis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE9662 Identification of new genes associated with breast cancer progression by gene expression analysis of predefined sets of neoplastic tissues. International journal of cancer 4.982 https://doi.org/10.1002/ijc.23660 {International journal of cancer (4.982): 10.1002/ijc.23660} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA103537 https://www.ebi.ac.uk/ena/browser/view/PRJNA103537 None [Overal design]From a group of 130 frozen tumor samples, 30 cases of ductal invasive carcinoma with recurrence within 72 months from surgery (high-risk) and 30 without recurrence (low-risk) were selected for microarray analysis. From each group, 6 RNA pools of 5 samples each were prepared and analyzed on GeneChip Human Genome U133A oligonucleotide microarrays. Hybridizations were performed in technical duplicates, in two experimental sessions.; [Treatment]'None'; [Growth]'None'; [Extraction]"RNA was isolated with Concert Cytoplasmic RNA Reagent (Invitrogen Corporation) from 20 to 50 mg tumor tissues, according to the manufacturer's guidelines. Frozen tumors were placed in this reagent and homogenized using a ball mill (MM200, Retsch, Düsseldorf, Germany). 10 µg aliquots of total RNA was treated with DNase I, using a commercially available kit (DNA free, Ambion, Inc., Austin, TX) to eliminate genomic DNA contamination. The quantity and quality of the RNA samples were determined using the Agilent 2100 Bioanalyzer and the RNA 6000 Nano Assay kit (Agilent Technologies, Palo Alto, CA)."; [Cell type]'Source: ''Sample name: pool 1 replicate a; ', 'Sample name: pool 1 replicate b; ', 'Sample name: pool 3 replicate a; ', 'Sample name: pool 3 replicate b; ', 'Sample name: pool 5 replicate a; ', 'Sample name: pool 5 replicate b; ', 'Sample name: pool 7 replicate a; ', 'Sample name: pool 7 replicate b; ', 'Sample name: pool 9 replicate a; ', 'Sample name: pool 9 replicate b; ', 'Sample name: pool 11 replicate a; ', 'Sample name: pool 11 replicate b; ', 'Sample name: pool 2 replicate a; ', 'Sample name: pool 2 replicate b; ', 'Sample name: pool 4 replicate a; ', 'Sample name: pool 4 replicate b; ', 'Sample name: pool 6 replicate a; ', 'Sample name: pool 6 replicate b; ', 'Sample name: pool 8 replicate a; ', 'Sample name: pool 8 replicate b; ', 'Sample name: pool 10 replicate a; ', 'Sample name: pool 10 replicate b; ', 'Sample name: pool 12 replicate a; ', 'Sample name: pool 12 replicate b; ' GSE110117 Homo sapiens 2 Expression profiling by array GPL10558 Effect of cold atmospheric plasma (CAP) on MCF-7 breast cancer cell (Illumina HumanHT-12 V4.0 beadchip) 2018-02-05 genom-wide expression profiling of MCF-7, MCF-7 and CAP-treated MCF-7 cell. In result, cold atmospheric plasma different effect the CAP-treated MCF-7 breast cancer cell. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE110117 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA432910 https://www.ebi.ac.uk/ena/browser/view/PRJNA432910 None [Overal design]Total RNA is obtained from MCF-7 and CAP treated MCF-7.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted and purified from MCF-10A using ZR Dyet DNA/RNA kit (Zymo research) according'; [Cell type]'breast cancer epithelial cell''cell line: MCF-7; cell type: breast cancer epithelial cell; treated with: none (control); ', 'cell line: MCF-7; cell type: breast cancer epithelial cell; treated with: Cold atmospheric plasma (CAP); ' GSE102907 Homo sapiens 61 Expression profiling by array GPL570 Transcriptome analysis by expression microarrays of breast cancer derived from the Cancer Institute Hospital of Japanese Foundation for Cancer Research. 2017-08-22 We performed the expression microarray experiments for mRNA of breast cancer tissue. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE102907 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA399252 https://www.ebi.ac.uk/ena/browser/view/PRJNA399252 None [Overal design]Messenger RNA were extracted from primary tumor of 29 breast cancer patients, hybridized and scanned with Affymetrix Human Genome GeneChip U133 Plus 2.0 array.; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was extracted using QIAGEN RNeasy mini kit following manufacturer's instruction."; [Cell type]'Source: ''age: 40-44; gender: female; ', 'age: 30-34; gender: female; ', 'age: 50-54; gender: female; ', 'age: 45-49; gender: female; ', 'age: 70-74; gender: female; ', 'age: 55-59; gender: female; ', 'age: 75-79; gender: female; ', 'age: 60-64; gender: female; ', 'age: 35-39; gender: female; ', 'age: 45-50; gender: female; ' GSE162815 Mus musculus 64 Expression profiling by high throughput sequencing GPL19057 Abi1 gene dose study in PyVT breast tumors 2020-12-07 To execute RNA-Seq analysis in PyMT tumors with and without Abi1 gene in heterozygous and homozygous state https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE162815 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA683072 https://www.ebi.ac.uk/ena/browser/view/PRJNA683072 https://www.ncbi.nlm.nih.gov/sra?term=SRP296845 [Overal design]64 total samples were analyzed: PyMT-positive animals, with wild-type Abi1 or homozygous or heterozygous Abi1 loss. Multiple sections from each tumor were analyzed in this cohort.; [Treatment]'None'; [Growth]'PyMT males were bred to homozygous Abi1 females to generate PyMT;Abi1 (fl/wt) males, which were then backcrossed to homozygous Abi1 females. The resulting progeny were used to establish PyMT animals with heterozygous or homozygous Abi1 floxed, with and without MMTV-cre expression'; [Extraction]'Tissue was homogenized in QIAzol reagent with a Qiagen TissueRuptor, and RNA was extracted using QIAzol/choloroform phase separation followed by purification with Qiagen RNeasy Mini Columns\nIllumina TruSeq Stranded Total RNA Kit with RiboZer Gold H/M/R'; [Cell type]'Source: ''date: 190617; mouse_id: G144; tumor_id: 6; lane: L001; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190617; mouse_id: G144; tumor_id: 6; lane: L002; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190617; mouse_id: G144; tumor_id: 6; lane: L003; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190617; mouse_id: G144; tumor_id: 6; lane: L004; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190617; mouse_id: G144; tumor_id: 8; lane: L001; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190617; mouse_id: G144; tumor_id: 8; lane: L002; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190617; mouse_id: G144; tumor_id: 8; lane: L003; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190617; mouse_id: G144; tumor_id: 8; lane: L004; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190617; mouse_id: G164; tumor_id: 3; lane: L001; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190617; mouse_id: G164; tumor_id: 3; lane: L002; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190617; mouse_id: G164; tumor_id: 3; lane: L003; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190617; mouse_id: G164; tumor_id: 3; lane: L004; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190617; mouse_id: G164; tumor_id: 6; lane: L001; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190617; mouse_id: G164; tumor_id: 6; lane: L002; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190617; mouse_id: G164; tumor_id: 6; lane: L003; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190617; mouse_id: G164; tumor_id: 6; lane: L004; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190617; mouse_id: G174; tumor_id: 1; lane: L001; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190617; mouse_id: G174; tumor_id: 1; lane: L002; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190617; mouse_id: G174; tumor_id: 1; lane: L003; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190617; mouse_id: G174; tumor_id: 1; lane: L004; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190617; mouse_id: G174; tumor_id: 6; lane: L001; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190617; mouse_id: G174; tumor_id: 6; lane: L002; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190617; mouse_id: G174; tumor_id: 6; lane: L003; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190617; mouse_id: G174; tumor_id: 6; lane: L004; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190617; mouse_id: G184; tumor_id: 6; lane: L001; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190617; mouse_id: G184; tumor_id: 6; lane: L002; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190617; mouse_id: G184; tumor_id: 6; lane: L003; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190617; mouse_id: G184; tumor_id: 6; lane: L004; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190617; mouse_id: G184; tumor_id: 9; lane: L001; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190617; mouse_id: G184; tumor_id: 9; lane: L002; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190617; mouse_id: G184; tumor_id: 9; lane: L003; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190617; mouse_id: G184; tumor_id: 9; lane: L004; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190618; mouse_id: G144; tumor_id: 6; lane: L001; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190618; mouse_id: G144; tumor_id: 6; lane: L002; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190618; mouse_id: G144; tumor_id: 6; lane: L003; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190618; mouse_id: G144; tumor_id: 6; lane: L004; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190618; mouse_id: G144; tumor_id: 8; lane: L001; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190618; mouse_id: G144; tumor_id: 8; lane: L002; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190618; mouse_id: G144; tumor_id: 8; lane: L003; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190618; mouse_id: G144; tumor_id: 8; lane: L004; abi1 genotype (all mice are pyvt+): fl/wt; cre: -; ', 'date: 190618; mouse_id: G164; tumor_id: 3; lane: L001; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190618; mouse_id: G164; tumor_id: 3; lane: L002; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190618; mouse_id: G164; tumor_id: 3; lane: L003; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190618; mouse_id: G164; tumor_id: 3; lane: L004; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190618; mouse_id: G164; tumor_id: 6; lane: L001; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190618; mouse_id: G164; tumor_id: 6; lane: L002; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190618; mouse_id: G164; tumor_id: 6; lane: L003; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190618; mouse_id: G164; tumor_id: 6; lane: L004; abi1 genotype (all mice are pyvt+): fl/wt; cre: +; ', 'date: 190618; mouse_id: G174; tumor_id: 1; lane: L001; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190618; mouse_id: G174; tumor_id: 1; lane: L002; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190618; mouse_id: G174; tumor_id: 1; lane: L003; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190618; mouse_id: G174; tumor_id: 1; lane: L004; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190618; mouse_id: G174; tumor_id: 6; lane: L001; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190618; mouse_id: G174; tumor_id: 6; lane: L002; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190618; mouse_id: G174; tumor_id: 6; lane: L003; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190618; mouse_id: G174; tumor_id: 6; lane: L004; abi1 genotype (all mice are pyvt+): fl/fl; cre: +; ', 'date: 190618; mouse_id: G184; tumor_id: 6; lane: L001; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190618; mouse_id: G184; tumor_id: 6; lane: L002; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190618; mouse_id: G184; tumor_id: 6; lane: L003; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190618; mouse_id: G184; tumor_id: 6; lane: L004; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190618; mouse_id: G184; tumor_id: 9; lane: L001; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190618; mouse_id: G184; tumor_id: 9; lane: L002; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190618; mouse_id: G184; tumor_id: 9; lane: L003; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ', 'date: 190618; mouse_id: G184; tumor_id: 9; lane: L004; abi1 genotype (all mice are pyvt+): fl/fl; cre: -; ' GSE39412 Homo sapiens 19 Genome variation profiling by SNP array GPL6801 Somatic cell fusions reveal extensive heterogeneity in basal-like breast cancer [SNP] 2012-07-17 Basal-like and luminal breast tumors have distinct clinical behavior and molecular profiles, yet the underlying mechanisms are poorly defined. To interrogate processes that determine these distinct phenotypes and their inheritance pattern, we generated somatic cell fusions and performed integrated genetic and epigenetic (DNA methylation and chromatin) profiling. We found that the basal-like trait is generally dominant and it is largely defined by epigenetic repression of luminal transcription factors. Definition of super-enhancers highlighted a core program common in luminal cells but high degree of heterogeneity in basal-like breast cancers that correlates with clinical outcome. We also found that protein extracts of basal-like cells is sufficient to induce luminal-to-basal phenotypic switch implying a trigger of basal-like autoregulatory circuits. We determined that KDM6A might be required for luminal-basal fusions, and identified EN1, TBX18, and TCF4 as candidate transcriptional regulators of luminal-to-basal switch. Our findings highlight the remarkable epigenetic plasticity of breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39412 Somatic Cell Fusions Reveal Extensive Heterogeneity in Basal-like Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2015.05.011 {Cell reports (7.815): 10.1016/j.celrep.2015.05.011} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA170834 https://www.ebi.ac.uk/ena/browser/view/PRJNA170834 None [Overal design]We investigated the potential contribution of genetic factors to defining cell type-specific gene expression patterns by analyzing allelic inheritance based on Affymetrix SNP6.0 array hybridization of DNA from parental and fusion cells; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was extracted from breast cancer cell lines and the fusion cell lines with a standard method using proteinase K digestion, phenol-chloroform extraction and ethanol precipitation. The DNA was subjected to genotyping.'; [Cell type]'Source: ''cell line: SUM159PT; ', 'cell line: MDA-MB-231; ', 'cell line: MCF7; ', 'cell line: T-47D; ', 'cell line: BT-474; ', 'cell line: heterofusion SUM159PT_MCF7; ', 'cell line: heterofusion SUM159PT_T-47D; ', 'cell line: heterofusion SUM159PT_BT-474; ', 'cell line: heterofusion MDA-MB-231_MCF7; ', 'cell line: CAL51; ', 'cell line: 21NT; ', 'cell line: ZR75-1; ', 'cell line: MDA-MB-453; ', 'cell line: heterofusion SUM159PT-21NT; ', 'cell line: heterofusion SUM159PT-ZR75-1; ', 'cell line: heterofusion SUM159PT-MDA-MB-453; ', 'cell line: heterofusion CAL51-MCF7; ' GSE54592 Homo sapiens 8 Genome binding/occupancy profiling by high throughput sequencing GPL9115; GPL10999; GPL11154 ER ChIP-seq of Androstenedione treated Letrozole Resistant Breast Cancer Cell line 2014-01-31 Acquired resistance to aromatase inhibitor (AI) therapy is a major clinical problem in the treatment of breast cancer. The detailed mechanisms of how tumour cells develop this resistance remain unclear. Here estrogen receptor ChIPseq analysis identifies adaptations of the ER in response to prolonged letrozole treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54592 Adaptation to AI Therapy in Breast Cancer Can Induce Dynamic Alterations in ER Activity Resulting in Estrogen-Independent Metastatic Tumors. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-15-1583 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-15-1583} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA237102 https://www.ebi.ac.uk/ena/browser/view/PRJNA237102 https://www.ncbi.nlm.nih.gov/sra?term=SRP036128 [Overal design]Let-R cells were treated with either Androstenedione or vehicle and immunoprecipitated with anti-ER; [Treatment]'Cells were maintained in steroid depleted medium for 72 hours prior to treatment with androstenedione (10-7 M; Sigma Aldrich, St. Louis, MO, USA) or Vehicle (10% ethanol) for 45minutes.', 'Cells were maintained in steroid depleted medium for 72 hours prior to treatment with Vehicle (10% ethanol) for 45minutes.', 'Input libraries were harvested without further treatment'; [Growth]'Estrogen receptor positive MCF-7 breast cancer cells were obtained from American Type Culture Collection (ATCC). MCF-7 cells were stably transfected with the aromatase gene (CYP19) (Invitrogen, Paisley, UK) to generate aromatase inhibitor sensitive cells (Aro cells). Letrozole-resistant (LetR) cells were then generated by long-term (>3 months) culture of Aro cells with letrozole (10-6M; Novartis, Switzerland) and androstenedione (25 x 10-5 mol/L; Sigma Aldrich) in MEM supplemented with 10% charcoal-dextran-stripped FCS, 1% L-Glutamine, 1% Pen/Strep, and 200 mg/mL Geneticin (G418, Gibco Invitrogen). All cells were maintained at 37degreesCelcius, 5% CO2 in a humidified incubator.', 'LY2 cells were grown in phenol red-free MEM with 2mM L-glutamine, 10% charcoal dextrin stripped fetal bovine serum, 50U/ml penicillin and 50ug/ml streptomycin in 37C incubator with 5% CO2.'; [Extraction]'Cells were treated and harvested for ChIP-seq as described previously (Schmidt et al, 2009, http://www.ncbi.nlm.nih.gov/pubmed/19275939). The anti-ER (sc-543) from Santa Cruz Biotechnologies was used as the antibody. Chromatin was extracted from the cells and the protein of interest, along with the DNA attached, was immunoprecipitated using the antibody attached to Dynal beads (Dynabeads® Protein A 10001D, Life Technologies). The proteins were then removed from the DNA by reverse crosslinking overnight and the DNA purified and amplified before being sequenced.\nDNA libraries were generated from ChIP output DNA by adaptor ligation, gel purification, and cycles of PCR as described by Illumina.', 'no entry'; [Cell type]'Letrozole-resistant breast cancer cells', 'Source: ''cell line: Let-R; cell type: Letrozole-resistant breast cancer cells; treated with: Androstenedione for 45min; chip antibody: anti-ER; chip antibody vendor: Santa Cruz Biotechnologies; chip antibody cat. #: sc-543; ', 'cell line: Let-R; cell type: Letrozole-resistant breast cancer cells; treated with: 10% ethanol (vehicle control) for 45min; chip antibody: anti-ER; chip antibody vendor: Santa Cruz Biotechnologies; chip antibody cat. #: sc-543; ', 'cell line: Let-R; cell type: Letrozole-resistant breast cancer cells; ', 'treatment: Untreated; cell line: LY2; chip antibody: ER; ', 'treatment: Untreated; cell line: LY2; ' GSE75802 Homo sapiens 22 Expression profiling by array GPL10558 Double-stranded microRNA mimics can induce length- and passenger strand-dependent effects in a cell type-specific manner (RNA 2015) 2015-12-08 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE75802 Double-stranded microRNA mimics can induce length- and passenger strand-dependent effects in a cell type-specific manner. RNA (New York, N.Y.) 3.949 https://doi.org/10.1261/rna.054072.115 {RNA (New York, N.Y.) (3.949): 10.1261/rna.054072.115} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA305401 https://www.ebi.ac.uk/ena/browser/view/PRJNA305401 None [Overal design]Refer to individual Series; [Treatment]'Cells were seeded on day prior to transfection, transfected with miRNA mimic or controls and submitted for cell density growth curve readings (Incucyte) [see Goldgraben et al. 2015]'; [Growth]'Cell lines were maintained and split regularly at 90% confluence, see Goldgraben et al. 2015'; [Extraction]'RNA was collected in QIAZOL and extracted with QIAGEN miRNeasy kit as per the manufacturers instructions. Quality control was performed with Agilent Bioanalyser before running on microarray'; [Cell type]'Source: ''cell line: MCF-7; ' GSE130513 Homo sapiens 6 Expression profiling by high throughput sequencing GPL16791 Modeling the MYC-driven normal-to-tumour switch in breast cancer. 2019-04-30 The potent MYC oncoprotein is deregulated in many human cancers, including breast carcinoma, and is associated with aggressive disease. To understand the mechanisms and vulnerabilities of MYC-driven breast cancer, we have generated an in vivo model that mimics human disease in response to MYC deregulation. MCF10A cells ectopically expressing a common breast cancer mutation in the PI3 kinase pathway (PIK3CAH1047R) lead to the development of organized acinar structures in mice. However, expressing both PIK3CAH1047R and deregulated-MYC lead to the development of invasive ductal carcinoma, thus creating a model in which a MYC-dependent normal-to-tumour switch occurs in vivo. These MYC-driven tumours exhibit classic hallmarks of human breast cancer at both the pathological and molecular levels. Moreover, tumour growth is dependent upon sustained deregulated MYC expression, further demonstrating addiction to this potent oncogene and regulator of gene transcription. We therefore provide a MYC-dependent model of breast cancer which can be assayed for in vivo tumour initiation, proliferation, and transformation from normal breast acini into invasive breast carcinoma. Taken together, we anticipate that this novel MYC-driven transformation model will be a useful research tool to both better understand MYC’s oncogenic function and identify therapeutic vulnerabilities. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130513 Modelling the MYC-driven normal-to-tumour switch in breast cancer. Disease models & mechanisms 4.028 https://doi.org/10.1242/dmm.038083 {Disease models & mechanisms (4.028): 10.1242/dmm.038083} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA540502 https://www.ebi.ac.uk/ena/browser/view/PRJNA540502 https://www.ncbi.nlm.nih.gov/sra?term=SRP194282 [Overal design]RNA-seq was conducted on 3 biological replicates of each 10A.PE and 10A.PM xenograft tumours.; [Treatment]'n/a'; [Growth]'1E6 cells (10A.PE or 10APM) were injected sub-cutaneously in female NOD-SCID mice. Tumours were harvested at them same time point and flash frozen.'; [Extraction]'RNA from xenograft tissue was harvested using the RNeasy Plus Universal Kit (Cat# 73404, Qiagen) following the manufacturer’s protocol.\nRNA libraries were prepared using standard Illumina protocol'; [Cell type]'breast cancer cell line''host strain: NOD-SCID; cell line source: MCF10A parental cell line; cell type: breast cancer cell line; ectopic alleles expressed: PIK3CA^H1047R + EV control; tissue: Xenograft tissue (derived from MCF10A parental cell line); ', 'host strain: NOD-SCID; cell line source: MCF10A parental cell line; cell type: breast cancer cell line; ectopic alleles expressed: PIK3CA^H1047R + MYC; tissue: Xenograft tissue (derived from MCF10A parental cell line); ' GSE32646 Homo sapiens 115 Expression profiling by array GPL570 GSTP1 expression predicts poor pathological complete response to neoadjuvant chemotherapy in ER-negative breast cancer 2011-10-05 The purpose of the present study was to investigate the association of glutathione S-transferase P1 (GSTP1) expression with resistance to neoadjuvant paclitaxel followed by 5-fluorouracil/epirubicin/cyclophosphamide (P-FEC) in human breast cancers. The relationship of GSTP1 expression and GSTP1 promoter hypermethylation with intrinsic subtypes was also investigated. In this study, primary breast cancer patients (n = 123, stage II-III) treated with neoadjuvant P-FEC were analyzed. Tumor samples were obtained by vacuum-assisted core biopsy before P-FEC. GSTP1 expression was determined using immunohistochemistry, GSTP1 promoter methylation index (MI) using bisulfite methylation assay and intrinsic subtypes using DNA microarray. The pathological complete response (pCR) rate was significantly higher in GSTP1-negative tumors (80.0%) than GSTP1-positive tumors (30.6%) (P = 0.009) among estrogen receptor (ER)-negative tumors but not among ER-positive tumors (P = 0.267). Multivariate analysis showed that GSTP1 was the only predictive factor for pCR (P = 0.013) among ER-negative tumors. Luminal A, luminal B and HER2-enriched tumors showed a significantly lower GSTP1 positivity than basal-like tumors (P = 0.002, P < 0.001 and P = 0.009, respectively), while luminal A, luminal B and HER2-enriched tumors showed a higher GSTP1 MI than basal-like tumors (P = 0.076, P < 0.001 and P < 0.001, respectively). In conclusion, these results suggest the possibility that GSTP1 expression can predict pathological response to P-FEC in ER-negative tumors but not in ER-positive tumors. Additionally, GSTP1 promoter hypermethylation might be implicated more importantly in the pathogenesis of luminal A, luminal B and HER2-enriched tumors than basal-like tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32646 GSTP1 expression predicts poor pathological complete response to neoadjuvant chemotherapy in ER-negative breast cancer. Cancer science 4.751 https://doi.org/10.1111/j.1349-7006.2012.02231.x {Cancer science (4.751): 10.1111/j.1349-7006.2012.02231.x} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA146953 https://www.ebi.ac.uk/ena/browser/view/PRJNA146953 None [Overal design]Fresh frozen tumor samples obtained by vacuum-assisted core biopsy from one hundred and fifteen patients were subjected to RNA extraction and hybridization on Affymetrix microarrays.; [Treatment]'Patients prospectively consented to a research biopsy by vacuum-assisted core-biopsy instrument (Mammotome 8G; HH Ethicon Endosurgery, Johnson and Johnson Company) under ultrasonographic guidance for histologic examination and gene expression analysis prior to any systemic therapy, and to the future assessment of pathologic response'; [Growth]'None'; [Extraction]'Trizol (Invitrogen, Carlsbad, Calif) was used to extract RNA from core-needle tumor biopsy samples that were obtained with the Mammotome.'; [Cell type]'Source: ''tissue: breast cancer tumor; age: 46; clinical t stage: 3; lymph node status: positive; clinical stage: IIIA; histological grade: 3; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 56; clinical t stage: 3; lymph node status: positive; clinical stage: IIIA; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 67; clinical t stage: 3; lymph node status: positive; clinical stage: IIIA; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 56; clinical t stage: 3; lymph node status: positive; clinical stage: IIIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 40; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 57; clinical t stage: 3; lymph node status: positive; clinical stage: IIIA; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 48; clinical t stage: 4; lymph node status: positive; clinical stage: IIIB; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 49; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 1; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 55; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 45; clinical t stage: 3; lymph node status: negative; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 36; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 58; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 33; clinical t stage: 3; lymph node status: positive; clinical stage: IIIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 44; clinical t stage: 4; lymph node status: positive; clinical stage: IIIB; histological grade: 1; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 51; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 46; clinical t stage: 3; lymph node status: positive; clinical stage: IIIA; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 48; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 46; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 65; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 52; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 30; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 40; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 35; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 59; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 1; er status ihc: positive; pr status ihc: positive; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 50; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 43; clinical t stage: 3; lymph node status: positive; clinical stage: IIIA; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 49; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 65; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 31; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 46; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 1; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 42; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 33; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 56; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 56; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 43; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 60; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 58; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 1; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 48; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 72; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 52; clinical t stage: 4; lymph node status: positive; clinical stage: IIIB; histological grade: 3; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 63; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 61; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 62; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 49; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 59; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 53; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 42; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 28; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 68; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 47; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 57; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 3; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 47; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 63; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 56; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 68; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 45; clinical t stage: 3; lymph node status: negative; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 27; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 58; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 37; clinical t stage: 3; lymph node status: negative; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 39; clinical t stage: 3; lymph node status: positive; clinical stage: IIIA; histological grade: 1; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 44; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 50; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 54; clinical t stage: 4; lymph node status: positive; clinical stage: IIIB; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 36; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 54; clinical t stage: 3; lymph node status: positive; clinical stage: IIIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 36; clinical t stage: 3; lymph node status: negative; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 61; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 43; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 3; er status ihc: positive; pr status ihc: positive; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 54; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 1; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 47; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 62; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 50; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 48; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 1; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 59; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 48; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 1; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 70; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 48; clinical t stage: 1; lymph node status: positive; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 49; clinical t stage: 1; lymph node status: positive; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 57; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 54; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 70; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 51; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 63; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 1; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 42; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 66; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 1; er status ihc: positive; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 61; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 49; clinical t stage: 3; lymph node status: positive; clinical stage: IIIA; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 63; clinical t stage: 3; lymph node status: positive; clinical stage: IIIA; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 53; clinical t stage: 1; lymph node status: positive; clinical stage: IIA; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 73; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 55; clinical t stage: 4; lymph node status: positive; clinical stage: IIIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 36; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 63; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 48; clinical t stage: 3; lymph node status: negative; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 60; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 60; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 39; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 68; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 55; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 45; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 48; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 3; er status ihc: positive; pr status ihc: positive; her2 status fish: positive; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 44; clinical t stage: 1; lymph node status: positive; clinical stage: IIA; histological grade: 1; er status ihc: positive; pr status ihc: positive; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 37; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 47; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 56; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 1; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 61; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 2; er status ihc: negative; pr status ihc: negative; her2 status fish: positive; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 68; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 3; er status ihc: negative; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: pCR; ', 'tissue: breast cancer tumor; age: 42; clinical t stage: 2; lymph node status: positive; clinical stage: IIB; histological grade: 1; er status ihc: positive; pr status ihc: positive; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 68; clinical t stage: 2; lymph node status: negative; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: nCR; ', 'tissue: breast cancer tumor; age: 61; clinical t stage: 1; lymph node status: positive; clinical stage: IIA; histological grade: 2; er status ihc: positive; pr status ihc: negative; her2 status fish: negative; pathologic response pcr ncr: pCR; ' GSE16200 Homo sapiens 12 Expression profiling by array GPL571 Loss of Syk in normal breast cells 2009-05-22 Loss of Syk in normal breast cells in vivo and in vitro: gene expression and phenotypic switch to stem-cell like with induction of invadopodia Morphological and gene microarray analysis following Syk knockdown in MCF10A reveals a loss of luminal and differentiated epithelial features with epithelial to mesenchymal transition and a gain in invadopodia and stem/ progenitor cell marker expression. These results support the role of Syk in limiting normal stem/progenitor proliferation and invasion during morphogenesis, and support the role of Syk as a critical tumor suppressor for breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE16200 Tumor suppressor function of Syk in human MCF10A in vitro and normal mouse mammary epithelium in vivo. PloS one 2.776 https://doi.org/10.1371/journal.pone.0007445 {PloS one (2.776): 10.1371/journal.pone.0007445} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA117139 https://www.ebi.ac.uk/ena/browser/view/PRJNA117139 None [Overal design]Global gene expression profiles were measured using Affymetrix U133A 2.0 microarrays in MCF10A cell lines (control and Syk siRNA knockdown cells on collagen gels or plastic).; [Treatment]'Syk siRNA knockdown or control'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''sirna: control; plate: collagen coated; cell line: MCF10A; ', 'sirna: control; plate: plastic; cell line: MCF10A; ', 'sirna: Syk siRNA knockdown; plate: collagen coated; cell line: MCF10A; ', 'sirna: Syk siRNA knockdown; plate: plastic; cell line: MCF10A; ' GSE56823 Homo sapiens 6 Expression profiling by array GPL17586 Expression data from MDA-MB-231 breast cancer cell lines exposed to DMSO control and UF010 2014-04-15 Breast cancer cell line MDA-MB-231 was treated with DMSO or UF010, a novel HDAC inhibitor for 24 hours. The impact of UF010 treatment on global gene expression was determined. We used Affymetrix Human Transcriptome Array 2.0 (HTA-2_0) to analyze genes that were up or downregulated upon UF010 exposure. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE56823 Identification of histone deacetylase inhibitors with benzoylhydrazide scaffold that selectively inhibit class I histone deacetylases. Chemistry & biology None https://doi.org/10.1016/j.chembiol.2014.12.015 {Chemistry & biology (None) doi:10.1016/j.chembiol.2014.12.015}; {Genomics data (None) doi:10.1016/j.gdata.2015.06.019}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA244687 https://www.ebi.ac.uk/ena/browser/view/PRJNA244687 None [Overal design]MDA-MB-231 cells were treated with DMSO (control) or 1.0 µM of UF010 for 24 hours.Total RNAs were isolated for hybridization on Affymetrix microarrays.; [Treatment]'DMSO (1 µl) was added to cell culture with 1 ml of medium. Similarly, 1 µl of 1 mM UF010 was added to the final concentration of 1 µM. Cells were cultured for 24 hours after treatment.'; [Growth]'MDA-MB-231 cells were seeded in a well in a 6-well plate and cultured in complete DMEM medium for 24 hours'; [Extraction]"Extraction of total RNA with the RNeasy mini kit was performed according to the manufacturer's instructions."; [Cell type]'Source: ''tissue: Cultured breast cancer cells; cell line: MDA-MB-231; ' GSE10917 Homo sapiens 14 Genome binding/occupancy profiling by genome tiling array GPL6639 Preferential localization of human origins of DNA replication at the 5' end of expressed genes 2008-03-21 Human DNA replication relies on the activation of thousands of origins distributed along the genome. Their organization and the functional significance of their distribution remains unknown. To map large number of origins in human cells, we have localized the distribution of short nascent DNA using a high-resolution DNA tiling array platform covering 33.9Mb. Results with three different cell lines reveal that origins are very closely spaced (average interval 3-5kb), and that their positions are largely conserved among the cell lines studied. Origins are non-randomly distributed, being preferentially enriched at the 5’-end of expressed genes and at evolutionary intergenic sequences. In MCF7 cells, a strong correlation is also found between origin positioning and histone H3K4me3 and of PolII binding to chromatin. This study provides a large scale view of the organization of DNA replication origins in human chromosomes and suggests a link between this distribution and underlying chromatin features related to chromosome structure, and gene expression Keywords: nascent strand DNA, histone, Pol-II ChIP-chip. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE10917 Preferential localization of human origins of DNA replication at the 5'-ends of expressed genes and at evolutionarily conserved DNA sequences. PloS one 2.776 https://doi.org/10.1371/journal.pone.0017308 {PloS one (2.776): 10.1371/journal.pone.0017308} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA107217 https://www.ebi.ac.uk/ena/browser/view/PRJNA107217 None [Overal design]To map initiation sites for DNA replication and the position of both H3K4Me3 and Pol-II chromatin binding sites in human cell lines on a custom made high density tiling DNA microarray covering 33.9 Mb of the human genome.; [Treatment]'None'; [Growth]'None'; [Extraction]'For the isolation of short nascent DNA from human cell lines a procedure employed in our laboratory (reference below) was followed with minor modifications. About 108 cells were washed in PBS and collected by centrifugation. Cells were lysed with SDS in presence of Proteinase K, DNA extracted with phenol and chloroform, precipitated by centrifugation with ethanol in 0.3M Sodium Acetate, and resuspended in TE (10mM Tris-HCl, pH 8.0; 1mM EDTA) buffer. The re-suspended DNA was denatured by incubation in boiling water for 12 min, followed by quenching in ice for 6 min, and applied onto to a 5-30% neutral sucrose gradient. After centrifugation of the gradient in a SW28 Beckman rotor for 24,000 rpm for 20 hrs at 15°C, the gradient was fractionated using an ISCO 185 fractionator. I ml fractions were collected and the linearity of the gradient assessed by measuring the refractive index of every third fraction. Only gradients with a regression line R2 value larger than 0.99 were further processed. The consistency of the gradients allowed us to identify fractions corresponding to the desired DNA size range, which in our experience falls around a refractive index of 1.35. About 80 ul of every gradient fraction was concentrated 10-fold in a speedvac and analyzed by gel electrophoresis in 1% agarose to confirm the fragment size range in the fractions. Fractions containing nascent DNA strands in the range of 0.7-1.5kb in length were pooled and dialyzed. The quality and abundance of short nascent strands in our nascent DNA preparation was assessed by real time PCR, and used for hybridization to DNA tiling microarrays. Reference: Hu, L., Xu, X., and Valenzuela, M.S. Initiation sites for human DNA replication at a putative ribulose-5-phosphate-3-epimerase gene. Biochem. Biophys. Res. Commun. 320:648-655 (2004)', 'The reference DNA sample, corresponded to DNA obtained from the same cell line from which the nascent strand preparation was originated, was extracted according to arrayCGH protocol. This DNA was sheared by sonication to yield an equivalent range in size fragments as the test DNA.', "Chromatin immunoprecipitation.(ChIP) was carried out according to standard protocols using a ChIP-IT kit from Active Motif (Carlsbad, CA), and following the manufacture’s instructions with minor modifications. Briefly, MCF7 cells were crosslinked with 1% formaldehyde at room temperature for 15 minutes. Then the cells were sheared with a VirSonic 100 sonicator for 10 cycles of ten 1-second pulses. After centrifugation, the chromatin contained in the supernatant was collected. Part of it was set aside and served as input fraction. The rest was immunoprecipitated overnight at 4°C. The antibodies used were: anti-polymerase II antibody (Upstate 05-623) and anti-trimethylated histone H3K4 (Abcam Ab8580). After reversal of crosslinking at 65°C overnight, the ChIP DNA was purified using spin columns provided by the kit. For ChIP-chip, the ChIP DNA was amplified using the ligation mediated-PCR method as described in the reference below. A second round amplification of 15 cycles was added to increase the yield of DNA. 3 ?g of amplified ChIP DNA and Input DNA was labeled with Cy5–dUTP and Cy3-dUTP, respectively, with BioPrime DNA Labeling System (Invitrogen). The labeled ChIP DNA and Input DNA were then combined and hybridized to the NimbleGen arrays. Reference: Li et al. (2003) A global transcriptional regulatory role for c-Myc in Burkitt's lymphoma cells Proc Natl Acad Sci U S A 100(14): 8164-9"; [Cell type]'Source: ''' GSE71141 Homo sapiens 2 Expression profiling by array GPL16025 Gene expression signatures in SPIN1 siRNA- and negative control-transfected breast cancer cell line MCF-7/ADM 2015-07-21 To screen potential target genes of SPIN1 in breast cancer, human gene expression microarray was performed to identify differentially expressed mRNAs in SPIN1 siRNA or negative control transfected MCF-7/ADM cells. After transfection with SPIN1 siRNA, 4409 genes were differentially expressed by >2-fold in MCF-7/ADM cells compared with negative control-transfected cells, of which 2413 were significantly downregulated and the other 1996 were upregulated. Differentially expressed genes were submitted to GO and KEGG pathway analysis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE71141 Suppression of SPIN1-mediated PI3K-Akt pathway by miR-489 increases chemosensitivity in breast cancer. The Journal of pathology None https://doi.org/10.1002/path.4743 {The Journal of pathology (None) doi:10.1002/path.4743}; {Journal of experimental & clinical cancer research : CR (None) doi:10.1186/s13046-018-0748-9}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA290447 https://www.ebi.ac.uk/ena/browser/view/PRJNA290447 None [Overal design]A two chip study using total RNA recovered from MCF-7/ADM breast cancer cells transfected with SPIN1 siRNA or negative control. Each chip measures the expression 45033 genes were collected from the authoritative data source including NCBI.; [Treatment]'MCF-7/ADM cells were transfected with SPIN1 siRNA or negative control.'; [Growth]'MCF-7/ADM cells were cultured in RPMI-1640 medium (Gibco) supplemented with 10% FBS.'; [Extraction]'Total RNA were extracted using Trizol. The RNA quantity and quality were measured by NanoDrop ND-1000. RNA integrity was assessed by standard denaturing agarose gel electrophoresis.'; [Cell type]'breast cancer''cell line: MCF-7/ADM; cell type: breast cancer; ' GSE98551 Homo sapiens 9 Genome binding/occupancy profiling by high throughput sequencing GPL18460 Chromatin structure and CTCF across the MCF10 breast cancer progression series (ChIP-Seq) 2017-05-04 Transcription and processing of histone mRNAs occurs at subnuclear domains known as Histone Locus Bodies (HLBs). Although it is known that higher-order chromatin organization is dysregulated in cancer, structural alterations within HLB across breast cancer progression are unclear. Differential expression across known as MCF10, a basal triple negative breast cancer progression model, followed by pathway analysis demonstrated many alterations in signaling cascades known to be related to proliferation. Positional gene enrichment identified the hist1 gene locus at chromosome 6p22 as the most significantly altered cluster of genes from the normal-like MCF10A to premalignant MCF10AT1. The malignant MCF10CA1a had a more varied expression pattern across the hist1 locus. Within this region there are three subclusters of hist1 genes which were generally upregulated while intervening genes were more frequently downregulated. Extending these findings to TCGA breast tumors revealed that normal adjacent tissue had lower expression within the subclusters than their matched tumor samples. Moreover, the expression pattern within the hist1 locus comparing normal versus tumors recapitulated a very similar pattern to that comparing 10A to AT1 or CA1a. Since the hist1 locus is transcribed and processed at a specific subnuclear microenvironment, the higher order chromatin organization of this locus may be a critical component of its regulation. We addressed whether CTCF, a key chromatin organizing protein, may play a role in organizing the hist1 HLB. Immunofluorescence for CTCF along with NPAT, a protein which decorates this locus, identified that CTCF may tether the hist1 HLB to the nuclear matrix. All three subclusters reside within a single topologically associating domain wherein interacting loops are bound by CTCF. Inter-subcluster interactions are lost in the premalignant AT1. Consistent with the varied expression across the hist1 HLB in CA1a, inter-subcluster interactions are regained in the malignant state. These data suggest a transient state in highly proliferative breast cancer cells in which the hist1 HLB is dynamically reorganized. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98551 Intranuclear and higher-order chromatin organization of the major histone gene cluster in breast cancer. Journal of cellular physiology 4.522 https://doi.org/10.1002/jcp.25996 {Journal of cellular physiology (4.522): 10.1002/jcp.25996} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA385492 https://www.ebi.ac.uk/ena/browser/view/PRJNA385492 https://www.ncbi.nlm.nih.gov/sra?term=SRP106469 [Overal design]CTCF ChIP-Seq; [Treatment]'Cells were seeded at 1x106 cells per 100 mm dish and grown to 80-90% confluence. Cells were washed twice with phosphate buffered saline (PBS), fixed with 1% methanol free formaldehyde, glycine neutralized on ice for 5 minutes, and pellets were stored at -80C.'; [Growth]'MCF10A and MCF10AT1 cells were grown in DMEM: F12 (Hyclone-SH30271), 5% (v/v) horse serum (Gibco #16050) + 10ug/ml human insulin (Sigma I-1882)+ 20ng/ml recombinant hEGF (Peprotech AF-100-15) + 100ng/ml Cholera toxin (Sigma C-8052) + 0.5 ug/ml Hydrocortisone (Sigma H-0888) Pen/Strep (Life Technologies) and Glutamine (Life Technologies). MCF10CA1a cells were grown in DMEM: F12 (Hyclone-SH30271) + 5% (v/v) horse serum (Gibco #16050) +Pen/Strep (Life Technologies)and Glutamine (Life Technologies) .'; [Extraction]'DNA was extracted in cell lysis buffer (5mM PIPES pH8, 85mM KCL, 1% IGEPAL, protease inhbitors) on ice for 15 minutes, dounce homogenized 20x, and nuclear lysis buffer (50mM Tris-Cl pH8.1, 10mM EDTA, 1%SDS, protease inhibitors) on ice for 30 minutes, and sonicated 12-14 minutes (140W, 10DF, 200c/b). Samples were diluted in RIPA and IP was carried out overnight at 4oC using the recommended antibody concentrations on 150ug of chromatin. Magnetic protein A/G beads were washed and added for an additional 4 hours. Beads were collected and washed 2x with RIPA minus protease inhibitors, and once with a second IP wash buffer (100mM Tris pH9, 500mM LiCl, 1% IGEPAL, 1% deoxycholic acid). Next the DNA was eluted using 50mM NaHCO3, 1%SDS 2 times 30 minutes on a shaker. Formaldehyde crosslinks were reversed using elution buffer plus .6M NaCl overnight at 67oC.\nChIPseq libraries were prepared for sequencing using standard Illumina protocols using the TruSeq ChIP kit (Illumina #IP-202-1012)\nBarcoded libraries (Illumina TruSeq) were then loaded onto an Illumina HiSeq 1500 and single-end 100-base (SE100) sequencing was performed at the Advanced Genome Technologies Core Massively Parallel Sequencing Facility at UVM.'; [Cell type]'basal epithelial, non-tumorigenic', 'basal, pre-metastatic', 'basal, metastatic''tissue: breast; cell type: basal epithelial, non-tumorigenic; neoplasia type: fibrocystic disease; atcc id: ATCC CRL-10317; ', 'tissue: breast; cell type: basal, pre-metastatic; neoplasia type: hyperplastic; atcc id: n/a; ', 'tissue: breast; cell type: basal, metastatic; neoplasia type: tumorigenic; atcc id: n/a; ' GSE131383 Homo sapiens 6 Expression profiling by high throughput sequencing GPL21290 The effects of chemokines CCL2/7 on MDA-MB-231-FOXC1 cells 2019-05-17 Our preliminary studies performed in vitro show that MDA-MB-231-FOXC1 cell, which were used to mimic the lung-colonizing triple-negative breast cancer cells, was an indispensable component for the induction of migration and tube formation of lung endothelial cells. Moreover, our results further show that mouse lung fibroblast-derived chemokines CCL2/7 act on MDA-MB-231-FOXC1 cells, which mediates the migration and tube formation of lung endothelial cells in vitro. To understand the signaling pathways activated by CCL2/7 in MDA-MB-231-FOXC1 cells, we performed RNA-Seq assay. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131383 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA543438 https://www.ebi.ac.uk/ena/browser/view/PRJNA543438 https://www.ncbi.nlm.nih.gov/sra?term=SRP198746 [Overal design]MDA-MB-231-FOXC1 cells were treated with recombinant mouse Ccl2 (10 nM)/7 (50 nM) for 6 hours.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was isolated from the using RNeasy Mini kit (Qiagen, Germany).\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'human breast cancer cell''cell type: human breast cancer cell; passages: 15-18; ' GSE48934 Homo sapiens 6 Expression profiling by RT-PCR GPL17456 MicroRNA profiling of brain metastasis competent cell-derived exosomes 2013-07-16 Objective of this work was to characterize the miRNA profile of exosomes isolated from brain-homing cell lines (MDA-MB-231BR, CTC1BMSM, and 70W) with their respective parental non-brain metastatic cell lines (MDA-MB-231P, CTC1P and MeWo). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48934 MicroRNA and protein profiling of brain metastasis competent cell-derived exosomes. PloS one 2.776 https://doi.org/10.1371/journal.pone.0073790 {PloS one (2.776): 10.1371/journal.pone.0073790} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA212330 https://www.ebi.ac.uk/ena/browser/view/PRJNA212330 None [Overal design]Exosomes derived from the six cell lines were isolated. Brain metastatic cell-derived exosomal miRNAs were compared with non brain metastatic cell lines (MDA-MB-231BR versus MDA-MB-231P, CTC1BMSM versus CTC1P, and 70W versus MeWo).; [Treatment]'None'; [Growth]'After 72 hours of cell culturing, 10 ml of culture media was centrifuged at 3000 x g for 15 min to remove cells and cell debris. The supernatant was mixed with 2 ml of ExoQuick-TC, refrigerated for 16 hours and then centrifuged at 1500 x g for 30 min at 4°C to obtain the exosomes pellet.'; [Extraction]'Total RNA from exosomes was isolated using mirVana miRNA isolation kit (Life Technologies, Grand Island, NY)'; [Cell type]'Breast cancer', 'Circulating tumor cell', 'Melanoma''parental non-brain metastatic cell line: MDA-MB-231P; cell type: Breast cancer; ', 'brain-homing cell line: MDA-MB-231BR; cell type: Breast cancer; ', 'parental non-brain metastatic cell line: CTC1P; cell type: Circulating tumor cell; ', 'brain-homing cell line: CTC1BMSM; cell type: Circulating tumor cell; ', 'parental non-brain metastatic cell line: MeWo; cell type: Melanoma; ', 'brain-homing cell line: 70W; cell type: Melanoma; ' GSE62230 Mus musculus 7 Expression profiling by array GPL11383 Expression of miR-200c in claudin-low breast cancer alters stem cell functionality, enhances chemosensitivity and reduces metastatic potential 2014-10-09 Claudin-low tumors are a highly aggressive breast cancer subtype with no targeted treatments and a clinically documented resistance to chemotherapy. They are significantly enriched in cancer stem cells (CSCs), which makes claudin-low tumor models particularly attractive for studying CSC behavior and developing novel approaches to minimize CSC therapy resistance. One proposed mechanism by which CSCs arise is via an epithelial-mesenchymal transition (EMT), and reversal of this process may provide a potential therapeutic approach for increasing tumor chemosensitivity. Therefore, we investigated the role of the miR-200 family of microRNAs in regulating the epithelial state, stem-like properties, and therapeutic response in an in vivo primary, syngeneic p53null claudin-low tumor model that is normally deficient in miR-200 expression. Using an inducible lentiviral approach, we expressed the miR-200c cluster in this claudin-low model and found that it changed the epithelial state, and consequently, impeded CSC behavior in these mesenchymal tumors. Moreover, these state changes were accompanied by a decrease in proliferation and an increase in the differentiation status. MiR-200c expression also forced a significant reorganization of tumor architecture, affecting important cellular processes involved in cell-cell contact, cell adhesion, and motility. Accordingly, induced miR200c expression also significantly enhanced the chemosensitivity and decreased the metastatic potential of this p53null claudin-low tumor model. Collectively, our data suggest that miR-200c expression in claudin-low tumors offers a potential therapeutic application to disrupt the EMT program on multiple fronts in this mesenchymal tumor subtype, by altering tumor growth, chemosensitivity, and metastatic potential in vivo. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE62230 Expression of miR-200c in claudin-low breast cancer alters stem cell functionality, enhances chemosensitivity and reduces metastatic potential. Oncogene 6.634 https://doi.org/10.1038/onc.2015.48 {Oncogene (6.634): 10.1038/onc.2015.48} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA263589 https://www.ebi.ac.uk/ena/browser/view/PRJNA263589 None [Overal design]reference x sample; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA isolated using Qiagen RNeasy Kit', 'Total RNA isolated using Qiagen miRNeasy Kit'; [Cell type]'Source: ''reference: common reference RNA sample for these experiments consisted of total RNA harvested from equal numbers of C57Bl6/J and 129 male and female Day1 pups; ', 'strain: Balbc; tissue: p53null mammary tumor; ' GSE21541 Homo sapiens 45 Expression profiling by array; Third-party reanalysis; Methylation profiling by array; SNP genotyping by SNP array; Genome variation profiling by genome tiling array GPL570; GPL2616; GPL3718; GPL3720; GPL8490 An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer 2010-04-27 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE21541 An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer. BMC systems biology 2.048 https://doi.org/10.1186/1752-0509-4-67 {BMC systems biology (2.048): 10.1186/1752-0509-4-67} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA126201 https://www.ebi.ac.uk/ena/browser/view/PRJNA126201 None [Overal design]Refer to individual Series; [Treatment]'None', 'standard Affymetrix protocol'; [Growth]'None', 'Normal growth media for MCF10As is DMEM:F12 (Cellgro) w/ 2mM glutamine, containing 5% horse serum, insulin (10 µg ml-1) (Gibco), hydrocortisone (0.5 µg ml-1) (Sigma), EGF (20 ng ml-1) (Upstate) and 1 I.U. ml-1 penicillin, 0.1 µg ml-1 streptomysin, 0.25 µg ml-1 amphotericin B (Cellgro).', 'see Nat Genet. 2004 Mar;36(3):299-303'; [Extraction]'Qiagen Mini prep', 'performed as recommended by the Illumina', 'Standard DNA extraction protocol', 'Total RNA from cells grown in monolayer and Transwell® cultures were extracted using Tri reagent (MRC, Cincinnati, OH) and cleaned using DNaseI (Promega, Madison, WI) followed by standard phenol/chloroform precipitation and extraction method.', 'standard Affymetrix protocol', 'see Nat Genet. 2004 Mar;36(3):299-303'; [Cell type]'Source: ''cell line: HCC38; catalog number: ATCC# CRL-2314; ', 'cell line: HCC1008; catalog number: ATCC# CRL-2320; ', 'cell line: HCC1143; catalog number: ATCC# CRL-2321; ', 'cell line: HCC1395; catalog number: ATCC# CRL-2324; ', 'cell line: HCC1599; catalog number: ATCC# CRL-2331; ', 'cell line: HCC1937; catalog number: ATCC# CRL-2336; ', 'cell line: HCC2218; catalog number: ATCC# CRL-2343; ', 'cell line: MCF10A; catalog number: ATCC# CRL-10317; ', 'cell line: BT474; catalog number: ATCC# HTB-20; ', 'cell line: MCF7; catalog number: ATCC# HTB-22; ', 'sample type: diploid male reference; ' GSE147356 Homo sapiens 240 Expression profiling by high throughput sequencing GPL18573 Pan-cancer drivers are recurrent transcriptional regulatory heterogeneities in early-stage luminal breast cancer 2020-03-23 The heterogeneous composition of solid tumors is known to impact disease progression and response to therapy. Malignant cells coexist in different regulatory states that can be accessed transcriptomically by RNA sequencing, but single-cell methods have many caveats related to sensitivity, noise, and sample handling. We revised a statistical fluctuation analysis called stochastic profiling to combine with 10-cell RNA sequencing, which was designed for laser-capture microdissection (LCM) and extended here for immuno-LCM. When applied to a cohort of late-onset, early-stage luminal breast cancers, the integrated approach identified thousands of candidate regulatory heterogeneities. Intersecting the candidates from different tumors yielded a relatively stable set of 710 recurrent heterogeneously expressed genes (RHEGs) that were significantly variable in >50% of patients. RHEGs were not confounded by dissociation artifacts, cell cycle oscillations, or driving mutations for breast cancer. Rather, we detected RHEG enrichments for epithelial-to-mesenchymal transition genes and, unexpectedly, the latest pan-cancer assembly of driver genes across all cancer types. Heterogeneous transcriptional regulation conceivably provides a faster, reversible mechanism for malignant cells to sample the effects of potential oncogenes or tumor suppressors on cancer hallmarks. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE147356 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA614000 https://www.ebi.ac.uk/ena/browser/view/PRJNA614000 https://www.ncbi.nlm.nih.gov/sra?term=SRP253662 [Overal design]10-cell samples from human breast cancer biopsies were captured by laser capture microdissection. mRNA was extracted and PCR amplified for RNA-sequencing; [Treatment]'None'; [Growth]'None'; [Extraction]'All samples were cryoembedded and sectioned on to glass slides (8µm sections). Cell samples were isolated with laser capture microdissection and poly(A) RNA extracted, reverse transcribed and poly(A) PCR amplified prior to library preparation\nAmplified cDNA samples were diluted to 0.2 µg/ml for tagmentation with the Nextera XT DNA Library Preparation Kit (Illumina) according to the manufacturer’s earlier recommendation to purify libraries with 180% (vol/vol) SPRI beads'; [Cell type]'Source: ''tumor: UVABC1; sample type: Pool-and-split control; stage/grade: Stage 1 Grade 2; ', 'tumor: UVABC1; sample type: 10-cell sample; stage/grade: Stage 1 Grade 2; ', 'tumor: UVABC2; sample type: Pool-and-split control; stage/grade: Stage 2 Grade 2; ', 'tumor: UVABC2; sample type: 10-cell sample; stage/grade: Stage 2 Grade 2; ', 'tumor: UVABC3; sample type: Pool-and-split control; stage/grade: Stage 1 Grade 3; ', 'tumor: UVABC3; sample type: 10-cell sample; stage/grade: Stage 1 Grade 3; ', 'tumor: UVABC4; sample type: Pool-and-split control; stage/grade: Stage 1 Grade 2; ', 'tumor: UVABC4; sample type: 10-cell sample; stage/grade: Stage 1 Grade 2; ', 'tumor: UVABC5; sample type: Pool-and-split control; stage/grade: Stage 1 Grade 1; ', 'tumor: UVABC5; sample type: 10-cell sample; stage/grade: Stage 1 Grade 1; ' GSE23593 Homo sapiens 50 Expression profiling by array GPL570 Intratumor Heterogeneity and Precision of Microarray-Based Predictors of Breast Cancer Biology and Clinical Outcome 2010-08-12 Genome-wide expression profiling was performed on 50 core needle biopsies from 18 breast cancer patients using Affymetrix GeneChip Human Genome Plus 2.0 Arrays. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23593 Intratumor heterogeneity and precision of microarray-based predictors of breast cancer biology and clinical outcome. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 28.245 https://doi.org/10.1200/JCO.2009.26.7245 {Journal of clinical oncology : official journal of the American Society of Clinical Oncology (28.245): 10.1200/JCO.2009.26.7245} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA131731 https://www.ebi.ac.uk/ena/browser/view/PRJNA131731 None [Overal design]Global profiles of expression were characterized using unsupervised clustering methods and variance components models. Precision of predictors of breast cancer biology and clinical outcome were evaluated by interclass correlation.; [Treatment]'Core needle biopsies ontained from breast cancer excisions following patient consent.'; [Growth]'None'; [Extraction]'Total RNA was extracted using a kit-based method (Rneasy, Qiagen, Valencia, CA)'; [Cell type]'Source: ''patient: A; disease state: Breast tumor; tumor grade: 3; er status: ER Positive; pr status: PR Positive; ', 'patient: B; disease state: Breast tumor; tumor grade: 2; er status: ER Positive; pr status: PR Positive; ', 'patient: C; disease state: Breast tumor; tumor grade: 2; er status: ER Positive; pr status: PR Positive; ', 'patient: D; disease state: Breast tumor; tumor grade: 2; er status: ER Positive; pr status: PR Positive; ', 'patient: E; disease state: Breast tumor; tumor grade: 3; er status: ER Negative; pr status: PR Negative; ', 'patient: F; disease state: Breast tumor; tumor grade: 2; er status: ER Positive; pr status: PR Negative; ', 'patient: G; disease state: Breast tumor; tumor grade: 3; er status: ER Negative; pr status: PR Negative; ', 'patient: H; disease state: Breast tumor; tumor grade: 3; er status: ER Negative; pr status: PR Negative; ', 'patient: I; disease state: Breast tumor; tumor grade: 2; er status: ER Positive; pr status: PR Positive; ', 'patient: J; disease state: Breast tumor; tumor grade: 3; er status: ER Positive; pr status: PR Positive; ', 'patient: K; disease state: Breast tumor; tumor grade: 2; er status: ER Positive; pr status: PR Positive; ', 'patient: L; disease state: Breast tumor; tumor grade: 3; er status: ER Positive; pr status: PR Positive; ', 'patient: M; disease state: Breast tumor; tumor grade: 2; er status: ER Positive; pr status: PR Positive; ', 'patient: N; disease state: Breast tumor; tumor grade: 2; er status: ER Positive; pr status: PR Positive; ', 'patient: O; disease state: Breast tumor; tumor grade: 1; er status: ER Positive; pr status: PR Positive; ', 'patient: P; disease state: Breast tumor; tumor grade: 3; er status: ER Negative; pr status: PR Negative; ', 'patient: Q; disease state: Breast tumor; tumor grade: 3; er status: ER Negative; pr status: PR Positive; ', 'patient: R; disease state: Breast tumor; tumor grade: 3; er status: ER Positive; pr status: PR Negative; ' GSE144036 Homo sapiens 3 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Acetylation of histone H3K27 signals the transcriptional elongation for estrogen receptor alpha 2020-01-22 As approximately 70% of human breast tumors are estrogen receptor α (ERα)-positive, estrogen and ERα play essential roles in breast cancer development. By interrupting the ERα signaling pathway, endocrine therapy has been proven to be an effective therapeutic strategy. In the present study, we identified a novel mechanism by which Transcription Start Site (TSS)-associated histone H3K27 acetylation signals the Super Elongation Complex (SEC) to regulate transcriptional elongation of the ERα gene. The SEC interacts with H3K27ac on ERα TSS through its scaffold protein AFF4. Depletion of AFF4 by siRNA or CRISPR/Cas9 dramatically reduces expression of ERα and its target genes, consequently inhibiting breast cancer cell growth. More importantly, AFF4 mutant which lacks H3K27ac interaction failed to rescue ERα gene expression, suggesting H3K27 acetylation at TSS region is a key mark bridging the transition from transcriptional initiation to elongation, and perturbing SEC function can be an alternative strategy for targeting ERα signaling pathway at the level of chromatin. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144036 Acetylation of histone H3K27 signals the transcriptional elongation for estrogen receptor alpha. Communications biology 0.12 https://doi.org/10.1038/s42003-020-0898-0 {Communications biology (0.12): 10.1038/s42003-020-0898-0} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA602595 https://www.ebi.ac.uk/ena/browser/view/PRJNA602595 https://www.ncbi.nlm.nih.gov/sra?term=SRP243863 [Overal design]Examination of chromatin association of AFF4 and histone H3K27 acetylation in MCF7 breast cancer cell line; [Treatment]'none'; [Growth]'MCF7 cells were maintained in RPMI 1640 medium supplemented with 10% FBS.'; [Extraction]"Cells were fixed with 1% formaldehyde for 15 mins, followed by incubation with a stop solution containing 0.125M of Glycine. Lysates were clarified from sonicated nuclei and chromatin fragemnts were isolated with antibody.\nThe library construction was performed by Active Motif according to the company's protocol"; [Cell type]'Source: ''antibody: AFF4 (Bethyl Labs, A302-538A); cell line: MCF7; ', 'antibody: H3K27ac (Active Motif, 39133); cell line: MCF7; ', 'antibody: none; cell line: MCF7; ' GSE108250 Mus musculus 38 Expression profiling by high throughput sequencing GPL17021 Modulating Bone Marrow Hematopoietic Lineage Potential to Prevent Breast Cancer Bone Metastasis 2017-12-18 The presence of disseminated tumor cells in patient bone marrow (BM) aspirates predicts decreased recurrence-free survival, yet little is known about whether hematopoietic BM cells impact bone metastases. Here, we report that the BM can be rendered metastasis-suppressive by the bone-targeting bisphosphonate, zoledronic acid (ZA). In particular, ZA modulates hematopoietic myeloid/osteoclast progenitor cell (M/OCP) lineage potential to render them metastasis-suppressive. Granulocyte-colony stimulating factor (G-CSF) promotes resistance to ZA by re-directing M/OCP differentiation. We identified BM transcriptional programs that associate with metastasis suppression and resistance to ZA. Analysis of patient blood samples taken at randomization revealed that women with plasma G-CSF levels >23 pg/mL experienced significantly worse outcome with adjuvant ZA than those on ZA who had lower plasma G-CSF levels. Our findings establish that hematopoietic cells and M/OCP lineage potential profoundly impact bone metastasis and support the discovery of biomarkers that stratify therapeutic responses in patients at risk of recurrence. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE108250 Modulating Bone Marrow Hematopoietic Lineage Potential to Prevent Bone Metastasis in Breast Cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-18-0548 {Cancer research (8.378): 10.1158/0008-5472.CAN-18-0548} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA422921 https://www.ebi.ac.uk/ena/browser/view/PRJNA422921 https://www.ncbi.nlm.nih.gov/sra?term=SRP126978 [Overal design]To test in murine bone marrow and osteoclast precursor cells the effects on gene expression of treatment with ZA and G-CSF. At least two replicates from each treatment were used (including no treatment and combination treatment) and analyzed in a pairwise fashion.; [Treatment]'Zoledronic acid (ZA) [1-hydroxy-2-(1H-imidazole-1-yl)ethylidene-bisphosphonic acid] (Novartis Pharmaceuticals, Cambridge, MA) was dissolved in 1X Hank’s Balanced Buffer Solution (Gibco) and stored at 4°C until use. ZA was administered to mice at a dose of 100 µg/kg (i.p.). Recombinant human granulocyte colony stimulating factor (G-CSF) (carrier-free, Biolegend #578604) was administered to nude mice each day for 3 days at a dose of 50 µg/kg (i.p.) beginning one day after administration of ZA, and C57BL/6 mice each day for 3 days at a dose of 50 µg/kg (i.p.) beginning 2 days after administration of ZA. For G-CSF depletion experiments, nude mice were treated with 100 µg/kg (i.p.) G-CSF antibody (R&D Systems, MAB414100) or the 100 µg/kg (i.p.) isotype control IgG (R&D Systems, MAB005) six hours prior to intracardiac injection of tumor cells.'; [Growth]'6-7 week old C57BL/6J female mice were purchased from The Jackson Laboratory (Bar Harbor, ME). All animal procedures were performed in accordance with the ethics and regulations of Brigham & Women’s Hospital Institutional Animal Care and Use Committee (protocol approval 2017N000056), Boston Children’s Hospital Institutional Animal Care and Use Committee (protocol approval 12-11-2308R), and Massachusetts General Hospital (protocol approval 2017N000023).'; [Extraction]'RNA isolated from mouse bone marrow was subject to quality control using the Bioanalyzer (Agilent). BMCs were prepared for flow cytometry by suspension in sterile PBS containing 2% FBS. Cells were labeled with appropriate antibodies for 30 minutes at 4°C. Gating was used to exclude debris, cell clumps, and dead cells (using 7-aminoactinomycin D; 7-AAD Viability Staining Solution (BioLegend, 420404).Prior to sorting of the M/OCP populations, the Murine Direct Lineage Cell Depletion Kit (Miltenyi Biotec Inc., 130-110-470) was used to enrich for Lin- populations, which was confirmed by flow cytometry for the markers in the lineage cocktail. Myeloid/osteoclast progenitor cell (M/OCP) populations were defined as Lineage- CD115+. Antibody panel includes: Pacific BlueTM anti-mouse Lineage Cocktail (BioLegend, 133310: CD3-, Ly-6G/Ly6-C-, Cd11b-, CD45R-, TER119-) and Alexa Fluor® 488 anti-mouse CD115 (CSF-1R; BioLegend, 135511).\nRNA was converted into a DNA library using the Ultra RNA Library Prep Kit for Illumina (New England BioLabs). After further quality control, libraries were sequenced on the HiSeq 2000 (Illumina).'; [Cell type]'Source: ''strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: ZA & G-CSF; biological replicate: 1; sequencing batch: NA; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: ZA & G-CSF; biological replicate: 3; sequencing batch: NA; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: No treatment; biological replicate: 1; sequencing batch: NA; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: No treatment; biological replicate: 2; sequencing batch: NA; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: G-CSF; biological replicate: 1; sequencing batch: NA; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: G-CSF; biological replicate: 2; sequencing batch: NA; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: G-CSF; biological replicate: 3; sequencing batch: NA; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: ZA; biological replicate: 2; sequencing batch: NA; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: ZA; biological replicate: 3; sequencing batch: NA; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: No treatment; biological replicate: 2; sequencing batch: 1; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: No treatment; biological replicate: 2; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: G-CSF; biological replicate: 2; sequencing batch: 1; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: G-CSF; biological replicate: 2; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: ZA; biological replicate: 2; sequencing batch: 1; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Bone marrow; treatment: ZA; biological replicate: 2; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: ZA & G-CSF; biological replicate: 1; sequencing batch: 1; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: ZA & G-CSF; biological replicate: 1; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: ZA & G-CSF; biological replicate: 2; sequencing batch: 1; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: ZA & G-CSF; biological replicate: 3; sequencing batch: 1; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: ZA & G-CSF; biological replicate: 3; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: ZA & G-CSF; biological replicate: 4; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: ZA & G-CSF; biological replicate: 5; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: No treatment; biological replicate: 2; sequencing batch: 1; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: No treatment; biological replicate: 2; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: No treatment; biological replicate: 7; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: G-CSF; biological replicate: 1; sequencing batch: 1; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: G-CSF; biological replicate: 1; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: G-CSF; biological replicate: 2; sequencing batch: 1; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: G-CSF; biological replicate: 2; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: G-CSF; biological replicate: 3; sequencing batch: 1; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: G-CSF; biological replicate: 3; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: G-CSF; biological replicate: 4; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: G-CSF; biological replicate: 5; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: ZA; biological replicate: 3; sequencing batch: 1; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: ZA; biological replicate: 5; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: ZA; biological replicate: 6; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: ZA; biological replicate: 7; sequencing batch: 2; ', 'strain: C57BL/6; age: 6-7 weeks; tissue: Osteoclast precursors; treatment: ZA; biological replicate: 8; sequencing batch: 2; ' GSE58383 Homo sapiens 6 Expression profiling by array GPL6883 Breast cancer tumor promoting cell transcriptome 2014-06-10 In this study we obtained gene expression profiles of MCFS and parental MCF7 cell lines using Illumina microarrays https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58383 In-depth characterization of breast cancer tumor-promoting cell transcriptome by RNA sequencing and microarrays. Oncotarget None https://doi.org/10.18632/oncotarget.5810 {Oncotarget (None): 10.18632/oncotarget.5810} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA252386 https://www.ebi.ac.uk/ena/browser/view/PRJNA252386 None [Overal design]Transcriptome analysis of tumor promoting mammospheres (MCFS) and parental MCF7 breast cancer cell line was run in triplicate on microarrays; [Treatment]'None'; [Growth]'None'; [Extraction]'Cell pellets (~106 cells) were immediately put on ice, homogenized in 1 mL of TRIzol® Reagent (Invitrogen, Life technologies, Foster City, CA, USA) and lysates were stored at -80 °C for not more than 2 weeks. Total RNA was extracted following the manufacturer instructions. Contaminating DNA was digested using the Ambion® (Austin, TX, USA) recombinant DNase I and RNA samples were purified using the RNeasy MinElute Cleanup Kit (Qiagen, Germantown, Maryland, USA).'; [Cell type]'Source: ', 'tumor promoting mammospheres''cell line: MCFS; cell line type: tumor promoting mammospheres; ', 'cell line: MCFS; cell type: tumor promoting mammospheres; ', 'cell line: MCF7; cell line type: parental; ' GSE112089 Mus musculus 14 Genome binding/occupancy profiling by high throughput sequencing GPL21103 Simultaneous epitope and epigenetic profile measurements with multi-index single-cell ATAC-sequencing [4T1] 2018-03-20 A novel scATAC-seq approach, Multi-Index single cell ATAC-seq (MI-ATAC), in which we not only index the accessible chromatin of individual cells, but also index their protein expression using index Fluorescence Activated Cell Sorting (FACS). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112089 Joint single-cell DNA accessibility and protein epitope profiling reveals environmental regulation of epigenomic heterogeneity. Nature communications 11.878 https://doi.org/10.1038/s41467-018-07115-y {Nature communications (11.878): 10.1038/s41467-018-07115-y} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA439285 https://www.ebi.ac.uk/ena/browser/view/PRJNA439285 https://www.ncbi.nlm.nih.gov/sra?term=SRP136105 [Overal design]scATAC-seq performed on 4T1 cells in normoxia or hypoxic conditions for 6h, 12h, 24h, 48h, 36h, 48h or 72h.; [Treatment]'4T1 cell line were cultured in a Ruskinn Invivo2 workstation maintained at 1% O2 and 5% CO2, and cells were collected with trypsin digestion in the Ruskinn Invivo2 workstation and fixed immediately after 6hs, 12hs, 24hs, 36hs, 48hs and 72hs incubation'; [Growth]'None'; [Extraction]'bulk MI-ATAC of 4T1 cells, cells were first fixed in hypoxia, then counted and lysed, followed by transposition. The transposition reaction is the same as for standard ATAC-seq except with 0.05% Igepal CA-630 in the lysis buffer. After 30 min transposition, at 37 degrees, the reaction was quenched using 40 mM EDTA, then cells were centrifuged and supernatant was discarded. 20 µl of reverse crosslinking solution was added to the cell pellet (with final concentration of 5 ng/ml proteinase K). Reverse crosslinking was performed 65 degree overnight and inactivated by a 10 min incubation at 80 degrees the next day. The 25 µl PCR master mix (NEB, M0541S) and 5 µl of two unique primer combinations were directly added to the reverse crosslinking mixture and PCR was performed as previous described12. The PCR product was purified with Qiagen MinElute purification kit and eluted in 20 µl Qiagen EB elution buffer'; [Cell type]'breast cancer cells''cell line: 4T1; cell type: breast cancer cells; timepoint: n/a; ', 'cell line: 4T1; cell type: breast cancer cells; timepoint: 6h; ', 'cell line: 4T1; cell type: breast cancer cells; timepoint: 12h; ', 'cell line: 4T1; cell type: breast cancer cells; timepoint: 24h; ', 'cell line: 4T1; cell type: breast cancer cells; timepoint: 36h; ', 'cell line: 4T1; cell type: breast cancer cells; timepoint: 48h; ', 'cell line: 4T1; cell type: breast cancer cells; timepoint: 72h; ' GSE26971 Homo sapiens 277 Expression profiling by array; Third-party reanalysis GPL96 Affymetrix data for training of Endopredict algorithm 2011-01-31 These data, combined with other cohorts (GSE6532, GSE12093, and qRT-PCR based cohorts), was used to construct the EP algorithm, which predicts the likelihood of developing of a distant recurrence of early stage breast cancer under endocrine treatment. In addition, EPclin, a combination of the EP score, the nodal status and the tumor size, was constructed. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26971 Prognostic Significance of Interferon-γ and Its Signaling Pathway in Early Breast Cancer Depends on the Molecular Subtypes. International journal of molecular sciences 4.183 https://doi.org/10.3390/ijms21197178 {Clinical cancer research : an official journal of the American Association for Cancer Research (None) doi:10.1158/1078-0432.CCR-11-0926}; {International journal of molecular sciences (4.183) doi:10.3390/ijms21197178}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA135911 https://www.ebi.ac.uk/ena/browser/view/PRJNA135911 None [Overal design]All samples used for the development of the EP algorithm were taken from patients who received adjuvant tamoxifen only. Fresh-frozen tumours obtained from three centers were profiled on HG-U133A arrays. In brief, starting from 5 µg total RNA, labeled cRNA was prepared using the Roche Microarray cDNA Synthesis, Microarray RNA Target Synthesis (T7) and Microarray Target Purification Kit (Roche Applied Science, Mannheim, Germany), according to the manufacturer’s instructions. Raw .cel file data were processed by MAS 5.0 software (AFFYMETRIX, Santa Clara, CA). In the analysis settings, the global scaling procedure was chosen which multiplied the output signal intensities of each array to a mean target intensity of 500. We selected those samples from the GSE6532 and GSE12093 cohorts that we considered appropriate for our analyses (n=130 and n=130) and calculated MAS5 expression values from the corresponding .CEL-Files. One of the selection criteria was the GPL96 platform we also used for our measurements. GSE26971_GSE12093_dataset.txt.gz and GSE26971_GSE6532_dataset.txt.gz files contain data for both cohorts including the GSM numbers in row A and MAS5 expression data in the remaining rows. Processing of .CEL-files of these samples was exactly the same as the processing of the .CEL-files of our own samples: GPL96, MAS5, TGT 500.; [Treatment]'none'; [Growth]'primary tumor tissue, fresh-frozen after surgery'; [Extraction]"RNeasy kit, Qiagen. according to the manufacturer's instructions"; [Cell type]'Source: ''center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 134.761643835616; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 141.205479452055; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 50.0383561643836; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 130.520547945205; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 141.271232876712; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 120.854794520548; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 122.301369863014; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 122.597260273973; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 114.279452054795; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 114.049315068493; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 110.695890410959; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 109.347945205479; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 127.002739726027; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 56.6465753424658; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 118.38904109589; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 107.934246575342; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 38.4328767123288; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 9.36986301369863; tumor size: unknown; positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 134.564383561644; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 111.715068493151; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 130.290410958904; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 132.624657534247; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 106.487671232877; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 102.805479452055; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 82.7506849315068; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 111.978082191781; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 66.3123287671233; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 21.0082191780822; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 94.8493150684932; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 103.331506849315; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 63.3205479452055; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 133.775342465753; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 123.221917808219; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 113.424657534247; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 78.641095890411; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 106.38904109589; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 30.213698630137; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 58.8821917808219; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 23.0794520547945; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 107.967123287671; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 20.7452054794521; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 83.4082191780822; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 105.6; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 103.331506849315; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 101.917808219178; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 84.6904109589041; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 78.7068493150685; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 15.8465753424658; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 66.772602739726; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 60.2630136986301; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 54.7068493150685; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 53.5890410958904; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 51.7808219178082; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 66.213698630137; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 22.5205479452055; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 42.7397260273973; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 30.641095890411; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 36.986301369863; tumor size: T2 (2-5cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 111.912328767123; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 114.706849315068; tumor size: T1c (1-2cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 101.030136986301; tumor size: T1c (1-2cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 90.8054794520548; tumor size: T1ab (<=1cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 39.4191780821918; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 118.060273972603; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 64.9972602739726; tumor size: T1ab (<=1cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 144.197260273973; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 18.7397260273973; tumor size: T2 (2-5cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 24.3945205479452; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 142.947945205479; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 145.87397260274; tumor size: T2 (2-5cm); positive lymph nodes: 4-10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 34.7835616438356; tumor size: T1c (1-2cm); positive lymph nodes: >10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 136.109589041096; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 148.306849315068; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 74.9917808219178; tumor size: T3 (>5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 27.1232876712329; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Hamburg; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 139.298630136986; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 4.69815195071869; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 0.492813141683778; tumor size: T1c (1-2cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 57.1006160164271; tumor size: T1c (1-2cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 4.36960985626283; tumor size: T3 (>5cm); positive lymph nodes: >10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 21.782340862423; tumor size: T2 (2-5cm); positive lymph nodes: 4-10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 21.5852156057495; tumor size: T2 (2-5cm); positive lymph nodes: >10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 51.8767967145791; tumor size: T2 (2-5cm); positive lymph nodes: 4-10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 12.4188911704312; tumor size: T2 (2-5cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 42.4804928131417; tumor size: T2 (2-5cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 12.4845995893224; tumor size: unknown; positive lymph nodes: >10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 11.8275154004107; tumor size: T3 (>5cm); positive lymph nodes: >10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 174.915811088296; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 12.1889117043121; tumor size: T2 (2-5cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 6.01232032854209; tumor size: T3 (>5cm); positive lymph nodes: >10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 17.6098562628337; tumor size: T1c (1-2cm); positive lymph nodes: 4-10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 72.476386036961; tumor size: T2 (2-5cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 68.6981519507187; tumor size: T2 (2-5cm); positive lymph nodes: >10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 60.1560574948665; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 68.1067761806981; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 87.2279260780287; tumor size: T1c (1-2cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 142.390143737166; tumor size: unknown; positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 170.874743326489; tumor size: T1ab (<=1cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; tumor size: unknown; positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 88.2464065708419; tumor size: T2 (2-5cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 8.83778234086242; tumor size: T2 (2-5cm); positive lymph nodes: >10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 80.0328542094456; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 106.250513347023; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 143.408624229979; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 95.7043121149897; tumor size: T1c (1-2cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 10.2505133470226; tumor size: T1ab (<=1cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 66.0698151950719; tumor size: T2 (2-5cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 104.640657084189; tumor size: T2 (2-5cm); positive lymph nodes: 4-10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 114.2340862423; tumor size: T1ab (<=1cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 25.6591375770021; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 3.7782340862423; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 40.2135523613963; tumor size: T2 (2-5cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 144.262833675565; tumor size: T2 (2-5cm); positive lymph nodes: 4-10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 86.3408624229979; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 84.2710472279261; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 141.667351129363; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 140.714579055441; tumor size: T2 (2-5cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; 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adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; tumor size: unknown; positive lymph nodes: 4-10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 113.70841889117; tumor size: T3 (>5cm); positive lymph nodes: >10; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 61.5359342915811; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 63.3100616016427; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 100.008213552361; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; 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', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 59; tumor size: T1ab (<=1cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 58; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 78; tumor size: T1ab (<=1cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 87; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 29; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 50; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 63; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 60; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 39; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 63; tumor size: T1ab (<=1cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 48; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 30; tumor size: T1ab (<=1cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 58; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 53; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 56; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 57; tumor size: T2 (2-5cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 41; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 64; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 36; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 43; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 61; tumor size: T1ab (<=1cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 42; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 56; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 13; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 51; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 42; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 60; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 77; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 68; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 57; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 42; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 5; tumor size: unknown; positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 34; tumor size: T2 (2-5cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 72; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 76; tumor size: T1c (1-2cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 24; tumor size: T2 (2-5cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 36; tumor size: T2 (2-5cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 66; tumor size: unknown; positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Frankfurt; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 24; tumor size: unknown; positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 72.1806981519507; tumor size: T2 (2-5cm); positive lymph nodes: unknown; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; tumor size: T3 (>5cm); positive lymph nodes: 1-3; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 1; metastasis free interval (months): 61.8973305954825; tumor size: T1c (1-2cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ', 'center/subcohort: Mainz; metastasis (1: yes, 0: no/censored): 0; metastasis free interval (months): 187.663244353183; tumor size: T2 (2-5cm); positive lymph nodes: none; adjuvant patient treatment: Tamoxifen; ' GSE46856 Homo sapiens 11 Expression profiling by array GPL13497 PLK1 signaling coopereates with estrogen receptor-dependent gene transcription. 2013-05-13 Analysis of MCF7 breast cancer cells treated with estadiol for 6 h in presence or absence of the specific PLK1 inhibitor BI2536. Together with CHIP and global phosphoproteome data, the results demonstrate a key role of PLK1 in the estrogen receptor-mediated gene response. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE46856 PLK1 signaling in breast cancer cells cooperates with estrogen receptor-dependent gene transcription. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2013.05.024 {Cell reports (7.815): 10.1016/j.celrep.2013.05.024} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA202861 https://www.ebi.ac.uk/ena/browser/view/PRJNA202861 None [Overal design]Hormone-deprived MCF7 cells were pretreated with BI2536 or vehicle (DMSO) followed by induction with estradiol (E2) or vehicle (ethanol). RNA of each condition was analysed in triplicate on an Agilent Human genome 4x44k v2 microarray [note: MCF7_DMSO_E2_rep3 sample was a clear technical outlier (poor hybridization), and was therefore excluded from the further analysis/this record].; [Treatment]'For hormonal starvation, MCF7 cells were cultured for 3 days in phenol-red free DMEM supplemented with 5% charcoal-dextran treated FBS. Cells were pretreated for 1h with 100nM BI2536 or vehicle (DMSO), followed by induction with 10 nM estradiol or vehicle (ethanol) for 6 h.'; [Growth]'MCF7 cells were cultured in DMEM with 10% FBS'; [Extraction]'RNA was extracted with the RNeasy extraction kit (Qiagen).'; [Cell type]'MCF7''cell type: MCF7; cell line: breast cancer cells; pretreated with: DMSO (vehicle) for 1hr; induced with: ethanol (vehicle) for 6 h; ', 'cell type: MCF7; cell line: breast cancer cells; pretreated with: DMSO (vehicle) for 1hr; induced with: 10 nM estradiol for 6 h; ', 'cell type: MCF7; cell line: breast cancer cells; pretreated with: 100nM BI2536 for 1h; induced with: ethanol (vehicle) for 6 h; ', 'cell type: MCF7; cell line: breast cancer cells; pretreated with: 100nM BI2536 for 1h; induced with: 10 nM estradiol for 6 h; ' GSE133075 Mus musculus; Homo sapiens 43 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL16791; GPL17021 TRPS1 acts as a context-dependent regulator of mammary epithelial cell growth/differentiation and breast cancer development 2019-06-20 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE133075 TRPS1 acts as a context-dependent regulator of mammary epithelial cell growth/differentiation and breast cancer development. Genes & development 8.990 https://doi.org/10.1101/gad.331371.119 {Genes & development (8.990): 10.1101/gad.331371.119} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA549878 https://www.ebi.ac.uk/ena/browser/view/PRJNA549878 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'Chromatin immunoprecipitations were performed as described previously, with adaptations (Schmidt et al., 2009). In short, cells were crosslinked in solution A (pH 7.4, 50mM Hepes, 100mM NaCl, 1mM EDTA, 0.5M EGTA) containing 2mM DSG for 35 minutes, then formaldehyde was added to a final concentration of 1% and incubated for another 10 minutes. After addition of Glycine to a final concentration of 125mM to quench the crosslinking reaction and washing with PBS, cells were collected. The Bioruptor Pico (Diagenode) was used for sonication. For ChIP, antibodies were used to detect TRPS1 (10ug, sc-26974, Santa Cruz; 5ug, AF4838, R&D) and GATA3 (10ug, sc-268, Santa Cruz) with 100 ml Protein A or G magnetic beads (Thermo Scientific).\nImmunoprecipitated DNA was processed for library preparation (Part# 0801-0303, KAPA biosystems kit).', 'RNA was extracted using the AllPrep DNA/RNA universal kit (Qiagen) according to the manufacturer’s instruction with Qiagen’s QIAcube robot. Samples with a RIN>8 were considered for library preparation.\nLibraries were generated with the Illumina TruSeq RNA Library Preparation kit (RS-122-2001/2, Illumina Inc.).'; [Cell type]'Source: ', 'Mammary epithelial cells', 'Primary mouse mammary tumor cells''cell-type: MTC (mouse tumor-derived cells); chip antibody: aTRPS1 (sc-26974, Santa Cruz); ', 'cell-type: MCF7; chip antibody: aTRPS1 (AF4838, R&D); ', 'cell-type: MCF7; chip antibody: aTRPS1 (AF4838 R&D); ', 'cell-type: MCF7; chip antibody: aGATA3 (sc-268, Santa Cruz); ', 'cell-type: MCF7; chip antibody: aGATA3 (sc-268, Santa Cruz); sgrna/sirna: sgScr; ', 'cell-type: MCF7; chip antibody: aGATA3 (sc-268, Santa Cruz); sgrna/sirna: sgTRPS1; ', 'cell-type: MCF7; chip antibody: aTRPS1 (sc-26974, Santa Cruz); sgrna/sirna: siNT; ', 'cell-type: MCF7; chip antibody: aTRPS1 (sc-26974, Santa Cruz); sgrna/sirna: siGATA3 (pool); ', 'cell-type: HC11; sgrna: sgScr #1; ', 'cell-type: HC11; sgrna: sgTrps1 #1; ', 'cell-type: Mammary organoids; genotype/strain: Cdh1F/F;Trps1+/+; treatment: AdCre transduction, harvested after 14 days; ', 'cell-type: Mammary organoids; genotype/strain: Cdh1+/F;Trps1F/F; treatment: AdCre transduction, harvested after 14 days; ', 'cell-type: Mammary organoids; genotype/strain: Cdh1F/F;Trps1F/F; treatment: AdCre transduction, harvested after 14 days; ', 'cell-type: Mammary organoids; genotype/strain: Cdh1F/F;Trps1+/+; treatment: AdCre transduction, harvested after 28 days; ', 'cell-type: Mammary organoids; genotype/strain: Cdh1+/F;Trps1F/F; treatment: AdCre transduction, harvested after 28 days; ', 'cell-type: Mammary organoids; genotype/strain: Cdh1F/F;Trps1F/F; treatment: AdCre transduction, harvested after 28 days; ', 'cell line: HC11; cell type: Mammary epithelial cells; treatment: DMSO; ', 'cell line: HC11; cell type: Mammary epithelial cells; treatment: 300nM Trichostatin A (24 hours); ', 'cell type: Primary mouse mammary tumor cells; genotype/strain: WAP-cre;Cdh1F/F;Trps1F/F; ', 'cell type: Primary mouse mammary tumor cells; genotype/strain: WAP-cre;Cdh1F/F;Trps1+/+; ' GSE128587 Homo sapiens 58 Genome variation profiling by SNP array GPL18602; GPL18637; GPL21558 Chromothripsis is a prognostic factor in early-onset breast cancer 2019-03-20 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE128587 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA528208 https://www.ebi.ac.uk/ena/browser/view/PRJNA528208 None [Overal design]Refer to individual Series; [Treatment]'Not applicable'; [Growth]'Not applicable'; [Extraction]"Genomic DNAs were extracted according to manufacturer's protocols."; [Cell type]'Source: ''ki67 ihq: <15; p53 ihq: -; histologic grade: 2; hormone receptor (hr): -; her2 ihq: -; subtype: TNC; brca status: BRCA+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: -; histologic grade: nd; hormone receptor (hr): -; her2 ihq: -; subtype: TNC; brca status: BRCA+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 3; hormone receptor (hr): -; her2 ihq: -; subtype: TNC; brca status: BRCA+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: -; histologic grade: 3; hormone receptor (hr): -; her2 ihq: -; subtype: TNC; brca status: BRCA+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: <15; p53 ihq: -; histologic grade: nd; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: BRCA+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: nd; hormone receptor (hr): -; her2 ihq: -; subtype: TNC; brca status: BRCA+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: nd; p53 ihq: nd; histologic grade: nd; hormone receptor (hr): -; her2 ihq: -; subtype: -; brca status: BRCA+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: nd; p53 ihq: nd; histologic grade: 3; hormone receptor (hr): -; her2 ihq: -; subtype: TNC; brca status: BRCA+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 2; hormone receptor (hr): +; her2 ihq: +; subtype: luminal B; brca status: BRCA+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: -; histologic grade: nd; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: BRCA+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: nd; histologic grade: 3; hormone receptor (hr): +; her2 ihq: +; subtype: luminal B; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: <15; p53 ihq: >50; histologic grade: 1; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: <15; p53 ihq: -; histologic grade: 1; hormone receptor (hr): -; her2 ihq: +; subtype: HER2; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: -; histologic grade: 3; hormone receptor (hr): +; her2 ihq: -; subtype: TNC; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: -; histologic grade: 2; hormone receptor (hr): +; her2 ihq: +; subtype: luminal B; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 3; hormone receptor (hr): +; her2 ihq: +; subtype: luminal B; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 3; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: -; histologic grade: 3; hormone receptor (hr): -; her2 ihq: -; subtype: TNC; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: nd; p53 ihq: nd; histologic grade: 3; hormone receptor (hr): +; her2 ihq: +; subtype: luminal B; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: -; histologic grade: 2; hormone receptor (hr): +; her2 ihq: -; subtype: -; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: -; histologic grade: 3; hormone receptor (hr): +; her2 ihq: +; subtype: luminal B; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: <15; p53 ihq: nd; histologic grade: 2; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: <15; p53 ihq: -; histologic grade: 2; hormone receptor (hr): +; her2 ihq: +; subtype: luminal B; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 3; hormone receptor (hr): +; her2 ihq: +; subtype: luminal B; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: <15; p53 ihq: -; histologic grade: nd; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 2; hormone receptor (hr): +; her2 ihq: +; subtype: luminal B; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: -; histologic grade: 3; hormone receptor (hr): +; her2 ihq: +; subtype: luminal B; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 2; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 3; hormone receptor (hr): -; her2 ihq: -; subtype: TNC; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: <15; p53 ihq: >50; histologic grade: 2; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: nd; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: <15; p53 ihq: >50; histologic grade: 1; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: -; histologic grade: 3; hormone receptor (hr): -; her2 ihq: +; subtype: HER2; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 3; hormone receptor (hr): -; her2 ihq: -; subtype: TNC; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 3; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: nd; p53 ihq: nd; histologic grade: 2; hormone receptor (hr): +; her2 ihq: -; subtype: -; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 2; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: BRCA+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 2; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: >50; histologic grade: 3; hormone receptor (hr): -; her2 ihq: +; subtype: HER2; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: -; histologic grade: 3; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC+; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: <15; p53 ihq: -; histologic grade: nd; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: <15; p53 ihq: -; histologic grade: 2; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: <15; p53 ihq: -; histologic grade: 3; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC-; tissue: FFPE breast cancer tissue; ', 'ki67 ihq: >15; p53 ihq: -; histologic grade: 2; hormone receptor (hr): +; her2 ihq: -; subtype: luminal A; brca status: FBC-; tissue: FFPE breast cancer tissue; ' GSE134655 Homo sapiens 72 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Characterization of FOXA1 mutations in breast cancer (ChIP-seq) 2019-07-22 Invasive Lobular Carcinoma (ILC) is the second most frequent breast cancer (BCa) type and encompasses 10-15% of BCa cases. FOXA1 specific mutations are enriched in this subtype of BCa, however their role in breast cancer pathogenesis is still ill-defined. FOXA1, together with estrogen receptor (ER), is a key transcription factor for the correct activation of estrogen-dependent gene expression and, consequently, for mammary gland development and BCa identity. FOXA1 has the capability to bind to and de-compact heterochromatin to render it accessible for other nuclear proteins, such as ER, and allow activation of their transcriptional programs upon estrogen stimulation. In this project, we aim to elucidate the role of FOXA1 missense mutations in altering its binding to DNA, chromatin accessibility, ER-dependent transcription and their implication in limiting the sensitivity to standard-of-care anti-hormonal therapy, commonly used in ER-positive BCa patients. To this end, we have generated BCa cell lines expressing these FOXA1 mutations and we will employ ATAC-Seq, RIME assays, ChIP-Seq and RNA-Seq to ascertain their effect on DNA accessibility, DNA binding capability, as well as binding of transcriptional coregulators, such as ER, to chromatin. We will extend our analyses to our internal BCa patient datasets with detailed clinical annotation to study the correlation between presence of FOXA1 mutations and response to anti-hormonal therapy of ER-positive BCa patients. The results of this project will allow to understand how the different mutations in the Forkhead domain can alter FOXA1 and ER function, transcriptional regulation and response to anti-hormonal therapy in ER-positive BCa patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE134655 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA556014 https://www.ebi.ac.uk/ena/browser/view/PRJNA556014 https://www.ncbi.nlm.nih.gov/sra?term=SRP215944 [Overal design]ChIP-Seq analysis of MCF7 cells overexpressing either empty vector (EV), FOXA1 wild-type (WTNS) or FOXA1 mutant (SY242CS, H247Y, S250F, F266L) constructs, in duplicates.; [Treatment]'DMSO and E2 conditions were subjected to DMSO or E2 treatment for 1h'; [Growth]'Cells were seeded in full media; the following day media was changed to either estrogen depleted media (for DMSO and E2 groups) or same DMEM/F12 50/50 full media (for FM); cells were incubated for 72h; the day of cell harvesting media was refreshed'; [Extraction]'Cells were crosslinked in adherent conditions, crosslinked cells were lysed to obtain nuclear extracts, lysates were clarified from sonicated nuclei and protein-DNA complexes were isolated with antibody.\nNEBNext ChIP-Seq Library Prep Master Mix Set for Illumina (prod. no: E6240L)'; [Cell type]'breast cancer''cell line: MCF7; cell type: breast cancer; chip antibody: FOXA1 (ab23738, lot:GR3241520-1); ', 'cell line: MCF7; cell type: breast cancer; chip antibody: none (input); ' GSE84114 Homo sapiens 17 Expression profiling by high throughput sequencing GPL18573; GPL19415 Profiling in vivo Bone Lesion and ex vivo Bone-In-Culture Array Samples by Next-Generation Sequencing 2016-07-06 Based on RNA-seq, we performed transcriptomic profiling to examine the similarities or differences between BICA (bone-in-culture array) and IVBL (in vivo bone lesion). CIBERSORT analysis reveals that the major local cellular components are comparable between BICA and IVBL, but differ dramatically in orthotopic tumors. Principle component analysis of human RNAs indicated that the transcriptomic profiles of cancer cells in BICA are more closely mimicking IVBL, as compared to cancer cells in 2D and in orthotopic tumors. These results provide transcriptome-wide evidence supporting BICA as a platform to mimic bone microenvironment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE84114 Bone-in-culture array as a platform to model early-stage bone metastases and discover anti-metastasis therapies. Nature communications 11.878 https://doi.org/10.1038/ncomms15045 {Nature communications (11.878): 10.1038/ncomms15045} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA328044 https://www.ebi.ac.uk/ena/browser/view/PRJNA328044 https://www.ncbi.nlm.nih.gov/sra?term=SRP078006 [Overal design]2D culture cells, orthotopic tumors, BICA samples and bone lesions, all developed by MCF-7, are subject to NGS and then analyzed.; [Treatment]'None'; [Growth]'For MCF-7, cells are cultured in DMEM with 2% FBS. For BICA, bone pieces were prepared from metaphysis of femurs and tibias harvested from mice receiving intra-iliac injection. The bones were crushed with a bone plier (F.S.T. 16025-14) and transferred to low attachment 96-well plate. Bone pieces bearing tumor cells were cultured in media comprised of DMEM/F12.'; [Extraction]'After homogenization, total RNA were extracted by Direct-zol RNA miniprep kit. The first and second strand cDNA were prepared by SuperScript III First-Strand Synthesis System and NEBNext mRNA Second Strand Synthesis Module from at least 200ng total RNA for each sample.\nIllumina Nextera XT DNA Sample Prep Kit was used with 1 ng of dsDNA for the construction of sequencing libraries.'; [Cell type]'breast cancer cell line', 'MCF-7 and local mouse cells''cell line: MCF-7; cell type: breast cancer cell line; passage: P140-P142; reporter gene: Firefly Luciferase (MCF-7); ', 'cell type: MCF-7 and local mouse cells; passage: P140-P142; reporter gene: Firefly Luciferase (MCF-7); ' GSE22513 Homo sapiens 28 Expression profiling by array GPL570 Markers of Taxane Sensitivity in Breast Cancer 2010-06-22 The purpose of this study was to identify molecular markers of pathologic response to neoadjuvant paclitaxel/radiation treatment, protein and gene expression profiling were done on pretreatment biopsies. Patients with high-risk, operable breast cancer were treated with three cycles of paclitaxel followed by concurrent paclitaxel/radiation. Tumor tissue from pretreatment biopsies was obtained from 19 of the 38 patients enrolled in the study. Protein and gene expression profiling were done on serial sections of the biopsies from patients that achieved a pathologic complete response (pCR) and compared to those with residual disease, non-pCR (NR). Proteomic and validation immunohistochemical analyses revealed that α-defensins (DEFA) were overexpressed in tumors from patients with a pCR. Gene expression analysis revealed that MAP2, a microtubule-associated protein, had significantly higher levels of expression in patients achieving a pCR. Elevation of MAP2 in breast cancer cell lines led to increased paclitaxel sensitivity. Furthermore, expression of genes that are associated with the basal-like, triple-negative phenotype were enriched in tumors from patients with a pCR. Analysis of a larger panel of tumors from patients receiving presurgical taxane-based treatment showed that DEFA and MAP2 expression as well as histologic features of inflammation were all statistically associated with response to therapy at the time of surgery. We show the utility of molecular profiling of pretreatment biopsies to discover markers of response. Our results suggest the potential use of immune signaling molecules such as DEFA as well as MAP2, a microtubule-associated protein, as tumor markers that associate with response to neoadjuvant taxane–based therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22513 Preoperative concurrent paclitaxel-radiation in locally advanced breast cancer: pathologic response correlates with five-year overall survival. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-010-1181-8 {Clinical cancer research : an official journal of the American Association for Cancer Research (None) doi:10.1158/1078-0432.CCR-09-1091}; {The Journal of clinical investigation (None) doi:10.1172/JCI45014}; {Breast cancer research and treatment (3.471) doi:10.1007/s10549-010-1181-8}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA128489 https://www.ebi.ac.uk/ena/browser/view/PRJNA128489 None [Overal design]Tumor tissues from pretreatment needle biopsies from patients enrolled on a paclitaxel/radiation clinical trial were laser capture microdissected for RNA extraction and hybridization to Affymetrix microarrays. We analyzed one array (sample A) from duplicate samples from each patient. 14 subject, 2 replicates each.; [Treatment]'all samples are from pretreatment patients'; [Growth]'all samples are from frozen primary breast needle biopsies'; [Extraction]"frozen biopsies were sectioned, laser capture microdissected for invasive tumor cells, and total RNA was isolated according to the manufacturer's instructions."; [Cell type]'Source: ''pathological complete response: no; tissue: Breast tumor biopsy; ', 'pathological complete response: yes; tissue: Breast tumor biopsy; ' GSE20417 Homo sapiens 2 Non-coding RNA profiling by high throughput sequencing GPL9186 Discovery of microRNAs and other small RNAs in solid human tumors: sequencing 2010-02-18 MicroRNAs (miRNAs) are ~22 nucleotide-long, non-coding RNAs that regulate gene silencing. It is known that many human miRNAs are deregulated in numerous types of tumors. Here we report the sequencing of small RNAs from 23 breast, bladder, colon, and lung tumor samples using high-throughput sequencing. We identified 49 novel miRNA and miRNA-like small RNAs. We further validated the expression of 10 novel small RNAs in 31 different types of blood, normal and tumor tissue samples using two independent platforms, namely microarray and RT-PCR. Some of the novel sequences show a large difference in expression between tumor and tumor-adjacent tissues, between different tumor stages, or between different tumor types. We also report the identification of novel small RNA classes in human: highly expressed small RNA derived from Y-RNA and endogenous siRNA. Finally, we identified dozens of new miRNA sequence variants that demonstrate the existence of miRNA-related SNP or post-transcriptional modifications. Our work extends the current knowledge of the tumor small RNA transcriptome and provides novel candidates for molecular biomarkers and drug targets. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE20417 Discovery of microRNAs and other small RNAs in solid tumors. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkq376 {Nucleic acids research (11.147): 10.1093/nar/gkq376} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA129825 https://www.ebi.ac.uk/ena/browser/view/PRJNA129825 None [Overal design]2 samples of pools of different tumor samples: pool1: breast (5 samples), bladder (5 samples); 2 replicates each pool2: colon (7 samples), lung (6 samples); 2 replicates each; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted twice from each sample of 23 human formalin-fixed paraffin-embedded (FFPE) samples derived from cancerous tissue. RNA was isolated using ten 10-µm-thick tissue sections using the miRdicatorTM extraction protocol developed at Rosetta Genomics. Briefly, the sample was incubated repeatedly in xylene at 57oC to remove excess paraffin, followed by washing in ethanol. Proteins were degraded by incubation in proteinase K solution at 45oC for a few hours. The RNA was extracted with acid phenol:chloroform followed by ethanol precipitation and DNAse digestion. Total RNA quantity and quality were checked by spectrophotometry (Nanodrop ND-1000). Pools of samples of the small RNA fraction within the total RNA were labeled and hybridized on arrays. After ensuring the presence and expression of more than 100 miRNAs per cancerous tissue pool, tissues were pooled together, resulting in a bladder+breast tumor pool and a colon+lung tumor pool. Array expression revealed the presence of 157 miRNAs from bladder cancer FFPEs, 260 miRNAs from breast cancer FFPEs, 135 miRNAs from lung cancer FFPEs, and 239 miRNAs from colon cancer FFPEs. Total RNA (75 µg) of seven different colon cancer FFPEs were pooled together with 75 µg of six different lung cancer FFPEs, while 75 µg total RNA of five different bladder cancer FFPEs were pooled together with 75 µg of five different breast cancer FFPEs.'; [Cell type]'Source: ''tissue: bladder tumors, breast tumors; ', 'tissue: colon tumors, lung tumors; ' GSE32669 Homo sapiens 8 Expression profiling by array GPL570 Time-course effect of estradiol and estradiol-BSA on early gene expression in SKBR3 cells 2011-10-06 Estrogens have been reported to activate several processes via membrane binding to either classic estrogen receptors (ERs) or GPR30. We have used either estradiol or BSA-conjugated estradiol in order to initiate membrane-initiated actions and ICI 172,780 (ICI) or G15 to explore ER- and GPR30-related transcription. Our results show that the majority of G15-inhibited transcription is depending on ERs, as it is also inhibited by ICI. However, a small number of transcripts, related to specific actions/pathways is either exclusively inhibited by G15, providing evidence about a specific GPR30 signature, or not inhibited by ICI or G15 suggesting the existence of another, yet unidentified estrogen receptor. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32669 Early membrane initiated transcriptional effects of estrogens in breast cancer cells: First pharmacological evidence for a novel membrane estrogen receptor element (ERx). Steroids 2.136 https://doi.org/10.1016/j.steroids.2012.02.011 {Steroids (2.136) doi:10.1016/j.steroids.2012.02.011}; {Steroids (2.136) doi:10.1016/j.steroids.2011.11.005}; {Steroids (2.136) doi:10.1016/j.steroids.2011.12.016}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA154465 https://www.ebi.ac.uk/ena/browser/view/PRJNA154465 None [Overal design]Cells after a 4h incubation with medium containing 10% charcoal stripped FBS were incubated with or without E2-BSA (10-6M) in the presence or absence of specific antagonists, in McCoys's 5A medium supplemented with 10% charcoal stripped FBS, for 3 hours. Total RNA was isolated using Nucleospin II columns (Macheray-Nagel, Dttren, Germany), according to the manufacturer’s instructions. RNA was labeled and hybridized according to the Affymetrix protocol (Affymetrix Gene-Chip Expression Analysis Technical Manual), using the HGU133A plus 2 chip, analyzing a total of 54675 transcripts. Signals were detected by an Affymetrix microarray chip reader.; [Treatment]'SKBR3 cells were incubated with or without Estradiol, E2-BSA, ICI, G15 or combinations of E2-BSA with ICI or G15 for 3 hours after preincubation for 4 hours with medium containing 10% charcoal stripped FBS.'; [Growth]'The human breast cancer cell line SKBR3 was obtained from DSMZ (Braunschweig, Germany) and cultured in McCoy′s 5A supplemented with 10% fetal bovine serum, at 37 °C, 5% CO2.'; [Extraction]'Total RNA was isolated using Nucleospin II columns (Macheray-Nagel, Dttren, Germany), according to the manufacturer’s instructions.'; [Cell type]'breast cancer derived cells''cell line: SKBR3; cell type: breast cancer derived cells; ' GSE72669 Homo sapiens 2 Expression profiling by array GPL16699 Genes induced by partial down-regulation of ARID1A in breast cancer cell 2015-09-02 Development of gene expression signatures for partial downreualtion of ARID1A protein. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72669 Downregulation of ARID1A, a component of the SWI/SNF chromatin remodeling complex, in breast cancer. Journal of Cancer 3.182 https://doi.org/10.7150/jca.16602 {Journal of Cancer (3.182): 10.7150/jca.16602} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA294615 https://www.ebi.ac.uk/ena/browser/view/PRJNA294615 None [Overal design]ARID1A was down-regulated by si-RNA in a breast cancer cell, MDA-MB-157. Subsequently, RNAs was extracted from control siRNA treated cells or partially ARID1A-down regulated cells. cDNAs were synthesized and cRNAs were labeled using low input quick Amp labeling kit (Agilent). Aftere washing and dry, scanned by Agilent Technologies Micorarrray Scanner and calculated using Agilent Feature 10.7.3.1. control siRNA treated MDA-MB-157 breast cancer cells (MOK) and siRNA-midiated ARID1A-downregulated MDA-MB157 breast cancer cells.; [Treatment]'None'; [Growth]'None'; [Extraction]"total RNAs were extracted using Rneasy mini kit (Qiagen) accoring to the the manufacturer's recommendations."; [Cell type]'Source: ''cell line: human invasive breast cancer cells MDA-MB-157 cells; ' GSE148312 Homo sapiens 3 Expression profiling by high throughput sequencing GPL18573 FGFR1 associates with gene promoters and regulates gene transcription: Implications for endocrine resistance in ER+/FGFR1-amplified breast cancer (RNA-seq) 2020-04-08 Using ChIP-Seq analysis of ER+/FGFR1-amplified breast cancer cells and PDXs, we found FGFR1 occupancy at transcription start sites with high overlap with histone modifications associated with active gene transcription. Mass spectrometry analysis of the nuclear and chromatin-bound FGFR1 interactome identified RNA-Polymerase II (Pol II) and FOXA1, with FOXA1 silencing impairing FGFR1 recruitment to chromatin. Transduction of FGFR1(SP-)(NLS) into MCF7 cells resulted in overexpression of nuclear FGFR1 and resistance to antiestrogens. Finally, an expression signature associated with nuclear FGFR1 correlated with endocrine resistance in patients treated with antiestrogens https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148312 Nuclear FGFR1 Regulates Gene Transcription and Promotes Antiestrogen Resistance in ER+ Breast Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-20-3905 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-20-3905} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA623904 https://www.ebi.ac.uk/ena/browser/view/PRJNA623904 https://www.ncbi.nlm.nih.gov/sra?term=SRP255745 [Overal design]Examination of transcriptome of ER+/FGFR1-amplified human breast cancer CAMA1 cells. Three biological replicates; [Treatment]'Cells were cultured for 48 h in estradiol-deprived media before RNA-extraction protocol'; [Growth]'Cells were cultured in 10-cm dishes'; [Extraction]'Cells were harvested and RNA was purified using a RNA purification kit (Maxwell, Promega).\nSamples were run on the Agilent Tapestation 4200 to ensure use of only high quality RNA (RIN Score ≥8).\xa0The Qubit fluorometer was used to determine sample concentration prior to preparation of libraries.\xa0One μg of total DNAse treated RNA was then prepared with the TruSeq Stranded mRNA Library Prep Kit from Illumina.\xa0Poly-A RNA was purified and fragmented before strand specific cDNA synthesis. cDNAs were then a-tailed and indexed adapters were ligated. After adapter ligation, samples were PCR amplified and purified with AmpureXP beads, then validated again on the Agilent Tapestation 4200.\xa0 Before being normalized and pooled, samples were quantified by Qubit then run on the Illumina NextSeq 500 using V2.5 reagents'; [Cell type]'ER+/FGFR1-amplified breast cancer cells''cell line: CAMA1; cell type: ER+/FGFR1-amplified breast cancer cells; passage: less than 10; ' GSE109396 Homo sapiens 6 Expression profiling by array GPL570 Expression data from SUM149 inflammatory breast cancer cells cultured in monolayer or Matrigel 2018-01-18 Inflammatory breast cancer (IBC) is a rare type of breast cancer but accounts for up to 10% of breast cancer-related deaths. Plasticity between epithelial and mesenchymal feature is reported to be crucial in metastasis of IBC. Using Matigel culture, we induced epithelial to mesenchymal transition (EMT) in epithelial-like SUM149 IBC cells and identified overexpressed genes in this EMT process. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE109396 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA430729 https://www.ebi.ac.uk/ena/browser/view/PRJNA430729 None [Overal design]SUM149 cells were plated on monolayer or Matrigel culture (triplicates each) on day 0. On day 2, SUM149 cells on monolayer culutre were collected by tripsinizing them and SUM149 cells on Matrigel culture were recovered by using Cell Recovery Solution for RNA extraction and hybridization on Affymetrix microarrays.; [Treatment]'Monolayer cultured SUM149 cells were tripsinized and tripsion was neutralized with 10% FBS containing medium. Matrigel cultured SUM149 cells were recovered by using Cell Recovery Solution (Corning).'; [Growth]'Single suspended SUM149 cells were plated in monolayer and Matrigel-coated dishes and cultured for 2 days. Cell suspension in Matrigel contained 2% Matrigel.'; [Extraction]'Total RNA was extracted using the RNeasy kit (Qiagen). The integrity of the obtained RNA was assessed using the Agilent 2100 BioAnalyzer (Agilent Technologies).'; [Cell type]'Source: ''cell line: SUM149; culture: monolayer; disease: Inflammatory breast cancer; gender: Female; ', 'cell line: SUM149; culture: matrigel; disease: Inflammatory breast cancer; gender: Female; ' GSE61198 Mus musculus 4 Genome binding/occupancy profiling by high throughput sequencing GPL9250; GPL17021 Distinct EMT programs control normal stem cells and cancer stem cells of mammary tissue 2014-09-08 Cancer stem cells (CSCs) are proposed to be responsible for metastatic dissemination and clinical relapse in a variety of cancers. Analogies between CSCs and normal tissue stem cells (SC) has led to the notion that CSCs often co-opt the normal SC program of their tissue-of-origin. The cell-biological program termed epithelial-mesenchymal transition (EMT) has been found to encourage entrance of normal and neoplastic mammary cells into the corresponding SC states. Using genetically engineered knock-in reporter mouse lines, we demonstrate that in the murine mammary lineage, the paralogous EMT-inducing transcription factors Snail and Slug, are selectively exploited by CSCs and normal SCs respectively. Slug, when expressed at physiological levels, only activates a partial EMT program and is dispensable in CSCs. In contrast, Snail drives a far more complete transition into the mesenchymal state and controls both tumor-initiation and metastatic dissemination. Consistent with their functional distinctions, Snail controls far more target genes than Slug, and their distinct functions are determined by their divergent N-terminal domains. Our findings underscore fundamental distinctions between the SC program operating in normal and neoplastic SCs, and hint for potential avenues of selective therapeutic elimination of breast CSCs. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE61198 Distinct EMT programs control normal mammary stem cells and tumour-initiating cells. Nature 43.070 https://doi.org/10.1038/nature14897 {Nature (43.070): 10.1038/nature14897} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA260499 https://www.ebi.ac.uk/ena/browser/view/PRJNA260499 https://www.ncbi.nlm.nih.gov/sra?term=SRP046313 [Overal design]We sought to understand differential ability to activate the EMT program in breast cancer cells by transcription factors Snail and Slug. Hence, we mapped genome-wide Snail and Slug binding sites in murine MMTV-PyMT breast cancer cell lines that express high level of Snail or high level of Slug respectively. Specifically, we performed Snail ChIP seq in the mesenchymal pBl.3G cells, and Slug ChIP-seq in the epithelial pBl.1G cells.; [Treatment]'None'; [Growth]'Cells were grown in DMEM/F12 + 5% adult bovine serum + Non-essential amino acide + Pen/Strep'; [Extraction]'the cells were cross-linked with 1% formaldehyde for 10 min at room temperature, and formaldehyde was then inactivated by the addition of 125mM glycine. Cells were lysed, and genomic DNA sonicated to generate DNA fragments that are about 200-500bp\nIllumina True-Seq Lirary Prep Kit'; [Cell type]'Source: ''cell line: MMTV-PyMT breast cancer cell line; genotype/variation: epithelial cell with high Slug expression; ', 'cell line: MMTV-PyMT breast cancer cell line; genotype/variation: Mesenchymal cell with high Snail expression; ', 'cell line: MMTV-PyMT breast cancer cell line; genotype/variation: epithelial cell with high Slug expression; chip antibody: Slug (C19G7) Rabbit mAb; chip antibody vendor: Cell Signalling Technology; chip antibody cat. #: 9585; ', 'cell line: MMTV-PyMT breast cancer cell line; genotype/variation: Mesenchymal cell with high Snail expression; chip antibody: Anti-SNAIL + SLUG antibody; chip antibody vendor: abcam; chip antibody cat. #: ab85931; ' GSE119147 Homo sapiens 4 Expression profiling by high throughput sequencing GPL18573 RNA-seq of MCF7 spheroids after macrophage infiltration. 2018-08-28 To determine effects of primary human macrophages on breast tumor cell mRNA levels, breast carcinoma cell line MCF7 were grown as spheroids in the presence or absence of infiltrating macrophages. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE119147 Macrophages attenuate the transcription of CYP1A1 in breast tumor cells and enhance their proliferation. PloS one 2.776 https://doi.org/10.1371/journal.pone.0209694 {PloS one (2.776): 10.1371/journal.pone.0209694} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA488257 https://www.ebi.ac.uk/ena/browser/view/PRJNA488257 https://www.ncbi.nlm.nih.gov/sra?term=SRP159019 [Overal design]Breast tumor profiles of MCF7 spheroids +/- infiltrated macrophages were generated by deep sequencing using Illumina TruSeq technology.; [Treatment]'CD14+ macrophages were cultured with spheroids for additional 48 hours.'; [Growth]'Cells were maintained in RPMI 1640 supplemented with 10% FBS, 1% sodium pyruvate, 100U/ml penicillin and 100 µg/ml streptomycin and cultivated at 37°C in a humidified atmosphere with 5% CO2. Multicellular spheroids were generated according to the liquid overlay technique and cultured for 5 days.'; [Extraction]'RNA was harvested using RNA Clean and Concentrator-25 protocol.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'MCF7 cells''cell type: MCF7 cells; infiltration: None; ', 'cell type: MCF7 cells; infiltration: MФ; ' GSE41227 Homo sapiens 22 Expression profiling by array GPL1352 Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 4 Epithelial) 2012-09-28 We used gene expression profiling of human DCIS and IBC to discover uniquely expressed genes that may also regulate progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41227 Differentially expressed genes regulating the progression of ductal carcinoma in situ to invasive breast cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-12-0636 {Cancer research (8.378): 10.1158/0008-5472.CAN-12-0636} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA176239 https://www.ebi.ac.uk/ena/browser/view/PRJNA176239 None [Overal design]RNA from human samples were extracted, purified, amplified, and evaluated for gene expression using Affymetrix U133-X3P gene expression arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'laser capture microdissection of target cells (Epithelial) to estimated >95% total cells using Ambion RNA extraction kit'; [Cell type]'epithelial''tissue: Breast; cell type: epithelial; disease state: ductal carcinoma in situ; ', 'tissue: Breast; cell type: epithelial; disease state: invasive breast cancer; ' GSE19615 Homo sapiens 115 Expression profiling by array GPL570 Integrated genomic and function characterization of the 8q22 gain 2009-12-22 Integrated DNA and expression array analysis in primary human breast tumors identified chromosome 8q22 copy number gain and a suite of over-expressed genes in this region highly relevant to subsequent recurrence. 8q copy gain is associated with increased risk of distant metastasis despite adjuvant chemotherapy and multiple genes from 8q22 are overexpressed and have pleiotropic effects, contributing to tumor growth, survival, and reduced killing of tumor cell by chemotherapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE19615 Amplification of LAPTM4B and YWHAZ contributes to chemotherapy resistance and recurrence of breast cancer. Nature medicine 30.641 https://doi.org/10.1038/nm.2090 {Nature medicine (30.641): 10.1038/nm.2090} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA122457 https://www.ebi.ac.uk/ena/browser/view/PRJNA122457 None [Overal design]Affymetrix U133plus2 from 115 tumor patients; [Treatment]'None'; [Growth]'None'; [Extraction]"extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 292; age: 53; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 2.3; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): NA; distant recurrence free survival (mo): 24; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 310; age: 60; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 0.9; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 38; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 316; age: 65; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 3.5; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 60; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 325; age: 48; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 1.8; lymph nodes: positive; adjuvant chemotherapy: AC-taxol(x1); chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): NA; distant recurrence free survival (mo): 9; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 330; age: 58; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 2.1; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 62; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 343; age: 45; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 2.5; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): NA; distant recurrence free survival (mo): 16; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 390; age: 49; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 1.2; lymph nodes: positive; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 64; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 397; age: 56; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 2.1; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 67; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 400; age: 85; histology type: Ductal; grade (modified, bloom, richardson): II; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 2.5; lymph nodes: positive; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): NA; distant recurrence free survival (mo): 27; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 451; age: 66; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 2.5; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 62; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 488; age: 58; histology type: Ductal; grade (modified, bloom, richardson): II; er: neg; pr: neg; her.2: neg; tumor size (cm): 1.8; lymph nodes: negative; adjuvant chemotherapy: Unknown; chemo class: Unknown; hormonal rx: none; time of followup (mo): 52; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 498; age: 79; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 5; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: none; time of followup (mo): NA; distant recurrence free survival (mo): 1; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 534; age: 58; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 2.1; lymph nodes: negative; adjuvant chemotherapy: Epirubicin, Cytoxan, Xeloda; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 53; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 538; age: 48; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 1; lymph nodes: negative; adjuvant chemotherapy: Unknown; chemo class: Unknown; hormonal rx: none; time of followup (mo): 54; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 554; age: 50; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 0.9; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 51; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 558; age: 40; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 2.2; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 48; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 582; age: 58; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 1; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 52; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 588; age: 63; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 3.5; lymph nodes: positive; adjuvant chemotherapy: AC-taxol/Herceptin; chemo class: Trastuzumab; hormonal rx: none; time of followup (mo): 50; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 591; age: 41; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 2.7; lymph nodes: negative; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 50; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 598; age: 74; histology type: Ductal; grade (modified, bloom, richardson): II; er: neg; pr: neg; her.2: neg; tumor size (cm): 2.5; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: none; time of followup (mo): 40; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 609; age: 48; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 3; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 49; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 613; age: 78; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 1.3; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: none; time of followup (mo): 53; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 653; age: 55; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 1.4; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 50; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 664; age: 43; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 1.7; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): NA; distant recurrence free survival (mo): 35; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 665; age: 72; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 2.3; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: none; time of followup (mo): 50; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 670; age: 49; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 3.4; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 36; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 799; age: 43; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 2.8; lymph nodes: negative; adjuvant chemotherapy: CAF; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 36; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 828; age: 56; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 2.2; lymph nodes: negative; adjuvant chemotherapy: AC-taxotere; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 39; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 396; age: 41; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: pos (3+); tumor size (cm): 1.1; lymph nodes: positive; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 65; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 92; age: 62; histology type: Lobular; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 3.5; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 80; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 129; age: 43; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: pos (3+); tumor size (cm): 1; lymph nodes: negative; adjuvant chemotherapy: Unknown; chemo class: Unknown; hormonal rx: unknown; time of followup (mo): 78; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 131; age: 54; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: low pos (2+); tumor size (cm): 1.7; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 78; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 96; age: 55; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos-low; pr: pos-low; her.2: pos (3+); tumor size (cm): 1.4; lymph nodes: positive; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 51; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 86; age: 46; histology type: Mixed; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 2.6; lymph nodes: positive; adjuvant chemotherapy: CMF; chemo class: Other; hormonal rx: Tam; time of followup (mo): NA; distant recurrence free survival (mo): 6; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 73; age: 46; histology type: Mixed; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 0.9; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 85; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 212; age: 44; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 0.8; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 73; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 74; age: 54; histology type: Ductal; grade (modified, bloom, richardson): II; er: pos; pr: pos-low; her.2: pos (3+); tumor size (cm): 2.2; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 82; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 196; age: 49; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 1.8; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 75; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 123; age: 84; histology type: Mixed; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 2.2; lymph nodes: positive; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 79; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 180; age: 43; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: neg; her.2: pos (3+); tumor size (cm): 4.2; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 52; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 249; age: 54; histology type: Ductal; grade (modified, bloom, richardson): II; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 2.5; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 81; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 207; age: 45; histology type: Lobular; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 2.3; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 59; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 65; age: 45; histology type: Ductal; grade (modified, bloom, richardson): II; er: pos-low; pr: pos-low; her.2: pos (3+); tumor size (cm): 1.7; lymph nodes: positive; adjuvant chemotherapy: AC-taxotere; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 83; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 157; age: 35; histology type: Lobular; grade (modified, bloom, richardson): II; er: pos; pr: neg; her.2: neg; tumor size (cm): 1.1; lymph nodes: positive; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 85; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 148; age: 53; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 3; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): NA; distant recurrence free survival (mo): 18; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 228; age: 60; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: pos-low; her.2: neg; tumor size (cm): 2.3; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 70; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 162; age: 32; histology type: Ductal; grade (modified, bloom, richardson): II; er: pos; pr: pos-low; her.2: neg; tumor size (cm): 1.5; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 83; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 175; age: 40; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: neg; her.2: neg; tumor size (cm): 4; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 74; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 14; age: 45; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 1.5; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 87; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 246; age: 46; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 1.1; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 86; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 60; age: 41; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 3; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 86; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 138; age: 46; histology type: Lobular; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: low pos (2+); tumor size (cm): 2.3; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 80; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 204; age: 36; histology type: Ductal; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 1; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 78; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 239; age: 68; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 1.1; lymph nodes: negative; adjuvant chemotherapy: Unknown; chemo class: Unknown; hormonal rx: unknown; time of followup (mo): 73; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 253; age: 54; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 1.1; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 56; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 11; age: 81; histology type: Lobular; grade (modified, bloom, richardson): I; er: pos; pr: pos-low; her.2: neg; tumor size (cm): 2.5; lymph nodes: positive; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 70; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 21; age: 45; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: low pos (2+); tumor size (cm): 3; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 83; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 214; age: 53; histology type: Lobular; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 5.2; lymph nodes: positive; adjuvant chemotherapy: AC x 2, Taxol; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): NA; distant recurrence free survival (mo): 14; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 12; age: 48; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 2.5; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 75; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 165; age: 53; histology type: Lobular; grade (modified, bloom, richardson): II; er: pos; pr: neg; her.2: neg; tumor size (cm): 2.5; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 77; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 126; age: 57; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: low pos (2+); tumor size (cm): 1.7; lymph nodes: positive; adjuvant chemotherapy: AC-taxol.taxotere; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 73; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 6; age: 57; histology type: Ductal; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 2.1; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 59; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 58; age: 46; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos-low; her.2: neg; tumor size (cm): 1.5; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 85; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 164; age: 50; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: low pos (2+); tumor size (cm): 1.9; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 77; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 119; age: 58; histology type: Mixed; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 3.5; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 81; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 154; age: 62; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 1.5; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 81; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 182; age: 44; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 2; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 57; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 35; age: 37; histology type: Ductal; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: pos (3+); tumor size (cm): 1.3; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 48; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 151; age: 55; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 2.5; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 58; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 203; age: 64; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: neg; tumor size (cm): 1.7; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: none; time of followup (mo): NA; distant recurrence free survival (mo): 21; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 187; age: 53; histology type: Ductal; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 3; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 77; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 237; age: 66; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos-low; pr: pos; her.2: neg; tumor size (cm): 1.1; lymph nodes: positive; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 82; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 238; age: 63; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: pos (3+); tumor size (cm): 1.2; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: none; time of followup (mo): 71; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 252; age: 66; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 1.2; lymph nodes: positive; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 55; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 206; age: 38; histology type: Mixed; grade (modified, bloom, richardson): III; er: pos-low; pr: pos-low; her.2: neg; tumor size (cm): 4.2; lymph nodes: positive; adjuvant chemotherapy: none; chemo class: none; hormonal rx: none; time of followup (mo): NA; distant recurrence free survival (mo): 2; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 230; age: 46; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: neg; tumor size (cm): 3; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 76; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 142; age: 60; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: neg; tumor size (cm): 2.2; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 88; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 168; age: 50; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 1.3; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 47; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 222; age: 37; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 1.2; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 83; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 219; age: 53; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos-low; her.2: pos (3+); tumor size (cm): 2; lymph nodes: negative; adjuvant chemotherapy: Unknown; chemo class: Unknown; hormonal rx: Tam; time of followup (mo): 54; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 91; age: 57; histology type: Mixed; grade (modified, bloom, richardson): I; er: pos; pr: neg; her.2: neg; tumor size (cm): 1.1; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 79; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 156; age: 57; histology type: Ductal; grade (modified, bloom, richardson): II; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 2.9; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): NA; distant recurrence free survival (mo): 15; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 227; age: 84; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: neg; tumor size (cm): 2.5; lymph nodes: positive; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): NA; distant recurrence free survival (mo): 18; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 177; age: 46; histology type: Lobular; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 1.2; lymph nodes: negative; adjuvant chemotherapy: CMF; chemo class: Other; hormonal rx: Tam; time of followup (mo): 76; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 231; age: 45; histology type: Lobular; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 1.5; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 81; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 150; age: 62; histology type: Lobular; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 5; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 83; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 221; age: 58; histology type: Mixed; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 1.5; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 54; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 174; age: 50; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: pos-low; her.2: neg; tumor size (cm): 1.4; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 79; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 178; age: 74; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 1.1; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 74; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 192; age: 57; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: neg; tumor size (cm): 1.1; lymph nodes: positive; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 74; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 87; age: 58; histology type: Ductal; grade (modified, bloom, richardson): I; er: pos; pr: neg; her.2: neg; tumor size (cm): 0.8; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 81; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 7; age: 59; histology type: Lobular; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 1; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 81; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 229; age: 46; histology type: Ductal; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 2.1; lymph nodes: negative; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 76; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 9; age: 54; histology type: Ductal; grade (modified, bloom, richardson): II; er: pos; pr: pos-low; her.2: low pos (2+); tumor size (cm): 1.5; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 65; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 224; age: 64; histology type: Mixed; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 1.3; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 83; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 666; age: 64; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: pos (3+); tumor size (cm): 2.1; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Arimidex; time of followup (mo): 48; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 643; age: 68; histology type: Mixed; grade (modified, bloom, richardson): III; er: neg; pr: neg; her.2: pos (3+); tumor size (cm): 5.5; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 51; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 552; age: 49; histology type: Mixed; grade (modified, bloom, richardson): I; er: pos; pr: pos; her.2: neg; tumor size (cm): 2; lymph nodes: pos.micromet; adjuvant chemotherapy: CMF; chemo class: Other; hormonal rx: Tam; time of followup (mo): 56; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 489; age: 37; histology type: Ductal; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 6.5; lymph nodes: positive; adjuvant chemotherapy: CAF; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 59; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 362; age: 63; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: neg; tumor size (cm): 4.5; lymph nodes: positive; adjuvant chemotherapy: CMF; chemo class: Other; hormonal rx: Tam; time of followup (mo): 69; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 537; age: 71; histology type: Lobular; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: pos (3+); tumor size (cm): 2.3; lymph nodes: positive; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 71; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 651; age: 45; histology type: Lobular; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 4; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 53; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 365; age: 78; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: neg; tumor size (cm): 2.3; lymph nodes: positive; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Arimidex; time of followup (mo): 53; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 612; age: 49; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: neg; tumor size (cm): 5.6; lymph nodes: pos.micromet; adjuvant chemotherapy: CAF; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 53; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 656; age: 42; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: neg; her.2: pos (3+); tumor size (cm): 4; lymph nodes: positive; adjuvant chemotherapy: AC-taxol/Herceptin; chemo class: Trastuzumab; hormonal rx: Tam; time of followup (mo): 54; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 254; age: 54; histology type: Ductal; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 2.5; lymph nodes: negative; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 71; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 260; age: 82; histology type: Ductal; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 2.5; lymph nodes: positive; adjuvant chemotherapy: none; chemo class: none; hormonal rx: Tam; time of followup (mo): 48; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 262; age: 48; histology type: Mixed; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: neg; tumor size (cm): 5; lymph nodes: positive; adjuvant chemotherapy: AC-taxotere; chemo class: Anthracycline-based; hormonal rx: unknown; time of followup (mo): 71; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 274; age: 49; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: pos (3+); tumor size (cm): 3; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 71; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 281; age: 45; histology type: Ductal; grade (modified, bloom, richardson): II; er: neg; pr: pos; her.2: neg; tumor size (cm): 1.2; lymph nodes: positive; adjuvant chemotherapy: AC-taxol; chemo class: Anthracycline-based; hormonal rx: none; time of followup (mo): 74; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 283; age: 47; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: pos (3+); tumor size (cm): 4; lymph nodes: positive; adjuvant chemotherapy: Unknown; chemo class: Unknown; hormonal rx: unknown; time of followup (mo): 36; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 300; age: 56; histology type: Lobular; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: neg; tumor size (cm): 1.6; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): NA; distant recurrence free survival (mo): 18; distant recur (yn): Y; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 308; age: 45; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos; her.2: pos (3+); tumor size (cm): 1.9; lymph nodes: negative; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 73; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): yes; patientid: 363; age: 41; histology type: Ductal; grade (modified, bloom, richardson): III; er: pos; pr: pos-low; her.2: neg; tumor size (cm): 4; lymph nodes: positive; adjuvant chemotherapy: AC x 4; chemo class: Anthracycline-based; hormonal rx: Tam; time of followup (mo): 67; distant recurrence free survival (mo): NA; distant recur (yn): N; ', 'tissue: breast tumor tissue; tumor recurrence (36mo): no; patientid: 621; age: 32; histology type: Mixed; grade (modified, bloom, richardson): II; er: pos; pr: pos; her.2: pos (3+); tumor size (cm): 4.5; lymph nodes: positive; adjuvant chemotherapy: AC-taxol/Herceptin; chemo class: Trastuzumab; hormonal rx: Tam; time of followup (mo): 55; distant recurrence free survival (mo): NA; distant recur (yn): N; ' GSE116869 Homo sapiens 3 Other GPL18573 Oncogenic Notch promotes long-range regulatory interactions within hyperconnected 3D cliques [MB157_HiChIP] 2018-07-10 Purpose: To investigate the impact of oncogenic Notch on the 3D genome organization of cancer cells. Methods: We generated cohesin HiChIP and 1D epigenomic data sets in two different Notch-dependent cancer cell types, triple-negative breast cancer (TNBC) and mantle cell lymphoma (MCL), in the Notch-on and -off states. Results: We report here that Notch transcription complexes control their direct target genes through two distinct regulatory modes: either through existing loops or by facilitating new long-range regulatory interactions. This combination of pre-existing and Notch-promoted loops coalesce enhancers and promoters to form highly interacting clusters, termed “3D cliques”. Notch preferentially activates enhancers and promotes looping interactions within highly connected 3D cliques that regulate key oncogenes. Conclusions: These observations suggest a general mechanism that oncogenic transcription factors can exploit to regulate the transcriptional outputs of cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE116869 Oncogenic Notch Promotes Long-Range Regulatory Interactions within Hyperconnected 3D Cliques. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2019.01.006 {Molecular cell (14.548): 10.1016/j.molcel.2019.01.006} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA480471 https://www.ebi.ac.uk/ena/browser/view/PRJNA480471 https://www.ncbi.nlm.nih.gov/sra?term=SRP152958 [Overal design]ChIP-seq, RNA-seq and HiChIP in Notch-on, -off, -recovery conditions in TNBC and MCL cell lines to profile Notch transcriptional complex binding, histone modification, Notch target genes and contact between regulatory elements.; [Treatment]'Untreated.', 'Cells were treated with the GSI compound E (1 μM, Calbiochem cat# 565790) for 72 hours.', 'Cells were treated with the GSI compound E (1 μM, Calbiochem cat# 565790) for 72 hours, washed, and then cultured for 3 days in media containing DMSO.'; [Growth]'MB157 (female) cells were grown in DMEM (Corning, cat# 10-013-CV) supplemented with 10% fetal bovine serum (Hyclone, cat# SH30070.03) and 100 U/mL and 100 μg/mL penicillin/streptomycin (Corning, cat# 30-002-CI). When passaged cells were detached with 0.25% trypsin, EDTA-free (Gibco, cat# 15090-046) to avoid activation of Notch signaling.'; [Extraction]'HiChIP was performed as described (Mumbach et al., 2016) using antibody against Smc1 (Bethyl, cat# A300-055A). Briefly, 2 x 10^7 cells were crosslinked with 1% formaldehyde (Thermo Scientific, cat# 28908) for 10 min and subsequently quenched with 0.125M glycine (Invitrogen, cat# 15527-013). Chromatin was digested using MboI restriction enzyme (NEB, Cat#R0147), followed by biotin incorporation with Biotin-14-dATP (Invitrogen, 19524-016) in end-repair step, ligation, and sonication. Sheared chromatin was 4-fold diluted with ChIP dilution buffer (16.7mM Tris pH 7.5, 167mM NaCl, 1.2mM EDTA, 0.01% SDS, 1.1% Triton X-100) and cleared and then incubated with anti-Smc1 antibody at 4°C for overnight. Chromatin-antibody complexes were captured by Protein-A magnetic beads (Pierce, cat# 88846) and subsequently washed with Low Salt Wash Buffer, High Salt Wash Buffer, LiCl Wash Buffer and eluted.\nDNA was purified with MinElute PCR Purification Kit (Qiagen, cat# 28004) and quantified using Qubit dsDNA HS Assay Kit (Invitrogen, cat# Q32851). 50-150ng was used for capture with Dynabeads MyOne Streptavidin C-1 (Invitrogen, cat# 65001) and an appropriate amount of Tn5 enzyme was added to captured DNA to generate sequencing library. Paired-end sequencing (38 bp+38 bp) was performed on a NextSeq 550.'; [Cell type]'Triple-negative breast cancer cell line''cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: SMC1a; drug treatment: untreated; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: SMC1a; drug treatment: GSI-treated; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: SMC1a; drug treatment: GSI-washout; ' GSE140848 Homo sapiens 4 Expression profiling by high throughput sequencing GPL20795 RNA sequencing analysis of shControl and shSASH1 in MDA-MB-468 cells 2019-11-22 We performed RNA-seq to determine the impact of SASH1 depletion on global gene expression profile.The results reveal that dysregulated genes were enriched for genes related to cell adhesion, extracellular matrix (ECM) organization and cell migration, suggesting SASH1 may play a critical role in determining the invasion and metastasis phenotype in breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE140848 SASH1 suppresses triple-negative breast cancer cell invasion through YAP-ARHGAP42-actin axis. Oncogene 6.634 https://doi.org/10.1038/s41388-020-1356-7 {Oncogene (6.634): 10.1038/s41388-020-1356-7} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA591154 https://www.ebi.ac.uk/ena/browser/view/PRJNA591154 https://www.ncbi.nlm.nih.gov/sra?term=SRP231434 [Overal design]Investigate transcriptomic difference between control and SASH1-depleted cells.; [Treatment]'Cells were infected with pGIPZ-CTRL and SASH1-shRNA lentiviruses, and stable clones were selected using puromycin.'; [Growth]'MDA-MBA-468 cells were routinely generated by re-plating with DMEM supplied with 5% FBS.'; [Extraction]"RNA was isolated from MDA-MBA-468-shSASH1 or MDA-MBA-468-shControl cells using TRIzol Reagent.\nThe sequencing libraries were prepared using NEBNext® UltraTM RNA Library Prep Kit for Illumina® (NEB, USA) according to the manufacturer's instructions."; [Cell type]'breast cancer epithelial cells''cell type: breast cancer epithelial cells; cell line: MDA-MB-468; tissue: breast; knockdown: control; ', 'cell type: breast cancer epithelial cells; cell line: MDA-MB-468; tissue: breast; knockdown: SASH1; ' GSE55070 Homo sapiens 12 Expression profiling by array GPL7504; GPL10481 Primary breast tumor-derived cellular models: characterization of tumorigenic, metastatic, and cancer-associated fibroblasts in dissociated tumor (DT) cultures 2014-02-17 The study of breast cancer pathogenesis relies heavily on the use of established cell lines often derived from metastatic lesions, which while having significantly contributed to the knowledge of breast cancer biology may inadvertently limit the understanding of the mechanisms governing the metastatic process. Our goal was to establish primary cultures from dissociation of breast tumors in order to provide cellular models that may better recapitulate breast cancer pathogenesis and the metastatic process. These cellular models differ from recently developed patient derived xenograft models (PDX) in that they can be used for both in vitro and in vivo studies. Here we report the characterization of six cellular models derived from the dissociation of primary breast tumor specimens, referred to as “dissociated tumor (DT) cells”. Among the DT cells are those that are tumorigenic and metastatic in immunosuppressed mice, and a group of cancer-associated fibroblasts (CAFs). In vitro, DT cells were characterized by proliferation assays, colony formation assays, protein and gene expression profiling, including PAM50 predictor analysis. The latter showed DT cultures similar to their paired primary tumor and as belonging to the basal and Her2-enriched subtypes, offering novel cellular models of these ER-negative breast cancer subtypes. In vivo, three DT cultures are tumorigenic in NOD/SCID and NSG mice, and one of these is metastatic to lymph nodes and lung after orthotopic inoculation into the mammary fat pad, without excision of the primary tumor. DT cultures comprised of CAFs were isolated from luminal-A, Her2-enriched and basal primary tumors, providing subtype-specific components of the tumor microenvironment. Altogether, these DT cultures provide closer-to-primary cellular models for the study of breast cancer pathogenesis, metastasis and tumor microenvironment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55070 Primary breast tumor-derived cellular models: characterization of tumorigenic, metastatic, and cancer-associated fibroblasts in dissociated tumor (DT) cultures. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-014-2887-9 {Breast cancer research and treatment (3.471): 10.1007/s10549-014-2887-9} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA238652 https://www.ebi.ac.uk/ena/browser/view/PRJNA238652 None [Overal design]reference x sample; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen Rneasy Kit'; [Cell type]'Source: ''reference: whole human total RNA; ', 'sample: Cell Line Hs578T p11; ', 'sample: DT13-Tumor; ', 'sample: DT19-Tumor; ', 'sample: DT21p11-Tumor; ', 'sample: DT21-Tumor; ', 'sample: DT22-Tumor; ', 'sample: DT23-Tumor; ', 'sample: Cell Line H2N+13-1-NT; ', 'sample: Cell Line +19-1-NT; ', 'sample: Cell Line H2N-22-1-NT; ', 'sample: Cell Line H2N-23-1-NT; ', 'sample: Cell Line H2N-28-1-NT; ' GSE61548 Homo sapiens 20 Expression profiling by array GPL201 Expression data in NK150460 treated breast cancer cell lines 2014-09-18 The purpose of this study is to investigate certain genes inuduced/reduced by NK150460, novel compound possessing antitumor activity. To identify genes, time course samples were prepared from NK150460 sensitive and insensitive breast cancer cell lines. By comparing patterns in both sensitive and resistant cell lines, we tried to identify genes specifically modulated by NK150460 treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE61548 A novel compound, NK150460, exhibits selective antitumor activity against breast cancer cell lines through activation of aryl hydrocarbon receptor. Molecular cancer therapeutics 4.856 https://doi.org/10.1158/1535-7163.MCT-14-0158 {Molecular cancer therapeutics (4.856): 10.1158/1535-7163.MCT-14-0158} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA261441 https://www.ebi.ac.uk/ena/browser/view/PRJNA261441 None [Overal design]Four breast cance cell lines (3 sensitive cell lines, 1 insensitive cell line) were treated with NK150460 in vitro. 0, 3, 6, 24 hr after drug addition, total RNA were prepared. In total, 16 samples were prepared and subjected to microarray analysis.; [Treatment]'NK150460 were added to each culture dish, then incubated for 0hr (untreated), 3hr, 6hr and 24hr.'; [Growth]'All cell lines were cultured at 37 degree C, 5% CO2 condition.'; [Extraction]'Total RNA were extracted with ISOGEN (Nippon Gene) and Purified with Rneasy Mini Kit (Qiagen).'; [Cell type]'Source: ''cell line: MCF-7; er status: ER(+); treated: untreated; ', 'cell line: MCF-7; er status: ER(+); treated: treated with NK150460 for 3hr; ', 'cell line: MCF-7; er status: ER(+); treated: treated with NK150460 for 6hr; ', 'cell line: MCF-7; er status: ER(+); treated: treated with NK150460 for 24hr; ', 'cell line: T-47D; er status: ER(+); treated: untreated; ', 'cell line: T-47D; er status: ER(+); treated: treated with NK150460 for 3hr; ', 'cell line: T-47D; er status: ER(+); treated: treated with NK150460 for 6hr; ', 'cell line: T-47D; er status: ER(+); treated: treated with NK150460 for 24hr; ', 'cell line: SK-BR-3; er status: ER(-); treated: untreated; ', 'cell line: SK-BR-3; er status: ER(-); treated: treated with NK150460 for 3hr; ', 'cell line: SK-BR-3; er status: ER(-); treated: treated with NK150460 for 6hr; ', 'cell line: SK-BR-3; er status: ER(-); treated: treated with NK150460 for 24hr; ', 'cell line: MDA-MB-231; er status: ER(-); treated: untreated; ', 'cell line: MDA-MB-231; er status: ER(-); treated: treated with NK150460 for 3hr; ', 'cell line: MDA-MB-231; er status: ER(-); treated: treated with NK150460 for 6hr; ', 'cell line: MDA-MB-231; er status: ER(-); treated: treated with NK150460 for 24hr; ' GSE48160 Homo sapiens 6 Expression profiling by array GPL10558 Identification of miRNA targets in breast cancer cells (DICER1 and DROSHA knockdown) 2013-06-20 miRNAs regulate mRNA stability and translation through the action of the RNAi-induced silencing complex. In this study, we systematically identified endogenous miRNA target genes by using AGO2 immunoprecipitation (AGO2-IP) and microarray analyses in two breast cancer cell lines, MCF7 and MDA-MB-231, representing luminal and basal-like breast cancer, respectively. The expression levels of ~70% of the AGO2-IP mRNAs were increased by DROSHA or DICER1 knockdown. In addition, integrated analysis of miRNA expression profiles, mRNA-AGO2 interaction, and the 3'-UTR of mRNAs revealed that >60% of the AGO2-IP mRNAs were putative targets of the fifty most abundantly expressed miRNAs. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48160 Comprehensive analysis of microRNA (miRNA) targets in breast cancer cells. The Journal of biological chemistry 4.106 https://doi.org/10.1074/jbc.M113.491803 {The Journal of biological chemistry (4.106): 10.1074/jbc.M113.491803} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA209069 https://www.ebi.ac.uk/ena/browser/view/PRJNA209069 None [Overal design]To identify mRNAs responsive to miRNA synthesis inhibition, total RNA was prepared from control cells and cells that stably express small hairpin RNA against DICER1 or DROSHA. Expression array analysis was performed with duplicates for each cell type.; [Treatment]'Cells were untreated.'; [Growth]'Cells were maintained in MEM medium (Invitrogen, Carlsbad, CA, USA) supplemented with 10% FBS and 100 units/ml penicillin.'; [Extraction]"Total RNA in cell lysates was prepared using Trizol according to the manufacturer's instructions."; [Cell type]'basal-like breast cancer cells''cell line: MDA-MB-231; cell type: basal-like breast cancer cells; shRNA expression: control; ', 'cell line: MDA-MB-231; cell type: basal-like breast cancer cells; shRNA expression: DICER1; ', 'cell line: MDA-MB-231; cell type: basal-like breast cancer cells; shRNA expression: DROSHA; ' GSE58574 Homo sapiens 4 Expression profiling by array GPL4133 Human MCF-7 breast cancer cells: control vs. treated with conditioned medium of cancer associated adipose tissue 2014-06-17 Transcriptional profiling of human MCF-7 breast cancer cells comparing MCF-7 cells treated with control medium (DMEM/F12 + 0,5% BSA) with MCF-7 cells treated with conditioned medium of cancer-associated adipose tissue (CMCAAT) obtained from 2 breast cancer patients. Goal was to determine the effects of CMCAAT treatment on global MCF-7 gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58574 Cancer-associated adipose tissue promotes breast cancer progression by paracrine oncostatin M and Jak/STAT3 signaling. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-14-0160 {Cancer research (8.378): 10.1158/0008-5472.CAN-14-0160} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA252929 https://www.ebi.ac.uk/ena/browser/view/PRJNA252929 None [Overal design]Two-condition experiment: MCF-7 control vs. CMCAAT treated cells. Biological replicates: 3 control replicates pooled as 1 (LL 1-2-4), 4 CMCAAT replicates (LL 6, LL 8, LL 9, LL 10); [Treatment]'MCF-7 cells were washed three times with serum-free DMEM supplemented with 100 U/mL penicillin, 100 μg/mL streptomycin and 2.5 μg/mL fungizone; afterwards MCF-7 cells were treated for 48h with control medium (DMEM/F12 + 0,5%BSA) or CMCAAT'; [Growth]'MCF-7 cells were grown in Dulbecco’s minimal essential medium (DMEM) supplemented with 10% fetal calf serum, 100 U/mL penicillin, 100 μg/mL streptomycin (Invitrogen, Carlsbad, CA) and 2.5 μg/mL fungizone (Bristol-Meyers Squibb, Brussels, Belgium)'; [Extraction]'Total RNA was isolated using the Nucleospin RNA II kit (Macherey-Nagel, Düren, Germany) including DNAse I treatment.'; [Cell type]'Source: ''tissue type: breast cancer; cell line: MCF-7; ' GSE17081 Mus musculus 9 Expression profiling by array GPL6238 KLF17 is a negative regulator of epithelial-mesenchymal transition and metastasis in breast cancer 2009-07-14 Metastasis is a complex multi-step process requiring the concerted action of many genes and is the primary cause of cancer deaths. Pathways that regulate metastasis enhancement and suppression both contribute to tumor dissemination process. In order to identify novel metastasis suppressors, we set up a forward genetic screen in a mouse model. We transduced a genome-wide RNAi library into the non-metastatic 168FARN breast cancer cell line, orthotopically transplanted the cells into mouse mammary fat pads, and then selected for cells that could metastasize to the lung and identified an RNAi for the KLF17 gene. Conversely, ectopic expression of KLF17 in highly metastatic 4T1 breast cancer cell line inhibited their ability to metastasize from the mammary fat pad to the lung. We showed that suppression of KLF17 expression promotes breast cancer cell invasion and epithelial-mesenchymal transition (EMT). We also showed that KLF17 functions by directly binding to the promoter of Id-1, a key metastasis regulator in breast cancer, to inhibit its transcription. Finally, we demonstrated that KLF17 expression is significantly down-regulated in primary human breast cancer samples and that the combined expression patterns of KLF17 and Id-1 can serve as a potential biomarker for lymph node metastasis in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17081 KLF17 is a negative regulator of epithelial-mesenchymal transition and metastasis in breast cancer. Nature cell biology 17.728 https://doi.org/10.1038/ncb1974 {Nature cell biology (17.728): 10.1038/ncb1974} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA119801 https://www.ebi.ac.uk/ena/browser/view/PRJNA119801 None [Overal design]Illumina mouse array was used for 168FARN cells stably expressing a control vector, KLF17 cDNA or KLF17 shRNA. Triplicate samples were used to perform gene expression analysis on each cell line.; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was extracted using Trizol according to manufacturer's protocol (Invitrogen)."; [Cell type]'Source: ''cell line: 168FARN; vector: control vector; ', 'cell line: 168FARN; vector: expressing a control vector; ', 'cell line: 168FARN; vector: expressing a KLF17 cDNA; ', 'cell line: 168FARN; vector: expressing a KLF17 shRNA; ' GSE95540 Homo sapiens 36 Expression profiling by high throughput sequencing GPL16791 Integrin-b4 identifies cancer stem cell-enriched populations of partially mesenchymal carcinoma cells 2017-02-28 We report the gene expression profiles of normal epithelial and carcinoma cell populations that differ in their relative levels of integrin-beta 4 expression. ITGB4 high, mesenchymal subtype, triple-negative breast cancer cells were found to be more epithelial than related ITGB4 low cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95540 Integrin-β4 identifies cancer stem cell-enriched populations of partially mesenchymal carcinoma cells. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1618298114 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1618298114} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA377346 https://www.ebi.ac.uk/ena/browser/view/PRJNA377346 https://www.ncbi.nlm.nih.gov/sra?term=SRP100883 [Overal design]RNA-seq was used to compare the expression of mesenchymal-like carcinoma cell subtypes isolated from polyclonal cell populations. Isolated cell populations that had high levels of ITGB4 were found to be more epithelial than those with low levels, despite the fact that they were within the mesenchymal-like cell state spectrum.; [Treatment]'RNA was collected 48 hours after seeding cells in their respective normal growth medium.'; [Growth]'NAMEC cell lines were grown in complete MEGM medium, MDA-MB231 cells were grown in DMEM + 10% FBS, and SUM159 cells were grown in F12 + 5% IFS + 5ug/ml insulin + 1ug/ml hydrocortisone.'; [Extraction]'Total RNA was prepared using a modified TRIzol protocol. To prepare total RNA, 1ml of TRIzol reagent was added to a sub-confluent 10cm dish of cells, scraped, then placed in a microfuge tube. Microfuge tubes were flash frozen on dry ice. Samples were then thawed and 200ul of chloroform was added to each tube, shaken vigorously by hand for 15 seconds, and incubated at room temperature for 3 minutes then centrifuged at 13,000g for 15 minutes. The aqueous phase was removed and placed into a gDNA elimination column from the RNeasy Plus kit (Qiagen). The eluate was mixed at a 1:1 ratio with 70% RNase-free EtOH and purified following the remaining steps outlined in the RNeasy Plus kit. Libraries were pooled together and sequenced on the HiSeq 2500 sequencer using the Standard sequencing protocols. Images analysis and base calling were done using the Standard Illumina pipeline, and then demultiplexed into fastq files.\nRNA-seq libraries were prepared using the TruSeq stranded polyA mRNA kits as described by the manufacturer (Illumina RS-122-2101).'; [Cell type]'Mammary epithelial cells', 'Mammary carcinoma cells''cell line: NAMEC8; cell type: Mammary epithelial cells; itgb4 level: lo; ', 'cell line: NAMEC8; cell type: Mammary epithelial cells; itgb4 level: hi; ', 'cell line: SUM159; cell type: Mammary carcinoma cells; itgb4 level: hi; ', 'cell line: SUM159; cell type: Mammary carcinoma cells; itgb4 level: lo; ', 'cell line: MDA231; cell type: Mammary carcinoma cells; itgb4 level: lo; ', 'cell line: MDA231; cell type: Mammary carcinoma cells; itgb4 level: hi; ', 'cell line: NAMEC1; cell type: Mammary epithelial cells; itgb4 level: lo; ', 'cell line: NAMEC5; cell type: Mammary epithelial cells; itgb4 level: lo; ' GSE78698 Mus musculus 23 Expression profiling by array GPL6246 Targeting metabolic symbiosis to overcome resistance to anti-angiogenic therapy 2016-02-25 Despite the approval of several anti-angiogenic therapies, clinical results remain unsatisfactory, and transient benefits are followed by rapid tumor recurrence. In the present study, we aimed to identify resistance mechanisms to the small-molecule tyrosine kinase inhibitor nintedanib in the Py2T murine breast cancer transplantation model. To identify differences in gene expression between short- and long-term nintedanib and untreaded FAC-sorted tumor and endothelial cells, we performed gene expression profiling by using affymetrix microarrays. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE78698 Targeting Metabolic Symbiosis to Overcome Resistance to Anti-angiogenic Therapy. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2016.04.028 {Cell reports (7.815): 10.1016/j.celrep.2016.04.028} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA313284 https://www.ebi.ac.uk/ena/browser/view/PRJNA313284 None [Overal design]The murine breast cancer cell line Py2T was injected into a mammary fat pad of FVB/N mice. Treatment with nintedanib was initiated when tumors reached a measurable size. After 1 week (short-term treatment) and 3 weeks of nintedanib treatment (long-term treatment), treated and untreated control (size-matched to the long-term nintedanib treatment group) tumor and endothelial cells were FAC-sorted, RNA was extracted and hybridized on Affymetrix microarrays.; [Treatment]'Mice were either kept untreated or treated with nintedanib (50mg/kg body weight)'; [Growth]'Py2T tumor cells were grown in the mammary fat pad of FVB/N female mice and were isolated by FAC-sorting together with endothelial cells'; [Extraction]'Total RNA was isolated using TRIzol® LS reagent (Ambion®), RNA Easy Mini Kit (Qiagen) and Absolutely RNA Nanoprep Kit (Stratagene)'; [Cell type]'Source: ''tissue: Py2T cells (murine breast cancer cell line); treatment: Untreated; ', 'tissue: Py2T cells (murine breast cancer cell line); treatment: short-term (7 days) nintedanib treated; ', 'tissue: Py2T cells (murine breast cancer cell line); treatment: long-term (21 days) nintedanib treated; ', 'tissue: tumor blood vessel endothelial cells; treatment: Untreated; ', 'tissue: tumor blood vessel endothelial cells; treatment: short-term (7 days) nintedanib treated; ', 'tissue: tumor blood vessel endothelial cells; treatment: long-term (21 days) nintedanib treated; ' GSE42024 Homo sapiens 6 Expression profiling by array GPL6480 Characterization of gene expression profiles induced by HIC-1 reactivation on breast cancer 2012-11-05 To explore the molecular mechanisms and signal pathways induced by restoring tumor suppressor gene HIC-1 on breast cancer cells. We have employed whole genome microarray expression profiling as a discovery platform to identify the differential genes induced by HIC-1 gene activation. Small activating RNA (saRNA) that targeted promoter region was used, and MCF-7 breast cancer cell line was selected as cell model. After 96h for saRNA transfection, the cells were collected and the whole genome expression profiles were analyzed. Three independent experiments were repeated for different groups. With the treshold of p<0.01 and fold change >=2 or <-2, there were 1375 differential expression genes, which are related to cell cycle, apoptosis, cell migration, cell invasion and cell proliferation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE42024 Small activating RNA restores the activity of the tumor suppressor HIC-1 on breast cancer. PloS one 2.776 https://doi.org/10.1371/journal.pone.0086486 {PloS one (2.776): 10.1371/journal.pone.0086486} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA178940 https://www.ebi.ac.uk/ena/browser/view/PRJNA178940 None [Overal design]SaRNA induced gene expression in human breast cancer cell MCF-7 was measured at 96 hours after transfection by 50 nM saRNA. Three independent experiments were performed for experimental group and control group.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted using TRIZOL Reagent (Cat#15596-018,Life technologies, Carlsbad, CA, US)following the manufacturer’s instructions and checked for a RIN number to inspect RNA integration by an Agilent Bioanalyzer 2100 (Agilent technologies, Santa Clara, CA, US).Qualified total RNA was further purified by RNeasy micro kit (Cat#74004, QIAGEN, GmBH, Germany)and RNase-Free DNase Set (Cat#79254, QIAGEN, GmBH, Germany).'; [Cell type]'Source: ''cell line: MCF-7; transfection: 50 nM saRNA; ', 'cell line: MCF-7; transfection: none; ' GSE133567 Homo sapiens 12 Expression profiling by high throughput sequencing GPL16791 Gene expression alterations associated with acquired-resistance to the CDK4/6 inhibitor palbociclib [Palbociclib resistance_RNASeq] 2019-07-01 RNA-seq was performed to compare the transcriptional programmes of palbociclib-resistant A375 and CHL1 cells compared to their parental counterparts Cyclin dependent kinase 4/6 (CDK4/6) inhibitors are an established treatment in estrogen receptor positive breast cancer and are currently in clinical development in melanoma; a tumour that exhibits high rates of CDK4 activation. We analyzed melanoma cells with acquired resistance to the CDK4/6 inhibitor palbociclib, and demonstrated that palbociclib-mediated inhibition of PRMT5 is essential for sensitivity to CDK4/6 inhibitors. Mechanistically, by inhibiting PRMT5 activity, palbociclib alters MDM4 pre-mRNA splicing leading to decreased MDM4 protein expression and subsequent p53 activation. In turn, p53 increases p21 leading to inhibition of CDK2, the main kinase substituting for CDK4/6 and a key driver of resistance to palbociclib. Loss of the ability of palbociclib to regulate the PRMT5-MDM4 axis leads to resistance. Importantly, combining palbociclib with the PRMT5 inhibitor GSK3326595 enhances the efficacy of palbociclib in treatment naïve and resistant models and also delays the emergence of resistance. Our studies have uncovered a novel mechanism of action of CDK4/6 inhibitors in regulating the MDM4 oncogene and the tumor suppressor, p53. Furthermore, we have established that palbociclib inhibition of the PRMT5-MDM4 axis is essential for robust melanoma cell sensitivity and provide pre-clinical evidence that co-inhibition of CDK4/6 and PRMT5 is an effective and well tolerated therapeutic strategy. Overall our data provides a strong rationale for further investigation of novel combinations of CDK4/6 and PRMT5 inhibitors in not only melanoma but other tumour types including breast, pancreatic and esophageal carcinoma. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE133567 Regulation of PRMT5-MDM4 axis is critical in the response to CDK4/6 inhibitors in melanoma. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1901323116 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1901323116} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA551944 https://www.ebi.ac.uk/ena/browser/view/PRJNA551944 https://www.ncbi.nlm.nih.gov/sra?term=SRP212665 [Overal design]Cells were treated with increasing concentrations of palbociclib for a prolonged period of time until resistance to the drug develop; [Treatment]'prior to RNA extraction cells were grown in palbociclib - free medium for 72 hr'; [Growth]'A375AR and CHL1AR991 cells were grown in fully supplemented RPMI medium containing gardually increasing concentrations of palbociclib, once resistance developed, cells were maintained in fully supplemented RPMI medium containing 4 μΜ palbociclib. Control cells were grown in fully supplemented RPMI medium'; [Extraction]"Total RNA was extracted RNeasy Mini Kit as per manufacturer's instructions\nRNA libraries were prepared for sequencing according to standard Illumina protocols (TruSeq RNA Sample Preparation Guide v2 Guide)"; [Cell type]'Source: ''cell line: A375AR991; tissue source: Melanoma; replicate: Replicate 1; treatment: increasing concentrations of palbociclib for 7 months; ', 'cell line: A375AR991; tissue source: Melanoma; replicate: Replicate 2; treatment: increasing concentrations of palbociclib for 7 months; ', 'cell line: A375AR991; tissue source: Melanoma; replicate: Replicate 3; treatment: increasing concentrations of palbociclib for 7 months; ', 'cell line: A375; tissue source: Melanoma; replicate: Replicate 1; treatment: No treatment; ', 'cell line: A375; tissue source: Melanoma; replicate: Replicate 2; treatment: No treatment; ', 'cell line: A375; tissue source: Melanoma; replicate: Replicate 3; treatment: No treatment; ', 'cell line: CHL1AR991; tissue source: Melanoma; replicate: Replicate 1; treatment: increasing concentrations of palbociclib for 3 months; ', 'cell line: CHL1AR991; tissue source: Melanoma; replicate: Replicate 2; treatment: increasing concentrations of palbociclib for 3 months; ', 'cell line: CHL1AR991; tissue source: Melanoma; replicate: Replicate 3; treatment: increasing concentrations of palbociclib for 3 months; ', 'cell line: CHL1; tissue source: Melanoma; replicate: Replicate 1; treatment: No treatment; ', 'cell line: CHL1; tissue source: Melanoma; replicate: Replicate 2; treatment: No treatment; ', 'cell line: CHL1; tissue source: Melanoma; replicate: Replicate 3; treatment: No treatment; ' GSE52783 Homo sapiens 16 Expression profiling by array GPL8269 Over-expression of miR-146a in basal-like breast cancer cells confers enhanced tumorigenic potential in association with altered p53 status 2013-11-26 The tumor suppressor p53 is the most frequently mutated gene in human cancers, mutated in 25-30% of breast cancers. However, mutation rates differ according to breast cancer subtype, being more prevalent in aggressive estrogen receptor (ER) negative tumors, basal-like and HER2 amplified subtypes. This heterogeneity suggests that p53 may function differently across breast cancer subtypes. We used RNAi-mediated p53 knockdown (KD) and antagomir-mediated KD of microRNAs to study how gene expression and cellular response to p53 loss differ in luminal vs. basal-like breast cancer. As expected, p53 loss caused down regulation of established p53 targets (e.g. p21 and miR-34 family) and increased proliferation in both luminal and basal-like cell lines. However, some p53-dependent changes were subtype-specific, including expression of miR-134, miR-146a, and miR-181b. To study the cellular response to miR-146a upregulation in p53-impaired basal-like lines, antagomir knockdown of miR-146a was performed. KD of miR-146a caused decreased proliferation and increased apoptosis, effectively ablating the effects of p53 loss. Furthermore, we found that miR-146a upregulation decreased NF-kB expression and downregulated the NF-kB-dependent extrinsic apoptotic pathway (including TNF, FADD, and TRADD) and antagomir-mediated miR-146a KD restored expression of these components, suggesting a plausible mechanism for miR-146a-dependent cellular responses. These findings are relevant to human basal-like tumor progression in vivo, since miR-146a is highly expressed in p53-mutant basal-like breast cancers. These findings suggest that targeting miR-146a expression may have value for altering the aggressiveness of p53 mutant basal-like tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE52783 Overexpression of miR-146a in basal-like breast cancer cells confers enhanced tumorigenic potential in association with altered p53 status. Carcinogenesis 4.004 https://doi.org/10.1093/carcin/bgu175 {Carcinogenesis (4.004): 10.1093/carcin/bgu175} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA230109 https://www.ebi.ac.uk/ena/browser/view/PRJNA230109 None [Overal design]reference x sample; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen Rneasy Mini'; [Cell type]'Source: ''reference: Stratagene Human Universal Reference that contained 1/10 added MCF7 and ME16C RNAs; ', 'treatment: wild-type p53 expression; cell line: HMECC; ', 'treatment: p53 knock down; cell line: HMECC; ', 'treatment: wild-type p53 expression; cell line: MCF7; ', 'treatment: p53 knock down; cell line: MCF7; ', 'treatment: wild-type p53 expression; cell line: SUM102; ', 'treatment: p53 knock down; cell line: SUM102; ', 'treatment: wild-type p53 expression; cell line: ZR751; ' GSE165407 Homo sapiens 28 Expression profiling by high throughput sequencing GPL11154 Mammary-specific expression of Trim24 establishes a mouse model of human metaplastic breast cancer and nominates c-Met and TRIM24 as therapeutic targets 2021-01-24 Conditional overexpression of histone reader Tripartite motif containing protein 24 (TRIM24) in mouse mammary epithelia (Trim24COE) drives spontaneous development of carcinosarcoma tumors, lacking ER, PR and HER2. Human carcinosarcomas or metaplastic breast cancers (MpBC) are a rare, chemorefractory subclass of triple-negative breast cancers (TNBC). Comparison of Trim24COE carcinosarcoma morphology, TRIM24 protein levels and a derived Trim24COE gene signature revealed strong correlation with human MpBC tumors and MpBC xenograft (PDX) models. Global and single-cell tumor profiling revealed Met as a direct oncogenic target of TRIM24, leading to aberrant PI3K/mTOR activation. Pharmacological inhibition of these pathways in primary Trim24COE tumor cells and TRIM24-PROTAC treatment of MpBC PDX tumorspheres revealed the therapeutic potential of targeting TRIM24. Altogether, global expression, single-cell immunophenotyping and mechanistic studies of tumors and MpBC PDX nominated TRIM24-activated c-MET/PI3K/mTOR pathways and TRIM24, which were validated as potential MpBC therapeutic targets. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE165407 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA694441 https://www.ebi.ac.uk/ena/browser/view/PRJNA694441 None [Overal design]We have obtained gene expression profiles of 8 treatment-naïve metaplastic tumors and 20 treatment-naïve non-metaplastic tumors from triple-negative breast cancer patients. -------------------------------------------------------- ***Submitter states the following: Due to IRB restrictions, we are required to use a controlled-access database for the raw data. Thus, we cannot upload the raw data to SRA. We are currently in the process of uploading it to EGA. --------------------------------------------------------; [Treatment]'None'; [Growth]'None'; [Extraction]'To perform deep sequencing of RNA (RNA-seq), total RNA was isolated from tumors, treated with Dnase I, and depleted of cytoplasmic and mitochondrial ribosomal RNA using Ribo-Zero Gold.\nTruSeq Stranded Total RNA'; [Cell type]'Source: ''subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: UNS; percent_vimentin: 1; response: RCB - III; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: MSL; percent_vimentin: 0; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: IM; percent_vimentin: <1; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: Y; subtype: IM; percent_vimentin: 5; response: RCB - III; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: LAR; percent_vimentin: 1; response: RCB - I; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: UNS; percent_vimentin: 5; response: RCB - I; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: IM; percent_vimentin: 30; response: RCB - 0; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: Y; subtype: IM; percent_vimentin: 15; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: Y; subtype: UNS; percent_vimentin: 15; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: LAR; percent_vimentin: 0; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: Y; subtype: M; percent_vimentin: 90; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: MSL; percent_vimentin: 10; response: RCB - III; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: BL1; percent_vimentin: 10; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: BL2; percent_vimentin: 1; response: RCB - III; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: IM; percent_vimentin: 0; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: UNS; percent_vimentin: 0; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: BL1; percent_vimentin: 75; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: Y; subtype: M; percent_vimentin: <1; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: BL1; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: MSL; percent_vimentin: 2; response: RCB - III; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: IM; percent_vimentin: 0; response: RCB - III; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: Y; subtype: M; percent_vimentin: 60; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: BL1; percent_vimentin: 50; response: RCB - III; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: BL1; response: RCB - I; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: Y; subtype: MSL; percent_vimentin: 95; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: LAR; percent_vimentin: 0; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: Y; subtype: IM; percent_vimentin: 90; response: RCB - II; ', 'subject status: triple-negative breast cancer patient; tissue: treatment-naive triple negative breast cancer tumor; is metaplastic: N; subtype: BL2; percent_vimentin: 15; response: RCB - III; ' GSE180775 Homo sapiens 41 Expression profiling by array GPL13607 Recurrence biomarkers of triple negative breast cancer treated with neoadjuvant chemotherapy combined with anti-EGFR antibodies [Agilent] 2021-07-25 To find metastatic recurrence biomarkers of triple negative breast cancer (TNBC) treated by neoadjuvant chemotherapy and anti-EGFR antibodies (NAT), we evaluated tumor genomic, transcriptomic and immune features, using MSK-IMPACT assay, gene arrays, Nanostring technology and TIL assessment on H&E. Six patients experienced a rapid fatal recurrence (RR) and other 6 had later non-fatal recurrences (LR). Before NAT, RR had low expression of 6 MHC class I and 13 MHC class II genes but were enriched in upregulated genes involved in the cell cycle-related pathways. Their TIL number before NAT in RR was very low (<5%) and did not increase after treatment. In post-NAT residual tumors, RR cases showed high expression of SOX2 and CXCR4. Our results indicate that high expression of cell cycle genes, combined with cold immunological phenotype, may predict strong TNBC resistance to NAT and rapid progression after it. This biomarker combination is worth validation in larger studies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE180775 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA749501 https://www.ebi.ac.uk/ena/browser/view/PRJNA749501 None [Overal design]Nucleic acids were extracted from frozen tumor tissue (pre-NAT samples) using AllPrep DNA/RNA mini kit (Qiagen France SAS, Courtaboeuf, France) according to the manufacturer’s protocol. RNA quality was verified using the 2100 BioAnalyzer (Agilent Technologies). The extracted material was sent to Helixio (Saint-Beauzire, France), where it was hybridized with gene arrays (Human SurePrint, Agilent Technologies France, Les Ullis, France).; [Treatment]'None'; [Growth]'None'; [Extraction]'Nucleic acids were extracted from frozen tumor tissue (pre-NAT samples) using AllPrep DNA/RNA mini kit (Qiagen France SAS, Courtaboeuf, France) according to the manufacturer’s protocol.'; [Cell type]'Source: ''age: 55; Stage: IIIA; tissue type: frozen tumor tissue; ', 'age: 44; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 42; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 57; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 65; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 53; Stage: IIIA; tissue type: frozen tumor tissue; ', 'age: 42; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 61; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 35; Stage: IIIA; tissue type: frozen tumor tissue; ', 'age: 29; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 62; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 53; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 34; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 47; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 60; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 59; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 37; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 35; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 48; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 50; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 47; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 61; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 64; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 54; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 48; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 33; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 31; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 49; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 52; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 27; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 41; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 56; Stage: IIB; tissue type: frozen tumor tissue; ', 'age: 30; Stage: IIA; tissue type: frozen tumor tissue; ', 'age: 40; Stage: IIA; tissue type: frozen tumor tissue; ' GSE179823 Homo sapiens 8 Genome binding/occupancy profiling by high throughput sequencing GPL24676 Cut and Run ChIP-seq of SUZ12 and EZH2 in cadmium resistant breast cancer MDA-231 cells 2021-07-09 In this study we compared genome wide SUZ12 and EZH2 Cut&RUN CHIP-seq of cadmium resistant MDA-231 breast cancer cells vs untreated controls. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE179823 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA745178 https://www.ebi.ac.uk/ena/browser/view/PRJNA745178 https://www.ncbi.nlm.nih.gov/sra?term=SRP327660 [Overal design]In this study we compared genome wide SUZ12 and EZH2 Cut&RUN CHIP-seq of cadmium resistant MDA-231 breast cancer cells vs untreated controls. Cells were passaged in the presence of increasing cadmium concentrations to induce heavy metal resistance, generating cadmium resistant cell lines. Parental cells were serially passaged in normal media to generate untreated controls.; [Treatment]'Cadmium-resistant cell (MDA-MB-231cadR) cell lines were selected by passage in medium containing CdSO4. The CdSO4 concentration was increased by increments of 5-25 μM after 10 passages at the current concentration and when cell count increased at least 1.8 times average daily over at least four passages consistently. Cells used in this study were adapted to CdSO4 containing medium for 7 months up to 10 μM CdSO4.'; [Growth]'MDA-MB-231 female breast cancer cell lines were maintained at 37°C in Dulbecco’s Modified Essential Medium (DMEM) with 10% FB essence (VWR), 1% penicillin/streptomycin, and L-glutamine.'; [Extraction]'CUT&RUN experiments were carried out following Epicypher CUT&RUN protocol (version 1.6, August 2020) with minor modifications. Briefly, nuclei from 5x105 cells were isolated with wash buffer (20 mM HEPES-KOH, pH 7.5, 150 mM NaCl, 0.5 mM Spermidine, and 1x protease inhibitor cocktails from Sigma), captured with Concanavalin A conjugated paramagnetic beads (Bangs Laboratory Inc.) and incubated while nutating with 0.5 µl primary antibody for EZH2 (Cell Signaling Technology), or SUZ12 (Cell Signaling Technology) in antibody buffer (20 mM HEPES-KOH, pH 7.5, 150 mM NaCl, 0.5 mM Spermidine, 0.02% digitonin, 2 mM EDTA and 1x protease inhibitor cocktails from Sigma) overnight. After washing with digitonin buffer (20 mM HEPES-KOH, pH 7.5, 150 mM NaCl, 0.5 mM Spermidine, 0.02% digitonin and 1x protease inhibitor cocktails from Sigma), pAG-MNase (Epicypher Inc) was added at a 1:20 ratio and incubated for 10 min at RT. The nuclei were washed again and placed on ice. To activate pAG-MNase, CaCl2 was added to a final concentration of 2 mM. The reaction was inubated for 2 hours while nutating at 4°C and stopped by addition of STOP buffer (340 mM NaCl, 20 mM EDTA, 4 mM EGTA, 50 mg/mL RNase A and 40 mg/mL glycogen). The protein-DNA complex was released by incubating for 10 min at 37°C. DNA was extracted using Qiagen Minelute PCR purification kit. Purified DNA was used for library preparation.\nCUT&RUN libraries were prepared using the Illumina NEBNext Ultra II ChIP-Seq sample kit, according to the manufacturer’s protocol. Libraries were validated using the Agilent Technologies 2100 Bioanalyzer'; [Cell type]'Source: ''treatment: 10uM cadmium resistance; chip target: EZH2; cell line: MDA-231; ', 'treatment: 10uM cadmium resistance; chip target: SUZ12; cell line: MDA-231; ', 'treatment: Untreated control; chip target: EZH2; cell line: MDA-231; ', 'treatment: Untreated control; chip target: SUZ12; cell line: MDA-231; ' GSE108980 Homo sapiens 8 Expression profiling by array GPL10904 Identification of the ERβ transcriptome in MDA-MB-231 cells [microarray] 2018-01-09 The goal of this study was to identify ERβ regulated genes in the triple negative MDA-MB-231 cell line which was engineered to express ERβ in a doxycycline inducible manner https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE108980 ERβ-mediated induction of cystatins results in suppression of TGFβ signaling and inhibition of triple-negative breast cancer metastasis. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1807751115 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1807751115} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA429299 https://www.ebi.ac.uk/ena/browser/view/PRJNA429299 None [Overal design]ERβ expressing MDA-MB-231 cells were treated with either vehicle control or 17-beta estradiol for 5 days. Treatments were conducted in replicates of 3. Upon original analysis, replicate 3 from each treatment showed a slight variation from the other two replicates. For this reason, a second sample of RNA from replicate 3 was submitted and the values between the original sample (#3) and the resubmitted sample (#3 rpt) were averaged together and analyzed along with the other two replicates for each treatment.; [Treatment]'MDA-MB-231-ER-beta cells were plated in 10 cm dishes and allowed to grow to approximately 80% confluence in DMEM/F12 medium containing 10% charcoal stripped FBS and Doxycycline (100 ng/ml, to induce ER-beta expression). Cells were subsequently treated with ethanol vehicle or 1 nM estradiol for 5 days. Media was changed on day 3 to refresh treatments.'; [Growth]'Doxycycline-inducible ER-beta expressing MDA-MB-231cells were maintained in phenol red-free DMEM/F12 medium supplemented with 10% fetal bovine serum (FBS), 1% antibiotic-antimycotic (AA), 5 mg/L blasticidin S and 500 mg/L zeocin.'; [Extraction]"Total RNA was extracted from cells using Trizol per the manufacturer's recommendation."; [Cell type]'Triple Negative Breast Cancer Cell Line''cell line: MDA-MB-231-ER-beta; cell type: Triple Negative Breast Cancer Cell Line; treated with: ethanol vehicle for 5 days; ', 'cell line: MDA-MB-231-ER-beta; cell type: Triple Negative Breast Cancer Cell Line; treated with: 17-beta estradiol for 5 days; ' GSE10613 Homo sapiens 20 Expression profiling by array GPL1708; GPL4133 Convergence of Mutation and Epigenetic Alterations Identifies Common Target Genes in Breast and Colon Cancer 2008-02-22 The identification and characterization of tumor suppressor genes has enhanced our understanding of the biology of cancer and enabled the development of new diagnostic and therapeutic modalities. Whereas in past decades, a handful of tumor suppressors have been slowly identified using techniques such as linkage analysis, large-scale sequencing of the cancer genome has enabled the rapid identification of a large number of genes that are mutated in cancer. However, determining which of these many genes play key roles in cancer development has proven challenging. Specifically, recent sequencing of human breast and colon cancers has revealed a large number of somatic gene mutations, but virtually all are heterozygous, occur at low frequency, and are tumor-type specific. Keywords: Microarray, Hypermethylome, DNA-hypermethylation, DAC, TSA, Epigenetic, Mutation, Colorectal Cancer, Breast Cancer https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE10613 Convergence of mutation and epigenetic alterations identifies common genes in cancer that predict for poor prognosis. PLoS medicine 11.048 https://doi.org/10.1371/journal.pmed.0050114 {PLoS medicine (11.048): 10.1371/journal.pmed.0050114} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA107789 https://www.ebi.ac.uk/ena/browser/view/PRJNA107789 None [Overal design]The candidate hypermethylome genes were identified as described below. These genes were compared to the CAN genes identified by Sjöblom T et al (Science, 2006). Cell culture and treatment. For drug treatments, log phase MCF7, T-47D, MDA-MB231 and MDA-MB-468 cells were cultured in McCoys 5A media (Invitrogen) containing 10% BCS and 1x penicillin/streptomycin with 5M 5aza-deoxycytidine (DAC) (Sigma; stock solution: 1mM in PBS) for 96 hours, replacing media and DAC every 24 hours. Cell treatment with 300nM Trichostatin A (Sigma; stock solution: 1.5mM dissolved in ethanol) was performed for 18 hours. Control cells underwent mock treatment in parallel with addition of equal volume of PBS or ethanol without drugs. Microarray analysis. Total RNA was harvested from log phase cells using the Qiagen kit according to the manufacturers instructions, including a DNAase step. RNA was quantified using the NanoDrop ND-100 followed by quality assessment with 2100 Bioanalyzer (Agilent Technologies). RNA concentrations for individual samples were greater than 200ng/ul, with 28s/18s ratios greater than 2.2 and RNA integrity numbers of 10 (highest). Sample amplification and labeling procedures were carried out using the Low RNA Input Fluorescent Linear Amplification Kit (Agilent Technologies) according to the manufacturers instructions. The labeled cRNA was purified using the RNeasy mini kit (Qiagen) and quantified. RNA spike-in controls (Agilent Technologies) were added to RNA samples before amplification. 0.75 microgram of samples labeled with Cy3 or Cy5 were mixed with control targets (Agilent Technologies), assembled on Oligo Microarray, hybridized, and processed according to the Agilent microarray protocol. Scanning was performed with the Agilent G2565BA microarray scanner under default settings recommended by Agilent Technologies. Data analysis. All arrays were subject to quality checks recommended by the manufacturer. Images were visually inspected for artifacts and distributions of signal and background intensity of both red and green channels were examined to identify anomalous arrays. No irregularities were observed, and all arrays were retained and used. All calculations were performed using the R statistical computing platform and packages from Bioconductor bioinformatics software project. The log ratio of red signal to green signal was calculated and Loess normalization as implemented in the limma package from Bioconductor.; [Treatment]'1x PBS for 96 hours', '5 micromolar 5-AZA for 96 hours', '300 nanomolar TSA for 18 hour', '300 nanomolar TSA for 18 hours'; [Growth]"McCoy's 5A medium with 10% BCS and 1x P/S"; [Extraction]'TriZol extraction followed by RNeasy kit (Qiagen) clean-up with on-column DNase treatment'; [Cell type]'Source: ''' GSE95461 Homo sapiens 34 Expression profiling by high throughput sequencing GPL20301 DNA methylation signature defines genes modulated by stromal cell contents of human breast tumors [RNA-seq] 2017-02-27 Using genome-wide approaches, we have identified groups of genes modulated by CAF-secreted factors from human breast cancer cell lines grown in different CAF-conditioned medium. The genes modulated by CAF secreted factors were characterized by a specific DNA methylation pattern: hypermethylation at transcription start site (TSS) and shore regions. Approximately 60% of them exhibited a methylation-dependent expression level and 20% of them were also dependent on the methyl-CpG-binding protein domain 2. Thus, these specific DNA methylation patterns were linked to an epigenetic control of their expression, upon CAF-secreted factors. We have therefore identified some molecular events defining the responsiveness of groups of genes to stromal cell contents in human breast tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95461 DNA methylation signal has a major role in the response of human breast cancer cells to the microenvironment. Oncogenesis 5.995 https://doi.org/10.1038/oncsis.2017.88 {Oncogenesis (5.995): 10.1038/oncsis.2017.88} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA377162 https://www.ebi.ac.uk/ena/browser/view/PRJNA377162 https://www.ncbi.nlm.nih.gov/sra?term=SRP100803 [Overal design]RNAseq of untreated SKBR3 cells and AU565 cells, CAF-conditionned medium treated cells, DAC treated cells, siMBD2 treated cells, siCtrl, in duplicates or in quadriplicates for untreated SKBR3 cells; [Treatment]'SKBR3 and AU565 were treated by CAF-CMs or DAC or sictrl and siMBD2 as specified in the methods section'; [Growth]'SKBR3 and AU565 cell lines were cultivated as the manufacturer’s instructions (ATCC).'; [Extraction]"Total RNA was extracted with the NucleoSpin RNA kit (Macherey-Nagel, Hoerdt, France) following the manufacturer's instructions. RNA purity and integrity were examined on agarose gel, and quantified with a NanoDrop 1000 (Thermo Scientific, Wilmington, DE).\nIllumina TruSeq RNA sample preparation Kit."; [Cell type]'Source: ''cell line: SKBR3; treatment: none; ', 'cell line: SKBR3; treatment: CAF-CM; ', 'cell line: SKBR3; treatment: DAC; ', 'cell line: SKBR3; treatment: siCtrl; ', 'cell line: AU565; treatment: none; ', 'cell line: AU565; treatment: CAF-CM; ', 'cell line: AU565; treatment: DAC; ', 'cell line: AU565; treatment: siCtrl; ', 'cell line: AU565; treatment: siMBD2; ' GSE74539 Homo sapiens 12 Expression profiling by array GPL10558 Effects of overexpression of hsa-miR-140-3p and its 5'isomiR in MCF10A and MDA-MB-231 breast cell lines 2015-10-30 miRNAs are small noncoding RNA molecules that play an important role in post-transcriptional regulation of gene expression. Length and/or sequence variants of the same miRNA are termed isomiRs. While most isomiRs are functionally redundant compared to their canonical counterparts, so-called 5’isomiRs exhibit a shifted 5’ end and therefore a shifted seed sequence resulting in a different target spectrum. However, not much is known about the functional relevance of these isoforms. Analysis of miRNA-seq data from breast cancer cell lines identified six pairs of highly expressed miRNAs and associated 5’isomiRs. Among them, hsa-miR-140-3p was of particular interest because its 5’isomiR showed higher expression compared to the canonical miRNA annotated in miRbase. This miRNA has previously been shown to control stemness of breast cancer cells. MiRNAseq data of breast cancer patients (TCGA dataset) showed that both the canonical hsa-miR-140-3p and its 5’isomiR-140-3p were highly expressed in patients compared to normal breast tissue. In the current work, we present the functional characterization of 5’isomiR-140-3p and the cellular phenotypes associated with its overexpression in MCF10A and MDA-MB-231 cell lines in comparison to the canonical hsa-miR-140-3p. Contrary to the effect of the canonical hsa miR 140-3p, overexpression of the 5’isomiR-140-3p led to a decrease in cell viability. The latter observation was supported by cell cycle analysis, where the 5’isomiR-140-3p but not the hsa-miR-140-3p caused cell cycle arrest in G0/G1-phase. Additionally, 5’ismoiR-140-3p overexpression was found to cause a decrease in cell migration in MCF10A cells. We identified three novel direct target genes of the 5’ isomiR-140-3p; COL4A1, ITGA6 and MARCKSL1. Finally, we have shown that knocking down these genes partially phenocopied the effects of the 5’isomiR-140-4p overexpression, where COL4A1 and ITGA6 knockdown led to reduced cell viability and cell cycle arrest, while MARCKSL1 knockdown resulted in a decrease in the migratory potential of cells. In summary, this work presents evidence that there is a functional synergy between the canonical hsa-miR-140-3p and the newly identified 5’isomiR-140-3p in suppressing growth and progression of breast cancer by simultaneously targeting genes related to differentiation, proliferation, and migration. With this array, we aimed to address the question which genes are regulated by either of the two forms of the miRNA. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74539 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA300673 https://www.ebi.ac.uk/ena/browser/view/PRJNA300673 None [Overal design]Samples were measured in one biological replicate of cells transfected with mimic-ctrl1 and mimic-ctrl2 (Dharmacon) as control samples and two biological replicates of cells transfected with hsa-miR-140-3p and 5'isomiR-140-3p (Exiqon) in 30nM concentration using Lipofectamin 2000 as transfection reagent.; [Treatment]'Cells were seeded in 6 well plates and transfected using Lipofectamin2000 and a final mimic concentration of 30nM. RNA was harvested 48h after transfection and microarray analysis was performed.'; [Growth]'MCF10A cells were cultured in DMEM-F12 medium and MDA-MB-231 cells were cultured in RPMI medium as described in the paper associated with this microarray.'; [Extraction]'RNA was extracted using the QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''cell line: MCF10A; ', 'cell line: MDA-MB-231; ' GSE50444 Homo sapiens 24 Expression profiling by array GPL3921; GPL4685 Gene expression in organized and disorganized human breast epithelial cells 2013-08-29 We have reported more than a dozen microenvironmental factors whose signaling must be integrated in order to effect an organized, functional tissue morphology. In order to identify underlying commonalities in gene transcription associated with the phenotype, we compared the gene expression of organized and disorganized epithelial cells of the HMT-3522 breast cancer progression series: the non-malignant S1 cells that form polarized spheres (‘acini’), the malignant T4-2 cells that form large tumor-like clusters, and the ‘phenotypically reverted’ T4-2 cells that polarize as a result of correction of the microenvironmental signaling. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50444 Inhibitors of Rho kinase (ROCK) signaling revert the malignant phenotype of breast cancer cells in 3D context. Oncotarget None https://doi.org/10.18632/oncotarget.9395 {Oncotarget (None): 10.18632/oncotarget.9395} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA217499 https://www.ebi.ac.uk/ena/browser/view/PRJNA217499 None [Overal design]24 samples were analyzed: 5 samples were non-malignant S1 cells that formed organized spherical structures ('acini'), 5 samples were the isogenic malignant counterpart of S1 cells, namely the T4-2 cells, which grow into disorganized large cell clusters; and 14 samples of T4-2 cells that had been treated with different reverting agents, these reverting agents cause the T4-2 cells to 'revert' in phenotype so that they resemble the structures formed by S1 cells.; [Treatment]'S1 and T4-2 cells were treated with different reverting agents with every feeding and isolated from 3D cultures with PBS/EDTA as previously described (Lee et al.,Nat Methods. 2007; 4(4):359-365)'; [Growth]'HMT-3522 S1 and T4-2 cells were maintained on tissue culture plastic as described in Petersen et al., Proc Natl Acad Sci U S A. 1992; 89(19):9064-9068. Three dimensional laminin-rich extracellular matrix (3D lrECM) on-top cultures (Lee et al., Nat Methods. 2007; 4(4):359-365) were prepared by trypsinization of cells from tissue culture plastic, seeding of single cells on top of a thin gel of Engelbreth-Holm-Swarm (EHS) tumor extract (Matrigel: BD Biosciences; Cultrex BME: Trevigen), and addition of medium containing 5% EHS. S1 cells were seeded at a density of 3.1×104 cells per cm2; T4-2 cells were seeded at 2.1 ×104 cells per cm2. S1 and T4-2 were maintained in their propagation medium with media change every 2 days.'; [Extraction]'Purified total cellular RNA was extracted using RNeasy Mini Kit with on-column DNase digestion (Qiagen).'; [Cell type]'mammary epithelial cells, non-malignant S1', 'mammary epithelial cells, malignant T4-2 with disorganized phenotype', 'mammary epithelial cells, malignant T4-2 with reverted phenotype''cell type: mammary epithelial cells, non-malignant S1; treatment: No treatment; ', 'cell type: mammary epithelial cells, non-malignant S1; treatment: Medium w/o glucose; ', 'cell type: mammary epithelial cells, malignant T4-2 with disorganized phenotype; treatment: Dominant active Rap1 overexpression plus tyrphostin\xa0(EGFR inhibitor); ', 'cell type: mammary epithelial cells, malignant T4-2 with disorganized phenotype; treatment: Overexpression of dominant active RAP1; ', 'cell type: mammary epithelial cells, malignant T4-2 with disorganized phenotype; treatment: No treatment; ', 'cell type: mammary epithelial cells, malignant T4-2 with reverted phenotype; treatment: 4mM 2-deoxy-D-glucose (2DG) treatment, glucose metabolism inhibitor; ', 'cell type: mammary epithelial cells, malignant T4-2 with reverted phenotype; treatment: Medium w/o glucose; ', 'cell type: mammary epithelial cells, malignant T4-2 with reverted phenotype; treatment: GM6001 treatment \xa0(MMP inhibitor); ', 'cell type: mammary epithelial cells, malignant T4-2 with reverted phenotype; treatment: LY(PI3K inhibitor) treatment; ', 'cell type: mammary epithelial cells, malignant T4-2 with reverted phenotype; treatment: AIIB2 - antibody interfering with beta1 integrin function; ', 'cell type: mammary epithelial cells, malignant T4-2 with reverted phenotype; treatment: EGFR blocking antibody; ', 'cell type: mammary epithelial cells, malignant T4-2 with reverted phenotype; treatment: PD treatment (MAPK inhibitor); ', 'cell type: mammary epithelial cells, malignant T4-2 with reverted phenotype; treatment: Dominant negative Rap1 overexpression; ', 'cell type: mammary epithelial cells, malignant T4-2 with reverted phenotype; treatment: TAPI2 treatment (TACE inhibitor); ', 'cell type: mammary epithelial cells, malignant T4-2 with reverted phenotype; treatment: Tyrphostin treatment (EGFR inhibitor); ', 'cell type: mammary epithelial cells, malignant T4-2 with reverted phenotype; treatment: Tyrphostin treatment\xa0 on top culture (EGFR inhibitor); ' GSE1456 Homo sapiens 318 Expression profiling by array GPL96; GPL97 Gene expression of breast cancer tissue in a large population-based cohort of Swedish patients 2004-06-04 Tissue material was collected from all breast cancer patients receiving surgery at Karolinska Hospital from 1994-1996. Material was frozen immediatley on dry ice or in liquid nitrogen and stored in -70°C freezers. This series contains expression data for n=159 tumors from which RNA could be collected in sufficient amounts and quality for analysis. Keywords: breast cancer, expression profiling, predictive gene signature, molecular classification of cancecr https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE1456 Hormone-replacement therapy influences gene expression profiles and is associated with breast-cancer prognosis: a cohort study. BMC medicine 8.285 https://doi.org/10.1186/1741-7015-4-16 {Breast cancer research : BCR (None) doi:10.1186/bcr1325}; {BMC medicine (8.285) doi:10.1186/1741-7015-4-16}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA90007 https://www.ebi.ac.uk/ena/browser/view/PRJNA90007 None [Overal design]All tumor specimens were assessed on U133 A and B arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen RNeasy Mini Kit'; [Cell type]'Source: ''' GSE24468 Homo sapiens 20 Expression profiling by array GPL570 Elucidation of the Mechanisms by which the Progesterone Receptor Inhibits Inflammatory Responses in Cellular Models of Breast Cancer 2010-09-30 Both pro- and anti-mitogenic activities have been ascribed to progesterone receptor (PR) agonists and antagonists in breast cancer cells, however, the transcriptional responses that underlie these paradoxical functions are not apparent. Using non-transformed, normal human mammary epithelial cells (hMECs) engineered to express PR, and standard microarray technology, we defined 2,370 genes that were significantly regulated by the PR agonist R5020. Gene Ontology (GO) analysis revealed that GO-terms involved in inflammation and NF-κB signaling were among the most significantly regulated. Interestingly, on those NF-κB responsive genes that were inhibited by agonist-activated PR, antagonists either (a) mimicked the actions of agonists or (b) reversed the inhibitory actions of agonists. This difference in pharmacological response could be attributed to the fact that although agonist and antagonist-activated PR is recruited to the promoters of NF-κB responsive promoters, the physical presence of PR tethered to the promoter of some genes is sufficient for transcriptional inhibition whereas on others an agonist-activated PR conformation is required for inhibition of NF-κB signaling. Importantly, the actions of PR on the latter class of genes were reversed by an AF-2 inhibiting, LXXLL-containing peptide. Consideration of the relative activities of these distinct anti-inflammatory pathways in breast cancer may be instructive with respect to the likely therapeutic activity of PR agonists or antagonists in the treatment of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24468 Mechanisms of progesterone receptor inhibition of inflammatory responses in cellular models of breast cancer. Molecular endocrinology (Baltimore, Md.) 3.628 https://doi.org/10.1210/me.2010-0289 {Molecular endocrinology (Baltimore, Md.) (3.628): 10.1210/me.2010-0289} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA132765 https://www.ebi.ac.uk/ena/browser/view/PRJNA132765 None [Overal design]Human mammary epithelial cells treated with R5020 or vehicle.; [Treatment]'Adenoviruses overexpressing hPR-B or β-Gal were generated using the ViraPower Adenoviral Expression System (Invitrogen), and were amplified and purified by CsCl2 centrifugation. Cells were infected at a multiplicity of infection (MOI) of 150 for 17.5 hr. Following infection, cells were treated with 10nM R5020 or vehicle for 16 hours.'; [Growth]'Human mammary epithelial cells were were maintained in MEBM (Lonza, Basel, Switzerland) supplemented with MEGM SingleQuots (Lonza) at 37 degrees C in 5% CO2 atmosphere'; [Extraction]'Total RNA was isolated by using either RNeasy kit (Qiagen, Valencia, CA) or Aurum total RNA mini kit (Bio-Rad, Hercules, CA).'; [Cell type]'mammary epithelial cell''ligand: R5020 10 nM; cell type: mammary epithelial cell; ', 'ligand: Ethanol; cell type: mammary epithelial cell; ' GSE52581 synthetic construct 1516 Protein profiling by protein array GPL14921 An Immunosignature system for diagnosis of cancer [Cancer immunosignaturing - test 2] 2013-11-20 This dataset contains peptide array information from 1516 patients from 12 different cancer types, 2 infectious diseases, and healthy controls using leave one out cross validation. This array is library 2 (GPL14921). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE52581 Immunosignature system for diagnosis of cancer. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1409432111 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1409432111} 'protein' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA229413 https://www.ebi.ac.uk/ena/browser/view/PRJNA229413 None [Overal design]A 1:500 dilution of human serum is added to a peptide array (GPL14921). This array is a one-up design, with 10286 peptides printed in duplicate on a standard glass microscope slide. 1516 patients samples from 14 different diseases and 1 control cohort were analyzed; [Treatment]'NA'; [Growth]'NA'; [Extraction]'NA'; [Cell type]'recurrent Breast cancer', 'Astrocytoma', 'Breast cancer', 'Breast cancer stage IVa', 'Glioblastoma multiformae', 'Lung cancer', 'Multiple myeloma', 'Mixed Oligo/Astrocytoma', 'Healthy normal donor', 'Oligodendroglioma', 'Ovarian cancer', 'Pancreatic cancer', 'Pancreatitis', 'Sarcoma', 'Valley Fever''cell type: recurrent Breast cancer; ', 'cell type: Astrocytoma; ', 'cell type: Breast cancer; ', 'cell type: Breast cancer stage IVa; ', 'cell type: Glioblastoma multiformae; ', 'cell type: Lung cancer; ', 'cell type: Multiple myeloma; ', 'cell type: Mixed Oligo/Astrocytoma; ', 'cell type: Healthy normal donor; ', 'cell type: Oligodendroglioma; ', 'cell type: Ovarian cancer; ', 'cell type: Pancreatic cancer; ', 'cell type: Pancreatitis; ', 'cell type: Sarcoma; ', 'cell type: Valley Fever; ' GSE73947 Homo sapiens 1 Genome binding/occupancy profiling by high throughput sequencing GPL10999 ZNF224 binding profiles in HEK293 cells 2015-10-13 ZNF224 is a Kruppel-associated box-containing zinc-finger protein which represses gene transcription by interacting with the KAP-1, WT1, PRMT5, and DEPDC1 co-repressors. In this study, we have found that ZNF224 functions as an oncogene in MCF7 cells. ZNF224 overexpression increases colony formation, cell growth, and cell survival against camptothecin (CPT) compared to control, and vice versa, upon siRNA knockdown of ZNF224. To examine the mechanism of ZNF224 as an oncogene, first we tried to identify DNA binding element (DBE) of ZNF224 through ChIP-sequencing, and found that ZNF224 could bind to elements containing 5'-CAGC-3' sequence, which was further confirmed by ELISA, SPR, qPCR, and luciferase activity assay. Based on these results, we found that ZNF224 binds to the MIR663A promoter. ZNF224 increased MIR663A transcription, which in turn binds to 3' UTR of p53 and p21 to decrease their expression. MIR663A antagonist abolished ZNF224-mediated suppression of p21 and p53, resulting in the enhanced apoptosis by CPT. The analyses using human breast ductal carcinoma tissues exhibited that the expression of ZNF224 and MIR663A was increased in cancer compared to its neighboring non-cancer region. Consequently, ZNF224 increases cell survival and decreases apoptosis by decreasing the expression of p53 and p21 via increasing the expression of MIR663A as a transcriptional activator. Taken together, we identified and characterized the DNA binding element of ZNF224 and its target genes, which provide novel insight into the role of ZNF224 in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE73947 ZNF224, Krüppel like zinc finger protein, induces cell growth and apoptosis-resistance by down-regulation of p21 and p53 via miR-663a. Oncotarget None https://doi.org/10.18632/oncotarget.8870 {Oncotarget (None): 10.18632/oncotarget.8870} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA298571 https://www.ebi.ac.uk/ena/browser/view/PRJNA298571 https://www.ncbi.nlm.nih.gov/sra?term=SRP064740 [Overal design]The information of genome-wide ZNF224 binding sites in HEK293 cells transiently expressing the protein was generated by deep sequencing using Illumina GAIIx. Note: The data for the sample immunoprecipitated with normal mouse IgG antibody was not provided by the submitter.; [Treatment]"HEK293 cells were transfected with 4ug of FLAG-ZNF224 using lipofectamine 2000 as following the manufacturer's instructions for 24 h."; [Growth]"Cells were maintained in Dulbecco's Modified Eagles Medium (DMEM, Hyclone) supplemented with 10% FBS (Fetal bovine serum, Hyclone) and 100 µg/ml penicillin-streptomycin (WelGENE Inc.), at 37°C, 5% CO2."; [Extraction]"Cells were allowed to crosslink with 1% formaldehyde for 10 minutes at room temperature (RT). To quench the crosslink, 0.125 M glycine was added for 5 minutes at RT. The cell pellets were eluted twice with 10 ml of ice-cold PBS and then incubated with 500 ul of swelling buffer (25mM HEPES, pH 7.8, 1.5mM MgCl2, 10mM KCl, 1mM DTT and 0.1% NP-40) containing a protease inhibitor cocktail (PIC, Roche) for 10 minutes on ice. After centrifugation, the cell pellets were incubated in 200 ul of sonication buffer (50mM HEPES, pH 7.9, 140mM NaCl, 1mM EDTA, 0.1% Na-deoxycholate, 0.1% SDS, 1% Triton X-100 and PIC). The cell lysate was sonicated for 70 seconds (10 sec pulse and 60 sec rest), and DNA lengths were sheared to between 200 and 1,000 bp. The mixture of nucleic acid and protein was incubated with M2 anti-Flag antibody (Sigma Aldrich, cat# F3165, lot# slbl1237v) or normal mouse IgG antibody (Santa Cruz Biotechnology), followed by immunoprecipitation using Protein A and G agarose bead mixture (Invitrogen). The beads were washed in high-salt, low-salt, LiCl and TE buffers. The protein-DNA complexes were separated from the beads by elution buffer (50mM Tris-HCl, pH 8.0, 1mM EDTA, 1% SDS, 50mM NaHCO3) and heated at 65 ℃ for 5 h with protease K to reverse the formaldehyde crosslink. Finally, the DNA was purified with the PCR Clean-up Kit (Promega).\nSequencing libraries were manually generated for high-throughput sequencing. Either end of DNA strands was filled using the Epicentre DNA END-Repair kit (Epicentre Biotechnologies, Madison, WI). Adenine was added at 3' ends by Taq DNA polymerase (New England Biolabs, Beverly, MA) under dATP conditions. Illumina's adaptor oligomers was ligated at both ends using Quick Ligation kit (Qiagen, Germantown, MD). After purified twice, DNA libraries were amplified using Solexa primers (Illumina, San Diego, CA) and Phusion PCR master mix (Thermo Scientific, Hudson, NH)."; [Cell type]'Source: ''cell line: HEK293; transfection: Flag-ZNF224; chip antibody: anti-Flag M2; ' GSE63427 Homo sapiens 74 Expression profiling by array GPL10558 Statin-induced transcriptional changes in breast cancer 2014-11-18 Global gene expression profiling was performed on [1] paired tumor biopsies collected before and after 2 weeks of statin treatment [2] a collection of breast cancer cells lines following 48hrs of atorvastatin treatment with the aim of detecting statin induced transcriptional changes in breast cancer cells in-vitro. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE63427 Insensitivity to atorvastatin is associated with increased accumulation of intracellular lipid droplets and fatty acid metabolism in breast cancer cells. Scientific reports 4.011 https://doi.org/10.1038/s41598-018-23726-3 {Clinical cancer research : an official journal of the American Association for Cancer Research (None) doi:10.1158/1078-0432.CCR-14-1403}; {Scientific reports (4.011) doi:10.1038/s41598-018-23726-3}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA267712 https://www.ebi.ac.uk/ena/browser/view/PRJNA267712 None [Overal design]In this phase II clinical study using the “window-of-opportunity” design, in which the treatment-free window between a cancer diagnosis and surgical tumor resection is used to study the biological effects of a certain drug, atorvastatin, a lipophilic statin, was prescribed to patients with primary breast cancer for two weeks pre-operatively. Tumor samples subjected to whole genome transcriptional profiling were collected before patients started treatment and after completing treatment. In addition, breast cancer cell lines were exposed to atorvastatin treatment for 48 hrs after which total RNA was extracted and subjected to whole genome transcriptional profiling. Vehicle (DMSO) treated samples were included as controls. Three biological replicates were included per sample (condition).; [Treatment]'None'; [Growth]'None'; [Extraction]'RNeasy protocol (Qiagen)'; [Cell type]'Source: ', 'Primary breast cancer cell line''treatment: 2 weeks atorvastatin; subject: FF15; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN15; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF16; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN16; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF41; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN41; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF42; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN42; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF4; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN4; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF22; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN22; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF39; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN39; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF50; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN50; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF1; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN1; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF44; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN44; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF2; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN2; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF17; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN17; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF24; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN24; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF6; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN6; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF28; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN28; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF29; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN29; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF11; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN11; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF43; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN43; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF48; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN48; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF10; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN10; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: FF19; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: MN19; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: FF26; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: MN26; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: FF33; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN33; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF25; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN25; tissue: breast cancer tumor biopsy; ', 'treatment: 2 weeks atorvastatin; subject: FF3; tissue: breast cancer tumor biopsy; ', 'treatment: no treatment (baseline); subject: MN3; tissue: breast cancer tumor biopsy; ', 'cell line: BT474; cell type: Primary breast cancer cell line; treated with: 5µM atorvastatin for 48hrs; ', 'cell line: BT474; cell type: Primary breast cancer cell line; treated with: DMSO (vehicle) for 48hrs; ', 'cell line: MCF7; cell type: Primary breast cancer cell line; treated with: 5µM atorvastatin for 48hrs; ', 'cell line: MCF7; cell type: Primary breast cancer cell line; treated with: DMSO (vehicle) for 48hrs; ', 'cell line: MDA231; cell type: Primary breast cancer cell line; treated with: 1µM atorvastatin for 48hrs; ', 'cell line: MDA231; cell type: Primary breast cancer cell line; treated with: DMSO (vehicle) for 48hrs; ', 'cell line: SKBR3; cell type: Primary breast cancer cell line; treated with: 5µM atorvastatin for 48hrs; ', 'cell line: SKBR3; cell type: Primary breast cancer cell line; treated with: DMSO (vehicle) for 48hrs; ' GSE115625 Mus musculus; Homo sapiens 33 Genome binding/occupancy profiling by high throughput sequencing GPL16791; GPL17021 Genome-wide fork-collapse sites in MEF and MDA-MB-231 from ATR inhibition 2018-06-11 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115625 Genome-wide Identification of Structure-Forming Repeats as Principal Sites of Fork Collapse upon ATR Inhibition. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2018.08.047 {Molecular cell (14.548): 10.1016/j.molcel.2018.08.047} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA475580 https://www.ebi.ac.uk/ena/browser/view/PRJNA475580 None [Overal design]Refer to individual Series; [Treatment]'None', 'DMSO treatment for 9hrs', '0.5 uM VE-822 + 0.2 uM aphidicolin for 9hrs', 'DMSO treatment for 18hrs', '1 uM ATR-45 inhibitor + 0.2 uM aphidicolin for 18hrs'; [Growth]'MEFs were grown in 150 mm tissue-culture plates in DMEM containing high glucose 4.5gm/L and supplemented with 10% FBS, 2mM L-glutamine and Pen/Strep to obtain 15 x 10^6 cells upon collection for RPA ChIP-Seq.', 'MEFs were grown in 150 mm tissue-culture plates in DMEM containing high glucose 4.5gm/L and supplemented with 10% FBS, 2mM L-glutamine and Pen/Strep to obtain 15 x 106 cells upon collection for RPA ChIP-Seq.', 'MDA-MB-231 cells were grown in 100 mm tissue-culture plates in DMEM containing high glucose 4.5gm/L and supplemented with 10% FBS, 2mM L-glutamine and Pen/Strep to obtain ~2 x 106 cells upon collection for BrITL.', 'MEFs were grown in 100 mm tissue-culture plates in DMEM containing high glucose 4.5gm/L and supplemented with 10% FBS, 2mM L-glutamine and Pen/Strep to obtain ~2 x 106 cells upon collection for BrITL.'; [Extraction]"Lysates were clarified from sonicated nuclei (sheared to obtain chromatin size <4 kb) and RPA-DNA complexes were isolated with anti-RPA32 antibody.\nLibraries were prepared according to the NEBNext kit. Briefly, DNA was sonicated to ~200 bp. DNA was end-repaired using a combination of T4 DNA polymerase, Klenow DNA polymerase and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (3' to 5' exo minus) and dATP to yield a protruding 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation, DNA fragments of ~200 bp (insert plus adaptor) were band isolated from a 2% agarose gel. The purified DNA was PCR amplified with Illumina primers for 18 cycles. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on Illumina HiSeq following the manufacturer's protocols.", "Cells were permeabilized, biotin end-labeld, and lysed. Genomic DNA was extracted and sonicated to 0.2-2 kb size fragments prior to pull-down of biotin-labeled fragments with streptaviding-coated Dynabeads.\nLibraries were prepared according to the NEBNext kit. Briefly, DNA was sonicated to ~200 bp. DNA was end-repaired using a combination of T4 DNA polymerase, Klenow DNA polymerase and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (3' to 5' exo minus) and dATP to yield a protruding 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation, DNA fragments of ~200 bp (insert plus adaptor) were band isolated from a 2% agarose gel. The purified DNA was PCR amplified with Illumina primers for 18 cycles. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on Illumina HiSeq following the manufacturer's protocols."; [Cell type]'ATR+/- MEFs', 'Human epithelial breast cancer cells; passage-immortalized', 'Mouse embryonic fibroblasts; passage-immortalized''cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: DMSO treatment for 18hrs; chip antibody: anti-RPA32 (EMD Millipore, NA19L-100UG, lot D00127062); ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: DMSO treatment for 18hrs; chip antibody: anti-RPA32 (EMD Millipore, NA19L-100UG, lot D00144219); ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: DMSO treatment for 18hrs; chip antibody: none; ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 1 uM ATR-45 inhibitor + 0.2 uM aphidicolin for 18hrs; chip antibody: anti-RPA32 (EMD Millipore, NA19L-100UG, lot D00127062); ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 1 uM ATR-45 inhibitor + 0.2 uM aphidicolin for 18hrs; chip antibody: anti-RPA32 (EMD Millipore, NA19L-100UG, lot D00144219); ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 1 uM ATR-45 inhibitor + 0.2 uM aphidicolin for 18hrs; chip antibody: anti-RPA32 (EMD Millipore, NA19L-100UG, lot D00153981); ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 1 uM ATR-45 inhibitor + 0.2 uM aphidicolin for 18hrs; chip antibody: none; ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 1 uM ATR-45 inhibitor + 0.2 uM aphidicolin for 9hrs; chip antibody: anti-RPA32 (EMD Millipore, NA19L-100UG, lot D00144219); ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 1 uM ATR-45 inhibitor + 0.2 uM aphidicolin for 9hrs; chip antibody: anti-RPA32 (EMD Millipore, NA19L-100UG, lot D00127062); ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 1 uM ATR-45 inhibitor + 0.2 uM aphidicolin for 9hrs; chip antibody: none; ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 1 uM ATR-45 inhibitor for 18hrs; chip antibody: anti-RPA32 (EMD Millipore, NA19L-100UG, lot D00127062); ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 1 uM ATR-45 inhibitor for 18hrs; chip antibody: none; ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 0.2 uM aphidicolin for 18hrs; chip antibody: anti-RPA32 (EMD Millipore, NA19L-100UG, lot D00127062); ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 0.2 uM aphidicolin for 18hrs; chip antibody: none; ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 1 uM ATR-45 inhibitor for 18hrs in TIM KD MEFs; chip antibody: anti-RPA32 (EMD Millipore, NA19L-100UG, lot D00144219); ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized MEFs; treatment: 1 uM ATR-45 inhibitor for 18hrs in TIM KD MEFs; chip antibody: none; ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized; treatment: 1 uM ATR-45 inhibitor for 18hrs; chip antibody: anti-RPA32 (EMD Millipore, NA19L-100UG, lot D00153981); ', 'cell type: ATR+/- MEFs; cell line: Passage-immortalized; treatment: 1 uM ATR-45 inhibitor for 18hrs; chip antibody: none; ', 'cell line: MDA-MB-231; cell type: Human epithelial breast cancer cells; passage-immortalized; treated with: DMSO for 9hrs; pull-down reagents: Biotin-16-ddUTP (Enzo Life Sciences, ENZ-42813); Dynabeads KilobaseBinder kit (Life Technologies, 601-01); ', 'cell line: MDA-MB-231; cell type: Human epithelial breast cancer cells; passage-immortalized; treated with: 0.5 uM VE-822 + 0.2 uM aphidicolin for 9hrs; pull-down reagents: Biotin-16-ddUTP (Enzo Life Sciences, ENZ-42813); Dynabeads KilobaseBinder kit (Life Technologies, 601-01); ', 'cell type: Mouse embryonic fibroblasts; passage-immortalized; genotype/variation: ATR+/- MEFs, Bcl-xL-expressing; treated with: DMSO for 18hrs; pull-down reagents: Biotin-16-ddUTP (Enzo Life Sciences, ENZ-42813); Dynabeads KilobaseBinder kit (Life Technologies, 601-01); ', 'cell type: Mouse embryonic fibroblasts; passage-immortalized; genotype/variation: ATR+/- MEFs, Bcl-xL-expressing; treated with: 1 uM ATR-45 inhibitor + 0.2 uM aphidicolin for 18hrs; pull-down reagents: Biotin-16-ddUTP (Enzo Life Sciences, ENZ-42813); Dynabeads KilobaseBinder kit (Life Technologies, 601-01); ' GSE143586 Mus musculus 22 Expression profiling by high throughput sequencing GPL21493 Ectopic Osx+ Cells Affect Tumor Growth 2020-01-13 Tumor growth and metastases are dependent on interactions between cancer cells and the local environment. Expression of the cell-cell adhesion molecule N-cadherin (Ncad) is associated with highly aggressive cancers, and its expression by osteogenic cells has been proposed to provide a molecular “dock” for disseminated tumor cells to establish pre-metastatic niches within the bone. Contrary to expectations, the breast cancer cells were able to form tumors in bone and to induce osteolysis in Cdh2-cKO as well as in control mice. Notably, subcutaneous tumors grew larger in Cdh2-cKO relative to control littermates. Cell tracking experiments using the Ai9 reporter revealed the presence of Osx+ and Ncad+ cells in the stroma of extra-skeletal tumors and in a small population of lung cells, a frequent site of breast cancer metastasis. Gene expression analysis by RNAseq of CD45- Osx+ cells isolated from extra-skeletal tumors revealed alterations of pro-tumorigenic signaling pathways in Cdh2-cKO cells relative to control Osx+ cells. Also surprisingly, we find Osx+ cells present in the circulation, and the majority of tumor-associated and circulating Osx+ cells express the hematopoietic marker CD45, have a phenotypic profile resembling that of tumor infiltrating myeloid and lymphoid populations, but with higher expression of lymphocytic immune suppressive genes. Our results indicate that Osx marks distinct tumor promoting CD45- and CD45+ populations and challenge the dogma that osteogenic and hematopoietic markers are mutually exclusive. They also show that Ncad in CD45- Osx+ cells is not necessary for the establishment of bone metastases, but in extra-skeletal tumors it regulates pro-tumorigenic support by the microenvironment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE143586 Osterix-Cre marks distinct subsets of CD45- and CD45+ stromal populations in extra-skeletal tumors with pro-tumorigenic characteristics. eLife 7.551 https://doi.org/10.7554/eLife.54659 {eLife (7.551): 10.7554/eLife.54659} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA600980 https://www.ebi.ac.uk/ena/browser/view/PRJNA600980 https://www.ncbi.nlm.nih.gov/sra?term=SRP241832 [Overal design]Profiling mRNA expression in Osx+ cells (CD45+ and CD45-) isolated from the stromal component of subcutaneous tumors grown in Cdh2-cKO and wild type mice; [Treatment]'None'; [Growth]'None'; [Extraction]'We inoculated 6 Cdh2-cKO;Ai9 and 4 Osx-cre;Ai9 (wild type) mice and selected, from these cell preparations, those samples that met the quality control test for RNA integrity (average RIN=8.95). Based on this protocol, we submitted 2-3 biological replicates per group of cells, per each genotype to RNAseq analysis.\nClontech SMARTer v1'; [Cell type]'Stromal cells from orthotopic MMTV-BO1 tumors''strain: C57BL/6; age: Postnatal day 56; genotype: wild type; phenotype: Osx+ CD45-; cell type: Stromal cells from orthotopic MMTV-BO1 tumors; ', 'strain: C57BL/6; age: Postnatal day 56; genotype: wild type; phenotype: Osx+ CD45+; cell type: Stromal cells from orthotopic MMTV-BO1 tumors; ', 'strain: C57BL/6; age: Postnatal day 56; genotype: wild type; phenotype: Osx- Cd45+; cell type: Stromal cells from orthotopic MMTV-BO1 tumors; ', 'strain: C57BL/6; age: Postnatal day 56; genotype: wild type; phenotype: Osx- Cd45-; cell type: Stromal cells from orthotopic MMTV-BO1 tumors; ', 'strain: C57BL/6; age: Postnatal day 56; genotype: Cdh2-cKO; phenotype: Osx+ CD45-; cell type: Stromal cells from orthotopic MMTV-BO1 tumors; ', 'strain: C57BL/6; age: Postnatal day 56; genotype: Cdh2-cKO; phenotype: Osx+ CD45+; cell type: Stromal cells from orthotopic MMTV-BO1 tumors; ', 'strain: C57BL/6; age: Postnatal day 56; genotype: Cdh2-cKO; phenotype: Osx- Cd45+; cell type: Stromal cells from orthotopic MMTV-BO1 tumors; ', 'strain: C57BL/6; age: Postnatal day 56; genotype: Cdh2-cKO; phenotype: Osx- Cd45-; cell type: Stromal cells from orthotopic MMTV-BO1 tumors; ' GSE113538 Homo sapiens 6 Expression profiling by high throughput sequencing GPL18573 Comparison between MCF7-IKKe overexpressing cells and MCF7 control cells 2018-04-23 Analysis of differentially expressed genes in MCF7 cancer cells transiently transfected with an expression vector containing the ORF of IKKe and as a control, cells were transfected with a vector containing the ORF of Lacz. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113538 IKKε regulates the breast cancer stem cell phenotype. Biochimica et biophysica acta. Molecular cell research None https://doi.org/10.1016/j.bbamcr.2019.01.002 {Biochimica et biophysica acta. Molecular cell research (None): 10.1016/j.bbamcr.2019.01.002} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA451476 https://www.ebi.ac.uk/ena/browser/view/PRJNA451476 https://www.ncbi.nlm.nih.gov/sra?term=SRP142315 [Overal design]Two groups were analyzed in triplicate each. The first group consisted on MCF7 transfected with an expression vector that overexpresses IKK and the other group was MCF7 cells transfected with a vector containing the ORF of Lacz; [Treatment]'None'; [Growth]'MCF7 cells were cultured in EMEM supplemented with 5% Fetal Bovine Serum and were transiently transfected with an expression vector containing the ORF of IKKe using Xfect (clontech) . An expression vector containing the ORF of Lacz was employed as a control. The cells were analyzed for IKKe expression 48 hours after transfection by qRTPCR and found a 200 fold increase expression in MCF7 IKKe overexpressing cells'; [Extraction]'RNA was isolated with Trizol\nLibrary was constructed using TruSeq stranded total RNA Illumina\nRNAseq 2x 76 Paired End'; [Cell type]'MCF7 cells''cell type: MCF7 cells; treatment: Transfected with a control vector; type of transfection: Transient; ', 'cell type: MCF7 cells; treatment: Transfected with an IKKe overexpressing vector; type of transfection: Transient; ' GSE76368 Homo sapiens 8 Expression profiling by array GPL21250 Identification of circadian-related gene expression profiles in entrained MCF7 2015-12-28 Cancer cells have broken circadian clocks as compared to their normal tissue counterparts. Moreover, it has been shown in breast cancer that disruption of common circadian oscillations are associated to worse prognosis. Numerous studies focused at conical circadian genes in breast cancer cell lines have suggested that there are no mRNA circadian-like oscillations. Nevertheless, cancer cell lines have not been extensively characterized and it is unknown to what extent the circadian oscillations are disrupted. We have chosen representative breast cancer cell lines (MCF-10A, MCF-7, ZR-75-30, MDA-MB-231, and HCC-1954) in order to determine the degree which the circadian clock is damaged. We used serum shock to synchronize the circadian clocks in culture. Our aim was to observe the time course of gene expression using cDNA microarrays in the noncancerous MCF-10A and the cancerous MCF-7 cells and characterize specific genes in other cell lines. We used a cosine function to select highly correlated profiles. Some of the identified genes were validated by qPCR and further evaluated in the other breast cancer cell lines. Interestingly, we observed that breast cancer and noncancerous cultured cells are able to generate specific circadian expression profiles in response to the serum shock. The rhythmic genes suggested via microarray and measured in each particular subtype suggest that each breast cancer cell type respond differently to the circadian synchronization. Future results could identify circadian-like genes that are altered in breast cancer and noncancerous cells which can be used to propose novel treatments. Breast cell lines are potential models for in vitro studies of circadian clocks and clock-controlled pathways. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76368 Identification of circadian-related gene expression profiles in entrained breast cancer cell lines. Chronobiology international 2.562 https://doi.org/10.3109/07420528.2016.1152976 {Chronobiology international (2.562): 10.3109/07420528.2016.1152976} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA307110 https://www.ebi.ac.uk/ena/browser/view/PRJNA307110 None [Overal design]There are 8 total samples representing 0 to 28 hours in 4 hour intervals in MFC-7 breast cancer epitheleal cell line.; [Treatment]'Cells seeded in 6-well plates were allowed to grow to full confluency and were entrained using the serum shock procedure previously described (Rossetti et al., 2012). Briefly, culture medium was removed and the cells were washed with 1X phosphate buffered saline (PBS, Gibco, Life Technologies). Confluent cells were starved overnight with FBS-free basal medium. For MCF-10A, ZR-75-30, and HCC-1954, the basal medium was RPMI-1640, and for MCF-7 and MDA-MB-231, D-MEM/F-12 was used as basal medium. Culture basal medium was removed and cells were then serum shocked with their respective growth basal medium supplemented with 50% horse serum (Biowest, France) and incubated for 2 hours. Following this, the cells were washed with PBS and basal culture medium was placed back into the culture dishes. The first time point was taken after the serum shock (t = 0) and then the cells were harvested every 4 hours for a period of 48 hours.'; [Growth]'MCF-7 breast cancer cells were grown in Gibco® Dulbecco’s modified eagle medium: nutrient mixture F-12 (D-MEM/F-12, Life Technologies) supplemented with 10% heat-inactivated FBS. All culture medium were supplemented with Gibco® Penicillin-Streptomycin (Life Technologies) antibiotics. All cell cultures were propagated in an incubator at 37°C under an atmosphere of 5.0% CO2 and 95.0% air.'; [Extraction]'Total RNA was isolated using the Ambion® RiboPure™ Kit (Life Technologies) according to the manufacturer’s instructions. Briefly, cell lysis was performed directly on the culture 6-well plates by adding 400μL of TRI Reagent® and incubated for 5 minutes. The homogenized sample was centrifuged at 13,000xg for 10 min at 4°C to remove insoluble material from homogenates and the supernatant was mixed with 40μL of bromo-chloro-propane (Aldrich-Sigma), mixed by vortex and incubated for 5 minutes at room temperature. Sample was centrifuged at 13,000xg for 5 min at 4°C, which produced fractionation phases. The upper aqueous phase was combined with molecular biology grade ethanol (Sigma-Aldrich). The RNA was isolated from the aqueous phase by binding to a glass-fiber filter by centrifugation at 13,000xg for 1 minute at room temperature. The filtrate was then rinsed twice with 500μL of the desalting Wash Solution by centrifugation at 13,000xg for 1 minute at room temperature. The purified RNA was then eluted off the filter using 100μL of Elution Buffer by centrifugation at 13,000xg for 1 minute at room temperature. RNA concentration and purity were determinated by spectrophotometry using BioTek’s Take3™ Multi-Volume Plate (BioTek Instruments, Inc., Vermont, USA) on the Synergy HT microplate reader (BioTek Instruments, Inc.). The quality of the RNA samples was also assessed by electrophoresis on a denaturing agarose gel. 500 ng of total RNA were reverse transcribed into cDNA using QuantiTect Reverse Transcription Kit (Qiagen, Valencia, CA, USA) according to the manufacturer‘s instructions. Briefly, RNA was first incubated with gDNA Wipeout Buffer to remove DNA contamination, then retrotranscribed with random primers in a PX2 thermal cycler (Thermo Electron Corporation, USA).'; [Cell type]'breast cancer epitheleal cell line''cell line: MCF-7; cell type: breast cancer epitheleal cell line; time point: 0 hr; ', 'cell line: MCF-7; cell type: breast cancer epitheleal cell line; time point: 4 hr; ', 'cell line: MCF-7; cell type: breast cancer epitheleal cell line; time point: 8 hr; ', 'cell line: MCF-7; cell type: breast cancer epitheleal cell line; time point: 12 hr; ', 'cell line: MCF-7; cell type: breast cancer epitheleal cell line; time point: 16 hr; ', 'cell line: MCF-7; cell type: breast cancer epitheleal cell line; time point: 20 hr; ', 'cell line: MCF-7; cell type: breast cancer epitheleal cell line; time point: 24 hr; ', 'cell line: MCF-7; cell type: breast cancer epitheleal cell line; time point: 28 hr; ' GSE57703 Homo sapiens 12 Expression profiling by array GPL17077 SSEA4 is a marker for chemotherapy resistance [mRNA] 2014-05-15 By coupling PDX and cell surface marker screening technologies, we have identified distinct tumor cell sub-populations that are associated with tumor resistance to chemotherapy. In the majority of relapsed tumors, the percentage of the marker-positive cells shifted back to pretreatment levels. SSEA4 is one of the cell surface molecules tested that could distinguish enriched residual tumor cells in all the different TNBC PDX models analyzed. The expression of SSEA4 is associated with tumor resistance to chemotherapy and SSEA4+ cells show increased gene expression of genes involved in response to toxins, cellular import/export, cell migration and EMT. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE57703 The sialyl-glycolipid stage-specific embryonic antigen 4 marks a subpopulation of chemotherapy-resistant breast cancer cells with mesenchymal features. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-015-0652-6 {Breast cancer research : BCR (5.676): 10.1186/s13058-015-0652-6} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA247770 https://www.ebi.ac.uk/ena/browser/view/PRJNA247770 None [Overal design]The dataset comprises four different sample groups including SSEA4- and SSEA4+ cell fractions isolated from mouse xenografts of human breast cancer cells. Two technical replicates were generated for each cell fraction. Microarray analysis was performed on the Agilent Whole Human Genome Oligo Microarray 8x60K (v2) platform.; [Treatment]'Whole tumors were dissected out together with the surrounding stromal tissue and were placed in a 50 mL falcon tube containing MACS® tissue storage solution (Miltenyi Biotec). Tumor tissue was dissociatied using the Tumor Dissociation Kit, human (Miltenyi Biotec). SSEA4+ and SSEA4- tumor cell subpopulations were isolated by magnetic activated cell sorting (MACS®). After dissociation and depletion of mouse cells, the cells were resuspended in PEB buffer (PBS, pH 7.2, 0.5% bovine serum albumin, and 2 mM EDTA; prepared by diluting MACS BSA Stock Solution 1:20 with autoMACS® Rinsing Solution) at a concentration of 1x10E7 cells per 100 µl. After adding 10 µl SSEA4-PE (Miltenyi Biotec) per 100 µl the suspension was incubated at 4°C under continuous agitation (MACSmix Tube Rotator, Miltenyi Biotec) for 10 min. Then the cells were pelleted at 300 g for 10 min, resuspended in 80 µl PEB per 1x10E7 cells, 20 µl of anti-PE MicroBeads (Miltenyi Biotec) were added and incubated at 4°C under continuous agitation for 15 min. Cells were washed in 1 ml PEB per 1x10E7 cells, pelleted and resuspended in 500 µl PEB per separation. SSEA4+ tumor cells were isolated using an MS-column (Miltenyi Biotec), SSEA4- tumor cells were isolated using an LD-column (Miltenyi Biotec). Purity of the isolated cells was evaluated using flow cytometry.'; [Growth]'Human breast cancer xenografts were established from patient’s primary tumor surgical specimens, by grafting tumor fragments into the interscapular fat pad of athymic nude mice, and maintained through in vivo passages as previously described (PMID: 17606733).'; [Extraction]'Total RNA was isolated using the miRNeasy Kit (QIAGEN).'; [Cell type]'Source: ''host mouse strain: Hsd:Athymic Nude-Foxn1nu (athymic nude mice); host mouse gender: female; xenograft tissue: human breast cancer; xenograft batch: 6; cell fraction: SSEA4-; ', 'host mouse strain: Hsd:Athymic Nude-Foxn1nu (athymic nude mice); host mouse gender: female; xenograft tissue: human breast cancer; xenograft batch: 6; cell fraction: SSEA4+; ', 'host mouse strain: Hsd:Athymic Nude-Foxn1nu (athymic nude mice); host mouse gender: female; xenograft tissue: human breast cancer; xenograft batch: 10; cell fraction: SSEA4-; ', 'host mouse strain: Hsd:Athymic Nude-Foxn1nu (athymic nude mice); host mouse gender: female; xenograft tissue: human breast cancer; xenograft batch: 10; cell fraction: SSEA4+; ', 'host mouse strain: Hsd:Athymic Nude-Foxn1nu (athymic nude mice); host mouse gender: female; xenograft tissue: human breast cancer; xenograft batch: 14; cell fraction: SSEA4-; ', 'host mouse strain: Hsd:Athymic Nude-Foxn1nu (athymic nude mice); host mouse gender: female; xenograft tissue: human breast cancer; xenograft batch: 14; cell fraction: SSEA4+; ' GSE28352 Homo sapiens 5 Genome binding/occupancy profiling by high throughput sequencing GPL9115 High resolution genome-wide mapping of HIF binding sites by ChIP-seq 2011-04-04 We report ChIP-Seq analysis of HIF-1 alpha, HIF-2 alpha, and HIF-1 beta binding in MCF-7 breast cancer cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28352 High-resolution genome-wide mapping of HIF-binding sites by ChIP-seq. Blood 16.562 https://doi.org/10.1182/blood-2010-10-314427 {Blood (16.562) doi:10.1182/blood-2010-10-314427}; {The Journal of biological chemistry (None) doi:10.1074/jbc.RA119.009827}; 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA139281 https://www.ebi.ac.uk/ena/browser/view/PRJNA139281 None [Overal design]Sample analysis compared to pre-immune serum chromatin immunoprecipitation; [Treatment]'Sub confluent cell cultures were exposed to 2 mM dimethyloxalylglycine (DMOG) or 0.5% hypoxia for 16 hours prior to harvest'; [Growth]'MCF-7 breast cancer cells were grown in Dulbeccoâ\x80\x99s modified Eagleâ\x80\x99s Medium, 2 mM L-glutamine and 10% fetal bovine serum (Sigma)'; [Extraction]'Libraries were prepared from immunoprecipitated chromatin using the Illumina ChIP-Seq kit'; [Cell type]'breast cancer cells''cell line: MCF-7; cell type: breast cancer cells; chip antibody: HIF-1 alpha; ', 'cell line: MCF-7; cell type: breast cancer cells; chip antibody: HIF-2 alpha; ', 'cell line: MCF-7; cell type: breast cancer cells; chip antibody: pre-immune serum; ', 'cell line: MCF-7; cell type: breast cancer cells; chip antibody: HIF-1 beta; ' GSE92504 Homo sapiens 6 Expression profiling by array GPL10558 The polycomb protein MEL-18/PCGF2 regulates ErbB phosphorylation in HER2-positive breast cancer 2016-12-16 Gene expression analysis on MEL-18-knockdown BT474 cells. MEL-18, a polycomb group protein and a member of the polycomb repressive complex 1 (PRC1), have suggested as a tumor suppressor in several cancer, including breast cancer. The results provides that the depletion of MEL-18 in HER2-positive breast cancer causes the activation of ErbB signaling pathway. We proposed that MEL-18 is a novel prognostic and therapeutic marker for HER2-positive breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE92504 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA357727 https://www.ebi.ac.uk/ena/browser/view/PRJNA357727 None [Overal design]Total RNA was isolated from the cells using Trizol reagent. BT474 cells stably infected with lentiviruses encoding MEL-18 shRNA (shMEL) compared to its control (shCon); [Treatment]'BT474 cells were infected with lentiviruses encoding either control or MEL-18 shRNA'; [Growth]'Cells were cultured in RPMI1640 supplemented with 10% FBS'; [Extraction]"RNA was extracted with Trizol reagent following the manufacturer's instructions. Quality control was peformed with Agilent Bioanalyzer."; [Cell type]'BT474''disease state: ductal carcinoma; cell type: BT474; lentivirus: shCon; ', 'disease state: ductal carcinoma; cell type: BT474; lentivirus: shMEL; ' GSE8516 Mus musculus 14 Expression profiling by array GPL2881 Characterization of mammary tumors from Brg1 heterozygous mice 2007-07-18 Mammalian SWI/SNF-related complexes have been implicated in cancer based on some of the subunits physically interacting with RB and other proteins involved in carcinogenesis. Additionally, several subunits are mutated or not expressed in tumor-derived cell lines. Strong evidence for a role in tumorigenesis in vivo, however, has been limited to SNF5 mutations that result primarily in malignant rhabdoid tumors (MRTs) in humans and MRTs as well as other sarcomas in mice. We previously generated a null mutation of the Brg1 catalytic subunit in the mouse and reported that homozygotes die during embryogenesis. Here, we demonstrate that Brg1 heterozygotes are susceptible to mammary tumors that are fundamentally different than Snf5 tumors. First, mammary tumors are carcinomas not sarcomas. Second, Brg1+/- tumors arise because of haploinsufficiency rather than loss of heterozygosity (LOH). Third, Brg1+/- tumors exhibit genomic instability but not polyploidy based on array CGH results. We monitored Brg1+/-, Brm-/- double-mutant mice but did not observe any tumors resembling those from Snf5 mutants, indicating that the Brg1+/- and Snf5+/- tumor phenotypes do not differ simply because Brg1 has a closely related paralog whereas Snf5 does not. These findings demonstrate that BRG1 and SNF5 are not functionally equivalent but protect against cancer in different ways. We also demonstrate that Brg1+/- mammary tumors have relatively heterogeneous gene expression profiles with similarities and differences compared to other mouse models of breast cancer. The Brg1+/- expression profiles are not particularly similar to mammary tumors from Wap-T121 transgenic line where RB is perturbed. We were also unable to detect a genetic interaction between the Brg1+/- and Rb+/- tumor phenotypes. These latter findings do not support a BRG1-RB interaction in vivo. Keywords: reference X sample https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE8516 Characterization of mammary tumors from Brg1 heterozygous mice. Oncogene 6.634 https://doi.org/10.1038/sj.onc.1210664 {Oncogene (6.634): 10.1038/sj.onc.1210664} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA101637 https://www.ebi.ac.uk/ena/browser/view/PRJNA101637 None [Overal design]14 microarrays consisting of 12 unique Brg1+/- murine mammary tumors; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen Rneasy Kit'; [Cell type]'Source: ''' GSE159979 synthetic construct 9 Non-coding RNA profiling by array GPL21572 miRNA expression data from MCF-7, LCC2 and LCC9 cells 2020-10-23 Acquired resistance to tamoxifen and fulvestrant is a challenging clinical problem in the treatment of hormone receptor-positive breast cancer patients. Non-coding RNAs (ncRNAs) could contribute to endocrine resistance but their specific roles in tamoxifen and fulvestrant resistance are not fully understood. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE159979 Comprehensive Transcriptomic Analysis Reveals Dysregulated Competing Endogenous RNA Network in Endocrine Resistant Breast Cancer Cells. Frontiers in oncology 4.137 https://doi.org/10.3389/fonc.2020.600487 {Frontiers in oncology (4.137): 10.3389/fonc.2020.600487} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA671456 https://www.ebi.ac.uk/ena/browser/view/PRJNA671456 None [Overal design]We performed microarray analysis of endocrine therapy sensitive (MCF-7), tamoxifen-resistant (LCC2), and dual tamoxifen and fulvestrant-resistant (LCC9) breast cancer cells. MCF-7, LCC2 and LCC9 cells were lysed to extract RNAs for microarray analysis.; [Treatment]'MCF-7, LCC2 or LCC9 cells were resuspended with phenol red free IMEM supplemented with 5% charcoal-stripped FBS and 1% penicillin/streptomycin and seeded in T75 flasks. Culture medium was changed once on day 2. Cells were washed with normal saline twice and harvested on day 4.'; [Growth]'MCF-7, LCC2 and LCC9 cells were grown in phenol red free IMEM supplemented with 5% charcoal-stripped FBS and 1% penicillin/streptomycin in a cell culture incubator at 37 ℃ and 5% CO2.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: LCC9; tamoxifen resistance: tamoxifen-resistant; fulvestrant resistance: fulvestrant-resistant; ', 'cell line: MCF-7; tamoxifen resistance: No; fulvestrant resistance: No; ', 'cell line: LCC2; tamoxifen resistance: tamoxifen-resistant; fulvestrant resistance: No; ' GSE22401 Homo sapiens 26 Genome variation profiling by genome tiling array GPL4560 CGH profiles of sporadic basal-like breast tumors 2010-06-17 Genomic DNA from sporadic breast tumours was isolated and analysed using array CGH. The NKI 1MB BAC/PAC micro array was used to identify chromosomal aberrations of all tumours. Other profiles are located at: GSE9114 Keywords: sporadic breast tumour, CGH. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22401 Prediction of BRCA1-association in hereditary non-BRCA1/2 breast carcinomas with array-CGH. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-008-0117-z {Breast cancer research and treatment (3.471): 10.1007/s10549-008-0117-z} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA128675 https://www.ebi.ac.uk/ena/browser/view/PRJNA128675 None [Overal design]Locate chromosomal aberrations in sporadic breast tumors.; [Treatment]'None'; [Growth]'None'; [Extraction]'As decribed in:\nPrediction of BRCA1-association in hereditary non-BRCA1/2 breast carcinomas with array-CGH.\nJoosse SA, et al.\nBreast Cancer Res Treat. 2008 Aug 14', 'Prediction of BRCA1-association in hereditary non-BRCA1/2 breast carcinomas with array-CGH.\nJoosse SA, et al.\nBreast Cancer Res Treat. 2008 Aug 14', 'DNA is extracted as described in: Joosse et al. (submitted)'; [Cell type]'Source: ', 'peripheral blood lymphocytes''organ: mammary gland; disease: infiltrating ductal carcinoma; type: sporadic breast tumor; ', 'sample: A pool of DNA from peripheral blood lymphocytes, from 7 apparently healthy women.; cell type: peripheral blood lymphocytes; disease: healthy appearing; ', 'organ: mammary gland; breast; disease: infiltrating ductal carcinoma; ' GSE24460 Homo sapiens 4 Expression profiling by array GPL571 Prolonged Drug Selection of Breast Cancer Cells and Enrichment of Cancer Stem Cell Characteristics. 2010-09-30 Background: Cancer stem cells are presumed to have virtually unlimited proliferative and self-renewal abilities and to be highly resistant to chemotherapy, a feature that is associated with overexpression of ATP-binding cassette transporters. We investigated whether prolonged continuous selection of cells for drug resistance enriches cultures for cancer stem-like cells. Methods: Cancer stem cells were defined as CD44+/CD24– cells that could self-renew (ie, generate cells with the tumorigenic CD44+/CD24– phenotype), differentiate, invade, and form tumors in vivo. We used doxorubicin-selected MCF-7/ADR cells, weakly tumorigenic parental MCF-7 cells, and MCF-7/MDR, an MCF-7 subline with forced expression of ABCB1 protein. Cells were examined for cell surface markers and side-population fractions by microarray and flow cytometry, with in vitro invasion assays, and for ability to form mammospheres. Xenograft tumors were generated in mice to examine tumorigenicity (n = 52). The mRNA expression of multidrug resistance genes was examined in putative cancer stem cells and pathway analysis of statistically significantly differentially expressed genes was performed. All statistical tests were two-sided. Results: Pathway analysis showed that MCF-7/ADR cells express mRNAs from ABCB1 and other genes also found in breast cancer stem cells (eg, CD44, TGFB1, and SNAI1). MCF-7/ADR cells were highly invasive, formed mammospheres, and were tumorigenic in mice. In contrast to parental MCF-7 cells, more than 30% of MCF-7/ADR cells had a CD44+/CD24– phenotype, could self-renew, and differentiate (ie, produce CD44+/CD24– and CD44+/CD24+ cells), and overexpressed various multidrug resistance-linked genes (including ABCB1, CCNE1, and MMP9). MCF-7/ADR cells were statistically significantly more invasive in Matrigel than parental MCF-7 cells (MCF-7 cells = 0.82 cell per field and MCF-7/ADR = 7.51 cells per field, difference = 6.69 cells per field, 95% confidence interval = 4.82 to 8.55 cells per field, P<.001). No enrichment in the CD44+/CD24– or CD133+ population was detected in MCF-7/MDR. Conclusion: The cell population with cancer stem cell characteristics increased after prolonged continuous selection for doxorubicin resistance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24460 Prolonged drug selection of breast cancer cells and enrichment of cancer stem cell characteristics. Journal of the National Cancer Institute 10.211 https://doi.org/10.1093/jnci/djq361 {Journal of the National Cancer Institute (10.211): 10.1093/jnci/djq361} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA132705 https://www.ebi.ac.uk/ena/browser/view/PRJNA132705 None [Overal design]PARALLEL study design with 4 samples Parental MCF-7 cell line versus Doxorubicin Resistant MCF-7 cell sublines Biological replicates: 2 parental controls, 2 drug resistant, independently grown and harvested. agent:Selection agent is multi-step doxorubicin selection: MCF7226ng, MCF7262ng biological replicate: MCF71, MCF72 biological replicate: MCF226ng, MCF7262ng; [Treatment]'MCF-7 cells were maintained in DMEM supplemented with 10 percent fetal calf serum, penicillin (100 units/mL), and streptomycin (100 ug/ml)'; [Growth]'None'; [Extraction]'RNA was isolated from approximately 1 million MCF-7 and MCF-7/ADR cells grown in two six-well plates. The medium and any detached cells were first removed from the wells, and total RNA was isolated from the cells that remained attached to the culture dish by use of the Qiagen RNeasy kit (Valencia, CA) by the manufacturers protocol. RNA was quantitated by use of a NanoDrop micro-volume spectrophotometer (Thermo Scientific, Wilmington, DE) and then the integrity of the mRNA was verified with an Agilent BioAnalyzer (Santa Clara, CA).'; [Cell type]'Source: ''cell line: MCF7; treatment: Control; ', 'cell line: MCF7-ADR; treatment: Multi-step doxorubicin-selected subline; ' GSE121657 synthetic construct 6 Non-coding RNA profiling by array GPL21572 MicroRNA expression data from an epithelial-mesenchymal transition (EMT) model of triple negative breast cancer (TNBC). 2018-10-23 Triple-negative breast cancer (TNBC) is the most aggressive form of breast cancer due to lack of effective targeted therapies. Here, we report that the expression of miR-4417 is suppressed during the progression of TNBC cells from non-malignant to the malignant stage. miR-4417 is localized to chromosome 1p36, a region with high loss of heterozygosity in multiple cancers, and its biogenesis is DICER-dependent. Low expression of miR-4417 is significantly associated with worse prognosis in TNBC patients, while overexpression of miR-4417 is sufficient to inhibit migration and tumorigenecity of TNBC cells in vitro. Overall, our findings suggest that miR-4417 exerts a tumor suppressive effect and thereby could serve as a prognostic biomarker and therapeutic tool against TNBC. We used microarrays to profile the global miRNA changes during EMT to identify putative tumor suppressors and prognostic biomarkers for TNBC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE121657 MicroRNA-4417 is a tumor suppressor and prognostic biomarker for triple-negative breast cancer. Cancer biology & therapy 2.879 https://doi.org/10.1080/15384047.2019.1595285 {Cancer biology & therapy (2.879): 10.1080/15384047.2019.1595285} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA498051 https://www.ebi.ac.uk/ena/browser/view/PRJNA498051 None [Overal design]Three biological replicates for each cell line (mesechymal MIIIshGFP vs epithelial MIIIshSMAD2) were selected for RNA extraction.; [Treatment]'Cells were washed with PBS prior to lysis with Trizol.'; [Growth]'MIII cells were maintained in DMEM/F12 medium supplemented with 5% Horse Serum (HS), 1% antibiotics, 10 mg/ml Insulin, 20ng/ml epidermal growth factor, 100ng/ml cholera toxin, and 500ng/ml hydrocortisone in a humidified incubator at 37°C with 5% CO2.'; [Extraction]"Total RNA was isolated from cells using Trizol (Life Technologies) and the miRNeasy Mini kit (Qiagen) according to the manufacturer's protocol."; [Cell type]'Source: ''shRNA: shGFP; cell line: MCF10A-derived cell line MIII; ', 'shRNA: shSMAD2; cell line: MCF10A-derived cell line MIII; ' GSE74141 Mus musculus; Homo sapiens 66 Genome binding/occupancy profiling by high throughput sequencing GPL13112; GPL18573 NAD+ Analog-sensitive PARPs Reveal a Role for PARP-1 in Transcription Elongation 2015-10-19 The PARP family of proteins comprises 17 members, about two thirds of which are active mono- or poly(ADP-ribosyl)transferase enzymes that transfer the ADP-ribose moiety of NAD+ onto target proteins. In many cases, ADP-ribosylation, which plays critical roles in human diseases (e.g., cancer, heart disease, and neuropathies) is associated with abrogation of the molecular functions of the target. Discerning ADP-ribosylation events mediated by a specific PARP is challenging, since all PARPs use the same substrate (i.e., NAD+) and the available inhibitors lack the specificity needed to make such conclusions. In order to identify the direct and specific targets of individual PARP family members, we have developed a chemical and genetic approach known as analog sensitivity, in which alteration of a single conserved amino acid in the active site of the PARP protein creates a pocket that allows use of an unnatural NAD+ analog containing a steric moiety. We have functionalized the steric moiety with alkyne for use in click chemistry reactions. This approach, which is transferable to other PARP family members, creates substrate specificity where none previously existed, allowing PARP-specific post-translational modification followed by target visualization, or isolation of ADP-ribosylated targets using click chemistry techniques. We have used this technology in conjunction with mass spectrometry to identify hundreds of targets both unique to, as well as shared among, the nuclear PARP proteins, PARP-1, PARP-2, and PARP-3. We have also determined the genome-wide distribution of PARP-1-specific ADP-ribosylation by coupling this analog-sensitive PARP approach with chromatin cross-linking in method that we call “Click-ChIP-seq”. We observed that PARP-1-specific ADP-ribosylation is enriched at transcriptionally active promoters in proximity to sites of PARP-1 enrichment. In addition, we observed that NELF, an important regulator of RNA Polymerase II (Pol II) pausing, is not only a target of ADP-ribosylation by PARP-1 but also spatially correlated with chromatin-associated ADP-ribose and PARP-1 in Click-ChIP-seq and ChIP-seq assays, respectively. Given these observations, we hypothesized that ADP-ribosylation might modulate NELF function and result altered Pol II pausing. We have explored this possibility using global run-on coupled with deep sequencing (GRO-seq) in MCF-7 cells in which PARP-1 was depleted by RNAi-mediated knockdown. PARP-1 depletion caused an increase in Pol II pausing genome-wide. Taken together, these results suggest the intriguing possibility that ADP-ribosylation of NELF by PARP-1 may be an important and heretofore unknown step in the release of Pol II into productive elongation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74141 Chemical genetic discovery of PARP targets reveals a role for PARP-1 in transcription elongation. Science (New York, N.Y.) 41.037 https://doi.org/10.1126/science.aaf7865 {Science (New York, N.Y.) (41.037): 10.1126/science.aaf7865} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA299154 https://www.ebi.ac.uk/ena/browser/view/PRJNA299154 https://www.ncbi.nlm.nih.gov/sra?term=SRP064969 [Overal design]Using ChIP-seq (knockdown of Luciferase [control] with or without CDK inhibitor [DRB] treatment, knockdown of PARP-1, knockdown of NELF-E, and re-expression of GFP [control], wild-type NELF-E, mutant NELF-E, or viral NELF inhibitor HDAg-S) in MCF-7 human breast cancer cells and using ChIP-seq (PARP-1 and click-ChIP-seq) in mouse embryonic fibroblasts (MEFs); [Treatment]'MEFs were harvested in cold PBS and collected by centrifugation. The cells were swollen in Nuclei Isolation Buffer (10 mM HEPES, pH 8.0, 2 mM MgCl2, 3 mM CaCl2, 300 mM sucrose, with freshly added 1 mM DTT, protease inhibitors, and phosphatase inhibitors) and the nuclei were released by the addition of 0.65% NP-40 with moderate vortexing. Following collection by centrifugation, the nuclei were resuspended in PARP Reaction Buffer (30 mM Tris•HCl, pH 7.5, 10 mM KCl, 5 mM MgCl2, 5 mM CaCl2, 0.01% NP-40, 0.05 mM EDTA, 20% glycerol, with freshly added 1 mM DTT, protease inhibitors, and phosphatase inhibitors) containing 250 μM 8-Bu(3-yne)T-NAD+ for 30 minutes at 25°C with occasional gentle mixing to allow ADP-ribosylation to occur in the isolated nuclei.', 'MCF-7 Cells were grown in (1) MEM supplemented 1 µg/mL doxycycline for four all four days, (2) MEM with charcoal stripped calf serum for three days, and (3) vehicle (DMSO) or DRB (100 µM) containing medium (1:1000 dilution of DMSO) for 1 hour prior to their crosslinking with 1% formaldehyde in PBS. Crosslinking was quenched with 0.1 M Glycine after 10 minutes at room temperature, and cells were harvested with cold PBS for sonication (200-500 bp) and chromatin immunoprecipitation. MEFs were harvested in cold PBS and collected by centrifugation. The cells were swollen in Nuclei Isolation Buffer (10 mM HEPES, pH 8.0, 2 mM MgCl2, 3 mM CaCl2, 300 mM sucrose, with freshly added 1 mM DTT, protease inhibitors, and phosphatase inhibitors) and the nuclei were released by the addition of 0.65% NP-40 with moderate vortexing. Following collection by centrifugation, the nuclei were resuspended in PARP Reaction Buffer (30 mM Tris•HCl, pH 7.5, 10 mM KCl, 5 mM MgCl2, 5 mM CaCl2, 0.01% NP-40, 0.05 mM EDTA, 20% glycerol, with freshly added 1 mM DTT, protease inhibitors, and phosphatase inhibitors) containing 250 μM 8-Bu(3-yne)T-NAD+ for 30 minutes at 25°C with occasional gentle mixing to allow ADP-ribosylation to occur in the isolated nuclei.'; [Growth]'PARP-1 knockout MEFs expressing analog-senstive PARP-1 were cultured in DMEM supplemented with 10% fetal bovine serum, penicillin, and streptomycin containing 1 µg/mL puromycin', 'MCF-7 cells were grown in culture as previously described (Hah et al. Cell 2011). PARP-1 knockout MEFs expressing analog-senstive PARP-1 were cultured in DMEM supplemented with 10% fetal bovine serum, penicillin, and streptomycin containing 1 µg/mL puromycin.'; [Extraction]'PARP-1 ChIP-seq: Following mock ADP-ribosylation in intact nuclei from MEFs, the nuclei were crosslinked with 0.5% formaldehyde and clicked to biotin. Nuclei were sonicated in a water bath sonicator to a DNA fragment size distribution of 200 to 500 bp and chromatin was used for chromatin immunoprecipitation. Click-ChIP-seq: Following 8-Bu(3-yne)T-ADP-ribosylation in intact nuclei from MEFs, the nuclei were crosslinked with 0.5% formaldehyde and clicked to biotin. Nuclei were sonicated in a water bath sonicator to a DNA fragment size distribution of 200 to 500 bp and bound to streptavidin-conjugated magnetic beads. Following extensive washing, the beads were collected in a magnetic field and de-crosslinked overnight at 65°C. DNA was to be sequenced was recovered by magnetic separation from the beads and purified by PCIAA extraction and ethanol precipitation\nAfter purification, 50 ng of ChIP’d DNA for each condition was used to generate libraries for sequencing, as previously described {Robertson, 2007 #41}, with some modifications. Briefly, the DNA was end-repaired and a single “A”-base overhang was added using the Klenow fragment of E. coli DNA polymerase. The A-modified DNA was ligated with Ilumina sequencing adaptors using the Illumina TruSeq DNA Sample Prep Kit. The ligated DNA (250 ± 25 bp) was size-selected by agarose gel electrophoresis and extraction, amplified by PCR, and purified using AmPure beads (Beckman Coulter). The final libraries were subjected to QC (size, purity, adapter contamination) and sequenced using an Illumina HiSeq 2000 per the manufacturer’s instructions.', 'PARP-1 ChIP-seq: Following mock ADP-ribosylation in intact nuclei from MEFs as described above, the nuclei were crosslinked with 0.5% formaldehyde and clicked to biotin. Nuclei were sonicated in a water bath sonicator to a DNA fragment size distribution of 200 to 500 bp and chromatin was used for chromatin immunoprecipitation. Click-ChIP-seq: Following 8-Bu(3-yne)T-ADP-ribosylation in intact nuclei from MEFs as described above, the nuclei were crosslinked with 0.5% formaldehyde and clicked to biotin. Nuclei were sonicated in a water bath sonicator to a DNA fragment size distribution of 200 to 500 bp and bound to streptavidin-conjugated magnetic beads. Following extensive washing, the beads were collected in a magnetic field and de-crosslinked overnight at 65°C. DNA was to be sequenced was recovered by magnetic separation from the beads and purified by PCIAA extraction and ethanol precipitation. All Other ChIP-seq: Cells were sonicated in a water bath sonicator to a DNA fragment size distribution of 200 to 500 bp and chromatin was used for chromatin immunoprecipitation.\nAfter purification, 50 ng of ChIP’d DNA for each condition was used to generate libraries for sequencing, as previously described {Robertson, 2007 #41}, with some modifications. Briefly, the DNA was end-repaired and a single “A”-base overhang was added using the Klenow fragment of E. coli DNA polymerase. The A-modified DNA was ligated with Ilumina sequencing adaptors using the Illumina TruSeq DNA Sample Prep Kit. The ligated DNA (250 ± 25 bp) was size-selected by agarose gel electrophoresis and extraction, amplified by PCR, and purified using AmPure beads (Beckman Coulter). The final libraries were subjected to QC (size, purity, adapter contamination) and sequenced using an Illumina HiSeq 2000 per the manufacturer’s instructions.'; [Cell type]'mouse embryonic fibroblasts', 'human breast cancer cells''cell type: mouse embryonic fibroblasts; ', 'cell type: human breast cancer cells; cell line: MCF-7; chip antibody: IgG; ', 'cell type: human breast cancer cells; cell line: MCF-7; chip antibody: NELFE; ', 'cell type: human breast cancer cells; cell line: MCF-7; chip antibody: PolII; ', 'cell type: human breast cancer cells; cell line: MCF-7; chip antibody: FLAG; ' GSE121396 synthetic construct 18 Non-coding RNA profiling by array GPL14613 miRNA expression in breast cancer cell lines 2018-10-17 We analyzed the miRNA expression in 6 breast cancer cell lines from young (HCC1500, HCC1937) and old (MCF-7, MDA-MB-231, HCC1806 and MDA-MB-468) patients with breast cancer using the GeneChip® miRNA 2.0 Array (Affymetrix, Santa Clara, CA, USA). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE121396 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA497259 https://www.ebi.ac.uk/ena/browser/view/PRJNA497259 None [Overal design]Total RNA from BC cell lines was isolated in passage 4 using High Pure RNA Isolation Kit from Roche following the manufacturer’s protocol. RNA concentration was measured using a NanoDrop ND 2000-UV-vis Spectrophotometer (Thermo Fisher Scientific Inc., Wilmington DE, USA). RNA integrity determined by RIN (RNA integrity number) value was assessed with the Agilent 2100 Bioanalyzer using RNA 6000 Nano Assay (Agilent Technologies Inc., Santa Clara, CA, USA). Microarray expression profiling was performed using GeneChip® miRNA 2.0 Array (Affymetrix, Santa Clara, CA, USA).; [Treatment]'None'; [Growth]'Cell lines were cultured in RPMI 1640 medium supplemented with 1% L-glutamine and 10% fetal bovine serum (GIBCO, New York, NY). The culture conditions were identical in all cell lines: 37 ̊C and 5% CO2.'; [Extraction]'Total RNA from BC cell lines was isolated in passage 4 using High Pure RNA Isolation Kit from Roche following the manufacturer’s protocol'; [Cell type]'breast cancer cell line''cell line: HCC1500; cell type: breast cancer cell line; patient age: young; ', 'cell line: HCC1806; cell type: breast cancer cell line; patient age: old; ', 'cell line: HCC1937; cell type: breast cancer cell line; patient age: young; ', 'cell line: MDA_MB_231; cell type: breast cancer cell line; patient age: old; ', 'cell line: MDA_MB_468; cell type: breast cancer cell line; patient age: old; ', 'cell line: MCF7; cell type: breast cancer cell line; patient age: old; ' GSE124409 Homo sapiens 20 Expression profiling by high throughput sequencing; Other; Genome binding/occupancy profiling by high throughput sequencing GPL20795; GPL24676 Nuclear peripheral chromatin-lamin B1 interaction is required for global integrity of chromatin architecture and dynamics in human cells 2018-12-27 Background: The eukaryotic genome is folded into higher-order conformation accompanied with constrained dynamics for coordinated genome functions. However, the molecular machinery underlying these hierarchically organized three-dimensional (3D) chromatin architecture and dynamics remains poorly understood. Results: Here by combining imaging and sequencing, we studied the role of lamin B1 in chromatin architecture and dynamics. We found that lamin B1 depletion leads to chromatin redistribution and decompaction. Consequently, lamina-associated domains (LADs) are detached from the nuclear periphery. The inter-chromosomal interactions and overlap between chromosome territories are increased. Moreover, Hi-C data revealed that lamin B1 is required for the integrity and segregation of chromatin compartments but not for the topologically associating domains (TADs). Using live cell single molecule tracking, we further proved that depletion of lamin B1 leads to increased chromatin dynamics, owing to chromatin decompaction and redistribution toward nucleoplasm. Conclusions: Taken together, our data suggest that lamin B1 and chromatin interactions at the nuclear periphery promote LAD maintenance, genomic compartmentalization into chromosome territories and A/B compartments and confine chromatin dynamics, supporting its crucial role in chromatin higher-order structure and chromatin dynamics. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124409 Nuclear peripheral chromatin-lamin B1 interaction is required for global integrity of chromatin architecture and dynamics in human cells. Protein & cell 7.575 https://doi.org/10.1007/s13238-020-00794-8 {Protein & cell (7.575): 10.1007/s13238-020-00794-8} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA511977 https://www.ebi.ac.uk/ena/browser/view/PRJNA511977 https://www.ncbi.nlm.nih.gov/sra?term=SRP174547 [Overal design]Analysis of chromatin 3D structure, lamina associated domains and gene expression data in wild-type and LMNB1-knockout MDA-MB-231 breast cancer cell lines. There are 2 replicates for each Hi-C sample, 3 replicates for each lamin A ChIP-seq sample and 3 replicates for each RNA-seq sample.; [Treatment]'Cells were grown to about 70-80 % confluence, washed with PBS, crosslinked with 1%, v/v formaldehyde solution, and the reaction was quenched by 0.2M glycine solution.', 'Cells were grown to about 70-80 % confluence, washed with PBS, crosslinked with 1%, v/v formaldehyde solution, and the reaction was quenched by 0.3M glycine solution.', 'Cells were grown to about 70-80 % confluence, washed with PBS, crosslinked with 1%, v/v formaldehyde solution, and the reaction was quenched by 0.4M glycine solution.', 'Cells were grown to about 70-80 % confluence, washed with PBS, crosslinked with 1%, v/v formaldehyde solution, and the reaction was quenched by 0.5M glycine solution.'; [Growth]'Human cell line MDA-MB-231 cells were maintained in Dulbecco’s modified Eagle medium with high glucose (Lifetech). The medium contained 10% Fetal bovine serum (FBS) (Lifetech), and 1% of penicillin and streptomycin antibiotics (Lifetech). Cells were maintained at 37 °C and 5% CO2 in a humidified incubator.'; [Extraction]"Cells were lysed and DNA was then cut with MboI and the overhangs were filled with a biotinylated base. Free ends were then ligated together in situ. Crosslinks were reversed, the DNA was sheared to 300-500bp and then biotinylated ligation junctions were recovered with streptavidin beads.\nSequencing libraries were generated using standard Illumina library construction protocol. Briefly, ends of sheared DNA were repaired and the blunt ends were added an “A” base to ligate with Illumina's adapters that have a single 'T' base overhang. Then DNA was PCR amplified for 8-12 cycles. At last, products were purified using AMPure XP system and sequenced through XTen (Illumina).", "Total RNA was collected using the TRIzol® Reagent (Life Technologies) following the manufacturer's instructions. mRNA was purified from total RNA using poly-T oligo-attached magnetic beads. Fragmentation was carried out using divalent cations under elevated temperature in NEBNext First Strand Synthesis Reaction Buffer (5X). First strand cDNA was synthesized using random hexamer primer and M-MuLV Reverse Transcriptase (RNaseH-). Second strand cDNA synthesis was subsequently performed using DNA Polymerase I and RNase H. Remaining overhangs were converted into blunt ends via exonuclease/polymerase activities. After adenylation of 3' ends of DNA fragments, NEBNext Adaptor with hairpin loop structure was ligated to prepare for hybridization. In order to select cDNA fragments with right length, the library fragments were purified with AMPure XP system (Beckman Coulter, Beverly, USA). Then, 3 μl USER Enzyme (NEB, USA) was used with size-selected, adaptor-ligated cDNA at 37°C for 15 min followed by 5 min at 95°C before PCR. Then, PCR was performed with Phusion High-Fidelity DNA polymerase, Universal PCR primers and Index (X) Primer. At last, products were purified (AMPure XP system) and library quality was assessed on the Agilent Bioanalyzer 2100 system.", 'Cells were collected and fixed with 1% formaldehyde (Sigma) at room temperature for 3 min, followed by 125 mM glycine (Amresco) quenching. About 0.8 M fixed cells for each replicate were resuspended with 1 ml hypotonic buffer (20 mM Hepes pH 7.9, 10 mM KCl, 1 mM EDTA, 10% Glycerol, 0.2% NP-40) and incubated in ice for 20 min. After centrifugation at 3000 rpm for 5 min at 4°C, the supernatant was discarded and the nuclei pellets were resuspended with 30 μl nuclei lysis buffer (1% SDS, 10 mM EDTA, 50 mM Tris-HCl pH 8.0). After lysis at 4°C for 30 min, add 70 μl dilution buffer ((0.01% SDS, 1% Triton X-100, 2 mM EDTA, 20 mM Tris-HCl pH8.0, 200 mM NaCl) to totally 100 μl with 0.3% SDS. The sample is transferred t 200 μl PCR tubes at this step. Chromatin was sheared into mainly 200-800 bp fragments with Q800R sonicator, at 80% power for 4 min, with 15 s ON and 30 s OFF. After sonication, the Triton X-100 in system was added to finally 1%. The chromatin was centrifuged at 20,000 g for 15 min at 4°C. The supernatant was saved to new PCR tubes and precleared with 8 μl protein A dynabeads (Invitrogen) at 4°C for 1 h, followed by adding lamin A antibody (ab26300, Abcam). About 1/50 of chromatin was taken out as the input. The chromatin-antibody mixture was incubated overnight at 4°C. Each 15 μl Protein A dynabeads blocked by 1% BSA/PBS were added into chromatin-antibody mixture and rotated together for 4 h at 4°C. Beads were washed with 150 μl low salt buffer for 3 min × 3 times, then for 1 min with 150 μl high salt buffer, and finally transferred into new tubes with 150 μl low salt buffer. Then ChIPmentation method was applied to add adaptors to ChIPed fragments and input fragments. After pheno-chloroform purification, the adaptor-ligated fragments were amplified by Q5 polymerase (NEB) to make libraries with Illumina Nextera index primers. Cycles were determined in advance. ChIPed groups were amplified for 10 cycles and input groups were amplified for 8 cycles. After size selection for 200-1000 bp fragments, the libraries were quantified with Qubit for concentrations and sequenced with paired-end 150 bp reads on Nova 6000 platform (Illumina).', '5×10e4 cells were collected for each library and washed with PBS. Cells were lysed and DNA was digested by Tn5 transposase in 37℃ water bath for 30 min. Then DNA was purified using Qiagen MinElute PCR Purification Kit and PCR amplified. PCR products were purified using AMPure XP system and sequenced through XTen (Illumina).', '5×104 cells were collected for each library and washed with PBS. Cells were lysed and DNA was digested by Tn5 transposase in 37℃ water bath for 30 min. Then DNA was purified using Qiagen MinElute PCR Purification Kit and PCR amplified. PCR products were purified using AMPure XP system and sequenced through XTen (Illumina).'; [Cell type]'epithelial, breast cancer cell line''cell line: MDA-MB-231; tissue: mammary gland/breast; cell type: epithelial, breast cancer cell line; age: 51 years adult; gender: female; genotype: wild type; ', 'cell line: MDA-MB-231; tissue: mammary gland/breast; cell type: epithelial, breast cancer cell line; age: 51 years adult; gender: female; genotype: LMNB1-/-; ', 'cell line: MDA-MB-231; tissue: mammary gland/breast; cell type: epithelial, breast cancer cell line; age: 51 years adult; gender: female; genotype: wild type; chip antibody: lamin A antibody (Abcam, catalog# ab26300, lot# GR3222248-1); ', 'cell line: MDA-MB-231; tissue: mammary gland/breast; cell type: epithelial, breast cancer cell line; age: 51 years adult; gender: female; genotype: LMNB1-/-; chip antibody: lamin A antibody (Abcam, catalog# ab26300, lot# GR3222248-1); ', 'cell line: MDA-MB-231; tissue: mammary gland/breast; cell type: epithelial, breast cancer cell line; age: 51 years adult; gender: female; genotype: wild type; chip antibody: lamin A antibody (ab26300, Abcam); ' GSE58729 Mus musculus 18 Expression profiling by array GPL6246 The ETS transcription factor Elf5 drives lung metastasis in luminal breast cancer via recruitment of Gr-1+CD11b+ myeloid derived suppressor cells 2014-06-23 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58729 ELF5 Drives Lung Metastasis in Luminal Breast Cancer through Recruitment of Gr1+ CD11b+ Myeloid-Derived Suppressor Cells. PLoS biology 8.386 https://doi.org/10.1371/journal.pbio.1002330 {PLoS biology (8.386): 10.1371/journal.pbio.1002330} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA253292 https://www.ebi.ac.uk/ena/browser/view/PRJNA253292 None [Overal design]Refer to individual Series; [Treatment]'Mice were exposed continuosly to a diet containing 700mg/Kg of Doxocyclin (Gordon’s Specialty Stockfeeds) for 1 week at 12-13 weeks old.', 'Mice were exposed continuosly to a diet containing 700mg/Kg of Doxocyclin (Gordon’s Specialty Stockfeeds) from week 6 of age until the ethical endpoint (8 weeks total treatment)'; [Growth]'MMTV-PyMT mouse mammary tumor samples were processed for single cell suspension and FACS sorted based on Lin- CD24+ markers. RNA was extracted from these populations straight after FACS sorting.', 'MMTV-PyMT mouse mammary tumor samples (and metastasis) were processed for single cell suspension and FACS sorted based on Lin- CD24+ markers. RNA was extracted from these populations straight after FACS sorting.'; [Extraction]'Total RNA was extracted by using the Qiagen RNeasy minikit (Qiagen, Doncaster, Vic, Australia) according to manufacturer’s protocol. Following extraction, RNA concentration and purity were analyzed using the NanoDrop® ND-1000 Spectrophotometer (Nano-Drop Technologies, Wilmington, DE, USA). For Affymetrix GeneChip® analysis, the integrity of RNA was analyzed using the Agilent Bioanalyser 2100 6000 Nano Assay (Agilent Technologies, Palo Alto, CA, USA) according to the manufacturer’s instructions.'; [Cell type]'Source: ''gender: female; tissue: mammary gland tumor; strain: FBV/N; genotype/variation: control; ', 'gender: female; tissue: mammary gland tumor; strain: FBV/N; genotype/variation: acute (1 week) Elf5 induced expression; ', 'gender: female; tissue: mammary gland tumor; strain: FBV/N; genotype/variation: WT PyMT; ', 'gender: female; tissue: mammary gland tumor; strain: FBV/N; genotype/variation: chronic (8 weeks) Elf5 induced expression; ', 'gender: female; tissue: lung metastasis; strain: FBV/N; genotype/variation: chronic (8 weeks) Elf5 induced expression; ' GSE135339 Homo sapiens 12 Expression profiling by high throughput sequencing GPL21290 Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [RNA-Seq] 2019-08-03 Estrogen receptor alpha (ERα) signaling mainly occupies on distal enhancers within genome and plays an essential role in ERα-positive breast cancer. ERα usually requires co-factors to regulate the enhancer activity. By analysis of genome-wide nascent transcript profiling in breast cancer cells, we identified a special group of eRNAs that are functionally important for estrogen-induced transcriptional repression. In addition to stabilizing promoter-enhancer looping structure, these eRNAs recruit ERα to particular enhancers of target genes, facilitate the hierarchical formation of a functional transcriptional complex, and cause gene silencing. Interestingly, we found that ERα directly binds to eRNAs and its DNA-binding domain mediates the interaction with RNA molecules. Our ChIP-seq data in MCF-7 cells indicating that ERαwas not able to bind to E2-activated enhancers, which is consistent with the DNA-binding function reported before; moreover the DBD-truncated ERα was not able to bind to E2-repressed enhancers as well, which further supports our hypothesis that eRNA from E2-repressed enhancers help to recruit ERα to specific enhancers through the interaction with DBD domain. Substitution of ERα-DDBD showed a global effect on both induction and repression of ERα target genes as examined by RNA-seq. Further, these eRNAs help with the formation of a specific ERα-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses transcription of target genes. Our work demonstrated that eRNAs, as a distinctive class of cis-acting molecules besides chromatin regulatory elements, play an important role in modulating and refining locus-specific transcriptional program. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE135339 Enhancer RNAs Mediate Estrogen-Induced Decommissioning of Selective Enhancers by Recruiting ERα and Its Cofactor. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2020.107803 {Cell reports (7.815): 10.1016/j.celrep.2020.107803} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA558468 https://www.ebi.ac.uk/ena/browser/view/PRJNA558468 None [Overal design]MCF7 cells were first infected with lentivirus-based ER truncations, and then transiently infected shControl(for vector group) or shER(for WT and dDBD group) targeting 3'UTR to knock down endogenous ER. Cells were kept in hormone stripped condition for at least three days before treating with 100 nM estradiol or corresponding condition of ethanol for six hours. total RNA etraction followed by high throughput sequencing (RNA-seq); [Treatment]"MCF7 cells were first infected with lentivirus-based ER truncations, and then transiently infected shControl(for vector group) or shER(for WT and dDBD group) targeting 3'UTR to knock down endogenous ER. Cells were kept in hormone stripped condition for at least three days before treating with 100 nM estradiol or corresponding condition of ethanol for six hours."; [Growth]'MCF7 obtained from ATCC were cultured in DMEM media supplemented with 10% FBS in a 5% CO2 humidified incubator at 37°C.'; [Extraction]'total RNA was extracted by Trizol Reagent from Invitrogen (Cat no 15596026).\nRNA library was prepared by the KAPA Stranded mRNA-Seq kit (KK8421), according to the manufacturer’s instructions.'; [Cell type]'Source: ''cell line: MCF7; transfection: Cells were infected with dDBD ER; treatment: 100 nM E2, 6hrs; ', 'cell line: MCF7; transfection: Cells were infected with dDBD ER; treatment: Veh; ', 'cell line: MCF7; transfection: Cells were infected with vector; treatment: 100 nM E2, 6hrs; ', 'cell line: MCF7; transfection: Cells were infected with vector; treatment: Veh; ', 'cell line: MCF7; transfection: Cells were infected with wild type ER; treatment: 100 nM E2, 6hrs; ', 'cell line: MCF7; transfection: Cells were infected with wild type ER; treatment: Veh; ' GSE34560 synthetic construct 8 Non-coding RNA profiling by array GPL8786 MicroRNA expression data from leukemia and breast cancer cell lines with/without treatment with microparticles 2011-12-19 Microparticles (MPs) comprise the major source of systemic RNA including microRNA (miRNA), the aberrant expression of which appears to be associated with stage, progression and spread of many cancers. We have shown MPs to transfer multidrug resistance proteins accross both haematological and and non-haematological cancers. using microarray miRNA profiling analysis we now analyze changes in miRNA profiles of both cancer types following microparticle transfer. We identified certain upregulated miRNAs in both cancer types. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE34560 Microparticles Mediate the Intercellular Regulation of microRNA-503 and Proline-Rich Tyrosine Kinase 2 to Alter the Migration and Invasion Capacity of Breast Cancer Cells. Frontiers in oncology 4.137 https://doi.org/10.3389/fonc.2014.00220 {Frontiers in oncology (4.137): 10.3389/fonc.2014.00220} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA151529 https://www.ebi.ac.uk/ena/browser/view/PRJNA151529 None [Overal design]Total RNA was extracted and pooled from duplicate experiments for hybridization on Affymetrix microarrays from (i) the parental drug sensitive leukaemia (CEM) or breast cancer (MCF-7) cells, (ii) their Multidrug Resistant strains leukaemia (VLB100) or breast cancer ( DX cells), (iii) the microparticles isolated from the resistant cells: VLBMP or DXMP, and (iv) the cocultured samples: sensitive cell co-incubated with MPs from their resistant cells ( leukaemia: CEM+VLBMP) or(breast cancer: MCF-7+DXMP). We sought to examine the miRNA profiles of the drug sensitve cells after MP transfer from drug resistant cells across leukaemia nd breact cancer cell lines.; [Treatment]'Unbound Microparticels were removed by washing with PBS and centrifuging at 500 g for 5 min at 25°C after 4 h from the MP co-incubated cells (CEM+VLBMP or MCF+DXMP). The control sensitive cells (CEM or MCF-7), the donor resistant cells (VLB or DX) and microparticles isolated from them (VLBMP or DXMP) were also washed with PBS as decribed.'; [Growth]'Microparticles from resistant leukaemia (VLBMP) breast cancer cells (DXMP) were coincubated with their sensitve counterparts CEM or MCF-7 cells, respectively, for 4 h in complete culture medium at 37°C and 5% CO2.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''sample type: total RNA; cell line: MCF-7; ', 'sample type: total RNA; treatment: DX microparticle; cell line: MCF-7; ', 'sample type: total RNA; cell line: DX; ', 'sample type: DX microparticle; cell line: DX; ', 'sample type: total RNA; cell line: CEM; ', 'sample type: total RNA; treatment: VLB100 microparticle; cell line: CEM; ', 'sample type: total RNA; cell line: VLB100; ', 'sample type: VLB100 microparticle; cell line: VLB100; ' GSE106605 Homo sapiens 4 Expression profiling by high throughput sequencing GPL16791 Covalent inhibitor of the Rho family inhibits the migration of breast cancer cells 2017-11-07 Small GTPase proteins usually serve as molecular switches in various biological process, such as the proliferation, survival, and migration of cells. Mutations or aberrant activations of small GTPase proteins, such as Ras, are frequently observed in various kinds of cancers. Drug discovery efforts that target the Ras family proteins are making breakthroughs, while the discovery of efficient inhibitors that target the Rho family proteins is still stagnant. Protein members from the Rho family, such as RhoA and Cdc42, are key regulators of the migration and invasion of cancer cells. Thus inhibitors of the Rho family proteins are promising to become drug candidates that target cancer metastasis, which is a principal cause of cancer recurrence and chemotherapy failure. Here we show the discovery and characterization of a novel covalent inhibitor named DC-RC-063 that targets the Rho family proteins, using a combined approach of computations and experiments. Revealed by solved crystal structures, compound DC-RC-063 inhibited the activation of RhoA, by disrupting protein-protein interactions, in an allosteric manner. As compound DC-RC-063 inhibited the migration and invasion of breast cancer MDA-MB-231 cells, our findings proved that the Rho family proteins are targetable for covalent inhibitors via an allosteric mechanism. The novel binding site revealed by this inhibitor can be exploited for further development of anti-cancer drugs that target cancer metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE106605 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA417393 https://www.ebi.ac.uk/ena/browser/view/PRJNA417393 https://www.ncbi.nlm.nih.gov/sra?term=SRP124462 [Overal design]RNA-Seq in breast cancer MDA-MB-231 cells in the presence or absence of Rho family covalent inhibitor; [Treatment]'treatment with compounds or DMSO, after 24 hours'; [Growth]'density 1x10e7 MDA-MB-231 cells in 15cm dish, 24 hours, to 70% confluentence'; [Extraction]'2100 Bioanalyzer for quality check, DNaseI (Takara, Japan) for digestion at 37 C and 30 mins\n100ng purified RNA, NEBNext® UltraTM RNA Library Prep Kit for Illumina (NEB, USA)'; [Cell type]'Source: ''cell line: MDA-MB-231 cells; agent: inhibitor; ', 'cell line: MDA-MB-231 cells; agent: DMSO; ' GSE43487 Mus musculus 25 Expression profiling by array; Non-coding RNA profiling by array GPL10740; GPL16502 Mammary tumors 2013-01-14 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43487 Inherited variation in miR-290 expression suppresses breast cancer progression by targeting the metastasis susceptibility gene Arid4b. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-12-3513 {Cancer research (8.378): 10.1158/0008-5472.CAN-12-3513} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA186557 https://www.ebi.ac.uk/ena/browser/view/PRJNA186557 None [Overal design]Refer to individual Series; [Treatment]'not applicable'; [Growth]'Mammary tumors were collected 30 days after orthotopic injection of 6dt1 cells.'; [Extraction]'Samples were snap frozen in liquid N2. Total RNA was isolated using RNAeasy Kit (Qiagen). RNA (100 ng) was reverse transcribed and amplified using WT Expression Kit (Ambion).', "Total RNA was extracted using the mirVana Isolation Kit (Ambion) following manufacturer's instructions."; [Cell type]'Source: ''strain: FVB/N; tissue: mammary tumor; treatment: orthotopic injection of 6dt1 cells expressing miR-290; ', 'strain: FVB/N; tissue: mammary tumor; treatment: orthotopic injection of 6dt1 cells expressing negative control; ', 'strain: [FVB/N-TgN(MMTV-PyVT)634Mul x AKXD R1]F1 sublines; tissue: mammary tumor; ', 'strain: Swiss Webster mice; tissue: various; ' GSE114447 Homo sapiens 6 Expression profiling by array GPL17586 Gene expression data from HepG2 SND1 knockdown stable cell lines after 5-Fu treatment 2018-05-15 SND1 protein is a highly conserved protein of eukaryotic cells and is involved in a group of cellular biological processes, such as gene transcription, pre-mRNA splicing, cell cycle, DNA damage repair, proliferation and programmed cell death degradome, adipogenesis and cancerogenesis. SND1 can promote the metastasis and proliferation of breast cancer cells by down-regulating the miR-127 expression. Herein, we used microarrays to detail the potential molecular mechanism in the chemotherapy drug-induced HCC apoptosis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE114447 SND1 acts as an anti-apoptotic factor via regulating the expression of lncRNA UCA1 in hepatocellular carcinoma. RNA biology 5.477 https://doi.org/10.1080/15476286.2018.1534525 {RNA biology (5.477): 10.1080/15476286.2018.1534525} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA471413 https://www.ebi.ac.uk/ena/browser/view/PRJNA471413 None [Overal design]HepG2 stable cell lines of shSND1-#1 and pLKO-Vector were treated with 6μg/mL 5-Fu, respectively. 48 h after treatment, total RNA was extracted. cDNA was synthesized and hybridised to Affymetrix microarrays.; [Treatment]'HepG2 stable cell lines of shSND1-#1 and pLKO-Vector were treated with 6μg/mL 5-Fu, respectively.'; [Growth]'HepG2 stable cell lines of shSND1-#1 and pLKO-Vector was grown in DMEM with 10% fetal bovine serum.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: HepG2; gene expression: normal; ', 'cell line: HepG2; gene expression: SND1 knockdown; ' GSE24027 Homo sapiens 4 Expression profiling by array GPL570 PCPTC screening 2010-09-08 Primary cultures of patient tumor cells (PCPTC) were used in a cell-based cytotoxicity screen. Microarray-based mRNA profiling was used to identify the mechanism-of-action for the small molecule VLX 50. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24027 Phenotype-based drug screening in primary ovarian carcinoma cultures identifies intracellular iron depletion as a promising strategy for cancer treatment. Biochemical pharmacology 4.825 https://doi.org/10.1016/j.bcp.2011.04.003 {Biochemical pharmacology (4.825): 10.1016/j.bcp.2011.04.003} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA130273 https://www.ebi.ac.uk/ena/browser/view/PRJNA130273 None [Overal design]MCF7 cells were treated with the PCPTC screening hit VLX 50 or DMSO control for 6h prior to RNA isolation. One sample per treatment. Data were analyzed using both MAS5.0 and RMA.; [Treatment]'MCF7 cells treated with 10 microM VLX 50 for 6 hours.', 'MCF7 control cells treated with 0.1% DMSO for 6 hours.'; [Growth]'None'; [Extraction]"Extraction of total RNA was performed using the Qiagen Rneasy minikit according to the manufacturer's instructions."; [Cell type]'breast cancer cells''cell line: MCF7; cell type: breast cancer cells; perturbagen: small molecule; treatment: VLX 50; concentration: 0.00001 M; vehicle: DMSO; duration: 6 h; sample type: treatment; ', 'cell line: MCF7; cell type: breast cancer cells; perturbagen: small molecule; treatment: DMSO; concentration: 0.1%; duration: 6 h; sample type: control; ' GSE76360 Homo sapiens 100 Expression profiling by array GPL6947 03-311 Trastzumab preoperative Trial of Early Stage HER2+ BRCA 2015-12-28 Tumor core biopsies were obtained at baseline and after brief-exposure to single-agent trastuzumab from patients enrolled on the 03-311 trial. Gene expression profiling was conducted on these tumor biopsies to identify signatures of response to preoperative therapy. This study was initiated to identify biomarkers of response to preoperative trastuzumab-conotaining therapy. We performed transcriptional profiling of patient tumor biopsies obtained at baseline and post brief-exposure to trastuzumab to test the hypothesis that transcriptional changes upon brief-exposure to therapy can provide an early readout of subsequent response. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76360 Immune Signatures Following Single Dose Trastuzumab Predict Pathologic Response to PreoperativeTrastuzumab and Chemotherapy in HER2-Positive Early Breast Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-15-2021 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-15-2021} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA307099 https://www.ebi.ac.uk/ena/browser/view/PRJNA307099 None [Overal design]A total of 50 patients generated quality microarray data at both both baseline and post-exposure timepoints. These 100 samples were analyzed for changes in immune subsets and pathway activities that correlated with subsequent response at surgery. Clinical response was assessed at the completion of preoperative therapy. Pathologic complete response (pCR) was scored by institutional pathologists and was defined as the absence of residual invasive disease in both the breast and any sampled axillary nodes; patients who failed to achieve pCR were grouped as objective responders (OBJR) category, which included complete and partial response (CR+PR), and non-responders (NOR) category including stable and progressive disease.; [Treatment]'The 03-311 trial was conducted at the Dana Farber Cancer Institute and the Yale Comprehensive Cancer Center (YCCC). Once a patient signed informed consent, pretreatment tumor biopsies were obtained, then she received a loading dose of trastuzumab (8 mg/kg). Repeat tumor biopsies were obtained approximately 14 days later, after which the patient started treatment with either vinorelbine 25 mg/m2 weekly x 12 weeks (NH) or docetaxel 75 mg/m2 and carboplatin AUC 6 every 3 weeks (TCH) with trastuzumab 2 mg/kg weekly for 12 weeks (TCH); the choice of chemotherapy regimen and subsequent surgical management of the breast and axilla were at the discretion of the treating physicians.'; [Growth]'None'; [Extraction]'200 ng RNA per sample was amplified using the Total PrepTM RNA Amplification Kit (Illumina, Inc.) according to manufacturer’s protocol.'; [Cell type]'Source: ''subject id: 119; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: NOR; er status: Neg; pr status: Neg; ', 'subject id: 119; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: NOR; er status: Neg; pr status: Neg; ', 'subject id: 120; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 120; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 122; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 122; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 123; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 123; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 125; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: NOR; er status: Pos; pr status: Pos; ', 'subject id: 125; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: NOR; er status: Pos; pr status: Pos; ', 'subject id: 126; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 126; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 128; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 128; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 129; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 129; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 130; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 130; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 132; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 132; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 133; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 133; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 134; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 134; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 135; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: pCR; er status: Neg; pr status: Neg; ', 'subject id: 135; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: pCR; er status: Neg; pr status: Neg; ', 'subject id: 137; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: NA; er status: Neg; pr status: Pos; ', 'subject id: 137; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: NA; er status: Neg; pr status: Pos; ', 'subject id: 139; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 139; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 140; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 140; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 142; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: NOR; er status: Pos; pr status: Neg; ', 'subject id: 142; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: NOR; er status: Pos; pr status: Neg; ', 'subject id: 143; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: NOR; er status: Pos; pr status: Pos; ', 'subject id: 143; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: NOR; er status: Pos; pr status: Pos; ', 'subject id: 145; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: pCR; er status: Pos; pr status: Pos; ', 'subject id: 145; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: pCR; er status: Pos; pr status: Pos; ', 'subject id: 146; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 146; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 147; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 147; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 148; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 148; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 149; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 149; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 151; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 151; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 152; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 152; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 153; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 153; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 154; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: pCR; er status: Neg; pr status: Neg; ', 'subject id: 154; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: pCR; er status: Neg; pr status: Neg; ', 'subject id: 156; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 156; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 157; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 157; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 160; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 160; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Neg; ', 'subject id: 161; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 161; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 162; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: pCR; er status: Neg; pr status: Neg; ', 'subject id: 162; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: pCR; er status: Neg; pr status: Neg; ', 'subject id: 164; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: NOR; er status: Neg; pr status: Neg; ', 'subject id: 164; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: NOR; er status: Neg; pr status: Neg; ', 'subject id: 165; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: pCR; er status: Neg; pr status: Neg; ', 'subject id: 165; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: pCR; er status: Neg; pr status: Neg; ', 'subject id: 166; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 166; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 169; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 169; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 170; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 170; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 181; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: pCR; er status: Pos; pr status: Pos; ', 'subject id: 181; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: pCR; er status: Pos; pr status: Pos; ', 'subject id: 182; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 182; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 184; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: NOR; er status: Pos; pr status: Neg; ', 'subject id: 184; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: NOR; er status: Pos; pr status: Neg; ', 'subject id: 185; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: pCR; er status: Neg; pr status: Pos; ', 'subject id: 185; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: pCR; er status: Neg; pr status: Pos; ', 'subject id: 187; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: pCR; er status: Neg; pr status: Neg; ', 'subject id: 187; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: pCR; er status: Neg; pr status: Neg; ', 'subject id: 189; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 189; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 190; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 190; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 191; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 191; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 192; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: NA; er status: Neg; pr status: Neg; ', 'subject id: 192; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: NA; er status: Neg; pr status: Neg; ', 'subject id: 194; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 194; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 195; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: pCR; er status: Pos; pr status: Neg; ', 'subject id: 195; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: pCR; er status: Pos; pr status: Neg; ', 'subject id: 196; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 196; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Neg; pr status: Neg; ', 'subject id: 197; patient status: HER2+ Breast Cancer; timepoint: baseline; response at surgery: OBJR; er status: Pos; pr status: Pos; ', 'subject id: 197; patient status: HER2+ Breast Cancer; timepoint: post; response at surgery: OBJR; er status: Pos; pr status: Pos; ' GSE136231 Homo sapiens 4 Expression profiling by high throughput sequencing GPL18573 MBNL2 knockdown in hypoxic breast cancer cells 2019-08-23 The transcriptome-wide response of hypoxic breast cancer cells upon MBNL2 knockdown was analyzed. Differential gene expression and alternative splicing were investigated. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE136231 Muscleblind-like 2 controls the hypoxia response of cancer cells. RNA (New York, N.Y.) 3.949 https://doi.org/10.1261/rna.073353.119 {RNA (New York, N.Y.) (3.949): 10.1261/rna.073353.119} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA561706 https://www.ebi.ac.uk/ena/browser/view/PRJNA561706 https://www.ncbi.nlm.nih.gov/sra?term=SRP219872 [Overal design]4 samples; 2 conditions: hypoxia control siRNA vs hypoxia MBNL2 siRNA; 2 replicates per condition; [Treatment]"200,000 MCF-7 cells were seeded in 12-well plates and incubated under normoxic conditions (37°C, 5% CO2, 21% O2). 24 h after seeding, cells were exposed to hypoxia (0.5% O2, 37°C, 5% CO2) for 48 h. For reverse transfection of siRNA, 200,000 MCF-7 were transfected after the manufacturer's protocol using Lipofectamine RNAiMAX. For subsequent RNA isolation, cells were transfected in a 12-well format with 200 pmol of an siRNA targeting MBNL2 (siMBNL2: 5'-CACCGUAACCGUUUGUAUG[dT][dT]-3', Paul, 2006, EMBO) or a nonsilencing control siRNA (siCTRL: 5'-UUCUCCGAACGUGUCACGU[dT][dT]-3', Qiagen)"; [Growth]'MCF-7 cells (DSMZ no. ACC-115) were cultured in T75 flasks in RPMI-1640 medium (Sigma-Aldrich), supplemented with 10% FBS (Thermo Fisher Scientific), 1 mM sodium pyruvate (Thermo Fisher Scientific) and Penicillin Streptomycin (Pen Strep, Thermo Fisher Scientific).'; [Extraction]'Total RNA was isolated using the miRNeasy Mini kit (Qiagen), including the optional on-column DNA digestion with the RNase-Free DNase Set (Qiagen).\nAfter isolation, total RNA was used to generate polyA-enriched strand-specific cDNA libraries (TruSeq stranded mRNA library preparation kit, Illumina). Libraries were sequenced on a Illumina NextSeq 500 sequencer with HighOutput'; [Cell type]'Source: ''cell line: MCF-7 (DSMZ no. ACC-115); genotype/variation: control siRNA; condition: hypoxia; ', 'cell line: MCF-7 (DSMZ no. ACC-115); genotype/variation: MBNL2 siRNA; condition: hypoxia; ' GSE7304 Homo sapiens 5 Expression profiling by array GPL3279 aTEA 40 uM 12 hour treatment for MDA-MB-435 cells 2007-03-19 In an effort to identify novel signaling molecules modulated by α-TEA, microarray analyses were performed. DNA array data obtained from human MDA-MB-435 breast cancer cells treated with 40 µM α-TEA for 12 h revealed over 400 genes that were consistently either up- or down-regulated. Thirty-four genes were selected based on their possible involvement in the known biological activities of α-TEA, and three: phorbol-12-myristate 13-acetate-induced protein (PMAPI) which codes for the protein NOXA, ABL2 which codes for the protein referred to as ARG (Abelson-related gene) and THBS1 which codes for thrombospondin 1, TSP-1 were chosen for further study. Keywords: Anti-cancer drug (aTEA at 40 uM 12 hour) treatment for MDA-MB-435 cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7304 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA98075 https://www.ebi.ac.uk/ena/browser/view/PRJNA98075 None [Overal design]The whole-genome cDNA microarrays were manufactured in the laboratory of Dr. Vishwanath Iyer (U.T. Austin). For the microarray experiments, MDA-MB-435 cells were cultured with 40 mM of a-TEA or ethanol control for 12 h. Messenger RNA was isolated using the FastTrack 2.0 kit (Invitrogen, Carlsbad, CA) then reverse transcribed by SuperScript II reverse transcriptase (Invitrogen) according to the manufacturers’ instructions. cDNA was purified using MinElute columns (Qiagen, Valencia, CA) and cDNA samples from vehicle treated controls were labeled with Cy3 and samples from a-TEA treated cells were labeled with Cy5. Array hybridizations were performed in humidity chambers at 65°C for 16 h. Slides were then washed, dried, and scanned using an Axon GenePix 4000 scanner (Axon Instruments, Union City, CA). Microarray images were quantified using GenePix 4.0 software (Axon). Data were uploaded to the Longhorn Array Database and filtered to pass minimum quality control thresholds before subsequent analysis. For a single comparison between two groups, a log2-transformed treatment/control signal ratio of 1 or –1 was chosen as the criterion for induction or repression, respectively. Data from 5 replica experiments were combined to eliminate variability and reduce misclassification.; [Treatment]'None'; [Growth]'None'; [Extraction]'Messenger RNA was isolated using the FastTRack 2.0 kit (Invitrogen, Carlsbad, CA).'; [Cell type]'Source: ''' GSE122849 Homo sapiens 34 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL16791 Cistromic re-programming by truncating GATA3 mutations promotes mesenchymal transformation in vitro, but not mammary tumour formation in mice 2018-11-23 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE122849 GATA3 Truncating Mutations Promote Cistromic Re-Programming In Vitro, but Not Mammary Tumor Formation in Mice. Journal of mammary gland biology and neoplasia 2.758 https://doi.org/10.1007/s10911-019-09432-4 {Journal of mammary gland biology and neoplasia (2.758): 10.1007/s10911-019-09432-4} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA506681 https://www.ebi.ac.uk/ena/browser/view/PRJNA506681 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'Chromatin immunoprecipitations were performed as described previously, with adaptations (Schmidt et al., 2009). In short, cells were crosslinked in solution A (pH 7.4, 50mM Hepes, 100mM NaCl, 1mM EDTA, 0.5M EGTA) containing 2mM DSG for 35 minutes, then formaldehyde was added to a final concentration of 1% and incubated for another 10 minutes. After addition of Glycine to a final concentration of 125mM to quench the crosslinking reaction and washing with PBS, cells were collected. The Bioruptor Pico (Diagenode) was used for sonication. For ChIP, antibodies were used to detect the HA-tag (25mg, 05-904, Millipore) and GATA3 (10 mg, sc-268, Santa Cruz) with 100 ml Protein A magnetic beads (Thermo Scientific).\nImmunoprecipitated DNA was processed for library preparation (Part# 0801-0303, KAPA biosystems kit).', 'RNA was extracted using the AllPrep DNA/RNA universal kit (Qiagen) according to the manufacturer’s instruction with Qiagen’s QIAcube robot. Samples with a RIN>8 were considered for library preparation.\nStrand-specific libraries were generated with the KAPA Stranded RNA-seq Library Preparation Kit (KAPA biosystems, KR0934).'; [Cell type]'Breast cancer cell line''cell line: T47D; cell type: Breast cancer cell line; chip antibody: aHA (05-904, Millipore); plasmid: control plasmid; ', 'cell line: T47D; cell type: Breast cancer cell line; chip antibody: aHA (05-904, Millipore); plasmid: HA_GATA3_wt plasmid; ', 'cell line: T47D; cell type: Breast cancer cell line; chip antibody: aHA (05-904, Millipore); plasmid: HA_GATA3_TR1 plasmid; ', 'cell line: T47D; cell type: Breast cancer cell line; chip antibody: aHA (05-904, Millipore); plasmid: HA_GATA3_TR2 plasmid; ', 'cell line: T47D; cell type: Breast cancer cell line; chip antibody: aHA (05-904, Millipore); plasmid: control plasmid; sirna: siNT; ', 'cell line: T47D; cell type: Breast cancer cell line; chip antibody: aHA (05-904, Millipore); plasmid: control plasmid; sirna: siFOXA1; ', 'cell line: T47D; cell type: Breast cancer cell line; chip antibody: aHA (05-904, Millipore); plasmid: HA_GATA3_wt plasmid; sirna: siNT; ', 'cell line: T47D; cell type: Breast cancer cell line; chip antibody: aHA (05-904, Millipore); plasmid: HA_GATA3_wt plasmid; sirna: siFOXA1; ', 'cell line: T47D; cell type: Breast cancer cell line; chip antibody: aHA (05-904, Millipore); plasmid: HA_GATA3_TR1 plasmid; sirna: siNT; ', 'cell line: T47D; cell type: Breast cancer cell line; chip antibody: aHA (05-904, Millipore); plasmid: HA_GATA3_TR1 plasmid; sirna: siFOXA1; ', 'cell line: T47D; cell type: Breast cancer cell line; chip antibody: aHA (05-904, Millipore); plasmid: HA_GATA3_TR2 plasmid; sirna: siNT; ', 'cell line: T47D; cell type: Breast cancer cell line; chip antibody: aHA (05-904, Millipore); plasmid: HA_GATA3_TR2 plasmid; sirna: siFOXA1; ', 'cell line: T47D; cell type: Breast cancer cell line; chip antibody: aGATA3 (sc-268, Santa Cruz); ', 'cell line: MCF7; cell type: Breast cancer cell line; chip antibody: aGATA3 (sc-268, Santa Cruz); ', 'cell line: T47D; cell type: Breast cancer cell line; plasmid: control plasmid; ', 'cell line: T47D; cell type: Breast cancer cell line; plasmid: HA_GATA3_wt plasmid; ', 'cell line: T47D; cell type: Breast cancer cell line; plasmid: HA_GATA3_TR1 plasmid; ', 'cell line: T47D; cell type: Breast cancer cell line; plasmid: HA_GATA3_TR2 plasmid; ' GSE115869 Homo sapiens 2 Expression profiling by high throughput sequencing GPL18573 Transcriptomic data of MCF7 cells adapted to culture in media containing different sugars (glucose or fructose) and cultured in 2D on plastic 2018-06-15 We report the single-cell RNA sequencing data obtained from MCF7 breast cancer cells cultured in standard DMEM with 25 mM glucose, or adapted to culture in DMEM with 10 mM fructose to reduce glycolysis, and cultures in 2D on plastic https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115869 p53 is regulated by aerobic glycolysis in cancer cells by the CtBP family of NADH-dependent transcriptional regulators. Science signaling 6.481 https://doi.org/10.1126/scisignal.aau9529 {Science signaling (6.481): 10.1126/scisignal.aau9529} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA476336 https://www.ebi.ac.uk/ena/browser/view/PRJNA476336 https://www.ncbi.nlm.nih.gov/sra?term=SRP150635 [Overal design]Examination of transcriptomic changes in MCF-7 breast cancer cells mammospheres in response to restriction of glycolysis; [Treatment]'Adapted cell cultures were plated on standard cell culture plate and grown to c. 70% confluency. Media was replaced 24 hours prior to assay.'; [Growth]'MCF-7 cells were adapted to culture in 2D in DMEM containing either 25 mM glucose or 10 mM fructose, for 30 days.'; [Extraction]'Trypsin/ EDTA disaggregated cells\nPCR on bead then Nextera XT'; [Cell type]'Source: ''protocol: 2D cultured; cell line: MCF-7; sugar source: 25 mM glucose; ', 'protocol: 2D cultured; cell line: MCF-7; sugar source: 10 mM fructose; ' GSE72013 Homo sapiens 13 Expression profiling by array; Non-coding RNA profiling by array GPL6244; GPL16601 MCF-7 human breast cancer cells treated with ethanol: DNA microarray expression data and microRNA prevalence data 2015-08-12 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72013 Long-term exposure of MCF-7 breast cancer cells to ethanol stimulates oncogenic features. International journal of oncology 3.571 https://doi.org/10.3892/ijo.2016.3800 {International journal of oncology (3.571): 10.3892/ijo.2016.3800} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA292714 https://www.ebi.ac.uk/ena/browser/view/PRJNA292714 None [Overal design]Refer to individual Series; [Treatment]'Cells were grown in culture in 6 well plates in minimal essentail medium Eagle plus 10 percent fetal bovine serum and 0.01 mg/ml bovine insulin. Ethanol was added to each well in a volume of 10 microliters to achieve concentrations ranging from 0 to 25 mM. The 25 mM and control (0 mM) treatments were carried on for 1 week or 4 weeks, and RNA was extracted for analysis.', 'Ethanol was added in 10 microliter volumes to fresh culture medium each 3 days throughout the treatment. Control wells received no ethanol.'; [Growth]'None', 'MCF-7 is an established cell line derived from a human breast cancer. Cells were maintained in culture in T-25 plastic flasks and transferred to 6 well plastic plates for experiments.'; [Extraction]'Cells were washed once with phosphate buffered saline pH 7.4 and RNA was extracted using the RNeasy Plus Micro kit.', "Total RNA was extracted using the Mirvana total RNA extraction kit and the manufacturer's procedure."; [Cell type]'non-malignant breast cancer', 'malignant breast cancer''cell line: MCF12-A; cell type: non-malignant breast cancer; ', 'cell line: MCF-7; cell type: malignant breast cancer; ' GSE175514 Homo sapiens 2 Non-coding RNA profiling by high throughput sequencing GPL15520 Identify LOC550643-regulated miRNAs in MDA-MB-231 cell (miRNA-Seq) 2021-05-25 The objective of this study is to unravel the metastasis-associated lncRNAs involved in the regulation of cell migration and invasion in breast cancer cells. Using next generation sequencing approach, we identify differential expression miRNAs in MDA-MB-231 cells with LOC550643 knockdown. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE175514 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA732679 https://www.ebi.ac.uk/ena/browser/view/PRJNA732679 None [Overal design]Total RNA samples were derived from MDA-MB-231-IV2 cells with/without LOC550643 knockdown. Small RNA expression levels of MB-231-IV2-C and MB-231-IV2-LOC550643 knockdown were examined by using a Next-generation sequencing approach (MiSeq V2 reagent kit ).; [Treatment]'After transfection with N.C and siLOC550643 for 48hr, RNA was extracted from two samples, MDA-MB-231-IV2-1 with LOC550643 knockdown and control cells'; [Growth]'MDA-MB-231 cells and IV2-1 cells were culturein in Dulbecco’s modified Eagle’s medium supplemented with 10% inactivated FBS'; [Extraction]"Total RNA of breast cancer cells was prepared using TRIZOL (Invitrogen, Carlsbad, CA, USA) according to the manufacturer’s protocol.\nRNA libraries were prepared for sequencing using standard Illumina protocols with MiSeq Reagent Kit v3 (MS-102-3001).\nLibraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit (Part# 0801-0303). Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation DNA was PCR amplified with Illumina primers for 15 cycles and library fragments of ~250 bp (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the Illumina HiSeq 2500 following the manufacturer's protocols."; [Cell type]'Source: ''cell line: MDA-MB-231; treatment: siRNA control transfection for 48hr; ', 'cell line: MDA-MB-231; treatment: siLOC550643 pool RNA transfection for 48hr; ' GSE148663 Homo sapiens 32 Methylation profiling by genome tiling array GPL13534 DNA methylation of leukocytes from sporadic breast cancer patients and healthy controls in Latin American population 2020-04-14 The study aimed to compare the DNA methylation differences between blood samples from sporadic breast cancer patients and healthy controls from a well-defined cohort in Uruguayan population. Infinium methylation arrays (450K Illumina) are used to identify genome-wide methylation differences between groups. The identified differently methylated CpG were further analyzed in an independent cohort of 80 breast cancer patients and 80 healthy controls. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148663 Discovery of novel DNA methylation biomarkers for non-invasive sporadic breast cancer detection in the Latino population. Molecular oncology 5.962 https://doi.org/10.1002/1878-0261.12842 {Molecular oncology (5.962): 10.1002/1878-0261.12842} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA625303 https://www.ebi.ac.uk/ena/browser/view/PRJNA625303 None [Overal design]The study aimed to compare the DNA methylation differences between blood samples from sporadic breast cancer patients and healthy controls from a well-defined cohort in Uruguayan population. Infinium methylation arrays (450K Illumina) are used to identify genome-wide methylation differences between groups.; [Treatment]'No treatment applied'; [Growth]'Not specified'; [Extraction]'Total DNA was isolated by standard procedures using using conventional phenol:chloroform:isoamylalcohol (Sigma) extraction'; [Cell type]'Peripheral blood leukocytes''disease state: sporadic breast cancer; individual: Patient 1; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 2; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 3; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 4; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 5; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 6; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 7; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 8; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 9; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 10; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 11; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 12; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 13; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 14; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 15; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 16; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 17; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 18; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 19; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 20; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 21; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: sporadic breast cancer; individual: Patient 22; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: healthy control; individual: Control 1; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: healthy control; individual: Control 2; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: healthy control; individual: Control 3; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: healthy control; individual: Control 4; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: healthy control; individual: Control 5; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: healthy control; individual: Control 6; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: healthy control; individual: Control 7; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: healthy control; individual: Control 8; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: healthy control; individual: Control 9; population: Uruguayan population; cell type: Peripheral blood leukocytes; ', 'disease state: healthy control; individual: Control 10; population: Uruguayan population; cell type: Peripheral blood leukocytes; ' GSE68973 Rattus norvegicus 35 Expression profiling by array GPL7294 Prenatal exposure to bisphenol A, genistein and indole-3-carbinol on early mammary gland development and carcinogenesis in female Sprague-Dawley offspring 2015-05-18 Rodent studies have indicated that gestational and perinatal bisphenol A (BPA) exposure increase the risk of developing breast cancer during adulthood. In contrast, some dietary compounds such as genistein (GEN) and indole 3-carbinol (I3C) present potential protective effects against inducing hormone-dependent cancers, including that of the mammary gland. Thus, we aimed to evaluate the role of these dietary compounds on early mammary gland development and carcinogenesis in female Sprague-Dawley offspring. Pregnant Sprague-Dawley (SD) rats were treated with BPA at 25 or 250µg/kg b.w./day by gavage from gestational day (GD) 10 to 21 with or without dietary GEN (250 mg/kg chow, ~5.5 mg/kg b.w./day) or I3C (2000 mg/kg chow, ~45.0 mg/kg b.w./day). At post-natal day (PND) 21, some female offspring from different litters were euthanized for mammary gland development and gene expression analyses while other female offspring received a single dose of N-methyl-N-nitrosourea (MNU) for mammary carcinogenesis initiation. The findings this study indicated the prenatal exposure to BPA, GEN and I3C did not significantly alter ductal elongation, number of terminal end buds (TEB) or cell proliferation, and estrogen receptor alpha (ER-α) immunostaining expression in epithelial mammary cells at PND 21. BPA treatment modulated the expression of several genes, but these changes were not associated with a dose dependent response. Dietary GEN and I3C treatment causally and consistent with the mammary gland structures outcomes. Besides, maternal BPA exposure associated with dietary GEN and I3C did not alter the susceptibility to the mammary cancer development in adulthood when the carcinogen was administered in a window of immature mammary gland development. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE68973 Global gene expression and morphological alterations in the mammary gland after gestational exposure to bisphenol A, genistein and indole-3-carbinol in female Sprague-Dawley offspring. Toxicology and applied pharmacology 3.585 https://doi.org/10.1016/j.taap.2016.05.004 {Toxicology and applied pharmacology (3.585): 10.1016/j.taap.2016.05.004} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA284241 https://www.ebi.ac.uk/ena/browser/view/PRJNA284241 None [Overal design]Pregnant Sprague-Dawley (SD) rats were treated with BPA at 25 or 250µg/kg b.w./day by gavage from gestational day (GD) 10 to 21 with or without dietary GEN (250 mg/kg chow, ~5.5 mg/kg b.w./day) or I3C (2000 mg/kg chow, ~45.0 mg/kg b.w./day). At post-natal day (PND) 21, some female offspring from different litters were euthanized for mammary gland development and gene expression analyses while other female offspring received a single dose of N-methyl-N-nitrosourea (MNU) for mammary carcinogenesis initiation.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted from the abdominal left mammary gland using the miRNeasy kit (QIAGEN Inc. USA Valencia, CA - USA) according to the manufacturer’s instructions. The extracted RNA was stored at -80°C. RNA was quantified in a spectrophotometer NanoVue (GE Healthcare UK Limited, UK) and the integrity was evaluated using the equipment Agilent 2100 Bioanalyzer (Agilent Technologies, Inc. Life Sciences and Chemical Analysis Group, Santa Clara, CA, USA) under standard conditions.'; [Cell type]'Source: ''strain: Sprague-Dawley; treatment (pregnant rat): negative control; gender (offspring): Female; tissue (offspring): Mammary gland; age (offspring): post-natal day 21; ', 'strain: Sprague-Dawley; treatment (pregnant rat): BPA25; gender (offspring): Female; tissue (offspring): Mammary gland; age (offspring): post-natal day 21; ', 'strain: Sprague-Dawley; treatment (pregnant rat): BPA250; gender (offspring): Female; tissue (offspring): Mammary gland; age (offspring): post-natal day 21; ', 'strain: Sprague-Dawley; treatment (pregnant rat): BPA25+genistein; gender (offspring): Female; tissue (offspring): Mammary gland; age (offspring): post-natal day 21; ', 'strain: Sprague-Dawley; treatment (pregnant rat): BPA250+genistein; gender (offspring): Female; tissue (offspring): Mammary gland; age (offspring): post-natal day 21; ', 'strain: Sprague-Dawley; treatment (pregnant rat): BPA25+indole; gender (offspring): Female; tissue (offspring): Mammary gland; age (offspring): post-natal day 21; ', 'strain: Sprague-Dawley; treatment (pregnant rat): BPA250+indole; gender (offspring): Female; tissue (offspring): Mammary gland; age (offspring): post-natal day 21; ' GSE36847 Homo sapiens 32 Expression profiling by array GPL14877 Distinct perturbation of the translatome by the anti-diabetic drug metformin 2012-03-27 Reduced cancer incidence has been reported among type II diabetics treated with metformin. Metformin exhibits anti-proliferative and anti-neoplastic effects associated with inhibition of mTORC1, but the mechanisms are poorly understood. We provide the first genome-wide analysis of translational targets of canonical mTOR inhibitors (rapamycin and PP242) and metformin, revealing that metformin controls gene expression at the level of mRNA translation to an extent comparable to that of canonical mTOR inhibitors. Importantly, metformin's anti-proliferative activity can be explained by selective translational suppression of mRNAs encoding cell cycle regulators via the mTORC1/4E-BP pathway. Thus, metformin selectively inhibits mRNA translation of encoded proteins that promote neoplastic proliferation, motivating further studies of this compound and related biguanides in cancer prevention and treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36847 Distinct perturbation of the translatome by the antidiabetic drug metformin. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1201689109 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1201689109} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA156903 https://www.ebi.ac.uk/ena/browser/view/PRJNA156903 None [Overal design]MCF7 cells were treated with rapamycin, metformin or PP242 at concentrations that inhibited proliferation to 50% of control. Both cytoplasmic and polysome-associated mRNA was extracted from treatments and a vehicle treated control and probed with microarrays.; [Treatment]'Cells were treated with vehicle, rapamycin (100nM), PP242 (1\uf06dM) and metformin (10mM) for 12h'; [Growth]'MCF7 cells were obtained from ATCC and grown in RPMI (Invitrogen), supplemented with 10% fetal bovine serum (FBS; Invitrogen), 2 mM L-glutamine, and 100 units/ml penicillin/streptomycin (all from Invitrogen) at 37oC and 5% CO2.'; [Extraction]'Polysome profile analysis was carried out as previously described (Dowling RJ, Zakikhani M, Fantus IG, Pollak M, & Sonenberg N (2007) Cancer Res 67, 10804-10812). A parallel sample was collected from post-nuclear lysates that are loaded onto the sucrose gradient and RNA was isolated using Trizol (Invitrogen) (“cytoplasmic mRNA”). Polysome fractions with mRNA associated with >3 ribosomes were pooled (“polysome-associated” mRNA) and RNA was isolated using Trizol.'; [Cell type]'Source: ''cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: metformin; experiment: 1; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: metformin; experiment: 1; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: rapamycin; experiment: 1; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: rapamycin; experiment: 1; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: vehicle; experiment: 1; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: vehicle; experiment: 1; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: PP242; experiment: 1; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: PP242; experiment: 1; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: rapamycin; experiment: 2; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: rapamycin; experiment: 2; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: vehicle; experiment: 2; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: vehicle; experiment: 2; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: PP242; experiment: 2; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: PP242; experiment: 2; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: metformin; experiment: 2; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: metformin; experiment: 2; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: vehicle; experiment: 3; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: vehicle; experiment: 3; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: PP242; experiment: 3; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: PP242; experiment: 3; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: metformin; experiment: 3; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: metformin; experiment: 3; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: rapamycin; experiment: 3; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: rapamycin; experiment: 3; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: PP242; experiment: 4; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: PP242; experiment: 4; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: metformin; experiment: 4; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: metformin; experiment: 4; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: rapamycin; experiment: 4; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: rapamycin; experiment: 4; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: polysome-associated; treatment: vehicle; experiment: 4; ', 'cell line: MCF7; tumor type: Breast cancer; rna source: cytosolic; treatment: vehicle; experiment: 4; ' GSE109809 Homo sapiens 4 Expression profiling by high throughput sequencing GPL16791 Transcriptome profiling of HCC1937 vector and wtBRCA1 cell lines which were treated with OTX-015 2018-01-29 Purpose: To compare the transcriptomes of HCC1937 vector and wtBRCA1 cells which were treated with OTX-015. Methods: HCC1937 vector and wtBRCA1 cells were treated with 5 micromolar OTX-015 for 24 hours. Total RNA was extracted and processed with NEBNext Ultra Directional RNA Library Prep Kit for cDNA library preparation. The data are in duplicate and raw data were generated by Illumina 2500 sequencer. The Fastq format data were then processed with Tophat for genome mapping. After getting the bam files, they were further analyzed with cuffdiff for gene expression of different groups. Results: From the transcriotome profiling and analysis, we got gene expression data of DMSO control group and OTX-015 treatment group for the HCC1937 BRCA1 isogenic cell lines. Conclusion: The gene expression data revealed the transcriptome variation by OTX-015 treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE109809 BRCA1 deficiency sensitizes breast cancer cells to bromodomain and extra-terminal domain (BET) inhibition. Oncogene 6.634 https://doi.org/10.1038/s41388-018-0408-8 {Oncogene (6.634): 10.1038/s41388-018-0408-8} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA432071 https://www.ebi.ac.uk/ena/browser/view/PRJNA432071 https://www.ncbi.nlm.nih.gov/sra?term=SRP131693 [Overal design]OTX-015 treated HCC1937 BRCA1 isogenic cells were used for RNA extraction and RNAseq analysis for transcriptome profiling; [Treatment]'None'; [Growth]'None'; [Extraction]'Cell culture medium was removed. Total RNA was extracted by Rneasy Plus Mini Kit and checked with Agilent bioanalyzer 2100 for RIN values. Then mRNA was isolated with NEBNext Poly(A) mRNA magnetic isolation module.\nRNA library was prepared for sequencing using NEBNext Ultra Directional RNA Library Prep Kit for Illunima'; [Cell type]'Source: ''cell line: HCC1937; tissue: Breast; genotype: BRCA1 -/-; treatment: DMSO; ', 'cell line: HCC1937; tissue: Breast; genotype: BRCA1 -/-; treatment: OTX-015 treated; ', 'cell line: HCC1937; tissue: Breast; genotype: wild type; treatment: DMSO; ', 'cell line: HCC1937; tissue: Breast; genotype: wild type; treatment: OTX-015 treated; ' GSE83292 Homo sapiens 12 Non-coding RNA profiling by array GPL22007 Differential miRNA expression profiles of primary and relapse lesions of breast cancer patients receiving tamoxifen 2016-06-13 Long-term tamoxifen treatment significantly improves the survival of hormone receptor-positive (HR+) breast cancer (BC) patients. However, tamoxifen resistance remains a big challenge for endocrine therapy. We aimed to identify prognostic biomarkers for tamoxifen treatment and explore their role in tamoxifen resistance. We used Exiqon miRCURY™ LNA Array (v.18.0) to detect the miRNA expression profiles in the primary tumors and their matched recurrent/metastatic lesions from six HR+ breast cancer patients who relapsed after TAM treatment. Fold changes ≥ 2 and P values < 0.05 were defined as differential expression. We found that 28 miRNAs were significantly downregulated in recurrent/metastatic lesions compared to primary tumors, and 54 miRNAs were significantly upregulated. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE83292 MiR-4653-3p and its target gene FRS2 are prognostic biomarkers for hormone receptor positive breast cancer patients receiving tamoxifen as adjuvant endocrine therapy. Oncotarget None https://doi.org/10.18632/oncotarget.11278 {Oncotarget (None): 10.18632/oncotarget.11278} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA325532 https://www.ebi.ac.uk/ena/browser/view/PRJNA325532 None [Overal design]In this study, 6 primary tumor samples and 6 matched recurrent/metastatic lesion samples from six HR+ breast cancer patients who relapsed after TAM treatment were analyzed by microRNA array.; [Treatment]'6 hormone receptor positive BC women (stage I~III) relapsed after standard adjuvant tamoxifen treatment in West China Hospital. MiRNA expression profiles in the primary tumors and their matched recurrent/metastatic lesions from those patients were compared.'; [Growth]'None'; [Extraction]'Total RNA was extracted from deparaffinized FFPE tissue sections using TRIzol (Invitrogen, Carlsbad, CA, USA) and miRNeasy mini kit (QIAGEN, Hilden, Germany) according to manufacturer’s instructions. RNA quality and quantity was measured by using nanodrop spectrophotometer (ND-1000, Nanodrop Technologies) .'; [Cell type]'Source: ''age at diagnosis: 40; Sex: Female; clincal stage: IIIA; tumor histology: Invasive ductal carcinoma; er: positive; pr: positive; ki67: ≥14%; her2: postive; menopause when receiving tamoxifen: Premenopause; adjuvant chemotherapy: Yes; disease-free survival following tamoxifen treatment_months: 96.7; death: Alive; ', 'age at diagnosis: 40; Sex: Female; clincal stage: N/A; tumor histology: Invasive ductal carcinoma; er: positive; pr: negative; ki67: ≥14%; her2: uncertain; menopause when receiving tamoxifen: Premenopause; adjuvant chemotherapy: Yes; disease-free survival following tamoxifen treatment_months: 96.7; death: Alive; ', 'age at diagnosis: 56; Sex: Female; clincal stage: IIIA; tumor histology: Invasive ductal carcinoma; er: positive; pr: positive; ki67: ≥14%; her2: uncertain; menopause when receiving tamoxifen: Postmenopause; adjuvant chemotherapy: Yes; disease-free survival following tamoxifen treatment_months: 80.6; death: Dead; ', 'age at diagnosis: 56; Sex: Female; clincal stage: N/A; tumor histology: Invasive ductal carcinoma; er: positive; pr: positive; ki67: ≥14%; her2: uncertain; menopause when receiving tamoxifen: Postmenopause; adjuvant chemotherapy: Yes; disease-free survival following tamoxifen treatment_months: 80.6; death: Dead; ', 'age at diagnosis: 41; Sex: Female; clincal stage: IIIA; tumor histology: Invasive ductal carcinoma; er: positive; pr: positive; ki67: ≥14%; her2: negative; menopause when receiving tamoxifen: Premenopause; adjuvant chemotherapy: Yes; disease-free survival following tamoxifen treatment_months: 26.8; death: Dead; ', 'age at diagnosis: 41; Sex: Female; clincal stage: N/A; tumor histology: Invasive ductal carcinoma; er: positive; pr: positive; ki67: ≥14%; her2: negative; menopause when receiving tamoxifen: Premenopause; adjuvant chemotherapy: Yes; disease-free survival following tamoxifen treatment_months: 26.8; death: Dead; ', 'age at diagnosis: 55; Sex: Female; clincal stage: Unknown; tumor histology: Invasive ductal carcinoma; er: positive; pr: positive; ki67: <14%; her2: negative; menopause when receiving tamoxifen: Postmenopause; adjuvant chemotherapy: Yes; disease-free survival following tamoxifen treatment_months: 98.9; death: Alive; ', 'age at diagnosis: 55; Sex: Female; clincal stage: N/A; tumor histology: Invasive ductal carcinoma; er: positive; pr: positive; ki67: <14%; her2: negative; menopause when receiving tamoxifen: Postmenopause; adjuvant chemotherapy: Yes; disease-free survival following tamoxifen treatment_months: 98.9; death: Alive; ', 'age at diagnosis: 40; Sex: Female; clincal stage: IIB; tumor histology: Invasive ductal carcinoma; er: negative; pr: positive; ki67: <14%; her2: negative; menopause when receiving tamoxifen: Premenopause; adjuvant chemotherapy: Yes; disease-free survival following tamoxifen treatment_months: 56.4; death: Alive; ', 'age at diagnosis: 40; Sex: Female; clincal stage: N/A; tumor histology: Invasive ductal carcinoma; er: positive; pr: positive; ki67: <14%; her2: negative; menopause when receiving tamoxifen: Premenopause; adjuvant chemotherapy: Yes; disease-free survival following tamoxifen treatment_months: 56.4; death: Alive; ', 'age at diagnosis: 34; Sex: Female; clincal stage: IIIA; tumor histology: Invasive ductal carcinoma; er: positive; pr: positive; ki67: <14%; her2: negative; menopause when receiving tamoxifen: Premenopause; adjuvant chemotherapy: Yes; disease-free survival following tamoxifen treatment_months: 26.2; death: Alive; ', 'age at diagnosis: 34; Sex: Female; clincal stage: N/A; tumor histology: Invasive ductal carcinoma; er: positive; pr: positive; ki67: <14%; her2: negative; menopause when receiving tamoxifen: Premenopause; adjuvant chemotherapy: Yes; disease-free survival following tamoxifen treatment_months: 26.2; death: Alive; ' GSE16989 Mus musculus 4 Expression profiling by array GPL8321 Expression Data from Normal or Tumor Fibroblasts With or Without Ets2 2009-07-07 The mechanisms involved in epithelium-stroma interactions remain poorly understood, despite the importance of the microenvironment during tumorigenesis. Here, we studied the role of the Ets2 transcription factor in tumor-associated fibroblasts in the MMTV-PyMT mammary tumor model. Inactivation of Ets2 specifically in fibroblasts using Fsp-cre significantly reduced tumor growth, in contrast to Ets2 inactivation in epithelium, in which no differences in tumor growth were observed. Microarray analysis on isolated fibroblasts demonstrated the important role of Ets2 in remodeling of the extracellular matrix and angiogenesis in these cells. At the molecular level, Ets2 regulated Mmp9 expression through direct binding to the promoter region. Tumors lacking Ets2 in fibroblasts had diminished blood vessels. We also found a significant correlation between phosphorylation of ETS2 and MMP9 levels in stroma of human breast cancer samples. Collectively, our results suggest Ets2 uniquely contributes to angiogenesis from fibroblasts in the tumor microenvironment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE16989 Ets2 in tumor fibroblasts promotes angiogenesis in breast cancer. PloS one 2.776 https://doi.org/10.1371/journal.pone.0071533 {PloS one (2.776): 10.1371/journal.pone.0071533} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA117337 https://www.ebi.ac.uk/ena/browser/view/PRJNA117337 None [Overal design]Primary mammary fibroblasts were isolated from mice without the PyMT oncogene with or without Ets2, and from mice with the PyMT oncogene with or without Ets2. RNA was extracted and samples were submitted for Affymetrix gene expression arrays.; [Treatment]'Fibroblasts were grown in 10% FBS DMEM in a 37º incubator with 7% CO2.'; [Growth]'Fibroblasts were isolated from mammary gland tissue using a modified protocol for gravity separation.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Fibroblasts''strain: FVB/N; age: 9 Weeks; tissue: Mammary Gland; cell type: Fibroblasts; genotype: Ets2db/loxP; ', 'strain: FVB/N; age: 9 Weeks; tissue: Mammary Gland; cell type: Fibroblasts; genotype: PyMT;Ets2db/loxP; ', 'strain: FVB/N; age: 9 Weeks; tissue: Mammary Gland; cell type: Fibroblasts; genotype: Fsp-cre;Ets2db/loxP; ', 'strain: FVB/N; age: 9 Weeks; tissue: Mammary Gland; cell type: Fibroblasts; genotype: PyMT;Fsp-cre;Ets2db/loxP; ' GSE13051 Homo sapiens 6 Genome binding/occupancy profiling by genome tiling array GPL7408 Postrecruitment Regulation of RNA Pol II Directs Rapid Signaling Responses at the Promoters of Estrogen Target Genes 2008-10-05 Under current models for signal-dependent transcription in eukaryotes, DNA-binding activator proteins regulate the recruitment of RNA polymerase II (Pol II) to a set of target promoters. Yet, recent studies, as well as our results herein, show that Pol II is widely distributed (i.e., "preloaded") at the promoters of many genes prior to specific signaling events. How Pol II recruitment and Pol II preloading fit within a unified model of gene regulation is unclear. In addition, the mechanisms through which cellular signals activate preloaded Pol II across mammalian genomes remain largely unknown. Here we show that the predominant genomic outcome of estrogen signaling is the post-recruitment regulation of Pol II activity through phosphorylation, rather than recruitment of Pol II. Furthermore, we show that negative elongation factor (NELF) binds to estrogen target promoters in conjunction with preloaded Pol II and represses gene expression until the appropriate signal is received. Finally, our studies reveal that the estrogen-dependent activation of preloaded Pol II facilitates rapid transcriptional and post-transcriptional responses which play important physiological roles in regulating estrogen signaling itself. Our results reveal a broad use of post-recruitment Pol II regulation by the estrogen signaling pathway, a mode of regulation that is likely to apply to a wide variety of signal-regulated pathways. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE13051 Postrecruitment regulation of RNA polymerase II directs rapid signaling responses at the promoters of estrogen target genes. Molecular and cellular biology 3.735 https://doi.org/10.1128/MCB.00841-08 {Molecular and cellular biology (3.735): 10.1128/MCB.00841-08} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA109965 https://www.ebi.ac.uk/ena/browser/view/PRJNA109965 None [Overal design]ChIP-chip analysis for RNA Pol II, Ser5 phosphorylated RNA Pol II and NELF-A in MCF7 breast cancer cells.; [Treatment]'None'; [Growth]'None'; [Extraction]'MCF-7 breast cancer cells were grown to ~80 to 90% confluence, cross-linked with 1% paraformaldehyde in PBS for 10 min. at 37°C, and quenched in 125 mM glycine in PBS for 5 min at 4°C. The cells were collected by centrifugation and sonicated in lysis buffer (1% SDS, 10 mM EDTA, 50 mM Tris•HCl, pH 7.9, 1x protease inhibitor cocktail) to generate chromatin fragments of ~500 bp in length. The material was clarified by centrifugation, diluted 10-fold in dilution buffer (0.5% Triton X-100, 2 mM EDTA, 150 mM NaCl, 20 mM Tris•HCl, pH 7.9, 1x protease inhibitor cocktail), and pre-cleared with protein A-agarose beads. The pre-cleared, chromatin-containing supernatant was used in immunoprecipitation reactions with antibodies against RNA Pol II. The immunoprecipitated genomic DNA was cleared of protein and residual RNA by digestion with proteinase K and RNase H, respectively. The DNA was then extracted with phenol:chloroform:isoamyl alcohol and precipitated with ethanol.', 'MCF-7 breast cancer cells were grown to ~80 to 90% confluence, cross-linked with 1% paraformaldehyde in PBS for 10 min. at 37°C, and quenched in 125 mM glycine in PBS for 5 min at 4°C. The cells were collected by centrifugation and sonicated in lysis buffer (1% SDS, 10 mM EDTA, 50 mM Tris•HCl, pH 7.9, 1x protease inhibitor cocktail) to generate chromatin fragments of ~500 bp in length. The material was clarified by centrifugation, diluted 10-fold in dilution buffer (0.5% Triton X-100, 2 mM EDTA, 150 mM NaCl, 20 mM Tris•HCl, pH 7.9, 1x protease inhibitor cocktail), and pre-cleared with protein A-agarose beads. The pre-cleared, chromatin-containing supernatant was extracted with phenol:chloroform:isoamyl alcohol and precipitated with ethanol. The DNA was then amplified by LM-PCR.', 'MCF-7 breast cancer cells were grown to ~80 to 90% confluence, cross-linked with 1% paraformaldehyde in PBS for 10 min. at 37°C, and quenched in 125 mM glycine in PBS for 5 min at 4°C. The cells were collected by centrifugation and sonicated in lysis buffer (1% SDS, 10 mM EDTA, 50 mM Tris•HCl, pH 7.9, 1x protease inhibitor cocktail) to generate chromatin fragments of ~500 bp in length. The material was clarified by centrifugation, diluted 10-fold in dilution buffer (0.5% Triton X-100, 2 mM EDTA, 150 mM NaCl, 20 mM Tris•HCl, pH 7.9, 1x protease inhibitor cocktail), and pre-cleared with protein A-agarose beads. The pre-cleared, chromatin-containing supernatant was used in immunoprecipitation reactions with antibodies against Ser5P RNA Pol II. The immunoprecipitated genomic DNA was cleared of protein and residual RNA by digestion with proteinase K and RNase H, respectively. The DNA was then extracted with phenol:chloroform:isoamyl alcohol and precipitated with ethanol.', 'MCF-7 breast cancer cells were grown to ~80 to 90% confluence, cross-linked with 1% paraformaldehyde in PBS for 10 min. at 37°C, and quenched in 125 mM glycine in PBS for 5 min at 4°C. The cells were collected by centrifugation and sonicated in lysis buffer (1% SDS, 10 mM EDTA, 50 mM Tris•HCl, pH 7.9, 1x protease inhibitor cocktail) to generate chromatin fragments of ~500 bp in length. The material was clarified by centrifugation, diluted 10-fold in dilution buffer (0.5% Triton X-100, 2 mM EDTA, 150 mM NaCl, 20 mM Tris•HCl, pH 7.9, 1x protease inhibitor cocktail), and pre-cleared with protein A-agarose beads. The pre-cleared, chromatin-containing supernatant was used in immunoprecipitation reactions with antibodies against NELFA. The immunoprecipitated genomic DNA was cleared of protein and residual RNA by digestion with proteinase K and RNase H, respectively. The DNA was then extracted with phenol:chloroform:isoamyl alcohol and precipitated with ethanol.'; [Cell type]'Source: ''' GSE84593 Homo sapiens 10 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Regulation of KMT2D by PI(3)K/AKT signalling orchestrates oestrogen receptor mediated transcriptional activation in breast cancer [ChIP-seq] 2016-07-19 We aim to elucidate the mechanisms of how PI3K inhibition is promoting oestrogen receptor (ER) activation and ER dependency in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE84593 PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D. Science (New York, N.Y.) 41.037 https://doi.org/10.1126/science.aah6893 {Science (New York, N.Y.) (41.037): 10.1126/science.aah6893} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA330542 https://www.ebi.ac.uk/ena/browser/view/PRJNA330542 https://www.ncbi.nlm.nih.gov/sra?term=SRP078949 [Overal design]Genome-wide analysis of ER, FOXA1 TF upon treatment with the PI3K inhibitor (BYL719).; [Treatment]'10 milion T47D cells were treated with DMSO or BYL719 1μM for 24hr.'; [Growth]'T47D cells were maintained in RPMI 1640 with 10% FBS, 1% L-glutamine and 1% penicillin-streptomycin.'; [Extraction]"Cells were lysed and sonicated leading to a DNA average size of 200bp. Protein G dynabeads were pre-incubated with 5μg of ER alpha (sc-543) or FOXA1 (ab5089) with pre cleared chromatin. The complexes were reverse cross-linked and DNA was purified.\nChIP-seq libraries were prepared using 10 ng of DNA and Illumina's TruSeq ChIP sample prep.Libraries were validated using the Agient Technologies 2100 Bioanalyzer and Qubit high sensitivity assay."; [Cell type]'Source: ''cell line: T47D; passages: 5 to 10; ', 'cell line: T47D; passages: 5 to 10; chip-antibody: ER alpha (sc543) Santa Cruz; ', 'cell line: T47D; passages: 5 to 10; chip-antibody: FOXA1 (ab5089) Abcam; ' GSE124127 Homo sapiens 15 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL16791 Insulin induced alterations in chromatin acetylation and transcriptome in triple negative breast cancer cells 2018-12-19 We have performed quantitative H3K9ac ChIP-seq and RNA-seq from untreated and 3h, 6h insulin treated MDA-MB-231 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124127 Hyperinsulinemia promotes aberrant histone acetylation in triple-negative breast cancer. Epigenetics & chromatin 4.185 https://doi.org/10.1186/s13072-019-0290-9 {Epigenetics & chromatin (4.185): 10.1186/s13072-019-0290-9} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA510812 https://www.ebi.ac.uk/ena/browser/view/PRJNA510812 https://www.ncbi.nlm.nih.gov/sra?term=SRP173943 [Overal design]Analysis of H3K9ac enrichment after insulin treatment and gene expression from insulin treated MDA-MB-231 cells.; [Treatment]'Insulin treatment, MDA-MB-231 cells were serum depleted in DMEM high glucose medium containing 0.2% BSA for 24h and stimulated without (untreated) or with 100 nM Insulin for indicated time periods.'; [Growth]"MDA-MB-231 cells were grown in Dulbecco's modified Eagle's medium (DMEM) with high glucose (25mM) supplemented with 10% heat-inactivated Fetal Bovine Serum (v/v) and 1X antibiotics containing penicillin and streptomycin at 37°C, 5% CO2 in a humidified chamber.", "MDA-MB-231 cells were grown in Dulbecco's modified Eagle's medium (DMEM) with high glucose (25mM) supplemented with 10% heat-inactivated Fetal Bovine Serum (v/v) and 1X antibiotics containing penicillin and streptomycinat 37°C, 5% CO2 in a humidified chamber."; [Extraction]'Chromatin lysates were clarified from sonicated cells and histone-DNA complexes were isolated with respective antibodies.\nSequencing library preparation and reactions were conducted at City of Hope’s Integrative Genomics Core. ChIP-seq libraries were made using Illumina Tru-Seq library preparation kit and multiplexing barcodes compatible with Illumina HiSeq 2500 technology. RNA-seq libraries were prepared using Kapa Hyper Prep Kit (Kapa Biosystems)', 'Chromatin lysates were clarified from sonicated cells and histone-DNA complexes were isolated with respective antibodies.\nSequencing library preparation and reactions were conducted at City of Hope’s Integrative Genomics Core. ChIP-seq libraries were made using Illumina Tru-Seq library preparation kit and multiplexing barcodes compatible with Illumina HiSeq 2500 technology. RNA-seq libraries were prepared using Kapa Hyper Prep Kit (Kapa Biosystems).', 'Chromatin lysates were clarified from sonicated cells and histone-DNA complexes were isolated with respective antibodies.\nSequencing library preparation and reactions were conducted at City of Hope’s Integrative Genomics Core. ChIP-seq libraries were made using Illumina Tru-Seq library preparation kit and multiplexing barcodes compatible with Illumina HiSeq 2500 technology. RMA-seq libraries were prepared using Kapa Hyper Prep Kit (Kapa Biosystems)'; [Cell type]'Triple negative breast cancer cells''cell line/tissue: MDA-MB-231; cell type: Triple negative breast cancer cells; passages: 3-6; treatment: none; chip antibody: H3K9ac, ab4441 (Abcam); ', 'cell line/tissue: MDA-MB-231; cell type: Triple negative breast cancer cells; passages: 3-6; treatment: none; chip antibody: input; ', 'cell line/tissue: MDA-MB-231; cell type: Triple negative breast cancer cells; passages: 3-6; treatment: Insulin for 3 hours; chip antibody: H3K9ac, ab4441 (Abcam); ', 'cell line/tissue: MDA-MB-231; cell type: Triple negative breast cancer cells; passages: 3-6; treatment: Insulin for 3 hours; chip antibody: input; ', 'cell line/tissue: MDA-MB-231; cell type: Triple negative breast cancer cells; passages: 3-6; treatment: Insulin for 6 hours; chip antibody: H3K9ac, ab4441 (Abcam); ', 'cell line/tissue: MDA-MB-231; cell type: Triple negative breast cancer cells; passages: 3-6; treatment: Insulin for 6 hours; chip antibody: input; ', 'cell line/tissue: MDA-MB-231; cell type: Triple negative breast cancer cells; passages: 3-6; treatment: none; ', 'cell line/tissue: MDA-MB-231; cell type: Triple negative breast cancer cells; passages: 3-6; treatment: Insulin for 3 hours; ', 'cell line/tissue: MDA-MB-231; cell type: Triple negative breast cancer cells; passages: 3-6; treatment: Insulin for 6 hours; ' GSE93784 Mus musculus 6 Expression profiling by array GPL20775 Stromal PTEN determines mammary epithelial response to radio-therapy 2017-01-18 It is well-described that the tumor stroma participates in cancer progression, but whether stromal factors can initiate breast tumorigenesis remains unclear. Using our previously described stromal-specific phosphatase and tensin homolog (PTEN) deletion mouse model, we investigated transformative events in young, non-tumor bearing animals. Here, we show stromal PTEN deletion initiates radiation-induced genomic instability on neighboring mammary epithelium through paracrine epidermal growth factor receptor (EGFR) activation. In these mice, a single low dose of whole-body radiation induces mammary hyperplasia, a result that is prevented by pre-treatment with an EGFR inhibitor. We reveal that stromal PTEN is lost in a subset of normal breast samples and is predictive of recurrence in breast cancer patients. Combined, these data suggest both diagnostic and therapeutic chest wall radiotherapy may inadvertently predispose patients with focal stromal PTEN loss to secondary breast cancer, and that this predisposition may be treated prophylactically through EGFR inhibition. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93784 Stromal PTEN determines mammary epithelial response to radiotherapy. Nature communications 11.878 https://doi.org/10.1038/s41467-018-05266-6 {Nature communications (11.878): 10.1038/s41467-018-05266-6} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA362364 https://www.ebi.ac.uk/ena/browser/view/PRJNA362364 None [Overal design]Each biological replicate of FACS sorted Lin-CD24+CD29loCD61- mature luminal epithelial subpopulations was collected by pooling pre-neoplastic mammary tissue from 6-8 virgin ErbB2;Ptenfl/fl or ErbB2;Fsp-cre;Ptenfl/fl (8-9 weeks of age) mice. Microarray on three mature luminal samples from both genetic groups was performed with GeneChip® Mouse Transcriptome Assay 1.0 (Affymetrix, Santa Clara, California, USA) at the OSUCCC Genomics Facility.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was isolated using TRIzol (Invitrogen) and treated with DNAse I (DNA-free, Ambion). RNA quality was assessed using a NanoDrop TM2000 Spectrophotometer (Thermo Scientific). Sample quality was further ensured by characterizing size distribution via fluorescent capillary electrophoresis using the Bioanalyzer 2100 RNA 6000 Pico-Chip and Degradometer software (Agilent Technologies, Santa Clara, California, USA).'; [Cell type]'Source: ''genotype/variation: MMTV-ErbB2;Ptenfl/fl; tissue: mature luminal cell population; ', 'genotype/variation: MMTV-ErbB2;Fsp-cre;Ptenfl/fl; tissue: mature luminal cell population; ' GSE115604 Homo sapiens 26 Expression profiling by high throughput sequencing; Other; Genome binding/occupancy profiling by high throughput sequencing GPL11154; GPL20301 Enhancer Release and Retargeting” Activates Disease Susceptibility Genes 2018-06-11 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115604 None None None None None 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA475556 https://www.ebi.ac.uk/ena/browser/view/PRJNA475556 None [Overal design]Refer to individual Series; [Treatment]'To induce the estrogen gene transcriptional responses, MCF-7 cells at 60-80% confluency were first hormone-stripped for 3 days in phenol-free DMEM media plus 5% charcoal dextran treated FBS (Omega Scientific, CA), and they were then treated with 100nM 17β-estradiol (E2) (Sigma) for indicated time points (usually for 1 hour).', "To induce the estrogen gene transcriptional responses, MCF-7 cells at 60-80% confluency were first hormone-stripped for 3 days in phenol-free DMEM media plus 5% charcoal dextran treated FBS (Omega Scientific, CA), and they were then treated with 100nM 17β-estradiol (E2) (Sigma) for indicated time points (usually for 1 hour). Transfection of small interfering RNAs (siRNAs) into MCF-7 cells was performed using Lipofectamine 2000 (Life technologies) following manufacturer's instructions. For all experiments, two rounds of siRNA transfection (40nM each time) were performed to achieve higher efficiency. The siRNAs used in this study include: Qiagen Negative Control siRNA (Qiagen Cat# 1027310) and/or Sigma Mission siRNA universal control #2 (SIC002); siRAD21 (Sigma SASI_Hs02_00341219 and SASI_Hs01_00195799)."; [Growth]'We originally purchased MCF-7 from ATCC, which were maintained in DMEM (Gibco® #10566) media supplemented with 10% FBS (Omega Scientific, CA) in a 5% CO2 humidified incubator at 37°C (MCF-7 without stripping).'; [Extraction]'Cells were cross-linked with 1% formaldehyde at room temperature for 10 min. Or for some cases, cells were double cross-linked with 1mM DSG (ProteoChem) for 1 hr first and then for 10minutes by 1% formaldehyde. In both situations, the crosslinking was quenched by addition of 0.125M glycine for 10 minutes. ChIP chromatin was fragmented using (Diagenode) Bioruptor®300 (20-40 cycles, 30sec on, 30sec off, 4°C). Subsequently, the soluble chromatin was harvested by 16,100g centrifugation, pre-cleared with 10-20ul Dynabeads G (Life Technologies), and was then incubated with 1-5 μg of antibodies at 4°C overnight. The next morning, immuno-precipitated complexes were collected using 30ul Dynabeads protein G (Invitrogen) per reaction. The immune-complexes were subjected to washes with wash buffer I for once, with wash buffer II for twice, and with Tris-EDTA (TE) + 0.1% triton x-100 for once, with TE for once, the beads were incubated at 55°C for 2hrs with proteinase K and de-crosslinked at 65°C for overnight. The final ChIP DNA was extracted and purified using QIAquick spin columns (Qiagen).\nThe library was processed that the extracted DNA was ligated to specific adaptors for Illumina’s HiSeq system using KAPA Hyper Prep Kit (Kapa Biosystems)', 'Methods: The transfected MCF7 cells were subjected to GRO-seq experiments. GRO-Seq experiments were performed as previously reported (Li et al., 2013, Nature). Briefly, ~10-20 millions of MCF-7 cells were washed 3 times with cold PBS and then sequentially swelled in swelling buffer (10mM Tris-Cl pH7.5, 2mM MgCl2, 3mM CaCl2) for 5 min on ice, harvested, and lysed in lysis buffer (swelling buffer plus 0.5% NP-40 and 10% glycerol). The resultant nuclei were washed one more time with 10mL lysis buffer and finally re-suspended in 100uL of freezing buffer (50mM Tris-Cl pH8.3, 40% glycerol, 5mM MgCl2, 0.1mM EDTA). For the run-on assay, re-suspended nuclei were mixed with an equal volume of reaction buffer (10mM Tris-Cl pH 8.0, 5mM MgCl2, 1mM DTT, 300mM KCl, 20 units of SUPERase-IN, 1% sarkosyl, 500uM ATP, GTP, and Br-UTP, 2uM CTP) and incubated for 5 min at 30°C . The resultant nuclear-run-on RNA (NRO-RNA) was then extracted with TRIzol LS reagent (Life Technologies) following manufacturer’s instructions. NRO-RNA was fragmented to ~300-500nt by alkaline base hydrolysis on ice and followed by treatment with DNase I and Antarctic phosphatase. These fragmented Br-UTP labeled nascent RNA was then immunoprecipitated with an anti-BrdU argarose beads (Sc32323ac, Santa Cruz Biotechnology) in binding buffer (0.5XSSPE, 1mM EDTA, 0.05% tween) for 3 hrs at 4°C with rotation. Subsequently, T4 PNK was used to repair the end of the immunoprecipitated BrU-NRO-RNA, at 37°C for 1hr. The RNA was extracted and precipitated using acidic phenol-chloroform. cDNA synthesis was performed as per a published method (54) with few modifications. The RNA fragments were subjected to poly-A tailing reaction by poly-A polymerase (NEB) for 30 min at 37°C. Subsequently, reverse transcription was performed using oNTI223 primer and superscript III RT kit (Life Technologies). The cDNA products were separated on a 10% polyacrylamide TBE-urea gel and only those migrated between ~100-500bp were excised and recovered by gel extraction. After that, the first-strand cDNA was circularized by CircLigase (Epicentre) and re-linearized by APE1 (NEB). Re-linearized single strand cDNA (sscDNA) was separated by a 10% polyacrylamide TBE gel as described above and the product of needed size was excised (~170-400bp) for gel extraction. Finally, sscDNA template was amplified by PCR (usually between 10-14 PCR cycles) using the Phusion High-Fidelity enzyme (NEB) according to the manufacturer’s instructions. The resulted library was subjected to deep sequencing.'; [Cell type]'MCF7 breast cancer cell', 'Source: ''cell type: MCF7 breast cancer cell; passages: ~200; chip antibody: SMC1a (bethyl, A300-055A); ', 'cell type: MCF7 breast cancer cell; passages: ~200; chip antibody: H3K4me3 (abcam, ab8580); ', 'cell type: MCF7 breast cancer cell; passages: ~200; chip antibody: H3K4me1 (abcam, ab8895); ', 'strain: MCF7 breast cancer cell; tissue: ~200; genotype: brU sc-32323 AC, Santa Cruz; ', 'strain: MCF7 breast cancer cell; tissue: ~100; genotype: brU sc-32323 AC, Santa Cruz; ' GSE108607 Homo sapiens 10 Expression profiling by array GPL570 SUMOylation Regulates Transcription by the Progesterone Receptor A Isoform in a Target Gene Selective Manner 2017-12-28 Luminal breast cancers express estrogen (ER) and progesterone (PR) receptors, and respond to endocrine therapies. However, some ER+PR+ tumors display intrinsic or acquired resistance, possibly related to PR. Two PR isoforms, PR-A and PR-B, regulate distinct gene subsets that may differentially influence tumor fate. A high PR-A:PR-B ratio is associated with poor prognosis and tamoxifen resistance. We speculate that excessive PR-A marks tumors that will relapse early. Here we address mechanisms by which PR-A regulate transcription, focusing on SUMOylation. We use receptor mutants and synthetic promoter/reporters to show that SUMOylation deficiency or the deSUMOylase SENP1 enhance transcription by PR-A, independent of the receptors’ dimerization interface or DNA binding domain. De-SUMOylation exposes the agonist properties of the antiprogestin RU486. Thus, on synthetic promoters, SUMOylation functions as an independent brake on transcription by PR-A. What about PR-A SUMOylation of endogenous human breast cancer genes? To study these, we used gene expression profiling. Surprisingly, PR-A SUMOylation influences progestin target genes differentially, with some upregulated, others downregulated, and others unaffected. Hormone-independent gene regulation is also PR-A SUMOylation dependent. Several SUMOylated genes were analyzed in clinical breast cancer database. In sum, we show that SUMOylation does not simply repress PR-A. Rather, it regulates PR-A activity in a target selective manner including genes associated with poor prognosis, shortened survival, and metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE108607 SUMOylation Regulates Transcription by the Progesterone Receptor A Isoform in a Target Gene Selective Manner. Diseases (Basel, Switzerland) None https://doi.org/10.3390/diseases6010005 {Diseases (Basel, Switzerland) (None): 10.3390/diseases6010005} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA427814 https://www.ebi.ac.uk/ena/browser/view/PRJNA427814 None [Overal design]T47D human breast cancer cells stably expressing WT or SUMOylation-deficient PR-AK388R were created by transfection of previously cloned PR-negative T47D-Y cells with expression vectors that encode WT PR-A or PR-AK388R mutant. These cell lines were treated with either vehicle control (ethanol) or 10 nM synthetic progestin R5020 for 24 hrs before total RNA harvest. Thus, the experiment contains three cell lines and two treatments. Total RNA was extracted, cRNA was labeled and hybridized to U133 Plus 2 microarrays.; [Treatment]'Cells were treated with ethanol or 10 nM synthetic progestin R5020.'; [Growth]"Cells were maintained in Dulbecco's modified eagle medium (DMEM, Life Technologies) containing 5% charcoal stripped fetal bovine serum (FBS, Japan Serum) in the presence or absence of 10 nM synthetic progestin R5020."; [Extraction]"Total RNA was extracted (PicoPure; Arcturus) following the manufacturer's recommendations."; [Cell type]'breast cancer cell line''originating cell line: T47D; cell type: breast cancer cell line; genotype/variation: WT PR-A; treatment: ethanol control; ', 'originating cell line: T47D; cell type: breast cancer cell line; genotype/variation: WT PR-A; treatment: synthetic progestin R5020; ', 'originating cell line: T47D; cell type: breast cancer cell line; genotype/variation: SUMOylation-deficient PR-AK388R mutant; treatment: ethanol control; ', 'originating cell line: T47D; cell type: breast cancer cell line; genotype/variation: SUMOylation-deficient PR-AK388R mutant; treatment: synthetic progestin R5020; ', 'originating cell line: T47D; cell type: breast cancer cell line; genotype/variation: PR-negative; treatment: ethanol control; ' GSE156968 Homo sapiens 138 Methylation profiling by genome tiling array GPL13534 Genome-wide DNA methylation and expression patterns of microRNAs in relation to breast cancer subtypes among American women of African and European ancestry [methylation array] 2020-08-27 We reAggressive high-grade, estrogen receptor negative (ER-) breast cancer is more common among American women of African ancestry (AA) than those of European ancestry (EA). The reasons remain largely unknown. Epigenetic mechanisms, particularly DNA methylation and altered microRNA (miRNA) expression, may contribute to racial differences in breast cancer. However, the characterization of this epigenetic modification in relation to ER+ and ER- breast cancer, and its functional role in the regulation of miRNA expression remains to be investigated, especially among high risk AA women. In this study, we evaluated methylation patterns of miRNA genes and their effect on miRNA expression in breast tumors from both AA and EA women. The genome-wide methylation screen identified a number of differentially methylated loci (DML) between ER- and ER+ tumor subtypes in tumors from both races, or specific to AA or EA women. Integrated analysis of DNA methylation and miRNA expression further identified certain DMLs whose methylation levels were significantly correlated with the expression of relevant miRNAs, such as multiple CpGs highly correlated with miR-190b and miR-135b. In summary, our results suggest that DNA methylation patterns in miRNA encoding genes differ between breast cancers according to cancer subtype and race, and that this altered methylation may affect miRNA expression. Further pathway analysis identified their potential role in modulating cancer-related key biological processes. These findings shed light on the epigenetic regulation of miRNA expression and provide insights into the relations of clinical-relevant miRNAs to their target genes and to serve as potential preventative and therapeutic targets. port the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mammalian cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse embryonic stem cells, neural progenitor cells and embryonic fibroblasts. We find that lysine 4 and lysine 27 trimethylation effectively discriminates genes that are expressed, poised for expression, or stably repressed, and therefore reflect cell state and lineage potential. Lysine 36 trimethylation marks primary coding and non-coding transcripts, facilitating gene annotation. Trimethylation of lysine 9 and lysine 20 is detected at satellite, telomeric and active long-terminal repeats, and can spread into proximal unique sequences. Lysine 4 and lysine 9 trimethylation marks imprinting control regions. Finally, we show that chromatin state can be read in an allele-specific manner by using single nucleotide polymorphisms. This study provides a framework for the application of comprehensive chromatin profiling towards characterization of diverse mammalian cell populations. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE156968 Differential methylation and expression patterns of microRNAs in relation to breast cancer subtypes among American women of African and European ancestry. PloS one 2.776 https://doi.org/10.1371/journal.pone.0249229 {PloS one (2.776): 10.1371/journal.pone.0249229} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA659707 https://www.ebi.ac.uk/ena/browser/view/PRJNA659707 None [Overal design]Geome-wide methylation assay on HM450 Bead Chip using genomic DNA extracted from flash frozen human breast tumor tissue; [Treatment]'NA'; [Growth]'NA'; [Extraction]'DNA was extracted using a MasterPure DNA purification kit (Epicentre).'; [Cell type]'Source: ''gender: Female; tissue: Flash frozen breast tumor tissue; ' GSE42310 Homo sapiens 14 Expression profiling by array; Methylation profiling by genome tiling array GPL6244; GPL13534; GPL16353 COHCAP: City of Hope CpG Island Analysis Pipeline 2012-11-15 COHCAP (City of Hope CpG Island Analysis Pipeline) is an algorithm to analyze single-nucleotide resolution DNA methylation data. It provides QC metrics, differential methylation for CpG Sites, differential methylation for CpG Islands, integration with gene expression data, and visualization of methylation values. COHCAP is currently the only DNA methylation package that can handle integration with gene expression data, and the results of this study show that COHCAP can identify regions of differential methylation with ~50% concordance with gene expression. COHCAP is scalable for analysis of both cell line data and heterogeneous patient data, and it can identify known cancer biomarkers as well as intriguing new roles of epigenetic regulation in cancer (such as methylation of estrogen receptor in breast cancer patients). This study also uses cell line data to show that COHCAP is capable of analyzing Illumina methylation array and targeted bisulfite sequencing data, with either 1-group or 2-group study designs. The accuracy of COHCAP is accessed using qPCR, EpiTect, and comparison of COHCAP regions of differential methylation with MIRA peaks. This software is freely available at https://sourceforge.net/projects/cohcap/. The following third-party datasets were utilized in the paper: BS-Seq data: GSE26826 Additional Microarray Data: GSE29290 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE42310 COHCAP: an integrative genomic pipeline for single-nucleotide resolution DNA methylation analysis. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkt242 {Nucleic acids research (11.147): 10.1093/nar/gkt242} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA181146 https://www.ebi.ac.uk/ena/browser/view/PRJNA181146 None [Overal design]Refer to individual Series.; [Treatment]'None', 'N/A'; [Growth]"Cells were cultured in McCoy's 5A medium supplemented with 10% FBS and antibiotics.", "HES-2 (ES02) human embryonic stem cells were adapted from mitotically inactive MEF feeders to matrigel substrate (BD Biosciences) and mTesR1 medium (STEMCELL Technologiesaccording to manufacturer's protocol. Adaptation was for 4 passages and the final passage number was p72. DNA was extracted from Tra 1-60+ cells isolated by flow cytometry. (Sigma).", 'Matrigel (BD)/mTesR1 (STEMCELL technologies) standard protocol'; [Extraction]'RNA was extracted with the RNeasy kit (Qiagen)', 'Genomic DNA was prepared using the DNeasy Tissue kit following manufacturer’s instructions', 'DNA was purified using Dneasy Blood and Tissue Kit (Qiagen) and Bisulfite converted using the EpiTect Bisulfite Kit (Qiagen)', "HES-2 (ES02) human embryonic stem cells were adapted from mitotically inactive MEF feeders to matrigel substrate (BD Biosciences) and mTesR1 medium (STEMCELL Technologiesaccording to manufacturer's protocol. Adaptation was for 4 passages and the final passage number was p72. DNA was extracted from Tra 1-60+ cells isolated by flow cytometry and prepared for MIRA-chip analysis. 500 ng of sonicated and fragmented DNA was enriched for methylated DNA using the MethylCollector Ultra Kit (Active Motif). Eluted DNA was purified with MinElute reaction cleanup kit (Qiagen). MIRA-enriched and 10 ng of sonicated input DNA was subsequently amplified using the Whole Genome Amplification kit2 (Sigma)."; [Cell type]'Source: ''cell line: HCT116; genotype/variation: parental; ', 'cell line: HCT116; genotype/variation: mutant with altered DNA methylation; ', 'cell line: embryonic stem cell line HES-2; ', 'cell line: embryonic stem cell line HES-2; sample type: MIRA enriched sample; ', 'sample type: input DNA; cell line: embryonic stem cell line HES-2; ' GSE82048 Homo sapiens 6 Expression profiling by array GPL13693 Transcriptional screening in MDA-231 cells treated with low-dose Paclitaxel for 24 and 48 hours 2016-05-31 Paclitaxel is the most commonly used chemotherapeutic agent in breast cancer treatment. Notably, a comprehensive understanding of paclitaxel’s effects requires insight into the dose-specific activities of paclitaxel and their influence on the cancer cells and host microenvironment. The aim of our study is to reveal the gene transcriptional changes in response to low-Paclitaxel (PTX) treatment in breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE82048 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA323815 https://www.ebi.ac.uk/ena/browser/view/PRJNA323815 None [Overal design]For genome-wide gene expression analysis, MDA-MB-231 cells (high-invasive breast cancer cell line) were treated with 5 ng/ml PTX for 24 and 48 hours respectively and then the cell lysates were prepared by TRIzol reagent. Then the total RNA in each group was extracted and the genome-wide gene expressing profile was detected through the Human One Array (HOA) Microarray system (Phalanx Biotech Group, Taiwan).; [Treatment]'MDA-231 cells were plated onto 6-well plate and cultured for 24 hours. After that, the cells were treated with 5 ng/ml (2 wells / time point) PTX for 24 and 48 hours respectively and then the cell lysates were prepared by TRIzol reagent.'; [Growth]'The breast cancer cell lines MDA-MB-231 were purchased from the American Type Culture Collection (Maryland, USA) and cultured with RPMI-1640 medium supplemented with 10% fatal bovine serum and 1% Pen/Strep in a humid incubator with 5% CO2.'; [Extraction]'RNA extraction by Trizol Reagent (Invitrogen). RNA purity was checked by optical density of NanoDrop ND-1000 and agarose electrophoresis with the result of A260/A280≧1.8, A260/A230≧1.5, no gDNA contamination. RNA integrity was measured by Agilent RNA 6000 Nano Assay (RIN≧6).'; [Cell type]'adherent epithelial cells''cell line: MDA-MB-231; gender: female; pathological type: high-invasive breast adenocarcinoma cells derived from metastatic site: pleural effusion; cell type: adherent epithelial cells; origin: 51 years adult,Caucasian; ' GSE76637 Mus musculus; Homo sapiens 9 Genome binding/occupancy profiling by high throughput sequencing GPL16791; GPL17021 A Surveillance System of Active Enhancers by a RACK7-histone Demethylase Complex (ChIP-Seq II) 2016-01-07 Primed enhancers are marked by histone H3K4 mono-methylation (H3K4me1), and the conversion to active enhancers involves acetylation of histone H3K27 (H3K27Ac). However, whether active enhancers are regulated remains unclear. Here we report a biochemical complex consisting of a potential chromatin reader (RACK7) and a histone demethylase (KDM5C) that occupies many active enhancers in a breast cancer cell line. Loss of RACK7 or KDM5C results in hyperactive enhancers marked by H3K4me3 and H3K27Ac, and characterized by an increased eRNA transcription and elevated expression of nearby genes. Loss of RACK7 or KDM5C also leads to increased cell invasion and migration, and enhanced tumor growth. We propose that RACK7/KDM5C functions as an enhancer “brake” to ensure appropriate enhancer activities in the cell. Our findings provide important insight into histone H3K4 methylation dynamics at enhancers and reveal a molecular mechanism that controls the activities of active enhancers, which when compromised, can contribute to tumorigenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76637 Suppression of Enhancer Overactivation by a RACK7-Histone Demethylase Complex. Cell 36.216 https://doi.org/10.1016/j.cell.2016.02.064 {Cell (36.216): 10.1016/j.cell.2016.02.064} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA308213 https://www.ebi.ac.uk/ena/browser/view/PRJNA308213 https://www.ncbi.nlm.nih.gov/sra?term=SRP068198 [Overal design]ChIP-seq data of RACK7, KDM5C and histone modifications in parental and RACK7-KO ZR-75-30 cells.; [Treatment]'none'; [Growth]'ZR-75-30 and MCF-7were cultured in Dulbecco’s Modified Eagle’s Medium (DMEM, Hyclone) supplemented with 10% fetal bovine serum (FBS, Gibco). mES cells were grown on 0.1% gelatinized (Sigma, G1890) tissue culture plates in ESC media. ESC media: DMEM supplemented with 10% fetal bovine serum, 1000 U/mL LIF, 100 µM nonessential amino acids (Invitrogen, 11140-050), 2 mM L-glutamine (Invitrogen, 25030-081), 100 U/mL penicillin, 100 µg/mL streptomycin (Invitrogen, 15140-122), and 1 μL/mL of 2-mercaptoethanol (Sigma, M7522).'; [Extraction]'Chromatin samples were incubated with specific antibodies in ChIP Lysis buffer (50mM HEPES pH7.5, 500mM NaCl, 1mM EDTA, 1%Triton, 0.1%Na-deoxylcholate, 0.1% SDS) overnight at 4℃. The protein-DNA complexes were immobilized on protein A/G beads (10μl per reaction). The bound fractions were washed 3 times with Lysis buffer, and 3 times with RIPA buffer (50mM Hepes, 300mM LiCl, 1mM EDTA, 0.5%NP-40, 0.7%Nadeoxylcholate), and once with TE. Elution and Reverse crosslinking were carried out in Elution buffer (50mM Tris, PH8.0, 1mM EDTA, 1% SDS) 65℃ for 6 hours. After RNase A and protease K digestion, DNA fraction was purified using PCR extraction kit (QIAGEN).\nChIP DNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'Source: ''antibody: Bethyl, A302-090A; cell line: ZR-75-30; genotype: parental; ', 'antibody: ActiveMotif, 39297; cell line: ZR-75-30; genotype: RACK7 knockout; ', 'antibody: Cell Signaling, 9751S; cell line: ZR-75-30; genotype: RACK7 knockout; ', 'antibody: ActiveMotif, 39297; cell line: ZR-75-30; genotype: parental; ', 'antibody: Cell Signaling, 9751S; cell line: ZR-75-30; genotype: parental; ', 'antibody: Millipore, 07-360; cell line: ZR-75-30; genotype: parental; ', 'antibody: Santa Cruz, SC-584; cell line: ZR-75-30; genotype: parental; ' GSE18955 Homo sapiens 20 Expression profiling by array GPL9550; GPL9551 Effects of IGF 1 on primary breast fibroblasts, MCF-7 breast cancer cells and CCL-171 fibroblasts 2009-11-09 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE18955 IGF-I induced genes in stromal fibroblasts predict the clinical outcome of breast and lung cancer patients. BMC medicine 8.285 https://doi.org/10.1186/1741-7015-8-1 {BMC medicine (8.285): 10.1186/1741-7015-8-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA120989 https://www.ebi.ac.uk/ena/browser/view/PRJNA120989 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None', 'Monoculture cell conditions.; MCF - 7 and CCL - 171 cells were expanded and propagated in Dulbeccos Modified Eagles Medium (DMEM) supplemented with: 10% FBS (GIBCO, Grand Island, N.Y.), L - glutamine, 4.5 g/L glucose, 100 U/ml penicillin and 100 ug/ml streptomycin (GIBCO, Grand Island, N.Y.). For mono-culture experiments the cells were cultivated for 6 hours at 30,000 cells/cm2 in DMEM medium with 5% FBS. After 6 hours medium was changed to DMEM medium with 0.2% FBS and the cells were cultured for 48 hours(starving period). After 48 hours medium was changed to a fresh DMEM medium with 0.2% FBS and the cells were cultured for 24 hours.; Protocol Type = Biological Sample; Performer: Michal,,Rajski'; [Extraction]'StratageneRef; RNA for the reference was pooled from 11 cell lines - obtained from Stratagene.; Protocol Type = Biological Sample; Performer: Michal,,Rajski', "RNeasy; Total RNA was isolated using the RNeasy mini kit (QIAGEN), according to the manufacturer's instructions.; Protocol Type = Extract preparation; Performer: Michal,,Rajski"; [Cell type]'Source: ', 'Human Primary breast Fibroblasts''reference: stratagene human reference plus doping controls.; ', 'cell type: Human Primary breast Fibroblasts; ', 'cell line: MCF-7 breast cancer cells; ', 'cell line: CCL 171 fibroblasts; ' GSE41718 Mus musculus 8 Expression profiling by array GPL11202 The ShcA PTB Domain Functions as a Biological Sensor of Phospho-tyrosine Signaling During Breast Cancer Progression 2012-10-19 The ShcA adaptor possesses two phosphotyrosine binding motifs, which include an SH2 and a PTB domain. In the majority of cases, ShcA utilizes its PTB domain to engage activated receptor tyrosine kinases (RTKs). To establish the mportance of this domain during mammary tumorigenesis, we employed a ShcA mutant (R175Q) that no longer binds phospho-tyrosine residues via its PTB domain. We demonstrate that the ShcR175Q mutant delays mammary tumor onset n MMTV/MT transgenic animals. Paradoxically, we observe a robust increase in the growth and angiogenesis of emerging mammary tumors. ShcR175Q-expressing breast cancer cells increase fibronectin secretion and possess elevated levels f integrin α5/β1, the principle fibronectin receptor. Sustained integrin engagement activates Src, which in turn phosphorylates pro-angiogenic RTKs, including PDGFR, FGFR and Met, leading to increased VEGF secretion from ShcR175Q-xpressing breast cancer cells. Finally, we describe a ShcR175Q-dependent gene signature that stratifies breast cancer patients with a high microvessel density. This is the first study to demonstrate that intracellular signaling pathways ownstream of the ShcA PTB domain both positively and negatively regulate tumorigenesis during the various stages of breast cancer progression https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41718 The ShcA PTB domain functions as a biological sensor of phosphotyrosine signaling during breast cancer progression. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-12-4178 {Cancer research (8.378): 10.1158/0008-5472.CAN-12-4178} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA178013 https://www.ebi.ac.uk/ena/browser/view/PRJNA178013 None [Overal design]ShcA mutant (R175Q) vs NT/ShcA cells; [Treatment]'None'; [Growth]'NMuMG-NT2197 cells were generated, cultured, and transfected with a pMSCV/hygro expression vector (Clontech) expressing a wildtype ShcA cDNA or a ShcA mutant harbouring an arginine to glutamine substitution at amino acid 175 (R175Q)'; [Extraction]'Total RNA (1-2.5ng) from microdissected material was subjected to two rounds of linear amplification using a RiboAmp HSPlus Amplification Kit (Cat. #: KIT0525, Applied Biosystems) following the manufacturer’s protocol.'; [Cell type]'Source: ''treatment: ShcA R175Q expression; cell line: NMuMG-NT2197; ', 'sample type: Universal Mouse Reference; ', 'treatment: ShcA wild type expression; cell line: NMuMG-NT2197; ' GSE26129 Homo sapiens 12 Expression profiling by array GPL4133 Alterations in tumour necrosis factor signaling pathways associated with cytotoxicity and resistance to taxanes in tumour cells. 2010-12-16 The taxanes are widely used in the treatment of breast and other cancers. While their cytotoxicity has been attributed to the induction of cell cycle arrest in mitosis through the stabilization of microtubules, we found that docetaxel promotes soluble tumor necrosis factor alpha (TNF-alpha production in MCF-7 breast tumor cells. TNF-alpha induces apoptotic cell death in a variety of cell types by binding to one of its receptors (TNFR1) which promotes death-inducing signaling complex (DISC) formation. Consistent with this view, we also report that selection of MCF-7 cells for survival in increasing concentrations of paclitaxel or docetaxel results in selection of drug-resistant variants that are resistant to TNF-alpha cytotoxicity. MCF-7 cells selected to 3-5 nM docetaxel produced >30-fold more TNF-alpha than control MCF-7CC cells but had strongly reduced levels of TNFR1. In contrast, expression of TNFR2 was unchanged, resulting in enhanced cell survival through the activation of the NF-kappaB p50 and p65 subunits. Gene expression profiling of docetaxel resistant MCF-7 cells compared to parental MCF-7 cells was performed for the changes of TNF related genes, and also confirmed in ovarian cell line A2780. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26129 Alterations in tumor necrosis factor signaling pathways are associated with cytotoxicity and resistance to taxanes: a study in isogenic resistant tumor cells. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr3083 {Breast cancer research : BCR (5.676): 10.1186/bcr3083} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA135373 https://www.ebi.ac.uk/ena/browser/view/PRJNA135373 None [Overal design]Two docetaxel resistant cell lines of breast MCF-7 and ovarian A2780 were generated for gene expression profilling. Two colour microarray of Agilent whole human genome nucleotide arrays was conducted with two replicate of both forward and reverse labellings for MCF-7. Four arrays were used for this experiments. And it was four replicate of both forward and reverse labellings for A2780 cells. Eight arrays were used for this experiments; [Treatment]'Cell were cultured and selected for survival in increasing doses of docetaxel as previously described (Guo B, Villeneuve DJ, Hembruff SLet al. Breast Cancer Res Treat. 2004;85(1):31-5126;27). MCF-7 cells selected to docetaxel concentrations of 5.00nM (dose 10, MCF-7Txt10), and A2780 cells selected to terminally tolerated dose at 405 nM of docetacel were used in this microarray study.'; [Growth]'Cells were grown in tissue culture flucks with DMEM H21 medium at 37C with 5% of CO2, and subcultured when cell density reached 80-90% confluence.'; [Extraction]'Total RNA was isolated using RNeasy Mini Kit (Qiagen), and quantity and quality were assessed using Agilent BioAnalyizer. 3 separate isolations with RIN at 10 were pooled together for labelling.'; [Cell type]'docetaxel sensitive', 'docetaxel resistant''cell lines: MCF-7; cell type: docetaxel sensitive; ', 'cell line: MCF-7Txt10; cell type: docetaxel resistant; ', 'cell lines: A2780; cell type: docetaxel sensitive; ', 'cell line: A2780Dxl; cell type: docetaxel resistant; ' GSE134787 Mus musculus 2 Expression profiling by high throughput sequencing GPL24247 Differential expression levels of mRNAs in control 4T1 versus M2 macrophages co-cultured 4T1 murine breast cancer cells 2019-07-24 Tumor-associated macrophages (TAMs) are closely related to poor prognosis in triple-negative breast cancer (TNBC). Thus, gaining insight into how TAMs support cancer progression could contribute to effective therapies. We utilized the 4T1 murine TNBC cell line and murine bone marrow-derived macrophages to assess TAMs mediated pro-proliferative effects in vivo and in vitro. Further, Transcriptional analysis was performed to identify pathways activated in TAMs stimulated 4T1 cells. To simulate tumor microenvironment, M2 macrophages and 4T1 cells were plated into upper and lower chambers of Transwell co-culture systems respectively. we performed RNA-sequencing analysis of 4T1 cells incubated with vehicle control or M2 macrophages. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE134787 Combined MEK inhibition and tumor-associated macrophages depletion suppresses tumor growth in a triple-negative breast cancer mouse model. International immunopharmacology 3.361 https://doi.org/10.1016/j.intimp.2019.105864 {International immunopharmacology (3.361): 10.1016/j.intimp.2019.105864} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA556415 https://www.ebi.ac.uk/ena/browser/view/PRJNA556415 https://www.ncbi.nlm.nih.gov/sra?term=SRP216227 [Overal design]A high throughput sequencing about mRNAs was perfomed in control 4T1 versus M2 macrophages co-cultured 4T1 cells, without replicate.; [Treatment]'M2 macrophages and 4T1 cells were plated into upper and lower chambers of transwell co-culture systems respectively for 3 days. we performed RNA-sequencing analysis of control 4T1 cells and M2 macrophages co-cultured 4T1 cells.'; [Growth]'All cells were maintained at 37°C in a 5% CO2 humidified incubator.'; [Extraction]'Total RNA was extracted from the 4T1 cells using TRIzol® Reagent according the manufacturer’s instructions (Invitrogen) and genomic DNA was removed using DNase I (TaKara).\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'Source: ''tissue: murine breast cancer cells; treatment: control 4T1; ', 'tissue: murine breast cancer cells; treatment: M2 macrophages co-cultured 4T1; ' GSE159317 Homo sapiens 17 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Targeted nanopore sequencing for the identification of ABCB1 promoter translocations in relapsed acute myeloid leukemia [ChIP-seq] 2020-10-09 Resistance to chemotherapy is the most common cause of treatment failure in acute myeloid leukemia and the drug efflux pump ABCB1 is a critical mediator. Here we demonstrate that in vitro daunorubicin exposure can induce activating ABCB1 promoter translocations in human myeloid cells, similar to those recently described in recurrent high-grade serous ovarian and breast cancer. We then develop a targeted nanopore sequencing approach that enables efficient identification of ABCB1 structural variants in high-grade serous ovarian cancer. Finally, we confirm that ABCB1high cases of relapsed AML are not characterized by ABCB1 promoter translocations but instead show high-level activity of native promoters, consistent with endogenous regulation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE159317 Targeted nanopore sequencing for the identification of ABCB1 promoter translocations in cancer. BMC cancer 2.933 https://doi.org/10.1186/s12885-020-07571-0 {BMC cancer (2.933): 10.1186/s12885-020-07571-0} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA668355 https://www.ebi.ac.uk/ena/browser/view/PRJNA668355 https://www.ncbi.nlm.nih.gov/sra?term=SRP286902 [Overal design]THP-1 cells were from DSMZ (Braunschweig, Germany) and cultured in RPMI 1640 medium (Sigma Aldrich) supplemented with 2mM L-Glutamine (Life Technologies, Carlsbad, CA) and 10% fetal bovine serum (Sigma Aldrich). Whilst under drug selection cells were counted and replated every third day. Cell lines were confirmed mycoplasma-free and authenticated by short tandem repeat DNA profiling. THP-1 were exposed to escalating doses of daunorubicin over 142 days, generating a resistant line (THP-1_R) which exhibited a 28.3-fold increase in daunorubicin IC50 compared with the sensitive parental cell line (THP-1_S). Primary human AML cells were obtained from the Manchester Cancer Research Centre Tissue Biobank (approved by the South Manchester Research Ethics Committee). The Biobank archive was searched for samples from patients with relapsed AML with high blast counts and sufficient viable cells from ChIP sequencing. H3K27 acetylation ChIP sequencing was performed using two replicates for both the sensitive (THP-1_S1 and THP-1_S2) and resistant (THP-1_R1 and THP-1_R2) lines and a single aliquot from each patient sample.; [Treatment]'None'; [Growth]'THP-1 and derived cell lines were cultured in RPMI 1640 medium (Sigma Aldrich) supplemented with 2mM L-Glutamine (Life Technologies) and 10% fetal bovine serum (Sigma Aldrich).', 'Cyropreserved primary cells were thawed and immediately crosslinked for ChIP.'; [Extraction]'ChIP was performed using anti-H3K27Ac (ab4729, Abcam, Cambridge, UK). 10^8 cells (THP-1) or 107 cells (primary AML samples) were used for each precipitation using the method described by Lee et al. (2006). Briefly, cells were cross-linked with 1% formaldehyde for 10 minutes at room temperature before the reaction was quenched with 0.125M glycine. Cell pellets were washed twice with PBS and nuclear lysates sonicated for 6 cycles using a Bioruptor® Pico (Diagenode, Liege, Belgium). 10μg of antibody bound to 100μl of magnetic beads (Dynabeads Protein G, Invitrogen, Carlsbad, CA) was added to each sample and immunoprecipitation performed overnight on a rotator at 4°C and 20rpm. After five washes with RIPA buffer (50mM HEPES pH 7.6, 1mM EDTA, 0.7% Na deoxycholate, 1% NP-40, 0.5M LiCl), chromatin IP-bound fractions were extracted by incubating for 15 min at 65°C with elution buffer (50mM TrisHCl pH8, 10mM EDTA, 1% SDS). Crosslinking was then reversed by incubation at 65°C for 6 hours. RNaseA (1mg/ml) and proteinase K (20mg/ml) were added to eliminate RNA and protein from the samples. DNA was extracted using phenol:chloroform:isoamyl alcohol and precipitated by adding 2 volumes of ice-cold 100% ethanol, glycogen (20μg/μl), 200mM NaCl and freezing at -80°C for at least 1hr. Pellets were washed with 70% ethanol and eluted in 50μl 10mM TrisHCl pH8.0.\nLibraries were prepared for sequencing using a Microplex Library Preparation Kit (Diagenode). 200-800bp fragments were selected using AMPure beads (Beckman Coulter, Brea, CA) and quantified by qPCR with a KAPA Library Quantification Kit (Kapa Biosystems, Basel, Switzerland). Sequencing was performed using a NextSeq desktop sequencing system (Illumina) with 75bp, paired-end high output generating 65-80M (THP-1_S and THP-1_R) and 34-45M reads per sample (primary AML samples).'; [Cell type]'Source: ', 'Primary AML''cell line: THP-1_R; phenotype: Resistant; chip antibody: none; ', 'cell line: THP-1_S; phenotype: Sensitive; chip antibody: anti-H3K27Ac (ab4729, Abcam, Cambridge, UK); ', 'cell line: THP-1_S; phenotype: Sensitive; chip antibody: none; ', 'cell line: THP-1_R; phenotype: Resistant; chip antibody: anti-H3K27Ac (ab4729, Abcam, Cambridge, UK); ', 'cell type: Primary AML; chip antibody: anti-H3K27Ac (ab4729, Abcam, Cambridge, UK); ', 'cell type: Primary AML; chip antibody: none; ' GSE33827 Homo sapiens 10 Expression profiling by array GPL570 Expression data from MDA-MB-231 parental and xenograft tumor cells treated with Smac mimetic SM-164. 2011-11-19 Small-molecule Smac mimetics target inhibitor of apoptosis (IAP) proteins to induce TNFα-dependent apoptosis in cancer cells and several Smac mimetics have been advanced into clinical development as a new class of anticancer drugs. However, preclinical studies have shown that only a small subset of cancer cell lines are sensitive to Smac mimetics used as single agents and these cell lines are at risk of developing drug resistance to Smac mimetics. Thus, it is important to understand the molecular mechanisms underlying intrinsic and acquired resistance of cancer cells to Smac mimetics in order to develop effective therapeutic strategies to overcome or prevent Smac mimetic resistance. We established Smac mimetic resistant sublines derived from MDA-MB-231 breast cancer cells, which exhibit exquisite sensitivity to the Smac mimetic SM-164, and used microarrays to detail the global programme of gene expression underlying SM-164 resistance in MDA-MB-231 cells and identified differentially expressed genes in SM-164-resistant and -sensitive MDA-MB-231 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE33827 LRIG1 modulates cancer cell sensitivity to Smac mimetics by regulating TNFα expression and receptor tyrosine kinase signaling. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-11-2428 {Cancer research (8.378): 10.1158/0008-5472.CAN-11-2428} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA148199 https://www.ebi.ac.uk/ena/browser/view/PRJNA148199 None [Overal design]SCID mice with MDA-MB-231 xenograft tumors were treated with 5 mg/kg of SM-164 intravenously for 5 days/week for 2 weeks. SM-164-regressed MDA-MB-231 tumors regrew after treatment ended. Tumor cells from these regrown MDA-MB-231 tumors were isolated and total RNAs were prepared for microarray analysis.; [Treatment]'SCID mice with MDA-MB-231 xenograft tumors were treated with 5 mg/kg of SM-164 intravenously for 5 days/week for 2 weeks. Regrown tumors were harvested and tumor cells were isolated.'; [Growth]'MDA-MB-231 parental cells were cultured under standard conditions.'; [Extraction]"Total RNA was isolated by RNA miniprep kit (Sigma) according to the manufacturer's instruction."; [Cell type]'breat cancer cells''background cell line: MDA-MB-231; cell type: breat cancer cells; ' GSE8193 Homo sapiens 47 Expression profiling by array GPL4685 Expression data from age-dichotomized ER+ breast tumors 2007-06-20 To investigate the biological basis between aging and sporadic breast cancer incidence and prognosis, RNA samples from matched ER+ invasive breast cancers diagnosed in either young (≤45) or old (≥70) women were analyzed by expression microarrays Keywords: biomarker identification https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE8193 Aging impacts transcriptomes but not genomes of hormone-dependent breast cancers. Breast cancer research : BCR None https://doi.org/10.1186/bcr1765 {Breast cancer research : BCR (None) doi:10.1186/bcr1765}; {Breast cancer research : BCR (None) doi:10.1186/bcr2120}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA101101 https://www.ebi.ac.uk/ena/browser/view/PRJNA101101 None [Overal design]ER+ breast cancers collected from either young or old women, well matched for other clinical parameters were analyzed using expression microarrays. Age associated tumor subtypes and enrichment of pre-defined gene signatures were identified. Age associated differential expression and an age signature (gene-based classifier) was assessed; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen RNAesy purification from formamide extracted samples'; [Cell type]'Source: ''' GSE123471 Homo sapiens 2 Expression profiling by high throughput sequencing GPL20795 Characterization of RNA context tumor associated macrophages and related extracellular vesicles [RNA-seq] 2018-12-06 Extracellular vesicles (EVs) are membrane vesicles released by all cell types and contain proteins and non-coding RNAs, which are transported into recipient cells to regulate their signal transduction and functions. Increasing evidence has demonstrated that EV shuttling is an effective means of bio-molecule transportation among various cell types in the tumor microenvironment, and thus plays a critical role in regulating cancer cell biology. Previous studies have shown that TAMs are an important source of extracellular vesicles and the extracellular vesicles released by TAMs can promote the invasiveness of breast cancer cells. In this study, we studied the differential expression of TAM EV and the donor cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE123471 Extracellular vesicle-packaged HIF-1α-stabilizing lncRNA from tumour-associated macrophages regulates aerobic glycolysis of breast cancer cells. Nature cell biology 17.728 https://doi.org/10.1038/s41556-019-0299-0 {Nature cell biology (17.728): 10.1038/s41556-019-0299-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA508813 https://www.ebi.ac.uk/ena/browser/view/PRJNA508813 https://www.ncbi.nlm.nih.gov/sra?term=SRP172793 [Overal design]Examination of RNA-seq in TAMs and TAM EV (mixture from 10 donors).; [Treatment]'Monocytes derived macrophages (MDMs) were as control macrophages, polarized-tumor associated macrophages (TAMs) were stimulated by 30% CM from MDA-MB-231 cells for 6 days.'; [Growth]'Peripheral blood monocytes (PBMs) from healthy donors were isolated by Ficoll density gradient centrifugation as previously described. Monocytes derived macrophages (MDMs) were grown in DMEM (GIBCO) supplemented with 10% fetal bovine serum, 50 U/ml penicillin (GIBCO) and 50 μg/ml streptomycin (GIBCO). To induce tumor associated macrophages (TAMs), MDMs were treated with 30% CM from MDA-MB-231 cells for 6 days.'; [Extraction]"Total RNA was isolated from TAMs or TAM EVs using RNeasy mini kit (Qiagen, Germany) or SeraMir Exosome RNA Purification for Media & Urine (RA806TC-1, System Biosciences, USA).\nAccording to the experimental instructions, the purified total RNA was subjected to rRNA isolation, fragmentation, first strand cDNA synthesis, second strand cDNA synthesis, terminal repair, 3' end plus A, ligation linker, enrichment and other steps to complete the library construction of the samples."; [Cell type]'tumor associated macrophages', 'extracellular vesicles from tumor associated macrophages''cell type: tumor associated macrophages; ', 'cell type: extracellular vesicles from tumor associated macrophages; ' GSE61723 Homo sapiens 65 Expression profiling by array GPL16686 Novel transcripts associated with lymph node metastasis in triple negative breast cancer [discovery cohort] 2014-09-24 Triple negative breast cancer (TNBC) is the most aggressive breast cancer subtype with the worst prognosis. It is characterised by the absence of hormone receptors for estrogen, progesterone, and human epidermal growth factor 2, and as a consequence there are no targeted endocrine treatments available. TNBC patients are more likely to develop metastases and disease relapse than patients with other breast cancer subtypes. The identification of biomarkers that can be used to predict which patient is likely to develop metastatic disease remains a priority since this is the major cause of cancer-related death in these women. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE61723 Novel genes associated with lymph node metastasis in triple negative breast cancer. Scientific reports 4.011 https://doi.org/10.1038/srep15832 {Scientific reports (4.011): 10.1038/srep15832} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA261957 https://www.ebi.ac.uk/ena/browser/view/PRJNA261957 None [Overal design]A total of 33 grade 3 invasive ductal carcinomas were used in this study, from which we were able to compare 17 matched normal adjacent tissues from the tumour specimens and 15 lymph node metastases. Gene expression microarray analysis was used to reveal which transcripts were differentially expressed between patients with lymph node involvement and those who only presented with a primary tumour.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted from 2mm punch biopsies of FFPE tissue using the RNeasy FFPE kit (Qiagen, Doncaster, VIC, Australia).'; [Cell type]'Source: ''patient id: patient 1; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 2; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 3; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 3; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 4; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 4; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: patient 5; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 5; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: patient 5; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 6; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 6; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 7; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 7; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: pateint 7; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 8; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 8; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 9; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 9; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: patient 9; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: pateint 10; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 10; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 11; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 11; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: patient 11; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 12; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 12; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 13; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 14; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 14; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: patient 15; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: pateint 16; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 16; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: pateint 17; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 18; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 18; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: patient 18; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 19; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 19; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 20; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 20; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: patient 21; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 22; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 23; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 23; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 24; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 25; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 25; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: patient 26; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 26; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 27; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 28; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 28; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 29; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 30; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 30; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: patient 30; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 31; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: patient 32; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 32; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: patient 32; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 33; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 33; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ', 'patient id: patient 33; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'patient id: patient 34; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: invasive ductal carcinomas (IDC); ', 'patient id: patient 35; patient status: triple negative breast cancer (TNBC); tumor grade: grade 3; tissue type: lymph node metastases (LN); ' GSE36131 Homo sapiens 16 Expression profiling by array GPL14550 Breast cancer cell lines treated with EZH2 inhibitor compounds 2012-02-28 Loss of H3K27me3 repressive chromatin histone marks, maintained by the histone methyltransferase (HKMT) EZH2, may lead to reversal of epigenetic silencing in tumor cells and have therapeutic potential. Using a cell-based assay, we have identified three compounds from a HKMT inhibitor chemical library which re-express H3K27me3 mediated, silenced genes. Chromatin immunoprecipitation verified a decrease in silencing marks (H3K27me3, H3K9me3) and importantly an increase in active marks (H3K4me2/3, H3K27ac) at the promoter of re-expressed genes. Compound treated breast tumor cells induced enrichment for genome-wide changes in expression of known target genes for EZH2 and induced cell growth inhibition: with most sensitive breast tumor cell lines having low EZH2 protein expression, while a normal epithelial breast line was least sensitive. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36131 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA152943 https://www.ebi.ac.uk/ena/browser/view/PRJNA152943 None [Overal design]Agilent SurePrint G3 Human 8x60k two-colour microarrays were used to profile gene expression changes induced by treatment with drug compounds in MDA MB-231 cells, both at 24h and 48h. 4 replicates were used for each drug, time combination. A separate untreated control sample was used for comparison with each replicate.; [Treatment]'Cell cultures were treated for either 48h or 72h with an EZH2/G9a inhibitor compound. Compounds were diluted in DMSO at Stocks of 10mM.'; [Growth]'MDA-MB-231 cells were cultured in DMEM-Medium supplemented with 10% FCS (#02.00.830, First Link (UK), 2mM L-Glutamine (#25030-024, Invitrogen), 100U/ml Penicillin and 100μg/ml Streptavidin (#15070-063, Invitrogen) until they were ~60% confluent and then treated for either 48h or 72h with a compound.'; [Extraction]'Total RNA was extracted using QIAshredder spin columns combined with RNeasy spin-columns. Briefly, medium was removed, cells were lysed and homogenised with 600 \uf06dof RTL Buffer and then put on a Qiashredder spin column. To the RNA containing flow-through 600\uf06dof 70% ethanol was added, mixed well and transferred onto RNeasy spin-columns. The columns were treated according to the manufactures protocol and RNA was eluted using 50µRNase free water and immediately stored at -80 °C.'; [Cell type]'Source: ''cell line: MDA-MB-231; ' GSE84917 Mus musculus 9 Expression profiling by array GPL16570 Whole-genome expression profiling of metastatic versus non-metastatic mammary tumors in MMTV-Wnt1 transgenic mice 2016-07-27 To identify genes that mediate lung metastasis in breast cancer, we compared expression profiles of metastatic versus non-metastatic mammary tumors in MMTV-Wnt1 transgenic mice. A subset of biologically relevant genes with statistically significant changes was selected for validation. These genes include Alox15, Ptn, Ror2, Sox9, Jag2 and Runx2. These genes encode proteins that play important roles in the immune and inflammatory responses as well as osteogenesis and skeletal morphogenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE84917 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA335632 https://www.ebi.ac.uk/ena/browser/view/PRJNA335632 None [Overal design]We performed whole-transcript array analysis of three normal mammary glands, three non-metastatic mammary tumors and three metastatic mammary tumors from MMTV-Wnt1 transgenic mice using Affymetrix GeneChip® Mouse Gene 2.0 ST Array.; [Treatment]'At six weeks of age, MMTV-Wnt1 transgenic mice and control littermates were placed into group housing with food provided ad lib and a 6% sucrose solution with 200 ug/ml of doxycycline. When the mammary tumor reached the size of 20 mm, the animal was euthanized and the tumor was collected.'; [Growth]'None'; [Extraction]'Total RNA was isolated from frozen mouse mammary tissues (normal or tumor) using mirVana RNA isolation kit, and cleaned-up by Qiagen RNeasy mini kit.'; [Cell type]'Source: ''strain: FVB; tissue: mammary; metastatic status: n/a; gender: Female; genotype: Wild-type Wnt1; age (onset): No tumor; age (sack): 533 days; ', 'strain: FVB; tissue: mammary; metastatic status: n/a; gender: Female; genotype: Wild-type Wnt1; age (onset): No tumor; age (sack): 556 days; ', 'strain: FVB; tissue: mammary; metastatic status: n/a; gender: Female; genotype: Wild-type Wnt1; age (onset): No tumor; age (sack): 538 days; ', 'strain: FVB; tissue: mammary tumor; metastatic status: non-metastatic; gender: Female; genotype: Wnt1+/-; age (onset): 306 days; age (sack): 354 days; ', 'strain: FVB; tissue: mammary tumor; metastatic status: non-metastatic; gender: Female; genotype: Wnt1+/-; age (onset): 192 days; age (sack): 222 days; ', 'strain: FVB; tissue: mammary tumor; metastatic status: non-metastatic; gender: Female; genotype: Wnt1+/-; age (onset): 247 days; age (sack): 298 days; ', 'strain: FVB; tissue: mammary tumor; metastatic status: metastatic; gender: Female; genotype: Wnt1+/-; age (onset): 251 days; age (sack): 300 days; ', 'strain: FVB; tissue: mammary tumor; metastatic status: metastatic; gender: Female; genotype: Wnt1+/-; age (onset): 194 days; age (sack): 281 days; ', 'strain: FVB; tissue: mammary tumor; metastatic status: metastatic; gender: Female; genotype: Wnt1+/-; age (onset): 242 days; age (sack): 284 days; ' GSE121947 Mus musculus; Homo sapiens 33 Expression profiling by array GPL1261; GPL19109; GPL25741 Lung metastasis of breast cancer 2018-10-29 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE121947 Metastasis-initiating cells induce and exploit a fibroblast niche to fuel malignant colonization of the lungs. Nature communications 11.878 https://doi.org/10.1038/s41467-020-15188-x {Nature communications (11.878): 10.1038/s41467-020-15188-x} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA499112 https://www.ebi.ac.uk/ena/browser/view/PRJNA499112 None [Overal design]Refer to individual Series; [Treatment]'None', 'Cells were stained with 5 μg PE-conjugated anti-human CD183 (CXCR3) antibody (clone G025H7, BioLegend) or PE-conjugated mouse IgG1, κ isotype control (BioLegend) per million cells in 100 μl FACS buffer for 30 min on ice in the dark. CXCR3+ and CXCR3- cells were sorted on a BD FACSAria1 machine into Arcturus PicoPure Extraction Buffer (ThermoFisher Scientific).', 'Cells were stimulated with 1 µM AMG-487 (CXCR3i)or 0.001% DMSO vehicle daily for 7 days.'; [Growth]'None', 'SUM-159-LM1 breast cancer cells were cultured for 7 days as spheres at a density of 25,000 cells/mlin into ultra-low attachment cell culture flasks with Onco2 medium, consisting of HuMEC-medium (Invitrogen) supplemented 50 U/ml penicillin (Sigma-Aldrich), 50 μg/ml streptomycin (Sigma-Aldrich), 10 ng/ml basic fibroblast growth factor (bFGF, Invitrogen), 20 ng/ml EGF (Sigma-Aldrich), 5 μg/ml human insulin (Sigma-Aldrich) and 2 % vol/vol B27 (Life Technologies).', 'CXCL9/10-OE MDA-MB-231 breast cancer cells were cultured for 7 days as spheres at a density of 25,000 cells/ml in into ultra-low attachment cell culture flasks with Onco2 medium, consisting of HuMEC-medium (Invitrogen) supplemented 50 U/ml penicillin (Sigma-Aldrich), 50 μg/ml streptomycin (Sigma-Aldrich), 10 ng/ml basic fibroblast growth factor (bFGF, Invitrogen), 20 ng/ml EGF (Sigma-Aldrich), 5 μg/ml human insulin (Sigma-Aldrich) and 2 % vol/vol B27 (Life Technologies). Cells were stimulated with 1 µM AMG-487 or 0.001% DMSO vehicle daily for 7 days.'; [Extraction]'RNA extraction was performed using the Arcturus PicoPure Extraction Kit (ThermoFisher Scientific) according to the manufacturer’s protocol. cDNA preamplification was conducted using the GeneChip WT Pico Reagent Kit (Affymetrix) according to the manufacturer’s protocol.', 'RNA extraction was performed using the Arcturus PicoPure Extraction Kit (ThermoFisher Scientific) according to the manufacturer’s protocol. cDNA preamplification was conducted using the Ovation Pico WTA System V2 Kit (NuGEN).', 'RNA extraction was performed using the Arcturus PicoPure Extraction Kit (ThermoFisher Scientific) according to the manufacturer’s protocol.', 'RNA extraction was performed using the QIAGEN RNeasy Mini Kit according to the manufacturer’s protocol.'; [Cell type]'Source: ''metastatic stage: Micrometastasis; source: in vivo (NSG mouse lung); ', 'sorted pairs: pair 1; ', 'sorted pairs: pair 2; ', 'sorted pairs: pair 3; ', 'metastatic stage: Healthy; ', 'metastatic stage: Micrometastasis; ', 'metastatic stage: Macrometastasis; ', 'treatment: CXCR3i; ', 'treatment: DMSO; ' GSE139928 Homo sapiens 8 Expression profiling by high throughput sequencing GPL11154 Genome wide analysis of transcripts regulated by PAX2 and Tamoxifen in MCF-7 cells 2019-11-05 The aim of the study is to understand the role of the transcription factor PAX2 in estrogen receptor positive breast cancer cell line by using GRO-seq. MCF-7-PAX2 stable cells were cultured in full media and treated with doxycycline (50ng/ml) for 16 hours to induce overexpression of PAX2. Then cells were treated with 4-OH-tamoxifen (1μM) for 6 hours. All 4 treatments (Veh, Tam, Dox, DoxTam) were performed in duplicates. After treatments, nuclei were isolated and used for nuclear run-on and subsequent GRO-seq library preparation. Libraries were sequenced and data analysis showed that PAX2 could repress estrogen target genes and induce genes enriched in cytokine (TNF-alpha and INF-gamma) related pathways. When combined with tamoxifen, PAX2 could further repress estrogen target genes to a higher degree, and induce genes enriched in p53 related pathway. Moreover, PAX2 could induce the transcription of some intergenic transcripts (potential enhancers) to activate the transcription of nearby genes with could predict good outcome in estrogen receptor positive breast cancer. Overall our finding suggests that PAX2 could benifit ER positive breast cancer by 1) repressing estrogen target genes, and this effect is enhanced by tamoxifen 2) activating cell death/growth arrest related pathways, which is enhanced by potential enhancer transcription induced by PAX2 itself. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE139928 The proapoptotic gene interferon regulatory factor-1 mediates the antiproliferative outcome of paired box 2 gene and tamoxifen. Oncogene 6.634 https://doi.org/10.1038/s41388-020-01435-4 {Oncogene (6.634): 10.1038/s41388-020-01435-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA587641 https://www.ebi.ac.uk/ena/browser/view/PRJNA587641 https://www.ncbi.nlm.nih.gov/sra?term=SRP228576 [Overal design]Transcriptome profiling of MCF-7 cells with PAX2 overexpression and in combination with tamoxifen; [Treatment]'Cells were treated with doxycycline (50ng/ml) to induce PAX2 oeverexpresson, followed by tamoxifen (1uM) treatment for 6 hours.'; [Growth]'MCF-7 cells were cultured in DMEM with 10% FBS'; [Extraction]'Nuclei were isolated after treatment, then they were used for nuclear run-on reaction (Br-UTP incorporation) followed by RNA isolation with TRIzol LS. Total RNA was used for library preparation.\n5 ×10^6 nuclei were used for each run-on reaction, 2 biological replicates were produced for both vehicle and estrogen treatments. Br-UTP was incorporated into on-going transcription by run-on reaction which was performed at 30 degree for 5 min. Total RNA was extracted with TRIzol and fragmented with RNA Fragmentation Reagent. Fragmented RNA was purified with P-30 column, which was followed by T4 polynucleotide kinase treatment to dephosphorylate the 3’ end of RNA fragments. Br-UTP labeled RNA was enriched twice with anti-BrdU beads and precipitated overnight.PolyA tailing was done using E.coli Poly(A) Polymerase, followed by reverse transcription with oNTI-223-index: /5Phos/GATCGTCGGACTGTAGAACTCTGAAC/iSp18/TCAGACGTGTGCTCTTCCGATCTTTTTTTTTTTTTTTTTTTTVN which allows custom barcoding. Exonuclease I was used to remove excess oligo after reverse transcription. DNA-RNA duplex was purified with ChIP DNA Clean & Concentrator Kit followed by RNAse H treatment. cDNA was circularized amplified with oNTI-201: AATGATACGGCGACCACCGACAGGTTCAGAGTTCTACAGTCCGACG and oNTI-200: CAAGCAGAAGACGGCATACGAGATXXXXXXGTGACTGGAGTTCAGACGTGTGCTCTTCCGATCT(XXXXXX is barcode used for specific sample) for 12 to 14 cycles. Final PCR product was purified by running 10% TBE gel and cleaned up.'; [Cell type]'Breast adenocarcinoma''cell type: Breast adenocarcinoma; gender: Female; cell line: MCF-7; agent: none; ', 'cell type: Breast adenocarcinoma; gender: Female; cell line: MCF-7; agent: tamoxifen; ', 'cell type: Breast adenocarcinoma; gender: Female; cell line: MCF-7; agent: doxycycline; ', 'cell type: Breast adenocarcinoma; gender: Female; cell line: MCF-7; agent: doxycycline + tamoxifen; ' GSE144713 Mus musculus 18 Expression profiling by high throughput sequencing GPL19057 Characterizing breast cancer lung metastatic lesions in host environments with or without NK cells by RNA-seq 2020-02-03 We demonstrated that natural killer (NK) cells selectively suppress single circulating tumor cells (CTCs) and monoclonal metastasis compared to multicellular CTC clusters and polyclonal metastasis. To better understand how NK cells influence overall metastatic evolution, we generated spontaneous AT3 breast cancer lung metastasis in immunodeficient Rag2-/-IL2rg-/- mice, and treated mice with or without adoptive transfer of NK cells. RNA-seq on individual laser-capture microdissected lesions confirmed the infiltration of NK cells. The expression of epithelial-to-mesenchymal transition (EMT) genes strongly correlated with expression of genes indicating NK cell activation, consistent with experimental data from our lab and others. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144713 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA604624 https://www.ebi.ac.uk/ena/browser/view/PRJNA604624 https://www.ncbi.nlm.nih.gov/sra?term=SRP246994 [Overal design]RNA-seq on AT3 breast cancer lung metastatic lesions from Rag2-/-IL2rg-/- mice (with or without adoptive transfer of NK cells).; [Treatment]'Mice receive intravenous injection of PBS or 60,000 in vitro activated murine NK cells on Day 11.'; [Growth]'GFP and mCherry-labelled AT3 cells were injected into the mammary fat pad of Rag1-/-IL2rg-/- mice to generate mammary gland tumors. Tumor cells then spontaneously metastasized to lungs.'; [Extraction]"Lungs were harvested, embedded in OCT and cut into frozen sections on a Leica CM3050 S Research Cryostat equipped with Cryojane. GFP and RFP+ Lung lesions were extracted by laser capture microdissection on a Leica LMD7000 instrument instrument. RNA was purified by RNeasy micro kit (Qiagen). 2ng of total RNA per sample was used to prepare the sequencing libraries.\nLibraries were then prepared using QIAseq FX single cell RNA library kit (Qiagen) following standard manufacturer's protocol. The cDNA library was inspected using using Agilent Bioanalyzer High Sensitivity DNA chips and quantitated by PicoGreen dsDNA Assay kit (ThermoFisher)."; [Cell type]'Source: ''strain: Rag2-/-IL2rg-/-; treatment: NK transferred; tissue: breast cancer lung metastatic lesion; ', 'strain: Rag2-/-IL2rg-/-; treatment: Ctrl; tissue: breast cancer lung metastatic lesion; ' GSE131857 Homo sapiens 23 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL9052; GPL11154 Nuclear receptor RORγ is a targetable master regulator of cholesterol in a subtype of breast cancer 2019-05-28 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131857 RORγ is a targetable master regulator of cholesterol biosynthesis in a cancer subtype. Nature communications 11.878 https://doi.org/10.1038/s41467-019-12529-3 {Nature communications (11.878): 10.1038/s41467-019-12529-3} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA545129 https://www.ebi.ac.uk/ena/browser/view/PRJNA545129 None [Overal design]Refer to individual Series; [Treatment]'HCC70 cells were seeded into15 cm dish and cultured in RPMI supplemented with 10% FBS, next day, cell were then treated with vehicle or XY018 (5µM) for another 24 hours.', 'HCC70 and MDA-MB468 cells were seeded into 6-well plates and cultured in growth medium. Next day, cell were treated with vehicle, XY018 (1.25 or 2.5 µM), atorvastatin (ATV, 1.25 µM) or the combination of XY018 (1.25 µM) and ATV for 24 hours. For MDA-MB468, cells were treated with vehicle or GSK805 (2.5 µM) for 24 hours before RNA extraction.'; [Growth]'HCC70 cells were cultured in RPMI supplemented with 10% FBS for maintenance for experiments. Cells were grown at 37℃ in 5% CO2 incubators.', 'HCC70 cells were cultured in RPMI supplemented with 10% FBS for maintenance for experiments. MDA-MB468 cells were cultured in RPMI supplemented with 10% FBS plus 1% insulin for maintenance for experiments. Cells were grown at 37℃ in 5% CO2 incubators.'; [Extraction]"Lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody.\nLibraries were prepared according to Illumina's paired-end DNA sample Prep kit.", '1 μg of total RNA was extracted for each sample.\nLibraries were prepared using Illumina Tru-Seq RNA Sample Prep Kit, according to the manufacturer’s instructions. Libraries were validated with an Agilent Bioanalyzer (Agilent Technologies, Palo Alto, CA).'; [Cell type]'Source: ''cell line: HCC70; passages: 6-9; treatment: vehicle; chip antibody: H3(acetyl K27) (Abcam; ab4729); ', 'cell line: HCC70; passages: 6-9; treatment: XY018; chip antibody: H3(acetyl K27) (Abcam; ab4729); ', 'cell line: HCC70; passages: 6-9; treatment: vehicle; chip antibody: none; ', 'cell line: HCC70; passages: 6-9; treatment: XY018; chip antibody: none; ', 'cell line: HCC70; passages: 6-9; treatment: vehicle; chip antibody: SREBP2 (Cayman, #10007663); ', 'cell line: HCC70; passages: 6-9; treatment: XY018; chip antibody: SREBP2 (Cayman, #10007663); ', 'cell line: HCC70; passages: 6-9; treatment: vehicle; chip antibody: anti-RORγ rabbit serum was generated by Covance, using purified GST-human RORγ fragment (amino acids 79-301) expressed in Escherichia coli.; ', 'cell line: HCC70; passages: 6-9; treatment: XY018; chip antibody: anti-RORγ rabbit serum was generated by Covance, using purified GST-human RORγ fragment (amino acids 79-301) expressed in Escherichia coli.; ', 'cell line: HCC70; passages: 6-9; treatment: Vehicle; ', 'cell line: HCC70; passages: 6-9; treatment: XY018_1.25uM; ', 'cell line: HCC70; passages: 6-9; treatment: XY018_2.5uM; ', 'cell line: HCC70; passages: 6-9; treatment: Atorvastatin_1.25uM; ', 'cell line: HCC70; passages: 6-9; treatment: XY018_1.25uM combined with Atorvastatin_1.25uM; ', 'cell line: MDA-MB468; passages: 6-9; treatment: Vehicle (for combination); ', 'cell line: MDA-MB468; passages: 6-9; treatment: XY018_1.25uM; ', 'cell line: MDA-MB468; passages: 6-9; treatment: XY018_2.5uM; ', 'cell line: MDA-MB468; passages: 6-9; treatment: XY018_1.25uM combined with Atorvastatin; ', 'cell line: MDA-MB468; passages: 6-9; treatment: Vehicle (for GSK805); ', 'cell line: MDA-MB468; passages: 6-9; treatment: GSK805_2.5uM; ' GSE17350 Homo sapiens 1 Non-coding RNA profiling by array GPL8935 MicroRNAome of highly metastatic and non-metastatic human breast cell lines 2009-07-27 MicroRNAs are noncoding, endogenous small RNAs that regulate target genes by cleavage of the targeted mRNA or translational repression. We investigated the microRNAome using 2-color microarrays in a highly invasive human breast cancer cell line, MDA-MB-231 (sub line 4175) and a non-invasive breast epithelial cell line, MCF10A. We found 13 miRNAs that were up-regulated and 9 were down-regulated significantly in 4175 cells (p <0.05, fold change >2) compared with MCF10A cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17350 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA119063 https://www.ebi.ac.uk/ena/browser/view/PRJNA119063 None [Overal design]We compared the highly metastatic human breast cell lines MDA-MB-231 (4175 subline) with non-metastatic MCF10A cell lines. Two 4175 sublines and two MCF10A cell lines, independently grown and harvested. Dye swap was performed.; [Treatment]'None'; [Growth]'Human breast cancer cell lines, MDA-MB-231 (subline 4175) was maintained in Dulbecco’s Modified Eagle’s Medium (DMEM) supplemented with 10% fetal bovine serum (FBS). The ERBB2-independent human mammary epithelial cell line, MCF10A, was maintained in DMEM/F12 medium supplemented with 5% FBS, 20 ng/mL of EGF, 0.5 μg/mL hydrocortisone, 100 ng/mL cholera toxin, and 10 μg/mL insulin.'; [Extraction]"Total RNA extracted using miRNeasy kit (QIAGEN) following manufacturer's instructions"; [Cell type]'Source: ''passage: 6; cell line: MDA-MB-231 cells (4175 subline); phenotype: highly metastatic; ', 'passage: 4; cell line: MCF10A; phenotype: non-metastatic; ' GSE176078 Homo sapiens 26 Expression profiling by high throughput sequencing GPL18573 A single-cell and spatially resolved atlas of human breast cancers 2021-06-03 This study presents a single cell and spatially resolved transcriptomics analysis of human breast cancers. We develop a single cell method of intrinsic subtype classification (scSubtype) to reveal recurrent neoplastic cell heterogeneity. Immunophenotyping using CITE-Seq provides high-resolution immune profiles, including novel PD-L1/PD-L2+ macrophage populations associated with clinical outcome. Mesenchymal cells displayed diverse functions and cell surface protein expression through differentiation within 3 major lineages. Stromal-immune niches were spatially organized in tumors, offering insights into anti-tumor immune regulation. Using single cell signatures, we deconvoluted large breast cancer cohorts to stratify them into nine clusters, termed ‘ecotypes’, with unique cellular compositions and clinical outcomes. This study provides a comprehensive transcriptional atlas of the cellular architecture of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE176078 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA734812 https://www.ebi.ac.uk/ena/browser/view/PRJNA734812 None [Overal design]We performed scRNA-Seq (Chromium, 10X Genomics) on 26 primary tumors from three major clinical subtypes of breast cancer, including 11 ER+, 5 HER2+ and 10 TNBC. We also performed bulk RNA-Seq on a total of 24 of these matched samples. ***Raw Data Disclaimer: Raw human data files are deposited to the EGA (EGAS00001005173) to adhere to ethics.***; [Treatment]'None'; [Growth]'None'; [Extraction]"Single-cell sequencing was performed using the Chromium Single-Cell v2 3’ and 5’ Chemistry Library, Gel Bead, Multiplex and Chip Kits (10X Genomics) according to the manufacturer's protocol. A total of 5,000 to 7,000 cells were targeted per well.\nLibraries were sequenced on the NextSeq 500 platform (Illumina) with pair-ended sequencing and dual indexing. A total of 26, 8 and 98 cycles were run for Read 1, i7 index and Read 2, respectively."; [Cell type]'Source: ''clinical_subtype: HER2+/ER+; gender: female; tissue: Primary Breast Tumor; ', 'clinical_subtype: HER2+; gender: female; tissue: Primary Breast Tumor; ', 'clinical_subtype: ER+; gender: female; tissue: Primary Breast Tumor; ', 'clinical_subtype: TNBC; gender: female; tissue: Primary Breast Tumor; ' GSE33167 Homo sapiens 15 Expression profiling by array GPL570 Phenotypic Plasticity in Aggressive Triple-Negative Breast Cancer: Human Biology is Recapitulated by a Novel Model System 2011-10-24 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE33167 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA149229 https://www.ebi.ac.uk/ena/browser/view/PRJNA149229 None [Overal design]Refer to individual Series; [Treatment]'DKAT, HMEC, or MDA-MB-231 cells were cultured in MEGM (Lonza).', 'DKAT cells (passage 10) in MEGM were split and grown for 14 days either in MEGM (Lonza) or SCGM (Lonza) in adherent culture.'; [Growth]'DKAT, HMEC, or MDA-MB-231 cells were cultured in MEGM (Lonza).', 'DKAT cells (passage 10) in MEGM were split and grown for 14 days either in MEGM (Lonza) or SCGM (Lonza) in adherent culture.'; [Extraction]"Extraction of total RNA was performed using the Qiagen RNeasy kit according to the manufacturer's instructions with option DNAse step."; [Cell type]'Source: ''cell line: Human breast cancer-derived cell line HMEC; culture medium: MEGM; ', 'cell line: Human breast cancer-derived cell line DKAT; culture medium: MEGM; ', 'cell line: Human breast cancer-derived cell line MDA-MB-231; culture medium: MEGM; ', 'cell line: Human breast cancer-derived cell line DKAT; culture medium: SCGM; ' GSE12122 Homo sapiens 6 Methylation profiling by genome tiling array GPL5082 Epigenetic mapping and functional analysis in a breast cancer metastasis model using whole genome tiling arrays 2008-07-15 We have used a human gene promoter tiling microarray platform to analyze a cell line model of lymph node metastasis comprised of a poorly metastatic MDA-MB-468GFP human breast adenocarcinoma cell line and its highly metastatic variant (468LN). Gene networks and pathways associated with metastasis were identified and target genes associated with epithelial-mesenchymal transition (EMT) was validated with respect to DNA methylation effects on gene expression. We integrated data from the tiling microarrays with targets identified by Ingenuity Pathway Analysis software and observed epigenetic variations in genes implicated in EMT and with tumor cell migration. We identified widespread genomic hyper- and hypo- methylation events in these cells and we confirmed functional associations between methylation status and expression of the CDH1, CST6, EGFR, SNAI2 and ZEB2 genes by quantitative RealTime PCR. Our data also suggest that the complex genomic reorganization present in cancer cells may be superimposed over promoter-specific methylation events that are responsible for gene-specific expression changes. Keywords: Lymph node metastatic vs non metastatic https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE12122 Epigenetic mapping and functional analysis in a breast cancer metastasis model using whole-genome promoter tiling microarrays. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr2121 {Breast cancer research : BCR (5.676): 10.1186/bcr2121} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA122647 https://www.ebi.ac.uk/ena/browser/view/PRJNA122647 None [Overal design]DNA derived from three biological replicates of a highly metastatic (via Lymph Nodes) Breast cancer cell line (468GFP-LN) was compared to 3 biological replicates of DNA prepared from the parental cell line, 468GFP.; [Treatment]'No treatment'; [Growth]'Cells were grown out to three passages in alpha-MEM containing 10% FBS in 5% CO2 to 70 % confluency'; [Extraction]"Genomic DNA was extracted using Sigma GeneElute kit using the Manufacturer's protocol"; [Cell type]'Source: ''' GSE46815 Mus musculus 4 Expression profiling by high throughput sequencing GPL13112 Effect of pubertal BPA exposure on mammary stem cells 2013-05-09 Perinatal exposure to bisphenol A (BPA) has been shown to cause aberrant mammary gland morphogenesis and mammary neoplastic transformation. Yet, the underlying mechanism is poorly understood. We tested the hypothesis that mammary glands exposed to BPA during a susceptible window may lead to its susceptibility to tumorigenesis through a stem-cell mediated mechanism. We exposed 21-day-old Balb/c mice to BPA by gavage (25 µg/kg/day) during puberty for 3 weeks, and a subset of animals were further challenged with one oral dose (30 mg/kg) of 7,12-dimethylbenz[a]anthracene (DMBA) at 2 months of age. Primary mammary cells were isolated at 6 weeks, and 2 and 4 months of age for mammary stem cell (MaSC) quantification and function analysis. Pubertal exposure to the low-dose BPA increased lateral branches and hyperplasia in adult mammary glands and caused an acute increase of MaSC in 6-week-old glands and a delayed increase of luminal progenitors in 4-month-old adult gland. Most importantly, pubertal BPA exposure altered the function of MaSC from different age groups, causing pre-neoplastic lesions in their regenerated glands similar to those induced by DMBA exposure, which indicates that MaSCs are susceptible to BPA-induced transformation. Deep sequencing analysis on MaSC-enriched mammospheres identified a set of aberrantly expressed genes associated with pre-neoplastic lesions in human breast cancer patients. Thus, our study for the first time shows that pubertal BPA exposure altered MaSC gene expression and function such that they induced early neoplastic transformation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE46815 Pubertal bisphenol A exposure alters murine mammary stem cell function leading to early neoplasia in regenerated glands. Cancer prevention research (Philadelphia, Pa.) 3.866 https://doi.org/10.1158/1940-6207.CAPR-13-0260 {Cancer prevention research (Philadelphia, Pa.) (3.866): 10.1158/1940-6207.CAPR-13-0260} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA202390 https://www.ebi.ac.uk/ena/browser/view/PRJNA202390 https://www.ncbi.nlm.nih.gov/sra?term=SRP022252 [Overal design]Four samples were analyzed (control, BPA, DMBA, BPA+DMBA), and for each treatment group, mammospheres from 5 animals were pooled for RNA extraction.; [Treatment]'Balb/C mice of 21 days old were intragastrically gavaged daily with sesame oil (vehicle control) or BPA at 25 μg/kg/day for 3 weeks. Beyond puberty, all mice were continued on low-phytoestrogen diet until the end of the experiment. At 2 months of age, a subgroup of vehicle control and pubertal BPA-treated mice were given a single oral gavage of 7,12-dimethylbenz[a]anthracene (DMBA) at 30 mg/kg. Mammary glands were harvested at 4 months of age for FACS analysis and sorting. Sorted basal cells were then used for mammosphere culture. Spheres were harvested at day 7 for RNA extraction.'; [Growth]'Sorted basal cells were cultured in ultralow attachment 96-well plates (Corning) with mouse EpiCult-B medium (150 μL per well) supplemented with 2% B27 (Invitrogen), 20 ng/mL bFGF, 20 ng/mL EGF, 10 µg/mL heparin, 10 µg/mL insulin, 1 µg/mL hydrocortisone, and 50 µg/mL gentamicin for 7 days.'; [Extraction]'Total RNA was isolated using miRNeasy Mini kit (Qiagen, cat #217004).\nSequencing libraries were constructed using the Illumina TruSeq RNA sample preparation protocol (Illumina, Catalog no. RS-122-2002).'; [Cell type]'FACS-sorted basal cells''strain/background: Balb/C; age: 4 months; tissue: mammary gland; cell type: FACS-sorted basal cells; treatment: control; ', 'strain/background: Balb/C; age: 4 months; tissue: mammary gland; cell type: FACS-sorted basal cells; treatment: BPA; ', 'strain/background: Balb/C; age: 4 months; tissue: mammary gland; cell type: FACS-sorted basal cells; treatment: DMBA; ', 'strain/background: Balb/C; age: 4 months; tissue: mammary gland; cell type: FACS-sorted basal cells; treatment: BPA+DMBA; ' GSE181524 Homo sapiens 16 Genome binding/occupancy profiling by high throughput sequencing GPL18573 H3K27ac ChIP-seq of MCF10A progression series 2021-08-05 This study takes an unbiased global analysis of super-enhancers that are acquired or lost in progression of breast cancer using the MCF10a progression series https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE181524 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA752355 https://www.ebi.ac.uk/ena/browser/view/PRJNA752355 https://www.ncbi.nlm.nih.gov/sra?term=SRP331234 [Overal design]Using the enhancer mark H3K27ac, we performed ChIP seq to identify enhancers, and subesquently, using ROSE to identify super-enhancers acquired or lost in progression of breast cancer.; [Treatment]'None'; [Growth]"MCF10A, MCF10A-AT1, DCIS.com, and MCF10A-CA1 cells were grown to a final count of 5 x 10^6. The cells were maintained in a culture of Dulbecco's modified Eagle's medium (DMEM) medium supplemented with 5% horse serum, 20\u2009ng/mL EGF, 0.5\u2009mg/mL hydrocortisone, 100\u2009ng/mL cholera toxin, 10\u2009μg/mL insulin and 1× antibiotic‐antimycotic (Gibco, Grand Island, NY)"; [Extraction]'Lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody.\n1 to 10 ng of DNA was prepared for sequencing using NEBNext Ultra II DNA Library Prep Kit (E7645S) and NEBNext® Multiplex Oligos for Illumina® (Index Primers Set 1) (E7335S)'; [Cell type]'epithelial cells''cell line: MCF10A; tissue: Breast; Mammary gland; disease state: normal; cell type: epithelial cells; chip antibody: H3K27ac (abcam ChIP Grade (ab4729)); treatment: Untreated; ', 'cell line: MCF10A; tissue: Breast; Mammary gland; disease state: normal; cell type: epithelial cells; chip antibody: IgG- Cell Signaling(Rabbit (DA1E) mAb IgG XP® Isotype Control #3900; treatment: Untreated; ', 'cell line: MCF10A-AT1; tissue: Breast; Mammary gland; disease state: atypical ductal hyperplasia; cell type: epithelial cells; chip antibody: H3K27ac (abcam ChIP Grade (ab4729)); treatment: Untreated; ', 'cell line: MCF10A-AT1; tissue: Breast; Mammary gland; disease state: atypical ductal hyperplasia; cell type: epithelial cells; chip antibody: IgG- Cell Signaling(Rabbit (DA1E) mAb IgG XP® Isotype Control #3900; treatment: Untreated; ', 'cell line: DCIS; tissue: Breast; Mammary gland; disease state: ductal carcinoma in situ; cell type: epithelial cells; chip antibody: H3K27ac (abcam ChIP Grade (ab4729)); treatment: Untreated; ', 'cell line: DCIS; tissue: Breast; Mammary gland; disease state: ductal carcinoma in situ; cell type: epithelial cells; chip antibody: IgG- Cell Signaling(Rabbit (DA1E) mAb IgG XP® Isotype Control #3900; treatment: Untreated; ', 'cell line: MCF10A-CA1; tissue: Breast; Mammary gland; disease state: invasive ductal carcinoma; cell type: epithelial cells; chip antibody: H3K27ac (abcam ChIP Grade (ab4729)); treatment: Untreated; ', 'cell line: MCF10A-CA1; tissue: Breast; Mammary gland; disease state: invasive ductal carcinoma; cell type: epithelial cells; chip antibody: IgG- Cell Signaling(Rabbit (DA1E) mAb IgG XP® Isotype Control #3900; treatment: Untreated; ' GSE121179 Homo sapiens 12 Expression profiling by high throughput sequencing GPL16791 Next generation seuquencing of 3D breast cancer cell culture in synthetic hydrogels presenting either a collagen mimic or laminin mimic 2018-10-12 MDA-MB-231 (ER-) and T47D (ER+) breast cancer cells were encapsulated in synthetic hydrogels, formed with a multi-arm bioinert polymer poly(ethylene glycol), cell-degradable peptide crosslinks, and receptor-binding pendant peptides, and cultured for 3 days to assess initial cell responses to different matrix compositions. The synthetic matrices had a Young's modulus (E) ~ 0.6 kPa, in the range of bone marrow and healthy mammary tissue, and biochemcial cues to mimic binding sites found in collagen (GFOGER peptide) or laminin (IKVAV peptide). After 3 days in culture, mRNA was collected and RNA-seq performed to compare cell responses between the collagen and laminin mimetic cultures. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE121179 Tunable synthetic extracellular matrices to investigate breast cancer response to biophysical and biochemical cues. APL bioengineering None https://doi.org/10.1063/1.5064596 {APL bioengineering (None): 10.1063/1.5064596} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA496024 https://www.ebi.ac.uk/ena/browser/view/PRJNA496024 https://www.ncbi.nlm.nih.gov/sra?term=SRP165292 [Overal design]Examination of two different peptide compositions, collagen (GFOGER) and laminin (IKVAV), on two breast cancer cell lines MDA-MB-231 (ER-) and T47D (ER+) cultured in three dimensional PEG hydrogels for 3 days.; [Treatment]"Cells were encapsulated in a hydrogel: 5 µL of the gel precusor solution with a single cell suspension of 5,000 cells/µL was polymersized on top of a pre-formed 15 µL base hydrogel without encapsulated cells (20 uL total hydrogel volume formed in 1-mL sterile syringe with end removed). Cells were formed by free-radical step growth-polymerization 'thiol-ene' click chemistry of a 4-arm PEG-SH and cell-degradable crosslinker (GPQGIWGQ) difunctional with allyloxycarbonyl groups. Two treatments per cell line were performed, consisting of a collagen (GFOGER peptide) or laminin (IKVAV peptide) environment."; [Growth]'MDA-MB-231 and T47Ds were cultured in DMEM (Corning 10-013CV) + 10% FBS + Pen/strep + Fungizone. Media was replaced every 2-3 days. Cells encapsulated within hydrogels were cultured in 48-well plates with 500 µL of culture media.'; [Extraction]'Hydrogels were degraded by incubating gels with 250 U collagenase for 20 minutes at 37 ℃ and 5% CO2. After gel degadation, cells were pelleted by centrifugation at 1000 RPM for 5 minutes, and PEG was removed. RNA was then extracted from cells by a Nucleospin miRNA kit (Takara), where cells were first placed into lysis buffer. Three gels of the same composition was used for one replicate of RNA. DNase treatment was performed duing RNA isolation.\nRNA Indexed libraries were constructed from 100-500 ng of total RNA using the Universal Plus mRNA-seq Workflow Kit (Nugen)\nStranded Poly-A capture RNA-Seq'; [Cell type]'epithelial''cell line: MDA-MB-231; tissue: Mammary Gland/Breast; Derived From Metastatic Site: Pleural Effusion; cell type: epithelial; disease state: Adenocarcinoma; time: 3 days; growth matrix peptide: IKVAV; ', 'cell line: MDA-MB-231; tissue: Mammary Gland/Breast; Derived From Metastatic Site: Pleural Effusion; cell type: epithelial; disease state: Adenocarcinoma; time: 3 days; growth matrix peptide: GFOGER; ', 'cell line: T47D; tissue: Mammary Gland/Breast; Derived From Metastatic Site: Pleural Effusion; cell type: epithelial; disease state: Ductal Carcinoma; time: 3 days; growth matrix peptide: IKVAV; ', 'cell line: T47D; tissue: Mammary Gland/Breast; Derived From Metastatic Site: Pleural Effusion; cell type: epithelial; disease state: Ductal Carcinoma; time: 3 days; growth matrix peptide: GFOGER; ' GSE39788 Rattus norvegicus 10 Expression profiling by array GPL1355 Mapping of Three Genetic Determinants of Susceptibility to Estrogen-Induced Mammary Cancer within the Emca8 Locus on Rat Chromosome 5 2012-07-31 We are using the ACI rat model of 17beta-estradiol induced mammary cancer to define the mechanisms through which estrogens contribute to breast cancer development; identify and functionally characterize the genetic variants that determine susceptibility; and define the hormone-gene-environment interactions that influence development of mammary cancer in this physiologically relevant rat model. Female ACI rats are uniquely susceptible to development of mammary cancer when treated continuously with physiologic levels of 17beta-estradiol. Induction of mammary cancer in female ACI rats occurs through a mechanism that is largely dependent upon estrogen receptor-alpha. Interval mapping analyses of progeny generated in intercrosses between susceptible ACI rats and resistant Brown Norway (BN) rats revealed seven quantitative trait loci (QTL), designated Emca3 (Estrogen-induced mammary cancer) through Emca9, each of which harbors one or more genetic determinants of mammary cancer susceptibility. Genes that reside within Emca8 on RNO5 and were differentially expressed between 17beta-estradiol treated ACI and ACI.BN-Emca8 congenic rats were identified as Emca8 candidates. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39788 Mapping of three genetic determinants of susceptibility to estrogen-induced mammary cancer within the Emca8 locus on rat chromosome 5. Cancer prevention research (Philadelphia, Pa.) 3.866 https://doi.org/10.1158/1940-6207.CAPR-12-0346-T {Cancer prevention research (Philadelphia, Pa.) (3.866): 10.1158/1940-6207.CAPR-12-0346-T} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA171714 https://www.ebi.ac.uk/ena/browser/view/PRJNA171714 None [Overal design]Two groups of 17beta-estradiol treated female rats were compared. Five ACI and five BN.ACI-Emca8 rats were treated with 17beta-estradiol for 12 weeks. Total RNA was isolated from the mammary glands of these animals, labeled, and hybridized to Affymetrix Rat Genome 230 2.0 Arrays (Affymetrix Inc.). Significantly differentially expressed genes were found between these groups.; [Treatment]'The rats were treated continuously with 17beta-estradiol delivered from subcutaneous implants, starting at 9 weeks of age. The rats were euthanized following 12 weeks of 17beta-estradiol treatment and the mammary glands were harvested, frozen in liquid nitrogen and stored at -80° C.'; [Growth]'None'; [Extraction]'Absolutely RNA Miniprep Kits (Stratagene, La Jolla, CA) were used to isolate RNA from mammary tissues that were dissected from individual ACI rats that had been treated with 17beta-estradiol for 12 weeks, a time point that precedes development of palpable mammary cancer.', 'Absolutely RNA Miniprep Kits (Stratagene, La Jolla, CA) were used to isolate RNA from mammary tissues that were dissected from individual ACI.BN-EMCA8 rats that had been treated with 17beta-estradiol for 12 weeks, a time point that precedes development of palpable mammary cancer.'; [Cell type]'Source: ''strain: ACI/SegHsd; gender: Female; age: 21 weeks; tissue: Mammary gland; 17beta-estradiol treatment time: 12 weeks; ', 'strain: ACI.BN-EMCA8 (RGD ID 5144110); gender: Female; age: 21 weeks; tissue: Mammary gland; 17beta-estradiol treatment time: 12 weeks; ' GSE137560 Homo sapiens 8 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL16791; GPL18460 Heat Shock Factor 1 (HSF1) acquires transcriptional competence under 17b-estradiol in ERa-positive breast cancer cells 2019-09-17 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE137560 17β-Estradiol Activates HSF1 via MAPK Signaling in ERα-Positive Breast Cancer Cells. Cancers 6.162 https://doi.org/10.3390/cancers11101533 {Cancers (6.162): 10.3390/cancers11101533} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA565913 https://www.ebi.ac.uk/ena/browser/view/PRJNA565913 None [Overal design]Refer to individual Series; [Treatment]'Cells were seeded on 10cm2 culture plates. Next day the medium was replaced into phenol-free DMEM/F12 medium supplemented with 5% dextran-activated charcoal-stripped FBS and 48 hours later cells were subjected to hyperthermia at 43°C for 15 minutes or 17β-estradiol was added to final concentration of 10nM for indicated time (1h and 2h).', 'Cells were seeded on culture plates. Next day the medium was replaced into phenol-free DMEM/F12 medium supplemented with 5% dextran-activated charcoal-stripped FBS and 48 hours later 17β-estradiol was added to final concentration of 100nM for 4hour or cells were subjected to hyperthermia (43°C) for 1hour with 2hours of recovery.'; [Growth]'The wild-type MCF7 cells were purchased from ATCC (HTB-22) and used as a primary model. Cells were grown in DMEM/F12 medium supplemented with 10% fetal bovine serum and antibiotic-antimycotic cocktail (penicillin, streptomycin, amphotericin) at 37 °C in a humidified 5% CO2 atmosphere.'; [Extraction]'At the appointed experimental points culture medium was removed and fixation was performed using 1% formaldehyde in PBS for 12 min at RT with rotating. Formaldehyde fixation was quenched by glycine (125 mM final concentration) and then nuclei were isolated using buffers and protocol from iDeal ChIP-seq Kit for Transcription Factors (Diagenode). Chromatin of nuclei re-suspended in 200 µl was sheared using Bioruptor® PLUS combined with the Bioruptor® Water cooler & Single Cycle Valve (at HIGH power setting) with 20 cycles of 30 sec shearing followed by 30 sec of standby; chromatin fragments with approximate length 100-600 bp were obtained. Chromatin immunoprecipitation was carried out using the iDeal ChIP-seq Kit for Transcription Factors (Diagenode) with 30μg of chromatin and 3µl/sample of anti-HSF1 polyclonal antibody (ADI-SPA-901, Enzo) or without antibody (mock-IP), according to the manufacturer protocol.\nImmunoprecipitated DNA fragments from six ChIP replicates was pooled. ChIP samples and input DNA were sequenced using the HiSeq 1500 system with TruSeq workflow (Illumina)', 'Total RNA from 10^6 cells was isolated using the Direct-ZolTM RNA MiniPrep Kit (Zymo Research) and digested with DNase I (Worthington Biochemical Corporation, NY, USA)\nRNA libraries were prepared for sequencing according to the standard Illumina protocols'; [Cell type]'Source: ''cell line: MCF7; tumor: adenocarcinoma; Sex: female; age: 69 years; tissue/cells: breast; chip antibody: none; ', 'cell line: MCF7; tumor: adenocarcinoma; Sex: female; age: 69 years; tissue/cells: breast; chip antibody: HSF1 polyclonal antibody (Enzo, ADI-SPA-901); ', 'cell line: MCF7; tumor: adenocarcinoma; Sex: female; age: 69 years; tissue/cells: breast; ' GSE98601 Homo sapiens 12 Expression profiling by array GPL10558 Analysis of the miR-34 family functions in breast cancer reveals annotation error of miR-34b 2017-05-05 The miR-34 family of microRNAs consisting of miR-34a, miR-34b and miR-34c are tumour suppressors. The annotated human miR-34b-5p has one additional base at the 5’ end of the common miR-34 family seed sequence, compared to miR-34a-5p and miR-34c-5p. This extra base results in a shift of the seed sequence, which would affect the target gene repertoire and have functional consequences. During our studies of miR-34 functions, we investigated the precise sequence of mature miR-34b-5p in human cells by deep sequencing. We found that a miR-34b-5p without the extra base was the predominant form in both non-malignant and malignant cells derived from several human tissues, indicating that the miR-34b annotation is misleading. We evaluated the functional implications of the seed shift, by comparing the effect of mimics representing the alternative miR-34b-5p sequences in MDA-MB-231 cells. In contrast to the annotated miR-34b, the endogenously expressed miR-34b displayed tumour suppressive characteristics in vitro similarly to miR-34c. These data demonstrate the importance of determining the precise sequence of a mature microRNA before exploring miRNA functions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98601 Analysis of the miR-34 family functions in breast cancer reveals annotation error of miR-34b. Scientific reports 4.011 https://doi.org/10.1038/s41598-017-10189-1 {Scientific reports (4.011): 10.1038/s41598-017-10189-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA385621 https://www.ebi.ac.uk/ena/browser/view/PRJNA385621 None [Overal design]Investigation of miR-34 family functions.; [Treatment]'24h after seeding, cells were transiently transfected using 18 nM mimics (Ambion) and INTERFERin (PolyPLUS), according to the manufacturer’s protocol.'; [Growth]'Cells were grown in RPMI-1640 (Sigma-Aldrich) supplemented with 10 % foetal calf serum (Sigma-Aldrich) and glutamax (Sigma-Aldrich), at 37°C with 5 % CO2. The cell line was routinely tested for mycoplasma, and always found negative. The cell line was also subject to short tandem repeat (STR)-DNA profiling of 15 loci and amelogenin (Genotyping core facility, Oslo University Hospital) and matched the STR-profile available from ATTC.'; [Extraction]'RNA was isolated 48h after transfection using standard TRIzol procedure (Invitrogen).'; [Cell type]'Triple-negative breast cancer cell line''cell line: MDA-MB-231; cell type: Triple-negative breast cancer cell line; sample origin: Pleural effusion; gender: Female; miRNA: miR-34a mimic; ', 'cell line: MDA-MB-231; cell type: Triple-negative breast cancer cell line; sample origin: Pleural effusion; gender: Female; miRNA: miR-34b mimic; ', 'cell line: MDA-MB-231; cell type: Triple-negative breast cancer cell line; sample origin: Pleural effusion; gender: Female; miRNA: miR-34c mimic; ', 'cell line: MDA-MB-231; cell type: Triple-negative breast cancer cell line; sample origin: Pleural effusion; gender: Female; miRNA: Negative Controls oligonucleotide; ' GSE108502 Homo sapiens 6 Expression profiling by high throughput sequencing GPL11154 KDM5 histone demethylases repress innate immune response via suppression of STING 2017-12-25 Tri-methylation on histone H3 lysine 4 (H3K4me3) is enriched near transcription start sites and correlates with active transcription. Like other histone marks, methylation on H3K4 is catalyzed by the respective methyltransferases and erased by demethylases. Lysine demethylase 5 (KDM5) family of Fe (II) and α-ketoglutarate-dependent dioxygenases removes the methyl groups from H3K4me3. All four family members of KDM5 demethylases (KDM5A-D) share sequence identity, have similar in vitro kinetic parameters, and display functional redundancy. To determine the effects of complete depletion of KDM5 activity, we treated MCF7 cells with DMSO, or two pan-KDM5 specific inhibitors, KDM5-C70 (our lab code 443) and CPI-48 (our lab code 278) and performed RNA sequencing to determine gene expression changes after KDM5 inhibitor treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE108502 KDM5 histone demethylases repress immune response via suppression of STING. PLoS biology 8.386 https://doi.org/10.1371/journal.pbio.2006134 {PLoS biology (8.386): 10.1371/journal.pbio.2006134} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA427473 https://www.ebi.ac.uk/ena/browser/view/PRJNA427473 https://www.ncbi.nlm.nih.gov/sra?term=SRP127521 [Overal design]RNA sequencing of MCF7 cells treated with DMSO or KDM5 inhibitors.; [Treatment]'At Day 0, 2x10e6 MCF7 cells were seeded into a 100 mm dish. At Day 1, Day 3, and Day 5, cells were refed with fresh medium plus indicated chemicals. At Day 7, cells were harvested from dishes for total RNA isolation.'; [Growth]'MCF7 cells were routinely generated by re-plating every four days (typically 2-4x10e6 cells into a 100 mm dish) with refeeding once between two splits in RPMI-1640 medium supplemented with 10% FBS.'; [Extraction]'Total RNA was isolated by using RNeasy mini kit (Qiagen) and following the handbook provided.\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'Breast cancer cell line''cell line: MCF7; cell type: Breast cancer cell line; treatment 1: DMSO; concentration 1: 0.10%; time: 6 days; ', 'cell line: MCF7; cell type: Breast cancer cell line; treatment 1: DMSO; concentration 1: 0.10%; treatment 2: CPI-48; concentration 2: 3 uM; time: 6 days; ', 'cell line: MCF7; cell type: Breast cancer cell line; treatment 1: DMSO; concentration 1: 0.10%; treatment 2: KDM5-C70; concentration 2: 3 uM; time: 6 days; ' GSE68683 Mus musculus 58 Non-coding RNA profiling by high throughput sequencing; Expression profiling by array GPL13188; GPL16417 Cell density, Her2 and progesterone signaling regulate dissemination of breast cancer cells 2015-05-08 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE68683 Early dissemination seeds metastasis in breast cancer. Nature 43.070 https://doi.org/10.1038/nature20785 {Nature (43.070): 10.1038/nature20785} 'polyA RNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA283387 https://www.ebi.ac.uk/ena/browser/view/PRJNA283387 None [Overal design]Refer to individual Series; [Treatment]'Transgenic Balb-NeuT mouse model of breast cancer (untreated)', 'None'; [Growth]'not applicable', 'Cells were cultured in DMEM, 10% FCS mediume'; [Extraction]'Laser microdissection (PALM MicroBeam from Carl Zeiss MicroImaging GmbH) was performed to dissect metastatic lesions from lung, primary tumors, epithelial layers of mammary glands of BALB-NeuT mice at the time point of ADH, and BALB/c mice at different age. Small pieces summing up to 100,000 um2 for each sample were catapulted into a cap with 10 ul paramagnetic oligo-dT bead suspension and lysis buffer. The extraction of mRNA and microarray experiments were performed as described previously (Klein et al., 2002).', 'Total RNA was isolated using TRIzol reagent (Life Technologies) following the manufacturer’s recommendations.\nIn short, an adenylated adapter was ligated to the 3’ end of the total RNA by a truncated T4 RNA Ligase 2, followed by the ligation of a 5’ RNA-adapter by T4 RNA Ligase 1 (NEB). After reverse-transcription using a specific primer, the cDNA was amplified by PCR. After gel-fractionation bands corresponding to miRNA inserts were cut out. PCR products from these bands were eluted in elution buffer, precipitated and dissolved in water. The quality of the libraries was assessed by qPCR and Bioanalyzer measurements.'; [Cell type]'Source: ''source: ADH tissue; ', 'source: normal tissue; ', 'source: tumor margin tissue; ', 'source: tumor center tissue; ', 'source: tumor tissue; ', 'source: lung metastasis tissue; ', 'source: Exosomes extracted from supernatant of TUBO cell cultures; ', 'source: MM3MG is a normal mammary epithelial cell line from BALB/c mouse strain; ', 'source: MM3MG is a normal mammary epithelial cell line from BALB/c mouse strain; transduction: Transduced wit pLSXN-Neu (Retro viral particles); ', 'source: supernatant from exosome-isolation; ', 'source: Mouse breast cancer cell line derived from primary tomors of Balb-NeuT; ' GSE26292 Homo sapiens 12 Expression profiling by array GPL6102 Gene expression of human cancer cells co-cultured with mouse astrocytes and fibroblasts after series of cross co-culture 2010-12-23 Brain metastases are highly resistant to chemotherapy. Brain metastases are surrounded and infiltrated by activated astrocytes. To examine the genes whose expression is associated with chemo-resistance of brain-metastasized cancer cells, gene expression data were collected and analyzed from breast cancer cells and lung cancer cells co-cultured with astrocytes. Fibroblast cells were used as control. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26292 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA142309 https://www.ebi.ac.uk/ena/browser/view/PRJNA142309 None [Overal design]Human lung cancer cell PC14 was co-cultured with mouse astrocytes or fibroblasts for two rounds. Total RNAs were extracted from co-cultured cells and hybridized to human microarray.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was isolated from tissues with mirVana RNA Isolation labeling kit (Ambion Inc) according to the manufacturer protocol. RNA quality and integrity were confirmed by ExperionTM Automated Electrophoresis System (BIO-RAD)'; [Cell type]'Source: ''protocol: astrocytes(first co-culture) and astrocytes(second co-culture); ', 'protocol: NIH 3T3(first co-culture) and astrocytes(second co-culture); ', 'protocol: astrocytes(first co-culture) and NIH 3T3(second co-culture); ', 'protocol: NIH 3T3(first co-culture) and NIH 3T3(second co-culture); ' GSE86538 Homo sapiens 18 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL18573 ChIP-seq of ER and RUNX2 in MCF7 breast cancer cell lines 2016-09-07 We performed ChIP-seq on MCF7 cells in an effort to discern differential binding patterns between wild type MCF7s and MCF7s that have acquired resistance to Tamoxifen and Estrogen deprivation. Furthermore, we also performed an HAtag ChIP on a DOX inducible RUNX2 overexpression MCF7 cell line. We also performed RNA-seq on MCF7 cells to determine transciptional changes after acquisition of Tamoxifen resistance, and also transciptional changes in a DOX inducible RUNX2 overexpression model. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE86538 Embryonic transcription factor SOX9 drives breast cancer endocrine resistance. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1620993114 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1620993114} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA342148 https://www.ebi.ac.uk/ena/browser/view/PRJNA342148 https://www.ncbi.nlm.nih.gov/sra?term=SRP087481 [Overal design]ER and HAtag ChIP on MCF7 cells, RNAseq on MCF7 cells; [Treatment]'None'; [Growth]'MCF7 cells were grown in DMEM supplemented with Penstrep and L-glutamine and 10% FBS.'; [Extraction]'Cell lines before ChIP were then either introduced to White Medium DMEM with or without supplemental E2 or Doxycycline, Cells were sonicated, then cell lysate was incubated with antibody to extract protein-DNA complex of interest, Library Preparation is performed using the Rubicon 48S kit', 'Cell lines were extracted using the Rneasy (Qiagen # 74104) kit with the substitution of Trizol instead of Buffer RLT. Preparation for sequaencing is done using the Illumina Truseq RNAseq v2 kit (15025063)'; [Cell type]'MCF7', 'Patient''cell type: MCF7; cell subtype: Wild Type; condition: White Medium + E2; ', 'cell type: MCF7; cell subtype: Tamoxifen Resistance; condition: White Medium; ', 'cell type: MCF7; cell subtype: Tamoxifen Resistance; condition: White Medium + E2; ', 'cell type: MCF7; cell subtype: Long Term Estrogen Deprivation; condition: White Medium; ', 'cell type: MCF7; cell subtype: Long Term Estrogen Deprivation; condition: White Medium + E2; ', 'cell type: MCF7; cell subtype: RUNX2 DOX inducible model; condition: Full Medium + Doxycycline; ', 'cell type: Patient; cell subtype: Pleural Effusion; condition: N/A; ', 'cell type: MCF7; cell subtype: Parental; ', 'cell type: MCF7; cell subtype: Tamoxifen Resistance; ', 'cell type: MCF7; cell subtype: RUNX2 DOX inducible model; condition: Full Medium; ' GSE85857 Homo sapiens 6 Expression profiling by high throughput sequencing GPL18460 Runx1 stabilizes the mammary epithelial cell phenotype and prevents epithelial to mesenchymal transition 2016-08-19 The Runx1 transcription factor is essential for hematopoietic differentiation and mutations underlie various leukemias. Here we demonstrate a role for Runx1 in the MCF10 cell series model of breast cancer progression. The highest level of Runx1 that occurs in normal like mammary epithelial cells (MCF10A) is decreased in tumorigenic (MCF10AT1) and metastatic (MCF10CA1a) breast cancer cells. We show that depletion of Runx1 in MCF10A cells results in striking changes in cell morphology and induction of epithelial-mesenchymal transition (EMT) via several signaling pathways. Analyses of breast tumors and patient survival data reveal that loss of Runx1 is associated with poor prognosis and decreased survival. Re-expressing Runx1 in MCF10AT1 breast cancer cells restores the epithelial phenotype. These results identify a novel function for Runx1 in sustaining normal epithelial morphology and preventing EMT. These mechanisms suggest Runx1 levels in early stage tumors can be used as a prognostic indicator of tumor progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE85857 Runx1 stabilizes the mammary epithelial cell phenotype and prevents epithelial to mesenchymal transition. Oncotarget None https://doi.org/10.18632/oncotarget.15381 {Oncotarget (None): 10.18632/oncotarget.15381} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA339558 https://www.ebi.ac.uk/ena/browser/view/PRJNA339558 https://www.ncbi.nlm.nih.gov/sra?term=SRP082418 [Overal design]RNA-Seq; two replicates each sample (6 total); [Treatment]'Cells were seeded at 1.5x106 cells per 100 mm dish and grown to 80% confluence. Cells were washed twice with phosphate buffered saline (PBS) and stored at -80C in TRIzol.'; [Growth]'MCF10a cells were grown in DMEM: F12 (Hyclone-SH30271), 5% (v/v) horse serum (Gibco #16050 lot #1075876) + 10ug/ml human insulin (Sigma I-1882)+ 20ng/ml recombinant hEGF (Peprotech AF-100-15) + 100ng/ml Cholera toxin (Sigma C-8052) + 0.5 ug/ml Hydrocortisone (Sigma H-0888) Pen/Strep (Life Technologies) and Glutamine (Life Technologies). MCF10A cells without growth factors were grown in DMEM: F12 (Hyclone-SH30271), 5% (v/v) horse serum (Gibco #16050 lot #1075876) + Pen/Strep (Life Technologies) and Glutamine (Life Technologies).'; [Extraction]'Total RNA was isolated from Trizol using Direct-zol RNA mini-prep kit (Zymo Research #R2050) with DNaseI digestion.\nRNA libraries were prepared for sequencing with the TruSeq Stranded Total RNA with Ribo-Zero Gold kit using standard Illumina protocols with the exception that library amplifcation was performed using KAPA HiFi™ Real-Time PCR Library Amplification Kit (Kapa Biosystems #KK2701).\nBarcoded libraries (Illumina TruSeq) were then loaded onto an Illumina HiSeq 1500 and single-end 100-base (SE100) sequencing was performed at the Advanced Genome Technologies Core Massively Parallel Sequencing Facility at UVM.'; [Cell type]'luminal ductal cells''tissue: breast; cell type: luminal ductal cells; neoplasia type: fibrocystic disease; atcc id: ATCC CRL-10317; cell line: MCF10A; ' GSE39539 Mus musculus 9 Expression profiling by array GPL6246 Fibrillar collagen implicated in pregnancy-induced protection of mammary cancer 2012-07-20 A suggested role for fibrillr collagen topology in the pregnancy-induced protection and invasive phenotype. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39539 Collagen architecture in pregnancy-induced protection from breast cancer. Journal of cell science 4.517 https://doi.org/10.1242/jcs.121590 {Journal of cell science (4.517): 10.1242/jcs.121590} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA171062 https://www.ebi.ac.uk/ena/browser/view/PRJNA171062 None [Overal design]Two conditions: RNA was isolated from murine mammary D2.OR cells cultured in fibrillar collagen I and non-fibrillar collagen I in 3D cell culture; [Treatment]'None'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: D2.OR mammary tumor cell line; growth protocol: cultured in fibrillar collagen I in 3D cell culture; ', 'cell line: D2.OR mammary tumor cell line; growth protocol: cultured in non-fibrillar collagen I in 3D cell culture; ' GSE158669 Homo sapiens 24 Expression profiling by high throughput sequencing; Other; Non-coding RNA profiling by high throughput sequencing GPL11154 BCDIN3D RNA methyltransferase stimulates Aldolase C expression and glycolysis through let-7 microRNA in breast cancer cells 2020-09-28 BCDIN3D is an RNA modifying enzyme that methylates specific precursor microRNAs and tRNAHis. In addition to breast cancer, BCDIN3D may also be linked to metabolism, as its gene locus is associated with obesity and T2D. In order to uncover metabolic pathways regulated by BCDIN3D in cancer, we performed an unbiased analysis of the metabolome, transcriptome, and proteome of breast cancer cells depleted for BCDIN3D. Intersection of these analyses showed that BCDIN3D-depleted cells have increased levels of Fructose 1,6 Bisphosphate (F1,6-BP), the last six-carbon glycolytic intermediate accompanied by reduced glycolytic capacity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE158669 BCDIN3D RNA methyltransferase stimulates Aldolase C expression and glycolysis through let-7 microRNA in breast cancer cells. Oncogene 6.634 https://doi.org/10.1038/s41388-021-01702-y {Oncogene (6.634): 10.1038/s41388-021-01702-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA666167 https://www.ebi.ac.uk/ena/browser/view/PRJNA666167 https://www.ncbi.nlm.nih.gov/sra?term=SRP285644 [Overal design]We performed combined RNA-Seq, miRNA-seq, and ribosome profiling in shBCDIN3D MDA-MB-231 breast cancer cells; [Treatment]'No treatment - collected 48h after seeding at 10^5 cells/mL', '24h with 10nM Rapamycin - collected 48h after seeding at 10^5 cells/mL'; [Growth]'DMEM+10%FBS+PSQ+1µg/mL puromycin'; [Extraction]'As in Ingolia at al, 2012\nAs in Ingolia at al, 2012', 'Norgen RNA/protein purification kit\nTruSeq Stranded Total RNA', 'Norgen RNA/protein purification kit followed by gel extraction of small RNAs < 35 nt\nAs in Ingolia at al, 2012'; [Cell type]'Source: ''cell line: MDA-MB-231; shRNA status: shNC; molecule type: ribosome-protected RNA; ', 'cell line: MDA-MB-231; shRNA status: shBCDIN3D; molecule type: ribosome-protected RNA; ', 'cell line: MDA-MB-231; shRNA status: shNC; molecule type: total RNA; ', 'cell line: MDA-MB-231; shRNA status: shBCDIN3D; molecule type: total RNA; ', 'cell line: MDA-MB-231; shRNA status: shNC; molecule type: Gel-fractionated small RNA; ', 'cell line: MDA-MB-231; shRNA status: shBCDIN3D; molecule type: Gel-fractionated small RNA; ' GSE153636 Homo sapiens 48 Methylation profiling by genome tiling array GPL5082 DNA methylation variations in familial female and male breast cancer 2020-07-01 About 25% of familial breast cancer (BC) is attributed to germline mutations of BRCA1 and BRCA2 genes while the rest of patients are included in the BRCAX group. BC also affects men with a worldwide incidence of 1%. The epigenetic alterations, including those DNA methylation, have been rarely studied in the male breast cancer (MBC) on a genome-wide level. The aim of the current work was to study the global DNA methylation profiles of BC patients to look for differences between familial female breast cancer (FBC) and MBC and according to BRCA1, BRCA2 and BRCAX mutation status. The genomic DNA from FFPE tissues of 17 female and 7 male patients with BC was subjected to methylated DNA immunoprecipitation (MeDIP) and hybridized on human promoter microarrays. The comparison between FBC and MBC showed 2846 differentially methylated regions (DMRs) corresponding to 2486 distinct annotated genes. The gene ontology enrichment analysis revealdrelevant molecular function terms such as the GTPase superfamily genes (in particular the GTPase Rho GAP/GEF and GTPase RAB) and cellular component terms associated to cytoskeletal architecture such as “cytoskeletal part”, “keratin filament”, “intermediate filament". By considering only FBC, several cancer-associated pathways were the most enriched KEGG pathways of differentially methylated genes between BRCA2 and BRCAX or BRCA1+BRCAX groups. The comparison between BRCA1 group vs BRCA2+BRCAX group displayed the enriched molecular function term “cytoskeletal protein binding”. Finally, the functional annotation of differentially methylated genes between BRCAX and BRCA1+BRCA2 groups indicated that the most enriched molecular function terms were related to GTPase activity. In summary, this is the first study that compares the global DNA methylation profile of familial FBC and MBC and the results may provide useful insights into the epigenomic subtyping of breast cancer and shed light on a possible new molecular mechanisms underlying BC carcinogenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE153636 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA643525 https://www.ebi.ac.uk/ena/browser/view/PRJNA643525 None [Overal design]The global DNA methylation profiles of 24 breast cancer cases were obtained by methylated DNA immunoprecipitation coupled with Affymetrix Human Promoter 1.0R Tiling Arrays (MeDip-chip). The genomic DNA from 24 breast cancer FFPE tissues was extracted using QIAamp DNA FFPE Tissue Kit supplied by Qiagen- The genomic DNA was digested using micrococcal nuclease (New England Biolabs) to obtain DNA fragments ranging from 200 to 500 nucleotides and used them as input (IN) DNA. Agilent Bioanalyzer with the RNA 6000 Nano LabChip Kit was used to check the size of fragmented DNA. Part of IN DNA (4 µg) was immunoprecipitated (IP) with 10 µl of anti-5-MethylCytosine Antibody (Eurogentec, BI-MECY-0100) using the MeDip protocol. The antibody-DNA complexes were immunoprecipitated using Dynabeads® Protein G immunoprecipitation kit (Life Technologies) and the methylated enriched DNA was purified by standard phenol/chloroform procedure and precipitated with isopropanol. A total of 200 ng of IN and IP DNA was amplified with the Affymetrix Chromatin Immunoprecipitation Assay Protocol. Totalling 2 arrays per each breast cancer case were performed (1 IP DNA and 1 IN DNA). The CEL files were imported into Partek® Genomics Suite® (PGS). We performed 9 different comparisons according to gender and mutation status (BRCA1, BRCA2 and BRCAX). For each comparison performed the significantly differentially methylated regions (DMR) were obtained using ANOVA followed by MAT algorithm (model-based analysis of tiling arrays algorithm). Using PGS function, each DMR was associated to its nearest gene of human genome. The genomic coordinates of each DMR were calculated based on UCSC human genomic assembly version 18.; [Treatment]'None'; [Growth]'None'; [Extraction]'The global DNA methylation profiles of 24 breast cancer cases were obtained by methylated DNA immunoprecipitation coupled with Affymetrix Human Promoter 1.0R Tiling Arrays (MeDip-chip). The genomic DNA from 24 breast cancer FFPE tissues was extracted using QIAamp DNA FFPE Tissue Kit supplied by Qiagen- The genomic DNA was digested using micrococcal nuclease (New England Biolabs) to obtain DNA fragments ranging from 200 to 500 nucleotides and used them as input (IN) DNA. Agilent Bioanalyzer with the RNA 6000 Nano LabChip Kit was used to check the size of fragmented DNA. Part of IN DNA (4 µg) was immunoprecipitated (IP) with 10 µl of anti-5-MethylCytosine Antibody (Eurogentec, BI-MECY-0100) using the MeDip protocol. The antibody-DNA complexes were immunoprecipitated using Dynabeads® Protein G immunoprecipitation kit (Life Technologies) and the methylated enriched DNA was purified by standard phenol/chloroform procedure and precipitated with isopropanol.'; [Cell type]'Source: ''gender: Female; tissue: Breast cancer FFPE tissue; mutation: BRCA 2 458stop; antibody: none; ', 'gender: Female; tissue: Breast cancer FFPE tissue; mutation: BRCA 2 458stop; antibody: anti-5-MethylCytosine; ', 'gender: Female; tissue: Breast cancer FFPE tissue; mutation: BRCA X; antibody: none; ', 'gender: Female; tissue: Breast cancer FFPE tissue; mutation: BRCA X; antibody: anti-5-MethylCytosine; ', 'gender: Female; tissue: Breast cancer FFPE tissue; mutation: BRCA 2 T703N; antibody: none; ', 'gender: Female; tissue: Breast cancer FFPE tissue; mutation: BRCA 2 T703N; antibody: anti-5-MethylCytosine; ', 'gender: Female; tissue: Breast cancer FFPE tissue; mutation: BRCA 1 C64R; antibody: none; ', 'gender: Female; tissue: Breast cancer FFPE tissue; mutation: BRCA 1 C64R; antibody: anti-5-MethylCytosine; ', 'gender: Female; tissue: Breast cancer FFPE tissue; mutation: BRCA 2 Q2960X; antibody: none; ', 'gender: Female; tissue: Breast cancer FFPE tissue; mutation: BRCA 2 Q2960X; antibody: anti-5-MethylCytosine; ', 'gender: Female; tissue: Breast cancer FFPE tissue; mutation: BRCA1 M1652I; antibody: none; ', 'gender: Female; tissue: Breast cancer FFPE tissue; mutation: BRCA1 M1652I; antibody: anti-5-MethylCytosine; ', 'gender: Male; tissue: Breast cancer FFPE tissue; mutation: BRCA 2 delA9158FS + 29 stop; antibody: none; ', 'gender: Male; tissue: Breast cancer FFPE tissue; mutation: BRCA 2 delA9158FS + 29 stop; antibody: anti-5-MethylCytosine; ', 'gender: Male; tissue: Breast cancer FFPE tissue; mutation: BRCA X; antibody: none; ', 'gender: Male; tissue: Breast cancer FFPE tissue; mutation: BRCA X; antibody: anti-5-MethylCytosine; ' GSE81373 Homo sapiens 4 Expression profiling by array GPL21185 Small extracellular vesicles secreted from senescent cells promote cancer cell proliferation through EphA2. 2016-05-12 Cellular senescence prevents the proliferation of cells at risk for neoplastic transformation. However, the altered secretome of senescent cells can promote the growth of the surrounding cancer cells. Although extracellular vesicles (EVs) have emerged as new players in intercellular communication, their role in the function of senescent cell secretome has been largely unexplored. Here, we show that exosome-like small EVs (sEVs) are important mediators of the pro-tumorigenic function of senescent cells. sEV-associated EphA2 secreted from senescent cells binds to ephrin-A1 that is highly expressed in several types of cancer cells and promotes cell proliferation through EphA2/ephrin-A1 reverse signalling. sEV sorting of EphA2 is increased in senescent cells due to its enhanced phosphorylation resulting from oxidative inactivation of PTP1B phosphatase. Our results demonstrate a novel mechanism of reactive oxygen species (ROS)-regulated cargo sorting into sEVs, which is critical for the potentially deleterious growth-promoting effect of the senescent cell secretome. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE81373 Small extracellular vesicles secreted from senescent cells promote cancer cell proliferation through EphA2. Nature communications 11.878 https://doi.org/10.1038/ncomms15728 {Nature communications (11.878): 10.1038/ncomms15728} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA321401 https://www.ebi.ac.uk/ena/browser/view/PRJNA321401 None [Overal design]To investigate the function of sEV-associated EphA2, we cultured breast cancer cell line MCF7 in the conditioned medium (CM) prepared from doxorubicin-induced senescent RPE1 expressing control or two different EphA2 shRNA. The effects of sEV-associated EphA2 on the gene expression profile of MCF7 were investigated using microarray. Microarray experiments were conducted using SurePrint G3 Human GE microarray 8 x 60K ver 2.0 (Agilent). Total RNA was isolated by Trizol Reagent. cDNA labelling, hybridizations, and scanning were performed by DNA ChiP Research Inc. (Japan), an Agilent-certified service provider. Data were then normalized to 75th percentile for inter-array comparison.; [Treatment]'Cells were cultured in control 10%FBS/DMEM or CM prepared from doxorubicin-treated RPE1 expressing control or two different EphA2 shRNA.'; [Growth]'Cells were cultured under atmospheric oxygen.'; [Extraction]'Total RNA was isolated by Trizol Reagent.'; [Cell type]'Source: ''cell line: breast cancer cell line MCF7; culture protocol: control medium; ', 'cell line: breast cancer cell line MCF7; culture protocol: conditioned medium prepared from senescent RPE1 expressing non-targeting shRNA; ', 'cell line: breast cancer cell line MCF7; culture protocol: conditioned medium prepared from senescent RPE1 expressing shEphA2-1; ', 'cell line: breast cancer cell line MCF7; culture protocol: conditioned medium prepared from senescent RPE1 expressing shEphA2-2; ' GSE120756 Homo sapiens 79 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing GPL18573 TET2 coactivates gene expression through demethylation of enhancers 2018-10-02 The tet methylcytosine dioxygenase 2 (TET2) enzyme catalyzes the conversion of the modified DNA base 5-methylcytosine to 5-hydroxymethylcytosine. TET2 is frequently mutated or dysregulated in multiple human cancers, and loss of TET2 is associated with changes in DNA methylation patterns. Here, using newly developed TET2-specific antibodies and the estrogen response as a model system for studying the regulation of gene expression, we demonstrate that endogenous TET2 occupies active enhancers and facilitates the proper recruitment of ERalpha. Knockout of TET2 by CRISPR-CAS9 leads to a global increase of DNA-methylation at enhancers resulting in attenuation of the estrogen response. We further identified a positive feedback loop between TET2 and ERalpha, which further requires MLL3/COMPASS at these enhancers. Together, this study reveals an epigenetic axis coordinating a transcriptional program through enhancer activation via DNA demethylation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE120756 TET2 coactivates gene expression through demethylation of enhancers. Science advances 12.804 https://doi.org/10.1126/sciadv.aau6986 {Science advances (12.804): 10.1126/sciadv.aau6986} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA494397 https://www.ebi.ac.uk/ena/browser/view/PRJNA494397 https://www.ncbi.nlm.nih.gov/sra?term=SRP163132 [Overal design]To examine changes in histone modifications, ER-alpha occupancy, MLL3 occupancy, and gene expression changes after depletion of TET2 in human breast cancer cell lines.; [Treatment]'Cells were grown in phenored free DMEM and 5% of stripped FBS for 96 hours. Then the cells were treated with E2 for either 45 minutes (ChIP-seq) or 4 hours (RNA-seq).'; [Growth]'Cell medium was composed as follows: DMEM 1X (Thermo Fisher), 10% serum (Corning), 1X glutamine (Life Technologies), 1X penicillin/streptomycin (Life Technologies). Cells were grown in a CO2 incubator (5% CO2) at 37˚C.'; [Extraction]'RNA was extracted using QIAGEN RNeasy kit. DNA after ChIP protocol was isolated using QIAGEN PCR purification kit.\nChIP-sequencing libraries were prepared using the KAPA HTP Library Preparation Kit complemented with NEXTflex DNA Barcodes from Bioo Scientific. 10 ng of DNA was used as starting material for input and ip samples. Libraries were amplified using 13 cycles on the thermocycler. Post amplification libraries were size selected at 250- 450bp in length using Agencourt AMPure XP beads from Beckman Coulter. Libraries were validated using the Agilent High Sensitivity DNA Kit. RNA-sequencing libraries were prepared using the Illumina TruSeq Stranded Total RNA Preparation Kit with Ribo-Depletion. Input RNA quality was validated using the Agilent RNA 6000 Nano Kit. 200ng-1 µg of total RNA was used as starting material. Libraries were validated using the Agilent DNA 1000 Kit. For Bisulfite-seq, genomic DNA was quantified with a Qubit 3.0 instrument. ~250 ng of genomic DNA was then digested with the restriction endonuclease MspI (New England BioLabs). Resulting fragments underwent size selection for fragments ~100-250-bp in length using SPRI beads (MagBio Genomics) and subsequent bisulfite conversion using the EZ DNA Methylation-Lightning Kit (Zymo Research) per the manufacturer’s protocol. Bisulfite conversion efficiency averaged > 99% as estimated by the measured percent of unmethylated CpGs in λ-bacteriophage DNA (New England BioLabs N3013S) added at a 1:200 ratio to each sample. Libraries for Illumina-based sequencing were prepared with the Pico Methyl-Seq Library Prep Kit (Zymo Research) using Illumina TruSeq DNA methylation barcodes. Libraries were run on a High Sensitivity chip using an Agilent TapeStation 4200 to assess size distribution and overall quality of the amplified library. Fluorometric quantitation and TapeStation size distribution estimates permitted equimolar pooling, and 6 pooled libraries per run were sequenced on an Illumina NextSeq 500 instrument using the NextSeq 500/550 V2 High Output reagent kit (1 x 75 cycles).'; [Cell type]'Breast cancer cell''cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); treatment: DMSO; chip antibody: anti-ERa (Santa Cruz Biotechnology, sc-543); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); treatment: DMSO; chip antibody: none; ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); treatment: E2; chip antibody: anti-ERa (Santa Cruz Biotechnology, sc-543); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); treatment: E2; chip antibody: none; ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: TET2 knockout; passages: Low passages (6-10); treatment: DMSO; chip antibody: anti-ERa (Santa Cruz Biotechnology, sc-543); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: TET2 knockout; passages: Low passages (6-10); treatment: DMSO; chip antibody: none; ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: TET2 knockout; passages: Low passages (6-10); treatment: E2; chip antibody: anti-ERa (Santa Cruz Biotechnology, sc-543); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: TET2 knockout; passages: Low passages (6-10); treatment: E2; chip antibody: none; ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); chip antibody: TET2_NTD (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: TET2 knockout; passages: Low passages (6-10); chip antibody: TET2_NTD (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); treatment: DMSO; chip antibody: anti-H3K4me3 (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); treatment: E2; chip antibody: anti-H3K4me3 (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); treatment: DMSO; chip antibody: anti-TET2_NTD (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); treatment: Tamoxifen; chip antibody: anti-TET2_NTD (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); treatment: DMSO; chip antibody: anti-MLL3 (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); treatment: E2; chip antibody: anti-MLL3 (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); treatment: DMSO; chip antibody: anti-H3K4me1 (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); treatment: E2; chip antibody: anti-H3K4me1 (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); treatment: DMSO; chip antibody: anti-H3k27Ac (Cell Signaling Technology); ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); treatment: E2; chip antibody: anti-H3k27Ac (Cell Signaling Technology); ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); treatment: DMSO; chip antibody: none; ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); treatment: E2; chip antibody: none; ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); shRNA: Non-targeting; chip antibody: anti-MLL3 (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); shRNA: MLL3; chip antibody: anti-MLL3 (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); shRNA: Non-targeting; chip antibody: none; ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); shRNA: MLL3; chip antibody: none; ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Parental cells; passages: Low passages (6-10); chip antibody: anti-H3K4me3 (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Parental cells; passages: Low passages (6-10); chip antibody: anti-H3K27me3 (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); shRNA: TET2; chip antibody: anti-TET2_NTD (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); shRNA: TET2; chip antibody: none; ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); chip antibody: anti-TET2 (Cell Signaling Technology); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: TET2 knockout; passages: Low passages (6-10); chip antibody: anti-TET2 (Cell Signaling Technology); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); chip antibody: none; ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: TET2 knockout; passages: Low passages (6-10); chip antibody: none; ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Parental cells; passages: Low passages (6-10); chip antibody: anti-UTX (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Parental cells; passages: Low passages (6-10); chip antibody: anti-H3K4me1 (homemade); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Parental cells; passages: Low passages (6-10); chip antibody: anti-H3k27Ac (Cell Signaling Technology); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); treatment: DMSO; ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); treatment: E2; ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: TET2 knockout; passages: Low passages (6-10); treatment: DMSO; ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: TET2 knockout; passages: Low passages (6-10); treatment: E2; ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); treatment: DMSO; ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); treatment: Tamoxifen; ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); shRNA: Non-targeting; treatment: DMSO; ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); shRNA: Non-targeting; treatment: E2; ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); shRNA: MLL3; treatment: DMSO; ', 'cell line: MCF7; cell type: Breast cancer cell; passages: Low passages (6-10); shRNA: MLL3; treatment: E2; ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: TET2 knockout; passages: Low passages (6-10); ', 'cell line: CAL51; cell type: Breast cancer cell; genotype/variation: Wild type TET2; passages: Low passages (6-10); ', 'cell line: CAL51; cell type: Breast cancer cell; genotype/variation: TET2 knockout; passages: Low passages (6-10); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: Wild type MLL3; passages: Low passages (6-10); ', 'cell line: MCF7; cell type: Breast cancer cell; genotype/variation: MLL3 knockout; passages: Low passages (6-10); ' GSE155510 Homo sapiens 12 Other GPL18573 Systematic functional interrogation of human pseudogenes 2020-07-31 Human genome encodes >14,000 pseudogenes that are evolutionary relics and have long been considered as nonfunctional genomic elements. Emerging evidence suggests that pseudogene can exert important regulatory function. However, function of most pseudogenes remains unknown. To fill this gap, we developed an integrated computational pipeline and performed to date the first set of pseudogene-focused CRISPRi screens in human cells. Our screens identified >100 pseudogenes that are important for cell fitness, with a more cell-type specific function compared to parent genes. In addition, we discovered a cancer-testis unitary pseudogene MGAT4EP that interacts with FOXA1, a key regulator in luminal A breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE155510 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA649966 https://www.ebi.ac.uk/ena/browser/view/PRJNA649966 https://www.ncbi.nlm.nih.gov/sra?term=SRP274630 [Overal design]5703 sgRNAs target pseudogenes and 3727 sgRNAs target their parent genes were included in the library. The CRISPRi screen was conducted in MCF7 cell line. MGAT4EP expression was down-regulated by sgRNA in dcas9 expressed MCF7 cells, and then next generation sequencing was performed to identify MGAT4EP regulated genes.; [Treatment]'MCF7-dCas9 and MDA-MB-231-dCas9 cell lines were infected with lenti virus containing the sgRNA library'; [Growth]'MCF7-dCas9, MDA-MB-231-dCas9 cell lines were cultured in Dulbecco’s modified Eagle’s medium (DMEM, Hyclone #SH30022.01), supplemented with 10% Fetal Bovine Serum, and 1% penicillin/streptomycin. The authenticated MCF7 and MDA-MB-231 cells were cultured in RPMI-1640 (Hyclone #SH30027.1) supplemented with 10% FBS (Gibco #10437-028) and 1% penicillin/streptomycin (Corning # 30-002-CI). All cell lines were cultured in an incubator (Thermo, HEARCELL VIOS 160i) with 5% CO2 at 37 °C.'; [Extraction]'Total genomic DNA was extracted from MCF7 and MDA-MB-231 cells using QIAamp DNA Mini Kit.Total RNA was extracted from MCF7 cells using the RNeasy Mini kit.\nTwo rounds of PCR were employed to prepare the next-generation-sequencing (NGS)-ready sgRNA libraries with the KAPA HiFi HotStart ReadyMix (Roche # KK2602). The first-round PCR was conduced for 16 cycles, using 40 \uf06dg of input genomic DNA from each replicate at D0 or D21 as a template. The PCR product of different samples was pooled and 20 \uf06dl of the mixed product was used as a template for the second-round PCR, which was conducted for 12 cycles to incorporate Illumina barcode sequences. The final PCR product was purified from 2% agarose gel with QIAquick Gel Extraction Kit. Concentration of different libraries was measured using the Qubit dsDNA HS (High Sensitivity) Assay Kit (Thermo # Q32851) on a Qubit Fluorometer (Thermo fisher). Two ug of RNA was used for RNA-seq library construction with TruSeq Stranded mRNA Library Prep kit (Illumina # 20020594).'; [Cell type]'Source: ''cell line: MCF7; time point: Day 0; replicate: 1; ', 'cell line: MCF7; time point: Day 0; replicate: 2; ', 'cell line: MCF7; time point: Day 0; replicate: 3; ', 'cell line: MCF7; time point: Day 21; replicate: 1; ', 'cell line: MCF7; time point: Day 21; replicate: 2; ', 'cell line: MCF7; time point: Day 21; replicate: 3; ', 'cell line: MCF7; genotype/variation: negative control; ', 'cell line: MCF7; genotype/variation: MGAT4EP knockdown; ' GSE154541 Mus musculus 6 Expression profiling by high throughput sequencing GPL21626 RNA seq analysis of Nfe2 expressing 4T1 and TS/A cells 2020-07-16 We founed enhanced Nfe2 mRNA expression in bone tropic mouse breast cancer cell lines, 4T1.3, grown in a bone cavity, compared with in vitro culture condition. Thus, we examined about the function of Nfe2 in tumor growth in bone microenvironment in this study. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE154541 Involvement of a Transcription factor, Nfe2, in Breast Cancer Metastasis to Bone. Cancers 6.162 https://doi.org/10.3390/cancers12103003 {Cancers (6.162): 10.3390/cancers12103003} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA646634 https://www.ebi.ac.uk/ena/browser/view/PRJNA646634 https://www.ncbi.nlm.nih.gov/sra?term=SRP272196 [Overal design]Total RNA was extracted from mouse breast cancer cell lines 4T1 and TS/A cells which wre transduced Nfe2 gene. The resultant total RNAs were subjected to RNAseq.; [Treatment]'4T1 or TS/A cells which were transduced Nfe2 expressing vector or empty vector'; [Growth]'RPMI supplemented with 10% FCS'; [Extraction]'Total RNAs were extracted by using RNeasy Mini Kit (Qiagen).\nWe used TruSeq RNA Library Preparation Kit v2.'; [Cell type]'Mouse breast cancer cell line''strain background: BALB/c; cell line: 4T1; cell type: Mouse breast cancer cell line; transduced vector: Empty vector; ', 'strain background: BALB/c; cell line: 4T1; cell type: Mouse breast cancer cell line; transduced vector: Nfe2 expressing vector; ', 'strain background: BALB/c; cell line: TS/A; cell type: Mouse breast cancer cell line; transduced vector: Empty vector; ', 'strain background: BALB/c; cell line: TS/A; cell type: Mouse breast cancer cell line; transduced vector: Nfe2 expressing vector; ' GSE86861 Homo sapiens 10 Expression profiling by array GPL570 Global Gene Expression Analyses of Three BCC Subsets, Based on the Relative Level of Oct4A 2016-09-13 Despite education and aggressive treatment, breast cancer (BC) remains a clinical problem. BC cells (BCCs) can migrate early to metastatic sites where they may exist in cellular dormancy for decades. Presently, there are no consensus markers for cancer stem cells (CSCs) that are involved in tumor initiation and progression, and drug resistance. The current designation of CSCs might comprise similar tumor initiating cells, but at different developmental phase. In order to understand these differences, we developed a working hierarchy of BCCs. We initiated the studies in which three BCC subsets were selected based on the relative expressions of the stem cell-linked genes, Octamer4A (Oct4A). The sorted BCCs were subjected to array analyses using Affymetrix gene chip. Hierarchical clustering indicated distinct gene expression among the three subsets. Differential gene expressions of membrane proteins validated three novel genes, TMEM-98, GPR64 and FAT4. These three genes, in combination of known markers for CSCs, CD44, CD24, aldehyde dehydrogenase 1 (ALDH1) and Oct4A, were used to stratify BCCs led to a working hierarchy of BCCs. The validity of the hierarchical BCCs was applied to blood samples from patients, during relapse, and before and after treatment. These studies resulted in the patients grouped with distinct BCCs in the circulation. The relevance of the latter findings are discussed with regards to prediction of treatment response and time of BC relapse. The findings require a larger cohort of patients in a prospective multi-center study. The stratification could be important to understand treatment response, strategies for alternative approaches, and an understanding of the interaction between particular BCC subsets and the tissue microenvironment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE86861 Evaluation of a developmental hierarchy for breast cancer cells to assess risk-based patient selection for targeted treatment. Scientific reports 4.011 https://doi.org/10.1038/s41598-017-18834-5 {Scientific reports (4.011): 10.1038/s41598-017-18834-5} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA342796 https://www.ebi.ac.uk/ena/browser/view/PRJNA342796 None [Overal design]MDA-MB-231 cells were transfected with pEGFP1-Oct3/4 and then selected with neomycin. Three groups of cells were isolated with the FACSDiva cell sorter. The top and lowest 5% of cells according to GFP expression were designated as Oct4hi and Oct4low while the Oct4med cells were in the middle of the two extreme subsets. Cells were counted and processed in quadruplicate in a random order. Due to limited reagents only duplicates of the Oct4med cells were processed.; [Treatment]'Stable transfectants were sorted based on GFP intensity using the FACSDiva (BD Biosciences). Sorting was done using the top and lower 5% GFP cells and the population in the middle of the two extreme subsets and were designated Oct4hi, Oct4med and Oct4lo.'; [Growth]'MDA-MB-231 cells from ATCC were transfected with pEGFP1-Oct3/4 and then selected with neomycin'; [Extraction]'Total RNA was isolated using the Qiagen RNeasy Mini Kit (Qiagen) and quality was assessed on the Agilent Bioanalyzer 2100.'; [Cell type]'Source: ''cell line: MDA-MB-231; tissue: Breast cancer cell derived from metastatic site; phenotype: MDA-MB-231 with OCT4-low; ', 'cell line: MDA-MB-231; tissue: Breast cancer cell derived from metastatic site; phenotype: MDA-MB-231 with OCT4-Medium; ', 'cell line: MDA-MB-231; tissue: Breast cancer cell derived from metastatic site; phenotype: MDA-MB-231 with OCT4-high; ' GSE124030 Homo sapiens 7 Expression profiling by high throughput sequencing GPL16791 Genome-wide maps of DNA methylation and gene expression for multiple regions within a breast tumor [RNA-Seq] 2018-12-18 As the differentiation state of the cells is affected by epigenetic modification regulation, the abnormal epigenetic modification is an important factor leading to the intratumoral heterogeneity. To further understand of the intratumoral epigenetic heterogeneity, we performed Reduced Representation Bisulfite Sequencing and RNA sequencing for multiple regions within a breast tumor and exhibited the epigenetic maps of different regions. We detected intratumoral heterogeneity-related molecular features and further explored the correlation between tumor heterogeneity and tumor hypoxic microenvironment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124030 Intratumor heterogeneity of breast cancer detected by epialleles shows association with hypoxic microenvironment. Theranostics 8.063 https://doi.org/10.7150/thno.53737 {Theranostics (8.063): 10.7150/thno.53737} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA510705 https://www.ebi.ac.uk/ena/browser/view/PRJNA510705 https://www.ncbi.nlm.nih.gov/sra?term=SRP173942 [Overal design]Our tumor samples were derived from a patient with HER2 breast invasive ductal carcinoma at stage II. The size of tumor was 45 mm×22 mm and the patient was without prior neoadjuvant therapy. For RNA and DNA libraries preparation, the tissues of tumor center, 12 o'clock, 3 o'clock, 6 o'clock and 9 o'clock of tumor periphery as well as adjacent of the tumor were taken for 0.6 mg, respectively. Another case of normal breast tissue was used as a control. Totally, 7 samples were examined by RRBS and RNA sequencing.; [Treatment]'None'; [Growth]'None'; [Extraction]'Tissues were ground in liquid nitrogen, and total RNAs were extracted and checked for quality.\nThe RNA libraries were quantified using Qubit Instruments after PCR enrichment and cluster generated using a Start cBot instrument, and then were sequenced using Hiseq2500 platform.'; [Cell type]'Source: ''tissue: breast tumor; tissue location: tumor center; ', "tissue: breast tumor; tissue location: 3 o'clock of tumor periphery; ", "tissue: breast tumor; tissue location: 6 o'clock of tumor periphery; ", "tissue: breast tumor; tissue location: 9 o'clock of tumor periphery; ", "tissue: breast tumor; tissue location: 12 o'clock of tumor periphery; ", 'tissue: adjacent tumor; ', 'tissue: normal breast tissue; ' GSE93892 Mus musculus 8 Expression profiling by array GPL16570 An ErbB2/c-Src axis drives mammary tumorigenesis through metabolically directed translational regulation of Polycomb Repressor Complex 2 [array] 2017-01-20 Perturbations in histone modifications alter transcription and promote carcinogenesis. Breast cancers frequently overexpress the histone methyltransferase EZH2, the catalytic subunit of Polycomb Repressor Complex 2 (PRC2). However, the mechanisms driving EZH2 overexpression are obscure and elucidating the role of PRC2 in breast cancer, which is highly heterogeneous, is challenging given its context-dependent oncogenic and tumor suppressive functions. Here, using genetically engineered mouse, PDX and cell line models, we show that the tyrosine kinase c-Src links energy sufficiency with PRC2 subunit overexpression via control of mRNA translation. In breast cancers initiated by the oncogene ErbB2, c-Src stimulates mitochondrial ATP production to suppress energy stress and permit sustained activation of the mammalian/mechanistic target of rapamycin complex 1 (mTORC1), which increases the translation of mRNAs encoding the PRC2 subunits Ezh2 and Suz12. We show that Ezh2 overexpression and activity are pivotal in ErbB2-mediated mammary tumorigenesis. These results reveal the hitherto unknown c-Src/mTORC1/PRC2 axis, which is essential for ErbB2-driven carcinogenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93892 An ErbB2/c-Src axis links bioenergetics with PRC2 translation to drive epigenetic reprogramming and mammary tumorigenesis. Nature communications 11.878 https://doi.org/10.1038/s41467-019-10681-4 {Nature communications (11.878): 10.1038/s41467-019-10681-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA362728 https://www.ebi.ac.uk/ena/browser/view/PRJNA362728 None [Overal design]We used microarrays to analyze transcriptional responses to c-Src ablation in the resulting c-Src-deficient mammary tumors. ErbB2-expressing tumors from mice without conditional Src alleles (hence expressing normal levels of c-Src) were used as the control. We extracted total RNA from four control tumors (MMTV-NIC/c-Src+/+) and four c-Src-deficient tumors (MMTV-NIC/c-SrcL/L) of equivalent size and subjected the RNA to Affymetrix microarray analysis.; [Treatment]'Mammary tumors were monitored by manual palpation and caliper measurements.'; [Growth]'Mammary tumors were excised from transgenic mice at tumor burden endpoint (total tumor burden 5cm3 or a single mass reaching 2.5cm3)'; [Extraction]"Qiagen Rneasy Mini Kit according to manufacturer's instructions"; [Cell type]'Source: ''strain: FVB/N; Sex: female; tissue: ErbB2-driven mammary tumor; genotype: MMTV-NIC; ', 'strain: FVB/N; Sex: female; tissue: ErbB2-driven mammary tumor; genotype: MMTV-NIC, FloxSrc Homozygous; ' GSE150319 Homo sapiens 6 Expression profiling by high throughput sequencing GPL18573 CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity [MDA-MB-231 RNA-seq] 2020-05-11 Epigenetic deregulation of gene transcription is central to cancer cell plasticity and malignant progression, but remains poorly understood. We found that the uncharacterized epigenetic factor Chromodomain on Y-like 2 (CDYL2) is commonly over-expressed in breast cancer, and that high CDYL2 levels correlate with poor prognosis. Supporting a functional role for CDYL2 in malignancy, it positively regulated breast cancer cell migration, invasion, stem-like phenotypes, and epithelial-to-mesenchymal transition (EMT). CDYL2 regulation of these plasticity-associated processes depended on signaling via p65/NF-kB and STAT3. This, in turn, was downstream of CDYL2 regulation of MIR124 gene transcription. CDYL2 co-immunoprecipitated with G9a/EHMT2 and GLP/EHMT1, and regulated the chromatin enrichment of G9a and EZH2 at MIR124 genes. We propose that CDYL2 contributes to poor prognosis in breast cancer by recruiting G9a and EZH2 to epigenetically repress MIR124 genes, thereby promoting NF-kB and STAT3 signaling, as well as downstream cancer cell plasticity and malignant progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE150319 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA631763 https://www.ebi.ac.uk/ena/browser/view/PRJNA631763 https://www.ncbi.nlm.nih.gov/sra?term=SRP261153 [Overal design]RNA was extracted from MDA-MB-231 cells transietly transfected with either CDYL2 siRNA or a control siLuciferase RNAi and differentially expressed genes identified.; [Treatment]"MDA-MB-231 cells were transfected with CDYL2 esiRNA (Sigma, EHU042511) or esiLuciferase (Sigma, EHUFLUC) using Interferin reagent (Polyplus, 409-10) according to the manufacturer's instructions. RNA was extracted 72h post-transfection."; [Growth]'MDA-MB-231 cells (ATCC, HTB-26) were grown in DMEM GlutaMAX (Gibco, 10566016) supplemented with 10 % of FBS (Gibco, 10270-106), 1 % penicillin/streptomycin (Gibco, 15140122). Cells were grown at 37°C and 5% CO2\xa0in a humidified incubator and passaged every 2 – 4 days by trypsinization. Cells were regularly tested for mycoplasma using a commercial kit (ATCC, 30-1012K), and cultures renewed from low passage stocks every two months or less.'; [Extraction]'RNA was extracted from sub-confluent cells using TRI-reagent (Sigma, T9424).\nRNA libraries were prepared with the TruSeq Stranded Total-RNA kit (Illumina).'; [Cell type]'Source: ''tissue: Breast cancer; transfection: Control; ', 'tissue: Breast cancer; transfection: CDYL2; ' GSE55649 Homo sapiens 6 Expression profiling by array GPL10558 Role of Ubc13 in Breast Cancer Metastasis 2014-03-06 We recently found that Ubc13 controls breast cancer metastasis. However, the underlying molecular mechanisms remain elusive. In order to gain a better understanding of the signaling pathways controlled by Ubc13 in metastasis, we performed a gene array analysis on xenografts derived from orthotopically implanted MDA-MB-231 LM2 cells, which preferentially metastazize to lung in NOD/SCID mice. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55649 Ubiquitin-conjugating enzyme Ubc13 controls breast cancer metastasis through a TAK1-p38 MAP kinase cascade. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1414358111 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1414358111} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA241030 https://www.ebi.ac.uk/ena/browser/view/PRJNA241030 None [Overal design]MDA-MB-231 LM2 cells were infected with lentivial shRNA constructs targeting either GFP (Control) or Ubc13 (ubc13). The resulting Control or Ubc13-silenced cells were implanted into fat pads of six weeks old female virgin NOD/SCID mice. After eight weeks, tumors were excised, followed by collagenase/hyaluronidase digestion to establish single cell suspension, from which epithelial cells were enriched by depleting mouse cells of hematopoietic, endothelial, and fibroblast origin (CD45, TER119, CD31 and BP-1). The enrihced epithelial cells (three Control and three Ubc13-KD cells) were lysed in TRIZOL to extract RNA, which were then used to run microarray.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted from cells using an RNAasy Mini Kit (Qiagen) as per manufacturers specifications. Extracted RNA was quantified on a Bioanalyser (Agilent) for quality control and used subsequently in microarray assay.'; [Cell type]'Source: ''sh transfrection: GFP; cell line: MDA-MB-231; ', 'sh transfrection: ubc13; cell line: MDA-MB-231; ' GSE141834 Homo sapiens 26 Expression profiling by high throughput sequencing GPL24676 Transcriptional Heterogeneity within the Glucocorticoid Response 2019-12-11 Steroid hormone receptors such as the Glucocorticoid Receptor (GR) mediate the transcriptional response to hormones and are frequently targeted in the treatment of human diseases. Experiments using bulk populations of cells have provided a detailed picture of the global transcriptional hormone response but are unable to interrogate cell-to-cell transcriptional heterogeneity. To examine the glucocorticoid response in individual cells, we performed single cell RNA sequencing (scRNAseq). The transcriptional response to hormone was robustly detected in individual cells and scRNAseq provided additional statistical power to identify over 100 GR-regulated genes that were not detected in bulk RNAseq. scRNAseq also revealed a large degree of cell-to-cell variability in the hormone response. On average, individual hormone-treated cells showed a response at only 30% of the total set of GR target genes. Understanding the basis of this heterogeneity will be critical for the development of more precise models of steroid hormone signaling. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE141834 Single-cell RNA sequencing reveals a heterogeneous response to Glucocorticoids in breast cancer cells. Communications biology 0.12 https://doi.org/10.1038/s42003-020-0837-0 {Communications biology (0.12): 10.1038/s42003-020-0837-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA594939 https://www.ebi.ac.uk/ena/browser/view/PRJNA594939 https://www.ncbi.nlm.nih.gov/sra?term=SRP236872 [Overal design]Single-cell RNAseq and bulk total RNAseq in A1-2 human breast cancer cells; [Treatment]'For Dexamethasone treatments, cells were initially cultured for 24 hours in reduced-serum, hormone-stripped media (Phenol-red free MEM (Gibco 51200) with 5% Charcoal/Dextran treated FBS (Atlanta S11650), 1X Penicillin/Streptomycin (Sigma P0781), 1% HEPES (Sigma H0887), 1X Glutamax (Gibco 35050), and 250 ug/ml G418 (Gibco 10131)). Subsequently, Dexamethasone (Sigma D4902) was added to the media at 100 nM for all treatments timepoints and 9.5 x 10e-4% ethanol was used as vehicle control. For both RNAseq experiments, control cells were treated with ethanol for 18 hours.'; [Growth]'Cells were cultured in modified Eagle medium (MEM) containing 10% fetal bovine serum, 1X Penicillin/Streptomycin (Sigma P0781), 1% HEPES (Sigma H0887), 1X Glutamax (Gibco 35050), and 250 ug/ml G418 (Gibco 10131).'; [Extraction]'For bulk RNAseq, Qiagen RNeasy kits with on-column DNase treatment were used to isolate total RNA. For single-cell RNAseq, cells were dissociated using 0.25% Trypsin-EDTA (Gibco 25200) into single cell suspension and the BioRad ddSeq Single-Cell Isolator was used to create single cell emulsions\nBulk RNAseq libraries were generated using Ribo-Zero Gold and the Illumina TruSeq RNA Stranded kit. Single-cell RNAseq libraries were generated using the Illumina SureCell WTA 3’ Library Prep kit'; [Cell type]'A1-2 breast cancer cells''cell type: A1-2 breast cancer cells; treatment: 18hr EtOH; ', 'cell type: A1-2 breast cancer cells; treatment: 1hr Dex; ', 'cell type: A1-2 breast cancer cells; treatment: 2hr Dex; ', 'cell type: A1-2 breast cancer cells; treatment: 4hr Dex; ', 'cell type: A1-2 breast cancer cells; treatment: 8hr Dex; ', 'cell type: A1-2 breast cancer cells; treatment: 18hr Dex; ' GSE30763 Homo sapiens 6 Non-coding RNA profiling by array GPL7723 Integration of BRCA1-mediated miRNA and mRNA signatures reveal miR-146a, miR-99b and miR-205 regulation of the TRAF2 and NFkB pathways (miRNA dataset) 2011-07-18 Microarray‐based techniques are being used to obtain miRNA and gene expression signatures associated with different samples. In order to deepen our understanding of BRCA1-associated tumorigenesis, we integrated data from microarray experiments to obtain significant miRNA-mRNA relationships associated with the presence of the BRCA1 gene. We obtained significant miRNA-gene-pathway relationships underlying the array signatures. Furthermore, we have demonstrated that miR-146a, miR-99b and miR-205, induced in HCC1937 BRCA1-expressing cells, commonly regulate the TRAF2 gene, a key regulator of NF-κB and MAPK pathways. In addition, re-expression of miR-146a, miR-99b or miR-205 in HCC1937 BRCA1-null cells was sufficient to modulate NF-κB activity. Thus, integration between miRNA-mRNA expression data allowed us to define genes and pathways controlled by miRNAs induced in the context of BRCA1 expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE30763 Integration of BRCA1-mediated miRNA and mRNA profiles reveals microRNA regulation of TRAF2 and NFκB pathway. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-011-1905-4 {Breast cancer research and treatment (3.471): 10.1007/s10549-011-1905-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA154713 https://www.ebi.ac.uk/ena/browser/view/PRJNA154713 None [Overal design]Comparison of miRNA expression profiles between two isogenic cell lines differing in BRCA1 gene expression status. Single-color experiments in a pairwise comparison design with three technical replicates per cell line.; [Treatment]'None'; [Growth]'Cell lines were grown in 10% FBS DMEM media with 2% penicillin/streptomycin at 37ºC, 5% CO2 atmosphere and 80% humidity.'; [Extraction]"Total RNA was extracted from cell pellets using Trizol following the manufacturer's recommendations."; [Cell type]'breast cancer cells''cell line: HCC1937/BRCA1; cell type: breast cancer cells; brca1 expression: yes; ', 'cell line: HCC1937; cell type: breast cancer cells; brca1 expression: no; ' GSE49333 Homo sapiens 10 Genome binding/occupancy profiling by genome tiling array GPL15802 Mapping of somatic linker histone H1 variants in T47D-MTVL and HeLa cells 2013-07-29 At least six histone H1 variants exist in mammalian somatic cells that bind to the linker DNA and stabilize the nucleosome particle contributing to higher order chromatin compaction. In addition, H1 seems to be involved in the active regulation of gene expression. It is not well known whether the different variants have specific roles, are distributed differentially along the genome, or regulate specific promoters. By taking advantage of specific antibodies to H1 variants and HA-tagged recombinant H1 variants expressed in a breast cancer-derived cell line, we have investigated the distribution of the different somatic H1 variants (H1.2 to H1.5, H1.0 and H1X) in particular promoters and genome-wide. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE49333 Mapping of six somatic linker histone H1 variants in human breast cancer cells uncovers specific features of H1.2. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gku079 {Nucleic acids research (11.147) doi:10.1093/nar/gku079}; {The Journal of biological chemistry (None) doi:10.1074/jbc.M114.617324}; 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA213642 https://www.ebi.ac.uk/ena/browser/view/PRJNA213642 None [Overal design]Analysis of H1 (H1.0, H1.2, H1.3, H1.4, H1.5 and H1X) and H3 abundance in promoter regions; [Treatment]'None'; [Growth]'RPMI 1640 medium + 10%FBS, 1%glutamine, 1%penicillin/streptomycin', 'DMEM GlutaMax medium + 10%FBS, 1%penicillin/streptomycin'; [Extraction]'T47D-MTVL or HeLa cells cells were fixed using 1% formaldehyde, harvested and sonicated using a Diagenode Bioruptor to generate chromatin fragments between 200 and 500 bp. To perform the chromatin immunoprecipitation, 30 µg of chromatin was immunoprecipitated overnight using the indicated antibody. Rabbit IgG (Santa Cruz Biothechnology) was used as a control for nonspecific interaction of DNA. Input was prepared with 10% of the chromatin material used for an immunoprecipitation. Immunocomplexes were recovered using Protein A magnetic beads from Millipore. Beads with bound antibody/protein/DNA complexes were washed, decross-linked at 65ºC overnight and immunoprecipitated DNA was recovered using the IPure Kit from Diagenode.'; [Cell type]'Source: ''cell line: T47D-MTVL; stably overexpressing: H1.0-HA; gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-HA (Abcam 9110); ', 'cell line: T47D-MTVL; stably overexpressing: H1.0; gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'cell line: T47D-MTVL; stably overexpressing: H1.2-HA; gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H1.2 (Abcam 4086); ', 'cell line: T47D-MTVL; stably overexpressing: H1.2; gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'cell line: T47D-MTVL; gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H1.2 (Abcam 4086); ', 'cell line: T47D-MTVL; gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'cell line: T47D-MTVL; stably overexpressing: H1.3-HA; gender: female; tissue: breast cancer ductal carcinoma; antibody: H1.3-HA histone protein immunoprecipitated DNA; ', 'cell line: T47D-MTVL; stably overexpressing: H1.3; gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'cell line: T47D-MTVL; stably overexpressing: H1.4-HA; gender: female; tissue: breast cancer ductal carcinoma; antibody: H1.4-HA histone protein immunoprecipitated DNA; ', 'cell line: T47D-MTVL; stably overexpressing: H1.4; gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'cell line: T47D-MTVL; stably overexpressing: H1.5-HA; gender: female; tissue: breast cancer ductal carcinoma; antibody: H1.5-HA histone protein immunoprecipitated DNA; ', 'cell line: T47D-MTVL; stably overexpressing: H1.5; gender: female; tissue: breast cancer ductal carcinoma; antibody: none; ', 'cell line: T47D-MTVL; gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H1X (Abcam 31972); ', 'cell line: T47D-MTVL; gender: female; tissue: breast cancer ductal carcinoma; antibody: anti-H3 (Abcam 1791); ', 'cell line: HeLa; gender: female; tissue: cervical cancer; antibody: anti-H1.2 (Abcam 4086); ', 'cell line: HeLa; gender: female; tissue: cervical cancer; antibody: none; ', 'cell line: HeLa; gender: female; tissue: cervical cancer; antibody: anti-H1X (Abcam 31972); ' GSE120796 Homo sapiens 8 Expression profiling by high throughput sequencing GPL20301 Next-generation RNA sequencing to determine changes in gene expression during breast cancer progression 2018-10-03 Purpose: The goal of the study is to compare NGS-derived transcriptome in an isogenic breast cancer progression model cell line system. By comparing the protein-coding and noncoding gene expression of normal versus tumorigenic breast cancer cell lines, we will be able to identify genes that show aberrant expression during breast cancer progression. Methods: We isolated poly A + RNA from four isogenic mammary epithelial cell lines showing various stages of breast cancer progression. The model system comprises of 4 isogenic cell lines, categorized as M1-M4. M1 represents the normal, non-tumorigenic, immortalized MCF10A cells. Transfection of MCF10A with activated T24-HRAS and selection by xenografting generated the M2 (MCF10AT1k.cl2) cell line, which is highly proliferative and gives rise to premalignant lesions with the potential for neoplastic progression. M3 (MCF10Ca1h) and M4 (MCF10CA1a.cl1) were derived from occasional carcinomas arising from xenografts of M2 cells. M3 gives predominantly well-differentiated low-grade carcinomas on xenografting, while M4 gives rise to relatively undifferentiated carcinomas and colonizes to the lung upon injection of these cells into the tail vein. We performed paired-end deep sequencing (190-260 million reads/sample) of poly A+ RNA isolated from these cells that were cultured as 3D acini in biological duplicates. Reads of the samples were trimmed for adapters and low-quality bases using Trimmomatic software before alignment with the reference genome (Human - hg19) and the annotated transcripts using STAR. The average mapping rate of all samples is 96%. Unique alignment is above 87%. There are 3.74 to 4.07% unmapped reads. The mapping statistics are calculated using Picard software. The samples have 0.59% ribosomal bases. Percent coding bases are between 67-72%. Percent UTR bases are 23-26%, and mRNA bases are between 94-96% for all the samples. Library complexity is measured in terms of unique fragments in the mapped reads using Picard’s MarkDuplicate utility. The samples have 31-52% non-duplicate reads. In addition, the gene expression quantification analysis was performed for all samples using STAR/RSEM tools. Both the normalized count and the raw count are provided as part of the data delivery. Results: Using an optimised data analysis workflow, we mapped ~190-250 million reads/sample and identified expression of 17396 protein-coding genes and 11509 long noncoding RNA genes. We initially compared gene expression between M1 and M4 cells. 4668 genes (2815 protein coding and 1853 lncRNAs) showed ~2 fold change in their expression between M1 and M4 cells in both biological repeats. 1159 out of the 1853 deregulated lncRNAs showed 2-fold upregulation in M4 cells in both repeats. On the other hand, 694 of lncRNAs displayed reduced levels in M4 compared to M1 cells. Further, we noticed that natural antisense transcripts (NATs) comprised one of the largest types of lncRNAs (504 out of 1853) that showed deregulation in M4 cells. Conclusion: Our study revealed differential expression of thousands of protein-coding and long noncoding RNAs during breast cancer progression using the isogenic cell line model system. This data set will act as a rich resource for downstream mechanistic studies to determine the role of these differentially expressed genes in breast cancer progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE120796 A natural antisense lncRNA controls breast cancer progression by promoting tumor suppressor gene mRNA stability. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1007802 {PLoS genetics (5.224): 10.1371/journal.pgen.1007802} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA494563 https://www.ebi.ac.uk/ena/browser/view/PRJNA494563 https://www.ncbi.nlm.nih.gov/sra?term=SRP163265 [Overal design]Poly A+ RNA from M1, M2, M3 and M4 cells (all grown in 3D acini in matrigel as biological duplicates) for 8-10 days were sequenced on HiSeq using Illumina TruSeq mRNA Prep Kit RS-122-2101 and paired-end sequencing. The samples have 163 to 256 million pass filter reads with a base call quality of above 94% of bases with Q30 and above.; [Treatment]'None'; [Growth]'Acinar culture of M1-M4 cells was performed similar to three-dimensional culture of MCF10A cells. Briefly, growth-factor reduced Matrigel was used to coat multi-well plates. A single-cell suspension of each of the cell lines M1-M4 was prepared. M1-M2 cells were suspended in an assay medium containing growth medium (DMEM/F12 containing 2% Horse serum, 1 mg/ml hydrocortisone, 1 mg/ml cholera toxin, 10 mg/ml insulin, 10 ng/ml EGF, and 1% penicillin/streptomycin as well as 2.5% Matrigel dissolved in the medium). M3-M4 cells are prepared in the same way but omitting the EGF in the medium. The cells were seeded at a concentration of 8000 cells/mL. Media was changed every fourth day. Cells were cultured for 8 days prior to harvesting.'; [Extraction]'Trizol reagent (Invitrogen) was used to extract total RNA according to manufacturer’s protocol. The concentration was measured using Nanodrop instrument (ThermoFisher SCIENTIFIC). RNA was treated with RNase-free DNase I (Sigma, USA).\n8 mRNA-seq samples were pooled and sequenced on HiSeq using Illumina TruSeq mRNA Prep Kit RS-122-2101 and paired-end sequencing.'; [Cell type]'mammary epithelial cells', 'M2-derived cells', 'M1-derived cells''cell line: MCF10A; cell type: mammary epithelial cells; ', 'cell line: MCF10Ca1h; cell type: M2-derived cells; ', 'cell line: MCF10CA1a.cl1; cell type: M2-derived cells; ', 'cell line: MCF10AT1k.cl2; cell type: M1-derived cells; ' GSE41972 Homo sapiens 6 Expression profiling by array GPL570 In vivo NCL-targeting affects breast cancer aggressiveness through miRNA regulation [Affymetrix] 2012-11-01 Numerous studies have described the altered expression and the causal role of miRNAs in human cancer. However, to date efforts to modulate miRNA levels for therapeutic purposes have been challenging to implement. Here, we find that Nucleolin (NCL), a major nucleolar protein, post-transcriptionally regulates the expression of a specific subset of miRNAs, including miR-21, miR-221, miR-222, and miR-103, causally involved in breast cancer initiation, progression and drug-resistance. We also show that NCL is commonly overexpressed in human breast tumors, and its expression correlates with that of NCL-dependent miRNAs. Finally, this study indicates that NCL-binding guanosine-rich aptamers affect the levels of NCL-dependent miRNAs and their target genes, reducing breast cancer cell aggressiveness, both in vitro and in vivo. These findings illuminate a path to novel therapeutic approaches based on NCL-targeting aptamers for the modulation of miRNA expression in the treatment of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41972 In vivo NCL targeting affects breast cancer aggressiveness through miRNA regulation. The Journal of experimental medicine 10.892 https://doi.org/10.1084/jem.20120950 {The Journal of experimental medicine (10.892): 10.1084/jem.20120950} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA178628 https://www.ebi.ac.uk/ena/browser/view/PRJNA178628 None [Overal design]MCF7 cells were treated with the control drug or AS1411 aptamer. After 72hours total RNA was collected and analyzed by Affymetrix U133 plus.; [Treatment]'MCF7 cells were treated with the control drug or AS1411 aptamer. After 72hours total RNA was collected and analyzed by Affymetrix U133 plus.'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MCF7; ' GSE28274 Homo sapiens 6 Expression profiling by array GPL570 Real-time Monitoring of Cisplatin Toxicity on Cancer Cells 2011-03-30 Treatment of MCF7 breast cancer cells by cisplatin leads to a very specific metabolic response and an onset of cell death about 10-11 h after beginning of treatment. For more detailed understanding of the molecular processes underlying the specific metabolic response, mRNA was isolated from MCF7 cells when the specific changes, (i) induction of glycolysis and (ii) onset of cell death, were detected during online measurement in the cell biosensor system. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28274 Real-time monitoring of cisplatin-induced cell death. PloS one 2.776 https://doi.org/10.1371/journal.pone.0019714 {PloS one (2.776): 10.1371/journal.pone.0019714} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA139373 https://www.ebi.ac.uk/ena/browser/view/PRJNA139373 None [Overal design]MCF7 breast cancer cells were treated with cisplatin in the BIONAS 2500 cell biosensor chip system, and samples were collected from the biosensor chip module at time points when glycolysis was induced (change of ph; 8-9h) and at the beginning of cell death (change of impedance; 10-11h).; [Treatment]'Drug activity testing: (a) 5 h equilibration with RM with and 8-min cycles (4 min exchange of medium and 4 min without flow); (b) drug incubation with freshly dissolved cisplatin at indicated concentration and the same 8-min cycles (4 min stop/ 4 min flow) for indicated time.'; [Growth]'Cells were first grown on BIONAS SC100 sensor chips in DMEM (pen/strep; 10% FCS) and incubated in a standard tissue culture incubator at 37 °C, 5% CO2, and 95% humidity for 24 h until 80–90% confluence. Sensor chips with cells were then transferred to Bionas 2500 workstation in which medium is continuously exchanged in 8-min cycles (4 min exchange of medium and 4 min without flow) during which metabolic parameters were measured. Running medium (RM) used during analysis was DMEM without carbonate buffer (PAN Cat. Nr. P03-0010), weakly buffered with 1 mM Hepes, reduced FCS (0.1%) and low glucose (1 g/l).'; [Extraction]'Cell lysis for RNA extraction was done directly on biosensor at indicated time points, using RNeasy Mini Kit (Qiagen) according to the manufacturer’s instructions. RNA quality was examined by agarose gel electrophoresis and concentration was determined by UV absorbance.'; [Cell type]'Source: ''cell line: MCF-7; ' GSE114421 Mus musculus 16 Non-coding RNA profiling by high throughput sequencing GPL21103 Paternal malnutrition programs offspring’s breast cancer risk and tumor metabolism in a mouse model (small RNA-seq) 2018-05-14 We found that LP daughters have lower birthweight, alterations in mammary gland morphology and higher rates of mammary cancer. Further, we found that mammary glands and tumors of LP daughters are metabolic rewired, with alterations in the AMPK and amino-acid metabolism pathways. These changes were associated with differential expression of miRNAs 451a, miR-200c and miR-92a. Importantly, some of the same miRNAs and target genes alterations were detected in breast tumors of women from populations with high rates of low birthweight. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE114421 Paternal malnutrition programs breast cancer risk and tumor metabolism in offspring. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-018-1034-7 {Breast cancer research : BCR (5.676): 10.1186/s13058-018-1034-7} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA471323 https://www.ebi.ac.uk/ena/browser/view/PRJNA471323 https://www.ncbi.nlm.nih.gov/sra?term=SRP145630 [Overal design]Male mice were fed AIN93G-based diets containing either 17.7% (control) or 8.9% (LP) energy from protein from 3 to 10 weeks of age. Males on either group were mated to females raised on a control diet. Female offspring from control and LP fathers were treated with 7,12-dimethylbenz[a]anthracene (DMBA) to initiate mammary carcinogenesis and used for mammary tissue collection. Mature sperm from fathers and normal mammary tissue from female offspring were used for RNA-seq analyses.; [Treatment]'Males were fed etiher a control or low-protein (LP) diet from 3 to 10 weeks of age.Mature sperm was collected from fathers and Mammary tissue from their female offspring.'; [Growth]'None'; [Extraction]"Mammary gland and sperm samples were removed.\xa0\xa0Frozen crushed tissue were\xa0used for\xa0RNA extraction\xa0according\xa0with the manufacturer's instructions. The total RNA was performed using\xa0miRNeasy\xa0Kit.\xa0\nRNA libraries were prepared for sequencing using standard Illumina protocols"; [Cell type]'Source: ''strain: C57BL/6; gender: female; tissue: mammary gland tissue; ', 'strain: C57BL/6; gender: male; tissue: mature sperm cells; ' GSE98012 Homo sapiens 44 Genome binding/occupancy profiling by high throughput sequencing GPL16791; GPL20301 Enhancer profiling in metastatic cancer [ChIP-Seq] 2017-04-20 Metastases cause the majority of cancer-related deaths. Yet, the origins of metastatic cancer phenotypes remain poorly understood. Few metastasis-specific driver mutations have been identified [1-3], raising the possibility that metastatic transcriptional programmes may emerge from perturbations in the oncogenic signalling cascades that support the development of primary tumours. Here, using genome-wide histone modification profiling, high-throughput chromatin conformation capture by Hi-C and functional analysis in human-derived metastasis models of renal and breast cancers, we identify transcriptional enhancers that drive metastatic cancer progression. We demonstrate that specific enhancers and enhancer clusters are activated in metastatic cancer cell populations. The activation status of these enhancers is associated with gene expression patterns predictive of poor patient outcome in clinical samples. CRISPRi-mediated inhibition of enhancer activity and genetic ablation of enhancer sequences demonstrated the requirement of metastasis-associated regulatory elements for metastatic colonization in vivo. We further show that metastatic cancer clones co-opt evolutionarily conserved enhancers that converge on shared metastasis driver genes, such as CXCR4. Thus, we provide functional evidence for the requirement of specific enhancers for metastatic colonization and show that metastatic traits can arise through tissue-specific commissioning of distal gene regulatory elements. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98012 NF-κB-Dependent Lymphoid Enhancer Co-option Promotes Renal Carcinoma Metastasis. Cancer discovery 26.370 https://doi.org/10.1158/2159-8290.CD-17-1211 {Cancer discovery (26.370): 10.1158/2159-8290.CD-17-1211} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA383670 https://www.ebi.ac.uk/ena/browser/view/PRJNA383670 https://www.ncbi.nlm.nih.gov/sra?term=SRP104404 [Overal design]Examination of 2 different histone modifications and transcription factors in experimental model systems of metastasis.; [Treatment]'None'; [Growth]'Cells grown under standard tissue culture conditions in RPMI + 10% FBS.Cells grown under standard tissue culture conditions in RPMI + 10% FBS.'; [Extraction]'Cells were crosslinked in 1% formaldehyde for 10min at room temperature, followed by 5 min quenching with 0.125M glycine. Cells were washed twice with PBS, the supernatant was aspirated and cell pellets were frozen in liquid nitrogen and stored at -80°C. 100µl of Protein A/G magnetic beads (Thermo 26162) were blocked with 0.5% BSA in PBS, followed by incubation with the antibody. Cross-linked cells were resuspendend and sonicated in lysis buffer (20 mM Tris-HCl pH 8.0, 150 mM NaCl, 2 mM EDTA pH 8.0, 0.1% SDS, and 1% Triton X-100). Sonication was performed using Bioruptor (Diagenode) for 14 cycles (30’’ on/ 30’’ off) at max output to obtain fragments of 100-500bp. Sonicated lysates were cleared and incubated overnight at 4°C with antibody-bound magnetic beads. Beads were sequentially washed three times with low salt buffer (50mM HEPES pH7.5, 140mM NaCl, 1% Triton) and once with high salt buffer (50mM HEPES pH7.5, 500mM NaCl, 1% Triton). DNA was eluted in elution buffer (50mM NaHCO3, 1%SDS) and cross-links were reversed for 3h (65°C, 1000rpm shaking). DNA was purified using the QuickClean II PCR Extraction Kit (Genescript L00419-100) according to the manufacturer’s recommendations and eluted with 100µl H2O.\nPurified ChIP DNA was used to prepare Illumina multiplexed sequencing libraries with the KAPA Hyper Prep Kit (KR0961) Illumina platforms sample preparation protocol (v1.14). Briefly, DNA was end-repaired and A-tailed to produce end-repaired, 5’-phosphorylated, 3’-dA-tailed, dsDNA fragments. These 3’-dA-tailed library fragments were then ligated with dsDNA adapters with 3’dTMP overhangs. After adapter ligation, libraries were size selected to 150-350bp using AMPure XP reagent (Agencourt A63880) according to the protocol recommendations. Size selected libraries were amplified for 15 cycles using the KAPA HiFi HotStart ReadyMix. PCR libraries were pooled in equimolar concentrations and sequenced.'; [Cell type]'Source: ''cell line type: breast cancer cell line; treatment: na; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: 1833-BoM; ', 'cell line type: breast cancer cell line; treatment: na; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: 4175-LM2; ', 'cell line type: renal cancer cell line; treatment: non-targeting CRISPRi; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: 786-M1A; ', 'cell line type: renal cancer cell line; treatment: CRISPRi – iMAE-1.1; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: 786-M1A; ', 'cell line type: renal cancer cell line; treatment: CRISPRi – iMAE-1.2; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: 786-M1A; ', 'cell line type: renal cancer cell line; treatment: CRISPRi – iMAE-126; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: 786-M1A; ', 'cell line type: renal cancer cell line; treatment: CRISPRi – iMAE-2; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: 786-M1A; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: 786-M1A; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: H3K4me1; antibody: ab8895 (Abcam); cell line: 786-M1A; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: HIF1B; antibody: NB100-110 (Novus); cell line: 786-M1A; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: na (input control); antibody: na; cell line: 786-M1A; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: p300; antibody: sc-585 (Santa Cruz); cell line: 786-M1A; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: 786-O; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: H3K4me1; antibody: ab8895 (Abcam); cell line: 786-O; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: HIF1B; antibody: NB100-110 (Novus); cell line: 786-O; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: na (input control); antibody: na; cell line: 786-O; ', 'cell line type: breast cancer cell line; treatment: na; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: MDA-MB-231; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: OS-LM1; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: HIF1B; antibody: NB100-110 (Novus); cell line: OS-LM1; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: na (input control); antibody: na; cell line: OS-LM1; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: OS-RC-2; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: HIF1B; antibody: NB100-110 (Novus); cell line: OS-RC-2; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: na (input control); antibody: na; cell line: OS-RC-2; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: 786-M2A; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: H3K27ac; antibody: ab4729 (Abcam); cell line: 786-M2B; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: HIF2A; antibody: ab199 (Abcam); cell line: 786-M1A; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: p65; antibody: ab16502 (Abcam); cell line: 786-M1A; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: HIF2A; antibody: ab199 (Abcam); cell line: 786-O; ', 'cell line type: renal cancer cell line; treatment: na; target molecule: p65; antibody: ab16502 (Abcam); cell line: 786-O; ' GSE97585 Homo sapiens 6 Genome binding/occupancy profiling by high throughput sequencing GPL20301 Next Generation Sequencing Facilitates Quantitative Analysis for H3K27ac mediated chromatin conformation capture of Wild Type and PVT1 Knockdown by CRISPRi in MDA-MB-231 human breast cancer cell line 2017-04-10 CRISPRi targeting PVT1 specifically decrease PVT1-MYC interaction https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE97585 Promoter of lncRNA Gene PVT1 Is a Tumor-Suppressor DNA Boundary Element. Cell 36.216 https://doi.org/10.1016/j.cell.2018.03.068 {Cell (36.216): 10.1016/j.cell.2018.03.068} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA382387 https://www.ebi.ac.uk/ena/browser/view/PRJNA382387 https://www.ncbi.nlm.nih.gov/sra?term=SRP103777 [Overal design]HiChIP performed with biological replicates for CRISPRi-PVT1 with H3K27ac; [Treatment]'lentivirus harboring mU6-sgRNA (control or PVT1 R2/R3). Selected by Puromycin 1 ug/ml for 4 days. Recovered for one day in media without Puromycin.'; [Growth]'Cultured in DMEM supplemented with 10% FBS + 1% pen-strep.'; [Extraction]'described in doi:10.1038/nmeth.3999 (2016)\nNextera'; [Cell type]'Source: ''cell line: MDA-MB-231; genotype: wild type; antibody: Abcam, #ab4729; ', 'cell line: MDA-MB-231; genotype: PVT1 Knockdown; antibody: Abcam, #ab4729; ' GSE7206 Homo sapiens 20 Expression profiling by array GPL4840 Gene expression profiling in T-47D breast cancer cells following inducible expression of estrogen receptor beta 2007-03-06 T-47D breast cancer cells were stably transfected with a tet-off inducible construct encoding estrogen receptor beta. Microarray experiments were carried out at multiple time points 1-30 hours following treatment with estradiol and under induction and non-induction conditions. Keywords: Inducible expression of ERbeta https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7206 Inhibitory effects of estrogen receptor beta on specific hormone-responsive gene expression and association with disease outcome in primary breast cancer. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr1667 {Breast cancer research : BCR (5.676): 10.1186/bcr1667} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA98323 https://www.ebi.ac.uk/ena/browser/view/PRJNA98323 None [Overal design]Single biological samples were taking at each time point for each of the four treatment condition (uninduced-untreated, induced-untreated, uninduced-treated, and induced-treated.; [Treatment]'None'; [Growth]'Cells were added to 150 mm plates at a confluency of 40%; after one day, the normal medium was replaced by the medium described above, supplemented with 5% dextran coated charcoal treated FBS (DCCFBS). After 24h, 10 nM ICI 182,780 was added to the cultures and incubation proceeded for an additional 48h. For expression of ERb, tetracycline was removed 12 h before initiation of treatment with 17b-estradiol. At time 0 h the medium was changed to 0.5% DCCFBS and 10 nM of 17b-estradiol or equivalent volume of DMSO for mock-treated controls were added.'; [Extraction]"Total RNA extracted using Trizol following manufacturer's instructions"; [Cell type]'Source: ''' GSE151072 Homo sapiens 9 Expression profiling by high throughput sequencing GPL16791 Transcriptional and functional analysis of CD1c+ human dendritic cells identifies a CD163+ subset priming CD8+CD103+ T cells [Breast_iLN] 2020-05-22 Dendritic cells (DC) are antigen presenting cells controlling T cell activation. In human, the diversity, ontogeny and functional capabilities of DC subsets are not fully understood. Here, we identified circulating CD88-CD1c+CD163+ DC (termed as DC3) as an immediate precursor of inflammatory CD88-CD14+CD1c+CD163+FcεRI+ DC. DC3 develop via a specific pathway activated by GM-CSF, independent from the cDC-restricted (CDP) and monocyte-restricted (cMoP) progenitors. As classical DC, but unlike monocytes, DC3 drove the activation of naïve T cells. In vitro, DC3 displayed a distinctive ability to prime CD8+ T cells expressing a tissue-homing signature and the epithelial homing alpha-E integrin (CD103) through transforming growth factor-b (TGF-β) signaling. In vivo, DC3 infiltrated luminal breast cancer primary tumors and DC3 infiltration correlated positively with CD8+CD103+CD69+ tissue-resident memory T cells. Altogether, these findings define DC3 as a lineage of inflammatory DC endowed with a strong potential to regulate tumor immunity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE151072 Transcriptional and Functional Analysis of CD1c+ Human Dendritic Cells Identifies a CD163+ Subset Priming CD8+CD103+ T Cells. Immunity 21.522 https://doi.org/10.1016/j.immuni.2020.06.002 {Immunity (21.522): 10.1016/j.immuni.2020.06.002} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA634547 https://www.ebi.ac.uk/ena/browser/view/PRJNA634547 https://www.ncbi.nlm.nih.gov/sra?term=SRP263000 [Overal design]Tumor-draining lymph nodes (tdLN) and primary tumors were collected and processed within few hours after the primary surgery. CD11c+HLADR+CD14-CD1a-CD206-CD1c+, CD11c+HLADR+CD1a-CD1c-CD14+ and CD11c+HLADR+CD1a-CD1c+CD14+ cells were sorted in triplicates with up to 1000 cells per sample.; [Treatment]'None'; [Growth]'None'; [Extraction]'Tumor-draining lymph nodes (tdLN) and primary tumors were collected in CO2 independent medium (Gibco) within few hours after the primary surgery. Tissue were cut into small fragments and submitted to enzymatic digestion using 0.1 mg/ml of Liberase TL (Roche) and 0.1 mg/ml of DNase (Roche) for 30 min. Cells were filtered on 40-μm cell strainer (BD), washed using CO2 independent medium (Gibco) containing 0.4g/ml of human albumin and resuspended for cell counting.\nT and B lymphocytes, NK cells, erythrocytes and myelomonocytic cells were depleted using monoclonal antibodies against: CD3, CD19, CD56, CD235a and CD15, respectively. Subsequently, cell suspensions were stained for 30 min with antibody-conjugated as the following: HLA-DR, CD11c, CD14, CD1c, CD304, CD1a, CD206, CD141. Around 1,000 cells of each DC subset were sorted by flow cytometry using BD FACS ARIA II cell sorter, (purity > 98%). Cells were centrifuged and lysed with TCL buffer (Qiagen) containing 1% of beta-mercaptoethanol before storage at -80°C. RNA were extracted and isolated using the Single Cell RNA purification kit (Norgen) according to the manufacturer’s instructions and the RNA integrity number was evaluated with an Agilent RNA 6000 pico kit.'; [Cell type]'CD11c+HLADR+CD14-CD1a-CD206-CD1c+ cells', 'CD11c+HLADR+CD1a-CD1c-CD14+ cells', 'CD11c+HLADR+CD1a-CD1c+CD14+ cells''tissue: Breast cancer iLN; donor: 1; cell type: CD11c+HLADR+CD14-CD1a-CD206-CD1c+ cells; ', 'tissue: Breast cancer iLN; donor: 1; cell type: CD11c+HLADR+CD1a-CD1c-CD14+ cells; ', 'tissue: Breast cancer iLN; donor: 1; cell type: CD11c+HLADR+CD1a-CD1c+CD14+ cells; ', 'tissue: Breast cancer iLN; donor: 2; cell type: CD11c+HLADR+CD14-CD1a-CD206-CD1c+ cells; ', 'tissue: Breast cancer iLN; donor: 2; cell type: CD11c+HLADR+CD1a-CD1c-CD14+ cells; ', 'tissue: Breast cancer iLN; donor: 2; cell type: CD11c+HLADR+CD1a-CD1c+CD14+ cells; ', 'tissue: Breast cancer iLN; donor: 4; cell type: CD11c+HLADR+CD14-CD1a-CD206-CD1c+ cells; ', 'tissue: Breast cancer iLN; donor: 4; cell type: CD11c+HLADR+CD1a-CD1c-CD14+ cells; ', 'tissue: Breast cancer iLN; donor: 4; cell type: CD11c+HLADR+CD1a-CD1c+CD14+ cells; ' GSE46590 Homo sapiens 6 Expression profiling by array GPL6244 Expression data from MDA-MB-231 cells treated with vehicle or YW3-56 2013-05-02 PAD4 is overexpressed in many cancer cells. We developed PAD inhibitors that efficiently inhibit the cancer cell growth. One inhibitor YW3-56 could efficently induce cell death of triple negative breast cancer MDA-MB-231 cells. We used microarray to detail the global gene expression of MDA-MB-231 before and after YW3-56 treatment and identify significant up-regulated or down-regulated genes by YW3-56 https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE46590 ATF4 Gene Network Mediates Cellular Response to the Anticancer PAD Inhibitor YW3-56 in Triple-Negative Breast Cancer Cells. Molecular cancer therapeutics 4.856 https://doi.org/10.1158/1535-7163.MCT-14-1093-T {Molecular cancer therapeutics (4.856): 10.1158/1535-7163.MCT-14-1093-T} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA201057 https://www.ebi.ac.uk/ena/browser/view/PRJNA201057 None [Overal design]MDA-MB-231 cells were cultured and treated with vehicle (DMSO) or YW3-56. Cells were washed with PBS and harvested for RNA extraction and hybridization on Affymetrix microarry.; [Treatment]'DMSO and YW3-56 were added when cells reached around 70% confluence. Cells were then treated with 10μM YW3-56 for 8hr.'; [Growth]'MDA-MB-231 cells were cultured in DMEM medium (Gibco) supplemented with 10% FBS and 1% penicillin-streptomycin in a 5% CO2 incubator at 37 °C.'; [Extraction]'Extraction of total RNA was performed using the RNeasy Mini Kit (Qiagen) following manufacturer’s instructions.'; [Cell type]'Source: ''cell line: MDA-MB-231; treatment: DMSO; ', 'cell line: MDA-MB-231; treatment: YW3-56; ' GSE32387 Homo sapiens 16 Expression profiling by array GPL11532 Prolactin stimulation of parathyroid adenomas 2011-09-26 Primary hyperparathyroidism is a common endocrine disorder frequently affecting postmenopausal women. In this study we have investigated expression of the prolactin receptor (PRLr) in a panel of 37 sporadic parathyroid tumours, as well as functionality in vitro in cultured parathyroid tumour cells. High levels of the prolactin receptor gene (PRLR) transcripts were demonstrated in parathyroid tissues as compared to other reference tissues and breast cancer cells. PRLr products of 60/70 kDa were highly expressed in all parathyroid tumours. In addition varying levels of the 80 kDa PRLr isoform, with known proliferative activity, were demonstrated. In parathyroid tumours PRLr immunoreactivity was observed in cytoplasm in all cases and in addition in the plasma membrane (n = 12) or enlarged lysosomes (n = 4). In normal parathyroid rim PRLr was expressed in cytoplasm and granulae. In in vitro studies of short-term cultured human parathyroid tumour cells prolactin stimulation was associated with transcriptional changes in JAK/STAT, RIG-I like receptor and type II interferon signaling pathways as documented by gene expression profiling. Moreover, PRLR gene expression in parathyroid tumors was significantly inversely correlated with plasma total Ca2+ levels. In conclusion, the prolactin receptor was found highly abundant in human parathyroid gland, parathyroid tumours, correlated with patient Ca2+ levels and functionally responsive to physiological levels of prolactin. These findings suggest a role for the prolactin receptor in human parathyroid adenomas. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32387 Prolactin receptor in primary hyperparathyroidism--expression, functionality and clinical correlations. PloS one 2.776 https://doi.org/10.1371/journal.pone.0036448 {PloS one (2.776): 10.1371/journal.pone.0036448} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA147951 https://www.ebi.ac.uk/ena/browser/view/PRJNA147951 None [Overal design]Expression profiling was done in parathyroid adenomas subjected to prolactin treatment in culture. In addition, corresponding paraffin sections were obtained for verification of PRLr expression by immunohistochemistry. 200 mg/L prolactin (recombinant human prolactin, Cat. No. JM-4687-50, MBL Woburn, MA) was added to 1× 10^6 attached parathyroid tumour cells. Cells were harvested using RNAlater (QIAGEN) and homogenized with QIAshredder for RNA extraction after 3 h and 24 h in culture, respectively. Negative controls were collected in parallel with each case at the same time points. RNA was extracted using QIA Cube, and quality assessed with Bioanalyser and Nanodrop. Expression array profiling and data analysis was done at the KI core facility Bioinformatics and Expression Analysis (BEA, Novum, Huddinge) using the Affymetrix platform and the TITAN ST 1.1 array. A total of 16 samples were analysed including 4 parathyroid adenomas cultured for 3 h or 24 h in the presence of prolactin plus control samples cultured in parallel without prolactin.; [Treatment]'Expression profiling was done in parathyroid adenomas subjected to prolactin treatment in culture. In addition, corresponding paraffin sections were obtained for verification of PRLr expression by immunohistochemistry. 200 mg/L prolactin (recombinant human\xa0prolactin, Cat. No. JM-4687-50, MBL Woburn, MA) was added to 1× 10^6 attached parathyroid tumour cells. Cells were harvested using RNAlater (QIAGEN) and homogenized with QIAshredder for RNA extraction after 3 h and 24 h in culture, respectively. Negative controls were collected in parallel with each case at the same time points. RNA was extracted using QIA Cube, and quality assessed with Bioanalyser and Nanodrop.'; [Growth]'None'; [Extraction]'Parathyroid\xa0adenoma samples for culturing and functional studies were obtained at surgery. Up to one third of the\xa0tumour was collected from each sample, while the majority of the tissue was sent to\xa0routine histopathological diagnostics. Fresh tissue samples were quickly transferred in cold culturing media to the nearby laboratory, and then isolated and cultured using previously described methods. All experiments were performed within 72 hours after isolation.'; [Cell type]'Source: ''tissue: Parthyroid Adenoma; ' GSE113380 Mus musculus 12 Expression profiling by high throughput sequencing GPL6246; GPL11002 A Syngeneic ErbB2 Mammary Cancer Model for Preclinical Immunotherapy Trials 2018-04-19 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113380 A Syngeneic ErbB2 Mammary Cancer Model for Preclinical Immunotherapy Trials. Journal of mammary gland biology and neoplasia 2.758 https://doi.org/10.1007/s10911-019-09425-3 {Journal of mammary gland biology and neoplasia (2.758): 10.1007/s10911-019-09425-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA450984 https://www.ebi.ac.uk/ena/browser/view/PRJNA450984 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'The NDL(UCD) SSM2(UCD) and Met1(UCD) transplantable mouse mammary tumor cell line was propagated in vitro and then injected as a bolus (0.1 – 2.0 x 10^6 cells) bilaterally into the uncleared #2, #3, and #4 mammary fat pads of 6- to 8-week-old female FVB/NJ mice. Tumors were harvested when they reached a maximum width of 5-10 mm, cut into 1-2mm sections, and then immediately snap-frozen.', 'The NDL(UCD) transplantable mouse mammary tumor cell line was propagated in vitro and then injected as a bolus (0.1 – 2.0 x 10^6 cells) bilaterally into the uncleared #2, #3, and #4 mammary fat pads of 6- to 8-week-old female FVB/NJ mice. Tumors were harvested when they reached a maximum width of 5-10 mm, cut into 1-2mm sections, and then immediately snap-frozen.'; [Extraction]'RNA was isolated from frozen samples using the miRNeasy FFPE Kit (Qiagen) according to the manufacturer’s protocols specific for each type of specimen.', 'RNA was isolated from frozen samples using the miRNeasy FFPE Kit (Qiagen) according to the manufacturer’s protocols. Total RNA was eluted from the columns in nuclease-free water and stored at -80°C.\nTotal RNA-Seq sequencing libraries were prepared from both intact RNA derived from flash-frozen samples and severely fragmented RNA isolated from FFPE samples. Briefly, rRNA-depleted RNA was prepared from total RNA input (1-5 ug) using the Ribo-Zero rRNA Removal Kit (Epicentre), which selectively depletes rRNA by hybridization to biotinylated capture probes followed by microsphere bead capture. Subsequently, directional Total RNA-Seq libraries were prepared from rRNA-depleted RNA (50 ng) using the ScriptSeq v2 RNA-Seq Library Preparation Kit (Epicentre) according to the manufacturer’s protocol. Briefly, 5’,3’-di-tagged cDNA was synthesized using tagged random hexamer-primed cDNA synthesis primers followed by annealing of 3’-terminal-tagging oligo (TTO) and extension with DNA Polymerase. The cDNA was then purified with Agencourt AMPure XP beads (Beckman Coulter, Inc.) or with the MinElute PCR Purification Kit (Qiagen), depending upon the source of RNA from flash-frozen or FFPE samples respectively. Illumina adaptor sequences and indexes were then incorporated during library amplification with the appropriate PCR primers and high-fidelity FailSafe PCR Enzyme Mix. Subsequently, the libraries were purified in a similar manner to that described above for the cDNA preparations. The ScriptSeq v2 libraries were then quantitated with the Qubit fluorometer (Invitrogen Life Sciences) and insert sizes determined with the Agilent 2100 Bioanalyzer. The molar concentration of PCR-competent sequencing templates in the libraries was then determined using by quantitative PCR with the KAPA Library Quantification Kit (Kapa Biosystems, Inc.).'; [Cell type]'Source: ''gender: female; strain: FVB/N; tissue: mammary tumor; cell line: SSM2; ', 'gender: female; strain: FVB/N; tissue: mammary tumor; cell line: Met1; ', 'gender: female; strain: FVB/N; tissue: mammary tumor; cell line: NDL; ', 'tissue: mammary tumor; strain: FVB/N; gender: female; ' GSE111838 Homo sapiens 3 Expression profiling by high throughput sequencing GPL16791 Gene expression changes in breast cancer cells upon USP1 knockdown [RNA-Seq] 2018-03-14 To explore the function of deubiquitinase USP1 in breast cancer cells, we performed RNA sequencing to analyze the expression pattern changes by knockdown of USP1 in MCF7 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE111838 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA438337 https://www.ebi.ac.uk/ena/browser/view/PRJNA438337 https://www.ncbi.nlm.nih.gov/sra?term=SRP135699 [Overal design]RNA-seq was preformed in breast cancer MCF7 cells transfected with control or USP1-specific siRNAs.; [Treatment]'Cells were maintained at 37 °C with 5% CO2, grown to 80% confluence, and then transfected with control siRNA or USP1-specific siRNA using Lipofectamine 2000 Transfection Reagent (Thermo Fisher Scientific).'; [Growth]'MCF7 cells were grown in Dulbecco’s Modified Eagle Medium plus 10% fetal bovine serum, 100 units/ml penicillin and 100 μg/mL streptomycin.'; [Extraction]'Total RNA was extracted by TRIZOL Reagent (Life Technologies, Inc) and quantified by Agilent Bioanalyzer 2100 (Agilent technologies).\nThe cDNA fragments were subjected to an end repair process, added a single ‘A’ base, and ligated with the adapters. The products were then purified and enriched with PCR to create the final cDNA library.'; [Cell type]'Source: ''cell line: MCF7; transfection: control siRNA; tissue: breast cancer cell line; ', 'cell line: MCF7; transfection: USP1 siRNA-1; tissue: breast cancer cell line; ', 'cell line: MCF7; transfection: USP1 siRNA-2; tissue: breast cancer cell line; ' GSE123603 Homo sapiens 12 Expression profiling by high throughput sequencing GPL18573 IL-6 augments IL-4-induced polarization of primary human macrophages through synergy of STAT3, STAT6 and BATF transcription factors 2018-12-11 Here we explored how cytokines of the tumor milieu, interleukin (IL)-6 and IL-4, interact to influence target gene expression in primary human monocyte-derived macrophages (hMDMs). We show that dual stimulation with IL-4 and IL-6 synergistically modified gene expression. Among the synergistically induced genes are several targets with known pro-tumorigenic properties, such as CC-chemokine ligand 18 (CCL18), transforming growth factor alpha (TGFA) or CD274 (programmed cell death 1 ligand 1 (PD-L1)). We found that transcription factors of the signal transducer and activator of transcription (STAT) family, STAT3 and STAT6 bind regulatory regions of synergistically induced genes in close vicinity. STAT3 and STAT6 co-binding further induces the basic leucine zipper ATF-like transcription factor (BATF), which participates in synergistic induction of target gene expression. Functional analyses revealed increased MCF-7 and MDA-MB 231 tumor cell motility in response to conditioned media from co-treated hMDMs compared to cells incubated with media from single cytokine-treated hMDMs. Flow cytometric analysis of T cell populations upon co-culture with hMDMs polarized by different cytokines indicated that dual stimulation promoted immunosuppressive properties of hMDMs in a PD-L1-dependent manner. Analysis of clinical data revealed increased expression of BATF together with TAM markers in tumor stroma of breast cancer patients as compared to normal breast tissue stroma. Collectively, our findings suggest that IL-4 and IL-6 cooperate to alter the human macrophage transcriptome, endowing hMDMs with pro-tumorigenic properties. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE123603 IL-6 augments IL-4-induced polarization of primary human macrophages through synergy of STAT3, STAT6 and BATF transcription factors. Oncoimmunology 5.333 https://doi.org/10.1080/2162402X.2018.1494110 {Oncoimmunology (5.333): 10.1080/2162402X.2018.1494110} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA509359 https://www.ebi.ac.uk/ena/browser/view/PRJNA509359 https://www.ncbi.nlm.nih.gov/sra?term=SRP173264 [Overal design]We compared synergistically induced genes in IL-4/IL-6 co-stimulation relative to IL-4, IL-6 and untreated monocyte derived human macrophages via RNA sequencing; [Treatment]'Treated with individual cytokines on Day 7 for 24hrs'; [Growth]'differentiated in 3% human plasma in RPMI, P/S'; [Extraction]'4µg of total RNA extracted from Macherey-Nagel NucleoSpin RNA extraction kit (#740955.250)\nLibraries were prepared using TruSeq Stranded mRNA LT - SetB library preparation kit (Illumina #RS-122-2102). cDNA was prepared for single end (SE) sequencing on NextSeq 500/550 High Output Kit v2 (75 cycles, Illumina # FC-404-2005).'; [Cell type]'human monocyte-derived primary macrophages''cell type: human monocyte-derived primary macrophages; Stage: 7 days differentiation from monocytes; treatment: untreated control; ', 'cell type: human monocyte-derived primary macrophages; Stage: 7 days differentiation from monocytes; treatment: IL4; ', 'cell type: human monocyte-derived primary macrophages; Stage: 7 days differentiation from monocytes; treatment: IL6; ', 'cell type: human monocyte-derived primary macrophages; Stage: 7 days differentiation from monocytes; treatment: IL-4/IL-6 co-stimulation; ' GSE6581 Mus musculus 3 Expression profiling by array GPL8321 Expression data from mammary glands of transgenic mice 2006-12-20 The aim of our work was the comparison of human and mouse gene expression data and to identify a conserved breast tumor gene set. The results encourage the usefulness of transgenic mice as a model for human breast cancer formation and therapy. Keywords: Comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE6581 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA104239 https://www.ebi.ac.uk/ena/browser/view/PRJNA104239 None [Overal design]The aim of our work was to establish a database for breast cancer gene expression data in order to compare human and mouse breast cancer. We identified human and mouse homologues genes and compared the expression profile of 24 human breast tumors with six WAP-SVT/t breast tumors (WAP-SVT/t animals, line 8). Our studies confirmed the heterogeneity in gene expression of human as well as mouse breast cancer cells. However, 63 genes were found to be differentially expressed (upregulated: 40; downregulated: 23 genes) in at least 75% of the breast tumors of both species.; [Treatment]'breast cancer'; [Growth]'breast cancer'; [Extraction]"RNAzol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''' GSE62383 Rattus norvegicus 24 Methylation profiling by array GPL19297 DNA Methylation Patterns in Rat Mammary Carcinomas Induced by Pre- and Post-Pubertal Irradiation 2014-10-15 Several lines of evidence indicate one's age at exposure to radiation strongly modifies the risk of radiation-induced breast cancer. We previously reported that rat mammary carcinomas induced by pre- and post-pubertal irradiation have distinct gene expression patterns, but the changes underlying these differences have not yet been characterized. The aim of this investigation was to see if differences in CpG DNA methylation were responsible for the differences in gene expression between age at exposure groups observed in our previous study. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE62383 DNA Methylation Patterns in Rat Mammary Carcinomas Induced by Pre- and Post-Pubertal Irradiation. PloS one 2.776 https://doi.org/10.1371/journal.pone.0164194 {PloS one (2.776): 10.1371/journal.pone.0164194} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA263958 https://www.ebi.ac.uk/ena/browser/view/PRJNA263958 None [Overal design]DNA was obtained from the mammary carcinomas arising in female Sprague-Dawley rats that were either untreated or irradiated (γ-rays, 2 Gy) during the pre- or post-pubertal period (3 or 7 weeks old). The DNA methylation was analyzed using CpG island microarrays and the results compared to the gene expression data from the original study.; [Treatment]'Rats were left untreated or were subjected to whole-body 137Cs gamma-irradiation (2 Gy, 0.6 Gy/min) at 3 or 7 weeks of age. Rats were fed AIN-76A diet containing 23.5% corn oil (Clea Japan) after 9 weeks of age.'; [Growth]'Rats were housed in autoclaved cages and maintained in a room with a controlled temperature (23 ± 1°C) and humidity (50 ± 5%) under a regular 12-hours light, 12-hours dark cycle. They were fed a standard laboratory animal diet (CE-2; Clea Japan, Tokyo, Japan) and sterilized water ad libitum.'; [Extraction]'Genomic DNA was isolated by proteinase K digestion, followed by phenol/chloroform extraction.'; [Cell type]'Source: ''disease status: normal; gender: female; strain: Sprague-Dawley; age at irradiation: non-irradiated; isolation of methylated dna: methyl-CpG binding domain-based protein; tissue: mammary gland; ', 'disease status: normal; gender: female; strain: Sprague-Dawley; age at irradiation: non-irradiated; isolation of methylated dna: none; tissue: mammary gland; ', 'disease status: carcinoma; gender: female; strain: Sprague-Dawley; age at irradiation: 3 weeks; isolation of methylated dna: methyl-CpG binding domain-based protein; tissue: mammary carcinoma; ', 'disease status: carcinoma; gender: female; strain: Sprague-Dawley; age at irradiation: 3 weeks; isolation of methylated dna: none; tissue: mammary carcinoma; ', 'disease status: carcinoma; gender: female; strain: Sprague-Dawley; age at irradiation: 7 weeks; isolation of methylated dna: methyl-CpG binding domain-based protein; tissue: mammary carcinoma; ', 'disease status: carcinoma; gender: female; strain: Sprague-Dawley; age at irradiation: 7 weeks; isolation of methylated dna: none; tissue: mammary carcinoma; ', 'disease status: carcinoma; gender: female; strain: Sprague-Dawley; age at irradiation: non-irradiated; isolation of methylated dna: methyl-CpG binding domain-based protein; tissue: mammary carcinoma; ', 'disease status: carcinoma; gender: female; strain: Sprague-Dawley; age at irradiation: non-irradiated; isolation of methylated dna: none; tissue: mammary carcinoma; ' GSE81510 Homo sapiens 16 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Glucocorticoid Receptor: MegaTrans Switching Mediates Repression of ERα-Regulated Transcriptional Program [ChIP-Seq] 2016-05-17 The mechanisms underlying GR-dependent inhibition of ERα-regulated gene activation programs at the global genomic level have been poorly understood. We found the binding of GR in trans on ERα-activated enhancers results in gene and enhancer repression by disassembling the MegaTrans Complex. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE81510 Glucocorticoid Receptor:MegaTrans Switching Mediates the Repression of an ERα-Regulated Transcriptional Program. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2017.03.019 {Molecular cell (14.548): 10.1016/j.molcel.2017.03.019} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA321838 https://www.ebi.ac.uk/ena/browser/view/PRJNA321838 https://www.ncbi.nlm.nih.gov/sra?term=SRP075269 [Overal design]All ChIP-Seq experiments were designed to elucidate the mechanism involving GR-mediated repression of ERα-Regulated Transcriptional Program; [Treatment]'Before experiment, the MCF7 cells were hormone-stripped in phenol red free DMEM medium plus 5% charcoal-treated FBS for 3-4 days, followed by treatment of 100 nM ICI for 3h, or 100nM 17β-estradiol (E2) ,100nM dexamethasone (Dex) or combine together for 1hr. To perform Biotin-ChIP experiments through Biotin-streptavidin pull-down, we used some BLRP-tagged MCF7 Tet-On inducible stable lines that can in vivo biotinylate BLRP-tagged proteins. To induce BLRP-tagged protein expression, 2μg/ml doxycycline was added into culture media for about 24 hours before hormone treatment and collection.'; [Growth]'MCF7 obtained from ATCC were cultured in DMEM media supplemented with 10% FBS in a 5% CO2 humidified incubator at 37°C.'; [Extraction]'For ChIP-seq, some samples were fixed for 10 minutes with 1% formaldehyde. Fixation was stopped by adding Glycine (0.125M). Chromatin DNA was sheared to 200–500 bp average in size by sonication. Soluble sheared chromatin was immunoprecipitated with specific antibodies or streptavidin beads overnight at 4°C. After washing and elution, the protein–DNA complex was decross-linked by heating at 65°C overnight. Immunoprecipitated DNA was purified by using iPure Diagenode kit.\nthe libraries were constructed following Illumina’s Chip-Seq Sample prep kit.'; [Cell type]'Source: ''cell line: MCF7; chip antibody used for chip or oligonucleotides used for chirp (chromatin isolation by rna purification): Santa Cruz Biotechnologies ERα (HC-20) sc-543; ', 'cell line: MCF7; chip antibody used for chip or oligonucleotides used for chirp (chromatin isolation by rna purification): streptavidin beads; ' GSE43097 Homo sapiens 8 Expression profiling by array GPL5175; GPL5188 Integrin α3b1-dependent gene expression in MDA-MB-231 breast cancer cells 2012-12-21 Gene-level and exon-level analysis of gene expression in MDA-MB-231 cells that stably express control shRNA or integrin α3-targeting shRNA. The laminin-332-binding integrin α3b1 is expressed highly in many breast cancer cells, but its roles in regulating gene expression programs that promote breast cancer progression have not been explored. In order to identify genes that are regulated by α3b1 in human breast cancer cells, we used a lentiviral approach to express an α3-targeting shRNA to suppress integrin α3b1 in MDA-MB-231 cells, and we identified subsequent changes in gene expression and alternate exon useage. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43097 Integrin α3β1 controls mRNA splicing that determines Cox-2 mRNA stability in breast cancer cells. Journal of cell science 4.517 https://doi.org/10.1242/jcs.131227 {Journal of cell science (4.517): 10.1242/jcs.131227} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA184388 https://www.ebi.ac.uk/ena/browser/view/PRJNA184388 None [Overal design]We used the Affymetrix Human Exon 1.0 ST platform to analyze biological replicates of MDA-MB-231 cells that were transduced with lentivirus to stably express either control shRNA or α3-targeting shRNA. Array data was processed by Affymetrix Exon Array Computational Tool.; [Treatment]'None'; [Growth]'MDA-MB-231 cells with stable expression of either control shRNA or α3-targeting shRNA were maintained at 37 degrees C, 5% CO2, on standard tissue culture plates. Cells were grown in DMEM supplemented with 10% FBS 100 units/ml penicillin and 100 μg/ml streptomycin.'; [Extraction]'Total cellular RNA was isolated from cells using the RNeasy Plus isolation kit (Qiagen, Valencia, CA), and quality was confirmed on an Agilent Bioanalyzer.'; [Cell type]'Source: ''cell line: MDA-MB-231; genotype/variation: control shRNA; ', 'cell line: MDA-MB-231; genotype/variation: alpha3-targeting shRNA; ' GSE26990 Homo sapiens 107 Methylation profiling by array; Expression profiling by array GPL6947; GPL8490 Analysis of Promoter Methylation in Breast Cancer 2011-02-01 Promoter methylation was assayed in a number of breast cancer and control normal samples along with the effects of 5'-aza-2'-deoxycytidine on breast cancer cell line transcriptomes. Aberrant promoter hypermethylation is frequently observed in cancer. The potential for this to contribute to tumour development depends on whether the genes affected are repressed because of their methylation. Many aberrantly methylated genes play important roles in development and are bivalently marked in ES cells suggesting that their aberrant methylation may reflect developmental processes. We investigated this possibility by analysing promoter methylation in 19 breast cancer cell lines, 10 normal tissues and 47 primary breast tumours. In order to determine the role of DNA methylation in silencing genes in breast cancer, we also examined the effects of the demethylating agent 5-aza-2?-deoxycytidine on gene expression in 3 breast cancer cell lines and HCT116 cells. Gene expression changes were also assayed in the DNA methyltransferase deficient HCT116 DKO cell line. Our findings implicate aberrant DNA methylation as a marker of cell lineage rather than tumour progression and suggest that, in most cases, it does not cause the repression with which it is associated. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26990 Tissue of origin determines cancer-associated CpG island promoter hypermethylation patterns. Genome biology 14.028 https://doi.org/10.1186/gb-2012-13-10-r84 {Proceedings of the National Academy of Sciences of the United States of America (9.580) doi:10.1073/pnas.1013224108}; {Genome biology (14.028) doi:10.1186/gb-2012-13-10-r84}; 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA135941 https://www.ebi.ac.uk/ena/browser/view/PRJNA135941 None [Overal design]A number of human breast cancer cell lines, breast tumours and normal tissues were analysed on Illumina Infinium Methylation27 Beadchips to assay promoter methylation. Selected cell lines were analysed on expression arrays before and after treatment with 5-aza-2'-deoxycytidine.; [Treatment]'None', "1µM 5'-aza-2'-deoxycytidine, refreshed every 24hrs, for a total of 72 h."; [Growth]'Standard culture conditions', 'None'; [Extraction]'Genomic DNA was extracted using standard molecular biology protocols (pK digestion, phenol-chloroform extraction and ethanol precipitation)', 'Total RNA was isolated using Trizol and standard molecular biology protocols'; [Cell type]'Source: ''tissue: breast; cell line: BT20; ', 'tissue: breast; cell line: BT474; ', 'tissue: breast; cell line: BT549; ', 'tissue: embryo; cell line: SHEF-6 human ES Cells; ', 'tissue: breast; cell line: HBL100; ', 'tissue: breast; cell line: HCC1569; ', 'tissue: breast; cell line: HCC1954; ', 'tissue: colon; cell line: wild-type HCT116 Cells; ', 'tissue: colon; cell line: DNA methyltransferase deficient HCT116 cells; ', 'tissue: breast; cell line: Human Mammary Epithelial Cells (HMEC); ', 'tissue: breast; cell line: HS578T; ', 'tissue: breast; cell line: MCF10A; ', 'tissue: breast; cell line: MCF7; ', 'tissue: breast; cell line: MDAMB157; ', 'tissue: breast; cell line: MDAMB231; ', 'tissue: breast; cell line: MDAMB361; ', 'tissue: breast; cell line: MDAMB453; ', 'tissue: breast; cell line: MDAMB468; ', 'tissue: Normal Breast; ', 'tissue: breast; cell line: SKBR3; ', 'tissue: breast; cell line: SUM1315MO2; ', 'tissue: breast; cell line: SUM159PT; ', 'tissue: breast; cell line: T47D; ', 'tissue: breast; cell line: ZR751; ', 'tissue: Normal Adult Brain; ', 'tissue: Normal Fetal Brain; ', 'tissue: Normal Testis; ', 'tissue: Normal Placenta; ', 'tissue: Normal Spleen; ', 'tissue: Normal Liver; ', 'tissue: Normal Blood; ', 'tissue: Normal Colon; ', 'tissue: Primary Breast Tumour; cell line: Fresh Frozen Primary Breast Tumour Sample; ', 'tissue: colon; cell line: wild type HCT116; agent: untreated; ', "tissue: colon; cell line: wild type HCT116; agent: 5'-aza-2'-deoxycytidine; ", 'tissue: colon; cell line: DNA methyltransferase deficient HCT116 cells; agent: untreated; ', 'tissue: breast; cell line: MCF7; agent: untreated; ', "tissue: breast; cell line: MCF7; agent: 5'-aza-2'-deoxycytidine; ", 'tissue: breast; cell line: BT20; agent: untreated; ', "tissue: breast; cell line: BT20; agent: 5'-aza-2'-deoxycytidine; ", 'tissue: breast; cell line: HBL100; agent: untreated; ', "tissue: breast; cell line: HBL100; agent: 5'-aza-2'-deoxycytidine; " GSE20483 Homo sapiens 97 Genome variation profiling by array GPL9077 Clinical implications of gene dosage and gene expression patterns in diploid breast carcinoma (CGH) 2010-02-23 Genomic and expression profiling using 38K BAC array-CGH and Illumina HT-12 beadchips were performed on 97 diploid invasive breast tumors to assess the impact of gene dosage on gene expression patterns and the effect of other mechanisms on transcriptional levels. Patient stratification was performed according to axillary lymph node status (node-negative, pN0; node-positive, pN1) and overall survival (>8-year survivors; breast cancer-specific mortality within 8 years of diagnosis). Array-CGH results was validated by FISH using tumors showing HER2/neu gene amplification and expression profiling was confirmed using qPCR for 16 transcripts. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE20483 Frequent MYC coamplification and DNA hypomethylation of multiple genes on 8q in 8p11-p12-amplified breast carcinomas. Oncogenesis 5.995 https://doi.org/10.1038/oncsis.2014.8 {Clinical cancer research : an official journal of the American Association for Cancer Research (None) doi:10.1158/1078-0432.CCR-10-0889}; {Oncogenesis (5.995) doi:10.1038/oncsis.2014.8}; 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA129867 https://www.ebi.ac.uk/ena/browser/view/PRJNA129867 None [Overal design]Genomic DNA was isolated from fresh-frozen tissue samples; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was isolated from fresh-frozen tissue specimens using the Wizard Genomic DNA extraction kit, including proteinase K treatment followed by phenol chloroform purification'; [Cell type]'Source: ''disease state: Human breast tumor; ', 'reference: Normal female genomic DNA; ' GSE134654 Homo sapiens 36 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Characterization of FOXA1 mutations in breast cancer (ATAC-seq) 2019-07-22 Invasive Lobular Carcinoma (ILC) is the second most frequent breast cancer (BCa) type and encompasses 10-15% of BCa cases. FOXA1 specific mutations are enriched in this subtype of BCa, however their role in breast cancer pathogenesis is still ill-defined. FOXA1, together with estrogen receptor (ER), is a key transcription factor for the correct activation of estrogen-dependent gene expression and, consequently, for mammary gland development and BCa identity. FOXA1 has the capability to bind to and de-compact heterochromatin to render it accessible for other nuclear proteins, such as ER, and allow activation of their transcriptional programs upon estrogen stimulation. In this project, we aim to elucidate the role of FOXA1 missense mutations in altering its binding to DNA, chromatin accessibility, ER-dependent transcription and their implication in limiting the sensitivity to standard-of-care anti-hormonal therapy, commonly used in ER-positive BCa patients. To this end, we have generated BCa cell lines expressing these FOXA1 mutations and we will employ ATAC-Seq, RIME assays, ChIP-Seq and RNA-Seq to ascertain their effect on DNA accessibility, DNA binding capability, as well as binding of transcriptional coregulators, such as ER, to chromatin. We will extend our analyses to our internal BCa patient datasets with detailed clinical annotation to study the correlation between presence of FOXA1 mutations and response to anti-hormonal therapy of ER-positive BCa patients. The results of this project will allow to understand how the different mutations in the Forkhead domain can alter FOXA1 and ER function, transcriptional regulation and response to anti-hormonal therapy in ER-positive BCa patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE134654 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA556013 https://www.ebi.ac.uk/ena/browser/view/PRJNA556013 https://www.ncbi.nlm.nih.gov/sra?term=SRP215943 [Overal design]Omni-ATAC analysis of MCF7 cells overexpressing either empty vector (EV), FOXA1 wild-type (WTNS) or FOXA1 mutant (SY242CS, H247Y, S250F, F266L) constructs, in duplicates; [Treatment]'DMSO and E2 conditions were subjected to DMSO or E2 treatment for 1h'; [Growth]'Cells were seeded in full media; the following day media was changed to either estrogen depleted media (for DMSO and E2 groups) or same DMEM/F12 50/50 full media (for FM); cells were incubated for 72h; the day of cell harvesting media was refreshed'; [Extraction]'Cells were deattached with accutase, spinned down, counted and 100K cells were used to perform Omni-ATAC protocol\nAmplification with barcode employing NEBNext Q5 Hot Start HiFi PCR Master Mix (prod. no: M0543L)'; [Cell type]'breast cancer''cell line: MCF7; cell type: breast cancer; ' GSE37754 Homo sapiens 72 Methylation profiling by array GPL13534 Molecular Profiles of Human Breast Cancer and Their Association with Tumor Subtypes and Disease Prognosis (Illumina) 2012-05-03 This study identified DNA methylation patterns that were associated with tumor subtypes, disease outcome, and distinct metabolome and gene expression patterns. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37754 Integrated proteotranscriptomics of breast cancer reveals globally increased protein-mRNA concordance associated with subtypes and survival. Genome medicine 10.886 https://doi.org/10.1186/s13073-018-0602-x {The Journal of clinical investigation (None) doi:10.1172/JCI71180}; {Genome medicine (10.886) doi:10.1186/s13073-018-0602-x}; {Neoplasia (New York, N.Y.) (None) doi:10.1016/j.neo.2014.05.007}; 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA169568 https://www.ebi.ac.uk/ena/browser/view/PRJNA169568 None [Overal design]This study performed a large scale DNA methylation (Illumina HumanMethylation450 BeadChip [HumanMethylation450 15017482 v.1.1], N=72), gene expression (Affymetrix Human Gene 1.0 ST Array [HuGene-1_0-st], N=108), and metabolome (Metabolon, Inc. Durham, NC) analysis of fresh-frozen human breast tumors from African-American and European-American patients from the greater Baltimore area, Maryland (US), with survival follow-up.; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was isolated from fresh frozen primary breast tumours following the Qiagen DNeasy Blood and Tissue Kit protocol. Briefly, tissues were pre-treated with Proteinase K at 55C over-night, then lysed, bound to the column, washed, and eluted. DNA was quantified using the nanodrop spectrophotomer.'; [Cell type]'Source: ''race: European-American; age: 51; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: IIA; node status: N0; survival (months): 97; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; age: 39; tissue type: Non-tumor; ', 'race: African-American; age: 39; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIA; tumor grade: 3; node status: N0; survival (months): 148; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 42; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIB; tumor grade: 2; node status: N1; survival (months): 10; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: Yes; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 42; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: I; tumor grade: 1; node status: N0; survival (months): 135; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: No; ', 'race: African-American; age: 91; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIIB; tumor grade: 2; node status: N0; survival (months): 1; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: No; ', 'race: African-American; age: 39; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIB; tumor grade: 3; node status: N0; survival (months): 10; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: Yes; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; age: 81; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIIB; tumor grade: 2; node status: N0; survival (months): 56; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: No; ', 'race: European-American; age: 65; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: II; tumor grade: 1; node status: N1; survival (months): 132; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: No; ', 'race: African-American; age: 30; tissue type: Non-tumor; ', 'race: African-American; age: 30; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIB; tumor grade: 3; node status: N0; survival (months): 23; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; age: 65; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: IIB; tumor grade: 3; node status: N1; survival (months): 13; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: Yes; ', 'race: European-American; age: 34; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIB; node status: N1; survival (months): 121; survival event: Alive; death due to cancer: No; neoadjuvant therapy: Yes; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 59; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIB; tumor grade: 1; node status: N1; survival (months): 29; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: No; ', 'race: European-American; age: 34; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIA; tumor grade: 3; node status: N0; survival (months): 120; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; age: 86; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIA; node status: N0; survival (months): 39; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: No; ', 'race: European-American; age: 55; tissue type: Tumor; estrogen receptor status: Negative; Stage: IIB; tumor grade: 3; node status: N0; survival (months): 13; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: Yes; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 74; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: IIA; tumor grade: 3; node status: N0; survival (months): 96; survival event: Dead; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: No; ', 'race: European-American; age: 62; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIB; tumor grade: 2; node status: N1; survival (months): 12; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: Yes; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; age: 48; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIA; tumor grade: 3; node status: N0; survival (months): 111; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 45; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIIB; tumor grade: 3; node status: N0; survival (months): 48; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: Yes; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 58; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIIB; tumor grade: 2; node status: N2; survival (months): 109; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; age: 46; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIA; node status: N1; survival (months): 99; survival event: Alive; death due to cancer: No; hormone-therapy: No; chemotherapy: No; ', 'race: European-American; age: 45; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIA; tumor grade: 3; node status: N0; survival (months): 98; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; ', 'race: African-American; age: 59; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIB; tumor grade: 3; node status: N1; survival (months): 15; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: No; ', 'race: European-American; age: 81; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIA; tumor grade: 3; node status: N0; survival (months): 70; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: Yes; hormone-therapy: Yes; chemotherapy: No; ', 'race: African-American; age: 76; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIA; tumor grade: 3; node status: N0; survival (months): 94; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: No; ', 'race: European-American; age: 84; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIIB; tumor grade: 2; node status: N2; survival (months): 0; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: Yes; hormone-therapy: Yes; chemotherapy: No; ', 'race: European-American; age: 57; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIIA; tumor grade: 2; node status: N1; survival (months): 90; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; age: 50; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: IIA; tumor grade: 3; node status: N0; survival (months): 91; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 40; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: IIIA; tumor grade: 2; node status: N2; survival (months): 11; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: Yes; hormone-therapy: Yes; chemotherapy: No; ', 'race: African-American; age: 43; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIB; tumor grade: 3; node status: N1; survival (months): 85; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: No; ', 'race: African-American; age: 44; tissue type: Non-tumor; ', 'race: African-American; age: 46; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: IIB; tumor grade: 3; node status: N1; survival (months): 29; survival event: Dead; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; age: 55; tissue type: Non-tumor; ', 'race: African-American; age: 55; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: IIIa; tumor grade: 3; node status: N2; survival (months): 17; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: No; ', 'race: European-American; age: 45; tissue type: Tumor; estrogen receptor status: Negative; Stage: II; node status: N0; survival (months): 86; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: No; ', 'race: European-American; age: 75; tissue type: Tumor; estrogen receptor status: Negative; Stage: I; tumor grade: 3; node status: N0; survival (months): 82; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: No; ', 'race: African-American; age: 34; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIIA; tumor grade: 2; node status: N1; survival (months): 83; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: Yes; ', 'race: European-American; age: 89; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIIA; tumor grade: 2; node status: N2; survival (months): 13; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: Yes; hormone-therapy: Yes; chemotherapy: No; ', 'race: European-American; age: 65; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIB; tumor grade: 3; node status: N0; survival (months): 92; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; age: 37; tissue type: Non-tumor; ', 'race: African-American; age: 37; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: IIB; tumor grade: 3; node status: N1; survival (months): 24; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 63; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIA; tumor grade: 2; node status: N0; survival (months): 80; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: No; ', 'race: African-American; age: 45; tissue type: Non-tumor; ', 'race: African-American; age: 45; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIB; tumor grade: 3; node status: N1; survival (months): 48; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; age: 73; tissue type: Non-tumor; ', 'race: African-American; age: 73; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: IIA; tumor grade: 3; node status: N0; survival (months): 16; survival event: Dead; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: No; ', 'race: African-American; age: 43; tissue type: Non-tumor; ', 'race: European-American; age: 93; tissue type: Non-tumor; ', 'race: African-American; age: 52; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: I; node status: N0; survival (months): 41; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; ', 'race: European-American; age: 52; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIA; tumor grade: 1; node status: N0; survival (months): 63; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: No; ', 'race: African-American; age: 45; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: I; tumor grade: 3; node status: N0; survival (months): 58; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: Yes; ', 'race: European-American; age: 53; tissue type: Tumor; estrogen receptor status: Negative; Stage: IIIB; survival (months): 3; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: Yes; hormone-therapy: No; chemotherapy: No; ', 'race: European-American; age: 61; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIA; tumor grade: 2; node status: N0; survival (months): 57; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 37; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIIA; tumor grade: 1; node status: N1; survival (months): 55; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 47; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: IIIA; tumor grade: 3; node status: N1; survival (months): 55; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: Yes; ', 'race: European-American; age: 36; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIB; tumor grade: 3; node status: N0; survival (months): 54; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 44; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: I; node status: N0; survival (months): 51; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: No; ', 'race: African-American; age: 51; tissue type: Non-tumor; ', 'race: African-American; age: 51; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIB; tumor grade: 3; node status: N1; survival (months): 36; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; age: 57; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIIA; tumor grade: 2; node status: N1; survival (months): 10; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; age: 67; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: IIA; tumor grade: 3; node status: N0; survival (months): 50; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 46; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: I; tumor grade: 2; node status: N0; survival (months): 50; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: No; ', 'race: European-American; age: 38; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIA; tumor grade: 2; node status: N0; survival (months): 50; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: No; ', 'race: African-American; age: 36; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIIA; tumor grade: 3; node status: N1; survival (months): 48; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: European-American; age: 52; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIA; tumor grade: 1; node status: N0; survival (months): 48; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: No; ', 'race: African-American; age: 36; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIB; tumor grade: 1; node status: N1; survival (months): 47; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: Yes; ', 'race: African-American; age: 46; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIA; tumor grade: 2; node status: N1; survival (months): 43; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: Yes; ', 'race: African-American; age: 66; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: No; Stage: IIB; tumor grade: 2; node status: N1; survival (months): 41; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: Yes; ', 'race: African-American; tissue type: Tumor; estrogen receptor status: Negative; triple negative or basal-like subtype: Yes; Stage: IIA; node status: N0; survival (months): 38; survival event: Alive; death due to cancer: No; neoadjuvant therapy: No; hormone-therapy: No; chemotherapy: Yes; ', 'race: African-American; tissue type: Tumor; estrogen receptor status: Positive; triple negative or basal-like subtype: No; Stage: IIB; tumor grade: 2; node status: N1; survival (months): 27; survival event: Dead; death due to cancer: Yes; neoadjuvant therapy: No; hormone-therapy: Yes; chemotherapy: No; ' GSE32466 Homo sapiens 24 Non-coding RNA profiling by array GPL10850 miRNA profiles in Primary and Recurrent GBM 2011-09-29 Glioblastoma (GBM) bears a dismal prognosis with rapid relapse following complete resection and radiochemotherapy. The involvement of microRNAs in tumor progression has been demonstrated in hepatoma, breast cancer, and prostate cancers. However, the microRNAs involved in modulating the progression and relapse of GBM are still unclear. Initially, we compared the miRNA expression profiles between primary and recurrent GBM tissues from the same patient in twelve independent cases. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32466 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA147879 https://www.ebi.ac.uk/ena/browser/view/PRJNA147879 None [Overal design]miRNA expression profiles between primary and recurrent GBM tissues from the same patient in twelve independent cases.; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was extracted using the mirVanaTM kit (Ambion, TX) according to manufacturer's protocol."; [Cell type]'primary GBM tissue', 'recurrent GBM tissue''cell type: primary GBM tissue; ', 'cell type: recurrent GBM tissue; ' GSE83232 Homo sapiens 516 Expression profiling by array GPL96; GPL97 caArray_mille-00271: Uppsala cohort 2016-06-10 breast cancer https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE83232 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA325311 https://www.ebi.ac.uk/ena/browser/view/PRJNA325311 None [Overal design]mille-00271 Assay Type: Gene Expression Provider: Affymetrix Array Designs: HG-U133A, HG-U133B Organism: Homo sapiens (ncbitax); [Treatment]'None'; [Growth]'None'; [Extraction]'See mage-tab files linked to series entry for additional details'; [Cell type]'Source: ''diagnosis: breast cancer; ' GSE136414 Homo sapiens 9 Expression profiling by high throughput sequencing GPL16791 Prolyl Hydroxylase Substrate Adenylosuccinate Lyase Is An Oncogenic Driver In Triple Negative Breast Cancer 2019-08-27 Protein hydroxylation extensively regulates cellular signaling by affecting protein stability, activity, and interactome, therefore contributing to the pathogenesis of various diseases including cancers. However, because of the transient nature of the hydroxylase-substrate interaction, identifying new prolyl hydroxylation substrates remains a daunting challenge. Here, by developing a novel enzyme-substrate trapping strategy coupled with TAP-TAG or orthogonal GST- purification followed by mass spectrometry, we identify Adenylosuccinate lyase (ADSL) as a bona fide EglN2 prolyl hydroxylase substrate in triple negative breast cancer (TNBC). ADSL expression is significantly higher in TNBC than other breast cancer subtypes or normal breast tissues. Functionally, ADSL knockout greatly impairs TNBC 2-D and 3-D cell proliferation and invasiveness in vitro, as well as TNBC tumorigenesis and lung colonization in xenograft models. Mechanistically, an integrated transcriptomics and metabolomics analysis revealed that ADSL promotes the activation of the oncogenic cMYC pathway by regulating cMYC protein level via a mechanism requiring ADSL hydroxylation on proline 24. Specifically, hydroxylation-proficient ADSL, by affecting adenosine levels, represses the expression of the long non-coding RNA MIR22HG, thus upregulating the oncogene cMYC protein level and its target gene expression. Our findings identify the critical role of ADSL hydroxylation in controlling cMYC and TNBC tumorigenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE136414 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA562516 https://www.ebi.ac.uk/ena/browser/view/PRJNA562516 https://www.ncbi.nlm.nih.gov/sra?term=SRP219378 [Overal design]Transcriptional profiling of MDA-MB-231 cells treated with sgRNA targeting ADSL or control sgRNA; [Treatment]'None'; [Growth]'None'; [Extraction]'Rneasy kit with on column Dnase digestion (Qiagen)\nTruSeq RNA Library Prep Kit v2 (Illumina) according to the manufacturer’s instructions'; [Cell type]'Source: ''cell line: MDA-MB-231; treatment: ADSL_sgRNA5; ', 'cell line: MDA-MB-231; treatment: ADSL_sgRNA6; ', 'cell line: MDA-MB-231; treatment: ctrl_sgRNA; ' GSE30597 Homo sapiens 10 Expression profiling by array GPL6883 Opposing effects of estrogen and Runx2 on breast cancer cell proliferation: identification of a reciprocally-regulated gene signature with clinical prognostic value. 2011-07-12 Analysis of reciprocal modulation of Runx2 and E2 signaling in BCA. Our objective was to investigate whether the interaction between estrogen and Runx2 signaling in breast cancer (BCa) could help refine an estrogen-responsive gene signature with improved prognostic value. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE30597 Opposing effects of Runx2 and estradiol on breast cancer cell proliferation: in vitro identification of reciprocally regulated gene signature related to clinical letrozole responsiveness. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-11-1530 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-11-1530} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA144569 https://www.ebi.ac.uk/ena/browser/view/PRJNA144569 None [Overal design]MCF7/Rx2dox BCa cells conditionally expressing Runx2 upon doxycycline treatment were treated with estradiol and/or doxycycline to induce Runx2, and global gene expression was profiled to define genes regulated by estradiol, Runx2, or both.; [Treatment]'MCF7/Runx2dox cells were treated with 0.5µg/ml doxycycline or 10nM estradiol and/or both for 48h'; [Growth]'MCF7/Runx2dox cells were maintained in DMEM supplemented with 10% FBS and 50µg of Hygromycin'; [Extraction]'RNA was extracted with Bio-Rad Aurum Total RNA mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with gel analysis.'; [Cell type]'Source: ''cell name: MCF7/Rx2dox cells; cell line: MCF7; transgene: Runx2 expression upon doxycycline treatment; treatment: Dox; ', 'cell name: MCF7/Rx2dox cells; cell line: MCF7; transgene: Runx2 expression upon doxycycline treatment; treatment: Control; ', 'cell name: MCF7/Rx2dox cells; cell line: MCF7; transgene: Runx2 expression upon doxycycline treatment; treatment: Dox + E2; ', 'cell name: MCF7/Rx2dox cells; cell line: MCF7; transgene: Runx2 expression upon doxycycline treatment; treatment: E2; ' GSE93710 Homo sapiens 8 Non-coding RNA profiling by array GPL22934 miR363-3p Mediates Maintenance and Chemoresistance of Breast Cancer Stem Cells 2017-01-17 There is increasing evidence that cancer recurrence and resistance to chemotherapy are linked to a subset of cancer stem cells. However, detecting these cells specifically and targeting them therapeutically remain challenging. As microRNAs (miRNAs) are emerging as key players in cancer biology, we set up to identify miRNAs involved in chemoresistance of breast cancer stem cells. In this study, we enriched populations of chemoresistant cancer stem cells from breast cancer and non-transformed breast cell lines using mammospheres. These mammospheres were treated or not with two chemoreagents, and we profiled surviving cells using miRNA microarray analysis. Comparison of the profiles from treated and untreated mammospheres as well as control and cancer cells yielded a six-miRNAs signature specific for chemoresistant stem cell-enriched subpopulations. From this signature miR-363-3p was found to be most highly overexpressed in various breast cancer cell lines and derived cancer stem cell-enriched populations, whereas non-tumorigenic cells had low levels. Inhibition of miR-363-3p was found to decrease cancer stem cell maintenance and tumorigenicity in vitro. Consistently, miR-363-3p downregulation decreased tumor growth and metastatization by human tumor cells transplanted in mice. Finally, miR363-3p levels in the sera of 38 breast cancer patients enrolled in a neoadjuvant trial correlated well with the response to the chemotherapeutic treatments. Altogether, miR363-3p was identified as a mediator of the breast cancer stem cell phenotype, and it may provide a predictor of the response to chemotherapy from a simple blood test, as well as a potential therapeutic approach for cancer stem cell targeting. This data set aims at identifying differentially expressed miRNAs in chemoresistant mammospheres, by the profiling of miRNA in MCF7 breast cancer cell-derived mammospheres selected to be resistant to 5 Fluorouracil (5FU) or Paclitaxel, as compared to unselected MCF7 mammospheres. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93710 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA362190 https://www.ebi.ac.uk/ena/browser/view/PRJNA362190 None [Overal design]miRNA expression was measured in eight samples. There are two untreated samples of normal breast cells (MCF10A) grown as mammospheres, two untreated samples of the breast cancer cell line MCF7 grown as mammospheres, two untreated samples of the breast cancer cell line MDA grown as mammospheres, and two additional samples from cell line MCF7 grown as mammospheres and treated with 5FU or Paclitaxel.; [Treatment]'To generate chemoresistant mammospheres, cells were maintained in mammospheres growth conditions 3 days before a 48h-treatment with paclitaxel (100nM, treatment a) or 5-fluorouracil (50mg/ml, treatment b).'; [Growth]'Cells (4000 cells/cm2) were grown in ultralow attachment plates (Corning, USA) and in the MammoCult culture medium (Stemcells technologies, France).'; [Extraction]'Cells were then harvested for RNA extraction. RNAs were extracted using TRIzol (Life Technologies, Fisher Scientific) following the manufacturer’s instructions, except that the volume of isopropanol used at the precipitation step was increased from 500 microL to 800 microL to enhance the recovery of small RNAs.'; [Cell type]'Source: ''cell line: MCF10A; ', 'cell line: MCF7; ', 'cell line: MDA; ' GSE28542 Homo sapiens 24 Expression profiling by array GPL6244 Expression Profiling of Inflammatory Breast Cancer Cells Treated with the Novel Histone Deacetylase Inhibitor, CG-1521 (Affymetrix HuGene-1_0) 2011-04-12 Studies of gene expression profiles using the whole genome wide microarray analysis in SUM149PT cells (ER-, p53mut) and SUM190PT cells (ER-, p53mut) when treated with 5 or 7.5 µM CG-1521 alone and in combination with 10 nM 17β-Estradiol. Comparisons between each treatment group provides evidence for the dysregulation of genes associated with the spindle assembly checkpoint. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28542 Histone deacetylase inhibitors modulate miRNA and mRNA expression, block metaphase, and induce apoptosis in inflammatory breast cancer cells. Cancer biology & therapy 2.879 https://doi.org/10.4161/cbt.25088 {Cancer biology & therapy (2.879): 10.4161/cbt.25088} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA143031 https://www.ebi.ac.uk/ena/browser/view/PRJNA143031 None [Overal design]Three independent experiments were carried out in SUM149PT and SUM190PT cells, which were treated with vehicle (ethanol/DMSO), 10nM 17β-Estradiol, 5 or 7.5µM CG-1521, and the combination of 17β-Estradiol and CG-1521. Total RNA was extracted from cell lysates using QIAGEN RNeasy mini kit after 48h of treatment.; [Treatment]'SUM149PT cells were plated at 1.5 x 10^6 cells per 150 x 25mm dish with 25mL of growth media, and allowed to adhere for 48h prior to treatment. The media in each plate was replaced with 25mL fresh media containing the drug treatment.', 'SUM190PT cells were plated at 1.5 x 10^6 cells per 150 x 25mm dish with 25mL of growth media containing 2%FBS and allowed to adhere for 24h. The media in each plate was then replaced with 25mL fresh media without FBS. After another 24h, each treatment was prepared at 6x concentration, so that 5mL of treatment solution was added to the 25mL growth media.'; [Growth]"SUM149PT cells were grown in Ham's F-12 media with 5% fetal bovine serume supplemented with 5 µg/mL insulin, 1 µg/mL hydrocortisone, 10 mM HEPES and Antimycotic/Antibiotic at 37°C with 5%CO2 and 85% humidity.", "SUM190PT cells were grown in Ham's F-12 media supplemented with 5 µg/mL insulin, 1 µg/mL hydrocortisone, 10 mM HEPES, 5mM Ethanolamine, 5µg/mL Transferrin, 10nM Triiodo Thyronine, 50nM Sodium Selenite, 1g/L Bovine Serum Albumin and Antibiotic/Antimycotic at 37° with 5% CO2 and 85% Humidity."; [Extraction]'Total RNA was extracted using the RNeasy Mini kit (Qiagen Inc., Valencia, CA, USA). RNA quality and concentration was determined by analysis with an Agilent 2100 bioanalyzer at the Center for Functional Genomics at State University of New York at Albany (Rensselaer, NY, USA)'; [Cell type]'Source: ''cell line: SUM149PT; er: ER(-); p53: mut (M237I); ', 'cell line: SUM190PT; er: ER(-); p53: mut (Q317X); ' GSE36598 Homo sapiens 8 Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing GPL570; GPL9052 Global transcriptional role of CtBP in breast cancer cells 2012-03-19 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36598 Genome-wide profiles of CtBP link metabolism with genome stability and epithelial reprogramming in breast cancer. Nature communications 11.878 https://doi.org/10.1038/ncomms2438 {Nature communications (11.878): 10.1038/ncomms2438} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA153683 https://www.ebi.ac.uk/ena/browser/view/PRJNA153683 None [Overal design]Refer to individual Series; [Treatment]"CtBP mRNA targetting oligos and the control oligos are from Dharmacon. Dharmafect1 transfection method was applied to introduce gene knockdown oligoes into the cells following manufacturer's manual."; [Growth]'MCF-7 cells were maintained in regular DMEM supplemented with 10% (v/v) FBS, penicillin-streptomycin (Invitrogen) and insulin.'; [Extraction]"Qiagen RNAeasy kit was applied to extract total RNA from MCF-7 cells following manufacturer's manual.", "Lysates were clarified from sonicated nuclei and CtBP-DNA complexes were isolated with antibody. Libraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit . Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation DNA was PCR amplified with Illumina primers for 15 cycles and library fragments of ~250 bp (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the Genome Analyzer following the manufacturer's protocols."; [Cell type]'Source: ', 'Immortalized breast cancer cells''cell line: MCF-7; treatment: CtBP KD for 72 hours; ', 'cell line: MCF-7; treatment: control KD for 72 hours; ', 'cell type: Immortalized breast cancer cells; passages: 15-18; chip antibody: CtBP; catalog#: H-440; vendor: Santa Cruz; ', 'cell type: Immortalized breast cancer cells; passages: 15-18; chip antibody: none; ' GSE6367 Homo sapiens 40 Expression profiling by array GPL8300 Gene profile of breast cancers with immunohistochemical phenotypes of ER+/- and/or HER2+/- 2006-11-26 Hormones and growth factors accelerate cell proliferation of breast cancer cells, and these molecules are well investigated targets for drug development and application. The mechanisms of cell proliferation of breast cancers lacking estrogen receptor (ER) and HER2 have not been fully understood. The purpose of the present study is to find genes that are differentially expressed in breast cancers and that might significantly contribute to cell proliferation in these cancers. Forty tumor samples, consisting of ten each of immunohistochemically ER(+)/HER2(-), ER(+)/HER2(+), ER(-)/HER2(+), and ER(-)/HER2(-) cancer were analyzed using oligonucleotide microarrays. Both genes and tumor samples were subjected to hierarchical clustering. ER(+)/HER2(-) breast cancers and ER(-)/HER2(-) cancers tended to form a tumor cluster, but HER2 positive breast cancers were split into different tumor clusters. Significant differential expression between IHC-ER(-)/HER2(-) and other tumors was defined as having an expression level at least 2-fold higher or 2-fold lower, and analyzed by multi-step two-way ANOVA. Genes overexpressed differently in IHC-ER(-)/HER2(-) breast cancers compared to other all three types were 8 genes (FABP7, GABRP, GAL, CXCL13, CDC42EP4, C2F, FOXM1, CSDA), and underexpressed genes were nine including ITGB5, KIAA0310, MAGED2, PRSS11, SORL1, TGFB3, KRT18, CPE, BCAS1. No gene was directly related to cell proliferation such as cyclins, cyclin-dependent kinase, p53, p16, and the pRb and p21 families. We had a particular focus on a transcriptional factor E2F-5 from a list of genes overexpressed in ER negative breast cancers compared to ER positive breast cancers, and further examined. Gene amplification of E2F-5 was detected in 5/57 (8.8%) in breast cancers by FISH. No point mutation was found at the binding domain with DNA or dimerization partner of E2F-5. Immunohistochemically E2F-5 positive cancers were more frequent in ER(-)/HER2(-) cancer (14/27, 51.9%) than in other types of cancer (5/30, 16.7%) (p=0.05). E2F-5 positive cancers had higher Ki-67 labeling index (59.5%) than E2F-5 negative cancers (36.3%). E2F-5 positive cancers showed higher histological grade including metaplastic carcinoma, and worse clinical outcome with shorter disease free survival in node negative patients. In conclusion, we demonstrated that there is a population of breast cancer with overexpression of a cell cycle related transcriptional factor E2F-5. E2F-5 positive breast cancers were frequent in ER(-)/HER2(-) group with high Ki-67 labeling index, high histological grade and worse clinical outcome. Keywords: immunohistochemical phenotype https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE6367 Overexpression of E2F-5 correlates with a pathological basal phenotype and a worse clinical outcome. British journal of cancer 5.416 https://doi.org/10.1038/sj.bjc.6604900 {British journal of cancer (5.416) doi:10.1038/sj.bjc.6604900}; {Cancer science (4.751) doi:10.1111/j.1349-7006.2012.02319.x}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA99585 https://www.ebi.ac.uk/ena/browser/view/PRJNA99585 None [Overal design]40 breast cancer consisted of ten each of immunohistochemically ER(+)/HER2(-), ER(+)/HER2(+), ER(-)/HER2(+), and ER(-)/HER2(-) cancers are compared.; [Treatment]'Tissues were surgically isolated and were immediately frozen in liquid nitrogen. Tissues were lysed and total RNA was extracted using the Sepasol-I (WAKO)'; [Growth]'not received any pre-operative adjuvant hormone or chemotherapy'; [Extraction]'Qiagen RNeasy kit'; [Cell type]'Source: ''' GSE76263 Homo sapiens 2 Genome variation profiling by array GPL13534 Oncometabolic nuclear reprogramming of cancer stemness 2015-12-22 By impairing histone demethylation and locking cells into a reprogramming-prone state, oncometabolites can partially mimic the process of induced pluripotent stem cell generation. Using a systems biology approach, combining mathematical modelling, computation, and proof-of-concept studies with live cells, we found that an oncometabolite-driven pathological version of nuclear reprogramming increases the speed and efficiency of dedifferentiating committed epithelial cells into stem-like states with only a minimal core of stemness transcription factors. Our biomathematical model, which introduces nucleosome modification and epigenetic regulation of cell differentiation genes to account for the direct effects of oncometabolites on nuclear reprogramming, demonstrates that oncometabolites markedly lower the “energy barriers” separating non-stem and stem cell attractors, diminishes the average time of nuclear reprogramming, and increases the size of the basin of attraction of the macrostate occupied by stem cells. These findings establish for the first time the concept of oncometabolic nuclear reprogramming of stemness as a novel metabolo-epigenetic mechanism for generation of cancer stem-like cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76263 Oncometabolic Nuclear Reprogramming of Cancer Stemness. Stem cell reports 5.499 https://doi.org/10.1016/j.stemcr.2015.12.012 {Stem cell reports (5.499): 10.1016/j.stemcr.2015.12.012} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA306745 https://www.ebi.ac.uk/ena/browser/view/PRJNA306745 None [Overal design]Total DNA was isolated according to standard procedures from MCF10A cells with heterozygous knock-in of IDH1 dominant-negative (R132H) point mutation (HD 101-013) and MCF10A isogenic parental cells (HD PAR-058), which were obtained from Horizon Discovery (HD) Ltd., Cambridge, UK; [Treatment]'No treatment'; [Growth]'Cells were routinely maintained in DMEM/F-12 including 2.5 mmol/L L-glutamine and 15 mmol/L HEPES, supplemented with 5% horse serum, 10 μg/mL insulin, 20 ng/mL hEGF, 0.5 μg/mL hydrocortisone, 0.1 μg/mL cholera toxin'; [Extraction]'Total DNA was isolated by standard procedures'; [Cell type]'Source: ''tissue: mammary gland; breast; cell line: MCF10A; ' GSE75292 Homo sapiens 6 Expression profiling by array GPL10558 Genome-wide analysis of gene expression by miR-204/211 in normal breast cell line MCF10A and breast cancer cell line MCF7 2015-11-23 Genome-wide expression analysis of MCF-10A and MCF-7 where miR-204 and miR-211 are overexpressed. The characteristics of differentially expressed genes in both cell lines derives the cells toward being oncogenic. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE75292 Genome-wide identification of target genes for miR-204 and miR-211 identifies their proliferation stimulatory role in breast cancer cells. Scientific reports 4.011 https://doi.org/10.1038/srep25287 {Scientific reports (4.011): 10.1038/srep25287} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA303137 https://www.ebi.ac.uk/ena/browser/view/PRJNA303137 None [Overal design]Total RNA is obtained from MCF-10A and 7 where miR-204/211 are overexpressed using lipofectamine RNAiMAX; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with QIAzol Lysis reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'epithelial''gender: female; tissue: breast; cell line: normal breast cell line MCF10A; cell type: epithelial; genotype/variation: control; ', 'gender: female; tissue: breast; cell line: normal breast cell line MCF10A; cell type: epithelial; genotype/variation: miR-204 overexpression; ', 'gender: female; tissue: breast; cell line: normal breast cell line MCF10A; cell type: epithelial; genotype/variation: miR-211 overexpression; ', 'gender: female; tissue: breast; cell line: breast cancer cell line MCF-7; cell type: epithelial; genotype/variation: control; ', 'gender: female; tissue: breast; cell line: breast cancer cell line MCF-7; cell type: epithelial; genotype/variation: miR-204 overexpression; ', 'gender: female; tissue: breast; cell line: breast cancer cell line MCF-7; cell type: epithelial; genotype/variation: miR-211 overexpression; ' GSE142525 Homo sapiens 2 Expression profiling by high throughput sequencing GPL23227 Effects of FZR1 knockout on gene expression of breast tumor cells treated with cisplatin 2019-12-23 We knockout FZR1 in T-47D breast cancer cell line, and treated the knockout and WT cells with cisplatin. The mRNA profiles were analyze. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE142525 FZR1 as a novel biomarker for breast cancer neoadjuvant chemotherapy prediction. Cell death & disease 5.959 https://doi.org/10.1038/s41419-020-03004-9 {Cell death & disease (5.959): 10.1038/s41419-020-03004-9} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA597321 https://www.ebi.ac.uk/ena/browser/view/PRJNA597321 https://www.ncbi.nlm.nih.gov/sra?term=SRP238586 [Overal design]mRNA profiles of 2 cisplatin treated breast cancer cell lines; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted using TRIZOL reagent (Invitrogen) following manufacturer’s instructions.'; [Cell type]'Source: ''cell line: T-47D; genotype: WT; drug: cisplatin; treatment dose: 2μg/mL; ', 'cell line: T-47D; genotype: FZR1 ko; drug: cisplatin; treatment dose: 2μg/mL; ' GSE5847 Homo sapiens 95 Expression profiling by array GPL96 Tumor and stroma from breast by LCM 2006-09-15 Tumor epithelium and surrounding stromal cells were isolated using laser capture microdissection of human breast cancer to examine differences in gene expression based on tissue types from inflammatory and non-inflammatory breast cancer Keywords: LCM https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE5847 A stromal gene signature associated with inflammatory breast cancer. International journal of cancer 4.982 https://doi.org/10.1002/ijc.23237 {International journal of cancer (4.982) doi:10.1002/ijc.23237}; {PloS one (2.776) doi:10.1371/journal.pone.0004531}; {The Journal of clinical investigation (None) doi:10.1172/JCI42059}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA97251 https://www.ebi.ac.uk/ena/browser/view/PRJNA97251 None [Overal design]We applied LCM to obtain samples enriched in tumor epithelium and stroma from 15 IBC and 35 non-IBC cases to study the relative contribution of each component to the IBC phenotype and to patient survival.; [Treatment]'None'; [Growth]'None'; [Extraction]'PicoPure kit (Arcturus)'; [Cell type]'Source: ''diagnosis: IBC; status: Deceased; ', 'diagnosis: IBC; status: Alive; ', 'diagnosis: non-IBC; status: Alive; patient_id: 1; race: European American; tnm_stage: I; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 2; race: African American; tnm_stage: IIA; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 4; race: European American; tnm_stage: I; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 5; race: European American; tnm_stage: IIA; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 6; race: African American; tnm_stage: IIA; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 7; race: European American; tnm_stage: IIB; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 8; race: European American; tnm_stage: IIA; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 12; race: European American; tnm_stage: IIA; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 9; race: European American; tnm_stage: IIA; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 10; race: African American; tnm_stage: IIA; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 13; race: European American; tnm_stage: IIB; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 14; race: European American; tnm_stage: IIIA; er_status: N/A; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 11; race: African American; tnm_stage: IIB; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 15; race: European American; tnm_stage: IIB; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 32; race: African American; tnm_stage: IIB; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 33; race: African American; tnm_stage: IIA; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 16; race: African American; tnm_stage: IIA; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 17; race: European American; tnm_stage: I; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 18; race: European American; tnm_stage: IIB; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 19; race: African American; tnm_stage: IIB; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 20; race: European American; tnm_stage: IIB; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 21; race: African American; tnm_stage: IIB; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 22; race: European American; tnm_stage: IIB; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 23; race: European American; tnm_stage: IIB; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 24; race: African American; tnm_stage: IIA; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 25; race: European American; tnm_stage: IIB; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 26; race: African American; tnm_stage: I; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 27; race: African American; tnm_stage: IIB; er_status: POS; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 34; race: African American; tnm_stage: IIIA; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 28; race: African American; tnm_stage: IIB; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 29; race: African American; tnm_stage: IIA; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 30; race: African American; tnm_stage: IIB; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 35; race: European American; tnm_stage: IIB; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 31; race: African American; tnm_stage: IIA; er_status: NEG; tissue: Stroma; ', 'diagnosis: non-IBC; status: Alive; patient_id: 1; race: European American; tnm_stage: I; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 2; race: African American; tnm_stage: IIA; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 3; race: African American; tnm_stage: IIA; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 4; race: European American; tnm_stage: I; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 5; race: European American; tnm_stage: IIA; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 6; race: African American; tnm_stage: IIA; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 7; race: European American; tnm_stage: IIB; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 8; race: European American; tnm_stage: IIA; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 12; race: European American; tnm_stage: IIA; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 9; race: European American; tnm_stage: IIA; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 10; race: African American; tnm_stage: IIA; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 13; race: European American; tnm_stage: IIB; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 14; race: European American; tnm_stage: IIIA; er_status: N/A; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 11; race: African American; tnm_stage: IIB; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Alive; patient_id: 15; race: European American; tnm_stage: IIB; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 32; race: African American; tnm_stage: IIB; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 33; race: African American; tnm_stage: IIA; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 16; race: African American; tnm_stage: IIA; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 17; race: European American; tnm_stage: I; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 18; race: European American; tnm_stage: IIB; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 19; race: African American; tnm_stage: IIB; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 20; race: European American; tnm_stage: IIB; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 21; race: African American; tnm_stage: IIB; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 22; race: European American; tnm_stage: IIB; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 23; race: European American; tnm_stage: IIB; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 24; race: African American; tnm_stage: IIA; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 25; race: European American; tnm_stage: IIB; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 26; race: African American; tnm_stage: I; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 27; race: African American; tnm_stage: IIB; er_status: POS; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 34; race: African American; tnm_stage: IIIA; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 28; race: African American; tnm_stage: IIB; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 29; race: African American; tnm_stage: IIA; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 30; race: African American; tnm_stage: IIB; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 35; race: European American; tnm_stage: IIB; er_status: NEG; tissue: Tumor; ', 'diagnosis: non-IBC; status: Deceased; patient_id: 31; race: African American; tnm_stage: IIA; er_status: NEG; tissue: Tumor; ' GSE163181 Mus musculus 25 Expression profiling by high throughput sequencing GPL19057 T11, AT3, PyMT-M, 2208L GEMM tumors treated with H3B-8800 2020-12-14 The objective is to identify splicing and expression changes that occur after spliceosome inhibition in triple-negative breast cancer using immune competent GEMM tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE163181 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA685157 https://www.ebi.ac.uk/ena/browser/view/PRJNA685157 https://www.ncbi.nlm.nih.gov/sra?term=SRP297915 [Overal design]4 different GEMM models of TNBC were transplanted orthotopically into C57BL/6 or Balbc females and then randomized onto 8800 or Vehicle. RNA was obtained from whole tumor. RNA from 3 or 4 biological replicate tumors were sequenced for each model for each condition.; [Treatment]'Mice were treated with 8800 or Vehicle each day prior to take down (as specified in manuscript) and tumor preservation in RNAlater.'; [Growth]'T11, AT3, PyMT-M, 2208L GEMM tumors were transplanted orthotopically into C57BL/6 or Balbc females and then randomized onto 8800 or Vehicle.'; [Extraction]'Bulk tumor RNA isolated using RNeasy kit (Qiagen).\n~300 bp insert strand specific library with polyA selection (TruSeq Stranded mRNA kit, Illumina).'; [Cell type]'Source: ''strain: Balb/c; tissue: Breast tumor; age: 4-5 week mice at transplant; genotype: Vehicle; phenotype: Nonresponder; ', 'strain: Balb/c; tissue: Breast tumor; age: 4-5 week mice at transplant; genotype: Drug; phenotype: Nonresponder; ', 'strain: C57BL/6; tissue: Breast tumor; age: 4-5 week mice at transplant; genotype: Vehicle; phenotype: Responder; ', 'strain: C57BL/6; tissue: Breast tumor; age: 4-5 week mice at transplant; genotype: Drug; phenotype: Responder; ', 'strain: C57BL/6; tissue: Breast tumor; age: 4-5 week mice at transplant; genotype: Vehicle; phenotype: Nonresponder; ', 'strain: C57BL/6; tissue: Breast tumor; age: 4-5 week mice at transplant; genotype: Drug; phenotype: Nonresponder; ', 'strain: Balb/c; tissue: Breast tumor; age: 4-5 week mice at transplant; genotype: Vehicle; phenotype: Responder; ', 'strain: Balb/c; tissue: Breast tumor; age: 4-5 week mice at transplant; genotype: Drug; phenotype: Responder; ' GSE115807 Homo sapiens 3 Expression profiling by array GPL21282 Regulating stem cell-related genes induces the plastic differentiation of cancer stem cells to treat cancer [in vitro] 2018-06-14 Relapse of cancer is associated with multi-directional differentiation, and unrestricted proliferative replication potential of cancer stem cells. Herein, we propose the plastic differentiation strategy for irreversible differentiation of cancer stem cells. Whole gene expression analysis revealed that salinomycin induced the cancer stem cells into normal cells, dormant cells, and mature cancer cells. Besides, the results indicated that the gatekeeper was related to the inhibition of PKC α signaling pathway. The differentiated normal or dormant cells were incorporated into normal tissue, while the rest were killed by chemotherapy. Our findings would offer the evidence for plastic differentiation of cancer stem cells, and propose an invert strategy for cancer therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115807 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA476108 https://www.ebi.ac.uk/ena/browser/view/PRJNA476108 None [Overal design]3 samples; [Treatment]'MDA-MB-435S stem cells were treated with salinomycin for 24h.'; [Growth]'MDA-MB-435S cells were maintained in serum-containing medium consisting of Leibovitz’s L15 medium supplemented with 10% fetal bovine serum (FBS), 100 units/mL penicillin, and 100 units/mL streptomycin. MDA-MB-435S stem cells were cultured in serum-free DMEM-Ham’s F12 medium supplemented with 10 ng/mL basic FGF, 20 ng/mL EGF, 5 mg/mL insulin, 0.4% BSA and 0.2% B27, 100 units/mL penicillin, and 100 units/mL streptomycin.'; [Extraction]'RNA extraction by Trizol Reagent (). RNA purity was checked by optical density of NanoDrop ND-1000 and agarose electrophoresis with the result of A260/A280≧1.8, A260/A230≧1.5, no gDNA contamination. RNA integrity was measured by Agilent RNA 6000 Nano Assay (RIN≧6).'; [Cell type]'breast cancer cells', 'breast cancer stem cells''treatment: serum-containing medium; cell line: MDA-MB-435S; gender: Female; cell type: breast cancer cells; ', 'treatment: Serum free culturing, one week; cell line: MDA-MB-435S; gender: Female; cell type: breast cancer stem cells; ', 'treatment: treated with salinomycin, 24h; cell line: MDA-MB-435S; gender: Female; cell type: breast cancer stem cells; ' GSE136277 Homo sapiens 1 Expression profiling by array GPL27139 Hyperglycemia promotes an aggressive phenotype in breast cancer cells 2019-08-23 Diabetes and breast cancer are common diseases with a major impact on the health sector in Mexico and worldwide. Epidemiological and experimental works support the link between type 2 diabetes and breast cancer; these data support that insulin resistance, hyperglycemia, hyperinsulinemia, and elevated levels of IGF-1 in patients with type II diabetes mellitus promote growth and invasiveness of tumor cells. The aim of the present work was to determine, by microarray, the mechanisms of action and signaling of a hyperglycemic microenvironment in the cell line (MDA-MB-231) and its effect to treatment with cisplatin (CCP). MDA-MB-231 breast cancer cells were cultured in DMEM medium, supplemented with 10% fetal bovine serum and antibiotics at 5% CO2, at 37 ˚C. We proceeded to extract total RNA for the analysis of microarrays under LG (low glucose) and HG (high glucose) conditions; for the cDNA synthesis, it was labeled with dUTP-Cy3 or dUTP-Cy5 fluorophores, using a CyScribe Firs-Strand cDNA kit. The analysis was carried out through the KEGG pathways program; some bioenergetic metabolism processes (glycolysis, biosynthesis of purines and pyrimidines, and metabolism of glycerol phospholipids) were found altered, which fulfill the feedback function to the cellular microenvironment, activating some signaling processes, such as the Hippo route, PI3K-Akt, Jak-STAT, MAPK, Ras, Wnt/β-catenin, apoptosis, and favoring an aggressive phenotype and drug resistance in a hyperglycemic microenvironment. The microarray analysis was validated by qRT-PCr of the tetraspanin and Frizzled genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE136277 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA561818 https://www.ebi.ac.uk/ena/browser/view/PRJNA561818 None [Overal design]The cells were cultured in BG and HG media; 10 μg of total RNA were obtained and used for cDNA synthesis and labeling with a Super Script II kit Invitrogen, using the dUTP-Cy3 incorporation array for BG (control) and dUTP-Cy5 for HG. Incorporation efficiency was analyzed measuring absorbance at 555 nm for Cy3 and 655 nm for Cy5. Similar quantities of fluorophores labeled cDNA were hybridized on the oligonucleotides collection 50-mer Human10K from MWG Biotech Oligo Bio Sets (Germany). Images of the microarrays were acquired and quantified in a Scan Array 4000 using the Quant Array software from Packard BioChips (USA). A first analysis of the images and the data was performed using the Array-Pro Analyzer software from Media Cybernetics (USA). Microarray data analysis was performed using the free software program genArise, allowing background correction, normalization, intensity filter, replicate analysis, and selection of differentially expressed genes; this program was developed in the Computing Unit of the Cellular Physiology Institute of the UNAM.; [Treatment]'None'; [Growth]'The cells were cultured in BG and HG media;'; [Extraction]'total RNA extraction'; [Cell type]'Source: ''cell line: MDA-MB-231; ' GSE34148 Homo sapiens 12 Expression profiling by array GPL10558 Phosphorylated and Sumoylation-Deficient Progesterone Receptors Drive Proliferative Gene Signatures During Breast Cancer Progression (Illumina gene expression analysis) 2011-12-05 Anlaysis of the differential gene expression between T47D cells expressing wild type (WT) progesterone receptor isoform B (PR) or SUMOylation-deficient PR molecules. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE34148 Phosphorylated and sumoylation-deficient progesterone receptors drive proliferative gene signatures during breast cancer progression. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr3211 {Breast cancer research : BCR (5.676): 10.1186/bcr3211} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA156473 https://www.ebi.ac.uk/ena/browser/view/PRJNA156473 None [Overal design]Total RNA obtained from T47D breast cancer cells that express either WT PR-B or mutant PR-B (K388R, SUMO-deficient), treated with or without synthetic PR ligand R5020 for 6 h.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''tissue: breast; genotype: PR null; parental cell line: T47D-Y; ligand treatment: vehicle; ', 'tissue: breast; genotype: PR null; parental cell line: T47D-Y; ligand treatment: R5020; ', 'tissue: breast; genotype: wild type PR; parental cell line: T47D-Y; ligand treatment: vehicle; ', 'tissue: breast; genotype: wild type PR; parental cell line: T47D-Y; ligand treatment: R5020; ', 'tissue: breast; genotype: mutant K388R PR; parental cell line: T47D-Y; ligand treatment: vehicle; ', 'tissue: breast; genotype: mutant K388R PR; parental cell line: T47D-Y; ligand treatment: R5020; ' GSE15632 Mus musculus 8 Expression profiling by array GPL4134 Gene expression profiling of Stat3flx/flx/NIC breast tumors compared to wild type NIC tumors. 2009-04-10 A Stat3-dependent transcription regulatory network involved in inflammation and metastasis is identified. Analyses of the gene expression data revealed that Stat3flx/flx/NIC tumors exhibited a significant reduction in the expression of factors involved in both tumor angiogenesis (fibronectin, von willebrand factor, annexin a3, thrombopoietin, fibulin 5) and in the acute phase inflammatory response (cebpd, osmr, saa1, saa2) https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15632 Identification of a Stat3-dependent transcription regulatory network involved in metastatic progression. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-09-1684 {Cancer research (8.378): 10.1158/0008-5472.CAN-09-1684} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA115629 https://www.ebi.ac.uk/ena/browser/view/PRJNA115629 None [Overal design]Common reference design. 8 samples including RNA extracted from 3 pools of Stat3wt/wt/NIC (WT) tumor tissues (5 individual tumor samples per pool) and 5 individual Stat3flx/flx/NIC (Homo) tumor tissue samples.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted from flash frozen mammary tumor samples using a Qiagen Rneasy Midi Kit'; [Cell type]'Source: ''tissue: mammary epithelial tumor; gender: female; parity: virgin; strain: Stat3flx/flx/MMTV-NIC; tumor stage: 6 weeks post palpation; ', 'reference: Stratagene universal mouse reference; ', 'tissue: mammary epithelial tumor; gender: female; parity: virgin; strain: Stat3wt/wt/MMTV-NIC; tumor stage: 6 weeks post palpation; ' GSE92443 Homo sapiens 7 Genome binding/occupancy profiling by high throughput sequencing GPL16791 TGF-beta signalling through SMAD1/5 is required for epithelial-to-mesenchymal transition 2016-12-15 TGF-beta treatment leads to SMAD1/5 phosphorylation. However, the ability of SMAD1/5 to bind chromatin downstream of TGF-beta signalling is unknown. We performed ChIP-sequencing for pSMAD1/5 and SMAD3 to identify binding sites for pSMAD1/5 upon TGF-beta stimulation and identified preferential pSMAD1/5 binding at SMAD1/5:SMAD4 consensus sites. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE92443 TGF-β uses a novel mode of receptor activation to phosphorylate SMAD1/5 and induce epithelial-to-mesenchymal transition. eLife 7.551 https://doi.org/10.7554/eLife.31756 {eLife (7.551): 10.7554/eLife.31756} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA357571 https://www.ebi.ac.uk/ena/browser/view/PRJNA357571 https://www.ncbi.nlm.nih.gov/sra?term=SRP095175 [Overal design]MDA-MB-231 cells untreated or treated with TGF-beta for 1 h and then examined with a SMAD3 or pSMAD1/5 antibody. The SMAD3 acts as a control as it is well known that SMAD3 is required for transcriptional regulation of many TGF-beta target genes.; [Treatment]'Either untreated or treated with 2ng/mL TGF-beta for 1 h.'; [Growth]'DMEM, 10% FCS, overnight starvation in OptiMEM prior to ligand stimulation.'; [Extraction]'Cross-linking with 4% formaldehyde for 5 min at room temperature followed by isolation of nuclei, sonication and immunoprecipitation.\nFollowing end repair, poly-A-tailing and adapter ligation, Illumina TruSeq ChIP sample preparation kits were used to generate the libraries. The Illumina kit Phusion enzyme was replaced by Kapa HiFi HotStart ready mix (Kapa Biosystems, Cape Town, South Africa). The PCR was run before gel isolation using the Invitrogen SizeSelect E-gel system (SizeSelect gel protocol, Thermo Fisher Scientific). Post PCR we used AMPure XP beads (AMPure bead protocol, Beckman Coulter, Inc.) at a 1:1 ratio to maintain size integrity. Samples were multiplexed and 101-bp single end reads were generated on an Illumina HiSeq 2500.'; [Cell type]'Breast cancer derived cell line''cell type: Breast cancer derived cell line; cell line: MDA-MB-231; treatment: Untreated; antibody: SMAD3, Abcam 28379; ', 'cell type: Breast cancer derived cell line; cell line: MDA-MB-231; treatment: Untreated; antibody: pSMAD1/5, Cell Signaling Technologies 11971; ', 'cell type: Breast cancer derived cell line; cell line: MDA-MB-231; treatment: TGF beta, 1 h; antibody: SMAD3, Abcam 28379; ', 'cell type: Breast cancer derived cell line; cell line: MDA-MB-231; treatment: TGF beta, 1 h; antibody: pSMAD1/5, Cell Signaling Technologies 11971; ', 'cell type: Breast cancer derived cell line; cell line: MDA-MB-231; treatment: Untreated; antibody: -; ', 'cell type: Breast cancer derived cell line; cell line: MDA-MB-231; treatment: TGF beta, 1 h; antibody: -; ' GSE101124 Homo sapiens 15 Non-coding RNA profiling by array GPL19978 circRNA expression in breast cancer 2017-07-11 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE101124 circTADA2As suppress breast cancer progression and metastasis via targeting miR-203a-3p/SOCS3 axis. Cell death & disease 5.959 https://doi.org/10.1038/s41419-019-1382-y {Cell death & disease (5.959) doi:10.1038/s41419-019-1382-y}; {American journal of translational research (3.266) pubmed_id = 33194025}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA393772 https://www.ebi.ac.uk/ena/browser/view/PRJNA393772 None [Overal design]Refer to individual Series; [Treatment]'Treated with Trizol for extraction', 'Tissues from surgury and promptly frozen in liquid nitrogen.'; [Growth]'Cells are cultured in EMEM containing 2 mM L-glutamine, 0.01 mg/mL bovine insulin (90%), fetal bovine serum (10%) and Earle’s BSS containing 1.5 g/L sodium bicarbonate, 0.1 mM non-essential amino acids and 1 mM sodium pyruvate.', 'breast cancer and non-tumor breast tissues'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: breast cancer; subtype: MCF-7; ', 'cell line: breast cancer; subtype: MDA-MB-231; ', 'cell line: breast cancer; subtype: Primary cells isolated from breast ductal carcinoma; ', 'cell line: breast cancer; subtype: Tamoxifen-Resistant MCF-7 cell; ', 'tissue: breast tumor; subtype: luminal A; gender: female; ', 'tissue: breast tumor; subtype: Triple-negative\xa0breast\xa0cancer; gender: female; ', 'tissue: mammary gland; subtype: non-tumor breast tissues; gender: female; ' GSE112852 Homo sapiens 47 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Next generation sequencing profiling experimental circulating tumor cells-derived metastatic variants [ATAC-seq] 2018-04-09 Hematogenous metastasis is initiated by a subset of circulating tumor cells (CTCs) shed from primary or metastatic tumors into the blood circulation. Thus, CTCs provide a unique patient biopsy resource to decipher the cellular subpopulations that initiate metastasis and their molecular properties. However, one crucial question is whether CTCs derived from patients recapitulate human metastatic disease in an animal model. Here, we show that CTC lines established from breast cancer patients are capable of generating metastases in mice with a pattern recapitulating most major organs from corresponding patients. We used ATAC-seq to assay chromatin accessibility in parental CTC and CTC-derived metastatic cells. Genome-wide sequencing analyses of metastatic variants identified novel chromatin accessibility domains predicting organ-specific metastasis identified from CTCs and facilitate the development of potential therapies targeting metastatis initiating cells in circulation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112852 Circulating Tumor Cells Exhibit Metastatic Tropism and Reveal Brain Metastasis Drivers. Cancer discovery 26.370 https://doi.org/10.1158/2159-8290.CD-19-0384 {Cancer discovery (26.370): 10.1158/2159-8290.CD-19-0384} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA449339 https://www.ebi.ac.uk/ena/browser/view/PRJNA449339 https://www.ncbi.nlm.nih.gov/sra?term=SRP139038 [Overal design]Profiling of 4 breast cancer CTC lines (4-8 replicates each) and -derived metastatic variants from brains (7 samples), bones (8 samples), lungs (5 samples), ovaries (5 samples) and kidney (1 sample).; [Treatment]'None'; [Growth]'CTC lines were cultured in ultra-low attachment plates with RPMI 1640 medium, supplemented with EGF (20ng/ml), bFGF (20ng/ml), 1X B27 and 1X antibiotic/antimycotic, in 4% O2 and 5% CO2. Metastatic tumors were established by inoculation of 100,000 GFP-LUC labeled CTCs in 100 µl of PBS into the left cardiac ventricles of 6-8 weeks old female NSG mice supplemented with subcutaneous slow release estrogen pills. Metastatic lesions were further dissociated into single-cell suspension by automated dissociation. CTC-derived metastatic cells (GFP+ cells) were sorted for ATAC sequencing.'; [Extraction]'Nuclei preparation was generated by resuspension of 25,000 or 50,000 sorted cells in nonionic lysis buffer (10 mM Tris pH7.4, 10 mM NaCl, 3 mM MgCl2, 0.1% (v/v) Igepal CA630).\nTransposition reaction was performed by using the Tn5 transposase (Nextera kit) at 37ºC for 30 minutes. Transposed DNA was further amplified by PCR, and the generated libraries were purified using Agencourt AMPure XP (Beckman Coulter). Library quality was controlled by using a Bioanalyzer high-sensitivity DNA analysis kit (Agilent)'; [Cell type]'Source: ''cell line: Brx07; parental or metastasis?: parental CTC; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: NA; generation: NA; ', 'cell line: Brx07; parental or metastasis?: parental CTC undergone dissociation protocol; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: lungdisso; generation: NA; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: Kidney; grown_in_culture: yes; dissociation_protocol: lungdisso; generation: 1; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: lung; grown_in_culture: no; dissociation_protocol: lungdisso; generation: 2; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: lung; grown_in_culture: yes; dissociation_protocol: lungdisso; generation: 2; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: lung; grown_in_culture: yes; dissociation_protocol: lungdisso; generation: 1; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: ovary; grown_in_culture: yes; dissociation_protocol: lungdisso; generation: 1; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: ovary; grown_in_culture: no; dissociation_protocol: lungdisso; generation: 2; ', 'cell line: Brx42; parental or metastasis?: parental CTC; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: NA; generation: NA; ', 'cell line: Brx42; parental or metastasis?: parental CTC undergone dissociation protocol; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: braindisso; generation: NA; ', 'cell line: Brx42; parental or metastasis?: metastatic sample; metastatic site: brain; grown_in_culture: no; dissociation_protocol: braindisso; generation: 1; ', 'cell line: Brx50; parental or metastasis?: parental CTC; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: NA; generation: NA; ', 'cell line: Brx50; parental or metastasis?: parental CTC undergone dissociation protocol; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: braindisso; generation: NA; ', 'cell line: Brx50; parental or metastasis?: metastatic sample; metastatic site: bone; grown_in_culture: no; dissociation_protocol: bonedisso; generation: 2; ', 'cell line: Brx50; parental or metastasis?: metastatic sample; metastatic site: brain; grown_in_culture: yes; dissociation_protocol: braindisso; generation: 3; ', 'cell line: Brx50; parental or metastasis?: metastatic sample; metastatic site: brain; grown_in_culture: yes; dissociation_protocol: braindisso; generation: 2; ', 'cell line: Brx50; parental or metastasis?: metastatic sample; metastatic site: brain; grown_in_culture: no; dissociation_protocol: braindisso; generation: 2; ', 'cell line: Brx68; parental or metastasis?: parental CTC; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: NA; generation: NA; ', 'cell line: Brx68; parental or metastasis?: parental CTC undergone dissociation protocol; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: bonedisso; generation: NA; ', 'cell line: Brx68; parental or metastasis?: metastatic sample; metastatic site: bone; grown_in_culture: yes; dissociation_protocol: bonedisso; generation: 1; ', 'cell line: Brx68; parental or metastasis?: metastatic sample; metastatic site: bone; grown_in_culture: no; dissociation_protocol: bonedisso; generation: 1; ', 'cell line: Brx68; parental or metastasis?: metastatic sample; metastatic site: bone; grown_in_culture: no; dissociation_protocol: bonedisso; generation: 2; ', 'cell line: Brx68; parental or metastasis?: metastatic sample; metastatic site: brain; grown_in_culture: yes; dissociation_protocol: braindisso; generation: 1; ', 'cell line: Brx68; parental or metastasis?: metastatic sample; metastatic site: lung; grown_in_culture: yes; dissociation_protocol: lungdisso; generation: 1; ' GSE14847 Homo sapiens 11 Expression profiling by array GPL6102 The effect of miRNA overexpression on gene expression profile of MCF-7 cells 2009-02-16 To identify microRNAs impacting estrogen receptor ERα expression in breast cancer, we have screened ER-positive breast cancer cells with a library of pre-miRs, and systematically monitored the ERα expression by protein lysate microarrays. There was a significant enrichment of the in silico predicted ERα targeting microRNAs among the hits. The most potent pre-miRs miR-18a/b, miR-193b, miR-206, and miR-302c, were confirmed to directly target ERα and to repress estrogen-responsive genes. The effect of miRNA overexpression on gene expression profile of MCF-7 cells was studied. Furthermore, miR-18a and miR-18b showed increased expression in ERα-negative as compared to ERα-positive clinical tumors. In summary, we present systematic and direct functional and correlative clinical evidence on microRNAs inhibiting ERα signaling in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE14847 Protein lysate microarray analysis to identify microRNAs regulating estrogen receptor signaling in breast cancer cell lines. Oncogene 6.634 https://doi.org/10.1038/onc.2009.241 {Oncogene (6.634): 10.1038/onc.2009.241} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA112123 https://www.ebi.ac.uk/ena/browser/view/PRJNA112123 None [Overal design]MCF-7 cells (300 000 per well on 6-well plates) were transfected with an siRNA for ERα or with Ambion pre-miR™ constructs for miR-18a, miR-193b, miR-206, miR-302c, or pre-miR negative control #1 (scrambled pre-miR) at 20 nM, and incubated for 24h.; [Treatment]'MCF-7 cells (300\xa0000 per well on 6-well plates) were transfected with Ambion pre-miR™ construct for miR-18a at 20 nM, and incubated for 24h.', 'MCF-7 cells (300\xa0000 per well on 6-well plates) were transfected with Ambion pre-miR™ construct for miR-193b at 20 nM, and incubated for 24h.', 'MCF-7 cells (300\xa0000 per well on 6-well plates) were transfected with Ambion pre-miR™ construct for miR-302c at 20 nM, and incubated for 24h.', 'MCF-7 cells (300\xa0000 per well on 6-well plates) were transfected with Ambion pre-miR™ construct for miR-206 at 20 nM, and incubated for 24h.', 'MCF-7 cells (300\xa0000 per well on 6-well plates) were transfected with Ambion pre-miR™ negative control #1 (scrambled pre-miR) at 20 nM, and incubated for 24h.', 'MCF-7 cells (300\xa0000 per well on 6-well plates) were transfected with an siRNA for ERα at 20 nM, and incubated for 24h.'; [Growth]'MCF-7 cells were grown at normal growth conditions.'; [Extraction]'The total cellular RNAs were isolated with MiRVana™ total RNA isolation kit (Ambion).'; [Cell type]'epithelial''atcc® number: HTB-22; designations: MCF7; gender: Female; growth properties: adherent; morphology: epithelial; organ: mammary gland; breast; disease: adenocarcinoma; derived from metastatic site: pleural effusion; cell type: epithelial; ' GSE49794 Homo sapiens 5 Methylation profiling by genome tiling array GPL13534 DNA methylation analysis of breast cancer cell-lines 2013-08-12 Recurrent mutations in histone modifying enzymes in multiple cancer types imply key roles in tumorigenesis. However, the functional relevance of these mutations remains unknown. Here we show that the JARID1B histone H3 lysine 4 demethylase is frequently amplified and overexpressed in luminal breast tumors and a somatic point mutation of JARID1B leads to the gain of luminal-specific gene expression programs. Downregulation of JARID1B in luminal breast cancer cells induces the expression of basal cell-specific genes and growth arrest, which is partially rescued by the inhibition of TGFBR thereby indicating a key role for TGFb signaling. Integrated genome-wide analysis of JARID1B chromatin binding, histone H3 lysine trimethyl (H3K4me3) and dimethyl (H3K4me2) patterns, and gene expression profiles in luminal and basal-like breast cancer cells suggest a key role for JARID1B in luminal cell-specific gene expression programs. A significant fraction of JARID1B binding-sites overlaps with CTCF in both luminal and basal-like breast cancer cells. CTCF also co-immunoprecipitates with JARID1B and it may influence its histone demethylase (HDM) activity as the H3K4me3/me2 ratio is lower at the CTCF-overlapping compared to JARID1B-unique sites. Additionally, a heterozygous JARID1B missense mutation (K1435R) in the HCC2157 basal-like breast cancer cell line is associated with unique JARID1B chromatin-binding and gene expression patterns implying gain of luminal features. In line with this, exogenous expression of this mutant in basal-like breast cancer cells leads to a gain of JARID1B binding at many luminal-specific genes. A PARADIGM score reflecting JARID1B activity in luminal breast cancer cells is associated with poor clinical outcome in patients with luminal breast tumors. Together, our data imply that JARID1B is a luminal lineage-driving oncogene and that its therapeutic targeting may represent a novel therapeutic strategy in treatment-resistant luminal breast tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE49794 JARID1B is a luminal lineage-driving oncogene in breast cancer. Cancer cell 23.916 https://doi.org/10.1016/j.ccr.2014.04.024 {Cancer cell (23.916): 10.1016/j.ccr.2014.04.024} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA214937 https://www.ebi.ac.uk/ena/browser/view/PRJNA214937 None [Overal design]Bisulphite converted DNA from 5 breast cancer cell lines were hybridised to the Illumina Infinium HumanMethylation450 BeadChip.; [Treatment]'None'; [Growth]'None'; [Extraction]'standard procedure'; [Cell type]'breast cancer''cell line: SUM159; cell type: breast cancer; subtype: Basal-like cells; ', 'cell line: T47D; cell type: breast cancer; subtype: Luminal cells; ', 'cell line: MCF7; cell type: breast cancer; subtype: Luminal cells; ', 'cell line: MDAMB231; cell type: breast cancer; subtype: Basal-like cells; ', 'cell line: HCC2157; cell type: breast cancer; subtype: Basal-like cells; ' GSE31364 Homo sapiens 72 Expression profiling by array GPL14378 A gene expression profile that predicts circulating tumor cell presence in breast cancer patients 2011-08-12 Development of a primary tumor gene expression profile that can predict the presence of circulating tumor cells in the blood of breast cancer patients. The detection of circulating tumor cells (CTCs) in the peripheral blood and microarray gene expression profiling of the primary tumor are two promising new technologies able to provide valuable prognostic data for patients with breast cancer. In the current study, we aimed to develop a novel profile which provided independent prognostic data by building a signature predictive of CTC status rather than outcome. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE31364 A prognostic gene expression profile that predicts circulating tumor cell presence in breast cancer patients. PloS one 2.776 https://doi.org/10.1371/journal.pone.0032426 {PloS one (2.776): 10.1371/journal.pone.0032426} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA145883 https://www.ebi.ac.uk/ena/browser/view/PRJNA145883 None [Overal design]Seventy-two primary breast cancer tumor have been analyzed against a breast cancer reference pool.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA isolation. We used sections of 30-µm thickness for total RNA isolation. Total RNA was isolated with Trizol, and finally dissolved in RNase-free H2O and treated with DNase using the Qiagen RNase-free DNase kit and RNeasy spin columns.'; [Cell type]'Source: ''gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 42; days between diagnosis and blood collection: 2961; metastatic: 1; ', 'sample type: combined total RNA isolated from multiple breast cancer samples.; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 51; days between diagnosis and blood collection: 2142; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 69; days between diagnosis and blood collection: 336; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: 0; age at diagnosis: 45; days between diagnosis and blood collection: 2352; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 71; days between diagnosis and blood collection: 989; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 53; days between diagnosis and blood collection: 24; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: 0; age at diagnosis: 52; days between diagnosis and blood collection: 10; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 1; age at diagnosis: 59; days between diagnosis and blood collection: 16; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 51; days between diagnosis and blood collection: 2023; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 46; days between diagnosis and blood collection: 2141; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 44; days between diagnosis and blood collection: 2209; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 59; days between diagnosis and blood collection: 1456; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 52; days between diagnosis and blood collection: 1243; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 40; days between diagnosis and blood collection: 6446; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: 0; age at diagnosis: 48; days between diagnosis and blood collection: 30; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 73; days between diagnosis and blood collection: 0; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 51; days between diagnosis and blood collection: 24; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 36; days between diagnosis and blood collection: 25; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 58; days between diagnosis and blood collection: 22; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 52; days between diagnosis and blood collection: 4; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: 0; age at diagnosis: 81; days between diagnosis and blood collection: 4; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 1; age at diagnosis: 59; days between diagnosis and blood collection: 4; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 1; age at diagnosis: 86; days between diagnosis and blood collection: 14; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: 1; age at diagnosis: 46; days between diagnosis and blood collection: 10; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 50; days between diagnosis and blood collection: 7; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: na; age at diagnosis: 54; days between diagnosis and blood collection: 9; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 1; age at diagnosis: 42; days between diagnosis and blood collection: 48; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 53; days between diagnosis and blood collection: 9; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 42; days between diagnosis and blood collection: 3; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: 1; age at diagnosis: 34; days between diagnosis and blood collection: 6; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 51; days between diagnosis and blood collection: 27; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 85; days between diagnosis and blood collection: 15; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 56; days between diagnosis and blood collection: 39; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 59; days between diagnosis and blood collection: 10; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 1; age at diagnosis: 71; days between diagnosis and blood collection: 0; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 65; days between diagnosis and blood collection: 7; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 41; days between diagnosis and blood collection: 24; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 36; days between diagnosis and blood collection: 31; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 43; days between diagnosis and blood collection: 3; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 52; days between diagnosis and blood collection: 7; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: 1; age at diagnosis: 70; days between diagnosis and blood collection: 24; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 56; days between diagnosis and blood collection: 31; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 64; days between diagnosis and blood collection: 14; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 50; days between diagnosis and blood collection: 19; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 1; age at diagnosis: 62; days between diagnosis and blood collection: 26; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 1; age at diagnosis: 46; days between diagnosis and blood collection: 10; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: na; age at diagnosis: 60; days between diagnosis and blood collection: 111; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 1; age at diagnosis: 71; days between diagnosis and blood collection: 17; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: 0; age at diagnosis: 53; days between diagnosis and blood collection: 4; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 59; days between diagnosis and blood collection: 7; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 0; lymph node metastasis: 0; age at diagnosis: 61; days between diagnosis and blood collection: 14; metastatic: 0; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: 0; age at diagnosis: 60; days between diagnosis and blood collection: 4325; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 44; days between diagnosis and blood collection: 1651; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 51; days between diagnosis and blood collection: 589; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: 0; age at diagnosis: 42; days between diagnosis and blood collection: 4918; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 51; days between diagnosis and blood collection: 989; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 68; days between diagnosis and blood collection: 3410; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 53; days between diagnosis and blood collection: 3072; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 61; days between diagnosis and blood collection: 2415; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 46; days between diagnosis and blood collection: 875; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 49; days between diagnosis and blood collection: 2047; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 52; days between diagnosis and blood collection: 1288; metastatic: 1; ', 'gender: female; tissue: breast; tumor type: primary tumor; ctc_status: 1; lymph node metastasis: na; age at diagnosis: 47; days between diagnosis and blood collection: 927; metastatic: 1; ' GSE68845 Homo sapiens 26 Other GPL11154 BRCA1, R-loops and Recombination defects in Ewing's sarcoma (DRIP-seq) 2015-05-13 Ewing’s sarcoma family of tumors (ESFT) is an aggressive pediatric bone and soft tissue cancer. It is the prototypical example of mesenchymal tumors driven by a fusion oncogene involving the ewing sarcoma break point region 1 (EWSR1) gene, most frequently– EWS-FLI1. We have discovered that loss of EWSR1 leads to accumulation of R-loops, replication stress and impaired homologous recombination, recapitulating breast cancer 1, early onset (BRCA1) deficiency. EWS-FLI1 acts dominant negatively in ESFT to impart the same phenotypes. Further we demonstrate that in ESFT, BRCA1 predominantly associates with the elongating transcription machinery and is unavailable for DNA strand break repair. Gene expression profiling identified upregulated compensatory mechanisms in ESFT cells to process increased R-loops (RNASEH2 and FEN1) and replication stress (Fanconi Anemia). Taken together, our data identifies BRCA1 sequestration due to transcription stress as the mechanistic basis for ESFT chemosensitivity and suggests potential targets for the much lacking second-line therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE68845 EWS-FLI1 increases transcription to cause R-loops and block BRCA1 repair in Ewing sarcoma. Nature 43.070 https://doi.org/10.1038/nature25748 {Nature (43.070): 10.1038/nature25748} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA283900 https://www.ebi.ac.uk/ena/browser/view/PRJNA283900 https://www.ncbi.nlm.nih.gov/sra?term=SRP058311 [Overal design]Examination of R-loops was conducted using DRIP-Seq. Three different Ewing's sarcoma cell lines, IMR90 control cell line and U2OS cells transfected with either siRNA against EWSR1 or EWS-FLI1 vector along with appropriate controls were used.Samples were further treated with either vehicle or LD65 dose of etoposide for 6 hours. Genomic DNA was extracted, digested with a restriction enzyme cocktail and used for pulldown of DNA:RNA hybrids.; [Treatment]'Samples were treated with either vehicle (DMSO) or indicated doses of etoposide for indicated amout of time before extraction of RNA'; [Growth]'Cells were passaged in 10cm corningware dishes using media described in Samples section in a 37°C humidified incubator'; [Extraction]'Genomic DNA was extracted from sub-confluent dishes and fragment with HindIII, EcoRI, BsrGI, XbaI and SspI (NEB). Half the samples were further treated to RNASEH (NEB). 10% of the samples from each cell line were pooled to form the Input. Monoclonal antibody S9.6 that recognizes DNA:RNA hybrids was used to enrich for R-loops.\nSequencing library was prepared using standard Illumina protocols'; [Cell type]"Ewing's sarcoma", 'Human fetal lung fibroblasts', 'Osteosarcoma'"cell type: Ewing's sarcoma; cell line: TC32; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; transfection protocol: none; treatment protocol: DMSO (NT: No Treatment); drip antibody: S9.6 (Kerafast, Cat#ENH001); ", "cell type: Ewing's sarcoma; cell line: TC32; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; transfection protocol: none; treatment protocol: 0.05μM Etoposide for 6 hours; drip antibody: S9.6 (Kerafast, Cat#ENH001); ", "cell type: Ewing's sarcoma; cell line: TC32; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; transfection protocol: none; treatment protocol: DMSO; sample preparation: pooled; drip antibody: none; ", "cell type: Ewing's sarcoma; cell line: EWS502; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; transfection protocol: none; treatment protocol: DMSO (NT: No Treatment); drip antibody: S9.6 (Kerafast, Cat#ENH001); ", "cell type: Ewing's sarcoma; cell line: EWS502; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; transfection protocol: none; treatment protocol: 0.25μM Etoposide for 6 hours; drip antibody: S9.6 (Kerafast, Cat#ENH001); ", "cell type: Ewing's sarcoma; cell line: EWS502; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; transfection protocol: none; treatment protocol: DMSO; sample preparation: pooled; drip antibody: none; ", "cell type: Ewing's sarcoma; cell line: CHLA10; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; transfection protocol: none; treatment protocol: DMSO (NT: No Treatment); drip antibody: S9.6 (Kerafast, Cat#ENH001); ", "cell type: Ewing's sarcoma; cell line: CHLA10; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; transfection protocol: none; treatment protocol: 0.15μM Etoposide for 6 hours; drip antibody: S9.6 (Kerafast, Cat#ENH001); ", "cell type: Ewing's sarcoma; cell line: CHLA10; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; transfection protocol: none; treatment protocol: DMSO; sample preparation: pooled; drip antibody: none; ", 'cell type: Human fetal lung fibroblasts; cell line: IMR90; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; transfection protocol: none; treatment protocol: DMSO (NT: No Treatment); drip antibody: S9.6 (Kerafast, Cat#ENH001); ', 'cell type: Human fetal lung fibroblasts; cell line: IMR90; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; transfection protocol: none; treatment protocol: 6μM Etoposide for 6 hours; drip antibody: S9.6 (Kerafast, Cat#ENH001); ', 'cell type: Human fetal lung fibroblasts; cell line: IMR90; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; transfection protocol: none; treatment protocol: DMSO; sample preparation: pooled; drip antibody: none; ', 'cell type: Osteosarcoma; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; cell line: U2OS; transfection protocol: Transfected with 20μg of empty vector (pMSCV, Clontech Cat#634401 ) using Lipofectamine 3000 (Invitrogen); treatment protocol: DMSO (NT: No Treatment); drip antibody: S9.6 (Kerafast, Cat#ENH001); ', 'cell type: Osteosarcoma; cell line: U2OS; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; transfection protocol: Transfected with 20μg of empty vector (pMSCV, Clontech Cat#634401 ) using Lipofectamine 3000 (Invitrogen); treatment protocol: 6μM Etoposide for 6 hours; drip antibody: S9.6 (Kerafast, Cat#ENH001); ', 'cell type: Osteosarcoma; cell line: U2OS; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; transfection protocol: Transfected with 40nmol of control siRNA (Santa Cruz,Cat#sc-37007) using Lipofectamine RNAiMax (Invitrogen); treatment protocol: DMSO (NT: No Treatment); drip antibody: S9.6 (Kerafast, Cat#ENH001); ', 'cell type: Osteosarcoma; cell line: U2OS; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; transfection protocol: Transfected with 40nmol of control siRNA (Santa Cruz, Cat#sc-37007) using Lipofectamine RNAiMax (Invitrogen); treatment protocol: 6μM Etoposide for 6 hours; drip antibody: S9.6 (Kerafast, Cat#ENH001); ', 'cell type: Osteosarcoma; cell line: U2OS; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; transfection protocol: Transfected with 40nmol of siRNA against EWSR1 (Santa Cruz, Cat#sc-35347) using Lipofectamine RNAiMax (Invitrogen); treatment protocol: DMSO (NT: No Treatment); drip antibody: S9.6 (Kerafast, Cat#ENH001); ', 'cell type: Osteosarcoma; cell line: U2OS; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; transfection protocol: Transfected with 40nmol of siRNA against EWSR1 (Santa Cruz, Cat#sc-35347) using Lipofectamine RNAiMax (Invitrogen); treatment protocol: 6μM Etoposide for 6 hours; drip antibody: S9.6 (Kerafast, Cat#ENH001); ', 'cell type: Osteosarcoma; cell line: U2OS; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; transfection protocol: Transfected with 40nmol of pooled siRNA against EWSR1 (ON-TARGETplus, Dharmacon, Cat#L-005119-02) using Lipofectamine RNAiMax (Invitrogen); treatment protocol: DMSO (NT: No Treatment); drip antibody: S9.6 (Kerafast, Cat#ENH001); ', 'cell type: Osteosarcoma; cell line: U2OS; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; transfection protocol: Transfected with 40nmol of pooled siRNA against EWSR1 (ON-TARGETplus, Dharmacon, Cat#L-005119-02) using Lipofectamine RNAiMax (Invitrogen); treatment protocol: 6μM Etoposide for 6 hours; drip antibody: S9.6 (Kerafast, Cat#ENH001); ', 'cell type: Osteosarcoma; cell line: U2OS; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; transfection protocol: none; treatment protocol: DMSO; sample preparation: pooled; drip antibody: none; ' GSE71402 Mus musculus 13 Methylation profiling by high throughput sequencing GPL17021 Tumor hypoxia causes DNA hypermethylation by reducing TET activity (TAB-Seq) 2015-07-27 Hypermethylation of tumor suppressor gene (TSG) promoters confers growth advantages to cancer cells, but how these changes arise is poorly understood. Here, we report that tumor hypoxia reduces the activity of oxygen-dependent TET enzymes, which catalyze DNA de-methylation through 5-methylcytosine oxidation. This occurs independently of hypoxia-associated alterations in TET gene expression, basal metabolism, HIF activity or nuclear reactive oxygen species, but directly depends on oxygen shortage. Hypoxia-induced loss of TET activity increases hypermethylation at gene promoters in vitro, while also in patients, gene promoters are markedly more methylated in hypoxic than normoxic tumors. Affected genes are frequently involved in DNA repair, cell cycle regulation, angiogenesis and metastasis, indicating cellular selection of hypermethylation events. Overall, up to 50% of the tumor-associated hypermethylation is ascribable to hypoxia across various cancer types. Accordingly, spontaneous murine breast tumors become hypermethylated when rendered hypoxic through vessel pruning, whereas vessel normalisation rescues this effect. Tumor hypoxia thus acts as a novel regulator underlying DNA methylation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE71402 Tumour hypoxia causes DNA hypermethylation by reducing TET activity. Nature 43.070 https://doi.org/10.1038/nature19081 {Nature (43.070): 10.1038/nature19081} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA291092 https://www.ebi.ac.uk/ena/browser/view/PRJNA291092 https://www.ncbi.nlm.nih.gov/sra?term=SRP061652 [Overal design]Shallow tet-assisted-bisulfite-sequencing of tumors with a normalized or truncated vasculature to assess global differences in 5hmC levels; [Treatment]'Mice were either WT or Phd heterozygotes, or hydrodynamically injected with an empty or sFlk1-overexpression plasmid. Whereas the Phd2+/-genotype restores vascularisation and oxygenation levels in the tumor, the latter treatment renders tumors more hypoxic'; [Growth]'breast tumors were isolated, flash-frozen in liquid nitrogen and stored at -150 until further processing'; [Extraction]'Nucleic acids were subsequently extracted using the Wizard Genomic DNA Purification (Promega, Leiden, The Netherlands) kit according to instructions, with all buffers supplemented with DFO (200 µM), dissolved in 80 µL PBS-DFO with RNAse A (200 units, NEB, Ipswich, MA, USA), incubated for 10 minutes at 37°C. After proteinase K addition (200 units) and incubation for 30 minutes at 56°C, DNA was purified using the QIAQuick blood and tissue kit (all buffers supplemented with DFO), eluted in 100 µL of a 10 mM Tris, 1mM EDTA solution (pH 8) and stored at -80°C until further processing.\nlibrary preparations and TAB-conversion were as described by Yu and colleagues (Nat Protoc 2012), except that bisulfite conversion was done using the EZ DNA Methylation-Lightning Kit (ZYMO), and libraries were amplified using the KAPA Uracil+ 2x master mix.\ntet-assisted-bisulfite-seq'; [Cell type]'Source: ''strain: FVB; hydrodynamically injected plasmid: NA; age: 16 weeks; replicate: A; ', 'strain: FVB; hydrodynamically injected plasmid: NA; age: 16 weeks; replicate: B; ', 'strain: FVB; hydrodynamically injected plasmid: NA; age: 16 weeks; replicate: C; ', 'strain: FVB, Phd2+/-; hydrodynamically injected plasmid: NA; age: 16 weeks; replicate: A; ', 'strain: FVB, Phd2+/-; hydrodynamically injected plasmid: NA; age: 16 weeks; replicate: B; ', 'strain: FVB, Phd2+/-; hydrodynamically injected plasmid: NA; age: 16 weeks; replicate: C; ', 'strain: FVB, Phd2+/-; hydrodynamically injected plasmid: NA; age: 16 weeks; replicate: D; ', 'strain: FVB; hydrodynamically injected plasmid: PRRL2-sFlk1; age: 12 weeks; replicate: A; ', 'strain: FVB; hydrodynamically injected plasmid: PRRL2-sFlk1; age: 12 weeks; replicate: B; ', 'strain: FVB; hydrodynamically injected plasmid: PRRL2-sFlk1; age: 12 weeks; replicate: C; ', 'strain: FVB; hydrodynamically injected plasmid: empty PRRL2; age: 12 weeks; replicate: A; ', 'strain: FVB; hydrodynamically injected plasmid: empty PRRL2; age: 12 weeks; replicate: B; ', 'strain: FVB; hydrodynamically injected plasmid: empty PRRL2; age: 12 weeks; replicate: C; ' GSE126675 Homo sapiens 8 Expression profiling by high throughput sequencing GPL16791 Inhibition of TNBC metastasis by Gpx1 2019-02-17 Gpx1 plays a vital role in the metastasis of TNBC cells by regulating cell adhesion. Depletion of Gpx1 reduces the survival, migration, and invasion of TNBC cells in vitro. Transcriptomic and signaling pathway analyses demonstrate that depletion of Gpx1 essentially impairs cell adhesion/spreading by down-regulating FAK/c-Src activation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE126675 Glutathione peroxidase-1 regulates adhesion and metastasis of triple-negative breast cancer cells via FAK signaling. Redox biology 7.793 https://doi.org/10.1016/j.redox.2019.101391 {Redox biology (7.793): 10.1016/j.redox.2019.101391} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA522914 https://www.ebi.ac.uk/ena/browser/view/PRJNA522914 https://www.ncbi.nlm.nih.gov/sra?term=SRP186127 [Overal design]Examination of transcriptome on control and Gpx1-depleted TNBC breast cancer cell lines by deep sequencing, in replicate.; [Treatment]'None'; [Growth]'None'; [Extraction]'The Illumina Qiagen RNeasy mini Kit (cat.No 74104) was used for the construction of sequencing libraries.\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'epithelial''tissue: Triple-negative breast cancer (TNBC) cell line HS578T; cell line: HS578T; tissue: mammary gland; breast; cell type: epithelial; genotype/variation: control; ', 'tissue: Triple-negative breast cancer (TNBC) cell line HS579T; cell line: HS578T; tissue: mammary gland; breast; cell type: epithelial; genotype/variation: control; ', 'tissue: Triple-negative breast cancer (TNBC) cell line HS580T; cell line: HS578T; tissue: mammary gland; breast; cell type: epithelial; genotype/variation: Gpx1-/-; ', 'tissue: Triple-negative breast cancer (TNBC) cell line HS581T; cell line: HS578T; tissue: mammary gland; breast; cell type: epithelial; genotype/variation: Gpx1-/-; ', 'tissue: Triple-negative breast cancer (TNBC) cell line MDA-MB-231; cell line: MDA-MB-231; tissue: mammary gland; breast; cell type: epithelial; genotype/variation: control; ', 'tissue: Triple-negative breast cancer (TNBC) cell line MDA-MB-232; cell line: MDA-MB-231; tissue: mammary gland; breast; cell type: epithelial; genotype/variation: control; ', 'tissue: Triple-negative breast cancer (TNBC) cell line MDA-MB-233; cell line: MDA-MB-231; tissue: mammary gland; breast; cell type: epithelial; genotype/variation: Gpx1-/-; ', 'tissue: Triple-negative breast cancer (TNBC) cell line MDA-MB-234; cell line: MDA-MB-231; tissue: mammary gland; breast; cell type: epithelial; genotype/variation: Gpx1-/-; ' GSE123604 Homo sapiens 40 Expression profiling by high throughput sequencing GPL18573 A novel computational complete deconvolution method using RNA-seq data 2018-12-11 The cell type composition of many biological tissues varies widely across samples. Such sample heterogeneity hampers efforts to probe the role of each cell type in the tissue microenvironment. Current approaches that address this issue have drawbacks. Cell sorting or single-cell based experimental techniques disrupt in situ interactions and alter physiological status of cells in tissues. Computational methods are flexible and promising; but they often estimate either sample-specific proportions of each cell type or cell-type-specific gene expression profiles, not both, by requiring the other as input. We introduce a computational Complete Deconvolution method that can estimate both sample-specific proportions of each cell type and cell-type-specific gene expression profiles simultaneously using bulk RNA-Seq data only (CDSeq). We assessed our method’s performance using several synthetic and experimental mixtures of varied but known cell-type composition and compared its performance to the performance of two state-of-the-art deconvolution methods on the same mixtures. The results showed CDSeq can estimate both sample-specific proportions of each component cell type and cell-type-specific gene expression profiles with high accuracy. CDSeq holds promise for computationally deciphering complex mixtures of cell types, each with differing expression profiles, using RNA-seq data measured in bulk tissue . https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE123604 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA509361 https://www.ebi.ac.uk/ena/browser/view/PRJNA509361 https://www.ncbi.nlm.nih.gov/sra?term=SRP173265 [Overal design]In brief, total mRNA was prepared from Namalwa (Burkitt’s lymphoma), Hs343T (fibroblast line derived from a mammary gland adenocarcinoma), hTERT-HME1 (normal mammary epithelial cells immortalized with hTERT), and MCF7 (estrogen receptor positive breast cancer cell line). mRNA samples were diluted to 100 ng/μl and mixed in different proportions (Supplementary Table 2). Global mRNA abundance of the four pure cell lines and of the mixed RNA samples was profiled by RNA-sequencing. Sequencing libraries were prepared using TruSeq RNA sample preparation kit v2 (Illumina). 75-bp single end sequencing was performed on the NextSeq sequencer (Illumina). After obtaining the fastq data, we first ran cutadapt (version 1.12) for trimming adapter sequences. Secondly, we mapped reads to the genome using STAR (version 020201). Lastly, we used featureCounts (version 1.5.1) to generate raw read counts data as the input for our algorithm.; [Treatment]'No treatment'; [Growth]'MCF7 cells were cultured in DMEM medium supplemented with 10% fetal bovine serum (FBS). Namalwa cells were a gift from Dr. Sandeep Dave, Duke University, and were cultured in RPMI medium supplemented with 10% FBS. Hs343T and hTERT-HME1 (ATCC) were cultured in HuMEC Ready medium (Thermo Fisher Scientific).'; [Extraction]'RNeasy kit\nTruSeq RNA sample preparation kit v2'; [Cell type]'Source: ''origin: cell line; sample name: Tumor-MCF7; tumor-mcf7 proportions: 100; cafs-hs_343.t proportions: 0; normal_breast-hmecs-htert proportions: 0; lymphocytes-namalwa proportions: 0; treatment: control; ', 'origin: cell line; sample name: CAFs-Hs_343.T; tumor-mcf7 proportions: 0; cafs-hs_343.t proportions: 100; normal_breast-hmecs-htert proportions: 0; lymphocytes-namalwa proportions: 0; treatment: control; ', 'origin: cell line; sample name: Normal_breast-hMECs-hTERT; tumor-mcf7 proportions: 0; cafs-hs_343.t proportions: 0; normal_breast-hmecs-htert proportions: 100; lymphocytes-namalwa proportions: 0; treatment: control; ', 'origin: cell line; sample name: Lymphocytes-Namalwa; tumor-mcf7 proportions: 0; cafs-hs_343.t proportions: 0; normal_breast-hmecs-htert proportions: 0; lymphocytes-namalwa proportions: 100; treatment: control; ', 'origin: cell line; sample name: Mixture_1; tumor-mcf7 proportions: 85; cafs-hs_343.t proportions: 5; normal_breast-hmecs-htert proportions: 5; lymphocytes-namalwa proportions: 5; treatment: control; ', 'origin: cell line; sample name: Mixture_2; tumor-mcf7 proportions: 85; cafs-hs_343.t proportions: 9; normal_breast-hmecs-htert proportions: 3; lymphocytes-namalwa proportions: 3; treatment: control; ', 'origin: cell line; sample name: Mixture_3; tumor-mcf7 proportions: 85; cafs-hs_343.t proportions: 3; normal_breast-hmecs-htert proportions: 9; lymphocytes-namalwa proportions: 3; treatment: control; ', 'origin: cell line; sample name: Mixture_4; tumor-mcf7 proportions: 85; cafs-hs_343.t proportions: 3; normal_breast-hmecs-htert proportions: 3; lymphocytes-namalwa proportions: 9; treatment: control; ', 'origin: cell line; sample name: Mixture_5; tumor-mcf7 proportions: 70; cafs-hs_343.t proportions: 10; normal_breast-hmecs-htert proportions: 10; lymphocytes-namalwa proportions: 10; treatment: control; ', 'origin: cell line; sample name: Mixture_6; tumor-mcf7 proportions: 70; cafs-hs_343.t proportions: 15; normal_breast-hmecs-htert proportions: 10; lymphocytes-namalwa proportions: 5; treatment: control; ', 'origin: cell line; sample name: Mixture_7; tumor-mcf7 proportions: 70; cafs-hs_343.t proportions: 15; normal_breast-hmecs-htert proportions: 5; lymphocytes-namalwa proportions: 10; treatment: control; ', 'origin: cell line; sample name: Mixture_8; tumor-mcf7 proportions: 70; cafs-hs_343.t proportions: 10; normal_breast-hmecs-htert proportions: 15; lymphocytes-namalwa proportions: 5; treatment: control; ', 'origin: cell line; sample name: Mixture_9; tumor-mcf7 proportions: 70; cafs-hs_343.t proportions: 10; normal_breast-hmecs-htert proportions: 5; lymphocytes-namalwa proportions: 15; treatment: control; ', 'origin: cell line; sample name: Mixture_10; tumor-mcf7 proportions: 70; cafs-hs_343.t proportions: 5; normal_breast-hmecs-htert proportions: 15; lymphocytes-namalwa proportions: 10; treatment: control; ', 'origin: cell line; sample name: Mixture_11; tumor-mcf7 proportions: 70; cafs-hs_343.t proportions: 5; normal_breast-hmecs-htert proportions: 10; lymphocytes-namalwa proportions: 15; treatment: control; ', 'origin: cell line; sample name: Mixture_12; tumor-mcf7 proportions: 55; cafs-hs_343.t proportions: 15; normal_breast-hmecs-htert proportions: 15; lymphocytes-namalwa proportions: 15; treatment: control; ', 'origin: cell line; sample name: Mixture_13; tumor-mcf7 proportions: 55; cafs-hs_343.t proportions: 30; normal_breast-hmecs-htert proportions: 10; lymphocytes-namalwa proportions: 5; treatment: control; ', 'origin: cell line; sample name: Mixture_14; tumor-mcf7 proportions: 55; cafs-hs_343.t proportions: 30; normal_breast-hmecs-htert proportions: 5; lymphocytes-namalwa proportions: 10; treatment: control; ', 'origin: cell line; sample name: Mixture_15; tumor-mcf7 proportions: 55; cafs-hs_343.t proportions: 10; normal_breast-hmecs-htert proportions: 30; lymphocytes-namalwa proportions: 5; treatment: control; ', 'origin: cell line; sample name: Mixture_16; tumor-mcf7 proportions: 55; cafs-hs_343.t proportions: 10; normal_breast-hmecs-htert proportions: 5; lymphocytes-namalwa proportions: 30; treatment: control; ', 'origin: cell line; sample name: Mixture_17; tumor-mcf7 proportions: 55; cafs-hs_343.t proportions: 5; normal_breast-hmecs-htert proportions: 30; lymphocytes-namalwa proportions: 10; treatment: control; ', 'origin: cell line; sample name: Mixture_18; tumor-mcf7 proportions: 55; cafs-hs_343.t proportions: 5; normal_breast-hmecs-htert proportions: 10; lymphocytes-namalwa proportions: 30; treatment: control; ', 'origin: cell line; sample name: Mixture_19; tumor-mcf7 proportions: 40; cafs-hs_343.t proportions: 20; normal_breast-hmecs-htert proportions: 20; lymphocytes-namalwa proportions: 20; treatment: control; ', 'origin: cell line; sample name: Mixture_20; tumor-mcf7 proportions: 40; cafs-hs_343.t proportions: 30; normal_breast-hmecs-htert proportions: 20; lymphocytes-namalwa proportions: 10; treatment: control; ', 'origin: cell line; sample name: Mixture_21; tumor-mcf7 proportions: 40; cafs-hs_343.t proportions: 30; normal_breast-hmecs-htert proportions: 10; lymphocytes-namalwa proportions: 20; treatment: control; ', 'origin: cell line; sample name: Mixture_22; tumor-mcf7 proportions: 40; cafs-hs_343.t proportions: 20; normal_breast-hmecs-htert proportions: 30; lymphocytes-namalwa proportions: 10; treatment: control; ', 'origin: cell line; sample name: Mixture_23; tumor-mcf7 proportions: 40; cafs-hs_343.t proportions: 20; normal_breast-hmecs-htert proportions: 10; lymphocytes-namalwa proportions: 30; treatment: control; ', 'origin: cell line; sample name: Mixture_24; tumor-mcf7 proportions: 40; cafs-hs_343.t proportions: 10; normal_breast-hmecs-htert proportions: 30; lymphocytes-namalwa proportions: 20; treatment: control; ', 'origin: cell line; sample name: Mixture_25; tumor-mcf7 proportions: 40; cafs-hs_343.t proportions: 10; normal_breast-hmecs-htert proportions: 20; lymphocytes-namalwa proportions: 30; treatment: control; ', 'origin: cell line; sample name: Mixture_26; tumor-mcf7 proportions: 25; cafs-hs_343.t proportions: 25; normal_breast-hmecs-htert proportions: 25; lymphocytes-namalwa proportions: 25; treatment: control; ', 'origin: cell line; sample name: Mixture_27; tumor-mcf7 proportions: 25; cafs-hs_343.t proportions: 35; normal_breast-hmecs-htert proportions: 25; lymphocytes-namalwa proportions: 15; treatment: control; ', 'origin: cell line; sample name: Mixture_28; tumor-mcf7 proportions: 25; cafs-hs_343.t proportions: 35; normal_breast-hmecs-htert proportions: 15; lymphocytes-namalwa proportions: 25; treatment: control; ', 'origin: cell line; sample name: Mixture_29; tumor-mcf7 proportions: 25; cafs-hs_343.t proportions: 25; normal_breast-hmecs-htert proportions: 35; lymphocytes-namalwa proportions: 15; treatment: control; ', 'origin: cell line; sample name: Mixture_30; tumor-mcf7 proportions: 25; cafs-hs_343.t proportions: 25; normal_breast-hmecs-htert proportions: 15; lymphocytes-namalwa proportions: 35; treatment: control; ', 'origin: cell line; sample name: Mixture_31; tumor-mcf7 proportions: 25; cafs-hs_343.t proportions: 15; normal_breast-hmecs-htert proportions: 35; lymphocytes-namalwa proportions: 25; treatment: control; ', 'origin: cell line; sample name: Mixture_32; tumor-mcf7 proportions: 25; cafs-hs_343.t proportions: 15; normal_breast-hmecs-htert proportions: 25; lymphocytes-namalwa proportions: 35; treatment: control; ' GSE137679 Homo sapiens 3 Expression profiling by array GPL16686 Transcriptomic analysis from ciprofloxacin treated human triple negative breast cancer cells 2019-09-18 A DNA microarray study was conducted to determine the impact of Mt-CFX on mRNA expression and pathway activation in human triple negative breast cancer cells. We used microarrays to detail the global program of gene expression underlying cellularisation and identified distinct classes of up- and down-regulated genes during this process. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE137679 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA566196 https://www.ebi.ac.uk/ena/browser/view/PRJNA566196 None [Overal design]MDA-MB-231 cells were treated with Mt-CFX, CFX, or 1% DMSO as a control for 72 h.; [Treatment]'The cells treated with 10 µM Mt-CFX, 10 µM CFX, and 1% DMSO as a control for 72 h.'; [Growth]'For microarray analysis, MDA-MB-231 cells (3 × 10e6 cells) were seeded in 100 mm dishes and were allowed to adhere for at least 24 h.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Triple negative breast cancer''cell line: MDA-MB-231; cell type: Triple negative breast cancer; treatment: DMSO control; ', 'cell line: MDA-MB-231; cell type: Triple negative breast cancer; treatment: CFX; ', 'cell line: MDA-MB-231; cell type: Triple negative breast cancer; treatment: Mt-CFX; ' GSE144099 Mus musculus 3 Expression profiling by high throughput sequencing GPL24247 Mal2 drives immune evasion by reducing antigen presentation on tumor cells 2020-01-22 Current cancer immunotherapies are assumed to improve infiltration and cytotoxicity of immune cells in the tumor. However, tumor cells have developed a variety of resistance mechanisms to suppress the MHC class I antigen presentation, and thereby impair the cytotoxicity of CD8+ T cells. Here, we identified Mal2 as a key player that mediates the turnover of the antigen-MHC-I complex and reduce the antigen presentation on tumor cells. Mal2 promotes the endocytosis of tumor antigen via direct interaction with the MHC-I complex and endosome-associated Rab5/7. In mouse and human breast tumor models, inhibition of Mal2 profoundly enhanced the cytotoxicity of tumor-infiltrating CD8+ T cells and suppressed breast tumor growth, suggesting that Mal2 is a potential target for breast cancer immunotherapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144099 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA602751 https://www.ebi.ac.uk/ena/browser/view/PRJNA602751 https://www.ncbi.nlm.nih.gov/sra?term=SRP244097 [Overal design]Examination of wildtype, knock out and overexpression of MAL2 in cancer microenvironment; [Treatment]'None'; [Growth]"Human triple-negative breast cancer cell line (MDA-MB-468) and murine triple-negative breast cancer cell lines (EO771 and 4T1) were cultured in Dulbecco's Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 1% penicillin/streptomycin. For lentivirus packaging, HEK293T cells were grown in DMEM with 10% FBS and 1% penicillin/streptomycin."; [Extraction]'Libraries were prepared for sequencing using standard 10X genomics protocols'; [Cell type]'CD3+ T cell''cell type: CD3+ T cell; genotype/variation: wild type; ', 'cell type: CD3+ T cell; genotype/variation: over expressed; ', 'cell type: CD3+ T cell; genotype/variation: knock out; ' GSE74968 Homo sapiens 8 Expression profiling by array GPL13667 Gene expression after knocking down of c-Met in breast cancer brain metastatic cell lines 2015-11-12 The purpose of this study is to identify the target genes of c-Met signaling in breast cancer brain metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74968 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA302058 https://www.ebi.ac.uk/ena/browser/view/PRJNA302058 None [Overal design]231BrM/Dox/shMet and SKBrM3/Dox/shMet cells were treated with or without doxycycline for 48hrs.; [Treatment]'100ng doxycycline for 48hrs'; [Growth]'cells were cultured in DMEM with 10%FBS'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'breast cancer cell line''cell type: breast cancer cell line; cell line: 231BrM; ', 'cell type: breast cancer cell line; cell line: SKBrM3; ' GSE29118 Homo sapiens 7 Genome binding/occupancy profiling by high throughput sequencing GPL10999 Genome-wide location analysis in breast cancer cells (HCC1954) 2011-05-06 While genetic mutation is a hallmark of cancer, many cancers also acquire epigenetic alterations during tumorigenesis including aberrant DNA hypermethylation of tumor suppressors as well as changes in chromatin modifications as caused by genetic mutations of the chromatin-modifying machinery. However, the extent of epigenetic alterations in cancer cells has not been fully characterized. Here, we describe the first complete methylome maps at single nucleotide resolution of a low-passage breast cancer cell line and primary human mammary epithelial cells. We find widespread DNA hypomethylation in the cancer cell, primarily at partially methylated domains (PMDs) in normal breast cells. Unexpectedly, genes within these regions are largely silenced in cancer cells. The loss of DNA methylation in these regions is accompanied by formation of repressive chromatin, with a significant fraction displaying allelic DNA methylation where one allele is DNA methylated while the other allele is occupied by histone modifications H3K9me3 or H3K27me3. Our results show a mutually exclusive and complementary relationship between DNA methylation and H3K9me3 or H3K27me3. These results suggest that global DNA hypomethylation in breast cancer is tightly linked to the formation of repressive chromatin domains and gene silencing, thus identifying a potential epigenetic pathway for gene regulation in cancer cells and suggesting a possible new approach toward the development of cancer therapeutics. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE29118 Global DNA hypomethylation coupled to repressive chromatin domain formation and gene silencing in breast cancer. Genome research 9.944 https://doi.org/10.1101/gr.125872.111 {Genome research (9.944): 10.1101/gr.125872.111} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA142885 https://www.ebi.ac.uk/ena/browser/view/PRJNA142885 https://www.ncbi.nlm.nih.gov/sra?term=SRP006725 [Overal design]ChIP-Seq on H3K4me1, H3K4me3, H3K9me3, H3K27ac, H3K27me3, H3K36me3, and input on breast cancer HCC1954. 36 cycles of sequencing on Illumina platform; [Treatment]'None'; [Growth]'None'; [Extraction]'To isolate chromatin, formaldehyde-cross-linked nuclei were sonicated using a Branson 450 Sonifier (Branson, Danbury, CT). Following ChIP performed with Dynal beads (Invitrogen, Carlsbad, CA), ChIP DNA was subjected to end repair, A-tailing, adaptor ligation, and gel purification. Following PCR amplification for 18 cycles, the final library underwent gel purification.'; [Cell type]'breast cancer cells''cell line: HCC1954; cell type: breast cancer cells; chip antibody: H3K4me1, catalog #ab8895-50, lot #720417; ', 'cell line: HCC1954; cell type: breast cancer cells; chip antibody: H3K4me3, cat #CS200580, lot #DAM1612220; ', 'cell line: HCC1954; cell type: breast cancer cells; chip antibody: H3K9me3, cat #ab8898-100, lot #699671; ', 'cell line: HCC1954; cell type: breast cancer cells; chip antibody: H3K27ac, cat #39133, lot #19208002; ', 'cell line: HCC1954; cell type: breast cancer cells; chip antibody: H3K27me3, cat #07-449, lot #DAM161288; ', 'cell line: HCC1954; cell type: breast cancer cells; chip antibody: H3K36me3, cat #ab9050-100, lot #707946; ', 'cell line: HCC1954; cell type: breast cancer cells; chip antibody: input; ' GSE38132 Homo sapiens 36 Expression profiling by array GPL6884 ZR-75-1 microarray expression data 2012-05-22 Testing the hormonal response of ZR-75-1 cells to estrogen, androgens, and a combination of both homones, with view determining the crosstalk between the transcriptional programs mediated by these hormones in breast cancer cells, and comparison with matched ChIP sequencing data for AR and ERalpha. Data analysis demonstrated reciprocal interference between 5α-dihydrotestosterone (DHT)- and estradiol (E2)-induced transcriptional programs. Specifically, regulation of 26% of E2 and 15% of DHT target genes was significantly affected by cotreatment with the other hormone, in the majority of cases (78-83%) antagonistically. Pathway analysis suggested that DHT co-treatment, for example, depleted E2-regulted pathways in cell survival and proliferation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE38132 Research resource: interplay between the genomic and transcriptional networks of androgen receptor and estrogen receptor α in luminal breast cancer cells. Molecular endocrinology (Baltimore, Md.) 3.628 https://doi.org/10.1210/me.2011-1314 {Molecular endocrinology (Baltimore, Md.) (3.628): 10.1210/me.2011-1314} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA169394 https://www.ebi.ac.uk/ena/browser/view/PRJNA169394 None [Overal design]Total RNA was extractd from luminal-like breast cancer ZR-75-1 cells in quadruplicate after treatment for 16h with 10nM of E2, DHT or E2+DHT.; [Treatment]'Plated 1.5x10e5 cells/well in 6-well dishes for 48h in phenol red-free RPMI 1640 containing 10% hormone stripped FCS and treated for 16h with 10nM E2 or 10nM DHT alone or in combination, or equivalent vehicle (ethanol).'; [Growth]'ZR-75-1 cells were maintained in RPMI 1640 medium containing 10% fetal bovine serum.'; [Extraction]'RNA was extracted using QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit.'; [Cell type]'Source: ''treatment: estradiol + medroxyprogesterone acetate; cell line: ZR-75-1; ', 'treatment: estradiol + 5a-dihydrotestosterone; cell line: ZR-75-1; ', 'treatment: estradiol + progesterone; cell line: ZR-75-1; ', 'treatment: vehicle; cell line: ZR-75-1; ', 'treatment: progesterone; cell line: ZR-75-1; ', 'treatment: medroxyprogesterone acetate; cell line: ZR-75-1; ', 'treatment: estradiol +; cell line: ZR-75-1; ', 'treatment: 5a-dihydrotestosterone; cell line: ZR-75-1; ' GSE60016 Homo sapiens 3 Expression profiling by array GPL13607 Gene expression of metabolically adaptable triple-negative breast cancer cells 2014-08-01 To gain insight into the characteristic of metabolically adaptable MA cells that enables them to survive severe metabolic challenge, i.e., prolonged lack of glutamine and other challenges [Singh et al., PLoS ONE 7: e36510, 2012], we used gene expression microarrays to compare these cells with the parental SUM149-Luc (luciferase-transfected) cells. We analyzed two independently selected cell populations, one from 0.5 million parental cells (designated MA1) and one from 1 million parental cells (designated MA2). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60016 Highly adaptable triple-negative breast cancer cells as a functional model for testing anticancer agents. PloS one 2.776 https://doi.org/10.1371/journal.pone.0109487 {PloS one (2.776): 10.1371/journal.pone.0109487} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA257281 https://www.ebi.ac.uk/ena/browser/view/PRJNA257281 None [Overal design]Comparing MA1 and MA2 variants to a common parental cell line SUM149-Luc. One sample each.; [Treatment]'No treatment. MA1 and MA2 are rare cells are derived from rare cells (less than 0.01% in pupulation) that were able to survive and grow without added glutamine in the culture medium.'; [Growth]'We cultured both MA1 and MA2 variants and the parental cell line in a medium containing Gln and dialyzed FBS; we used dialyzed FBS since it was used for selecting the MA variants in Gln-free medium.'; [Extraction]'RNA was isolated using standard RNA extraction protocols (NucleoSpin RNA II, Macherey-Nagel, Bethlehem, PA) and quality checked with the 2100 Bioanalyzer (Agilent Technologies).'; [Cell type]'Source: ''tissue: breast cancer; gender: female; strain: Parental; cell line: SUM149-Luc; ', 'tissue: breast cancer; gender: female; cell line: MA1 variant; strain: derived from SUM149-Luc; ', 'tissue: breast cancer; gender: female; cell line: MA2 variant; strain: derived from SUM149-Luc; ' GSE98528 Homo sapiens 48 Expression profiling by array GPL10558 LobSig a prognostic gene expression signature for invasive lobular carcinoma -Gene Expression Profiling 2017-05-03 Analysis of invasive lobular carcinoma (ILC) at gene expression level. Samples are annotated with breast cancer specific survival (BCSS) and tumour grade. Results are part of a larger study about molecular signatures that are associated with distinct clinical outcomes in ILC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98528 LobSig is a multigene predictor of outcome in invasive lobular carcinoma. NPJ breast cancer 32.43 https://doi.org/10.1038/s41523-019-0113-y {NPJ breast cancer (32.43): 10.1038/s41523-019-0113-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA385344 https://www.ebi.ac.uk/ena/browser/view/PRJNA385344 None [Overal design]Total RNA was extracted from fresh tumor tissues comprising ≥40% invasive tumor cells and hybridized on Illumina microarrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''tissue: invasive lobular carcinoma; tumour grade: 2; patient survival status: Alive; ', 'tissue: invasive lobular carcinoma; tumour grade: 3; patient survival status: Alive; ', 'tissue: invasive lobular carcinoma; tumour grade: 2; patient survival status: NA; ', 'tissue: invasive lobular carcinoma; tumour grade: 2; patient survival status: Dead; ', 'tissue: invasive lobular carcinoma; tumour grade: 3; patient survival status: NA; ', 'tissue: invasive lobular carcinoma; tumour grade: NA; patient survival status: Alive; ', 'tissue: invasive lobular carcinoma; tumour grade: 1; patient survival status: NA; ', 'tissue: invasive lobular carcinoma; tumour grade: 1; patient survival status: Alive; ' GSE59531 Homo sapiens 12 Expression profiling by high throughput sequencing GPL11154 TNFα Signaling Exposes Latent Estrogen Receptor Binding Sites in Breast Cancer Cells [GRO-seq] 2014-07-17 The interplay between mitogenic and proinflammatory signaling pathways play key roles in determining the phenotypes and clinical outcomes of breast cancers. We have used global nuclear run-on coupled with deep sequencing to characterize the immediate transcriptional responses of MCF-7 breast cancer cells treated with estradiol, TNFα, or both. In addition, we have integrated these data with chromatin immunoprecipitation coupled with deep sequencing for estrogen receptor alpha (ERα), the pioneer factor FoxA1 and the p65 subunit of the NF-κB transcription factor. Our results indicate extensive transcriptional interplay between these two signaling pathways, which is observed for a number of classical mitogenic and proinflammatory protein-coding genes. In addition, GRO-seq has allowed us to capture the transcriptional crosstalk at the genomic locations encoding for long non-coding RNAs, a poorly characterized class of RNAs which have been shown to play important roles in cancer outcomes. The synergistic and antagonistic interplay between estrogen and TNFα signaling at the gene level is also evident in the patterns of ERα and NF-κB binding, which relocalize to new binding sites that are not occupied by either treatment alone. Interestingly, the chromatin accessibility of classical ERα binding sites is predetermined prior to estrogen treatment, whereas ERα binding sites gained upon co-treatment with TNFα require NF-κB and FoxA1 to promote chromatin accessibility de novo. Our data suggest that TNFα signaling recruits FoxA1 and NF-κB to latent ERα enhancer locations and directly impact ERα enhancer accessibility. Binding of ERα to latent enhancers upon co-treatment, results in increased enhancer transcription, target gene expression and altered cellular response. This provides a mechanistic framework for understanding the molecular basis for integration of mitogenic and proinflammatory signaling in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59531 TNFα signaling exposes latent estrogen receptor binding sites to alter the breast cancer cell transcriptome. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2015.02.001 {Molecular cell (14.548): 10.1016/j.molcel.2015.02.001} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA255508 https://www.ebi.ac.uk/ena/browser/view/PRJNA255508 https://www.ncbi.nlm.nih.gov/sra?term=SRP044608 [Overal design]Using GRO-seq and ChIP-seq (ER, FoxA1 and p65) to assay the molecular crosstalk of MCF-7 cells treated with E2, TNFα or both E2+TNFα.; [Treatment]'Prior to all treatments, the cells were grown for 3 days in phenol red-free MEM Eagle medium supplemented with 5% charcoal-dextran-treated calf serum. All treatments were performed for 40 min with 100 nM 17β-estradiol, 25 ng/mL TNFα, or both.'; [Growth]'MCF-7 breast cancer cells were obtained from the ATCC and maintained in Minimum Essential Medium Eagle supplemented with 5% calf serum.'; [Extraction]'MCF-7 cells were seeded at 2.5 million cells per 15 cm dish and treated with Vehicle, E2, TNFα, or E2 + TNFα, as described above. The cells were washed three times with ice-cold PBS, swollen in hypotonic buffer, and collected in ice-cold lysis buffer [10 mM Tris•HCl, pH 7.4, 0.5% NP-40, 10% Glycerol, 3 mM CaCl2, 2 mM MgCl2, 1 mM DTT, 1X protease inhibitor cocktail (Sigma-Aldrich), and SUPERase-In (Ambion)] at 1000 x g for 10 min at 4°C. The cells were then resuspended in 1.5 ml of lysis buffer and pipetted up and down through a narrow opening 30 to 50 times to release the nuclei. The nuclei were pelleted again by centrifugation and washed once with 1 mL of lysis buffer. The nuclear pellets were resuspended in 500 μL of freezing buffer (50 mM Tris•HCl, pH 8.3, 40% glycerol, 5 mM MgCl2, 0.1 mM EDTA, and 4 units of SUPERase-In per mL), counted, and stored in 100 μl aliquots containing 5 x 106 nuclei.\nNuclear run-on and library preparation was performed as previously described (Danko et al., 2013; Hah et al., 2011), with modifications. Briefly, cells were treated for 40 min with 100 nM E2, 25 ng/ml TNFα, or both E2 + TNFα and libraries were prepared from two biological replicates using a circularized ligation-based protocol for adaptor addition used to improve the efficiency of library preparation, reduce sequence bias, and allow for barcoding. The libraries were amplified with indexed primers containing barcodes according to the Illumina TrueSeq small-RNA library prep kit, then sequenced using an Illumina HiSeq 2000. A more detailed protocol is available from the corresponding author (W.L.K.).'; [Cell type]'ER Positive Breast Cancer Cells''cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treated with: Vehicle for 40min; molecule subtype: nascent RNA; ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treated with: 100 nM 17β-estradiol (E2) for 40min; molecule subtype: nascent RNA; ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treated with: 25 ng/mL TNFα for 40min; molecule subtype: nascent RNA; ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treated with: 100 nM 17β-estradiol + 25 ng/mL TNFα for 40min; molecule subtype: nascent RNA; ' GSE117951 Homo sapiens 24 Expression profiling by array GPL17586 The thyroid hormone receptor β inhibits self-renewal capacity of breast cancer stem cells 2018-07-31 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE117951 Thyroid Hormone Receptor β Inhibits Self-Renewal Capacity of Breast Cancer Stem Cells. Thyroid : official journal of the American Thyroid Association 7.786 https://doi.org/10.1089/thy.2019.0175 {Thyroid : official journal of the American Thyroid Association (7.786): 10.1089/thy.2019.0175} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA483781 https://www.ebi.ac.uk/ena/browser/view/PRJNA483781 None [Overal design]Refer to individual Series; [Treatment]'When indicated, T3 was added to a final concentration of 25 nM.'; [Growth]"Cells were maintained in Dulbecco's Modified Eagle Medium GlutaMAX™ supplemented with 1% L-glutamine (Gibco-BRL Life Technologies), 10% fetal bovine serum (Sigma) and 1% penicillin/streptomycin (Gibco-BRL Life Technologies) at 37°C in a humidified atmosphere of 5% CO2.", "Mammospheres were grown in Ultralow attachment plates (Corning) in Dulbecco's Modified Eagle Medium GlutaMAX™ (Gibco-BRL Life Technologies) supplemented with 1% penicillin/streptomycin (Gibco-BRL Life Technologies), 2% B27 (Gibco), 10 ng/ml FGFb (PeproTech) and 20 ng/ml EGF (PeproTech) at 37°C in a humidified atmosphere of 5% CO2."; [Extraction]"Total RNA was extracted from cells using RNeasy Mini Kit (Qiagen) according to the manufacturer's instructions."; [Cell type]'Luminal breast cancer cell line', 'mammospheres made from luminal breast cancer cell line''cell type: Luminal breast cancer cell line; cell line: MCF7; ', 'cell type: mammospheres made from luminal breast cancer cell line; cell line: MCF7; ' GSE15134 Homo sapiens 123 Expression profiling by array; Genome variation profiling by genome tiling array GPL4091; GPL8253 PI3K inhibition in ER+ breast cancer microarray data 2009-03-05 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15134 PIK3CA and PIK3CB inhibition produce synthetic lethality when combined with estrogen deprivation in estrogen receptor-positive breast cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-08-4450 {Cancer research (8.378): 10.1158/0008-5472.CAN-08-4450} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA114891 https://www.ebi.ac.uk/ena/browser/view/PRJNA114891 None [Overal design]Refer to individual Series; [Treatment]'All tissue used for this study was taken prior to patient therapy.', 'Samples were taken from patients prior to treatment.', 'Normal growing conditions.'; [Growth]'None', 'Tissue biopsies were frozen in oct and stored in liquid nitrogen.', 'Grown under subconfluent conditions in growth media (RPMI 1640, pyruvate, 10 mM Hepes, glucose to 4.5g/L, 10% FBS, antibiotics).'; [Extraction]'Trizol extractions followed by DNase treatment and column purification.', 'DNA was isolated using Qiagen DNA Isolation kits.', 'Qiagen QiaAmp DNA Micro kit.'; [Cell type]'Source: ''cell lines: 1_Adenocarcinoma, mammary gland 2_Hepatoblastoma, liver 3_Adenocarcinoma, cervix 4_Embryonal carcinoma, testis 5_Glioblastoma, brain 6_Melanoma 7_Liposarcoma 8_Histiocytic Lymphoma; macrophage; histocyte 9_ Lymphoblastic leukemia, T lymphoblast 10_Plasmacytoma; myeloma; B lymphocyte; spike-ins: mRNA from MCF7 and ME16C; ', 'disease: breast cancer; subtype: LumA; pik3ca: wt; tissue: breast; tumor cellularity: at least 50%; stroage: oct blocks from fine needle biopsies; ', 'disease: breast cancer; subtype: LumB; pik3ca: wt; tissue: breast; tumor cellularity: at least 50%; stroage: oct blocks from fine needle biopsies; ', 'disease: breast cancer; subtype: LumB; pik3ca: mut; tissue: breast; tumor cellularity: at least 50%; stroage: oct blocks from fine needle biopsies; ', 'disease: breast cancer; subtype: LumA; pik3ca: mut; tissue: breast; tumor cellularity: at least 50%; stroage: oct blocks from fine needle biopsies; ', 'disease: breast cancer; subtype: LumB; pik3ca: nd; tissue: breast; tumor cellularity: at least 50%; stroage: oct blocks from fine needle biopsies; ', 'tissue: whole blood or cell pellets; ', 'disease: breast cancer; tissue: breast; tumor cellularity: at least 70%; storage: oct embedded; ', 'tissue: blood; gender: female; ', 'cell line: MCF7; ', 'cell line: T47D; ', 'cell line: ZR75-1; ', 'cell line: CAMA1; ', 'cell line: HCC712; ', 'cell line: HCC1419; ', 'cell line: SKBR3; ', 'cell line: HCC1806; ', 'cell line: MDAMB231; ', 'cell line: BT549; ', 'cell line: HCC38; ', 'cell line: HCC1937; ', 'cell line: HCC_1187; ' GSE99860 Homo sapiens 16 Expression profiling by array GPL570 The effect of GPAM silencing in MCF7 breast cancer cells 2017-06-09 GPAM is well characterized in triglyceride synthesis, but has never been implicated in cancer. Our study report a role for GPAM in cell migration. Gene expression changes after GPAM silencing was investigated to gain insight into possible mechanisms underlying GPAM's role in cell migration. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99860 Glycerol-3-phosphate Acyltransferase 1 Promotes Tumor Cell Migration and Poor Survival in Ovarian Carcinoma. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-16-2065 {Cancer research (8.378): 10.1158/0008-5472.CAN-16-2065} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA389798 https://www.ebi.ac.uk/ena/browser/view/PRJNA389798 None [Overal design]GPAM was silenced in MCF7 cells using two independent siRNA oligos targeting two different exons. Non-transfected cells and cells transfected with a scrambled siRNA were used as controls. Four biological replicates were performed.; [Treatment]"Cells were transfected with 20 nM scrambled or GPAM siRNA using Invitrogen's reverse transfection protocol. After three days, cells were harvested for RNA collection."; [Growth]'Cells were maintained in a humidified incubator at 37°C with 5% CO2.'; [Extraction]'Total RNA was isolated using the RNeasy Mini extraction kit (Qiagen). RNA concentration was measured using a NanoDrop N-1000 spectrophotometer and RNA integrity assessed using an automated gel electrophoresis system (Experion, Bio-Rad). The RNA was only further used if the RNA quality indicator (RQI) value was higher than 8.'; [Cell type]'breast cancer cell line''cell line: MCF7; cell type: breast cancer cell line; ' GSE32603 Homo sapiens 248 Expression profiling by array GPL14668 Serial gene expression analysis in locally advanced breast cancer patients who failed to respond to neoadjuvant chemotherapy 2011-10-04 To elucidate candidate genes and pathways associated with poor response, we retrospectively analyzed gene expression profiles in serial biopsies from women with locally advanced breast cancer who failed to respond to anthracycline-based chemo followed by taxane in the I-SPY https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32603 Serial expression analysis of breast tumors during neoadjuvant chemotherapy reveals changes in cell cycle and immune pathways associated with recurrence and response. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-015-0582-3 {Breast cancer research : BCR (5.676): 10.1186/s13058-015-0582-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA147177 https://www.ebi.ac.uk/ena/browser/view/PRJNA147177 None [Overal design]Of the 221 patients who completed neoadjuvant chemotherapy, 215 patients had surgery with 73% not achieving a pathologic complete response (pathCR). In these patients, cDNA microarray expression profiles from pretreatment biopsy (T1) were compared to those biopsy specimens obtained 24-72 hours after initiation of treatment (T2) or in tumors surgically removed after chemotherapy (TS). Paired expression data for T1vsT2 and T1vsTS were available for 29 and 39 patients with no pathCR, respectively. Paired differential expression analyses were performed via Significance Analysis of Microarrays (SAM) and differentially expressed genes were subjected to Ingenuity Pathway Analysis; [Treatment]'Patients with invasive breast cancer greater than 3 cm and/or at least one tumor-positive axillary lymph node were eligible for the study. Patients were treated with an anthracycline-based chemotherapy followed by taxane in the I-SPY TRIAL (CALGB150007/150012/ACRIN 6657)..'; [Growth]'None'; [Extraction]'One 5-µm tissue section (usually after 15 30-µm sections) of each biopsy and the first and the last section of each remaining tumor were hematoxylin and eosin stained to monitor the tumor cell percentage of the tissue. Only specimens with ≥ 50% of tumor cells were included in further analysis.A #10 scalpel blade was used to scrape tissue from the pathologic area of interest. Tissue was homogenized [Polytron 1200C, Brinkmann, Westbury, NY, at setting 4 for 30 sec] with 600µl of RNA lysis buffer plus 1% 2-mercaptoethanol, and RNA was isolated using RNEasy columns (Qiagen, Valencia, Ca).'; [Cell type]'Source: ''patient: 1001; tissue: Breast; treatment: F2; biopsy time: T1; rfs_days: 751; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.884; ', 'reference: Stratagene Reference Pooled RNA; ', 'patient: 1012; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 2425; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.899; ', 'patient: 1013; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 2383; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.673; ', 'patient: 1002; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1043; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.764; ', 'patient: 1005; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 2520; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1022; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1924; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.239; ', 'patient: 1017; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 916; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.947; ', 'patient: 1019; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 2370; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.718; ', 'patient: 1024; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1242; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.196; ', 'patient: 1021; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 639; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1016; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 759; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.5; ', 'patient: 1011; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 2340; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1009; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 2355; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.764; ', 'patient: 1008; tissue: Breast; treatment: F2; biopsy time: T1; rfs_days: 2341; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 1; rcb index: 1.03; ', 'patient: 1007; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 2449; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.648; ', 'patient: 1004; tissue: Breast; treatment: F2; biopsy time: T1; rfs_days: 2436; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1028; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 273; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1031; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1555; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1027; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1058; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.411; ', 'patient: 1035; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 729; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: NA; rcb class: NA; rcb index: NA; ', 'patient: 1032; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1384; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.84; ', 'patient: 1026; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 2213; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1033; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1942; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.808; ', 'patient: 1034; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 410; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.373; ', 'patient: 1064; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 369; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: NA; rcb class: NA; rcb index: NA; ', 'patient: 1061; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 524; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.208; ', 'patient: 1057; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 179; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.571; ', 'patient: 1077; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1926; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1049; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 179; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.048; ', 'patient: 1048; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1907; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.735; ', 'patient: 1047; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 2240; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.039; ', 'patient: 1046; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1992; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.891; ', 'patient: 1045; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 475; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1044; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 225; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.024; ', 'patient: 1043; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 224; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.996; ', 'patient: 1085; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1895; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 1; rcb index: 1.266; ', 'patient: 1051; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 912; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1054; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 303; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.481; ', 'patient: 1095; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1802; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.742; ', 'patient: 1038; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1843; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 1; rcb index: 1; ', 'patient: 1042; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 2033; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.4; ', 'patient: 1041; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1679; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.582; ', 'patient: 1110; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1652; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.617; ', 'patient: 1111; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1808; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.102; ', 'patient: 1055; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1738; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.622; ', 'patient: 1127; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 571; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.426; ', 'patient: 1128; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1887; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 1; rcb index: 0.917; ', 'patient: 1129; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 499; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1132; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1719; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.513; ', 'patient: 1058; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1655; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1114; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1756; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.039; ', 'patient: 1062; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 216; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.181; ', 'patient: 1075; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1891; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1069; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1947; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.766; ', 'patient: 1078; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1939; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1106; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 677; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.47; ', 'patient: 1100; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1906; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.99; ', 'patient: 1099; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1967; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1088; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1967; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1082; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1812; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.633; ', 'patient: 1086; tissue: Breast; treatment: F2; biopsy time: T1; rfs_days: 1643; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.931; ', 'patient: 1065; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1273; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.492; ', 'patient: 1126; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1720; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1135; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1596; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.474; ', 'patient: 1083; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1560; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.278; ', 'patient: 1073; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1725; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1134; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1816; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.615; ', 'patient: 1121; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1498; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1118; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1516; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1136; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 360; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.972; ', 'patient: 1109; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1349; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.509; ', 'patient: 1107; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1420; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.034; ', 'patient: 1113; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1432; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 1; rcb index: 1.217; ', 'patient: 1139; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1679; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1138; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1329; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1123; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1415; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.041; ', 'patient: 1149; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1534; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.109; ', 'patient: 1147; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 903; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.544; ', 'patient: 1148; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1646; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1144; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1261; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: NA; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1150; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1617; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.724; ', 'patient: 1151; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1544; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.117; ', 'patient: 1162; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1470; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 1; rcb index: 1.335; ', 'patient: 1165; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1330; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.918; ', 'patient: 1163; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1280; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1166; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1224; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.402; ', 'patient: 1155; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1615; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1158; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1581; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.841; ', 'patient: 1161; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1190; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 1; rcb index: 1.297; ', 'patient: 1160; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1595; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1152; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 981; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.544; ', 'patient: 1154; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1190; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.71; ', 'patient: 1142; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 718; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: NA; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.864; ', 'patient: 1145; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 371; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1146; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 283; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.594; ', 'patient: 1173; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1379; recurrence_yes is 1: 0; hr-positive_yes is 1: NA; her2-positive_yes is 1: NA; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.74; ', 'patient: 1179; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1456; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.057; ', 'patient: 1175; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1344; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.84; ', 'patient: 1176; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 855; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1164; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1624; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.577; ', 'patient: 1169; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 315; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.295; ', 'patient: 1202; tissue: Breast; treatment: F2; biopsy time: T1; rfs_days: 1441; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1074; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1981; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.422; ', 'patient: 1087; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1513; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1122; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1481; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.392; ', 'patient: 1130; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1375; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1192; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1311; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: NA; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1191; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1238; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.606; ', 'patient: 1215; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 478; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1208; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1309; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1206; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 481; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.189; ', 'patient: 1205; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 185; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: NA; rcb class: NA; rcb index: NA; ', 'patient: 1203; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1303; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1225; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1332; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.222; ', 'patient: 1213; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1113; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1226; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1272; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.131; ', 'patient: 1227; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1234; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1231; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1251; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.145; ', 'patient: 1237; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1031; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.517; ', 'patient: 1232; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1197; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.115; ', 'patient: 1236; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 510; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.827; ', 'patient: 1211; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1159; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.118; ', 'patient: 1239; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1155; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 1; rcb index: 1.261; ', 'patient: 1209; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 970; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.91; ', 'patient: 1216; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 644; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1218; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1379; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.375; ', 'patient: 1220; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1227; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1223; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1303; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.658; ', 'patient: 1222; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1148; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.588; ', 'patient: 1187; tissue: Breast; treatment: F2; biopsy time: T1; rfs_days: 1454; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.11; ', 'patient: 1219; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1183; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.985; ', 'patient: 1184; tissue: Breast; treatment: F2; biopsy time: T1; rfs_days: 929; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: NA; rcb index: NA; ', 'patient: 1193; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1425; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.602; ', 'patient: 1200; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1111; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.296; ', 'patient: 1199; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 274; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.46; ', 'patient: 1221; tissue: Breast; treatment: F2; biopsy time: T1; rfs_days: 644; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.216; ', 'patient: 1228; tissue: Breast; treatment: F2; biopsy time: T1; rfs_days: 1251; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1060; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 1622; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 1; rcb index: 1.141; ', 'patient: 1081; tissue: Breast; treatment: F2; biopsy time: T1; rfs_days: 1982; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.409; ', 'patient: 1194; tissue: Breast; treatment: F1; biopsy time: T1; rfs_days: 636; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.162; ', 'patient: 1094; tissue: Breast; treatment: F2; biopsy time: T1; rfs_days: 1793; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.943; ', 'patient: 1001; tissue: Breast; treatment: F4; biopsy time: T2; rfs_days: 751; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.884; ', 'patient: 1004; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 2436; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1009; tissue: Breast; treatment: F4; biopsy time: T2; rfs_days: 2355; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.764; ', 'patient: 1012; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 2425; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.899; ', 'patient: 1016; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 759; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.5; ', 'patient: 1017; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 916; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.947; ', 'patient: 1022; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1924; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.239; ', 'patient: 1026; tissue: Breast; treatment: F4; biopsy time: T2; rfs_days: 2213; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1027; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1058; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.411; ', 'patient: 1029; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 2413; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.651; ', 'patient: 1031; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1555; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1032; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1384; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.84; ', 'patient: 1033; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1942; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.808; ', 'patient: 1034; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 410; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.373; ', 'patient: 1035; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 729; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: NA; rcb class: NA; rcb index: NA; ', 'patient: 1036; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 391; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 1; rcb index: 0.587; ', 'patient: 1037; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1806; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.65; ', 'patient: 1038; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1843; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 1; rcb index: 1; ', 'patient: 1039; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 2030; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1041; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1679; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.582; ', 'patient: 1042; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 2033; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.4; ', 'patient: 1043; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 224; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.996; ', 'patient: 1044; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 225; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.024; ', 'patient: 1045; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 475; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1049; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 179; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.048; ', 'patient: 1051; tissue: Breast; treatment: F4; biopsy time: T2; rfs_days: 912; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1054; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 303; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.481; ', 'patient: 1057; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 179; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.571; ', 'patient: 1058; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1655; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1059; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1775; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.437; ', 'patient: 1063; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1862; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 1; rcb index: 1.237; ', 'patient: 1069; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1947; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.766; ', 'patient: 1077; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1926; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1078; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1939; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1081; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1982; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.409; ', 'patient: 1084; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1766; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.054; ', 'patient: 1086; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1643; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.931; ', 'patient: 1095; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1802; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.742; ', 'patient: 1100; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1906; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.99; ', 'patient: 1101; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 483; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.613; ', 'patient: 1110; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1652; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.617; ', 'patient: 1114; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1756; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.039; ', 'patient: 1125; tissue: Breast; treatment: F4; biopsy time: T2; rfs_days: 1615; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1127; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 571; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.426; ', 'patient: 1132; tissue: Breast; treatment: F3; biopsy time: T2; rfs_days: 1719; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.513; ', 'patient: 1002; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1043; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.764; ', 'patient: 1003; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 2387; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.73; ', 'patient: 1004; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 2436; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1005; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 2520; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1008; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 2341; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 1; rcb index: 1.03; ', 'patient: 1009; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 2355; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.764; ', 'patient: 1016; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 759; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.5; ', 'patient: 1032; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1384; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.84; ', 'patient: 1039; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 2030; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1040; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 413; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.28; ', 'patient: 1044; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 225; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.024; ', 'patient: 1049; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 179; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.048; ', 'patient: 1054; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 303; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.481; ', 'patient: 1055; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1738; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.622; ', 'patient: 1061; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 524; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.208; ', 'patient: 1062; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 216; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.181; ', 'patient: 1063; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1862; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 1; rcb index: 1.237; ', 'patient: 1069; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1947; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.766; ', 'patient: 1084; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1766; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.054; ', 'patient: 1091; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1154; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.93; ', 'patient: 1095; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1802; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.742; ', 'patient: 1104; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1472; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1110; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1652; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.617; ', 'patient: 1111; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1808; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.102; ', 'patient: 1112; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1510; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1115; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1802; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1121; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1498; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1129; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 499; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1139; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1679; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 1; rcb class: 0; rcb index: 0; ', 'patient: 1143; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 862; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1146; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 283; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.594; ', 'patient: 1149; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1534; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.109; ', 'patient: 1154; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1190; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.71; ', 'patient: 1159; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 428; recurrence_yes is 1: 1; hr-positive_yes is 1: NA; her2-positive_yes is 1: NA; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.789; ', 'patient: 1160; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1595; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1164; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1624; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.577; ', 'patient: 1167; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1289; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1169; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 315; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.295; ', 'patient: 1170; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1190; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.263; ', 'patient: 1173; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1379; recurrence_yes is 1: 0; hr-positive_yes is 1: NA; her2-positive_yes is 1: NA; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.74; ', 'patient: 1175; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1344; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.84; ', 'patient: 1179; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1456; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.057; ', 'patient: 1181; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1542; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.958; ', 'patient: 1183; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1456; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.025; ', 'patient: 1185; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1322; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.694; ', 'patient: 1188; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1318; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.078; ', 'patient: 1191; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1238; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.606; ', 'patient: 1192; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1311; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: NA; pcr_yes is 1: 1; rcb clas s: 0; rcb index: 0; ', 'patient: 1193; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1425; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.602; ', 'patient: 1194; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 636; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.162; ', 'patient: 1197; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1050; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.652; ', 'patient: 1199; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 274; recurrence_yes is 1: 1; hr-positive_yes is 1: 0; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.46; ', 'patient: 1200; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1111; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 3.296; ', 'patient: 1203; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1303; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: NA; rcb index: NA; ', 'patient: 1206; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 481; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.189; ', 'patient: 1219; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1183; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.985; ', 'patient: 1221; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 644; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 3; rcb index: 4.216; ', 'patient: 1222; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1148; recurrence_yes is 1: 0; hr-positive_yes is 1: 0; her2-positive_yes is 1: 1; pcr_yes is 1: 0; rcb class: 2; rcb index: 1.588; ', 'patient: 1225; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1332; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.222; ', 'patient: 1226; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1272; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 2.131; ', 'patient: 1230; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 180; recurrence_yes is 1: 1; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 3; rcb index: 5.291; ', 'patient: 1231; tissue: Breast; treatment: FS; biopsy time: TS; rfs_days: 1251; recurrence_yes is 1: 0; hr-positive_yes is 1: 1; her2-positive_yes is 1: 0; pcr_yes is 1: 0; rcb class: 2; rcb index: 3.145; ' GSE122743 Homo sapiens 14 Expression profiling by high throughput sequencing GPL20301 Single-cell Transcriptomics reveals multi-step adaptations to endocrine therapy 2018-11-20 Resistant tumours are thought to arise from the action of Darwinian selection on intratumoral genetic heterogeneity. However, clonal selection is incompatible with the late recurrence often characterising luminal breast cancers treated with endocrine therapy (ET), suggesting a more complex interplay between genetic and non-genetic factors. In the present study, we dissect the contributions of clonal genetic diversity and transcriptional plasticity during the early and late phases of ET at single-cell resolution. Using single-cell RNA-sequencing and imaging we disentangle the transcriptional variability of plastic cells and define a rare sub-population of pre-adapted (PA) cells which undergoes further transcriptomic reprogramming and copy number changes to acquire full resistance. PA cells show reduced oestrogen receptor α activity but increased features of quiescence and migration. We find evidence for sub-clonal expression of this PA signature in primary tumours and for dominant expression in clustered circulating tumour cells. We propose a multi-step model for ET resistance development and advocate the use of stage-specific biomarkers. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE122743 Single-cell transcriptomics reveals multi-step adaptations to endocrine therapy. Nature communications 11.878 https://doi.org/10.1038/s41467-019-11721-9 {Nature communications (11.878): 10.1038/s41467-019-11721-9} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA506208 https://www.ebi.ac.uk/ena/browser/view/PRJNA506208 https://www.ncbi.nlm.nih.gov/sra?term=SRP169873 [Overal design]Single-cell RNA-seq libraries from cell lines or FACS-sorted subpopulations, generated using 10x Chromium and subjected to high-throughput sequencing.; [Treatment]'MCF7 cells were treated with E2 depleted medium at 2, 4, and 7 days and sorted into CD44high and CD44low subpopulation.', 'T47D cells were treated with E2 depleted medium for 2 days.'; [Growth]'MCF7 cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM) containing 10% fetal calf serum (FCS). Long-term oestrogen-deprived cells (LTED) were derived from MCF7 after one year oestrogen deprivation as previously described and were maintained in phenol-red free DMEM containing 10% charcoal stripped fetal calf serum (SFCS) (PMID: 26610607). Both media were supplemented with 2 mM L-glutamine, 100 units/mL penicillin and streptomycin. 10−8 M estradiol (E2758 Sigma) was added routinely to MCF7.', 'T47D cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM) containing 10% fetal calf serum (FCS). T47D Long-term oestrogen-deprived cells (LTED) were derived from T47D after one year oestrogen deprivation as previously described and were maintained in phenol-red free DMEM containing 10% charcoal stripped fetal calf serum (SFCS) (PMID: 2632259). Both media were supplemented with 2 mM L-glutamine, 100 units/mL penicillin and streptomycin.'; [Extraction]'Single cells were prepared from a full population of MCF7 or LTED, or from sorting MCF7 CD44-GFP reporter cells by the level of GFP expression at different time points of E2 deprivation. After centrifugation, single cells were washed with PBS and were re-suspended with a buffer (Ca++/Mg++ free PBS + 0.04% BSA) at 1,000 cells/µl. Captures were performed using the 10x Genomics Chromium platform, according to manufacturer guidelines and in order to obtain 5,000 cells per capture.\nLibraries were generated using the 10x Genomics Chromium platform.', 'Single cells were prepared from a full population of T47D or LTED, or from sorting T47D CD44-GFP reporter cells by the level of GFP expression after 2 days of E2 deprivation. After centrifugation, single cells were washed with PBS and were re-suspended with a buffer (Ca++/Mg++ free PBS + 0.04% BSA) at 1,000 cells/µl. Captures were performed using the 10x Genomics Chromium platform, according to manufacturer guidelines and in order to obtain 5,000 cells per capture.\nLibraries were generated using the 10x Genomics Chromium platform.'; [Cell type]'Source: ''cell line: MCF7 full population; treatment: E2 supplement; ', 'cell line: MCF7 CD44low facs-sorted; treatment: E2 supplement; ', 'cell line: MCF7 CD44high facs-sorted; treatment: E2 supplement; ', 'cell line: MCF7 CD44low facs-sorted; treatment: E2 starvation for 2 days; ', 'cell line: MCF7 CD44high facs-sorted; treatment: E2 starvation for 2 days; ', 'cell line: MCF7 CD44low facs-sorted; treatment: E2 starvation for 4 days; ', 'cell line: MCF7 CD44high facs-sorted; treatment: E2 starvation for 4 days; ', 'cell line: MCF7 CD44low facs-sorted; treatment: E2 starvation for 7 days; ', 'cell line: MCF7 CD44high facs-sorted; treatment: E2 starvation for 7 days; ', 'cell line: LTED; treatment: E2 starvation; ', 'cell line: T47D full population; treatment: E2 supplement; ', 'cell line: T47D CD44high facs-sorted; treatment: E2 supplement; ', 'cell line: T47D CD44high facs-sorted; treatment: E2 starvation for 2 days; ', 'cell line: Long-term estrogen deprivation; treatment: E2 starvation; ' GSE46563 Homo sapiens 94 Expression profiling by array GPL6884 Prognostic value of gene signatures and proliferation in lymph node negative breast cancer 2013-05-01 Analyses whether, and if so, gene expression can add prognostic information in the subgroups of patients with tumours with low or high proliferative activity. As proliferation measured with MAI and PPH3 has repeatedly been shown to be the best prognosticator in node-negative breast cancer (high sensitivity, little overtreatment). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE46563 Prognostic value of gene signatures and proliferation in lymph-node-negative breast cancer. PloS one 2.776 https://doi.org/10.1371/journal.pone.0090642 {PloS one (2.776): 10.1371/journal.pone.0090642} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA200966 https://www.ebi.ac.uk/ena/browser/view/PRJNA200966 None [Overal design]Total RNA were extracted from 94 lymph node negative breast cancer patients; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with MirVANA total RNA isolation kit (Ambion/Applied Biosystems) according to the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''tissue: breast cancer tissue; follow-up (months): 121; efous_2: distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 150; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 157; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 154; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 78; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 123; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 148; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 69; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 151; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 141; efous_2: distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 109; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 150; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 156; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 148; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 3; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 119; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 149; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 154; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 35; efous_2: distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 144; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 92; efous_2: distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 63; efous_2: distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 139; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 150; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 154; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 81; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 152; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 151; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 142; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 134; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 130; efous_2: distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 137; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 124; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 51; efous_2: distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 146; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 142; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 110; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 145; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 50; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 143; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 142; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 59; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 60; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 14; efous_2: distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 92; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 94; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 90; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 76; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 100; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 94; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 92; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 83; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 108; efous_2: distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 94; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 138; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 138; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 72; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 positive; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 139; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 140; efous_2: distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 41; efous_2: distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 64; efous_2: distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 137; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 28; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 135; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 137; efous_2: distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 56; efous_2: distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 112; efous_2: distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 20; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 123; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 110; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 88; efous_2: distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 118; efous_2: distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 1; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 73; efous_2: distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 132; efous_2: distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 29; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 171; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 143; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 151; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 129; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 157; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 165; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 71; efous_2: distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 117; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 49; efous_2: distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 124; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 121; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 160; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 150; efous_2: no distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 1; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 135; efous_2: distant metastasis; tsize2: Less then 2 cm; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 positive; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 161; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI under 10; h3_13: PPH3 under 13; her2_pos_neg: HER2 negative; er: ER positive; ', 'tissue: breast cancer tissue; follow-up (months): 122; efous_2: distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 2; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ', 'tissue: breast cancer tissue; follow-up (months): 112; efous_2: no distant metastasis; tsize2: 2 cm or more; nottgrade: Grade 3; mai10: MAI = 10 or more; h3_13: PPH3 = 13 or more; her2_pos_neg: HER2 negative; er: ER negative; ' GSE161423 Homo sapiens 64 Expression profiling by high throughput sequencing; Genome variation profiling by high throughput sequencing GPL18573; GPL19415 Divergent resistance mechanisms to HER2-targeted therapies in breast cancer 2020-11-13 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE161423 The impact of tumor epithelial and microenvironmental heterogeneity on treatment responses in HER2+ breast cancer. JCI insight 6.014 https://doi.org/10.1172/jci.insight.147617 {JCI insight (6.014): 10.1172/jci.insight.147617} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA678280 https://www.ebi.ac.uk/ena/browser/view/PRJNA678280 None [Overal design]Refer to individual Series; [Treatment]'mice were randomized when tumors reached 5mm diameter and treated for 3 weeks; paclitaxel weekly 6.5mg/kg, lapatinib 6x/week 30mg/kg, T-DM1 weekly 3.6mg/kg, trastuzumab weekly 6mg/kg, pertuzumab weekly 20mg/kg'; [Growth]'PDX1 and PDX2 cells were injected into mammary fat pads of NOG mice'; [Extraction]'RNA and DNA was extracted using Quiagen Blood and Tissue kits\nRNAseq libraries were constructed with Illumina kit; for exome seq libraries were perpared with Agillent SureSelect Human All Exome kit V6', 'Tumors were dissociated to single cell and processed according to the 10xGenomics sample preparation protocol (Chromium Single Cell 3’ v2 Reagent Kit, 10xGenomics).\nLibraries were constructed according to the 10xGenomics sample preparation protocol (Chromium Single Cell 3’ v2 Reagent Kit, 10xGenomics).'; [Cell type]'Source: ''treatment: untreated; animal id: mouse 1; ', 'treatment: untreated; animal id: mouse 2; ', 'treatment: untreated; animal id: mouse 3; ', 'treatment: lapatinib; animal id: mouse 1; ', 'treatment: lapatinib; animal id: mouse 2; ', 'treatment: lapatinib; animal id: mouse 3; ', 'treatment: paclitaxel; animal id: mouse 1; ', 'treatment: paclitaxel; animal id: mouse 2; ', 'treatment: paclitaxel; animal id: mouse 3; ', 'treatment: T-DM1; animal id: mouse 1; ', 'treatment: T-DM1; animal id: mouse 2; ', 'treatment: T-DM1; animal id: mouse 3; ', 'treatment: trastuzumab; animal id: mouse 1; ', 'treatment: trastuzumab; animal id: mouse 2; ', 'treatment: trastuzumab; animal id: mouse 3; ', 'treatment: pertuzumab; animal id: mouse 1; ', 'treatment: pertuzumab; animal id: mouse 2; ', 'treatment: pertuzumab; animal id: mouse 3; ', 'cell line: PDX1; animal id: mouse 1; ', 'cell line: PDX2; animal id: mouse 1; ', 'cell line: PDX1; animal id: mouse 2; ', 'cell line: PDX2; animal id: mouse 2; ' GSE59734 Homo sapiens 115 Expression profiling by array GPL571; GPL18990 Gene expression profiling in response to radiation treatment in breast cancer 2014-07-24 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59734 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA256080 https://www.ebi.ac.uk/ena/browser/view/PRJNA256080 None [Overal design]Refer to individual Series; [Treatment]'16 cell lines representing luminal HER2- (MCF7, T47D, ZR751, CAMA-1), luminal-HER2+ (BT474, SKBR3, AU565), HER2+ (HCC1954) and basal (SUM149, SUM159, MDA-MB-231, MCF10A, MCF12A, BT549, HBL100, and DKAT) breast cancer cell lines were evaluated for response to a single dose of 5Gy.', 'Formalin fixed and paraffin-embedded (FFPE) samples were obtained at the time of diagnosis. Patients then received a single large dose of radiation to the intact tumor and proceeded to surgical resection within 10 days of treatment. A second post-radiation sample was obtained at the time of surgical excision.'; [Growth]"In order to identify differences in the radiation response gene expression profiles of specific breast cancer subtypes, we exposed 16 biologically-diverse breast tumor cell lines to 0 or 5GY radiation. Microarray analysis was performed on RNA harvested from those cell lines. Microarray analysis was performed on RNA harvested from those cell lines. Samples were run in triplicate. Breast cancer cell lines displaying gene expression patterns consistent with distinct clinical breast subtypes were selected (25, 26) as follows: Luminal - MCF7, T47D, ZR751, CAMA-1, BT474 (Her2+), SKBR3 (Her2+), AU565 (Her2+); Basal - SUM149, SUM159, MDA-MB-231, MCF10A, MCF12A, BT549, HBL100, HCC1954 (Her2+) and DKAT. These cell lines reflect the heterogeneity of human breast cancer, thereby, providing a valid biological model for study of phenotype specific mechanisms. Cell lines growth conditions: MCF7, ZR751, MDAMB231, and SUM159 were cultured in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum (Hyclone, SH30071.03) and 1X Antibiotic-Antimycotic (Gibco, 15240-062). SUM149 cells were grown in Ham's F-12 medium supplemented with 5% fetal bovine serum (Hyclone, SH30071.03), 5ug/ml Insulin (Sigma-Aldrich®, I- 5500), 1ug/ml Hydrocortisone (Sigma-Aldrich®, H-4001) and 1X Antibiotics / Antimycotic (Gibco, 15240-062). T47D cells were grown in MEM-alpha medium (Gibco, 12561) supplemented with 6% of fetal bovine serum (Hyclone, SH30071.03), 12mM Hepes (Gibco15630), 1XMEM NEAA(Gibco 11140), 1mM Sodium Pyruvate (Gibco, 11360), 1ug/ml insulin (Sigma-Aldrich®, I-5500), 1ug/ml Hydrocortisone (Sigma-Aldrich®, H-4001), 12.5ng/ml EGF (Sigma-Aldrich®, E4127) and 1X Antibiotic-Antimycotic (Gibco, 15240-062). AU565 and HCC1965 cells were grown in RPMI1640 medium supplemented with 10% of fetal bovine serum (Hyclone, SH30071.03), 1XSodium Pyruvate (Gibco 11360-070), 10mM Hepes(Gibco, 15630) and 1X Antibiotic-Antimycotic (Gibco, 15240-062). BT474 and SKBR3 cells were grown in RPMI1640 medium supplemented with 10% of fetal bovine serum (Hyclone, SH30071.03) and 1X Antibiotic-Antimycotic(Gibco, 15240-062). BT549 were grown in RPMI1640 medium supplemented with 10% of fetal bovine serum (Hyclone, SH30071.03), 1XSodium Pyruvate (Gibco 11360-070), 10mM Hepes(Gibco, 15630), 8ug/ml Insulin(life technology 12585014) and 1X Antibiotic-Antimycotic(Gibco, 15240-062). CAMA1 cells were grown in MEM (Gibco 11095-080) medium supplemented with 10% of fetal bovine serum (Hyclone, SH30071.03), 1XSodium Pyruvate (Gibco 11360-070), 1XNEAA (Gibco 11140) and 1X Antibiotic-Antimycotic (Gibco, 15240-062). HBL100 cells were grown in McCoy’s 5a medium (Gibco 16600-082) supplemented with 10% of fetal bovine serum (Hyclone, SH30071.03) and1X Antibiotic-Antimycotic (Gibco, 15240-062). MCF10A cells were grown in DMEM/F12 (GIBCO 11330-032) medium supplemented with 5% of Horse Serum (Invitrogen #16050-122), 0.5ug/ml of hydrocortisone(Sigma-Aldrich®,H4001), 10ug/ml of Insulin (life technology 12585014), 20ng/ml of EGF(Sigma-Aldrich® , e9644) and 1X Antibiotic-Antimycotic (Gibco, 15240-062). MCF12A cells were grown in DMEM/F12 (GIBCO11330-032) medium supplemented with 10% of fetal bovine serum (Hyclone, SH30071.03), 1ug/ml of hydrocortisone (Sigma-Aldrich, H-4001), 5ug/ml of Insulin (life technology 12585014) and 1X Antibiotic-Antimycotic (Gibco, 15240-062). DKAT cells were grown in MEGM (Lonza, CC-3150) medium and 1X Antibiotic-Antimycotic (Gibco, 15240-062). All cell lines were maintained in a humidified incubator with 5% CO2 atmosphere at 37o C."; [Extraction]'Microarray analysis was performed on RNA harvested from those cell lines. Samples were run in triplicate. Isolation of RNA. Total RNA was collected from approximately 1x10^6 cells in each of the sixteen cell lines. RNA was isolated from the treated cell lines (5Gy) 24 hours after radiation using the RNeasy Mini Isolation Kit (QIAGEN, Valencia, CA). The same protocol was used for control cell lines but with 0Gy radiation. Samples were run in triplicate. RNA was hybridized to Affymetrix U133A2 arrays and processed in the Duke Microarray Core facility.', "Microarray analysis of human samples: The same FFPE samples were also used for RNA extraction in a subset of the human tumors (n=9 patients, 18 paired samples) using the RNeasy FFPE kit from Qiagen (catalog # 73504). The SensationPlus 3' IVT A&L FFPE kit was used for the labeling and amplification of the RNA (Affymetrix, Inc. catalog # 902028)."; [Cell type]'breast cancer''cell line: T47D; cell type: breast cancer; clinical subtype: luminal (Her2-); ', 'cell line: ZR751; cell type: breast cancer; clinical subtype: luminal (Her2-); ', 'cell line: MCF7; cell type: breast cancer; clinical subtype: luminal (Her2-); ', 'cell line: MDA-MB-231; cell type: breast cancer; clinical subtype: basal; ', 'cell line: SUM159; cell type: breast cancer; clinical subtype: basal; ', 'cell line: SUM149; cell type: breast cancer; clinical subtype: basal; ', 'cell line: AU565; cell type: breast cancer; clinical subtype: luminal (Her2+); ', 'cell line: BT474; cell type: breast cancer; clinical subtype: luminal (Her2+); ', 'cell line: BT549; cell type: breast cancer; clinical subtype: basal; ', 'cell line: CAMA1; cell type: breast cancer; clinical subtype: luminal (Her2-); ', 'cell line: DKAT; cell type: breast cancer; clinical subtype: basal; ', 'cell line: HBL100; cell type: breast cancer; clinical subtype: basal; ', 'cell line: HCC1954; cell type: breast cancer; clinical subtype: basal (Her2+); ', 'cell line: MCF10A; cell type: breast cancer; clinical subtype: basal; ', 'cell line: MCF12A; cell type: breast cancer; clinical subtype: basal; ', 'cell line: SKBR3; cell type: breast cancer; clinical subtype: luminal (Her2+); ', 'tissue: breast; cell type: breast cancer; ' GSE138505 Homo sapiens 10 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Peptidylarginine deiminase IV (PADI4) has a novel tumor cell-autonomous suppressor role in regulating breast cancer stem cells [ChIP-Seq] 2019-10-07 Peptidylarginine deiminases (PADIs) catalyze post-translational modification of many target proteins and have been suggested to play a role in carcinogenesis. Since citrullination of histones by PADI4 was recently implicated in regulating embryonic stem and hematopoietic progenitor cells, here we investigated a possible role for PADI4 in regulating breast cancer stem cells. We showed by genetic and pharmacologic approaches that PADI4 activity limits the number of cancer stem cells (CSCs) in vitro and in vivo in multiple breast cancer models. A gene signature reflecting tumor cell-autonomous PADI4 inhibition is associated with poor outcome in human breast cancer datasets, consistent with a tumor suppressive role for PADI4. Mechanistically, PADI4 inhibition resulted in a global redistribution of histone H3 with accumulation around transcriptional start sites. Interestingly, epigenetic effects of PADI4 on the bulk tumor cell population did not explain the CSC phenotype. However, in sorted tumor cell populations, PADI4 down-regulated expression of the master transcription factors of stemness, NANOG and POU5F1, specifically in the cancer stem cell compartment, by reducing the transcriptionally activating H3R17me2a histone mark at those loci. This effect was not seen in the non-stem cells. Our findings reveal a novel role for PADI4 as a tumor suppressor in regulating breast cancer stem cells, and provide insights into context-specific effects of PADI4 in epigenetic modulation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE138505 Peptidylarginine Deiminase IV Regulates Breast Cancer Stem Cells via a Novel Tumor Cell-Autonomous Suppressor Role. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-19-3018 {Cancer research (8.378): 10.1158/0008-5472.CAN-19-3018} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA576214 https://www.ebi.ac.uk/ena/browser/view/PRJNA576214 https://www.ncbi.nlm.nih.gov/sra?term=SRP224615 [Overal design]MCF10Ca1h cells were cultured in DMEM/F12 media supplemented with 5% horse serum. Cells were treated with PADI4 inhibitor (GSK484) or control compound (GSK107) for 72 hours.; [Treatment]'Cells were treated with PADI4 inhibitor (GSK484) or control compound (GSK107) for 72 hours.'; [Growth]'MCF10Ca1h cells were cultured in DMEM/F12 media supplemented with 5% horse serum.'; [Extraction]'ChIPs were done with SimpleChIP Enzymatic chromatin IP kit (Cell Signaling technologies).\nSequencing libraries were prepared using standard Illumina protocols.\nSequencing libraries were run on Illumina NextSeq platform SR 75bp cycle runs of 50M reads/sample'; [Cell type]'Source: ''cell line: MCF10Ca1h human breast cancer cell line; treatment: CON; in vivo timepoint: 72 hrs; chip antibody: Histone H3 (D2B12) XP®\xa0Rabbit mAb, Cell Signaling Tech #4620; 1:50; ', 'cell line: MCF10Ca1h human breast cancer cell line; treatment: CON; in vivo timepoint: 72 hrs; chip antibody: Histone H3 (citrulline R2 + R8 + R17), Abcam ab5103; 1:50; ', 'cell line: MCF10Ca1h human breast cancer cell line; treatment: CON; in vivo timepoint: 72 hrs; chip antibody: Tri-Methyl-Histone H3 (Lys27) (C36B11) Rabbit mAb, Cell Signaling Tech #9733; 1:50; ', 'cell line: MCF10Ca1h human breast cancer cell line; treatment: GSK484; in vivo timepoint: 72 hrs; chip antibody: Tri-Methyl-Histone H3 (Lys4) (C42D8), Cell Signaling Tech #9751; 1:50; ', 'cell line: MCF10Ca1h human breast cancer cell line; treatment: GSK484; in vivo timepoint: 72 hrs; chip antibody: Normal Rabbit IgG, Cell Signaling Tech #2729; 2ul/IP; ', 'cell line: MCF10Ca1h human breast cancer cell line; treatment: GSK484; in vivo timepoint: 72 hrs; chip antibody: Histone H3 (D2B12) XP®\xa0Rabbit mAb, Cell Signaling Tech #4620; 1:50; ', 'cell line: MCF10Ca1h human breast cancer cell line; treatment: GSK484; in vivo timepoint: 72 hrs; chip antibody: Histone H3 (citrulline R2 + R8 + R17), Abcam ab5103; 1:50; ', 'cell line: MCF10Ca1h human breast cancer cell line; treatment: GSK484; in vivo timepoint: 72 hrs; chip antibody: Tri-Methyl-Histone H3 (Lys27) (C36B11) Rabbit mAb, Cell Signaling Tech #9733; 1:50; ' GSE149635 Mus musculus 50 Expression profiling by high throughput sequencing GPL19057 Single cell mapping of breast tumor stroma reveals dynamically evolving compositions of cancer-associated fibroblasts along tumor progression (scRNA-seq dataset) 2020-04-30 Tumors are complex ecosystems, in which malignant and non-malignant cells engage in continuous interactions. Cancer associated fibroblasts (CAFs) are the most abundant non-malignant cells in the majority of carcinomas. The wide range of activities that CAFs perform suggests a dynamic and heterogeneous composition, yet tumor infiltrating CAF subpopulations remain poorly characterized. Here we used single-cell RNA sequencing, index sorting and bulk RNA sequencing to map CAFs at various stages of tumor progression and metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE149635 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA629492 https://www.ebi.ac.uk/ena/browser/view/PRJNA629492 https://www.ncbi.nlm.nih.gov/sra?term=SRP259312 [Overal design]BALB/c female mice were orthotopically injected with 4T1-luc cells into the mammary pat pad. Tumors were harvested two weeks or four weeks following the injection. Mammary tissue was harvested from naïve mice (normal mammary fat pad), and lung metastases were harvested five weeks after the injection. The tissues were then dissociated and single-cell sorted for MARS-sequencing, using the follwing gating strategy to select for stromal cells: PI- /Ter119-/ CD45-/ EpCAM-.; [Treatment]'BALB/c females were injected under anaesthesia with 100,000 4T1-luc cells suspended in PBS, directly into the lower left mammary fat pad. To obtain CAFs from primary tumors, mice were sacrificed and tumors were immediately excised post mortem. To obtain CAFs from lung metastases, primary tumors were surgically removed under anesthesia 2 weeks after the injection. 2-3 weeks post primary tumor removal the animals were sacrificed, metastases bearing lungs were immediately excised and metastases were isolated from the lungs.'; [Growth]'8 to 13 weeks-old mice housed at the Weizmann Institute animal facility under specific pathogen-free conditions.'; [Extraction]'Normal mammary fat pad: Tissue was minced using scissors and placed and disrupted for 25 min at 37oC in a gentleMACS C tube using gentleMACS dissociator, in the presence of enzymatic digestion solution containing 1 mg ml-1 collagenase II, 1 mg ml-1collagenase IV and 70 unit ml-1 DNase. Primary tumor: Tissue was minced using scissors and treated with enzymatic digestion solution containing 3 mg ml-1 collagenase A and 70 unit ml-1 DNase in RPMI 1640 for 20 min at 37oC, with pipetting every 3 min. Lung metastases: Metastases bearing lungs were harvested and placed in gentleMACS C tubes with an enzymatic digestion solution containing collagenase A 1.5 mg ml-1, dispase II 2.5 unit ml-1 and DNase I 70 unit ml-1 in RPMI 1640. The tissue was disrupted for 30 min at 37oC using gentleMACS dissociator. Following dissociation, all tissues were washed, filtered through a 70 μm cell strainer and pelleted by centrifugation at 350 g, 5min, 4°C.\nSingle-cell RNA-seq libraries were prepared as previously described {Jaitin, 2014}. In brief, mRNA from single cells sorted into capture plates were barcoded and converted into cDNA and then pooled using an automated pipeline. The pooled sample was linearly amplified by T7 in vitro transcription, and the resulting RNA was fragmented and converted into a sequencing-ready library by tagging the samples with pool barcodes and Illumina sequences during ligation, RT, and PCR. Each pool of cells was tested for library quality and concentration as described previously {Jaitin, 2014}'; [Cell type]'Non-immune stromal cells''strain: BALB/c; Sex: female; tissue: Normal mammary fat pad; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: n/a; time point: Time zero; replicate id: NMF rep. 1; mouse age: 8 weeks; ', 'strain: BALB/c; Sex: female; tissue: Normal mammary fat pad; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: n/a; time point: Time zero; replicate id: NMF rep. 2; mouse age: 8 weeks; ', 'strain: BALB/c; Sex: female; tissue: Normal mammary fat pad; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: n/a; time point: Time zero; replicate id: NMF rep. 3; mouse age: 8 weeks; ', 'strain: BALB/c; Sex: female; tissue: Breast tumor; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: Orthotopic breast injection of 4T1-luc cells; time point: two weeks after injection; replicate id: 2W rep. 1; mouse age: 10 weeks; ', 'strain: BALB/c; Sex: female; tissue: Breast tumor; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: Orthotopic breast injection of 4T1-luc cells; time point: two weeks after injection; replicate id: 2W rep. 2; mouse age: 10 weeks; ', 'strain: BALB/c; Sex: female; tissue: Breast tumor; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: Orthotopic breast injection of 4T1-luc cells; time point: two weeks after injection; replicate id: 2W rep. 3; mouse age: 10 weeks; ', 'strain: BALB/c; Sex: female; tissue: Breast tumor; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: Orthotopic breast injection of 4T1-luc cells; time point: four weeks after injection; replicate id: 4W rep. 1; mouse age: 12 weeks; ', 'strain: BALB/c; Sex: female; tissue: Breast tumor; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: Orthotopic breast injection of 4T1-luc cells; time point: four weeks after injection; replicate id: 4W rep .2; mouse age: 12 weeks; ', 'strain: BALB/c; Sex: female; tissue: Breast tumor; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: Orthotopic breast injection of 4T1-luc cells; time point: four weeks after injection; replicate id: 4W rep. 3; mouse age: 12 weeks; ', 'strain: BALB/c; Sex: female; tissue: Breast tumor; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: Orthotopic breast injection of 4T1-luc cells; time point: four weeks after injection; replicate id: 4W rep .4; mouse age: 12 weeks; ', 'strain: BALB/c; Sex: female; tissue: Breast tumor; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: Orthotopic breast injection of 4T1-luc cells; time point: four weeks after injection; replicate id: 4W rep. 5; mouse age: 12 weeks; ', 'strain: BALB/c; Sex: female; tissue: Breast tumor; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: Orthotopic breast injection of 4T1-luc cells; time point: four weeks after injection; replicate id: 4W rep. 6; mouse age: 12 weeks; ', 'strain: BALB/c; Sex: female; tissue: Lung metastases; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: Orthotopic breast injection of 4T1-luc cells; surgical removal of primary tumor; time point: Five weeks after injection; replicate id: Met rep. 1; mouse age: 13 weeks; ', 'strain: BALB/c; Sex: female; tissue: Lung metastases; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: Orthotopic breast injection of 4T1-luc cells; surgical removal of primary tumor; time point: Five weeks after injection; replicate id: Met rep. 2; mouse age: 13 weeks; ', 'strain: BALB/c; Sex: female; tissue: Lung metastases; cell type: Non-immune stromal cells; selection marker: Ter119- CD45- EpCAM-; treatment: Orthotopic breast injection of 4T1-luc cells; surgical removal of primary tumor; time point: Five weeks after injection; replicate id: Met rep. 3; mouse age: 13 weeks; ' GSE47862 Homo sapiens 321 Expression profiling by array GPL17279 Expression profiling of peripheral blood gene expression of women with hereditary breast cancer and controls 2013-06-11 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47862 Integrative analyses reveal signaling pathways underlying familial breast cancer susceptibility. Molecular systems biology 9.800 https://doi.org/10.15252/msb.20156506 {Molecular systems biology (9.800): 10.15252/msb.20156506} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA208223 https://www.ebi.ac.uk/ena/browser/view/PRJNA208223 None [Overal design]Refer to individual Series; [Treatment]'Not applicable.'; [Growth]'Not applicable.'; [Extraction]'RNA was extracted using the RiboPure RNA Isolation Kit.'; [Cell type]'peripheral blood mononuclear cells''cell type: peripheral blood mononuclear cells; breast_cancer_family_history: no; developed_breast_cancer: no; cohort: Utah; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: no; developed_breast_cancer: yes; cohort: Utah; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: no; cohort: Utah; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: yes; cohort: Utah; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: yes; cohort: Utah; carries_brca_mutation: yes; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: no; cohort: Utah; carries_brca_mutation: yes; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: no; cohort: Ontario; carries_brca_mutation: yes; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: no; cohort: Ontario; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: no; developed_breast_cancer: yes; cohort: Ontario; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: yes; cohort: Ontario; carries_brca_mutation: yes; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: yes; cohort: Ontario; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: no; developed_breast_cancer: no; cohort: Ontario; carries_brca_mutation: no; ' GSE31397 Homo sapiens 6 Expression profiling by array GPL570 Expression profile of miR-101 transfection in MCF-7 cells compared with scramble control 2011-08-16 Autophagy is an evolutionarily conserved mechanism of cellular self-digestion in which proteins and organelles are degraded through delivery to lysosomes. Defects in this process are implicated in numerous human diseases including cancer. To further elucidate regulatory mechanisms of autophagy, we performed a functional screen in search of microRNAs (miRNAs), which regulate the autophagic flux in breast cancer cells. In this study we identified the tumor suppressive miRNA, miR-101, as a potent inhibitor of basal, etoposide- and rapamycin-induced autophagy. Through transcriptome profiling, we identified three novel miR-101 targets, STMN1, RAB5A and ATG4D. siRNA-mediated depletion of these genes phenocopied the effect of miR-101 overexpression, demonstrating their importance in autophagy regulation. Importantly, overexpression of STMN1 could partially rescue cells from miR-101-mediated inhibition of autophagy, indicating a functional importance for this target. Finally, we show that miR-101-mediated inhibition of autophagy can sensitize breast cancer cells to 4-hydroxytamoxifen (4-OHT) mediated cell death. Collectively, these data establish a novel link between two highly important and rapidly growing research fields and present a new role for miR-101 as a key regulator of autophagy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE31397 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA145871 https://www.ebi.ac.uk/ena/browser/view/PRJNA145871 None [Overal design]MCF-7 cells were seeded in 6-cm plates and independent triplicate transfections were performed the following day with 50 nM miR-101 or scramble control using Lipofectamine 2000. Total RNA was harvested 24 h after transfection using Trizol reagent. There are a total of six arrays included in this experiment, including three biological replicates of mRNA expression after miR-101 over-expression and three scramble controls in MCF-7 cells.; [Treatment]'None'; [Growth]'None'; [Extraction]'MCF-7 cells were seeded in 6-cm plates and independent triplicate transfections were performed the following day with 50 nM miR-101 or scramble control using Lipofectamine 2000. Total RNA was harvested 24 h after transfection using Trizol reagent.'; [Cell type]'Source: ''cell line: MCF-7 cells; conditions: transfection with 50 nM miR-101; ', 'cell line: MCF-7 cells conditions: transfection with 50 nM miR-101; ', 'cell line: MCF-7 cells; conditions: transfection with 50 nM scramble control; ' GSE58048 Homo sapiens 2 Expression profiling by array GPL570 Histone methyltransferase SMYD3 knockdown effects in MCF7 breast cancer cell line 2014-05-28 The study aims to elucidate the effect of histone methyltransferase SMYD3 on gene expression in MCF-7 breast cancer cell line. Knockdown luciferase control v.s. knockdown SMYD3 in MCF-7 breast cancer cell line were conducted. Results identify a large proportion of cell cycle-related genes regulated by SMYD3. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58048 SMYD3-Mediated H2A.Z.1 Methylation Promotes Cell Cycle and Cancer Proliferation. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-16-0500 {Cancer research (8.378) doi:10.1158/0008-5472.CAN-16-0500}; {Scientific reports (4.011) doi:10.1038/s41598-017-03385-6}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA248758 https://www.ebi.ac.uk/ena/browser/view/PRJNA248758 None [Overal design]SMYD3 was knockdowned in MCF-7 cells and shLuc was used as control. Their total RNA were isolated for genomic expression profiling with Affymetrix GeneChip Human Genome U133 Plus 2.0 Array.; [Treatment]'None'; [Growth]'Breast cancer cell lines MCF7 was maintained in DMEM containing 10% fetal bovine serum (FBS), non-essential amino acid (HyClone), sodium pyruvate (HyClone), and antibiotics (HyClone). The siRNA vector construct targeting control luciferase and SMYD3 and sequence were generated by usingLentiviral packaging system (National RNAi Core Facility, Institute of Molecular Biology / Genomic Research Center, Academia Sinica, Taiwan, ROC). The shLuc and shSMYD3 knockdown cell lines were selected by incubating them in the feeding medium with inclusion of 1 microgram/ml puromycin for 3 days.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'epithelial''cell line: MCF-7; cell type: epithelial; tissue: mammary gland/breast; ' GSE145471 Mus musculus; Homo sapiens 23 Expression profiling by high throughput sequencing GPL16791; GPL17021 Mutant SF3B1 promotes AKT and NF-kB driven mammary tumorigenesis 2020-02-18 Mutations in the core RNA splicing factor SF3B1 are prevalent in leukemias and uveal melanoma, but also recurrent in epithelial malignancies such as breast cancer. Whereas hotspot mutations in SF3B1 alter hematopoietic differentiation, whether SF3B1 mutations contribute to epithelial cancer development and progression is unknown. Here, we identify that SF3B1 mutations in mammary epithelial and breast cancer cells induce a recurrent pattern of aberrant splicing leading to activation of AKT and NF-kB, enhanced cell migration, and accelerated tumorigenesis. Transcriptomic analysis of human cancer specimens, MMTV-cre Sf3b1K700E/WT mice, and isogenic mutant cell lines identified hundreds of aberrant 3’ splice sites induced by mutant SF3B1, a portion of which were breast-specific. Across mouse and human tumors, mutant SF3B1 promoted aberrant splicing (dependent on aberrant branchpoints as well as pyrimidines downstream of the aberrant branchpoint) and consequent suppression of PPP2R5A and MAP3K7, critical negative regulators of AKT and NF-kB. Coordinate activation of NF-kB and AKT signaling was observed in the knock-in models, leading to accelerated cell migration and tumor development in combination with mutant PIK3CA but also hypersensitizing cells to AKT kinase inhibitors. These data identify mutations in SF3B1 as drivers of breast tumorigenesis and reveal unique vulnerabilities in cancers harboring them. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE145471 Mutant SF3B1 promotes AKT- and NF-κB-driven mammary tumorigenesis. The Journal of clinical investigation 12.282 https://doi.org/10.1172/JCI138315 {The Journal of clinical investigation (12.282): 10.1172/JCI138315} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA607270 https://www.ebi.ac.uk/ena/browser/view/PRJNA607270 https://www.ncbi.nlm.nih.gov/sra?term=SRP249914 [Overal design]23 samples, including 11 mouse and 12 human samples with varying SF3B1 status; [Treatment]'MCF7 and T47D cell were treated with doxycycline to induce wild-type or mutant SF3B1 expression for 48 hours before hearvesting cells.'; [Growth]'All mice were housed at Memorial Sloan Kettering Cancer Center and All mouse procedures were completed in accordance with the Guidelines for the Care and Use of Laboratory Animals and were approved by the Institutional Animal Care and Use Committees at MSKCC. Cell lines were maintained in 37°C incubator with 5% CO2 in humidified atmosphere. MCF7 cells were grown in DMEM/F12 supplemented with 10% FBS (Gibco), 100 μg/mL penicillin, 100 mg/mL streptomycin (Corning), and 4 mM glutamine, and MCF10A cells were grown in DMEM/F12 supplemented with 5% horse serum (Gibco), 20ng/mL EGF (Sigma-Aldrich), 10μg/mL insulin (Sigma-Aldrich), 0.5μg/mL hydrocortisone (Sigma-Aldrich), 0.1μg/mL cholera toxin (Sigma-Aldrich), 100 μg/mL penicillin, and 100 mg/mL streptomycin (Corning). T47D cells were cultured in RPMI1640 with 10% FBS (Gibco), 100 μg/mL penicillin and 100 mg/mL streptomycin (Corning).'; [Extraction]'Mammary gland epithelial cells were isolated from 4-month old mice. Breifly, mammary glands dissected from 4-month-old female mice were minced and digested with collagenase/trypsin mixture for 4 hours at 37\uf0b0C. After washed with L15 medium supplemented with 10% FBS, the red blood cells were lysed with Hybri-Max Red Blood Cell Lysing Buffer (Sigma). After washing with L15/10% FBS medium, the samples were incubated in serum-free Joklik’s medium and then treated with 0.05% trypsin and DNase I (Fisher Scientific). Trypsin was neutralized by adding L15/10% FBS medium and the samples were filtered through a 40\uf06dm cell strainer to remove cell clumps and debris. Cells were pelleted and resuspended in L15/10% FBS medium. Fluorescence-activated cell sorting (FACS) was used to isolate mammary epithelial cells. The cells were incubated with antibodies against CD24 and CD45 in L15/10% FBS medium on ice for 45 min. DAPI was used to exclude dead cells. The mammary epithelial cells were sorted as CD24+/CD45- cells on FACS Aria sorter. Human cell lines were hearvested at 70% to 80% confluence. Total RNA was extracted with Direct-Zol RNA miniprep kit (Zymo).\nLibraries were constructed with TruSeq RNA-seq prep kit by Genewiz or MSKCC Integrated Genomics Operation Core Facility.'; [Cell type]'Mouse mammary epithelial cells', 'Source: ''cell type: Mouse mammary epithelial cells; genotype: wild type; ', 'cell type: Mouse mammary epithelial cells; genotype: Sf3b1 K700E; ', 'cell type: Mouse mammary epithelial cells; genotype: Pik3ca H1047R; ', 'cell type: Mouse mammary epithelial cells; genotype: Sf3b1 K700E & Pik3ca H1047R; ', 'cell line: MCF7 breast cancer cell line; genotype: wild type; ', 'cell line: MCF7 breast cancer cell line; genotype: SF3B1 K700E; ', 'cell line: T47D breast cancer cell line; genotype: wild type; ', 'cell line: T47D breast cancer cell line; genotype: SF3B1 K700E; ', 'cell line: MCF10A breast cell line; genotype: wild type; ', 'cell line: MCF10A breast cell line; genotype: SF3B1 K700E; ' GSE23891 Homo sapiens 25 Genome variation profiling by array GPL2879; GPL5477 Gene copy number variation in male breast cancer by aCGH 2010-08-31 Characterization of DNA imbalances in a set of 25 MBC samples analyzed by high resolution CGH arrays in order to detect DNA copy number aberrations (CNAs). These results have been then compared with a female breast cancer dataset deposited with the Gene Expression Omnibus. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23891 Gene copy number variation in male breast cancer by aCGH. Analytical cellular pathology (Amsterdam) None https://doi.org/10.3233/ACP-CLO-2010-0544 {Analytical cellular pathology (Amsterdam) (None) doi:10.3233/ACP-CLO-2010-0544}; {Cellular oncology (Dordrecht) (None) doi:10.1007/s13402-011-0041-9}; 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA130449 https://www.ebi.ac.uk/ena/browser/view/PRJNA130449 None [Overal design]Male patients affected by breast cancer have been consecutively selected for this retrospective study: 15 received the primary diagnosis of breast cancer at the NCC of Bari, while 10 at Regina Elena Institute of Rome, Italy. This dataset was compared to GSE12659 (female breast cancer).; [Treatment]'None'; [Growth]'None'; [Extraction]'standard Agilent CGH protocol'; [Cell type]'Source: ''gender: male; tissue: breast cancer tumor; ' GSE59246 Homo sapiens 105 Expression profiling by array GPL13607 Molecular features of subtype-specific progression from ductal carcinoma in situ to invasive breast cancer [gene expression data] 2014-07-09 Breast cancer consists of at least five main molecular “intrinsic” subtypes, which are reflected in both pre-invasive and invasive disease. Although previous studies have suggested that many of the molecular features of invasive breast cancer are established early, it is unclear what mechanisms drive progression, and whether the mechanisms of progression are dependent or independent of subtype. We have generated mRNA, miRNA and DNA copy number profiles from a total of 59 in situ lesions and 85 invasive tumors, in order to comprehensively identify those genes, signaling pathways, processes, and cell types that are involved in breast cancer progression. Our work provides evidence that there are molecular features associated with disease progression that are unique to the intrinsic subtypes. We additionally establish subtype-specific signatures that are able to identify a small proportion of pre-invasive tumors with expression profiles that resemble invasive carcinoma, indicating a higher likelihood of future disease progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59246 Molecular Features of Subtype-Specific Progression from Ductal Carcinoma In Situ to Invasive Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2016.06.051 {Cell reports (7.815): 10.1016/j.celrep.2016.06.051} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA254806 https://www.ebi.ac.uk/ena/browser/view/PRJNA254806 None [Overal design]One-color design, totaling 105 arrays and 103 unique tissues. Arrays consist of 3 normal controls (1 unique), 46 DCIS lesions (46 unique), and 56 small invasive breast cancers (56 unique).; [Treatment]'None'; [Growth]'None'; [Extraction]'Tumor tissues were homogenized using TRIzol Reagent (Invitrogen, Life Technologies, USA), and purified with RNeasy mini columns (Qiagen, Netherlands). The quality of RNA was assessed using NanoDrop ND-1000 Spectrophotometer, version 3.7.1 (NanoDrop Technologies, Thermo Fisher Scientific Inc, USA).'; [Cell type]'Source: ''tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 57; size (mm): 20; pam50: Normal; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 47; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 1; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 50; size (mm): NA; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 241; source: Oslo; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 1; grade (elston): 1; grade (eortc): NA; lymph node: 0; age (years): 40; size (mm): 10; pam50: Her2; death event: 1; iPSilateral event: 1; dmfs event: 1; recurrence event: 1; recurrence location: Skin and brain; recurrence type: Invasive; follow-up time: 51; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 44; size (mm): NA; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 48; size (mm): 12; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 56; size (mm): NA; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 67; size (mm): 12; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 0; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 55; size (mm): NA; pam50: LumB; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 50; source: Uppsala; ', 'tissue type: Normal breast tissue; er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: NA; age (years): NA; size (mm): NA; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Ambion Human Breast Total RNA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): 2; grade (eortc): NA; lymph node: 0; age (years): 78; size (mm): 10; pam50: LumB; death event: 1; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 47; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 71; size (mm): 23; pam50: Basal; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 108; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 0; her2 (ihc): NA; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 78; size (mm): NA; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): NA; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 42; size (mm): 11; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 69; size (mm): NA; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 0; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 69; size (mm): 26; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 232; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 55; size (mm): 20; pam50: Her2; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 270; source: Oslo; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 57; size (mm): 13; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 72; size (mm): 19; pam50: LumA; death event: 1; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 50; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 65; size (mm): 19; pam50: LumA; death event: 0; iPSilateral event: 1; dmfs event: 0; recurrence event: 1; recurrence location: Ipsilateral invasive; recurrence type: Invasive; follow-up time: 93; source: Oslo; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 40; size (mm): 15; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 57; size (mm): 14; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 48; size (mm): 60; pam50: LumA; death event: 0; iPSilateral event: 1; dmfs event: 0; recurrence event: 1; recurrence location: Ipsi situ; recurrence type: Non-Invasive; follow-up time: 37; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 56; size (mm): 25; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): 2; grade (eortc): NA; lymph node: 0; age (years): 52; size (mm): 9; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 244; source: Oslo; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 79; size (mm): NA; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 60; size (mm): NA; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 1; grade (combined): 2; grade (elston): 2; grade (eortc): NA; lymph node: 0; age (years): 60; size (mm): 10; pam50: LumB; death event: 0; iPSilateral event: 1; dmfs event: 0; recurrence event: 1; recurrence location: Ipsilateral invasive; recurrence type: Invasive; follow-up time: 215; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 57; size (mm): NA; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 1; grade (combined): 1; grade (elston): 1; grade (eortc): NA; lymph node: 0; age (years): 72; size (mm): 10; pam50: LumA; death event: 1; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 33; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 54; size (mm): 17; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 1; recurrence event: 1; recurrence location: contra invasive then liver +skeleton; recurrence type: Invasive; follow-up time: 267; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 48; size (mm): NA; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 42; size (mm): 35; pam50: LumB; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 40; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 82; size (mm): 28; pam50: Her2; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 48; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 65; size (mm): 10; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 47; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 56; size (mm): 7; pam50: Her2; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 48; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 66; size (mm): NA; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): NA; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 83; size (mm): 14; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 47; size (mm): NA; pam50: LumB; death event: 1; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 63; source: Oslo; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): NA; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 48; size (mm): 14; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): NA; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 53; size (mm): 1; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 57; size (mm): 50; pam50: Normal; death event: 1; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 166; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 59; size (mm): 9; pam50: Normal; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 50; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 66; size (mm): 20; pam50: Normal; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 43; source: Uppsala; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): NA; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 53; size (mm): 13; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 63; size (mm): 14; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 43; size (mm): NA; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 60; size (mm): NA; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 56; size (mm): 45; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 45; size (mm): 24; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 64; size (mm): NA; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 0; her2 (ihc): 0; grade (combined): 2; grade (elston): 2; grade (eortc): NA; lymph node: 0; age (years): 62; size (mm): 10; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 1; recurrence location: contralateral in situ then contra invasive; recurrence type: Mixed; follow-up time: 231; source: Oslo; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): NA; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 64; size (mm): 15; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 46; size (mm): 15; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 53; size (mm): NA; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 36; size (mm): 45; pam50: Her2; death event: 0; iPSilateral event: 1; dmfs event: 0; recurrence event: 1; recurrence location: Ipsi inv; recurrence type: Invasive; follow-up time: 12; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 74; size (mm): 25; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 266; source: Oslo; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 57; size (mm): 30; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 49; size (mm): 35; pam50: LumB; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 51; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 66; size (mm): 17; pam50: Her2; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 245; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 54.8; size (mm): NA; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 60.9; size (mm): 15; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 53.8; size (mm): 25; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 51.1; size (mm): 25; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 75.1; size (mm): 44; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: NA; age (years): NA; size (mm): NA; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 47.9; size (mm): 45; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 78; size (mm): 12; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 75.3; size (mm): 11; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 52.1; size (mm): 10; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 60.6; size (mm): 11; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 61.4; size (mm): 11; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 37.9; size (mm): 11; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 55.1; size (mm): 7; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 61.9; size (mm): 13; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 50.1; size (mm): 12; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 69.9; size (mm): 9; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 52.1; size (mm): 8; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 43.1; size (mm): 7; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 62.4; size (mm): 9; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 1; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 60.2; size (mm): 12; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 58.5; size (mm): 13; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 75.1; size (mm): 14; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 75.5; size (mm): 12; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 52.7; size (mm): 11; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 52.1; size (mm): 6; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 56.9; size (mm): 11; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 51.3; size (mm): 11; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 63.8; size (mm): 10; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 50.7; size (mm): 8; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 72.4; size (mm): 11; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 0; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 74.6; size (mm): 10; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 49.1; size (mm): 9; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 44.6; size (mm): 11; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 59.3; size (mm): 14; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 65.1; size (mm): 9; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 40.7; size (mm): 12; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 67.6; size (mm): 12; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 0; her2 (ihc): 0; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 69.1; size (mm): 4; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 64.1; size (mm): 11; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 0; her2 (ihc): 1; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 46.1; size (mm): 9; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 52; size (mm): 7; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 64.3; size (mm): 11; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 67.5; size (mm): 11; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; ' GSE64350 Homo sapiens 4 Expression profiling by array GPL17077 GLI1-regulated genes in human mammary epithelial cells and human breast cancer cells 2014-12-19 To clarify transcriptional target genes of GLI1 in human mammary epithelial cells and breast cancer cells, primary culture cells of human mammary epithelium HMEC and breast cancer cell line MCF-7 were lentivirally transduced by either GLI1 or its control LacZ. Their RNA samples were served for expression analysis using AGILENT human 8x60K cDNA microarray. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64350 GLI1 orchestrates CXCR4/CXCR7 signaling to enhance migration and metastasis of breast cancer cells. Oncotarget None https://doi.org/10.18632/oncotarget.5203 {Oncotarget (None): 10.18632/oncotarget.5203} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA270805 https://www.ebi.ac.uk/ena/browser/view/PRJNA270805 None [Overal design]Array analysis of HMEC and MCF-7 expressing either GLI1 or LacZ. 1 color method was employed.; [Treatment]'None'; [Growth]'None'; [Extraction]'Not provided.'; [Cell type]'primary human mammary epithelium cells (HMEC)', 'MCF-7''cell type: primary human mammary epithelium cells (HMEC); genotype/variation: expressing LacZ; ', 'cell type: primary human mammary epithelium cells (HMEC); genotype/variation: expressing GLI1; ', 'cell type: MCF-7; genotype/variation: expressing LacZ; ', 'cell type: MCF-7; genotype/variation: expressing GLI1; ' GSE50470 Homo sapiens 105 Expression profiling by array GPL7504 Characterization of Cell Lines Derived from Breast Cancers and Normal Mammary Tissues for the Study of the Intrinsic Molecular Subtypes 2013-08-29 Five molecular subtypes (Luminal A/B, HER2-enriched, Basal-like, and Claudin-low) with clinical implications have been identified. In this report, we evaluated molecular and phenotypic relationships of a large in vitro panel of human breast cancer cell lines (BCCLs), human mammary fibroblasts (HMFs) and human mammary epithelial cells (HMECs) with (1) breast tumors, (2) normal breast cell-enriched subpopulations and (3) human embryonic stem cells (hESCs) and bone marrow-derived mesenchymal stem cells (hMSC). First, by integrating genomic data of 337 breast samples with 93 cell lines we were able to identify all the intrinsic tumor subtypes in vitro, except for the Luminal A. Secondly, we observed that cell lines recapitulate the differentiation hierarchy observed in the mammary gland, with Claudin-low BCCLs and HMFs cells showing a stromal phenotype, HMECs showing a mammary stem cell/bipotent progenitor phenotype, Basal-like cells showing a luminal progenitor phenotype, and Luminal B cells showing a luminal phenotype. Thirdly, we identified Basal-like and highly migratory Claudin-low subpopulations of cells within a subset of triple-negative BCCLs (SUM149PT, HCC1143 and HCC38). Interestingly, both subpopulations within SUM149PT where found to have Tumor Initiating Cell (TIC) features, but the Basal-like subpopulation grew faster than the Claudin-low subpopulation. Finally, Claudin-low BCCLs were found to resemble the phenotype of hMSCs, whereas hESCs cells were found to have an epithelial phenotype without basal and luminal differentiation. The results presented here should help improve our understanding of the cell line model system through the appropriate pairing of cell lines with relevant in vivo tumor and normal cell counterparts. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50470 Characterization of cell lines derived from breast cancers and normal mammary tissues for the study of the intrinsic molecular subtypes. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-013-2743-3 {Breast cancer research and treatment (3.471): 10.1007/s10549-013-2743-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA217714 https://www.ebi.ac.uk/ena/browser/view/PRJNA217714 None [Overal design]reference x sample; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA isolated by Stratagene.', 'Qiagen Rneasy Kit', 'Total RNA isolated by stratagene'; [Cell type]'Source: ', 'SUM149 sorted 5a/R1 HuMEC CD49f+/EpCAM+', 'SUM149 sorted 5a/R6 HuMEC CD49f+/EpCAM-', 'SUM149 sorted 5b/R5 HuMEC CD49f+/EpCAM-', 'SUM149 sorted 6a/R5 HuMEC+FBS CD49f+/EpCAM-', 'SUM149 sorted 6a/R6 HuMEC+FBS CD49f+/EpCAM+''reference: Stratagene Human Universal Reference that contained 1/10 added MCF7 and ME16C RNAs; ', 'tissue: Breast Cancer Cell Line; cell type: SUM149 sorted 5a/R1 HuMEC CD49f+/EpCAM+; ', 'tissue: Breast Cancer Cell Line; cell type: SUM149 sorted 5a/R6 HuMEC CD49f+/EpCAM-; ', 'tissue: Breast Cancer Cell Line; cell type: SUM149 sorted 5b/R5 HuMEC CD49f+/EpCAM-; ', 'tissue: Breast Cancer Cell Line; cell type: SUM149 sorted 6a/R5 HuMEC+FBS CD49f+/EpCAM-; ', 'tissue: Breast Cancer Cell Line; cell type: SUM149 sorted 6a/R6 HuMEC+FBS CD49f+/EpCAM+; ', 'cell line: vHMEC-1; origin tissue: breast; ', 'cell line: HME-CC; origin tissue: breast; ', 'cell line: vHMEC-2; origin tissue: breast; ', 'cell line: vHMEC-3; origin tissue: breast; ', 'cell line: ME16C; origin tissue: breast; ', 'cell line: MCF12F; origin tissue: breast; ', 'cell line: MCF10A; origin tissue: breast; ', 'cell line: MCF12A; origin tissue: breast; ', 'reference: whole human total RNA; ', 'sample: Cell Line Hs578T p11; ', 'references: Whole human total RNA; ', 'sample: Cell Line; ' GSE34555 Homo sapiens 60 Protein profiling by protein array GPL15009 Evaluation of auto-antibody serum biomarkers for breast cancer screening 2011-12-19 Using protein microarrays, derived from 642 His-tag proteins, we could distinguish sera from breast-nodule positive patients and healthy control individuals. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE34555 None None None None None 'protein' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA151535 https://www.ebi.ac.uk/ena/browser/view/PRJNA151535 None [Overal design]Each Protein microarray was divided in to 4 sub-arrays. Each protein was spotted in duplicates in each sub-array. For evaluation 24 malignant, 16 benign breast cancer serum samples and 20 healthy control serum samples were used.; [Treatment]'None'; [Growth]'None'; [Extraction]'The His-tag recombiant proteins were expressed in E. coli using autoinduction and purified using Ni-NTA agarose. Elution of the purified recombinant proteins was done using 50 mM Imidazole. These proteins were used for the generation of protein microarrays. The serum autoantibody profiling of the sera from breast cancer patients (benign & malignant) and healthy controls was done using the protein micrarrays'; [Cell type]'Source: ''disease state: Carcinoma, intraductal, noninvasive; age: 75; ', 'disease state: Invasive ductal carcinoma; age: 49; ', 'disease state: Borderline tumour (ovarian); age: 45; ', 'disease state: Invasive ductal carcinoma; age: 64; ', 'disease state: Invasive lobular carcinoma (10-20%); age: 62; ', 'disease state: Carcinoma, intraductal, noninvasive; age: 64; ', 'disease state: Invasive lobular carcinoma (10-20%); age: 51; ', 'disease state: Invasive ductal carcinoma; age: 63; ', 'disease state: Invasive ductal carcinoma; age: 51; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 45; ', 'disease state: Invasive ductal carcinoma; age: 55; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 42; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 44; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 61; ', 'disease state: Invasive ductal carcinoma; age: 44; ', 'disease state: Invasive ductal carcinoma; age: 71; ', 'disease state: Carcinoma, intraductal, noninvasive; age: 80; ', 'disease state: Invasive ductal carcinoma; age: 47; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 33; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 66; ', 'disease state: Muzinous carcinoma; age: 57; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 36; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 69; ', 'disease state: Invasive ductal carcinoma; age: 53; ', 'disease state: Invasive ductal carcinoma; age: 57; ', 'disease state: Invasive ductal carcinoma; age: 52; ', 'disease state: Invasive lobular carcinoma (10-20%); age: 80; ', 'disease state: intraductal Carcinoma with microinvasion; age: 60; ', 'disease state: Invasive lobular carcinoma (10-20%); age: 65; ', 'disease state: Carcinoma, intraductal, noninvasive; age: 61; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 29; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 39; ', 'disease state: Invasive ductal carcinoma; age: 59; ', 'disease state: Invasive ductal carcinoma; age: 75; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 47; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 46; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 53; ', 'disease state: mastopathy/fibroadenoma/mammaparenchym/papilloma; age: 48; ', 'disease state: Carcinoma, intraductal, noninvasive; age: 53; ', 'disease state: Healthy controls; age: 63; ', 'disease state: Healthy controls; age: 75; ', 'disease state: Healthy controls; age: 79; ', 'disease state: Healthy controls; age: 81; ', 'disease state: Healthy controls; age: 83; ', 'disease state: Healthy controls; age: 71; ', 'disease state: Healthy controls; age: 66; ', 'disease state: Healthy controls; age: 77; ', 'disease state: Healthy controls; age: 64; ', 'disease state: Healthy controls; age: 82; ', 'disease state: Healthy controls; age: 61; ', 'disease state: Healthy controls; age: 88; ', 'disease state: Healthy controls; age: 74; ' GSE72010 Homo sapiens 9 Expression profiling by array GPL6244 The effect of ethanol on the cultured human breast cancer line MCF-7 2015-08-12 Alcohol consumption is a known risk factor for breast cancer in humans. We used the established breast cancer cell line MCF-7 to analyze the effects of ethanol on gene expression at the RNA level. In addition, we carried out studies on protein levels and the ability of cells to grow in an anchorage independent manner. The DNA microarray results are deposited here. We also provide the results of studies on microRNA levels as a separate data set. Cells grown in culture for 1 to 4 weeks were treated with 0-25 mM ethanol. RNA was extracted using the RNeasy Plus Micro kit and subjected to analysis by DNA microarray, using the Affymetrix human Gene 1.0 ST array (platform GPL19142). RNA samples from different treatments were analysed by the UCLA DNA Core lab. Data were returned as rma values. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72010 Long-term exposure of MCF-7 breast cancer cells to ethanol stimulates oncogenic features. International journal of oncology 3.571 https://doi.org/10.3892/ijo.2016.3800 {International journal of oncology (3.571): 10.3892/ijo.2016.3800} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA292716 https://www.ebi.ac.uk/ena/browser/view/PRJNA292716 None [Overal design]There are control experiments in which cells were grown without added ethanol, and there are experiments in which cells were grown in the presence of 25 mM ethanol for either 1 week or 4 weeks. One column shows the gene expression values for another cell line MCF12-A, which was established using non-malignant human breast cells and which was grown in the absence of ethanol. In this particular Affymetrix array, most genes are evaluated as a single Probe Set, but there are some which are included in the array as 2 or more Probe Sets.; [Treatment]'Cells were grown in culture in 6 well plates in minimal essentail medium Eagle plus 10 percent fetal bovine serum and 0.01 mg/ml bovine insulin. Ethanol was added to each well in a volume of 10 microliters to achieve concentrations ranging from 0 to 25 mM. The 25 mM and control (0 mM) treatments were carried on for 1 week or 4 weeks, and RNA was extracted for analysis.'; [Growth]'None'; [Extraction]'Cells were washed once with phosphate buffered saline pH 7.4 and RNA was extracted using the RNeasy Plus Micro kit.'; [Cell type]'non-malignant breast cancer', 'malignant breast cancer''cell line: MCF12-A; cell type: non-malignant breast cancer; ', 'cell line: MCF-7; cell type: malignant breast cancer; ' GSE64033 Homo sapiens 65 Expression profiling by array GPL10558 PI3K inhibition results in enhanced estrogen receptor function and dependence in hormone receptor-positive breast cancer 2014-12-10 Activating mutations of PIK3CA are the most frequent genomic alterations in estrogen receptor (ER)-positive breast tumors and selective PI3Kα inhibitors are in clinical development. The activity of these agents, however, is not homogenous and only a fraction of patients bearing PIK3CA-mutant ER-positive tumors benefit from single agent administration. Searching for mechanisms of resistance, we observed that suppression of PI3K signaling with different agents results in induction of ER-dependent transcriptional activity as demonstrated by changes in expression in genes containing ER binding sites, enhanced ER transcription and increased occupancy by the ER of promoter regions of upregulated genes. Furthermore, expression of ESR1 mRNA and ER protein levels themselves were also increased upon PI3K inhibition. These changes in gene expression were confirmed in vivo in xenograft and patient derived models and in tumors from patients undergoing treatment with the PI3Kα inhibitor BYL719. The observed effects on transcription were enhanced by the addition of estradiol and suppressed by the anti-ER therapies fulvestrant and tamoxifen. Fulvestrant markedly sensitized ER-positive tumors to PI3Kα inhibition. We propose that increased ER transcriptional activity may be a compensatory mechanism that limits the activity of PI3K inhibitors and that combined PI3K and ER inhibition is a rational approach to target these tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64033 PI3K inhibition results in enhanced estrogen receptor function and dependence in hormone receptor-positive breast cancer. Science translational medicine 17.161 https://doi.org/10.1126/scitranslmed.aaa4442 {Science translational medicine (17.161): 10.1126/scitranslmed.aaa4442} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA269919 https://www.ebi.ac.uk/ena/browser/view/PRJNA269919 None [Overal design]The aim of our study was to explore the mechanism by which combination of PI3K pathway inhibitors and estrogen receptor function blockade results in superior antitumor activity. We aimed to evaluate whether changes in ER function were influencing the clinical response to anti-PI3K therapy in ER-positive breast tumors that harbor PI3K pathway activation. For this purpose, we planned to use various specific PI3K inhibitors, namely: BYL719 (p110α specific catalytic inhibitor), GDC0941 (pan-PI3K inhibitor), GDC0032 and BAY80-6946 (p110sparing PI3K inhibitors) in a panel of ER-positive breast cancer cell lines and xenografts that harbor PIK3CA activating mutations. We also used MK2206 (pan-AKT allosteric inhibitor) to inhibit the PI3K pathway in ER-positive cell lines which activate this pathway through PTEN loss. Finally, in order to evaluate the role of ER up-regulation as a pro-survival signal in our in vitro and in vivo models, we planned to use the selective ER modulator 4-hydroxy-tamoxifen (4-OHT) and degrader fulvestrant. For the in vivo experiments, the number of animals in each group was calculated to measure a 25% difference between the means of placebo and treatment groups with a power of 80% and a p value of 0.01. Host mice carrying xenografts were randomly and equally assigned to either control or treatment groups. Animal experiments were conducted in a controlled and non-blinded manner. Moreover, we evaluated by means of RNAseq gene expression changes breast cancer patients that underwent BYL719 based therapy to validate our in vitro findings in terms of ER expression. In vitro experiments were performed at least two times and at least in triplicate for each replica.; [Treatment]'None'; [Growth]'None'; [Extraction]'For microarray-gene expression analyisis total RNA was extracted from MCF7, T47D, CAMA1 cell lines using the QIAGEN RNeasy kit. Total RNA from MCF7 xenografts and patient derived xenografts was obtained using the same kit preceded by tissue homogenization with TRIzol® (Thermo Fisher Scientific Inc).'; [Cell type]'Breast cancer cell line''cell line: CAMA1; treatment (drug): Ctrl; treatment (time): Control; cell type: Breast cancer cell line; ', 'cell line: CAMA1; treatment (drug): AKT inhibitor (MK2206); treatment (time): 4h; cell type: Breast cancer cell line; ', 'cell line: CAMA1; treatment (drug): AKT inhibitor (MK2206); treatment (time): 8h; cell type: Breast cancer cell line; ', 'cell line: CAMA1; treatment (drug): AKT inhibitor (MK2206); treatment (time): 12h; cell type: Breast cancer cell line; ', 'cell line: CAMA1; treatment (drug): AKT inhibitor (MK2206); treatment (time): 24h; cell type: Breast cancer cell line; ', 'cell line: CAMA1; treatment (drug): AKT inhibitor (MK2206); treatment (time): 48h; cell type: Breast cancer cell line; ', 'cell line: MCF7; treatment (drug): Ctrl; treatment (time): Control; cell type: Breast cancer cell line; ', 'cell line: MCF7; treatment (drug): PI3K inhibitor (BYL719); treatment (time): 4h; cell type: Breast cancer cell line; ', 'cell line: MCF7; treatment (drug): PI3K inhibitor (BYL719); treatment (time): 8h; cell type: Breast cancer cell line; ', 'cell line: MCF7; treatment (drug): PI3K inhibitor (BYL719); treatment (time): 2h; cell type: Breast cancer cell line; ', 'cell line: MCF7; treatment (drug): PI3K inhibitor (BYL719); treatment (time): 48h; cell type: Breast cancer cell line; ', 'cell line: T47D; treatment (drug): Ctrl; treatment (time): Control; cell type: Breast cancer cell line; ', 'cell line: T47D; treatment (drug): PI3K inhibitor (BYL719); treatment (time): 4h; cell type: Breast cancer cell line; ', 'cell line: T47D; treatment (drug): PI3K inhibitor (BYL719); treatment (time): 8h; cell type: Breast cancer cell line; ', 'cell line: T47D; treatment (drug): PI3K inhibitor (BYL719); treatment (time): 12h; cell type: Breast cancer cell line; ', 'cell line: T47D; treatment (drug): PI3K inhibitor (BYL719); treatment (time): 24h; cell type: Breast cancer cell line; ', 'cell line: T47D; treatment (drug): PI3K inhibitor (BYL719); treatment (time): 48h; cell type: Breast cancer cell line; ', 'cell line: Patient derived xenograft; treatment (drug): Ctrl; cell type: Breast cancer cell line; ', 'cell line: Patient derived xenograft; treatment (drug): PI3K inhibitor (BYL719); cell type: Breast cancer cell line; ', 'cell line: MCF7 xenograft; treatment (drug): Ctrl; cell type: Breast cancer cell line; ', 'cell line: MCF7 xenograft; treatment (drug): PI3K inhibitor (BYL719); cell type: Breast cancer cell line; ' GSE132851 Homo sapiens 4 Expression profiling by high throughput sequencing GPL24676 Overexpression of eukaryotic translation initiation factor, eIF4E confers tamoxifen resistance in breast cancer via the ERα/FOXM1 axis 2019-06-17 We report the application of RNA sequencing technology for high-throughput profiling of mRNA expression in breast cancer cell line https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132851 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA549272 https://www.ebi.ac.uk/ena/browser/view/PRJNA549272 https://www.ncbi.nlm.nih.gov/sra?term=SRP201635 [Overal design]Examination of the effect of eIF4E overexpression on the alteration of mRNA expression profile in breast cancer cell lines MCF-7 and ZR-75; [Treatment]'None'; [Growth]'MCF-7 and MCF-7 eIF4E OE cells were cultured in DMEM containing 10% (v/v) FBS and 1% (v/v) antibiotics (penicillin, 100 U/ml; streptomycin sulfate, 100 ug/ml). ZR-75 and ZR-75 eIF4E OE were cultured in phenol-free modified IEME supplemented with 10% (v/v) FBS and 1% (v/v) PS. All cells were maintained in 370C humidified atmosphere supplemented with 5% CO2.'; [Extraction]'Trizol total RNA extraction\ncDNA libraries were prepared by KAPA Stranded mRNA-Seq Kit (KR0960-v3.15)'; [Cell type]'Source: ''cell line: MCF-7; passage: 20-24; er status: positive; ', 'cell line: ZR-75; passage: 20-24; er status: positive; ' GSE53531 Homo sapiens 3 Genome binding/occupancy profiling by high throughput sequencing GPL9115 Genome-wide activity of unliganded Estrogen Receptor alpha in breast cancer cells [ChIP-Seq] 2013-12-20 Estrogen Receptor α (ERα) has central role in hormone-dependent breast cancer and its ligand-induced functions have been extensively characterized. However, evidence exists that ERα has functions which are independent of ligands. In the present work, we investigated the binding of ERα to chromatin in absence of ligands, and its function(s) on gene regulation. We demonstrated that in MCF7 breast cancer cells unliganded ERα binds to more than four thousands chromatin sites. Unexpectedly, although almost entirely comprised in the larger group of estrogen-induced binding sites, we found that unliganded-ERα binding is specifically linked to genes with developmental functions, as compared to estrogen-induced binding. Moreover, we found that siRNA-mediated downregulation of ERα in absence of estrogen is accompanied by changes in the expression levels of hundreds of coding and noncoding RNAs. Downregulated mRNAs showed enrichment in genes related to epithelial cell growth and development. Stable ERα downregulation using shRNA, which caused cell-growth arrest, was accompanied by increased H3K27me3 at ERα binding sites. Finally, we found that FOXA1 and AP2γ binding to several sites is decreased upon ERα silencing, suggesting that unliganded ERα participates, together with other factors, to the maintenance of the luminal-specific cistrome in breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53531 Genome-wide activity of unliganded estrogen receptor-α in breast cancer cells. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1315445111 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1315445111} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA232304 https://www.ebi.ac.uk/ena/browser/view/PRJNA232304 https://www.ncbi.nlm.nih.gov/sra?term=SRP034656 [Overal design]Examination of unliganded estrogen receptor alpha (ERα) DNA interactions in control and ERα siRNA treated MCF7 cells.; [Treatment]'Cells were transfected with siRNA using Lipofectamine2000 (Invitrogen) on day 2, according to the manufacture protocol. Stealth RNAiTM siRNAs (ESR1HSS103376, ESR1HSS103377, ESR1HSS176619) from Invitrogen were used to target ERα. Stealth RNAiTM siRNA Negative Control LO GC from Invitrogen was used as a negative control.'; [Growth]'MCF7 were routinely grown in DMEM containing 10% heat-inactivated FBS, 2mM L-glutamine, 50 U/ml penicillin and 50 μg/ml streptomycin. Before to perform any experiments, MCF7 cells were grown in phenol red-free DMEM supplemented with 5% charcoal-dextran-treated serum for 3 days.'; [Extraction]'Cells were crosslinked by adding 1% formaldehyde, immunoprecipitation was performed as described using antibodies against ERα. DNA purification was achieved with Phenol:Chloroform:IAA (25:24:1) according to the manufacturer’s instructions.\nChIP-Seq was performed using 10ng of immunoprecipitated DNA obtained from 240 μg of chromatin for each sample, followed by library amplification and Illumina sequencing.'; [Cell type]'Source: ''cell line: MCF-7; chip antibody: ERα (Santa Cruz Biotechnology; sc-534X, sc-7207X); transfection: siCTL; ', 'cell line: MCF-7; chip antibody: ERα (Santa Cruz Biotechnology; sc-534X, sc-7207X); transfection: siERα; ', 'cell line: MCF-7; chip antibody: Rabbit Control IgG ChIP Grade ab46540; ' GSE60689 Homo sapiens 4 Non-coding RNA profiling by array GPL16956 Identification of LncRNA Expression Signatures for Triple-negative Breast Cancer 2014-08-22 To identify biologically and clinically novel lncRNAs potentially involved in the progression of breast cancer, we profiled the expression of lncRNAs in two stage III triple-negativebreast cancer tissues and their paired adjacent noncancerous tissues by LncRNA Array 3.0 (ArrayStar). Expression of the mostly upregulated lncRNA (BCAR4) from this signature was quantified in the breast caner tissue microarray by RNA In situ Hybridization and bioinformatic analysis of Oncomine database, confirming its correlation with breast cancer metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60689 lncRNA directs cooperative epigenetic regulation downstream of chemokine signals. Cell 36.216 https://doi.org/10.1016/j.cell.2014.10.013 {Cell (36.216): 10.1016/j.cell.2014.10.013} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA259367 https://www.ebi.ac.uk/ena/browser/view/PRJNA259367 None [Overal design]LncRNA Expression profiling analysis of the 4 samples including 2 triple-negative breast cancer tissues and their matched adjacent normal breast tissues by Arraystar Human LncRNA Array v3.0.; [Treatment]'None'; [Growth]'None'; [Extraction]"RNA was extracted from human breast cancers and their matched adjacent normal tissues using the TRIzol® Plus RNA Purification Kit (Life Technologies, Grand Island NY) following the manufacturer's recommendations. RNA quantity and quality were measured by NanoDrop ND-2000 and RNA integrity was assessed by standard denaturing agarose gel electrophoresis."; [Cell type]'Source: ''tissue: Breast; gender: Female; age: 73; ', 'tissue: Breast; gender: Female; age: 67; ' GSE24124 Homo sapiens 119 Expression profiling by array; Third-party reanalysis GPL887 The inferred mechanisms for prognostic features of signal transducer and activator of transcription 3 in an ER(+) breast cancer model system 2010-09-14 Abstract Aberrantly expressed signal transducer and activator of transcription 3 (STAT3) predicts poor prognosis primarily in estrogen receptor positive (ER(+)) breast cancers and activated STAT3 is overexpressed in luminal A subtype cells. The mechanisms contributing to the prognosis and/or subtype relevant features of *STAT3* in ER(+) breast cancers are* *through multiple interacting regulatory pathways including STAT3-MYC, STAT3-ER , STAT3-MYC-ER interactions and the direct action of activated STAT3. These results predict malignant events, treatment responses and a novel enhancer of tamoxifen resistance. The inferred crosstalk between ER and STAT3 in regulating their shared target gene-*METAP2* is partially validated in the luminal B breast cancer cell line-MCF7. Taken together, we identify a poor prognosis relevant gene set within the *STAT3* network and a robust one in a subset of patients. *VEGFA*, *ABL1*, *LYN*, *IGF2R* and* STAT3* are suggested therapeutic targets for further study based upon the degree of differential expression in our model. Keywords: STAT3 transcriptional regulatory network, prognosis, tamoxifen resistance, tumorigenesis, breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24124 Identifying gene set association enrichment using the coefficient of intrinsic dependence. PloS one 2.776 https://doi.org/10.1371/journal.pone.0058851 {International journal of genomics (2.303) doi:10.1155/2015/403576}; {PloS one (2.776) doi:10.1371/journal.pone.0058851}; {Cancer informatics (None) doi:10.4137/CIN.S8470}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA130065 https://www.ebi.ac.uk/ena/browser/view/PRJNA130065 None [Overal design]181 surgical specimens of primary infiltrating ductal carcinoma (IDC) were obtained from patients who underwent surgery at National Taiwan University Hospital (NTUH) between 1998 and 2007. They include 90 ER(+) IDCs and 91 ER(-) IDCs. Tissue samples were excised, snap frozen in liquid nitrogen, and stored at -80℃. Breast cancer samples containing relatively pure cancer as defined by greater than 50% tumor cells per high-power field examined in an adjacent section of tumor sample were for this study (Lien HC, et al. Oncogene 2007; 26: 7859-71). Twenty five non-tumor samples were surgically taken from breast cancer patients in 181 IDC patients to generate 25 gene expression profiles as a control in this study. All patients had given informed consent according to the guidelines approved by the Institutional Review Board at NTUH. The matrix file linked to the bottom of this Series includes reanalyzed data from the 119 Samples of this Series and 87 Samples from Series GSE9309 and GSE17040.; [Treatment]'The surgical removed tumors and non-tumor part of breast specimens were excised, collected and snap-frozen in liquid nitrogen immediately before RNA extraction.'; [Growth]'The fresh samples used for this study were immediately frozen by liquid nitrogen without any additional growth procedure applied before RNA extraction.'; [Extraction]'Trizol reagent combined with RNAeasy mini kit'; [Cell type]'Source: ''gender: female; tissue: non tumor part of breast tissue.; ', "sample type: Stratagene's human common reference RNA; ", 'er/pr/her status: NA; gender: female; tissue: non tumor part of breast tissue.; ', 'status: ER(+), PR(+); gender: female; tissue: primary tumor; ', 'er/pr/her status: ER(-) PR(-)HER(-); status: ER(-), PR(-); gender: female; tissue: primary tumor; ', 'status: ER(-), PR(-); gender: female; tissue: primary tumor; ', 'er/pr/her status: ER(-)PR(-)HER(+); status: ER(-), PR(-); gender: female; tissue: primary tumor; ', 'er/pr/her status: ER(-) PR(+)HER(+); status: ER(-), PR(+); gender: female; tissue: primary tumor; ', 'status: ER(+), PR(-); gender: female; tissue: primary tumor; ', 'er/pr/her status: ER(-)PR(+)HER(-); status: ER(-), PR(+); gender: female; tissue: primary tumor; ' GSE80526 Homo sapiens 120 Genome variation profiling by SNP array GPL6801 Genomewide copy number profiles for breast cancer from Taiwanese women 2016-04-21 The incidence of breast cancer has been rapidly increasing in East Asia. This is the first study of genome wide copy number of breast cancer in East Asia. We conducted this study to compare the genetic alterations between East and West. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80526 High prevalence of APOA1/C3/A4/A5 alterations in luminal breast cancers among young women in East Asia. NPJ breast cancer 32.43 https://doi.org/10.1038/s41523-021-00299-5 {NPJ breast cancer (32.43): 10.1038/s41523-021-00299-5} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA319199 https://www.ebi.ac.uk/ena/browser/view/PRJNA319199 None [Overal design]A total of 120 tumor samples from different patients were subjected to genomic DNA extract. The DNAs were hybridized to Affymetrix SNP 6.0 arrays per the manufacturer’s instructions (Affymetrix, Santa Clara, CA. USA) to obtain the copy number alterations profilings.; [Treatment]'None'; [Growth]'None'; [Extraction]'QIAamp DNA Mini Kit (Qiagen Inc., Valencia, CA, USA)'; [Cell type]'Source: ''disease: Breast cancer; tissue: tumor; gender: Female; age: 45; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 46; grade: 2; er: 1; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 43; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 58; grade: 3; er: 1; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 43; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 51; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 41; grade: 3; er: 1; pr: 1; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 59; grade: 2; er: 1; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 53; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 57; grade: 3; er: 1; pr: 1; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 58; grade: 2; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 70; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 56; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 55; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 50; grade: 3; er: 1; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 74; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 43; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 40; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 38; grade: 2; er: 1; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 50; grade: 2; er: 1; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 30; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 67; grade: 2; er: 1; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 62; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 47; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 40; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 54; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 54; grade: 2; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 56; grade: 2; er: 1; pr: 1; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 39; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 37; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 50; grade: 3; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 64; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 77; grade: 2; er: 1; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 58; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 31; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 42; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 46; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 56; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 52; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 53; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 39; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 54; grade: 3; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 50; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 42; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 78; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 37; grade: 3; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 42; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 59; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 38; grade: 2; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 29; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 59; grade: 3; er: 1; pr: 1; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 44; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 44; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 46; grade: 3; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 43; grade: 3; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 58; grade: 3; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 50; grade: 3; er: 1; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 51; grade: 3; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 46; grade: 1; er: 1; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 56; grade: 2; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 51; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 58; grade: 2; er: 1; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 34; grade: 2; er: 1; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 52; grade: 3; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 36; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 58; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 65; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 69; grade: 3; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 47; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 51; grade: 3; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 34; grade: NA; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 55; grade: 2; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 64; grade: 3; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 41; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 71; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 29; grade: 3; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 61; grade: 3; er: 1; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 24; grade: 3; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 37; grade: 2; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 52; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 39; grade: 2; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 55; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 46; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 48; grade: 2; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 37; grade: 2; er: 1; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 42; grade: 2; er: 1; pr: 1; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 35; grade: 3; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 49; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 39; grade: 2; er: 1; pr: 1; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 70; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 76; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 41; grade: 3; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 34; grade: 2; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 59; grade: 3; er: 1; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 40; grade: 3; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 42; grade: 3; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 32; grade: 3; er: 1; pr: 1; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 34; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 29; grade: 3; er: 0; pr: 1; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 56; grade: 3; er: 0; pr: 0; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 40; grade: 3; er: 0; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 44; grade: 3; er: 1; pr: 0; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 33; grade: 3; er: 1; pr: 1; her2: 1; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 79; grade: 1; er: 1; pr: 1; her2: 0; ', 'disease: Breast cancer; tissue: tumor; gender: Female; age: 33; grade: 2; er: 1; pr: 1; her2: 0; ' GSE130031 Mus musculus 4 Expression profiling by high throughput sequencing GPL17021 Estrogen receptor-depended gene signatures in the mouse mammary gland after acute estradiol treatment (RNA-Seq) 2019-04-18 Estrogen receptor α (ERα) is the major driving transcription factor in normal mammary gland development as well as breast cancer initiation and progression.However,the fundamental mechanisms,including global cistromic and genomic transcriptional responses that are required to elicit mammary epithelial cell proliferation in response to estradiol, have not been elucidated. We used RNA-seq analysis to identify global gene expression signatures that are acutely regulated by estroegn receptors in the mouse mammary gland after acute estradiol treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130031 The genomic landscape of estrogen receptor α binding sites in mouse mammary gland. PloS one 2.776 https://doi.org/10.1371/journal.pone.0220311 {PloS one (2.776): 10.1371/journal.pone.0220311} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA533618 https://www.ebi.ac.uk/ena/browser/view/PRJNA533618 https://www.ncbi.nlm.nih.gov/sra?term=SRP193003 [Overal design]Mammary gland gene expression data from 6-week-old ovariectomized wildtype mice treated subcutaneously with 17β-Estradiol for 2 hours . Two replicate pools were tested with five mice per pool.; [Treatment]'All mice were treated with vehicle (seasame oil) or 17β-estradiol (100ng) for2 h'; [Growth]'At 6 weeks of age, mice were ovariectomized and rested for 10 days and then mice were injected with vehicle (seasame oil) or 17β-estradiol (100ng) for 2 hours.'; [Extraction]"RNA extraction using the Qiagen RNeasy Lipid Tissue Midi Kit according to the manufacturer's instructions.\nRNA libraries were prepared for sequencing using standard Illumina protocols"; [Cell type]'Source: ''strain: BALB/c; age: 6 weeks; genotype/variation: wild type; tissue: Mammary gland (#4); ', 'strain: BALB/c; age: 6 weeks; genotype/variation: wild type; treatment: 17β-Estradiol for 2 hours; tissue: Mammary gland (#4); ' GSE41632 Mus musculus 30 Genome variation profiling by genome tiling array GPL2884 Met synergizes with p53 loss to induce mammary tumors that possess features of claudin-low breast cancer (aCGH data). 2012-10-16 Transcriptional profiling of normal and tumorigenic mouse mammary tissue. Mouse genotypes consist of wildtype, MMTV-Met, MMTV-Met;Trp53fl/+;Cre, and Trp53fl/+;Cre. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41632 Met synergizes with p53 loss to induce mammary tumors that possess features of claudin-low breast cancer. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1210353110 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1210353110} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA177952 https://www.ebi.ac.uk/ena/browser/view/PRJNA177952 None [Overal design]Two-color common reference design. Samples consist of 4 normal tissues, 8 MMTV-Met tumors, 10 MMTV-Met;Trp53fl/+;Cre tumors, and 8 Trp53;Cre tumors.; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was isolated from snap frozen tissue pieces using the Qiagen Allprep kit (as described for RNA isolation).'; [Cell type]'Source: ''gender: Female; strain: FVB; tissue: Tumor; genotype: MMTV-Met; pathology: Other; ', 'tissue: Normal Splenic DNA; ', 'gender: Female; strain: FVB; tissue: Tumor; genotype: MMTV-Met; pathology: Spindloid; ', 'gender: Female; strain: FVB; tissue: Tumor; genotype: MMTV-Met; pathology: Solid Nodular Carcinoma; ', 'gender: Female; strain: FVB; tissue: Tumor; genotype: MMTV-Met;Trp53fl/+; pathology: Spindloid; ', 'gender: Female; strain: FVB; tissue: Tumor; genotype: MMTV-Met;Trp53fl/+; pathology: Other; ', 'gender: Female; strain: FVB; tissue: Tumor; genotype: MMTV-Met;Trp53fl/+; pathology: Poorly Differentiated Adenocarcinoma; ', 'gender: Female; strain: FVB; tissue: Normal; genotype: Wild-Type; pathology: NA; ', 'gender: Female; strain: FVB; tissue: Normal; genotype: MMTV-Met;Trp53fl/+; pathology: NA; ', 'gender: Female; strain: FVB; tissue: Tumor; genotype: Trp53fl/+; pathology: Other; ', 'gender: Female; strain: FVB; tissue: Tumor; genotype: Trp53fl/+; pathology: Spindloid; ', 'gender: Female; strain: FVB; tissue: Tumor; genotype: Trp53fl/+; pathology: Poorly Differentiated Adenocarcinoma; ' GSE70552 Homo sapiens 1022 Expression profiling by RT-PCR GPL20665 Single-cell analysis reveals a stem cell program in human metastatic breast cancer cells (PDX mice - cancer cells) 2015-07-06 Despite major advances in understanding the molecular and genetic basis of cancer, metastasis remains the cause of >90% of cancer-related mortality1. Understanding metastasis initiation and progression is critical to develop new therapeutic strategies to treat and prevent metastatic disease. Prevailing theories hypothesize that metastases are seeded by rare tumor cells with unique properties, which may function like stem cells in their ability to initiate and propagate metastatic tumors.2 3-5 However, the identity of metastasis-initiating cells in human breast cancer remains elusive, and whether metastases are hierarchically organized is unknown.2 Here we show at the single-cell level that early stage metastatic cells possess a distinct stem-like gene expression signature. To identify and isolate metastatic cells from patient-derived xenograft (PDX) models of human breast cancer, we developed a highly sensitive FACS-based assay, which allowed us to enumerate metastatic cells in mouse peripheral tissues. We compared gene signatures in metastatic cells from tissues with low vs. high metastatic burden. Metastatic cells from low-burden tissues were distinct due to their increased expression of stem cell, EMT, pro-survival, and dormancy-associated genes. In contrast, metastatic cells from high-burden tissues were similar to primary tumor cells, which were more heterogeneous and expressed higher levels of luminal differentiation genes. Transplantation of stem-like metastatic cells from low-burden tissues showed that they have significant tumor-initiating capacity, and differentiate to produce luminal-like cancer cells. Progression to high metastatic burden was associated with increased proliferation and cMYC expression, which could be attenuated by treatment with cyclin dependent kinase (CDK) inhibitors. These findings support a hierarchical model for metastasis, where metastases are initiated by stem-like cells that proliferate and differentiate to produce advanced metastatic disease. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE70552 Single-cell analysis reveals a stem-cell program in human metastatic breast cancer cells. Nature 43.070 https://doi.org/10.1038/nature15260 {Nature (43.070): 10.1038/nature15260} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA289001 https://www.ebi.ac.uk/ena/browser/view/PRJNA289001 None [Overal design]1022 sampels; [Treatment]'n/a'; [Growth]'Patient-derived xenograft model'; [Extraction]'Enzymatic tissue digest'; [Cell type]'Lung metastatic cell', 'Primary tumor cell', 'Lymph node metastatic cell', 'Peripheral blood metastatic cell', 'Bone marrow metastatic cell', 'Primary tumor cell (transplanted)', 'Brain metastatic cell', 'Lung metastatic cell (resected)', 'Primary tumor cell (resected)''model: Model HCI-001; cell type: Lung metastatic cell; ', 'model: Model HCI-001; cell type: Primary tumor cell; ', 'model: Model HCI-001; cell type: Lymph node metastatic cell; ', 'model: Model HCI-002; cell type: Lung metastatic cell; ', 'model: Model HCI-002; cell type: Peripheral blood metastatic cell; ', 'model: Model HCI-002; cell type: Primary tumor cell; ', 'model: Model HCI-002; cell type: Bone marrow metastatic cell; ', 'model: Model HCI-002; cell type: Lymph node metastatic cell; ', 'model: Model HCI-002; cell type: Primary tumor cell (transplanted); ', 'model: Model HCI-010; cell type: Brain metastatic cell; ', 'model: Model HCI-010; cell type: Primary tumor cell; ', 'model: Model HCI-010; cell type: Lymph node metastatic cell; ', 'model: Model HCI-010; cell type: Lung metastatic cell; ', 'model: Model HCI-010; cell type: Lung metastatic cell (resected); ', 'model: Model HCI-010; cell type: Primary tumor cell (resected); ' GSE67919 Homo sapiens 96 Methylation profiling by genome tiling array GPL13534 Epigenome analysis of tumor adjacent normal tissue from breast cancer patients 2015-04-15 Genome wide DNA methylation profiling of tumor adjacent normal tissue from patients with invasive breast cancer, as well as tissue from women undergoing reduction mammoplasty or prophylactic surgery. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 485,577 CpGs in snap frozen breast tissue. Samples included 70 tumor-adjacent normal breast tissue with invasive disease, 8 tissues from breast prophylactic patients, and 18 tissues from breast reduction patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE67919 Body mass index associated with genome-wide methylation in breast tissue. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-015-3401-8 {Breast cancer research and treatment (3.471): 10.1007/s10549-015-3401-8} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA281205 https://www.ebi.ac.uk/ena/browser/view/PRJNA281205 None [Overal design]Bisulphite converted DNA from the 96 samples were hybridized to the Illumina Infinium 450k Human Methylation Beadchip.; [Treatment]'None'; [Growth]'None'; [Extraction]'genomic DNA was extracted and purified from snap frozen tissue using Qiagen DNeasy Kit according to standard instructions'; [Cell type]'Source: ''tissue: breast; gender: female; race: white; bmi: 42.7; alcohol use: yes; menopausal status: pre; age at surgery: 49; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 53.4; alcohol use: yes; menopausal status: post; age at surgery: 51; diagnosis at surgery: IDC w/lobular, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 39.0; alcohol use: yes; menopausal status: post; age at surgery: 64; diagnosis at surgery: IDC; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 45.8; alcohol use: no; menopausal status: post; age at surgery: 63; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 44.3; alcohol use: no; menopausal status: post; age at surgery: 59; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 34.6; alcohol use: no; menopausal status: post; age at surgery: 62; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 39.8; alcohol use: yes; menopausal status: post; age at surgery: 53; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 33.4; alcohol use: yes; menopausal status: post; age at surgery: 60; diagnosis at surgery: IDC; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 45.5; alcohol use: yes; menopausal status: post; age at surgery: 50; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 22.0; alcohol use: yes; menopausal status: post; age at surgery: 57; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: other; bmi: 25.4; alcohol use: yes; menopausal status: pre; age at surgery: 29; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 23.4; alcohol use: yes; menopausal status: post; age at surgery: 59; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 24.2; alcohol use: yes; menopausal status: post; age at surgery: 57; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: other; bmi: 26.0; alcohol use: yes; menopausal status: pre; age at surgery: 41; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 35.2; alcohol use: yes; menopausal status: post; age at surgery: 83; diagnosis at surgery: IDC w/lobular, LCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 34.0; alcohol use: yes; menopausal status: post; age at surgery: 71; diagnosis at surgery: IDC NOS, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 32.9; alcohol use: yes; menopausal status: unkn; age at surgery: 54; diagnosis at surgery: IDC NOS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 31.3; alcohol use: yes; menopausal status: post; age at surgery: 63; diagnosis at surgery: IDC w/lobular, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 27.4; alcohol use: yes; menopausal status: unkn; age at surgery: 84; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 27.1; alcohol use: yes; menopausal status: pre; age at surgery: 51; diagnosis at surgery: IDC NOS, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 43.8; alcohol use: yes; menopausal status: post; age at surgery: 59; diagnosis at surgery: IDC NOS, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 33.3; alcohol use: yes; menopausal status: pre; age at surgery: 42.0; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 26.5; alcohol use: yes; menopausal status: post; age at surgery: 45; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: other; bmi: 21.1; alcohol use: yes; menopausal status: pre; age at surgery: 41; diagnosis at surgery: IDC NOS, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 22.0; alcohol use: yes; menopausal status: post; age at surgery: 62; diagnosis at surgery: IDC W/lobular, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: other; bmi: 21.1; alcohol use: yes; menopausal status: post; age at surgery: 52; diagnosis at surgery: IDC NOS, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 26.2; alcohol use: no; menopausal status: pre; age at surgery: 38; diagnosis at surgery: IDC NOS, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 35.1; alcohol use: yes; menopausal status: post; age at surgery: 47; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: white; bmi: 27.6; alcohol use: yes; menopausal status: post; age at surgery: 41; diagnosis at surgery: prophylactic; tissue type: prophylactic; ', 'tissue: breast; gender: female; race: white; bmi: 28.3; alcohol use: yes; menopausal status: post; age at surgery: 47; diagnosis at surgery: prophylactic; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 17.8; alcohol use: yes; menopausal status: pre; age at surgery: 40; diagnosis at surgery: prophylactic; tissue type: prophylactic; ', 'tissue: breast; gender: female; race: white; bmi: 20.3; alcohol use: yes; menopausal status: unkn; age at surgery: 42; diagnosis at surgery: prophylactic; tissue type: prophylactic; ', 'tissue: breast; gender: female; race: other; bmi: 29.6; alcohol use: no; menopausal status: post; age at surgery: 76; diagnosis at surgery: prophylactic; tissue type: prophylactic; ', 'tissue: breast; gender: female; race: white; bmi: 18.7; alcohol use: yes; menopausal status: pre; age at surgery: 23; diagnosis at surgery: prophylactic; tissue type: prophylactic; ', 'tissue: breast; gender: female; race: white; bmi: 19.6; alcohol use: yes; menopausal status: peri; age at surgery: 52; diagnosis at surgery: prophylactic; tissue type: prophylactic; ', 'tissue: breast; gender: female; race: white; bmi: 23.8; alcohol use: yes; menopausal status: pre; age at surgery: 27; diagnosis at surgery: prophylactic; tissue type: prophylactic; ', 'tissue: breast; gender: female; race: black; bmi: 26.4; alcohol use: no; menopausal status: pre; age at surgery: 35; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: white; bmi: 27.3; alcohol use: yes; menopausal status: post; age at surgery: 69; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: white; bmi: 34.8; alcohol use: yes; menopausal status: pre; age at surgery: 32; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: white; bmi: 24.7; alcohol use: yes; menopausal status: pre; age at surgery: 19; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: black; bmi: 31.9; alcohol use: no; menopausal status: post; age at surgery: 53; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: black; bmi: 28.2; alcohol use: yes; menopausal status: pre; age at surgery: 35; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: white; bmi: 30.6; alcohol use: yes; menopausal status: pre; age at surgery: 49; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: white; bmi: 33.2; alcohol use: yes; menopausal status: pre; age at surgery: 44; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: white; bmi: 23.9; alcohol use: yes; menopausal status: post; age at surgery: 61; diagnosis at surgery: IDC; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 32.8; alcohol use: yes; menopausal status: pre; age at surgery: 34; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: other; bmi: 25.7; alcohol use: yes; menopausal status: pre; age at surgery: 24; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: white; bmi: 31.3; alcohol use: yes; menopausal status: post; age at surgery: 54; diagnosis at surgery: IDC; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 21.7; alcohol use: yes; menopausal status: post; age at surgery: 63; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: other; bmi: 34.0; alcohol use: no; menopausal status: post; age at surgery: 49; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: white; bmi: 27.5; alcohol use: yes; menopausal status: post; age at surgery: 72; diagnosis at surgery: IDC w/lobular, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 16.5; alcohol use: yes; menopausal status: post; age at surgery: 57; diagnosis at surgery: IDC w/lobular, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 21.5; alcohol use: yes; menopausal status: post; age at surgery: 58; diagnosis at surgery: IDC NOS, DCIS, LCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 27.3; alcohol use: yes; menopausal status: post; age at surgery: 66; diagnosis at surgery: Mixed-IDC Dominant; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 27.5; alcohol use: yes; menopausal status: peri; age at surgery: 52; diagnosis at surgery: IDC; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 24.7; alcohol use: yes; menopausal status: post; age at surgery: 61; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 38.8; alcohol use: yes; menopausal status: pre; age at surgery: 42; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 24.1; alcohol use: yes; menopausal status: post; age at surgery: 69; diagnosis at surgery: IDC, apocrine carcino; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 28.6; alcohol use: yes; menopausal status: post; age at surgery: 48; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: black; bmi: 33.8; alcohol use: no; menopausal status: post; age at surgery: 54; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 21.6; alcohol use: nR; menopausal status: unkn; age at surgery: 34; diagnosis at surgery: IDC; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 43.8; alcohol use: no; menopausal status: post; age at surgery: 56; diagnosis at surgery: IDC NOS, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 35.0; alcohol use: yes; menopausal status: pre; age at surgery: 39; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 31.0; alcohol use: no; menopausal status: post; age at surgery: 71; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 30.0; alcohol use: yes; menopausal status: pre; age at surgery: 46; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 26.8; alcohol use: no; menopausal status: post; age at surgery: 66; diagnosis at surgery: IDC; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 35.3; alcohol use: nR; menopausal status: unkn; age at surgery: 51; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 27.2; alcohol use: yes; menopausal status: peri; age at surgery: 53; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: black; bmi: 22.9; alcohol use: yes; menopausal status: pre; age at surgery: 50; diagnosis at surgery: IDC w/lobular, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 18.7; alcohol use: yes; menopausal status: peri; age at surgery: 36; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 24.9; alcohol use: yes; menopausal status: pre; age at surgery: 42; diagnosis at surgery: IDC, ILC, LCIS, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 28.3; alcohol use: yes; menopausal status: post; age at surgery: 67; diagnosis at surgery: IDC; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: other; bmi: 23.0; alcohol use: no; menopausal status: post; age at surgery: 47; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: other; bmi: 29.1; alcohol use: yes; menopausal status: post; age at surgery: 56; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: other; bmi: 26.6; alcohol use: yes; menopausal status: pre; age at surgery: 39; diagnosis at surgery: IDC - papillary; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 36.7; alcohol use: no; menopausal status: post; age at surgery: 65; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 29.2; alcohol use: yes; menopausal status: pre; age at surgery: 40; diagnosis at surgery: IDC w/medullary; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 31.2; alcohol use: yes; menopausal status: post; age at surgery: 81; diagnosis at surgery: IDC; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 39.3; alcohol use: no; menopausal status: post; age at surgery: 58; diagnosis at surgery: mixed-IDC Dominant, D; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 26.6; alcohol use: yes; menopausal status: post; age at surgery: 71; diagnosis at surgery: IDC; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 21.2; alcohol use: yes; menopausal status: post; age at surgery: 61; diagnosis at surgery: IDC NOS, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 38.6; alcohol use: yes; menopausal status: post; age at surgery: 62; diagnosis at surgery: IDC NOS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 25.7; alcohol use: no; menopausal status: pre; age at surgery: 42; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 23.5; alcohol use: yes; menopausal status: post; age at surgery: 56; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 35.1; alcohol use: yes; menopausal status: post; age at surgery: 54; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 29.6; alcohol use: yes; menopausal status: pre; age at surgery: 23; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: other; bmi: 27.0; alcohol use: yes; menopausal status: pre; age at surgery: 35; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: white; bmi: 24.1; alcohol use: yes; menopausal status: post; age at surgery: 55; diagnosis at surgery: IDC w/mucinous, DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 28.5; alcohol use: yes; menopausal status: pre; age at surgery: 29; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: white; bmi: 29.0; alcohol use: nR; menopausal status: unkn; age at surgery: 54; diagnosis at surgery: IDC; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: black; bmi: 39.2; alcohol use: no; menopausal status: post; age at surgery: 66; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 21.7; alcohol use: yes; menopausal status: post; age at surgery: 66; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 29.6; alcohol use: yes; menopausal status: pre; age at surgery: 40; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 23.2; alcohol use: yes; menopausal status: post; age at surgery: 56; diagnosis at surgery: reduction; tissue type: reduction; ', 'tissue: breast; gender: female; race: black; bmi: 30.2; alcohol use: nR; menopausal status: peri; age at surgery: 37; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ', 'tissue: breast; gender: female; race: white; bmi: 31.4; alcohol use: yes; menopausal status: post; age at surgery: 58; diagnosis at surgery: IDC w/DCIS; tissue type: mastectomy; ' GSE26834 Homo sapiens 17 Expression profiling by array GPL571 Expression data from MCF-7 cells stimulated by Estrogen or IGF-I 2011-01-24 Although estrogen receptor (ER) and insulin-like growth factor (IGF) signaling are important for normal mammary development and breast cancer, cross-talk between these pathways, particularly at the level of gene transcription, remains poorly understood. We performed microarray analysis on MCF-7 breast cancer cells treated with estradiol (E2) or IGF-I for 3hr or 24hr. IGF-I regulated mRNA of 5-10-fold more genes than estradiol, and many genes were co-regulated by both ligands. Importantly, expression of these co-regulated genes correlated with poor prognosis of human breast cancer. Closer examination revealed enrichment of repressed transcripts. Interestingly, a number of potential tumor suppressors were down-regulated by IGF-I and estradiol. In fact, BLNK, one of the top repressed genes, is a potential growth suppressor in breast cancer cells. Analysis of three down-regulated genes showed that E2-mediated repression occurred independently of IGF-IR, and IGF-I-mediated repression occurred independently of ER. However, repression by IGF-I or estradiol required common downstream kinases. In conclusion, E2 and IGF-I co-regulate a set of genes that affect breast cancer outcome. There is enrichment of repressed transcripts, and the down-regulation is independent at the receptor level. This may be important clinically, as tumors with active ER and IGF-IR signaling may require co-targeting of both pathways. KEYWORDS: multiple group comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26834 Estrogen and insulin-like growth factor-I (IGF-I) independently down-regulate critical repressors of breast cancer growth. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-011-1540-0 {Breast cancer research and treatment (3.471): 10.1007/s10549-011-1540-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA136041 https://www.ebi.ac.uk/ena/browser/view/PRJNA136041 None [Overal design]Microarray analysis on MCF-7 breast cancer cells treated with estradiol (E2) or IGF-I for 3hr or 24hr.; [Treatment]'None'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MCF-7 breast cancer cell line; agent: SFM (control); time: 3hr; ', 'cell line: MCF-7 breast cancer cell line; agent: estradiol (E2); time: 3hr; ', 'cell line: MCF-7 breast cancer cell line; agent: IGF; time: 3hr; ', 'cell line: MCF-7 breast cancer cell line; agent: SFM (control); time: 24hr; ', 'cell line: MCF-7 breast cancer cell line; agent: estradiol (E2); time: 24hr; ', 'cell line: MCF-7 breast cancer cell line; agent: IGF; time: 24hr; ' GSE115623 Homo sapiens 6 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Genome-wide fork-collapse sites in MDA-MB-231 cells from ATR inhibition [human] 2018-06-11 Transient obstruction of DNA polymerase progression activates the ATR checkpoint kinase, which suppresses fork breakage, strand resection, and RPA accumulation. Herein, we use a developed DNA break-detection assay, BrITL, to identify replication-problematic loci that become processed into persistent double-strand breaks across the human genome from ATR inhibition. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115623 Genome-wide Identification of Structure-Forming Repeats as Principal Sites of Fork Collapse upon ATR Inhibition. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2018.08.047 {Molecular cell (14.548): 10.1016/j.molcel.2018.08.047} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA475583 https://www.ebi.ac.uk/ena/browser/view/PRJNA475583 https://www.ncbi.nlm.nih.gov/sra?term=SRP150251 [Overal design]Examination of double-strand break sites in human triple-negative breast cancer cells arising from low-dose aphidicolin treatment and ATR inhibition. Two replicates of each condition are included, in addition to one input per condition, totaling 6 samples. This includes DMSO-treated controls. Samples were deep-sequenced through Illumina HiSeq.; [Treatment]'DMSO treatment for 9hrs', '0.5 uM VE-822 + 0.2 uM aphidicolin for 9hrs'; [Growth]'MDA-MB-231 cells were grown in 100 mm tissue-culture plates in DMEM containing high glucose 4.5gm/L and supplemented with 10% FBS, 2mM L-glutamine and Pen/Strep to obtain ~2 x 106 cells upon collection for BrITL.'; [Extraction]"Cells were permeabilized, biotin end-labeld, and lysed. Genomic DNA was extracted and sonicated to 0.2-2 kb size fragments prior to pull-down of biotin-labeled fragments with streptaviding-coated Dynabeads.\nLibraries were prepared according to the NEBNext kit. Briefly, DNA was sonicated to ~200 bp. DNA was end-repaired using a combination of T4 DNA polymerase, Klenow DNA polymerase and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (3' to 5' exo minus) and dATP to yield a protruding 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation, DNA fragments of ~200 bp (insert plus adaptor) were band isolated from a 2% agarose gel. The purified DNA was PCR amplified with Illumina primers for 18 cycles. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on Illumina HiSeq following the manufacturer's protocols."; [Cell type]'Human epithelial breast cancer cells; passage-immortalized''cell line: MDA-MB-231; cell type: Human epithelial breast cancer cells; passage-immortalized; treated with: DMSO for 9hrs; pull-down reagents: Biotin-16-ddUTP (Enzo Life Sciences, ENZ-42813); Dynabeads KilobaseBinder kit (Life Technologies, 601-01); ', 'cell line: MDA-MB-231; cell type: Human epithelial breast cancer cells; passage-immortalized; treated with: 0.5 uM VE-822 + 0.2 uM aphidicolin for 9hrs; pull-down reagents: Biotin-16-ddUTP (Enzo Life Sciences, ENZ-42813); Dynabeads KilobaseBinder kit (Life Technologies, 601-01); ' GSE16838 Homo sapiens 8 Expression profiling by array GPL6244 Expression data from MDA-MB-231 reference and in vitro-derived subpopulations with distinct invasive potentials 2009-06-25 To understand the link between invasion behavior and the steps of metastasis formation, we isolated invasive subpopulations from MDA-MB-231 cells in vitro using matrigel coated boyden chambers. Whole genome transcriptional profiling was used to characterize the expression changes uniquely related to invasive abilities of these cells. In this dataset, we include expression data obtained from MDA-MB-231 invasive cells (INV cells) and those that failed to invade the coated membrane during selection (REF cells). These subpopulations have been characterized in vitro by the differences in motility and invasion, cell morphology, adhesion properties to endothelial cells or fibronectin, proliferation, and resistance to doxorubicin as well as to growth factor starvation. INV tumors xenografted in nude mice presented higher volume with more angiogenesis. In addition, when injected into blood circulation, INV cells induced more sites of metastasis in nude mice as compared to REF cells, and dramatically diminished survival by about 80%. Transcriptomic analysis showed differences in genes involved in proliferation, chemotaxis and cytoskeleton, but particularly up-regulated genes involved in negative regulation of apoptosis and down-regulated genes involved in cell adhesion or cell-cell junction. In conclusion, invasive behavior was sufficient to reveal 134 differentially expressed genes correlated with invasive cell aggressivity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE16838 Invading basement membrane matrix is sufficient for MDA-MB-231 breast cancer cells to develop a stable in vivo metastatic phenotype. PloS one 2.776 https://doi.org/10.1371/journal.pone.0023334 {PloS one (2.776): 10.1371/journal.pone.0023334} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA117603 https://www.ebi.ac.uk/ena/browser/view/PRJNA117603 None [Overal design]8 total samples were analyzed (4 for each condition). To determine differentially expressed genes, differences between both conditions were calculated on each day of measurement and analyzed using a two-sided paired t-test implemented in the anapuce R package (http://www.agroparistech.fr/mia/outil.html). Pairing was made to remove variation due to the day of measurement in the comparison between the two conditions. The variance was split between subgroups of genes with homogeneous variance (Delmar P, Robin S, Daudin J.-J. VarMixt: efficient variance modelling for the differential analysis of replicated gene expression data. Bioinformatics, 2005, 21: 4,502-508). Statistical raw p-values were adjusted for multiple comparisons using the Benjamini-Hochberg procedure (Benjamini Y, Hochberg Y. Controlling the false discovery rate: a practical and powerful approach to multiple testing. J. R. Statist. Soc. B, 1995, 57:1, 289-300) which controls the False Discovery Rate (FDR) after the estimation of the proportion of genes not differentially expressed using the smoother method (Storey JD, Tibshirani R, Statistical significance for genome-wide experiments. Proc. Nat. Acad. Sci. USA, 2003, 100, 9440-9445). The level of statistical significance was set at 0.05 for all the comparisons.; [Treatment]'None'; [Growth]'INV and REF subpopulations of MDA-MB-231 cell line were maintained in DMEM supplemented with 10% fetal bovine serum (FBS), 1% sodium pyruvate and 1% penicillin sodium and 1% streptomycin antibiotics (10% FCS-DMEM) at 37°C in a humidified atmosphere containing 5% carbon dioxide.'; [Extraction]'Total RNA from 8 cell cultures (i.e., four biological replicates corresponding to four different passages of INV and REF cells) were isolated using RNeasy mini kit (Qiagen) by direct lysis on the 10cm culture dish with 600 μl RLT Buffer following manufacturer’s instructions. cDNA synthesis and amplification was performed using the WT cDNA synthesis and amplification kit (Affymetrix) starting from 300 ng total RNA.'; [Cell type]'Source: ''cell line: MDA-MB-231; cell line origin: breast cancer; cell line subpopulation: invasive; ', 'cell line: MDA-MB-231; cell line origin: breast cancer; cell line subpopulation: reference; ' GSE88883 Homo sapiens 100 Methylation profiling by array GPL13534 Breast cancer risk factors are associated with DNA methylation in non-diseased breast tissue independent of cell type 2016-10-18 The underlying biology through which established breast cancer risk factors contribute to disease risk is not well characterized. One key risk factor for breast cancer is age, and age-related DNA methylation alterations may contribute to increased risk of disease. Here we assessed normal breast tissues and tested the relation of DNA methylation with known breast cancer risk factors. Cancer-free women donated breast tissue biopsy specimens through the Susan G. Komen Foundation and provided detailed risk factor data (n=100). Bisulfite modified DNA was profiled for DNA methylation genome-wide using the Infinium 450K DNA methylation array. We tested the relation of known breast cancer risk factors such as age, BMI, parity, and family history of disease with DNA methylation adjusted for variation in cell type proportions using a novel cellular mixture deconvolution algorithm. We identified 787 CpGs that exhibited significant (FDR adjusted, q-value < 0.01) differential DNA methylation associated with subject age, but not with other breast cancer risk factors. We observed an enrichment among the risk factor-related CpGs for Polycomb group target genes (Fisher’s Exact test, P = 1.74E-06), and breast myoepithelial cell enhancer regions (H3K4me1; Fisher’s Exact test, P = 7.1E-20). We validated our risk factor-related findings in two independent populations of normal breast tissue (n=18 and n=97). In addition, age-related CpGs were further deregulated in both pre-invasive (DCIS, n=40) and invasive breast cancers (TCGA, n=731). Overall, our results suggest that the breast cancer risk factor age contributes to epigenetic dysregulation in normal breast tissue that exhibit progressive changes in cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE88883 Normal breast tissue DNA methylation differences at regulatory elements are associated with the cancer risk factor age. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-017-0873-y {Breast cancer research : BCR (5.676): 10.1186/s13058-017-0873-y} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA349021 https://www.ebi.ac.uk/ena/browser/view/PRJNA349021 None [Overal design]Bisulfite converted DNA from 100 healthy breast biopsy samples that were hybridised to the Illumina Infinium 450K Human Methylation beadchip; [Treatment]'None'; [Growth]'None'; [Extraction]'Frozen normal breast tissue DNA was extracted with the QIAmp DNeasy tissue kit (Qiagen) according to the manufacturer’s instructions.'; [Cell type]'Source: ''tissue: breast biopsy; Sex: female; subject age: 43; body mass index: 33.89; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 7.9; ', 'tissue: breast biopsy; Sex: female; subject age: 30; body mass index: 25.82; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 42; body mass index: 31.07; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 11.9; ', 'tissue: breast biopsy; Sex: female; subject age: 41; body mass index: 19.57; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 13.1; ', 'tissue: breast biopsy; Sex: female; subject age: 40; body mass index: 26.57; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 13.6; ', 'tissue: breast biopsy; Sex: female; subject age: 47; body mass index: 28.32; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 9.5; ', 'tissue: breast biopsy; Sex: female; subject age: 46; body mass index: 25.86; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 17.8; ', 'tissue: breast biopsy; Sex: female; subject age: 20; body mass index: 29.76; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 43; body mass index: 38.27; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 10.8; ', 'tissue: breast biopsy; Sex: female; subject age: 37; body mass index: 19.58; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 11.2; ', 'tissue: breast biopsy; Sex: female; subject age: 37; body mass index: 31.32; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 19; ', 'tissue: breast biopsy; Sex: female; subject age: 45; body mass index: 33.28; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 11.7; ', 'tissue: breast biopsy; Sex: female; subject age: 39; body mass index: 24.44; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): NA; gail risk model score (for women over 36 years old): 11.1; ', 'tissue: breast biopsy; Sex: female; subject age: 26; body mass index: 18.02; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 31; body mass index: 22.13; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 50; body mass index: 35.01; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 8; ', 'tissue: breast biopsy; Sex: female; subject age: 40; body mass index: 30.22; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 7.5; ', 'tissue: breast biopsy; Sex: female; subject age: 61; body mass index: 28.29; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 6.7; ', 'tissue: breast biopsy; Sex: female; subject age: 19; body mass index: 28.34; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 36; body mass index: 24.33; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 13.8; ', 'tissue: breast biopsy; Sex: female; subject age: 38; body mass index: 44.62; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 9.7; ', 'tissue: breast biopsy; Sex: female; subject age: 32; body mass index: 22.71; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 28; body mass index: 22.48; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 40; body mass index: 33.06; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 9.6; ', 'tissue: breast biopsy; Sex: female; subject age: 65; body mass index: 32.45; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 12; ', 'tissue: breast biopsy; Sex: female; subject age: 55; body mass index: 42.6; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 7.5; ', 'tissue: breast biopsy; Sex: female; subject age: 42; body mass index: 25.74; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): NA; gail risk model score (for women over 36 years old): 17.2; ', 'tissue: breast biopsy; Sex: female; subject age: 39; body mass index: 27.43; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 8.6; ', 'tissue: breast biopsy; Sex: female; subject age: 25; body mass index: 27.29; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 26; body mass index: 25.85; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 42; body mass index: 30.91; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 22.6; ', 'tissue: breast biopsy; Sex: female; subject age: 24; body mass index: 25.01; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 37; body mass index: 34.38; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): NA; gail risk model score (for women over 36 years old): 5.7; ', 'tissue: breast biopsy; Sex: female; subject age: 34; body mass index: 29.43; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 35; body mass index: 29.99; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 7.5; ', 'tissue: breast biopsy; Sex: female; subject age: 39; body mass index: 24.56; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 8.3; ', 'tissue: breast biopsy; Sex: female; subject age: 33; body mass index: 37.41; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): NA; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 38; body mass index: 37.36; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 8.1; ', 'tissue: breast biopsy; Sex: female; subject age: 41; body mass index: 20.95; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 13.5; ', 'tissue: breast biopsy; Sex: female; subject age: 50; body mass index: 27.98; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 9.9; ', 'tissue: breast biopsy; Sex: female; subject age: 35; body mass index: 32.92; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): NA; gail risk model score (for women over 36 years old): 12.3; ', 'tissue: breast biopsy; Sex: female; subject age: 27; body mass index: 26.09; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): NA; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 28; body mass index: 21.97; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 46; body mass index: 19.97; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 18.2; ', 'tissue: breast biopsy; Sex: female; subject age: 28; body mass index: 19.69; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 33; body mass index: 19.3; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 22; body mass index: 53.74; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 21; body mass index: 6.07; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 51; body mass index: 22.15; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 11.2; ', 'tissue: breast biopsy; Sex: female; subject age: 24; body mass index: 24.27; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 26; body mass index: 45.17; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 21; body mass index: 23.62; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): NA; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 34; body mass index: 35.84; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 21; body mass index: 26.79; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 19; body mass index: 31.88; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 44; body mass index: 37.56; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 10.7; ', 'tissue: breast biopsy; Sex: female; subject age: 39; body mass index: 31.58; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 11.1; ', 'tissue: breast biopsy; Sex: female; subject age: 18; body mass index: 29.08; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 50; body mass index: 16.78; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): NA; gail risk model score (for women over 36 years old): 7; ', 'tissue: breast biopsy; Sex: female; subject age: 47; body mass index: 23.38; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 6.8; ', 'tissue: breast biopsy; Sex: female; subject age: 19; body mass index: 22.59; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 22; body mass index: 21.45; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 22; body mass index: 29.78; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 32; body mass index: 34.33; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 30; body mass index: 29.86; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 27; body mass index: 21.77; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 57; body mass index: 36.61; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 14.6; ', 'tissue: breast biopsy; Sex: female; subject age: 69; body mass index: 31.35; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 11.6; ', 'tissue: breast biopsy; Sex: female; subject age: 20; body mass index: 22.49; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 49; body mass index: 37.94; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 10.5; ', 'tissue: breast biopsy; Sex: female; subject age: 30; body mass index: 22.3; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 22; body mass index: 28.35; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 20; body mass index: 21.97; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 20; body mass index: 20.67; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): NA; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 19; body mass index: 21.13; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): NA; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 22; body mass index: 24.27; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 20; body mass index: 25.54; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 67; body mass index: 29.35; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 6.4; ', 'tissue: breast biopsy; Sex: female; subject age: 20; body mass index: 22.14; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 50; body mass index: 21.92; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 15.9; ', 'tissue: breast biopsy; Sex: female; subject age: 22; body mass index: 21.21; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 18; body mass index: 24.62; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 32; body mass index: 28.66; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 43; body mass index: 27.43; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 12.1; ', 'tissue: breast biopsy; Sex: female; subject age: 52; body mass index: 35.32; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 12.8; ', 'tissue: breast biopsy; Sex: female; subject age: 45; body mass index: 24.53; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 10.5; ', 'tissue: breast biopsy; Sex: female; subject age: 59; body mass index: 22.86; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 13.2; ', 'tissue: breast biopsy; Sex: female; subject age: 41; body mass index: 20.47; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 10; ', 'tissue: breast biopsy; Sex: female; subject age: 56; body mass index: 25.24; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 11.6; ', 'tissue: breast biopsy; Sex: female; subject age: 82; body mass index: 25; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 2.9; ', 'tissue: breast biopsy; Sex: female; subject age: 69; body mass index: 27.46; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 5.6; ', 'tissue: breast biopsy; Sex: female; subject age: 41; body mass index: 22.14; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 13.4; ', 'tissue: breast biopsy; Sex: female; subject age: 49; body mass index: 41.8; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 11; ', 'tissue: breast biopsy; Sex: female; subject age: 56; body mass index: 16.81; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): 6.4; ', 'tissue: breast biopsy; Sex: female; subject age: 48; body mass index: 22.63; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 17.5; ', 'tissue: breast biopsy; Sex: female; subject age: 50; body mass index: 28.35; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 12; ', 'tissue: breast biopsy; Sex: female; subject age: 34; body mass index: 24.2; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): No; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 25; body mass index: 24.03; pregnancy (ever): No; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): NA; ', 'tissue: breast biopsy; Sex: female; subject age: 42; body mass index: 28.79; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 10.9; ', 'tissue: breast biopsy; Sex: female; subject age: 46; body mass index: 23.72; pregnancy (ever): Yes; family history (first-degree relative with breast or ovarian cancer): Yes; gail risk model score (for women over 36 years old): 10.5; ' GSE68086 Homo sapiens 285 Expression profiling by high throughput sequencing GPL16791 RNA-seq of tumor-educated platelets enables blood-based pan-cancer, multiclass and molecular pathway cancer diagnostics 2015-04-21 We report RNA-sequencing data of 283 blood platelet samples, including 228 tumor-educated platelet (TEP) samples collected from patients with six different malignant tumors (non-small cell lung cancer, colorectal cancer, pancreatic cancer, glioblastoma, breast cancer and hepatobiliary carcinomas). In addition, we report RNA-sequencing data of blood platelets isolated from 55 healthy individuals. This dataset highlights the ability of TEP RNA-based 'liquid biopsies' in patients with several types with cancer, including the ability for pan-cancer, multiclass cancer and companion diagnostics. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE68086 RNA-Seq of Tumor-Educated Platelets Enables Blood-Based Pan-Cancer, Multiclass, and Molecular Pathway Cancer Diagnostics. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2015.09.018 {Cancer cell (23.916): 10.1016/j.ccell.2015.09.018} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA281708 https://www.ebi.ac.uk/ena/browser/view/PRJNA281708 https://www.ncbi.nlm.nih.gov/sra?term=SRP057500 [Overal design]Blood platelets were isolated from whole blood in purple-cap BD Vacutainers containing EDTA anti-coagulant by standard centrifugation. Total RNA was extracted from the platelet pellet, subjected to cDNA synthesis and SMARTer amplification, fragmented by Covaris shearing, and prepared for sequencing using the Truseq Nano DNA Sample Preparation Kit. Subsequently, pooled sample libraries were sequenced on the Illumina Hiseq 2500 platform. All steps were quality-controlled using Bioanalyzer 2100 with RNA 6000 Picochip, DNA 7500 and DNA High Sensitivity chips measurements. For further downstream analyses, reads were quality-controlled using Trimmomatic, mapped to the human reference genome using STAR, and intron-spanning reads were summarized using HTseq. The processed data includes 285 samples (columns) and 57736 ensemble gene ids (rows). The supplementary data file (TEP_data_matrix.txt) contains the intron-spanning read counts, after data summarization by HTseq.; [Treatment]'None'; [Growth]'None'; [Extraction]'Blood platelets were isolated from whole blood in purple-cap BD Vacutainers containing the EDTA anti-coagulant. The cells and aggregates were removed by centrifugation at room temperature for 20 minutes at 120g, resulting in platelet-rich plasma. The platelets were isolated from the platelet-rich plasma by centrifugation at room temperature for 20 minutes at 360g. The platelet pellet was collected in 30 μl RNAlater (Life Technologies), incubated overnight at 4°C and frozen at -80°C for further use. Frozen platelets were thawed on ice and total RNA was isolated using the mirVana RNA isolation kit (Life Technologies) according to the manufacturers’ protocol. Complementary purification of small RNAs was included in the isolation procedure by addition of miRNA homogenate (Life Technologies). Total RNA was dissolved in 30 μl Elution Buffer (Life Technologies) and RNA quality and quantity was measured using Bioanalyzer 2100 with RNA 6000 Picochip (Agilent).\n100-500 pg of platelet total RNA (Bioanalyzer RIN values >7 and/or distinctive rRNA curves) diluted in nuclease free H2O was subjected to cDNA synthesis and amplification using the SMARTer Ultra Low RNA Kit for Illumina Sequencing v1 (Clontech, cat. nr. 634936) according to the manufacturers’ protocol. Conversion and efficient amplification of cDNA was quality-controlled using the Bioanalyzer 2100 with DNA High Sensitivity chip (Agilent). Samples with detectable fragments in the 300-7500 bp region were selected for further processing and Covaris shearing by sonication (Covaris Inc). Sample preparation for Illumina sequencing was performed using the Truseq DNA Sample Preparation Kit (Illumina, cat nr. FC-121-2001) or Truseq Nano DNA Sample Preparation Kit (Illumina, cat nr. FC-121-4001). Sample quality and quantity was measured using the DNA 7500 chip or DNA High Sensitivity chip (Agilent). High-quality samples with product sizes between 300-500 bp were pooled in equimolar concentrations (8-12 samples per Hiseq lane) and submitted for 100 bp Single Read sequencing on the Hiseq 2500 platform (Illumina).'; [Cell type]'Thrombocytes', 'thrombocytes''tissue: blood; cell type: Thrombocytes; patient id: Breast-03; cancer type: Breast; batch: Batch03; mutational subclass: HER2+; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-08; cancer type: Breast; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-10; cancer type: Breast; batch: Batch03; mutational subclass: HER2+; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-100; cancer type: Breast; batch: Batch04; mutational subclass: Triple Negative; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-15; cancer type: Breast; batch: Batch03; mutational subclass: HER2+; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-16; cancer type: Breast; batch: Batch03; mutational subclass: Triple Negative; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-21; cancer type: Breast; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-33; cancer type: Breast; batch: Batch03; mutational subclass: HER2+; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-42; cancer type: Breast; batch: Batch03; mutational subclass: HER2+, PIK3CA; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-454; cancer type: Breast; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-48; cancer type: Breast; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-50; cancer type: Breast; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-55; cancer type: Breast; batch: Batch03; mutational subclass: Triple Negative; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-56; cancer type: Breast; batch: Batch03; mutational subclass: PIK3CA; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-564; cancer type: Breast; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-59; cancer type: Breast; batch: Batch03; mutational subclass: PIK3CA; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-590; cancer type: Breast; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-60; cancer type: Breast; batch: Batch04; mutational subclass: Triple Negative; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-603; cancer type: Breast; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-61; cancer type: Breast; batch: Batch03; mutational subclass: Triple Negative; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-85; cancer type: Breast; batch: Batch04; mutational subclass: Triple Negative; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-86; cancer type: Breast; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-97; cancer type: Breast; batch: Batch03; mutational subclass: HER2+, PIK3CA; ', 'tissue: blood; cell type: Thrombocytes; patient id: Breast-ALK-82; cancer type: Breast; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Chol-292; cancer type: Hepatobiliary; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Chol-316; cancer type: Hepatobiliary; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Chol-341; cancer type: Hepatobiliary; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Chol-376; cancer type: Hepatobiliary; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Chol-379; cancer type: Hepatobiliary; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Chol-410; cancer type: Hepatobiliary; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Chol-442; cancer type: Hepatobiliary; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Chol-460; cancer type: Hepatobiliary; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Chol-611; cancer type: Hepatobiliary; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Chol-ALK-28; cancer type: Hepatobiliary; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-256; cancer type: CRC; batch: Batch02; mutational subclass: PIK3CA; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-258; cancer type: CRC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-272; cancer type: CRC; batch: Batch02; mutational subclass: PIK3CA; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-276; cancer type: CRC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-304; cancer type: CRC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-329; cancer type: CRC; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-342; cancer type: CRC; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-351; cancer type: CRC; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-354; cancer type: CRC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-356; cancer type: CRC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-357; cancer type: CRC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-374; cancer type: CRC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-378; cancer type: CRC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-420; cancer type: CRC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-429; cancer type: CRC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-450; cancer type: CRC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-453; cancer type: CRC; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-459; cancer type: CRC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-462; cancer type: CRC; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-463; cancer type: CRC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-466; cancer type: CRC; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-474; cancer type: CRC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-487; cancer type: CRC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-496; cancer type: CRC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-497; cancer type: CRC; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-504; cancer type: CRC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-511; cancer type: CRC; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-523; cancer type: CRC; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-524; cancer type: CRC; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-527; cancer type: CRC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-531; cancer type: CRC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-543; cancer type: CRC; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-546; cancer type: CRC; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-548; cancer type: CRC; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-552; cancer type: CRC; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-556; cancer type: CRC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-565; cancer type: CRC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: CRC-576; cancer type: CRC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-280; cancer type: GBM; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-284; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-306; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-360; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-372; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-378; cancer type: GBM; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-383; cancer type: GBM; batch: Batch01; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-393; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-394; cancer type: GBM; batch: Batch01; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-398; cancer type: GBM; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-402; cancer type: GBM; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-406; cancer type: GBM; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-408; cancer type: GBM; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-417; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-418; cancer type: GBM; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-419; cancer type: GBM; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-421; cancer type: GBM; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-422; cancer type: GBM; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-425; cancer type: GBM; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-429; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-430; cancer type: GBM; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-431; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-436; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-438; cancer type: GBM; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-439; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-440; cancer type: GBM; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-443; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-445; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-454; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-456; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-468; cancer type: GBM; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-471; cancer type: GBM; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-475; cancer type: GBM; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-476; cancer type: GBM; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-480; cancer type: GBM; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-484; cancer type: GBM; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-485; cancer type: GBM; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-486; cancer type: GBM; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-499; cancer type: GBM; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: GBM-505; cancer type: GBM; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-01; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-02; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-03; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-04; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-05; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-06; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-07; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-08; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-09; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-10; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-11; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-12; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-13; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-14; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-15; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-16; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-17; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-18; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-19; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-20; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-21; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-22; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-23; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-24; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-25; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-26; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-27; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-28; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-29; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-30; cancer type: HC; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-31; cancer type: HC; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-32; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-33; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-34; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-35; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-36; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-37; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-38; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-39; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-40; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-41; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-42; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-43; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-44; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-45; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-46; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-47; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-48; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-49; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-50; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-51; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-52; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-53; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-54; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: HC-55; cancer type: HC; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Liver-274; cancer type: Hepatobiliary; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Liver-297; cancer type: Hepatobiliary; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Liver-366; cancer type: Hepatobiliary; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-0082; cancer type: Lung; batch: Batch04; mutational subclass: MET; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-0096; cancer type: Lung; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-01; cancer type: Lung; batch: Batch02; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-0100; cancer type: Lung; batch: Batch04; mutational subclass: EGFR, MET; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-0101; cancer type: Lung; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-0102; cancer type: Lung; batch: Batch04; mutational subclass: EGFR, MET; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-0104; cancer type: Lung; batch: Batch04; mutational subclass: EGFR, MET; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-0110; cancer type: Lung; batch: Batch04; mutational subclass: EGFR, MET; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-0112; cancer type: Lung; batch: Batch04; mutational subclass: EGFR, MET; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-0119; cancer type: Lung; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-04; cancer type: Lung; batch: Batch03; mutational subclass: EGFR, MET; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-06; cancer type: Lung; batch: Batch02; mutational subclass: EGFR; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-07; cancer type: Lung; batch: Batch02; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-08; cancer type: Lung; batch: Batch02; mutational subclass: EGFR; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-12; cancer type: Lung; batch: Batch02; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-14; cancer type: Lung; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-15; cancer type: Lung; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-16; cancer type: Lung; batch: Batch02; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-17; cancer type: Lung; batch: Batch02; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-20; cancer type: Lung; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-20-1; cancer type: Lung; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-24-1; cancer type: Lung; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-25; cancer type: Lung; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-26; cancer type: Lung; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-271; cancer type: Lung; batch: Batch02; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-29; cancer type: Lung; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-30; cancer type: Lung; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-37; cancer type: Lung; batch: Batch02; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-40; cancer type: Lung; batch: Batch02; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-42; cancer type: Lung; batch: Batch02; mutational subclass: KRAS, MET; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-46; cancer type: Lung; batch: Batch02; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-58; cancer type: Lung; batch: Batch03; mutational subclass: EGFR, MET; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-61; cancer type: Lung; batch: Batch03; mutational subclass: EGFR, MET; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-62; cancer type: Lung; batch: Batch03; mutational subclass: EGFR; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-74; cancer type: Lung; batch: Batch03; mutational subclass: EGFR; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-L.13; cancer type: Lung; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-L.15; cancer type: Lung; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-L.26; cancer type: Lung; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-L.33; cancer type: Lung; batch: Batch04; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Lung-L.4; cancer type: Lung; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-260; cancer type: Pancreas; batch: Batch02; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-286; cancer type: Pancreas; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-314; cancer type: Pancreas; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-327; cancer type: Pancreas; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-328; cancer type: Pancreas; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-331; cancer type: Pancreas; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-335; cancer type: Pancreas; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-367; cancer type: Pancreas; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-369; cancer type: Pancreas; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-370; cancer type: Pancreas; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-371; cancer type: Pancreas; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-380; cancer type: Pancreas; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-382; cancer type: Pancreas; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-387; cancer type: Pancreas; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-388; cancer type: Pancreas; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-389; cancer type: Pancreas; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-390; cancer type: Pancreas; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-391; cancer type: Pancreas; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-431; cancer type: Pancreas; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-434; cancer type: Pancreas; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-435; cancer type: Pancreas; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-448; cancer type: Pancreas; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-449; cancer type: Pancreas; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-451; cancer type: Pancreas; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-461; cancer type: Pancreas; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-477; cancer type: Pancreas; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-488; cancer type: Pancreas; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-493; cancer type: Pancreas; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-498; cancer type: Pancreas; batch: Batch03; mutational subclass: wt; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-501; cancer type: Pancreas; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-503; cancer type: Pancreas; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-512; cancer type: Pancreas; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-553; cancer type: Pancreas; batch: Batch03; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-593; cancer type: Pancreas; batch: Batch04; mutational subclass: KRAS; ', 'tissue: blood; cell type: Thrombocytes; patient id: Panc-597; cancer type: Pancreas; batch: Batch04; mutational subclass: wt; ', 'patient id: Breast-H11; cancer type: Breast; batch: Batch05; mutational subclass: PIK3CA; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H31; cancer type: Breast; batch: Batch06; mutational subclass: wt; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H38; cancer type: Breast; batch: Batch06; mutational subclass: wt; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H59; cancer type: Breast; batch: Batch05; mutational subclass: wt; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H63; cancer type: Breast; batch: Batch06; mutational subclass: wt; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H66; cancer type: Breast; batch: Batch05; mutational subclass: wt; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H68; cancer type: Breast; batch: Batch05; mutational subclass: wt; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H74; cancer type: Breast; batch: Batch05; mutational subclass: HER2+; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H75; cancer type: Breast; batch: Batch05; mutational subclass: PIK3CA; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H76; cancer type: Breast; batch: Batch06; mutational subclass: HER2+; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H81; cancer type: Breast; batch: Batch06; mutational subclass: HER2+; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H83; cancer type: Breast; batch: Batch06; mutational subclass: HER2+; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H84; cancer type: Breast; batch: Batch06; mutational subclass: HER2+; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H89; cancer type: Breast; batch: Batch06; mutational subclass: wt; tissue: blood; cell type: thrombocytes; ', 'patient id: Breast-H92; cancer type: Breast; batch: Batch06; mutational subclass: HER2+; tissue: blood; cell type: thrombocytes; ', 'patient id: Chol-BRAF4; cancer type: Hepatobiliary; batch: Batch06; mutational subclass: wt; tissue: blood; cell type: thrombocytes; ', 'patient id: CRC-368; cancer type: CRC; batch: Batch05; mutational subclass: wt; tissue: blood; cell type: thrombocytes; ', 'patient id: CRC-412; cancer type: CRC; batch: Batch06; mutational subclass: wt; tissue: blood; cell type: thrombocytes; ', 'patient id: CRC-BRAF5; cancer type: CRC; batch: Batch06; mutational subclass: wt; tissue: blood; cell type: thrombocytes; ', 'patient id: CRC-BRAF6; cancer type: CRC; batch: Batch06; mutational subclass: wt; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-49; cancer type: Lung; batch: Batch05; mutational subclass: KRAS; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-57; cancer type: Lung; batch: Batch05; mutational subclass: KRAS; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-59; cancer type: Lung; batch: Batch05; mutational subclass: KRAS; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L01; cancer type: Lung; batch: Batch06; mutational subclass: EGFR; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L03; cancer type: Lung; batch: Batch06; mutational subclass: KRAS; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L07; cancer type: Lung; batch: Batch06; mutational subclass: EGFR; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L11; cancer type: Lung; batch: Batch06; mutational subclass: EGFR; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L12; cancer type: Lung; batch: Batch06; mutational subclass: EGFR; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L18; cancer type: Lung; batch: Batch06; mutational subclass: EGFR; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L19; cancer type: Lung; batch: Batch06; mutational subclass: KRAS; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L20; cancer type: Lung; batch: Batch06; mutational subclass: EGFR; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L22; cancer type: Lung; batch: Batch06; mutational subclass: KRAS; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L23; cancer type: Lung; batch: Batch06; mutational subclass: EGFR; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L25; cancer type: Lung; batch: Batch06; mutational subclass: EGFR; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L39; cancer type: Lung; batch: Batch06; mutational subclass: KRAS; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L40; cancer type: Lung; batch: Batch06; mutational subclass: KRAS; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L51; cancer type: Lung; batch: Batch06; mutational subclass: KRAS; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L58; cancer type: Lung; batch: Batch06; mutational subclass: EGFR; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L59; cancer type: Lung; batch: Batch06; mutational subclass: KRAS; tissue: blood; cell type: thrombocytes; ', 'patient id: Lung-L65; cancer type: Lung; batch: Batch06; mutational subclass: KRAS; tissue: blood; cell type: thrombocytes; ' GSE64522 Mus musculus 159 Expression profiling by array GPL6246 Expression data from mammary tumors from a generation 7 Diversity Outcross x PyMT cross 2014-12-24 Mouse genetic crosses were established between the PyMT model of metastatic breast cancer and the G7 generation of the Diversity Outcross (DO). Tumors were harvested from the animals for gene expression analysis to identify genes association with progression to distant metastatic disease. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64522 An Integrated Genome-Wide Systems Genetics Screen for Breast Cancer Metastasis Susceptibility Genes. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1005989 {PLoS genetics (5.224): 10.1371/journal.pgen.1005989} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA271173 https://www.ebi.ac.uk/ena/browser/view/PRJNA271173 None [Overal design]Gene expression of 159 samples from the PyMT x Diversity Outcross were assayed on Affymetrix chips.; [Treatment]'No treatment.'; [Growth]'DO x PyMT tumors spontaneously developed and were permitted to grow until animals reached approximately 100 days of age. Tumors were harvested, snap frozen in LN2 and stored at -80oC until RNA preparation.'; [Extraction]"Total RNA was extracted by Trizol, following manufacturer's recommended protocol."; [Cell type]'Source: ''strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14815; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14819; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14823; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14824; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14825; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14826; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14852; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14857; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14859; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14863; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14551; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14864; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14873; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14877; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14879; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14880; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14884; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14887; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14888; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14891; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14893; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14552; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14894; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14896; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14897; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14902; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14903; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14904; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14907; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14908; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14909; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14911; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14553; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14913; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14914; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14917; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14919; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14922; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14924; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14926; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14928; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14929; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14930; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14554; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14936; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14938; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14939; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14941; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14944; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14945; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14946; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14947; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14948; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14951; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14556; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14954; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14956; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14957; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14958; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14959; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 15002; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 15007; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 15025; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 15026; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 15029; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14558; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14562; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14576; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14578; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14579; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14540; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14580; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14587; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14590; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14591; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14593; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14595; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14596; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14597; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14601; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14602; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14541; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14603; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14606; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14607; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14608R; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14611R; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14612; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14613; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14616; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14617; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14618; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14542; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14619; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14620; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14623; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14624; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14625; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14628; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14629; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14630; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14631; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14632; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14543; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14633; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14635; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; 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', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14771; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14775; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14776; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14780; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14783; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14788; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14789; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14548; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14790; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14794; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14795; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14797; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14799; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14800; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14803; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14808; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14809; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14812; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; gender: female; age: 100 days; animal #: 14550; ' GSE96996 Homo sapiens 2 Genome binding/occupancy profiling by high throughput sequencing GPL16791 UTX ChIP sequencing in non-treated MCF-7 cells 2017-03-24 UTX is implicated in embryonic development and lineage specification. However, how this X-linked histone demethylase contributes to the development and progression of breast cancer remains to be investigated. Here we report that UTX is physically associated with estrogen receptor (ER) and functions in ER-regulated transcription. We showed that UTX coordinates with JHDM1D and CBP to direct H3K27 methylation-acetylation transition and to create a permissive chromatin state on ER targets. Genome-wide analysis of the transcriptional targets of UTX by ChIP-seq identified a cohort of genes including chemokine receptor CXCR4 that are critically involved in breast cancer tumorigenesis and metastasis. We demonstrated that UTX promotes the proliferation and migration of ER+ breast cancer cells. Interestingly, UTX itself is transactivated by ER, forming a feed-forward loop in the regulation of hormone response. Indeed, UTX is upregulated during ER+ breast cancer progression, and the level of its expression is positively correlated with that of CXCR4 and negatively correlated with the overall survival of ER+ breast cancer patients. Our study identified a feed-forward loop between UTX and ER in the regulation of hormonally responsive breast cancer carcinogenesis, supporting the pursuit of UTX as a potential target for the intervention of certain ER+ breast cancer with specific epigenetic vulnerability. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE96996 UTX promotes hormonally responsive breast carcinogenesis through feed-forward transcription regulation with estrogen receptor. Oncogene 6.634 https://doi.org/10.1038/onc.2017.157 {Oncogene (6.634): 10.1038/onc.2017.157} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA380353 https://www.ebi.ac.uk/ena/browser/view/PRJNA380353 https://www.ncbi.nlm.nih.gov/sra?term=SRP102437 [Overal design]Examination of UTX target genes in MCF-7 cells; [Treatment]'None'; [Growth]"MCF-7 cells were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% fetal bovine serum (FBS). Cells were maintained in a humidified incubator equilibrated with 5% CO2 at 37°C."; [Extraction]'MCF-7 cells were maintained in DMEM supplemented with 10% fetal bovine serum. Approximately 5 x 107 cells were used for each ChIP-seq assay. The chromatin DNA precipitated by polyclonal antibodies against UTX. The DNA was purified with the Qiagen PCR purification kit.\nThe 1st strand cDNA was synthesized with random primer flanked by 7 nt sequence to track infromation. The 2nd strand DNA was generated with N6 adaptor. The resulting DNA libraries were amplified with Phusion High-Fidelity DNA Polymerase.'; [Cell type]'Source: ''cell line: MCF-7; ' GSE131512 Homo sapiens 128 Expression profiling by high throughput sequencing GPL20301 Extracellular RNA in a single droplet of human serum reflects physiologic and disease states 2019-05-20 We developed SILVER-seq (Small Input Liquid Volume Extracellular RNA Sequencing) to efficiently sequence both integral and fragmented cfRNAs from a small droplet (5-7 microliters) of liquid biopsy. We carried out SILVER-seq on more than 150 serum droplets from male and female donors ranging from 19 to 48 years of age. SILVER-seq detected cfRNAs from more than a quarter of the human genes, including small RNAs and fragments of mRNAs and long non-coding RNAs (lincRNAs). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131512 Extracellular RNA in a single droplet of human serum reflects physiologic and disease states. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1908252116 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1908252116} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA543872 https://www.ebi.ac.uk/ena/browser/view/PRJNA543872 https://www.ncbi.nlm.nih.gov/sra?term=SRP198979 [Overal design]128 different samples, consisting of 32 samples from self-reported non-breast-cancer donors, 28 samples from cancer recurrence donors and 68 samples from cancer non-recurrence donors, were constructed to mols-seq libraries for cancer-normal and recurrence-nonrecurrence study.; [Treatment]'None'; [Growth]'None'; [Extraction]'Sequencing libraries were constructed with SILVER-seq from serum.'; [Cell type]'Source: ''age: 34.44; gender: Female; condition: breast cancer serum (with recurrence); equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; 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equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 46.32; gender: Female; condition: breast cancer serum (without recurrence); equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 47.21; gender: Female; condition: breast cancer serum (without recurrence); equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 27.52; gender: Female; condition: breast cancer serum (without recurrence); equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 28.53; gender: Female; condition: breast cancer serum (without recurrence); equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 39.83; gender: Female; condition: breast cancer serum (without recurrence); equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 40.66; gender: Female; condition: breast cancer serum (without recurrence); equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 40.49; gender: Female; condition: breast cancer serum (without recurrence); equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 40.77; gender: Female; condition: breast cancer serum (without recurrence); equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 43.44; gender: Female; condition: breast cancer serum (without recurrence); equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 43.90; gender: Female; condition: breast cancer serum (without recurrence); equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 39.77; gender: Female; condition: breast cancer serum (without recurrence); equivalent serum volume used (ul): 7; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 41.00; gender: Female; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 40.00; gender: Female; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 29.00; gender: Female; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 31.00; gender: Female; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 27.00; gender: Female; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 19.00; gender: Female; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 36.00; gender: Female; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 18.00; gender: Female; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 41.00; gender: Male; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 28.00; gender: Male; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 32.00; gender: Male; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 38.00; gender: Male; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 27.00; gender: Male; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 36.00; gender: Male; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 34.00; gender: Male; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 20.00; gender: Male; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 42.00; gender: Male; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 40.00; gender: Male; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 21.00; gender: Female; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 37.00; gender: Male; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 26.00; gender: Female; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 29.00; gender: Male; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 32.00; gender: Female; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ', 'age: 42.00; gender: Female; condition: normal serum; equivalent serum volume used (ul): 5; rna extration (y/n): N; library construction method: SILVER-seq; ' GSE36326 Homo sapiens 2 Protein profiling by protein array GPL15319 Targeted inhibition of human breast cancer cell lines selected as model systems of ERBB2-positive/EGFR high breast cancer [RPPA-SKBR3] 2012-03-07 EGFR-inhibition is required for targeted therapies of ERBB2-positive/EGFR high breast cancer. Approximately 30% of human ERBB2-positive breast tumors also express EGFR. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36326 Strong EGFR signaling in cell line models of ERBB2-amplified breast cancer attenuates response towards ERBB2-targeting drugs. Oncogenesis 5.995 https://doi.org/10.1038/oncsis.2012.16 {Oncogenesis (5.995): 10.1038/oncsis.2012.16} 'protein' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA155575 https://www.ebi.ac.uk/ena/browser/view/PRJNA155575 None [Overal design]Three targeted therapeutics (erlotinib, pertuzumab, trastuzumab) and two ligands (EGF, HRG) were analyzed in all possible combinations. Each experiment involving inhibition with targeted drugs was performed in three, and measurements without inhibitors were performed in five biological replicates. This resulted in 780 samples. HRG stimulated cells under the triple drug combination exceptionally have two biological replicates. Incubation with therapeutics only and dilution series of control lysated were included as controls.; [Treatment]'The inhibitors trastuzumab (10\xa0ng/µL), pertuzumab (10\xa0ng/µL), and erlotinib (1\xa0µM) (Roche, Penzberg, Germany) were added to cells in starvation medium either alone or in combinations 1\xa0h prior to stimulation with EGF or HRG (5\xa0nM) for 0, 4, 8, 12, 16, 20, 30, 40, 50 and 60 min. After stimulation, medium was removed and ice-cold PBS was added to the plates.'; [Growth]'Cells were seeded in 6-well plates, cultivated for 24h, and serum-starved for additional 24h.'; [Extraction]'Medium was replaced by ice-cold PBS, transferred on ice, and cells were harvested manually by scraping in M-PER lysis buffer (Pierce, Bonn, Germany) containing protease inhibitor Complete Mini and phosphatase inhibitor PhosSTOP (Roche, Mannheim, Germany). Cells were lyzed for 20\xa0min on an end-over-end shaker and lysates were cleared at 16,000\xa0x\xa0g by centrifugation.'; [Cell type]'Source: ''protein target: phospho-ERK1/2; phospho site: T202Y204; antibody id: CST 4370; ', 'protein target: phospho-AKT; phospho site: S473; antibody id: CST 9271; ' GSE71076 Mus musculus 4 Expression profiling by high throughput sequencing GPL17021 Cbx8 acts non-canonically with Wdr5 to promote mammary tumorigenesis [RNA-Seq] 2015-07-20 Here we show that in MMTV-Myc cells (1) MS culture enriches for aggressive breast cancer cells compared to the bulk cells, (2) Cbx8 knockdown reduces Notch-network gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE71076 Cbx8 Acts Non-canonically with Wdr5 to Promote Mammary Tumorigenesis. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2016.06.002 {Cell reports (7.815): 10.1016/j.celrep.2016.06.002} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA290315 https://www.ebi.ac.uk/ena/browser/view/PRJNA290315 https://www.ncbi.nlm.nih.gov/sra?term=SRP061312 [Overal design]Gene expression of (1) bulk vs MS MMTV-Myc cells, (2) control vs Cbx8 knockdown MMTV-Myc cells; [Treatment]'Lentiviral infections with pLKO.1 based Cbx8 shRNAs, 2 days after infection cells were selected with 2ug/ml of puromycin for at least 4 days. Cells were passaged with constant selection under 2ug/ml puromycin.'; [Growth]'MMTV-Myc cells were cultured in DMEM/F12 (Cellgro) with 2% FBS, 10μg/ml insulin, 1X glutamine, 10mM HEPES, 1X nonessential amino acids and 1X Penicillin/Streptomycin. MS were cultured in DMEM/F12 (Cellgro) or MEBM (Lonza) with 20ng/ml EGF, 20ng/ml bFGF, 1X Gem21 supplement (Gemini Bio-products) and 1X Penicillin/Streptomycin on Ultra-low attachment plates (Corning) at a density <1X106 cells per 10ml media. MS were dissociated with trypsin into single cells and passaged every 4 days.'; [Extraction]'Total RNA was extracted with the QIAGEN RNeasy Mini Kit\nRNA samples were quality checked (RIN score of 8 or higher) using the RNA 6000 Nano chip on a 2100 Bioanalyzer (Agilent). mRNA was then isolated using Sera-Mag oligo-dT beads (Thermo Fisher Scientific), and cDNA library was synthesized by SuperScript II (Invitrogen) with random primers. The cDNA library was quality checked.\nPooled libraries were loaded on high throughput HiSeq 2500 flow cells, using v3 reagents, and sequenced 100nt, single-end.'; [Cell type]'bulk cells (day 0)', 'mammosphere cells (day 20)', 'Source: ''cell line: MMTV-Myc; cell type: bulk cells (day 0); genotype: wild type; ', 'cell line: MMTV-Myc; cell type: mammosphere cells (day 20); genotype: wild type; ', 'cell line: MMTV-Myc; genotype: wild type (shLuc); ', 'cell line: MMTV-Myc; genotype: Cbx8 knockdown (sh68); ' GSE130453 Mus musculus 4 Expression profiling by high throughput sequencing GPL17021; GPL19057 Single cell RNA-Seq data for Trp53/Brca1-null premalignant mammary epithelial cells and tumor cells with a K8+ luminal origin 2019-04-29 BRCA1 mutation-carriers are predisposed to develop Basal-like breast cancer (BLBC), and p53 mutations are present in the majority of human BLBC cases, suggesting loss of these two tumor suppressors play key roles in development of BLBC. Recent studies suggest that the majority of human breast cancers, including BLBC, may originate from mammary epithelial cells (MECs) in the luminal lineage. However, how loss of p53 and BRCA1 contributes to development of BLBC from luminal MECs remains largely elusive. We developed a novel genetic targeting and lineage tracing approach based on intraductal injection of Cre-expressing adenovirus under the control of the pan-luminal Keratin 8 (K8) promoter (Ad-K8-Cre). We performed intraductal injection of Ad-K8-Cre to female mice carrying conditional knockout alleles of Brca1 (Brca1L) and Trp53 (Trp53L). The injected females developed mammary tumors similar to human BLBC within 12 months after injection. Here we characterized MECs targeted by Ad-K8-Cre at different time points after the intraductal injection, as well as mammary tumors developed in this model, by single cell expression analysis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130453 Inadequate DNA Damage Repair Promotes Mammary Transdifferentiation, Leading to BRCA1 Breast Cancer. Cell 36.216 https://doi.org/10.1016/j.cell.2019.06.002 {Cell (36.216): 10.1016/j.cell.2019.06.002} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA540878 https://www.ebi.ac.uk/ena/browser/view/PRJNA540878 https://www.ncbi.nlm.nih.gov/sra?term=SRP194662 [Overal design]YFP+ p53/BRCA1-deficient mammary epithelial cells were sorted from Trp53L/L;Brca1L/L;Rosa26-Stop-YFP (R26Y) female mice ~2 weeks or 5 months after intraductal induction of Ad-K8-Cre adenovirus, respectively, and were subjected to single cell RNA-seq analysis. In addition, single cell suspensions were prepared from two mammary tumors developed in this mouse model and were subjected to single cell RNA-seq analysis.; [Treatment]'None'; [Growth]'None'; [Extraction]'YFP+ premalignant mammary epithelial cells or mammary tumor cells from Trp53L/L;Brca1L/L;R26Y mice post Ad-K8-Cre injection (at the indicated time points) were sorted into Dulbecco’s PBS\u2009+\u20090.04% BSA and retained on ice reagent.\nBarcoded single cell RNA-seq libraries were generated as per the manufacturer’s instructions of 10×\u2009Chromium Single Cell 3’ v2 reagent kit (10×\u2009Genomics, Pleasanton, CA, USA).'; [Cell type]'Sorted YFP+ mammary epithelial cells', 'Sorted YFP+ mammary epithelial cells and CD45+ leukocytes', 'Sorted DAPI- live cells from the tumor mass''strain/background: Mixed genetic background; genotype/variation: Trp53/Brca1-null; gender: Female; cell type: Sorted YFP+ mammary epithelial cells; condition: ~Two weeks after Ad-K8-Cre intraductal injection; ', 'strain/background: Mixed genetic background; genotype/variation: Trp53/Brca1-null; gender: Female; cell type: Sorted YFP+ mammary epithelial cells and CD45+ leukocytes; condition: ~Five months after Ad-K8-Cre intraductal injection; ', 'strain/background: Mixed genetic background; genotype/variation: Trp53/Brca1-null; gender: Female; cell type: Sorted DAPI- live cells from the tumor mass; condition: Tumor #1 emerged in the mammary gland after Ad-K8-Cre intraductal injection; ', 'strain/background: Mixed genetic background; genotype/variation: Trp53/Brca1-null; gender: Female; cell type: Sorted DAPI- live cells from the tumor mass; condition: Tumor #2 emerged in the mammary gland after Ad-K8-Cre intraductal injection; ' GSE23061 Homo sapiens 20 Expression profiling by array GPL3921 The expression programme of ERR-alphain human mammary epithelial cells 2010-07-21 This dataset is part of the manuscript titled "The metabolic regulator ERRalpha, a downstream target of HER2/IGF1, as a therapeutic target in breast cancer" (in review). The expression data obtained in human mammary epithelial cells were used to generate a list of ERRalpha-regulated genes that was later refined in clinical breast cancer datasets to generate a clinically relevant signature of ERalpha activity (referred to as Cluster 3 signature). Using this signature of the estrogen-related receptor alpha (ERRa) to profile more than eight-hundred breast tumors, we found that patients with tumors exhibiting higher ERRa activity were predicted to have shorter disease free survival. Further, the ability of an ERRa antagonist, XCT790, to inhibit breast cancer cell proliferation correlates with the cell’s intrinsic ERRa activity. These findings highlight the potential of using the ERRa signature and antagonists in targeted therapy for breast cancer. Using a chemical genomic approach we determined that activation of the HER2/IGF1 signaling pathways upregulates the expression of PGC-1b, an obligate cofactor for ERRa activity. Knockdown of PGC-1b in HER2 positive breast cancer cells impaired ERRa signaling and reduced cell proliferation, implicating a functional role of PGC1b/ERRa in the pathogenesis HER2 positive breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23061 The metabolic regulator ERRα, a downstream target of HER2/IGF-1R, as a therapeutic target in breast cancer. Cancer cell 23.916 https://doi.org/10.1016/j.ccr.2011.08.023 {Cancer cell (23.916): 10.1016/j.ccr.2011.08.023} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA129885 https://www.ebi.ac.uk/ena/browser/view/PRJNA129885 None [Overal design]Primary human mammary epithelial cells were a gift from Dr. J. Marks (Duke University, Durham, NC) and cultured in MEBM (Cambrex, East Rutherford, NJ) with MEGM bullet kit and supplemented with 5mg/ml transferrin and 10-5M isoproterenol. To generate ERR-alpha signature, hMECs were serum starved for 36h followed by infection with MOI=150 of adenoviruses expressing two variants of PGC1alpha, a protein ligand for ERRalpha: PGC-1alpha2x9 or PGC-1alpha L2L3M. PGC-1-2x9 is specific to ERRalpha, while PGC-1-L2L3M lacks the NR box and does not interact with ERRalpha or other nuclear receptors. The generation and purification of variant PGC-1alpha viruses were described previously (Gaillard et al., Molecular Cell 24:5, 2006). Comparable expression levels of the two PGC-1alpha variants were verified by Western immonoblot analysis (data not shown). RNA was collect 16h after infection and purified using RNeasy mini kit (Qiagen, Valencia, CA). Ten independent biological replicates from each virus infection were collected.; [Treatment]'hMECs were serum starved for 36h followed by infection with MOI=150 of adenoviruses expressing two variants of PGC1alpha, a protein ligand for ERRalpha: PGC-1alpha2x9 or PGC-1alpha L2L3M.'; [Growth]'Primary human mammary epithelial cells were cultured in MEBM (Cambrex, East Rutherford, NJ) with MEGM bullet kit and supplemented with 5mg/ml transferrin and 10-5M isoproterenol.'; [Extraction]'RNeasy mini kit (Qiagen, Valencia, CA)'; [Cell type]'mammary epitheliel''cell type: mammary epitheliel; ' GSE52404 Homo sapiens 7 Expression profiling by array GPL6244 The effects of chronic cadmium exposure on gene expression in MCF7 breast cancer cells 2013-11-15 Cadmium is a metalloestrogen known to activate the estrogen receptor and promote breast cancer cell growth. Previous studies have implicated cadmium in the development of more malignant tumors; however the molecular mechanisms behind this cadmium-induced malignancy remain elusive. Using clonal cell lines derived by exposing breast cancer cells to cadmium for over 6 month (MCF7-Cd4, -Cd6, -Cd7, -Cd8 and -Cd12), this study aims to identify gene expression signatures associated with chronic cadmium exposure. Our results demonstrate that prolonged exposure does not merely result in the deregulation of genes but actually leads to a distinctive expression profile. The genes deregulated in cadmium-exposed cells are involved in multiple biological processes (i.e cell growth, apoptosis, etc.) and molecular functions (i.e. cadmium/metal ion binding, transcription factor activity, etc). Hierarchical clustering demonstrates that the five clonal cadmium cell lines share a common gene expression signature of breast cancer associated genes, clearly differentiating control from cadmium exposed cells. The results presented in this study offer insights into the cellular and molecular impacts of cadmium on breast cancer carcinogenesis and emphasize the importance of studying chronic cadmium exposure as one possible mechanism of promoting breast cancer progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE52404 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA227800 https://www.ebi.ac.uk/ena/browser/view/PRJNA227800 None [Overal design]To understand the effects of chronic cadmium exposure on gene expression in breast cancer, two control MCF7 parental cell lines and five different clonal cadmium-adapted cell lines (MCF7-Cd4, -Cd6, -Cd7, -Cd8, and -Cd12) - previously derived from cells chronically exposed to cadmium - were used for microarray analysis.; [Treatment]'None'; [Growth]'None'; [Extraction]'extract protocol'; [Cell type]'Source: ''cell line: MCF7; ', 'cell line: cadmium MCF7-Cd4; ', 'cell line: cadmium MCF7-Cd6; ', 'cell line: cadmium MCF7-Cd7; ', 'cell line: cadmium MCF7-Cd8; ', 'cell line: cadmium MCF7-Cd12; ' GSE55897 Homo sapiens 36 Expression profiling by array GPL10904 Indole-3-Carbinol Preferentially Target ERα-Positive Breast Cancer Cells. 2014-03-13 Indole-3-carbinol (I3C) is a natural anti-carcinogenic compound found at high concentrations in Brassica vegetables. ER-positive cell lines demonstrated the greatest sensitivity to the anti-tumor effects of I3C compared to ER-negative breast cancer cell lines. Gene expression analysis was performed to identify genes and pathways that accounted for sensitivity to I3C. Microarray analysis performed using Illumina HT-12 v4 expression arrays https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55897 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA241265 https://www.ebi.ac.uk/ena/browser/view/PRJNA241265 None [Overal design]A total of 36 samples were analyzed with six breast cancer cell lines treated with either the vehicle control or the drug Indole-3-carbinol in triplicate. The cell lines were: MCF-7, T47D, ZR751(sensitive to the drug, apoptosis/growth arrest) and MDA-MB-231, MDA-MB-157, and MDA-MB-436 (insensitive to the drug). Sensitive cell lines are of the luminal subtype and insensitive cell lines are of the basal subtype.; [Treatment]'Microarray analysis was performed on three I3C sensitive cell lines (luminal ERa-positive: MCF-7, ZR751, and T47D) and three I3C insensitive cell lines (non-luminal ERa-negative: MDA-MB-231, MDA-MB-436, and MDA-MB-157) treated in triplicate with either 200 micromolar I3C or an equivalent volume of DMSO for 24 hours.'; [Growth]'All cell lines were maintained in a humidified tissue culture incubator at 37ºC and 6.5% CO2. All cell lines were obtained from ATCC and were routinely authenticated and tested for mycoplasma contamination using the MycoAlert assay kit (Lonza). The culture media was a-MEM supplemented with 10% fetal calf serum (Atlanta Biological), 0.01M HEPES, 2 mM L-glutamine, and 0.01 mg/mL of ciprofloxacin, 0.1 mM non-essential amino acids and 1 mM sodium pyruvate.'; [Extraction]'Total RNA was extracted from 2 x106 cells using the RNAeasy kit (Qiagen) and subjected to on column DNase I (NEB) digestion (all performed according to manufactures instructions). RNA integrity was confirmed using an Agilent Technologies Bioanalyzer 2100.'; [Cell type]'Source: ''treatment: DMSO; concentration i3c: 0 micromolar; tissue: breast cancer; cell line: ZR75-1; ', 'treatment: I3C; concentration i3c: 200 micromolar; tissue: breast cancer; cell line: ZR75-1; ', 'treatment: DMSO; concentration i3c: 0 micromolar; tissue: breast cancer; cell line: MDA-MB-436; ', 'treatment: I3C; concentration i3c: 200 micromolar; tissue: breast cancer; cell line: MDA-MB-436; ', 'treatment: DMSO; concentration i3c: 0 micromolar; tissue: breast cancer; cell line: MDA-MB-157; ', 'treatment: I3C; concentration i3c: 200 micromolar; tissue: breast cancer; cell line: MDA-MB-157; ', 'treatment: DMSO; concentration i3c: 0 micromolar; tissue: breast cancer; cell line: MDA-MB-231; ', 'treatment: I3C; concentration i3c: 200 micromolar; tissue: breast cancer; cell line: MDA-MB-231; ', 'treatment: DMSO; concentration i3c: 0 micromolar; tissue: breast cancer; cell line: MCF-7; ', 'treatment: I3C; concentration i3c: 200 micromolar; tissue: breast cancer; cell line: MCF-7; ', 'treatment: DMSO; concentration i3c: 0 micromolar; tissue: breast cancer; cell line: T47D; ', 'treatment: I3C; concentration i3c: 200 micromolar; tissue: breast cancer; cell line: T47D; ' GSE69240 Homo sapiens 35 Expression profiling by high throughput sequencing GPL11154 A Molecular Portrait Of High-Grade Ductal Carcinoma In Situ (DCIS) [RNA-seq] 2015-05-26 DCIS is a non-invasive precursor lesion to invasive breast carcinoma. We still have no understanding on why only some DCIS lesions evolve to invasive cancer while others appear not to do so during the life span of the patient. Here, we performed full exome (tumor vs. matching normal), transcriptome and methylome analysis of 30 pure high-grade DCIS (HG-DCIS) and 10 normal breast epithelial samples. Sixty two percent of HG-DCIS cases displayed mutations affecting cancer driver genes or potential drivers. Mutations were observed affecting PIK3CA (21% of cases), TP53 (17%), GATA3 (7%), MLL3 (7%) and single cases of mutations affecting CDH1, MAP2K4, TBX3, NF1, ATM and ARID1A. Significantly, 83% of lesions displayed numerous large chromosomal copy number alterations, suggesting they might precede selection of cancer driver mutations. Integrated pathway-based modeling analysis of RNA-seq data allowed us to identify two DCIS subgroups (DCIS-C1 and DCIS-C2) based on their tumor intrinsic subtypes, proliferative, immune scores and in the activity of specific signaling pathways. The more aggressive DCIS-C1 (highly proliferative, basal-like or ERBB2+) displayed signatures characteristic of activated Treg cells (CD4+/CD25+/FOXP3+) and CTLA4+/CD86+ complexes indicative of a tumor-associated immune suppressive phenotype. Strikingly, all lesions showed evidence of TP53 pathway inactivation. Similarly ncRNA and methylation profiles reproduce changes observed post-invasion. Among the most significant findings we observed upregulation of lncRNA HOTAIR in DCIS-C1 lesions and hypermethylation of HOXA5 and specific SOX genes. We conclude that most HG-DCIS lesions, in spite of representing a pre-invasive stage of tumor progression, displayed molecular profiles indistinguishable from invasive breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE69240 A Molecular Portrait of High-Grade Ductal Carcinoma In Situ. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-15-0506 {Cancer research (8.378): 10.1158/0008-5472.CAN-15-0506} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA284949 https://www.ebi.ac.uk/ena/browser/view/PRJNA284949 https://www.ncbi.nlm.nih.gov/sra?term=SRP058722 [Overal design]RNAs from 25 out of 30 (83%) pure HG-DCIS and 10 normal breast organoids (total 35 samples) were subjected to RNA-Seq analysis by using Illumina HiSeq2000 platform Please note that description of samples employed for the NGS analyses including age, race, ER/PR immunohistochemistry results, ITIL/STIL scores and PAM50 classification is provided the 'Supplementary Data1_Samples data.xlsx' (available on Superseries record); [Treatment]'None'; [Growth]'None'; [Extraction]"RNA was isolated and purified using TRIzol reagent (Life Technologies) and RNeasy mini kit (Qiagen). RNA concentration and integrity were measured on a Agilent 2100 Bioanalyzer (Agilent Technologies). Only RNA samples with RNA integrity values (RIN) over 8.0 were considered for subsequent analysis.\nmRNA from normal breast epithelial samples and DCIS samples were processed for directional mRNA-seq library construction using the ScriptSeq v2 RNA-Seq Library Preparation Kit (Epicentre) according to the manufacturer's protocol."; [Cell type]'Source: ''tissue: normal breast epithelial organoid; age: 44; race: White; ', 'tissue: normal breast epithelial organoid; age: 19; race: Black; ', 'tissue: normal breast epithelial organoid; age: 35; race: White; ', 'tissue: normal breast epithelial organoid; age: 37; race: White; ', 'tissue: normal breast epithelial organoid; age: 43; race: Black; ', 'tissue: normal breast epithelial organoid; age: 20; race: Black; ', 'tissue: normal breast epithelial organoid; age: 38; race: White; ', 'tissue: normal breast epithelial organoid; age: 34; race: White; ', 'tissue: normal breast epithelial organoid; age: 28; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 71; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 39; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 33; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 49; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 46; race: Black; ', 'tissue: breast ductal carcinoma in situ; age: 47; race: Asian; ', 'tissue: breast ductal carcinoma in situ; age: 66; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 57; race: Hispanic; ', 'tissue: breast ductal carcinoma in situ; age: 54; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 58; race: Black; ', 'tissue: breast ductal carcinoma in situ; age: 45; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 53; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 52; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 41; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 50; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 54; race: Hispanic; ', 'tissue: breast ductal carcinoma in situ; age: 46; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 48; race: White; ', 'tissue: breast ductal carcinoma in situ; age: 82; race: Asian; ', 'tissue: breast ductal carcinoma in situ; age: 47; race: AMIndian/AlaskaNativ; ', 'tissue: breast ductal carcinoma in situ; age: 51; race: Black; ', 'tissue: breast ductal carcinoma in situ; age: 74; race: White; ' GSE55561 Homo sapiens 30 Expression profiling by array GPL11532 Gene expression profiles of PDX models with acquired resistance to endocrine treatments 2014-03-04 Acquired resistance to endocrine therapy occurs with high frequency in patients with luminal breast cancer (LBC). We report here the establishment of four patient-derived xenograft models of LBC with acquired resistance in vivo to tamoxifen and estrogen deprivation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55561 Acquired resistance to endocrine treatments is associated with tumor-specific molecular changes in patient-derived luminal breast cancer xenografts. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-13-3230 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-13-3230} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA239992 https://www.ebi.ac.uk/ena/browser/view/PRJNA239992 None [Overal design]CEL files represent expresison data generated from 5 replicates (independent mice) of the following tumor models: HBCx22 (parental), HBCx22 TamR (tamoxifen-resistant), HBCx22 OvaR (ovariectomy-resistant), HBCx34 (parental), HBCx34 TamR (tamoxifen-resistant), HBCx34 OvaR (ovariectomy-resistant); [Treatment]'NA'; [Growth]'NA'; [Extraction]'Total RNA were extracted by miRNeasy kit (Qiagen)'; [Cell type]'Source: ''model: HBCx22; resistance: N/A; tissue: luminal breast cancer tumor; ', 'model: HBCx22; resistance: ovariectomy-resistant; tissue: luminal breast cancer tumor; ', 'model: HBCx22; resistance: tamoxifen-resistant; tissue: luminal breast cancer tumor; ', 'model: HBCx34; resistance: N/A; tissue: luminal breast cancer tumor; ', 'model: HBCx34; resistance: ovariectomy-resistant; tissue: luminal breast cancer tumor; ', 'model: HBCx34; resistance: tamoxifen-resistant; tissue: luminal breast cancer tumor; ' GSE93529 Homo sapiens 8 Expression profiling by array GPL570 Mechanical cues control mutant p53 stability through a Mevalonate/RhoA axis 2017-01-11 To investigate the genes differentially expressed upon plating on top of matrixes with different stiffness, we compared the expression profiles of MDA-MB-231 breast cancer cells plated on a stiff substrate (plastic) with the same cells plated on a soft substrate (hydrogels 0.7 kPa). Keywords: expression profiling by array https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93529 Mechanical cues control mutant p53 stability through a mevalonate-RhoA axis. Nature cell biology 17.728 https://doi.org/10.1038/s41556-017-0009-8 {Nature cell biology (17.728): 10.1038/s41556-017-0009-8} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA361002 https://www.ebi.ac.uk/ena/browser/view/PRJNA361002 None [Overal design]We collected RNA from MDA-MB-231 cells plated and cultured from 2 days on a stiff substrate and on a soft substrate. Samples were then processed for total RNA extraction and hybridization on Affymetrix microarrays. Four biological replicas (A, B, C, D) were used for each condition for a total of 8 samples.; [Treatment]'MDA-MB-231 cells were cultured either on a stiff substrate or on a soft substrate in MDA-MB-231 medium.'; [Growth]'MDA-MB-231 cells were cultured in MDA-MB-231 medium (DMEM/F12 supplemented with 10% FBS, glutamine and antibiotics).'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MDA-MB-231; substrate quality: stiff; ', 'cell line: MDA-MB-231; substrate quality: soft; ' GSE80035 Homo sapiens 15 Expression profiling by array GPL10558 Gene expression profile of human fibroblasts stimulated by breast cancer cell lines secretome 2016-04-07 Normal human dermal fibroblasts (NHDF) were treated under serum-free conditions with cell culture media conditioned by breast cancer cell lines (SkBr3, MDA-MB-468, T47D) for 72 hours and subjected to gene expression profiling with Illumina platform. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80035 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA317670 https://www.ebi.ac.uk/ena/browser/view/PRJNA317670 None [Overal design]NHDF treatments with c.m. was performed on independent biological triplicates and RNA derived from each replicate was separately extracted. Three hundred ng of total RNA were used for gene expression profiling by microarray using Illumina HumanHT-12 v4 Expression BeadChips.; [Treatment]'Conditioned media (c.m.) were collected from breast cancer cell lines (SkBr3, MDA-MB-468, T47D) separately plated (1.65x10^6cells) in F25 cm2 flasks, in DMEM F/12 5% FBS/FBM 2% FBS (1:1). After cell attachment, the medium was replaced with 7 mL of serum-free MIX medium and collected at 72 hours. After collection, media were clarified by centrifugation (1,400 x g for 3 minutes). Conditioned media produced by SkBr3, MDA-MB-468, T47D were used for the treatment (72 h) of NHDF (NAF) plated in 6-wells plate at a density of 750,000 cells.'; [Growth]'Human breast cancer cell lines, cultured in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 5% fetal bovine serum (T47D) or with 10% fetal bovine serum (MDA-MB-468) or in McCoy’s medium supplemented with 10% fetal bovine serum (SkBr3), were used to stimulate the normal human fibroblast cell line NHDF cultured in Fibroblast Basal Medium (FBM) supplemented with Fibroblast Growth Medium-2 (FGM-2) Bullet kit containing 2% fetal bovine serum (FBS), 0.1% Insulin, 0.1% GA 1000, 0.1% FGF. All cell lines were cultured at 37 °C in 95% humidified air in the presence of 5% CO2.'; [Extraction]'Total RNA was extracted from treated NHDF cells using QIAzol reagent followed by a clean-up treatment with the RNeasy Mini kit by Qiagen according to manufacturer’s recommendations to remove contaminating genomic DNA. RNA integrity and purity were assessed by Bioanalyzer and concentration was evaluated using a NanoDrop 2000c spectrophotometer.'; [Cell type]'normal human dermal fibroblasts''cell line: NHDF; cell type: normal human dermal fibroblasts; conditioned medium: T47D; ', 'cell line: NHDF; cell type: normal human dermal fibroblasts; conditioned medium: MDA-MB-468; ', 'cell line: NHDF; cell type: normal human dermal fibroblasts; conditioned medium: ctrl_DMEM; ', 'cell line: NHDF; cell type: normal human dermal fibroblasts; conditioned medium: SkBr3; ', 'cell line: NHDF; cell type: normal human dermal fibroblasts; conditioned medium: ctrl_McCoy; ' GSE47375 Mus musculus 6 Expression profiling by array GPL1261 Microarray expression profiling study of Runx1-null and wild type luminal mammary epithelial cells 2013-05-25 RUNX1 encodes a RUNX family transcription factor (TF) and was recently identified as a novel mutated gene in human luminal breast cancers. We found that Runx1 is expressed in all subpopulations of murine mammary epithelial cells (MECs) except the secretory alveolar luminal cells. Conditional knockout of Runx1 in MECs by MMTV-Cre led to a decrease in luminal MECs, largely due to a profound reduction in the estrogen receptor (ER)-positive mature luminal subpopulation, a phenotype that could be rescued by loss of either Trp53 or Rb1. Mechanistically RUNX1 represses Elf5, a master regulatory TF gene for alveolar cells, and activates Foxa1, a key mature luminal TF gene involved in the ER program. Collectively, our data identified a key regulator of the ER+ luminal lineage whose disruption may contribute to development of ER+ luminal breast cancer when under the background of either TP53 or RB1 loss. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47375 RUNX1, a transcription factor mutated in breast cancer, controls the fate of ER-positive mammary luminal cells. eLife 7.551 https://doi.org/10.7554/eLife.03881 {eLife (7.551): 10.7554/eLife.03881} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA205362 https://www.ebi.ac.uk/ena/browser/view/PRJNA205362 None [Overal design]Thoracic and inguinal mammary glands from 3 MMTV-Cre;Runx1L/L;R26Y and 3 MMTV-Cre;Runx1+/+;R26Y adult virgin females were dissected out, minced and digested to single cell suspension. Runx1L is the floxed conditional knockout allele of Runx1. R26Y is a conditional YFP reporter that would be turned on upon Cre-mediated recombination. FACSaria machine was used to sort out the YFP-marked luminal epithelial cell population of each of these 6 mice. Total RNA was isolated with Qiagen RNeasy kit and subsequently amplified by Nugen V2 and applied to Affymetrix mouse genome 430 2.0 arrays.; [Treatment]'Mammary glands were minced and digested with enzyme mix to generate single cell suspensions. YFP-marked luminal epithelial cells were sorted by FACS.'; [Growth]'Mammary tissues were isolated from adult virgin female mice of their corresponding genotypes.'; [Extraction]"RNeasy kit (Qiagen, #74134) was used according to manufacturer's protocol."; [Cell type]'mammary gland luminal epithelial cells''strain/background: mixed B6/129/FVB; genotype: MMTV-Cre;Runx1+/+;R26Y; gender: female; developmental stage: adult virgin; cell type: mammary gland luminal epithelial cells; ', 'strain/background: mixed B6/129/FVB; genotype: MMTV-Cre;Runx1L/L;R26Y; gender: female; developmental stage: adult virgin; cell type: mammary gland luminal epithelial cells; ' GSE53975 Homo sapiens 12 Expression profiling by array GPL5188 Calcitriol Induces Endoplasmic Reticulum Stress Response in Breast Cancer Cells 2014-01-10 Effects of calcitriol on expressions of ER stress related genes were evaluated with microarray. Calcitriol, the active form of vitamin D, is known to induce apoptosis in cancer cells and increase intracellular calcium. Increase in cytopalsmic calcicium levels may indicate a decrease in endoplasmic reticulum (ER) calcium levels since ER is the main storage unit for calcium. Decrease in ER calcium levels are known to induce ER stress which can lead to apoptosis. However the effects of calcitriol on ER stress have not been reported before. Here we hypotesized that the cellular effects of calcitriol can be explained by induction of ER stress. We have tested this hypothesis by assessing calcitriol induced transcriptomic alterations with a focus on ER stress related genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53975 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA234099 https://www.ebi.ac.uk/ena/browser/view/PRJNA234099 None [Overal design]We analyzed MCF-7 and MDA-MB-231 cells treated with calcitriol or DMSO (Each group consists of 3 replicates) using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by Partek Genomic Suite. No technical replicates were performed.; [Treatment]'MCF-7 cells were treated with 40 μM calcitriol or 0.20% DMSO; MDA-MB-231 cells were treated with 50 μM calcitriol or 0.25% DMSO for 24 hours.'; [Growth]'All cells were grown in DMEM medium (Lonza) with 10% fetal bovine serum and %1 penicillin/streptomycin supplement and maintained in a CO2 incubator with standard incubation conditions.'; [Extraction]"RNA was isolated from the cells with RNAeasy mini kit (Qiagen) according to manufacturer's instructions."; [Cell type]'ER+ breast cancer cells', 'ER- breast cancer cells''cell line: MCF-7; cell type: ER+ breast cancer cells; treated with: 40 μM calcitriol for 24 hrs; ', 'cell line: MCF-7; cell type: ER+ breast cancer cells; treated with: 0.20% DMSO for 24 hrs; ', 'cell line: MDA-MB-231; cell type: ER- breast cancer cells; treated with: 50 μM calcitriol for 24 hrs; ', 'cell line: MDA-MB-231; cell type: ER- breast cancer cells; treated with: 0.25% DMSO for 24 hrs; ' GSE59530 Homo sapiens 40 Genome binding/occupancy profiling by high throughput sequencing GPL16791 TNFα Signaling Exposes Latent Estrogen Receptor Binding Sites in Breast Cancer Cells [ChIP-seq] 2014-07-17 The interplay between mitogenic and proinflammatory signaling pathways play key roles in determining the phenotypes and clinical outcomes of breast cancers. We have used global nuclear run-on coupled with deep sequencing to characterize the immediate transcriptional responses of MCF-7 breast cancer cells treated with estradiol, TNF?, or both. In addition, we have integrated these data with chromatin immunoprecipitation coupled with deep sequencing for estrogen receptor alpha (ER?), the pioneer factor FoxA1 and the p65 subunit of the NF-?B transcription factor. Our results indicate extensive transcriptional interplay between these two signaling pathways, which is observed for a number of classical mitogenic and proinflammatory protein-coding genes. In addition, GRO-seq has allowed us to capture the transcriptional crosstalk at the genomic locations encoding for long non-coding RNAs, a poorly characterized class of RNAs which have been shown to play important roles in cancer outcomes. The synergistic and antagonistic interplay between estrogen and TNF? signaling at the gene level is also evident in the patterns of ER? and NF-?B binding, which relocalize to new binding sites that are not occupied by either treatment alone. Interestingly, the chromatin accessibility of classical ER? binding sites is predetermined prior to estrogen treatment, whereas ER? binding sites gained upon co-treatment with TNF? require NF-?B and FoxA1 to promote chromatin accessibility de novo. Our data suggest that TNF? signaling recruits FoxA1 and NF-?B to latent ER? enhancer locations and directly impact ER? enhancer accessibility. Binding of ER? to latent enhancers upon co-treatment, results in increased enhancer transcription, target gene expression and altered cellular response. This provides a mechanistic framework for understanding the molecular basis for integration of mitogenic and proinflammatory signaling in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59530 TNFα signaling exposes latent estrogen receptor binding sites to alter the breast cancer cell transcriptome. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2015.02.001 {Molecular cell (14.548): 10.1016/j.molcel.2015.02.001} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA255509 https://www.ebi.ac.uk/ena/browser/view/PRJNA255509 https://www.ncbi.nlm.nih.gov/sra?term=SRP044607 [Overal design]Using GRO-seq and ChIP-seq (ER, FoxA1 and p65) to assay the molecular crosstalk of MCF-7 cells treated with E2, TNFa or both E2+TNFa.; [Treatment]'Prior to all treatments, the cells were grown for 3 days in phenol red-free MEM Eagle medium supplemented with 5% charcoal-dextran-treated calf serum. All treatments were performed for 40 min with 100 nM 17β-estradiol, 25 ng/mL TNFα, or both.'; [Growth]'MCF-7 breast cancer cells were obtained from the ATCC and maintained in Minimum Essential Medium Eagle supplemented with 5% calf serum.'; [Extraction]'ChIP-seq libraries were generated from two biological replicates for each condition. The immunoprecipitated DNA was purified using a MiniElute PCR Purification Kit from Qiagen. After purification, 50 ng of ChIPed DNA for each condition was used to generate libraries for deep sequencing, as previously described (Quail et al., 2008), with some modifications. Briefly, the DNA was end-repaired and a single “A”-base overhang was added using the Klenow fragment of E. coli DNA polymerase. The A-modified DNA was ligated to Illumina sequencing adaptors using the Illumina TruSeq DNA Sample Prep Kit. The ligated DNA (250-300 bp) was size-selected by agarose gel electrophoresis and purified using a Qiagen Gel Extraction Kit.\nThe size-selected fragments were amplified using Illumina TruSeq P5 and P7 PCR primers, and purified using AMPure beads (Beckman Coulter). Quality control was performed to determine the size, purity, and concentration of the final libraries, which were sequenced using an Illumina HiSeq 2000 per the manufacturer’s instructions.'; [Cell type]'ER Positive Breast Cancer Cells''cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: Vehicle; chip antibody: input; ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: E2; chip antibody: input; ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: TNFa; chip antibody: input; ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: E2+TNFa; chip antibody: input; ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: Vehicle; chip antibody: ER alpha (rabbit polyclonal generated in the Kraus Lab); ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: E2; chip antibody: ER alpha (rabbit polyclonal generated in the Kraus Lab); ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: TNFa; chip antibody: ER alpha (rabbit polyclonal generated in the Kraus Lab); ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: E2+TNFa; chip antibody: ER alpha (rabbit polyclonal generated in the Kraus Lab); ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: Vehicle; chip antibody: p65 (Abcam ab7970); ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: E2; chip antibody: p65 (Abcam ab7970); ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: TNFa; chip antibody: p65 (Abcam ab7970); ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: E2+TNFa; chip antibody: p65 (Abcam ab7970); ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: Vehicle; chip antibody: FoxA1 (Abcam ab23738); ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: E2; chip antibody: FoxA1 (Abcam ab23738); ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: TNFa; chip antibody: FoxA1 (Abcam ab23738); ', 'cell line: MCF-7; cell type: ER Positive Breast Cancer Cells; treatment: E2+TNFa; chip antibody: FoxA1 (Abcam ab23738); ' GSE54330 Homo sapiens 36 Expression profiling by array GPL18190 Interleukin-6 is a Potential Therapeutic Target in Interleukin-6 Dependent Estrogen Receptor-alpha Positive Breast Cancer [patient tumor tissue] 2014-01-23 Interleukin-6 (IL-6) is an important growth factor for estrogen receptor-alpha (ERα) positive breast cancer, and elevated serum IL-6 is associated with poor prognosis. We firstly demonstrated that pSTAT3 is the primary downstream IL-6 signaling pathway in ERα-positive breast cancer, using ten different breast cancer cell lines. Three-dimensional cultures of these cell lines were also used to develop a 17-gene IL-6 specific gene signature that could be used to identify IL-6 driven disease. This signature included a variety of genes involved in immune cell function and migration, cell growth and apoptosis, and the tumor microenvironment. To further validate this IL-6 signature, we obtained 36 human ERα-positive breast cancer tumor samples with matched serum for gene expression profiling and determination of an IL-6 pathway activation score (PAS). Patients with high IL-6 PAS were also enriched for elevated serum IL-6 (>=10 pg/ml). We then utilized a murine MCF-7 xenograft model to determine the role of IL-6 in ERα-positive breast cancer and potential anti-IL-6 therapy in vivo. When IL-6 was administered in vivo, MCF-7 cells engrafted without the need for estrogen supplementation. Subsequently, we prophylactically treated mice at MCF-7 engraftment with an anti-IL-6 antibody (siltuximab), fulvestrant or combination therapy. Siltuximab alone was able to blunt MCF-7 engraftment. Similarly, when tumors were allowed to grow to 125 mm3 before treatment, siltuximab alone demonstrated tumor regressions in 90% (9/10) of tumors. Given the established role for IL-6 in ERα+ breast cancer, this data demonstrates the potential for anti-IL-6 therapeutics. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54330 Interleukin-6 is a potential therapeutic target in interleukin-6 dependent, estrogen receptor-α-positive breast cancer. Breast cancer (Dove Medical Press) 2.044 https://doi.org/10.2147/BCTT.S92414 {Breast cancer (Dove Medical Press) (2.044): 10.2147/BCTT.S92414} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA236222 https://www.ebi.ac.uk/ena/browser/view/PRJNA236222 None [Overal design]Matched formalin-fixed paraffin-embedded (FFPE) tissue and serum from 36 ERα-positive breast tumors were purchased from Asterand USA (Detroit, MI, USA).; [Treatment]'None'; [Growth]'None'; [Extraction]'From each block four slices of 10 µm each were cut and transferred to a 1.5 ml Eppendorf tube. Paraffin was removed using Deparaffinization Solution (Qiagen). The tissue was then lyzed in proteinase K digestion (PKD) buffer (Qiagen). RNA isolation was continued using the RNeasy FFPE kit (Qiagen) according to the manufacturer’s instructions. The RNA concentration of all the samples was determined on a Nanodrop-8000 UV-Vis Spectrophotometer (Thermo Scientific). For a selection of samples, the RNA quality was determined with the RNA 6000 Nano LabChip on an Agilent 2100 Bioanalyzer (Agilent Technologies, Inc., Santa Clara, CA, USA) according to the manufacturer’s instructions. SenseRNA was generated from 200 ng of total RNA using the Sensation RNA Amplification Kit (Genisphere, Hatfield, PA, USA).'; [Cell type]'Source: ''tissue type: FFPE tumor sample; panoptic il6: 9.77; ', 'tissue type: FFPE tumor sample; panoptic il6: 24.39; ', 'tissue type: FFPE tumor sample; panoptic il6: 21.39; ', 'tissue type: FFPE tumor sample; panoptic il6: 32.18; ', 'tissue type: FFPE tumor sample; panoptic il6: 21.14; ', 'tissue type: FFPE tumor sample; panoptic il6: 24.92; ', 'tissue type: FFPE tumor sample; panoptic il6: 22.72; ', 'tissue type: FFPE tumor sample; panoptic il6: 58.16; ', 'tissue type: FFPE tumor sample; panoptic il6: 13.63; ', 'tissue type: FFPE tumor sample; panoptic il6: 38.16; ', 'tissue type: FFPE tumor sample; panoptic il6: 28.05; ', 'tissue type: FFPE tumor sample; panoptic il6: 25.8; ', 'tissue type: FFPE tumor sample; panoptic il6: 37.25; ', 'tissue type: FFPE tumor sample; panoptic il6: 96.25; ', 'tissue type: FFPE tumor sample; panoptic il6: 49.59; ', 'tissue type: FFPE tumor sample; panoptic il6: 10.65; ', 'tissue type: FFPE tumor sample; panoptic il6: 41.08; ', 'tissue type: FFPE tumor sample; panoptic il6: 112.56; ', 'tissue type: FFPE tumor sample; panoptic il6: 803.75; ', 'tissue type: FFPE tumor sample; panoptic il6: 50.53; ' GSE4006 Homo sapiens 12 Expression profiling by array GPL96 Estrogen effects on MCF-7 breast cancer cells co-expressing ERa and ERb 2006-01-10 Two subtypes of the estrogen receptor, ERalpha and ERbeta, mediate the actions of estrogens, and the majority of human breast tumors contain both ERalpha and ERbeta. To examine the possible interactions and modulatory effects of ERbeta on ERalpha activity, we have used adenoviral gene delivery to produce human breast cancer (MCF-7) cells expressing ERbeta, along with their endogenous ERalpha. We have examined the effects of ERβ expression on genome-wide gene expression by Affymetrix GeneChip microarrays. We find that ERbeta modulated estrogen gene expression on nearly 24% of E2-stimulated genes but only 8% of E2-inhibited genes. We find that ERbeta modulation is gene-specific, enhancing or counteracting ERalpha regulation for distinct subsets of estrogen target genes. Introduction of ERbeta into ERalpha-containing cells induced up/down-regulation of many estrogen target in the absence of any added ligand. In addition, ERbeta presence elicited the expression of a unique set of genes that were not regulated by ERalpha alone. ERbeta modulated the expression of genes in many functional categories, but the greatest numbers were associated with transcription factor and signal transduction pathways. Regulation of multiple components in the TGF beta, SDF1, and semaphorin pathways, may contribute to the suppression of proliferation observed with ERbeta both in the presence and absence of estrogen. Hence, ERbeta modulates ERalpha gene regulation in diverse ways that may contribute to its growth-inhibiting beneficial effects in breast cancer Keywords: modulatory effects of ERb on ERa https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE4006 Impact of estrogen receptor beta on gene networks regulated by estrogen receptor alpha in breast cancer cells. Endocrinology 3.800 https://doi.org/10.1210/en.2006-0563 {Endocrinology (3.800): 10.1210/en.2006-0563} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA95225 https://www.ebi.ac.uk/ena/browser/view/PRJNA95225 None [Overal design]MCF-7 cells expressing endogenous ERalpha were infected with adenovirus carrying either estrogen receptor beta (AdERb) or no insert (Ad) at multiplicity of infection (moi) of 5 or 50. Cells were infected with adenovirus for a period of 48hr before treatment with ligand (vehicle control or 10nM 17beta-estradiol) for a additional period of 24hr before harvest.; [Treatment]'None'; [Growth]'None'; [Extraction]'MCF-7 cells expressing endogenous ERalpha were plated in 100mm dish in 5% CD-stripped calf serum. Cells were infected with adenovirus carrying either estrogen receptor beta (AdERb) or no insert (Ad) at multiplicity of infection (moi) of 5 or 50. Cells were infected with adenovirus for a period of 48hr before treatment with ligand (vehicle control or 10nM 17beta-estradiol) for a additional period of 24hr before harvest. Total RNA was extracted using 1mL of TRIzol (Invitrogen) per 100mm dish.'; [Cell type]'Source: ''' GSE103218 synthetic construct 6 Non-coding RNA profiling by array GPL16384 MiR-1287-5p has inhibitory effects on breast cancer growth mediated by interaction with phosphoinositide 3-kinase CB 2017-08-29 Background: Non-coding RNAs and especially microRNAs have been discovered as master regulators of cancer initiation and progression. The aim of our study was to discover and characterize the function of yet uncharacterized microRNAs in human breast carcinogenesis. Methods: In an unbiased approach, we made use of a commonly used model system for breast cancer (BC) stem cells (“mammospheres”) to identify whole miRNome alterations with a special focus on previously uncharacterized miRNAs in BC. We further characterized the influence of microRNA-1287-5p, a yet uncharacterized microRNA in BC, in patient samples (n=1262) and on several hallmarks of cancer in vitro and in vivo with a special focus on triple negative BC. The molecular mode of action was further characterized using whole transcriptome analysis, in silico prediction tools, miRNA-interaction luciferase assays and pheno-copy assays. Results: We identified miR-1287-5p among many others as differentially expressed in mammospheres. Clinical validation indicated that miR-1287-5p is significantly downregulated in human BC and associated with poor prognosis. This clinical finding can be explained by miR-1287-5p mediated growth inhibitory effects, G1 cell cycle arrest, decreased anchorage-independent growth and tumor growth in vivo. Finally, we identified PIK3CB as a direct molecular interactor of miR-1287-5p and a pheno-copy factor for miR-1287-5p. Finally, targeting PI3K-signaling pathway with chemical inhibitors together with miR-1287-5p mimics increased the pharmacological growth inhibitory potential. Conclusion: In conclusion, our data identified for the first time an involvement of miR-1287-5p in human BC and suggest a potential for therapeutic interventions in hardly to treat triple negative BC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE103218 MiR-1287-5p inhibits triple negative breast cancer growth by interaction with phosphoinositide 3-kinase CB, thereby sensitizing cells for PI3Kinase inhibitors. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-019-1104-5 {Breast cancer research : BCR (5.676): 10.1186/s13058-019-1104-5} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA400558 https://www.ebi.ac.uk/ena/browser/view/PRJNA400558 None [Overal design]Comparison af adherent growing breast cancer cell lines versus mammospheres under ultra-low attachment and serum-free conditions; [Treatment]'Comparison of standard adherent growing cells compared to mammospheres in ultra-low attachment conditions.'; [Growth]"SUM159 cells were grown in Ham`s F12 containing 1 mmol/L L-glutamine, 2 mmol/L HEPES buffer, 5µg/ml insulin actrapid, 1µg/ml hydrocortisone, 1% penicillin/streptomycin ( (50 units per ml of penicillin, 50μg/ml of streptomycin) and 5% FBS gold. MCF-7 cells were grown in MEM with Earle's salts containing 2 mmol/L L-Glutamine, 1% sodium pyruvate, 1% penicillin/streptomycin and 10% FBS gold. BT474 were cultured in RPMI 1640 (with L-Glutamine), 20% FBS gold, 1% penicillin/streptomycin and 10µg/ml insulin Actrapid. For Mammospheres, the adherent growing breast cancer cell lines were dissociated into single cells using trypsin/EDTA and 2,000 single cells per well seeded in ultra-low attachment 6-well plates using serum-free MEBM medium supplemented with 1xB27 supplement, 20 ng/ml human epidermal growth factor EGF, 10 ng/ml human basic fibroblast growth factor FGF, 20 IU/ml Heparin and 1% antibiotic/antimycotic solution containing 10,000 units/mL of penicillin, 10,000 µg/mL of streptomycin, and 25 µg/mL of Gibco Amphotericin B). Cells were incubated in a 5% CO2 humidified atmosphere at 37°C."; [Extraction]'miRNeasy'; [Cell type]'breast cancer (BC) cell line''cell line: BT474; cell type: breast cancer (BC) cell line; growth type: standard adherent growing cells; ', 'cell line: MCF7; cell type: breast cancer (BC) cell line; growth type: standard adherent growing cells; ', 'cell line: SUM159; cell type: breast cancer (BC) cell line; growth type: standard adherent growing cells; ', 'cell line: BT474; cell type: breast cancer (BC) cell line; growth type: mammospheres in ultra-low attachment condition; ', 'cell line: MCF7; cell type: breast cancer (BC) cell line; growth type: mammospheres in ultra-low attachment condition; ', 'cell line: SUM159; cell type: breast cancer (BC) cell line; growth type: mammospheres in ultra-low attachment condition; ' GSE118390 Homo sapiens 1539 Expression profiling by high throughput sequencing; Other GPL9052; GPL16791 Unravelling subclonal heterogeneity and aggressive disease states in TNBC through single-cell RNA-seq 2018-08-10 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE118390 Unravelling subclonal heterogeneity and aggressive disease states in TNBC through single-cell RNA-seq. Nature communications 11.878 https://doi.org/10.1038/s41467-018-06052-0 {Nature communications (11.878): 10.1038/s41467-018-06052-0} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA485423 https://www.ebi.ac.uk/ena/browser/view/PRJNA485423 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'total nucleic acid was extracted from formalin-fixed paraffin embedded tissues using a standard protocol.\nlibraries were prepared using standard Illumina protocols.', 'Fresly collected human tumor samples were mechanically and enzymatically digested using tumor dissociation kit (Miltenyi Biotec). Single cells were sorted by flow cytometry, lysed and snap frozen on dry ice immediately.\nRNA libraries were prepared using Smart-seq2 protocol (Picelli et al., 2014)'; [Cell type]'Source: ''tissue: breast; breast cancer subtype: TNBC; ', 'breast cancer subtype: NA; cell line: CEPH1408 lymphoblastoid cell line; ', 'tissue: breast; breast cancer subtype: TNBC; patient: PT089; ', 'tissue: breast; breast cancer subtype: TNBC; patient: PT039; ', 'tissue: breast; breast cancer subtype: TNBC; patient: PT058; ', 'tissue: breast; breast cancer subtype: TNBC; patient: PT081; ', 'tissue: breast; breast cancer subtype: TNBC; patient: PT084; ', 'tissue: breast; breast cancer subtype: TNBC; patient: PT126; ' GSE32905 Mus musculus; Homo sapiens 17 Expression profiling by array GPL570; GPL1261 EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors 2011-10-12 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32905 EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors in transgenic mice. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1002723 {PLoS genetics (5.224): 10.1371/journal.pgen.1002723} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA146583 https://www.ebi.ac.uk/ena/browser/view/PRJNA146583 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'Cells were grown in DMEM/HAMF12 medium supplemented with penicillin/strptomycin, L-glutamin, 10% fetal bovine serum, 10ng/ml hEGF, 0.5µg/ml hydrocortisone and 10µg/ml insulin.', 'cells were grown in DMEM/HAMF12 medium supplemented with penicillin/strptomycin, L-glutamin, 10% fetal bovine serum, 10ng/ml hEGF, 0.5µg/ml hydrocortisone and 10µg/ml insulin'; [Extraction]'Total RNAs were extract with with the Qiagen RNeasy minikit (Qiagen), then 100 ng of total RNAs were amplified using Kit GeneChip 3’ IVT Express (Affymetrix).', 'Total RNA were extract with with the Qiagen RNeasy minikit (Qiagen), then 100 ng of total RNA were amplified using Kit GeneChip 3’ IVT Express (Affymetrix).', 'Total RNAs were extract with with the Qiagen RNeasy minikit (Qiagen), then 100 ng of total RNAs were amplified using Kit GeneChip 3’ IVT Express (Affymetrix)'; [Cell type]'expressed hTert', 'expressed hTert, Twist1 and HRasG12V', 'expressed hTert, zeb1 and HRasG12V', 'expressed hTert, Zeb2 and HRasG12V', 'luminal cell', 'basal B cell', 'Twist1 + Ras- transgenic mouse-derived metaplastic breast tumor', 'Source: ', 'expressed HRasG12V', 'expressed hTert, zeb1', 'expressed hTert, Zeb2', 'expressed hTert, Twist1''cell line: HMEC immortalized; cell type: expressed hTert; ', 'cell line: HMEC-derivatives; cell type: expressed hTert, Twist1 and HRasG12V; ', 'cell line: HMEC-derivatives; cell type: expressed hTert, zeb1 and HRasG12V; ', 'cell line: HMEC-derivatives; cell type: expressed hTert, Zeb2 and HRasG12V; ', 'cell line: MCF7; cell type: luminal cell; ', 'cell line: MDAMB157; cell type: basal B cell; ', 'cell type: Twist1 + Ras- transgenic mouse-derived metaplastic breast tumor; ', 'cell line: luminal MMTV-ErbB2-breast tumor-derived cell line; ', 'cell line: HMEC-derivatives; cell type: expressed HRasG12V; ', 'cell line: HMEC-derivatives; cell type: expressed hTert, zeb1; ', 'cell line: HMEC-derivatives; cell type: expressed hTert, Zeb2; ', 'cell line: HMEC-derivatives; cell type: expressed hTert, Twist1; ' GSE103531 Homo sapiens 12 Expression profiling by high throughput sequencing GPL16791 SILAC identifies LAD1 as an oncogenic filamin binder regulating actin dynamics in response to EGF and marking aggressive breast tumors 2017-09-06 Mutations mimicking growth factor-induced proliferation and motility characterize some aggressive subtypes of mammary tumors. To unravel novel players, we applied phosphoproteomics on untransformed mammary cells, which were pre-stimulated with the epidermal growth factor (EGF). This analysis identified ladinin-1 (LAD1), a hitherto poorly characterized protein, as a phosphor-effector of the EGF-to-ERK pathway. We report that LAD1 is essential for mammary cell proliferation and migration. LAD1 is transcriptionally induced, undergoes phosphorylation by EGF and co-localizes with actin stress fibers. Yeast 2-hybrids and co-immunoprecipitation screens revealed that LAD1 binds with filamins, actin cross-linking proteins. Co-sedimentation analyses attribute to LAD1 a role in actin treadmilling, probably in conjuction with SFN/14-3-3sigma. Depletion of LAD1 led to a decrease in viability related transcripts, and inhibited growth of mammary xenografts in an animal model. Furthermore, LAD1 is highly expressed in two aggressive subtypes of breast cancer, as well as predicts poor patient prognosis. These studies identify a new cytoskeletal component essential for signal transduction and for the acquisition of oncogenic attributes by human mammary tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE103531 SILAC identifies LAD1 as a filamin-binding regulator of actin dynamics in response to EGF and a marker of aggressive breast tumors. Science signaling 6.481 https://doi.org/10.1126/scisignal.aan0949 {Science signaling (6.481): 10.1126/scisignal.aan0949} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA401815 https://www.ebi.ac.uk/ena/browser/view/PRJNA401815 https://www.ncbi.nlm.nih.gov/sra?term=SRP117048 [Overal design]RNA-Seq – EGF treatemnt for 0, 40 and 240 minutes of HCC70 cell-line stably expressing LAD1 targeting shRNA (or scrambled control); [Treatment]'Cells were starved overnight in medium without serum and then stimulated with 50ng/ml EGF 0,40,240 minutes before sequencing'; [Growth]'HCC70 cells were cultured in RPMI Medium supplemented with 10% fetal bovine serum'; [Extraction]'RNA was extracted using the 5-prime kit and poly-A selected on magnetic beads using the TruSeq RNA Library Preparation Kit v2\nLibrary were constructed using the TruSeq RNA Library Preparation Kit v2'; [Cell type]'Source: ''cell line: HCC70; genotype/variation: stably expressing scramble shRNA control; treated with: none (untreated); ', 'cell line: HCC70; genotype/variation: stably expressing scramble shRNA control; treated with: EGF; treated with: 50ng/ml EGF for 40min; ', 'cell line: HCC70; genotype/variation: stably expressing scramble shRNA control; treated with: 50ng/ml EGF for 40min; ', 'cell line: HCC70; genotype/variation: stably expressing scramble shRNA control; treated with: 50ng/ml EGF for 240min; ', 'cell line: HCC70; genotype/variation: stably expressing LAD1 targeting shRNA; treated with: none (untreated); ', 'cell line: HCC70; genotype/variation: stably expressing LAD1 targeting shRNA; treated with: 50ng/ml EGF for 40min; ', 'cell line: HCC70; genotype/variation: stably expressing LAD1 targeting shRNA; treated with: 50ng/ml EGF for 240min; ' GSE37945 Homo sapiens 8 Expression profiling by array GPL6480 Effect of HIC1 and miR-212/132 expression on MCF7 cells 2012-05-11 To identify the target of miR-212, miR-132 and HIC1, we have employed whole genome microarray expression profiling on the human breast cancer MCF7 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37945 miR-212 and miR-132 are dispensable for mouse mammary gland development. Nature genetics 25.455 https://doi.org/10.1038/ng.2990 {Nature genetics (25.455): 10.1038/ng.2990} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA165657 https://www.ebi.ac.uk/ena/browser/view/PRJNA165657 None [Overal design]To generate miR-212/132 or HIC1 inducible MCF7 cells, doxycycline-dependent miR-212/132 or HIC1 gene expression system was used. Either Tet-ON miR-212/132 MCF7 or Tet-ON HIC1 MCF7 were treated with 1μg/ml of Doxycycline for 36 hours with EMEM containing 0.01 mg/ml bovine insulin and 10% FCS. Two independent experiments were performed.; [Treatment]'Either Tet-ON miR-212/132 MCF7 or Tet-ON HIC1 MCF7 were treated with 1μg/ml of Doxycycline and incubated for 36 hours'; [Growth]'Doxycycline-dependent gene inducible MCF7 cells were grown in EMEM medium containing 10% FCS, 0.01 mg/ml bovine insulin, Antibiotics, 100μg/ml of G418 and 100μg/ml at 37℃ in a humidified incubator with 5% CO2.Doxycycline-dependent gene inducible MCF7 cells were grown in EMEM medium containing 10% FCS, 0.01 mg/ml bovine insulin, Antibiotics, 100μg/ml of G418 and 100μg/ml at 37℃ in a humidified incubator with 5% CO2.'; [Extraction]'Total RNA was prepared using the RNeasy Kit (QIagen) following the manufacturer’s recommendations. The protocol includes on-column DNase digestion. RNA was quantified using a NanoDrop-1000 spectrophotometer.'; [Cell type]'epithelial''organ: mammary gland; breast; disease: adenocarcinoma; cell type: epithelial; treatment: Tet-ON HIC1 MCF7 cells treated with DOX; ', 'organ: mammary gland; breast; disease: adenocarcinoma; cell type: epithelial; treatment: Tet-ON HIC1 MCF7 cells treated without DOX; ', 'organ: mammary gland; breast; disease: adenocarcinoma; cell type: epithelial; treatment: Tet-ON miR-212/132 MCF7 cells treated with DOX; ', 'organ: mammary gland; breast; disease: adenocarcinoma; cell type: epithelial; treatment: Tet-ON miR-212/132 MCF7 cells treated without DOX; ' GSE18953 Homo sapiens 4 Expression profiling by array GPL9550 Effects of IGF 1 on MCF-7 breast cancer cells 2009-11-09 To characterize the effects of IGF 1 on MCF 7 breast cancer cells, we cultured pre-starved MCF 7 cells with or without 50ng/ml IGF 1 for 24 h. We then profiled gene expression changes using Human Exonic Evidence Based Oligonucleotide (HEEBO) microarrays. After stimulation, total RNA was extracted and amplified using a modified Eberwine procedure. The amplified RNA was labeled with the fluorescent dye Cy5 and pooled with Cy3 labeled reference RNA, and then the pooled RNA was hybridized onto HEEBO microarrays. After hybridization and washing, arrays were scanned on a fluorescent microscope scanner. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE18953 IGF-I induced genes in stromal fibroblasts predict the clinical outcome of breast and lung cancer patients. BMC medicine 8.285 https://doi.org/10.1186/1741-7015-8-1 {BMC medicine (8.285): 10.1186/1741-7015-8-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA123881 https://www.ebi.ac.uk/ena/browser/view/PRJNA123881 None [Overal design]An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract.; [Treatment]'None'; [Growth]'None', 'Monoculture cell conditions.; MCF - 7 and CCL - 171 cells were expanded and propagated in Dulbeccos Modified Eagles Medium (DMEM) supplemented with: 10% FBS (GIBCO, Grand Island, N.Y.), L - glutamine, 4.5 g/L glucose, 100 U/ml penicillin and 100 ug/ml streptomycin (GIBCO, Grand Island, N.Y.). For mono-culture experiments the cells were cultivated for 6 hours at 30,000 cells/cm2 in DMEM medium with 5% FBS. After 6 hours medium was changed to DMEM medium with 0.2% FBS and the cells were cultured for 48 hours(starving period). After 48 hours medium was changed to a fresh DMEM medium with 0.2% FBS and the cells were cultured for 24 hours.; Protocol Type = Biological Sample; Performer: Michal,,Rajski'; [Extraction]'StratageneRef; RNA for the reference was pooled from 11 cell lines - obtained from Stratagene.; Protocol Type = Biological Sample; Performer: Michal,,Rajski', "RNeasy; Total RNA was isolated using the RNeasy mini kit (QIAGEN), according to the manufacturer's instructions.; Protocol Type = Extract preparation; Performer: Michal,,Rajski"; [Cell type]'Source: ''reference: stratagene human reference plus doping controls.; ', 'cell line: MCF-7 breast cancer cells; ' GSE128796 Mus musculus; Homo sapiens 720 Other; Expression profiling by high throughput sequencing GPL18573; GPL19057 Bulk DNA seq, GTO-seq, and RNA-seq with murin and human cell lines 2019-03-25 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE128796 None None None None None 'genomic DNA', 'total RNA', 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA528890 https://www.ebi.ac.uk/ena/browser/view/PRJNA528890 None [Overal design]Refer to individual Series; [Treatment]'No treatment', '50000 KPC1199-EGFP cells in matrigel were injected orthotopically into the pancreas of 6-8 week old C57BL/6 male mice. Tumors were allowed to grow for 6-8 weeks before tumors were extracted.'; [Growth]'Cells were cultured in respective media at 37C, 5% CO2', 'KPC1199-EGFP cells were thawed and passaged in DMEM supplemented with 10% Fetal Bovine Serum, 1% Pencillin/streptomycin'; [Extraction]"Cells were trypsinized and spun down to get a pellet. The cells were processed using Qiagen DNeasy blood and tissue kit.\n2ug of DNA was fragmented to 400bp using Covaris sonicator. Following this, libraries for sequencing were prepared by subjecting the resulting DNA fragments to end-repair, 3′ adenylation and ligation of TruSeq barcoded adapters. After ligation, DNA fragments were size selected using Ampure XP beads. A 0.75 ratio of beads to sample was used to select fragments larger than 200bp and avoid adapter dimers. These fragments were further amplified by PCR, cleaned using Qiaquick PCR Purification Kit and then once again size selected using Ampure XP beads with a 0.75 ratio of beads to sample. The final libraries were then quantified on Nanodrop and Bioanalyzer using Agilent's High Sensitivity DNA Analysis Kit. 10nM of each sample was then pooled together and the resulting pool was then sequenced single read 76bp length on the Illumina NextSeq", 'Cells were trypsinized, diluted to 1000cells/ml and handpicked as single cells in 10x Lysis buffer\nSingle cells isolated into 10x Lysis Buffer with Rnase inhibitor were processed for mRNA transcription for first strand synthesis and cDNA amplification following SMART-Seq2 protocol. Samples were then treated ionically to fragment gDNA and cDNA to 400-700bp fragments. Later gDNA was amplified using SeqXE kit from Sigma Aldirch using manufacturer instructions. Libraries were made by end repair, Adenylation, Adapter ligation and PCR steps.', "Cells were trypsinized and spun down to get a pellet. The cells were processed using Qiagen Rneasy kit. RNA was qunatified and then a reverse transcription step was done using Oligo dT primer and Clontech Reverse Transcriptase to generate cDNA. 2ug of cDNA was used for library preparation\n2ug of cDNA was fragemented to 400bp using Covaris somicator. Following this, libraries for sequencing were prepared by subjecting the resulting DNA fragments to end-repair, 3′ adenylation and ligation of TruSeq barcoded adapters. After ligation, DNA fragments were size selected using Ampure XP beads. A 0.75 ratio of beads to sample was used to select fragments larger than 200bp and avoid adapter dimers. These fragments were further amplified by PCR, cleaned using Qiaquick PCR Purification Kit and then once again size selected using Ampure XP beads with a 0.75 ratio of beads to sample. The final libraries were then quantified on Nanodrop and Bioanalyzer using Agilent's High Sensitivity DNA Analysis Kit. 10nM of each sample was then pooled together and the resulting pool was then sequenced single read 76bp length on the Illumina NextSeq", "Adherent cells were trypsinzed, counted and resuspended in NST-DAPI buffer. Cells were sorted on flow cytometer based on the DNA content to obtain single nuclei for scWGS\nSingle cells isolated into 10x Lysis and Fragmentation Buffer were processed for genomic DNA amplification using SeqXE kit from Sigma Aldrich. Manufacturer's instructions very followed for gDNA amplification. Library preparation was done by end repair, adenylation, adapter ligation and PCR steps.", "Primary tumors were dissociated using collagenase D and trypsin. They were treated with ACK lysis buffer to remove contaminating red blood cells. These dissociated cells were stained with EpCam, CD45 antibodies. Single cells were isolated by flow cytometry for GFP+, EpCAM+, GFP+EpCAM+ and CD45+ from primary tumors. GFP+ cells were isolated from various metastases\nSingle cells isolated into 10x Lysis Buffer with Rnase inhibitor. Next they were processed for mRNA transcription for first strand synthesis using Oligo-dT primer and cDNA generated is amplified for 15 cycles following SMART-Seq2 PCR primers. Samples were then treated ionically to fragment gDNA and cDNA to 400-700bp fragments. Later gDNA was amplified using SeqXE kit from Sigma Aldirch using manufacturer instructions. resulting cDNA and gDNA fragments are quantified. Following this, libraries for sequencing were prepared by subjecting the 1ug of gDNA and cDNA fragments to end-repair, 3′ adenylation and ligation of TruSeq barcoded adapters. After ligation, DNA fragments were size selected using Ampure XP beads. A 0.75 ratio of beads to sample was used to select fragments larger than 200bp and avoid adapter dimers. These fragments were further amplified by PCR, cleaned using Qiaquick PCR Purification Kit and then once again size selected using Ampure XP beads with a 0.75 ratio of beads to sample. The final libraries were then quantified on Nanodrop and Bioanalyzer using Agilent's High Sensitivity DNA Analysis Kit. 10nM of each sample was then pooled together and the resulting pool was then sequenced single read 76bp length on the Illumina NextSeq", "Trypsinzed to create suspension of adherent cells\nSingle cells were isolated and cDNA amplified on medium sized IFC from Fluidigm on the C1 system following the manufacturer's instructions. Library was constucted using nextera XT kit again following the guildlines from Fluidigm"; [Cell type]'Adherent cell line', 'Suspension cell line', 'Source: ', 'Pancreatic cancer tumor cell line', 'Stromal', 'Tumor', 'Pancreatic cancer''cell line: A375 Melanoma cancer cell line; cell line source: Skin; cell type: Adherent cell line; labelling for flow: DMEM with 10% FBS and 1% Pencillin/Streptomycin; ', 'cell line: BT549 Triple negative breast cancer cell line; cell line source: Breast; cell type: Adherent cell line; labelling for flow: RPMI with 10% FBS and 1% Pencillin/Streptomycin; ', 'cell line: SKBR3 Her2 overexpresson breast cancer cell line; cell line source: Breast; cell type: Adherent cell line; labelling for flow: DMEM with 10% FBS and 1% Pencillin/Streptomycin; ', 'cell line: 315A Diploid lymphoblastoid cell line; cell line source: Lymphoblastoid; cell type: Suspension cell line; labelling for flow: RPMI with 10% FBS and 1% Pencillin/Streptomycin; ', 'cell line: A375_Melanoma cancer cell line; cell line source: Skin; culture type: Adherent cell line; media: DMEM with 10% FBS and 1% Pencillin/Streptomycin; molecule type: genomic DNA and mRNA; ', 'cell line: BT549_Triple negative breast cancer cell line; cell line source: Breast; culture type: Adherent cell line; media: RPMI with 10% FBS and 1% Pencillin/Streptomycin; molecule type: genomic DNA and mRNA; ', 'cell line: SKBR3_Her2 overexpresson breast cancer cell line; cell line source: Breast; culture type: Adherent cell line; media: DMEM with 10% FBS and 1% Pencillin/Streptomycin; molecule type: genomic DNA and mRNA; ', 'cell line: 315A_Diploid lymphoblastoid cell line; cell line source: Lymphoblastoid; culture type: Suspension cell line; media: RPMI with 10% FBS and 1% Pencillin/Streptomycin; molecule type: genomic DNA and mRNA; ', 'cell line: A375 Melanoma cancer cell line; cell line source: Skin; cell type: Adherent cell line; culture condition: DMEM with 10% FBS and 1% Pencillin/Streptomycin; ', 'cell line: BT549 Triple negative breast cancer cell line; cell line source: Breast; cell type: Adherent cell line; culture condition: RPMI with 10% FBS and 1% Pencillin/Streptomycin; ', 'cell line: SKBR3 Her2 overexpresson breast cancer cell line; cell line source: Breast; cell type: Adherent cell line; culture condition: DMEM with 10% FBS and 1% Pencillin/Streptomycin; ', 'cell line: 315A Diploid lymphoblastoid cell line; cell line source: Lymphoblastoid; cell type: Suspension cell line; culture condition: RPMI with 10% FBS and 1% Pencillin/Streptomycin; ', 'strain background: C57BL\\6; cell line: KPC1199EGFP; cell type: Pancreatic cancer tumor cell line; labelling for flow: EGFP expression; molecule subtype: genomic DNA in nuclei; ', 'strain: C57Bl/6; Sex: male; tumor type: Primary; tissue: Pancreas; cell type: Stromal; marker: CD45, Calcien Violet for Live/Dead; molecule type: genomic DNA and mRNA; ', 'strain: C57Bl/6; Sex: male; tumor type: Primary; tissue: Pancreas; cell type: Tumor; marker: GFP, EpCam, Calcien Violet for Live/Dead; molecule type: genomic DNA and mRNA; ', 'strain: C57Bl/6; Sex: male; tumor type: Primary; tissue: Pancreas; cell type: Tumor; marker: EpCam, Calcien Violet for Live/Dead; molecule type: genomic DNA and mRNA; ', 'strain: C57Bl/6; Sex: male; tumor type: Metastasis; tissue: Peritoneum; cell type: Tumor; marker: GFP, Calcien Violet for Live/Dead; molecule type: genomic DNA and mRNA; ', 'strain: C57Bl/6; Sex: male; tumor type: Primary; tissue: Pancreas; cell type: Tumor; marker: GFP, Calcien Violet for Live/Dead; molecule type: genomic DNA and mRNA; ', 'strain: C57Bl/6; Sex: male; tumor type: Metastasis; tissue: Kidney; cell type: Tumor; marker: GFP, Calcien Violet for Live/Dead; molecule type: genomic DNA and mRNA; ', 'strain: C57Bl/6; Sex: male; tumor type: Metastasis; tissue: Liver; cell type: Tumor; marker: GFP, Calcien Violet for Live/Dead; molecule type: genomic DNA and mRNA; ', 'strain: C57Bl/6; Sex: male; tumor type: Metastasis; tissue: Spleen; cell type: Tumor; marker: GFP, Calcien Violet for Live/Dead; molecule type: genomic DNA and mRNA; ', 'strain background: C57BL\\6; cell type: Pancreatic cancer; genotype/variation: EGFP expression; ' GSE124933 Mus musculus 10 Expression profiling by high throughput sequencing GPL13112 Gene expression profiling of alveolar macrophages from normal lung and metastasis-associated macrophages 2019-01-10 To profile the gene expression of macrophages associated with lung metastases and identify mechanisms by which macrophages regulate metasetatic growth https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124933 Induction of interferon signaling and allograft inflammatory factor 1 in macrophages in a mouse model of breast cancer metastases. Wellcome open research None https://doi.org/10.12688/wellcomeopenres.16569.2 {Wellcome open research (None): 10.12688/wellcomeopenres.16569.2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA514343 https://www.ebi.ac.uk/ena/browser/view/PRJNA514343 https://www.ncbi.nlm.nih.gov/sra?term=SRP178254 [Overal design]Lung metastases were induced by tail vein injection of syngenic mouse mammary tumor cells, dissected and processed in parallel with normal lungs for FACS sorting for the CD11B+ and CD11C+ subsets of CD45+;F4/80+;LY6C-;MRC1+;FSC hi cells. RNA from these cells was analyzed by RNA-seq.; [Treatment]'None'; [Growth]'None'; [Extraction]'Lung metastases were induced by tail vein injection of 1 x 106 E0771-LG to syngenic C57BL6/J female mice (6-8 wk old). Lungs were perfused with PBS through the right ventricle, dissected and minced. Lung metastases (<1 mm in diameter) were dissected with aid of a dissection microscope and pooled from 2-4 mice. The tissues were then digested with an enzyme mix of Liberase DL (Sigma-Aldrich 5466202001, 0.52 U/mL) and TL (Sigma-Aldrich 5401020001, 0.26 U/mL) and DNase I (Sigma-Aldrich DN25, 150 µg/mL) diluted in basal DMEM medium with rotation for 30 min at 37°C and filtered (70-µm member). Transcription inhibitors alpha-amanitin (Sigma-Aldrich A2263, 5 µg/mL) and actinomycin D (Sigma-Aldrich A1410, 1 µg/mL) were also added in the digestion buffer. Red blood cells were removed by incubation with RBC lysis buffer (Biolegend, 420301) for 5 min on ice (once for tissues and twice for blood). Cells were stained with DAPI to distinguish live/dead cells and were blocked with anti-mouse CD16/CD32 antibody (BD Biosciences 553141) for 10 min on ice, followed by antibody staining. Target cells were sorted directly into the Extraction Buffer in the Picopure RNA isolation kit (Arcturus KIT0202) for isolation.\nRNA sequencing of mouse total RNA was performed at Beijing Genomic Institute, using the Ovation® RNA-Seq System V2 kit for library construction, pair-end 100 bp and Hiseq 4000, which generated 60-80M reads per sample.'; [Cell type]'CD45+;F4/80+;LY6C-;MRC1+;FSC hi;CD11C-;CD11B+ macrophages', 'CD45+;F4/80+;LY6C-;MRC1+;FSC hi;CD11C+;CD11B- macrophages''cell type: CD45+;F4/80+;LY6C-;MRC1+;FSC hi;CD11C-;CD11B+ macrophages; tissue: Lung; age: 8-10 weeks; genotype: Wild type; ', 'cell type: CD45+;F4/80+;LY6C-;MRC1+;FSC hi;CD11C+;CD11B- macrophages; tissue: Lung; age: 8-10 weeks; genotype: Wild type; ' GSE76608 Homo sapiens 8 Expression profiling by high throughput sequencing GPL18460 Expression profiling of MCF-7 cells with 10nM treatment of TCDD 2016-01-06 The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that is regulated by environmental toxicants that function as AHR agonists such as 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD). L-Type Amino Acid Transporter 1 (LAT1) is a leucine uptake transporter that is overexpressed in cancer. The regulation of LAT1 by AHR in MCF-7 and MDA-MB-231 breast cancer cells (BCCs) was investigated in this report. Ingenuity pathway analysis (IPA) revealed a significant association between TCDD-regulated genes (TRGs) and molecular transport. Overlapping the TCDD-RNA-Seq dataset in this report with a published TCDD-ChIP-seq dataset identified that LAT1 was a direct TCDD/AHR gene target. Short interfering RNA (siRNA)-directed knockdown of AHR confirmed that TCDD-stimulated increases in LAT1 mRNA and protein required AHR. TCDD-stimulated increases in LAT1 mRNA was also inhibited by the AHR antagonist CH-223191. Upregulation of LAT1 by TCDD coincided with increases in leucine uptake by MCF-7 cells in response to TCDD. Chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR) assays revealed increases in AHR, AHR nuclear translocator (ARNT) and p300 binding and histone H3 acetylation at an AHR binding site in the LAT1 gene in response to TCDD. In MDA-MB-231 cells, which exhibit high levels of endogenous AHR activity, the levels of endogenous LAT1 mRNA and protein were reduced in response to knockdown of AHR with AHR-siRNA. The regulation of LAT1 by AHR stimulated MDA-MB-231 proliferation. Collectively, these findings have provided a deeper mechanistic understanding of extrinsic and intrinsic regulation of LAT1 by AHR. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76608 Aryl hydrocarbon receptor (AHR) regulation of L-Type Amino Acid Transporter 1 (LAT-1) expression in MCF-7 and MDA-MB-231 breast cancer cells. Biochemical pharmacology 4.825 https://doi.org/10.1016/j.bcp.2016.02.020 {Biochemical pharmacology (4.825): 10.1016/j.bcp.2016.02.020} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA308136 https://www.ebi.ac.uk/ena/browser/view/PRJNA308136 https://www.ncbi.nlm.nih.gov/sra?term=SRP068163 [Overal design]Expression profiling of four replicates of MCF-7 cells treated with 10nM TCDD were compared to expression profiles of four control replicates of MCF-7 cells treated with DMSO by RNA-Seq; [Treatment]'6hrs treatment with either vehicle (DMSO) or TCDD'; [Growth]'250,000 MCF-7 cells were seeded in 35 mm plates in DMEM supplemented with 10 % FBS for 24 hr, followed by overnight serum-starvation in phenol red-free DMEM'; [Extraction]'Total RNA purification kits from Qiagen (Valencia, CA) were used according to manufacturers instructions\nLibraries were prepared from 1 µg of total RNA using a TruSeq RNA Prep Kit (Illumina Inc., San Diego, CA)'; [Cell type]'Source: ''treatment: DMSO; concentration: N/A; ', 'treatment: TCDD; concentration: 10nM; ' GSE150576 Homo sapiens 288 Expression profiling by array; Protein profiling by protein array GPL16233; GPL20078; GPL28470 AKT/mTOR/HER/PI3K family genes and phospho-proteins as predictors of pCR for early stage breast cancer patients treated with the AKT inhibitor MK2206 in the I-SPY 2 TRIAL 2020-05-14 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE150576 Mechanism of action biomarkers predicting response to AKT inhibition in the I-SPY 2 breast cancer trial. NPJ breast cancer 32.43 https://doi.org/10.1038/s41523-020-00189-2 {NPJ breast cancer (32.43): 10.1038/s41523-020-00189-2} 'total RNA', 'protein' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA632842 https://www.ebi.ac.uk/ena/browser/view/PRJNA632842 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'not provided'; [Cell type]'Source: ''her2: 1; hr: 1; pcr: 0; arm: MK2206 Arm; ', 'her2: 0; hr: 0; pcr: 0; arm: MK2206 Arm; ', 'her2: 0; hr: 1; pcr: 0; arm: MK2206 Arm; ', 'her2: 0; hr: 0; pcr: 1; arm: MK2206 Arm; ', 'her2: 1; hr: 1; pcr: 1; arm: MK2206 Arm; ', 'her2: 1; hr: 0; pcr: 1; arm: MK2206 Arm; ', 'her2: 1; hr: 0; pcr: 0; arm: MK2206 Arm; ', 'her2: 0; hr: 1; pcr: 1; arm: MK2206 Arm; ', 'her2: 1; hr: 1; pcr: 0; arm: Control Arm; ', 'her2: 1; hr: 0; pcr: 0; arm: Control Arm; ', 'her2: 1; hr: 1; pcr: 1; arm: Control Arm; ', 'her2: 0; hr: 1; pcr: 0; arm: Control Arm; ', 'her2: 0; hr: 0; pcr: 1; arm: Control Arm; ', 'her2: 0; hr: 0; pcr: 0; arm: Control Arm; ', 'her2: 0; hr: 1; pcr: 1; arm: Control Arm; ', 'her2: 0; hr: 0; pcr: -1; arm: Control Arm; ', 'her2: 1; hr: 0; pcr: 1; arm: Control Arm; ', 'tissue: breast cancer biopsy; her2: 0; hr: 1; pcr: 0; arm: Control arm; rppa normalization key: RPPA.1; ', 'tissue: breast cancer biopsy; her2: 0; hr: 0; pcr: 1; arm: Control arm; rppa normalization key: RPPA.1; ', 'tissue: breast cancer biopsy; her2: 1; hr: 1; pcr: 0; arm: Control arm; rppa normalization key: RPPA.1; ', 'tissue: breast cancer biopsy; her2: 1; hr: 1; pcr: 0; arm: MK2206 arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 0; hr: 1; pcr: 0; arm: MK2206 arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 0; hr: 0; pcr: 0; arm: Control arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 0; hr: 1; pcr: 0; arm: Control arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 1; hr: 0; pcr: 1; arm: MK2206 arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 0; hr: 0; pcr: 1; arm: MK2206 arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 0; hr: 1; pcr: 1; arm: MK2206 arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 0; hr: 0; pcr: 1; arm: Control arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 0; hr: 0; pcr: 0; arm: MK2206 arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 1; hr: 0; pcr: 0; arm: MK2206 arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 1; hr: 1; pcr: 1; arm: MK2206 arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 1; hr: 0; pcr: 1; arm: Control arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 1; hr: 0; pcr: 0; arm: Control arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 0; hr: 1; pcr: 1; arm: Control arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 1; hr: 1; pcr: 0; arm: Control arm; rppa normalization key: RPPA.2; ', 'tissue: breast cancer biopsy; her2: 1; hr: 1; pcr: 1; arm: Control arm; rppa normalization key: RPPA.2; ' GSE87008 Homo sapiens 51 Expression profiling by array GPL570 CDK4 phosphorylation status and a linked gene expression profile predict sensitivity to Palbociclib 2016-09-16 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE87008 CDK4 phosphorylation status and a linked gene expression profile predict sensitivity to palbociclib. EMBO molecular medicine 10.624 https://doi.org/10.15252/emmm.201607084 {EMBO molecular medicine (10.624): 10.15252/emmm.201607084} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA343224 https://www.ebi.ac.uk/ena/browser/view/PRJNA343224 None [Overal design]Refer to individual Series; [Treatment]'Cells were kept in normal culture medium without treatment.', 'Not applicable'; [Growth]'Cells lines were cultured in the indicated medium and split following the indicated ratios (see characteristics). Cells were incubated in 10-cm petri dishes at 37 ºC at 5% CO2 until 70% confluency was reached. Pellets were harvested, flash frozen, and stored at -80 ºC for no more than one week until nucleic acid extraction.', 'Not applicable'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: BT20 breast cancer cell line; culture medium used: DMEM 10 % serum; split ratio: 1 out of 3; molecular subtype: Basal; pd0332991 ic50 (brdu): 3; ', 'cell line: BT474 breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 3; molecular subtype: Her2; pd0332991 ic50 (brdu): 15; ', 'cell line: BT549 breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 3; molecular subtype: Basal; pd0332991 ic50 (brdu): >1000; ', 'cell line: HCC1500 breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 3; molecular subtype: Basal; pd0332991 ic50 (brdu): 10; ', 'cell line: HCC1569 breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 3; molecular subtype: Her2; pd0332991 ic50 (brdu): >1000; ', 'cell line: HCC1806 breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 5; molecular subtype: Basal; pd0332991 ic50 (brdu): 10; ', 'cell line: HCC1937 breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 3; molecular subtype: Basal; pd0332991 ic50 (brdu): >1000; ', 'cell line: HCC1954 breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 5; molecular subtype: Her2; pd0332991 ic50 (brdu): 25; ', 'cell line: HCC202 breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 2; molecular subtype: Her2; pd0332991 ic50 (brdu): 25; ', 'cell line: HCC38 breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 3; molecular subtype: Basal; pd0332991 ic50 (brdu): 15; ', 'cell line: HCC70 breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 4; molecular subtype: Basal; pd0332991 ic50 (brdu): >1000; ', 'cell line: MCF7 breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 3; molecular subtype: Lum; pd0332991 ic50 (brdu): 15; ', 'cell line: MDAMB134VI breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 3; molecular subtype: Lum; pd0332991 ic50 (brdu): 3; ', 'cell line: MDAMB231 breast cancer cell line; culture medium used: DMEM 10 % serum; split ratio: 1 out of 5; molecular subtype: Basal; pd0332991 ic50 (brdu): 15; ', 'cell line: MDAMB361 breast cancer cell line; culture medium used: DMEM 10 % serum; split ratio: 1 out of 3; molecular subtype: Her2; pd0332991 ic50 (brdu): 10; ', 'cell line: MDAMB436 breast cancer cell line; culture medium used: DMEM 10 % serum; split ratio: 1 out of 5; molecular subtype: Basal; pd0332991 ic50 (brdu): >1000; ', 'cell line: MDAMB468 breast cancer cell line; culture medium used: DMEM 10 % serum; split ratio: 1 out of 5; molecular subtype: Basal; pd0332991 ic50 (brdu): >1000; ', 'cell line: SKBR3 breast cancer cell line; culture medium used: DMEM 10 % serum; split ratio: 1 out of 3; molecular subtype: Her2; pd0332991 ic50 (brdu): 15; ', 'cell line: T47D breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 3; molecular subtype: Lum; pd0332991 ic50 (brdu): 15; ', 'cell line: ZR751 breast cancer cell line; culture medium used: RPMI 10% serum; split ratio: 1 out of 3; molecular subtype: Her2; pd0332991 ic50 (brdu): 15; ', 'grade: 3; er: 0; pr: 0; her2: 1; cellularity: 30; ki67: 50; tissue: breast cancer tumor; molecular subtype: Her2; ', 'grade: 3; er: 0; pr: 0; her2: 1; cellularity: 70; ki67: 30; tissue: breast cancer tumor; molecular subtype: Her2; ', 'grade: 2; er: 0; pr: 0; her2: 1; cellularity: 30; ki67: 50; tissue: breast cancer tumor; molecular subtype: Her2; ', 'grade: 3; er: 0; pr: 0; her2: 1; cellularity: 35; ki67: 80; tissue: breast cancer tumor; molecular subtype: Her2; ', 'grade: 2; er: 0; pr: 0; her2: 1; cellularity: 30; ki67: 30; tissue: breast cancer tumor; molecular subtype: Her2; ', 'grade: 3; er: 0; pr: 0; her2: 1; cellularity: 30; ki67: NA; tissue: breast cancer tumor; molecular subtype: Her2; ', 'grade: 1; er: 1; pr: 1; her2: 0; cellularity: 30; ki67: <10; tissue: breast cancer tumor; molecular subtype: LumA; ', 'grade: 1; er: 1; pr: 1; her2: 0; cellularity: 50; ki67: 10; tissue: breast cancer tumor; molecular subtype: LumA; ', 'grade: 1; er: 1; pr: 1; her2: 0; cellularity: 30; ki67: 5; tissue: breast cancer tumor; molecular subtype: LumA; ', 'grade: 3; er: 1; pr: 1; her2: 0; cellularity: 40; ki67: 50; tissue: breast cancer tumor; molecular subtype: LumB; ', 'grade: 3; er: 1; pr: 1; her2: 0; cellularity: 40; ki67: 40; tissue: breast cancer tumor; molecular subtype: LumB; ', 'grade: 3; er: 1; pr: 1; her2: 0; cellularity: 50; ki67: 80; tissue: breast cancer tumor; molecular subtype: LumB; ', 'grade: 3; er: 1; pr: 1; her2: 0; cellularity: 40; ki67: 30; tissue: breast cancer tumor; molecular subtype: LumB; ', 'grade: 3; er: 1; pr: 1; her2: 0; cellularity: 50; ki67: 40; tissue: breast cancer tumor; molecular subtype: LumB; ', 'grade: 3; er: 1; pr: 1; her2: 0; cellularity: 70; ki67: 30; tissue: breast cancer tumor; molecular subtype: LumB; ', 'grade: 3; er: 1; pr: 1; her2: 0; cellularity: 80; ki67: 20; tissue: breast cancer tumor; molecular subtype: LumB; ', 'grade: 3; er: 1; pr: 1; her2: 0; cellularity: 60; ki67: 30; tissue: breast cancer tumor; molecular subtype: LumB; ', 'grade: 3; er: 1; pr: 1; her2: 0; cellularity: 80; ki67: 80; tissue: breast cancer tumor; molecular subtype: LumB; ', 'grade: 3; er: 0; pr: 0; her2: 0; cellularity: 90; ki67: 70; tissue: breast cancer tumor; molecular subtype: TN; ', 'grade: 3; er: 0; pr: 0; her2: 0; cellularity: 80; ki67: 95; tissue: breast cancer tumor; molecular subtype: TN; ', 'grade: 3; er: 0; pr: 0; her2: 0; cellularity: 40; ki67: 90; tissue: breast cancer tumor; molecular subtype: TN; ', 'grade: 3; er: 0; pr: 0; her2: 0; cellularity: 50; ki67: 90; tissue: breast cancer tumor; molecular subtype: TN; ', 'grade: 3; er: 0; pr: 0; her2: 0; cellularity: 80; ki67: 40; tissue: breast cancer tumor; molecular subtype: TN; ', 'grade: 3; er: 0; pr: 0; her2: 0; cellularity: 40; ki67: 80; tissue: breast cancer tumor; molecular subtype: TN; ', 'grade: 3; er: 0; pr: 0; her2: 0; cellularity: 80; ki67: 50; tissue: breast cancer tumor; molecular subtype: TN; ', 'grade: 3; er: 0; pr: 0; her2: 0; cellularity: 80; ki67: 70; tissue: breast cancer tumor; molecular subtype: TN; ', 'grade: 3; er: 0; pr: 0; her2: 0; cellularity: 70; ki67: 80; tissue: breast cancer tumor; molecular subtype: TN; ' GSE81217 Homo sapiens 24 Expression profiling by array GPL571 Gene expression data from MCF7 breast adenocarcinoma cells treated with prolactin and/or bufexamac 2016-05-06 The hormone prolactin is implicated in the pathogenesis of breast cancer, and a subset of prolactin-induced gene expression is mediated by HDAC6 activity. The NSAID, bufexamac, is a fairly specific inhibitor of HDAC6 and HDAC10. We used bufexamac in combination with prolactin treatment in MCF7 cells to determine differential expression under these conditions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE81217 HDAC6 Deacetylates HMGN2 to Regulate Stat5a Activity and Breast Cancer Growth. Molecular cancer research : MCR 4.484 https://doi.org/10.1158/1541-7786.MCR-16-0109 {Molecular cancer research : MCR (4.484): 10.1158/1541-7786.MCR-16-0109} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA320900 https://www.ebi.ac.uk/ena/browser/view/PRJNA320900 None [Overal design]MCF7 cells were serum starved for 24 hours prior to treatment with bufexamac and/or prolactin, and subsequent RNA extraction.; [Treatment]'Cells were then treated for 4 hours with either DMSO (0.1%) or Bufexamac (100 uM) before stimulation with prolactin (PRL; 250 ng/mL). After 2 hours PRL stimulation, cells were washed with PBS and RNA was extracted.'; [Growth]'Prior to RNA isolation, MCF7 cells were plated in DMEM with 10% FBS at 60% confluency in 6 cm plates and incubated for 24 hours followed by an additional 24 hours of serum starvation in DMEM and 1X ITS Liquid Media Supplement.'; [Extraction]'RNA was extracted using the MagMAX-96 for Microarrays Total RNA Isolation Kit (Invitrogen, Life Technologies, Carlsbad, CA) in an automated fashion using the magnetic particle processors MagMAX Express. RNA purity was judged by spectrophotometry at 260, 270, and 280 nm. RNA integrity was assessed by running 1 µL of every sample in RNA 6000 Nano LabChips on the 2100 Bioanalyzer (Agilent Technologies, Foster City, CA).'; [Cell type]'epithelial''cell line: MCF7; gender: female; tissue: breast; cell type: epithelial; cancer type: breast adenocarcinoma; ' GSE62074 Homo sapiens 7 Expression profiling by high throughput sequencing GPL11154 Mutation independent activation of the Notch pathway is associated with Lapatinib resistance in Her2+ breast cancer cell lines 2014-10-06 We compared untreated HCC1419 cells with Lapatinib resistant HCC1419 cells that were either treated with Lapatinib for only 9 days before harvesting (drug tolerant persisters, DTPs) or were growing in the presence of Lapatinib (>70 days) (drug tolerant expanded persisters, DTEPs). We show that the Notch pathway is significantly over-expressed in DTEPs when compared to untreated cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE62074 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA263155 https://www.ebi.ac.uk/ena/browser/view/PRJNA263155 https://www.ncbi.nlm.nih.gov/sra?term=SRP048664 [Overal design]RNA-Seq of HCC1419 cells either untreated, treated with 1μM Lapatinib for 9 days or treated with 1μM Lapatinib for greater than 70 days; [Treatment]'None'; [Growth]'HCC1419 cells (ATCC, CRL-2326, purchased 1/31/11) were grown in RPMI containing 1% penicillin streptomycin (PenStrep) and 10% Gibco certified fetal bovine serum (FBS) (Invitrogen) (RPMI-complete) conditioned with mouse embryonic fibroblasts (MEF). Media was changed every 3 days.'; [Extraction]'Trizol + RNEasy cleanup, followed by ribozero rRNA depletion\nStrand-specific dUTP followed by TruSeq DNA library prep kit'; [Cell type]'Source: ''cell line: HCC1419; treatment: untreated; sample id: par_mg01; ', 'cell line: HCC1419; treatment: untreated; sample id: par_mg03; ', 'cell line: HCC1419; treatment: 1μM Lapatinib 9 days; sample id: dtp_mg02; ', 'cell line: HCC1419; treatment: 1μM Lapatinib 9 days; sample id: dtp_mg05; ', 'cell line: HCC1419; treatment: 1μM Lapatinib indefinitely; sample id: dep_mgA6; ', 'cell line: HCC1419; treatment: 1μM Lapatinib indefinitely; sample id: dep_mg07; ', 'cell line: HCC1419; treatment: 1μM Lapatinib indefinitely; sample id: dep_mg08; ' GSE162069 Homo sapiens 14 Expression profiling by high throughput sequencing GPL16791 Ferroptotic cell death triggered by conjugated linolenic acids is mediated by ACSL1 2020-11-24 Ferroptosis is associated with lipid hydroperoxides generated by oxidation of polyunsaturated acyl chains. Lipid hydroperoxides are reduced by glutathione peroxidase 4 (GPX4) and GPX4 inhibitors induce ferroptosis. However, the therapeutic potential of triggering ferroptosis in cancer cells with polyunsaturated fatty acids is unknown. We identified conjugated linoleates including α-eleostearic acid (αESA) as novel ferroptosis inducers. αESA did not alter GPX4 activity but was incorporated into cellular lipids and promoted lipid peroxidation and cell death in diverse cancer cell types. αESA-triggered death was mediated by acyl-CoA synthetase long-chain isoform 1, which promoted αESA incorporation into neutral lipids including triacylglycerols. Interfering with triacylglycerol biosynthesis suppressed ferroptosis triggered by αESA but not by GPX4 inhibition. Orally administered tung oil, naturally rich in αESA, limited tumor growth and metastasis with transcriptional changes consistent with ferroptosis. Overall, these findings illuminate a novel approach to ferroptosis, complementary to GPX4 inhibition, with therapeutic potential. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE162069 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA680497 https://www.ebi.ac.uk/ena/browser/view/PRJNA680497 https://www.ncbi.nlm.nih.gov/sra?term=SRP293964 [Overal design]Three independent replicates of MDA-MB-231 cells incubated for 5 hours with ML162 (125 nM) or ESA (100 µM) and 2 replicates for the control incubated with the vehicle for ESA (methanol) were sequenced.; [Treatment]'MDA-MB-231 cells were incubated for 5 hours with ML162 (125 nM) or \uf061ESA (100 µM) and 2 replicates for the control incubated with the vehicle for \uf061ESA (methanol).Orthotopic MDA-MB-231 xenografts in NSG mice were treated orally with either 100 uL of safflower oil (control) or tung oil 5 days a week for 24 days'; [Growth]'MDA-MB-231 cells were grown on 10 cm culture plates to approximately 40% confluence.Orthotopic xenografts were generated by implanting 2.5 million MDA-MB-231 cells in 100 µL phosphate-buffered saline (PBS) mixed with 100 µL growth factor-reduced Matrigel (Corning) bilaterally into the fourth inguinal fat pad of four- to six-week-old female NOD.Cg-PrkdcscidIl2rgtm1Wjl/SzJ (NSG) mice. After 14 days, when tumors were roughly 50-75 mm3, animals were randomized into treatment groups.'; [Extraction]'Three biological replicate tung-oil or control MDA-MB-231 xenograft tumor samples were homogenized in ice-cold PBS using a dounce homogenizer and total RNA was isolated using the RNeasy kit (Qiagen).\nThe stranded mRNA-seq library was generated from 1000 ng of total RNA from each sample using Truseq stranded mRNA library kit (Illumina) according to the product instructions. In short, mRNAs were enriched twice via poly-T-based RNA purification beads, and subjected to fragmentation at 94 \uf0b0C for 8 minutes via the divalent cation method. The first strand cDNA was synthesized by SuperscriptII (ThermoFisher Scientific) and random primers at 42 \uf0b0C for 15 mins, followed by second strand synthesis at 16 \uf0b0C for 1 hour. During second strand synthesis, the dUTP was used to replace dTTP, thereby the second strand was quenched during amplification. A single ‘A’ nucleotide is added to the 3’ ends of the blunt fragments at 37 \uf0b0C for 30 minutes. Adapters with illuminaP5, P7 sequences as well as indices were ligated to the cDNA fragment at 30 \uf0b0C for 10 minutes. After Ampure bead (BD) purification (Beckman Coulter), a 15-cycle PCR reaction was used to enrich the fragments. PCR was set at 98 \uf0b0C for 10 s, 60 \uf0b0C for 30 s and extended at 72 \uf0b0C for 30 s. Libraries were again purified using AmPure beads, checked for quality check with a Bioanalyzer (Agilent Technologies) and quantified with Qubit (Invitrogen). Sample libraries were subsequently pooled and loaded to the HiSeq2500 and sequenced using a Hiseq rapid SRcluster kit and HiSeq rapid SBS kit (Illumina). Single 50bp were generated for the bioinformatic analysis.'; [Cell type]'Source: ''cell line: MDA-MB-231; cell line origin: triple-negative breast cancer; agent: vehicle, methanol; ', 'cell line: MDA-MB-231; cell line origin: triple-negative breast cancer; agent: ML162, GPX4 inhibitor; ', 'cell line: MDA-MB-231; cell line origin: triple-negative breast cancer; agent: alpha-eleostearic acid; ', 'cell line: MDA-MB-231; cell line origin: triple-negative breast cancer; agent: safflower oil, high-oleic; ', 'cell line: MDA-MB-231; cell line origin: triple-negative breast cancer; agent: tung oil; ' GSE65238 Homo sapiens 36 Expression profiling by array GPL15640 Transcriptome analysis of Wnt3a-treated triple-negative breast cancer cell lines. 2015-01-23 We analyzed the transcriptome of two different triple negative breast cancer (TNBC) cell lines to define a comprehensive list of Wnt target genes. Cells were treated with Wnt3a for 6h, 12h or 24h. We found up-regulated and down-regulated genes in response to Wnt3a treatment. They are involved in the Wnt pathway itself, and also in TGFß, p53 and Hedgehog pathways. Thorough characterization of these novel potential Wnt target genes may reveal new regulators of the canonical Wnt pathway. The comparison of our list of Wnt target genes with those published in other cellular contexts confirms the notion that Wnt target genes are tissue-, cell line- and treatment-specific. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE65238 Transcriptome analysis of Wnt3a-treated triple-negative breast cancer cells. PloS one 2.776 https://doi.org/10.1371/journal.pone.0122333 {PloS one (2.776): 10.1371/journal.pone.0122333} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA273488 https://www.ebi.ac.uk/ena/browser/view/PRJNA273488 None [Overal design]Cells were seeded in six-well plates, serum starved overnight then treated with Wnt3a for the indicated times (6, 12 and 24 hours). Triplicates for each condition were included in the experiment.; [Treatment]'Cells were seeded in six-well plates, serum starved overnight, and then treated with Wnt3a for the indicated times (6, 12 or 24 hours). Triplicates for each condition were included in the experiment.'; [Growth]'HCC38 and MDA-MB-468 cells were obtained from the American Type Culture Collection and authenticated in 2013 by short tandem repeat profiling. MDA-MB-468 cells were maintained in RPMI-1640 containing Glutamax and supplemented with 10% FBS. HCC38 cells were cultured in RPMI-1640 with Glutamax containing 10% FBS, 1.5g/L sodium bicarbonate, 10mM Hepes and 1mM sodium pyruvate. Cells were cultured at 37°C in a 5% CO2 humidified incubator.'; [Extraction]'Total RNA was extracted with the RNeasy Mini Kit from Qiagen (Courtaboeuf, France) following the manufacturer’s recommendations.'; [Cell type]'Source: ''wnt3a treatment: no; time after treatment (hours): 6; cell line: MDA-MB-468; ', 'wnt3a treatment: yes; time after treatment (hours): 6; cell line: MDA-MB-468; ', 'wnt3a treatment: no; time after treatment (hours): 12; cell line: MDA-MB-468; ', 'wnt3a treatment: yes; time after treatment (hours): 12; cell line: MDA-MB-468; ', 'wnt3a treatment: no; time after treatment (hours): 24; cell line: MDA-MB-468; ', 'wnt3a treatment: yes; time after treatment (hours): 24; cell line: MDA-MB-468; ', 'wnt3a treatment: no; time after treatment (hours): 6; cell line: HCC38; ', 'wnt3a treatment: yes; time after treatment (hours): 6; cell line: HCC38; ', 'wnt3a treatment: no; time after treatment (hours): 12; cell line: HCC38; ', 'wnt3a treatment: yes; time after treatment (hours): 12; cell line: HCC38; ', 'wnt3a treatment: no; time after treatment (hours): 24; cell line: HCC38; ', 'wnt3a treatment: yes; time after treatment (hours): 24; cell line: HCC38; ' GSE72956 Homo sapiens 43 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL11154; GPL16791 Transcriptomic and Epigenetic analysis of cell line derivatives from H2087 and HCC1954 cell lines 2015-09-11 We profiled the transcriptomes of latency-competent cells derived from the human cancer cell lines H2087 (lung adenocarcinoma) and HCC1954 (breast adenocarcinoma) in mitogen-rich and mitogen-low media (MRM and MLM, respectively). In addition, we analyzed the epigenetic landscape of these cell lines under MLM conditions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72956 Metastatic Latency and Immune Evasion through Autocrine Inhibition of WNT. Cell 36.216 https://doi.org/10.1016/j.cell.2016.02.025 {Cell (36.216): 10.1016/j.cell.2016.02.025} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA295409 https://www.ebi.ac.uk/ena/browser/view/PRJNA295409 https://www.ncbi.nlm.nih.gov/sra?term=SRP063623 [Overal design]H2087 and HCC1954 parental and latency-competent cell derivatives (LCCs) were grown for 48hr in mitogen-rich or mitogen-low conditions in vitro, and whole RNA was extracted for RNA-seq profiling. Cell lines were also grown in MLM conditions and DNA extracted for ChIP-Seq experiments.; [Treatment]'None'; [Growth]'Cells were grown under mitogen-rich or mitogen-low conditions for 48hr (subconfluent).', 'Cells were grown in mitogen-low media for 48 hours on standard tissue culture plates'; [Extraction]"Cells were immediately lysed and total RNA was extracted using the PrepEASE RNA Spin Kit according to the manufacturer's protocols.\nLibraries were constructed using standard Illumina protocols.", 'Cells were grown to 90–95% confluence, fixed with 1% formaldehyde for 15 min at room temperature followed by addition of glycine (1.25mM) for 10 minutes to stop cross linking. Nuclei were prepared and sonicated in lysis buffer (150 mM NaCl, 1% Triton X-100, 20 mM Tris pH 8.0, 0.1% SDS) using a Bioruptor to fragment chromatin to less than 500 base pairs (bp).\nChromatin was pre-cleared with 35 μl Protein-G Dyna magnetic beads, and then immunoprecipitated with 5 μg of antibody over night at 4 °C. The chromatin antibody mix was incubated with 35 μl protein G-conjugated Dyna beads for 4 h at 4 °C, washed three times with wash buffer (1% Triton X-100, 50 mM Tris pH 8.0, 10% glycerol) with increasing concentrations of NaCl (150 mM, 300 mM and 400 mM), and two times with Tris-EDTA buffer. DNA was eluted in 1% SDS in Tris-EDTA buffer for 45 min at 37 °C, crosslinking was reversed overnight at 65 °C, and DNA was purified using Qiagen columns. For each ChIP, one fifth of the cells from 15cm plates were used.'; [Cell type]'established breast cancer cell line', 'HCC1954 derivative isolated from BLI-negative mouse organ', 'established lung cancer cell line', 'H2087 derivative isolated from BLI-negative organ', 'Source: ''original cell line: HCC1954; cell type: established breast cancer cell line; growth condition: mitogen-rich media (MRM); growth time: 48hr; ', 'original cell line: HCC1954; cell type: HCC1954 derivative isolated from BLI-negative mouse organ; growth condition: mitogen-rich media (MRM); growth time: 48hr; ', 'original cell line: HCC1954; cell type: established breast cancer cell line; growth condition: mitogen-low media (MLM); growth time: 48hr; ', 'original cell line: HCC1954; cell type: HCC1954 derivative isolated from BLI-negative mouse organ; growth condition: mitogen-low media (MLM); growth time: 48hr; ', 'original cell line: H2087; cell type: established lung cancer cell line; growth condition: mitogen-rich media (MRM); growth time: 48hr; ', 'original cell line: H2087; cell type: H2087 derivative isolated from BLI-negative organ; growth condition: mitogen-rich media (MRM); growth time: 48hr; ', 'original cell line: H2087; cell type: established lung cancer cell line; growth condition: mitogen-low media (MLM); growth time: 48hr; ', 'original cell line: H2087; cell type: H2087 derivative isolated from BLI-negative organ; growth condition: mitogen-low media (MLM); growth time: 48hr; ', 'cell line source: H2087; source cell type: lung adenocarcinoma cell line; cell subtype: Parental Population; chip antibody: none (Input); ', 'cell line source: H2087; source cell type: lung adenocarcinoma cell line; cell subtype: Latency Competent Cancer Cell (LCC) Derivative; chip antibody: none (Input); ', 'cell line source: HCC1954; source cell type: breast adenocarcinoma cell line; cell subtype: Parental Population; chip antibody: none (Input); ', 'cell line source: HCC1954; source cell type: breast adenocarcinoma cell line; cell subtype: Latency Competent Cancer Cell (LCC) Derivative; chip antibody: none (Input); ', 'cell line source: H2087; source cell type: lung adenocarcinoma cell line; cell subtype: Parental Population; chip antibody: H3K27Ac; chip antibody vendor: Active Motif; chip antibody cat. #: 39133; ', 'cell line source: H2087; source cell type: lung adenocarcinoma cell line; cell subtype: Latency Competent Cancer Cell (LCC) Derivative; chip antibody: H3K27Ac; chip antibody vendor: Active Motif; chip antibody cat. #: 39133; ', 'cell line source: HCC1954; source cell type: breast adenocarcinoma cell line; cell subtype: Parental Population; chip antibody: H3K27Ac; chip antibody vendor: Active Motif; chip antibody cat. #: 39133; ', 'cell line source: HCC1954; source cell type: breast adenocarcinoma cell line; cell subtype: Latency Competent Cancer Cell (LCC) Derivative; chip antibody: H3K27Ac; chip antibody vendor: Active Motif; chip antibody cat. #: 39133; ', 'cell line source: H2087; source cell type: lung adenocarcinoma cell line; cell subtype: Parental Population; chip antibody: PolII; chip antibody vendor: Abcam; chip antibody cat. #: ab817; ', 'cell line source: H2087; source cell type: lung adenocarcinoma cell line; cell subtype: Latency Competent Cancer Cell (LCC) Derivative; chip antibody: PolII; chip antibody vendor: Abcam; chip antibody cat. #: ab817; ', 'cell line source: HCC1954; source cell type: breast adenocarcinoma cell line; cell subtype: Parental Population; chip antibody: PolII; chip antibody vendor: Abcam; chip antibody cat. #: ab817; ', 'cell line source: HCC1954; source cell type: breast adenocarcinoma cell line; cell subtype: Latency Competent Cancer Cell (LCC) Derivative; chip antibody: PolII; chip antibody vendor: Abcam; chip antibody cat. #: ab817; ' GSE75201 Homo sapiens 4 Genome binding/occupancy profiling by high throughput sequencing GPL9052 CHIP-SEQ of FOXA1 in parental MCF7 cells and tamoxifen resistant MCF7 cells 2015-11-19 ChIP sequencing of FOXA1 in MCF7 cells and tamoxifen resistant MCF7 cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE75201 FOXA1 overexpression mediates endocrine resistance by altering the ER transcriptome and IL-8 expression in ER-positive breast cancer. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1612835113 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1612835113} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA303962 https://www.ebi.ac.uk/ena/browser/view/PRJNA303962 https://www.ncbi.nlm.nih.gov/sra?term=SRP066602 [Overal design]ChIP sequencing for FOXA1 in MCF7 cells and tamoxifen resistant derivatives; [Treatment]'None'; [Growth]'None'; [Extraction]'chromatin from approximately 1 × 107 fixed cells was sonicated to a size range of 200-300 bp. Solubilized chromatin was subjected to immunoprecipitation with the FOXA1 antibody bound to protein A and protein G beads. A fraction of the sample was not exposed to antibody to be used as control (input). The samples were reversed crosslinked, treated with proteinase K, and DNA was extracted. DNA sequencing libraries were prepared using the ThruPLEX-FD Prep Kit (Rubicon Genomics). Libraries were sequenced using 50-bp reads on the Illumina platform\nDNA sequencing libraries were prepared using the ThruPLEX-FD Prep Kit (Rubicon Genomics per manual). Libraries were sequenced using Illumina platform'; [Cell type]'Source: ''antibody: FOXA1; ', 'antibody: none; ' GSE94363 Homo sapiens 84 Expression profiling by array GPL10558 Posttranslationally modified progesterone receptors direct ligand-specific expression of breast cancer stem cell-associated gene programs 2017-02-01 Background Estrogen and progesterone are potent breast mitogens. In addition to steroid hormones, multiple signaling pathways input to estrogen receptor (ER) and progesterone receptor (PR) actions via posttranslational events. Protein kinases commonly activated in breast cancers phosphorylate steroid hormone receptors (SRs) and profoundly impact their activities. Methods To better understand the role of modified PRs in breast cancer, we measured total and phospho-Ser294 PRs in 209 human breast tumors represented on 2754 individual tissue spots within a tissue microarray and assayed the regulation of this site in human tumor explants cultured ex vivo. To complement this analysis, we assayed PR target gene regulation in T47D luminal breast cancer models following treatment with progestin (promegestone; R5020) and antiprogestins (mifepristone, onapristone, or aglepristone) in conditions under which the receptor is regulated by Lys388 SUMOylation (K388 intact) or is SUMO-deficient (via K388R mutation to mimic persistent Ser294 phosphorylation). Selected phospho-PR-driven target genes were validated by qRT-PCR and following RUNX2 shRNA knockdown in breast cancer cell lines. Primary and secondary mammosphere assays were performed to implicate phospho-Ser294 PRs, epidermal growth factor signaling, and RUNX2 in breast cancer stem cell biology. Results Phospho-Ser294 PR species were abundant in a majority (54%) of luminal breast tumors, and PR promoter selectivity was exquisitely sensitive to posttranslational modifications. Phospho-PR expression and target gene programs were significantly associated with invasive lobular carcinoma (ILC). Consistent with our finding that activated phospho-PRs undergo rapid ligand-dependent turnover, unique phospho-PR gene signatures were most prevalent in breast tumors clinically designated as PR-low to PR-null (luminal B) and included gene sets associated with cancer stem cell biology (HER2, PAX2, AHR, AR, RUNX). Validation studies demonstrated a requirement for RUNX2 in the regulation of selected phospho-PR target genes (SLC37A2). In vitro mammosphere formation assays support a role for phospho-Ser294-PRs via growth factor (EGF) signaling as well as RUNX2 as potent drivers of breast cancer stem cell fate. Conclusions We conclude that PR Ser294 phosphorylation is a common event in breast cancer progression that is required to maintain breast cancer stem cell fate, in part via cooperation with growth factor-initiated signaling pathways and key phospho-PR target genes including SLC37A2 and RUNX2. Clinical measurement of phosphorylated PRs should be considered a useful marker of breast tumor stem cell potential. Alternatively, unique phospho-PR target gene sets may provide useful tools with which to identify patients likely to respond to selective PR modulators that block PR Ser294 phosphorylation as part of rational combination (i.e., with antiestrogens) endocrine therapies designed to durably block breast cancer recurrence. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE94363 Posttranslationally modified progesterone receptors direct ligand-specific expression of breast cancer stem cell-associated gene programs. Journal of hematology & oncology 8.731 https://doi.org/10.1186/s13045-017-0462-7 {Journal of hematology & oncology (8.731): 10.1186/s13045-017-0462-7} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA369476 https://www.ebi.ac.uk/ena/browser/view/PRJNA369476 None [Overal design]The study contains 3 different cell lines (PR-null, PRB-wildtype, PRB-K388R) tested with 8 different treatments in triplicate (8 x 3 x 3 = 72 individual samples). We also included 12 previously published samples (GSE34148) with the same treatments, which increased our total number of samples to 84. From parental T47D-Y (PR-null) human breast cancer cell lines, we created stable clones expressing either (1) an empty vector (pIRESneo3) or (2) the wild type progesterone receptor isoform B (pIRESneo3-PR-B), or (3) pIRESneo3-PR-B-K388R. These three cell lines were co-treated with either (1) vehicle control (ethanol) or (2) progesterone/R5020 10e-8 M, (3) RU486 10e-7 M, (4) onapristone 10e-7 M, (5) aglepristone 10e-7 M, (6) progesterone plus RU486, (7) progesterone plus onapristone, or (8) progesterone plus aglepristone. Treatments were for 6 hours before total RNA harvest. Standard Illumina HT-12v4 chip was used for gene expression analysis.; [Treatment]'Samples treated in IMEM medium, with or without progestin (10e-8 M) and/or antiprogestin (10e-7 M) for 6 hr.'; [Growth]'Samples grown in complete medium (MEM, 5% FBS, 1% NEAA, 1% pen/strep, 6ng/ml insulin, 200 ug/ml G418) before 1 day starvation in IMEM medium, then treated in IMEM medium for 6 hr.'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-empty; treatment: ethanol and ethanol; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-empty; treatment: ethanol; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-empty; treatment: ethanol and progesterone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-empty; treatment: R5020; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-empty; treatment: ethanol and RU486; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-empty; treatment: ethanol and onapristone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-empty; treatment: ethanol and aglepristone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-empty; treatment: progesterone and RU486; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-empty; treatment: progesterone and onapristone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-empty; treatment: progesterone and aglepristone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-wildtype; treatment: ethanol and ethanol; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-wildtype; treatment: ethanol; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-wildtype; treatment: ethanol and progesterone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-wildtype; treatment: R5020; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-wildtype; treatment: ethanol and RU486; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-wildtype; treatment: ethanol and onapristone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-wildtype; treatment: ethanol and aglepristone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-wildtype; treatment: progesterone and RU486; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-wildtype; treatment: progesterone and onapristone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-wildtype; treatment: progesterone and aglepristone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-K388R; treatment: ethanol and ethanol; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-K388R; treatment: ethanol; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-K388R; treatment: ethanol and progesterone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-K388R; treatment: R5020; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-K388R; treatment: ethanol and RU486; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-K388R; treatment: ethanol and onapristone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-K388R; treatment: ethanol and aglepristone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-K388R; treatment: progesterone and RU486; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-K388R; treatment: progesterone and onapristone; time point: 6 hr; ', 'parental cell line: T47D-Y; tissue: Breast; stable vector integration: pIRESneo3-PRB-K388R; treatment: progesterone and aglepristone; time point: 6 hr; ' GSE83669 Homo sapiens 6 Non-coding RNA profiling by high throughput sequencing GPL15520 Plasma Exosome microRNAs are Indicative of Breast Cancer 2016-06-23 Introduction: microRNAs are promising candidate breast cancer biomarkers due to their cancer-specific expression profiles. However, efforts to develop circulating breast cancer biomarkers are challenged by the heterogeneity of microRNAs in the blood. To overcome this challenge, we aimed to develop a molecular profile of microRNAs specifically secreted from breast cancer cells. Our first step towards this direction relates to capturing and analyzing the contents of exosomes, which are small secretory vesicles that selectively encapsulate microRNAs indicative of their cell of origin. To our knowledge, circulating exosome microRNAs have not been well evaluated as biomarkers for breast cancer diagnosis or monitoring. Methods: Exosomes were collected from the conditioned media of human breast cancer cell lines, mouse plasma of patient-derived orthotopic xenograft models (PDX), and human plasma samples. Exosomes were verified by electron microscopy, nanoparticle tracking analysis, and western blot. Cellular and exosome microRNAs from breast cancer cell lines were profiled by next-generation small RNA sequencing. Plasma exosome microRNA expression was analyzed by qRT-PCR analysis. Results: Small RNA sequencing and qRT-PCR analysis showed that several microRNAs are selectively encapsulated or highly enriched in breast cancer exosomes. Importantly, the selectively enriched exosome microRNA, human miR-1246, was detected at significantly higher levels in exosomes isolated from PDX mouse plasma, indicating that tumor exosome microRNAs are released into the circulation and can serve as plasma biomarkers for breast cancer. This observation was extended to human plasma samples where miR-1246 and miR-21 were detected at significantly higher levels in the plasma exosomes of 16 breast cancer patients as compared to the plasma exosomes of healthy control subjects. Receiver Operating Characteristic (ROC) curve analysis indicated that the combination of plasma exosome miR-1246 and miR-21 levels is a better indicator of breast cancer than their individual levels. Conclusions: Our results demonstrate that certain microRNA species, such as miR-21 and miR-1246, are selectively enriched in human breast cancer exosomes and significantly elevated in the plasma of breast cancer patients. These findings indicate a potential new strategy to selectively analyze plasma breast cancer microRNAs indicative of the presence of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE83669 Plasma exosome microRNAs are indicative of breast cancer. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-016-0753-x {Breast cancer research : BCR (5.676): 10.1186/s13058-016-0753-x} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA326670 https://www.ebi.ac.uk/ena/browser/view/PRJNA326670 https://www.ncbi.nlm.nih.gov/sra?term=SRP077010 [Overal design]The small RNA in the cells and exosomes of the normal mammary epithelial cell line (MCF10A) and two breast cancer cell lines (MCF7 and MDA-MB-231) were analyzed by Next Gen RNA Sequencing.; [Treatment]'None'; [Growth]'The human mammary epithelial cell line MCF10A, and breast cancer cell lines MCF7 and MDA-MB-231 were obtained from the American Type Culture Collection (Manassas, VA). MCF10A cells were cultured in DMEM/F12 medium supplemented with 5% exosome-depleted horse serum, 20ng/ml epithelial growth factor, 0.5mg/ml hydrocortisone, 100ng/ml cholera toxin, 10 μg/ml insulin, 100 IU/mL penicillin and 100 μg/mL streptomycin. MCF7 and MDA-MB-231 cells were cultivated in DMEM medium supplemented with 10% exosome-depleted fetal bovine serum (FBS), 100 IU/mL penicillin and 100 μg/mL streptomycin (Corning/Mediatech, Inc. Manassas, VA). Exosome-depleted FBS and horse serum were prepared by pelleting the serum exosomes by ultracentrifugation at 100,000 x g for 2 h at 4°C, and the resulting supernatant was filtered through a 0.2 μm pore filter. Cells were routinely maintained in a humidified chamber at 37°C and 5% CO2.'; [Extraction]'Exosomes were isolated utilizing a combination of centrifugation, ultracentrifugation, and filtration as we have previously described [16] or with the Exoquick-TC reagent (System Biosciences, Mountain View, CA) following the manufacturer’s protocol. For ultracentrifugation isolation, conditioned cell culture media was collected and centrifuged at 10,000 x g for 30 min at 4°C, to remove cells and large debris. The supernatant was filtered using a 0.22-μm pore filter and the exosomes were pelleted at 100,000 x g for 1 h at 4°C. The exosome pellet was washed with 10 ml of 1X PBS and pelleted again by centrifugation at 100,000 x g for 1 h at 4°C. The resulting pellet was either suspended in 1X PBS for whole exosome applications or further processed for RNA or protein extraction. Total RNA was extracted from exosome pellet using the TRIzol reagent (Invitrogen/Life Technologies) following the manufacturer’s protocol. RNA concentration was quantitated using the NanoDrop ND-100 Spectrophotometer (NanoDrop Technologies, Wilmington, DE).\nSmall RNA libraries were constructed using New England Biolabs (NEB) NEBNext Multiplex Small RNA Library Prep Set for Illumina sequencers and the NEB standard protocol. Individual libraries were constructed using 1µg of total RNA isolated from each sample.'; [Cell type]'normal mammary epithelial', 'breast cancer''cell line: MCF10A; cell type: normal mammary epithelial; ', 'cell line: MCF7; cell type: breast cancer; ', 'cell line: MDA-MB-231; cell type: breast cancer; ' GSE37954 Mus musculus 18 Expression profiling by array GPL2872; GPL6585 β-catenin signaling is a critical event in ErbB2-mediated mammary tumor progression. 2012-05-14 Although ERBB2 amplification and overexpression is correlated with poor outcome in breast cancer, the molecular mechanisms underlying the aggressive nature of these tumors has not been fully elucidated. To investigate this further, we have used a transgenic mouse model of ErbB2-driven tumor progression (ErbB2KI model) that recapitulates clinically relevant events, including selective amplification of the core erbB2 amplicon. By comparing the transcriptional profiles of ErbB2KI mammary tumors and human ERBB2-positive breast cancers, we demonstrate that ErbB2KI tumors possess molecular features of the basal subtype of ERBB2-positive human breast cancer, including activation of canonical β-catenin signaling. Inhibition of β-catenin-dependent signaling in ErbB2KI-derived tumor cells using RNA interference impaired tumor initiation and metastasis. Furthermore, treatment of ErbB2KI or human ERBB2-overexpressing tumor cells with a selective β-catenin/CBP inhibitor significantly decreased proliferation and ErbB2 expression. Collectively, our data indicate that ERBB2-mediated breast cancer progression requires β-catenin signaling and can be therapeutically targeted by selective β-catenin/CBP inhibitors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37954 β-Catenin signaling is a critical event in ErbB2-mediated mammary tumor progression. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-12-3925 {Cancer research (8.378): 10.1158/0008-5472.CAN-12-3925} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA166849 https://www.ebi.ac.uk/ena/browser/view/PRJNA166849 None [Overal design]Common reference design. 9 samples (including 2 normal tissue, 2 NIC tumors, and 5 KI tumor tissue samples) replicated twice as dye swaps, generating a total of 18 arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'No extraction', 'RNeasy Midi Kit (Qiagen)'; [Cell type]'Source: ''sample identifier: None; sample type: Stratagene universal mouse reference; ', 'sample identifier: FVBmg.10; Sex: Female; Strain: FVB/N; gender: female; genetic background: FVB/N; tissue: Normal tissue from whole murine mammary gland; ', 'sample identifier: FVBmg.18PI; Sex: Female; Strain: FVB/N; gender: female; genetic background: FVB/N; tissue: Normal tissue from whole murine mammary gland; ', 'sample identifier: T.NICp1; Type: Pool from 5 NIC tumors (equal amounts); Sex: Female; Strain: FVB/N; gender: female; genetic background: FVB/N; tissue: NIC tumor pool from whole murine mammary gland; ', 'sample identifier: T.NICp2; Type: Pool from 5 NIC tumors (equal amounts); Sex: Female; Strain: FVB/N; gender: female; genetic background: FVB/N; tissue: NIC tumor pool from whole murine mammary gland; ', 'sample identifier: FVBmg.10; Sex: Female; Strain: FVB/N; gender: female; genetic background: FVB/N; tissue: normal mammary gland; ', 'sample identifier: FVBmg.18PI; Sex: Female; Strain: FVB/N; gender: female; genetic background: FVB/N; tissue: normal mammary gland; ', 'sample identifier: T.5710; Sex: Female; Strain: FVB/N; genetic background: FVB/N; tissue: ErbB2 KI tumor from whole murine mammary gland; genotype: ErbB2 knock-in; ', 'sample identifier: T.5710; Sex: Female; Strain: FVB/N; gender: female; genetic background: FVB/N; tissue: ErbB2 KI tumor from whole murine mammary gland; genotype: ErbB2 knock-in; ', 'sample identifier: T.5901; Sex: Female; Strain: FVB/N; genetic background: FVB/N; tissue: ErbB2 KI tumor from whole murine mammary gland; genotype: ErbB2 knock-in; ', 'sample identifier: T.5901; Sex: Female; Strain: FVB/N; gender: female; genetic background: FVB/N; tissue: ErbB2 KI tumor from whole murine mammary gland; genotype: ErbB2 knock-in; ', 'sample identifier: T.5906; Sex: Female; Strain: FVB/N; genetic background: FVB/N; tissue: ErbB2 KI tumor from whole murine mammary gland; genotype: ErbB2 knock-in; ', 'sample identifier: T.1498; Sex: Female; Strain: FVB/N; genetic background: FVB/N; tissue: ErbB2 KI tumor from whole murine mammary gland; genotype: ErbB2 knock-in; ', 'sample identifier: T.1498; Sex: Female; Strain: FVB/N; gender: female; genetic background: FVB/N; tissue: ErbB2 KI tumor from whole murine mammary gland; genotype: ErbB2 knock-in; ', 'sample identifier: T.5906; Sex: Female; Strain: FVB/N; gender: female; genetic background: FVB/N; tissue: ErbB2 KI tumor from whole murine mammary gland; genotype: ErbB2 knock-in; ', 'sample identifier: T.6297; Sex: Female; Strain: FVB/N; genetic background: FVB/N; tissue: ErbB2 KI tumor from whole murine mammary gland; genotype: ErbB2 knock-in; ', 'sample identifier: T.6297; Sex: Female; Strain: FVB/N; gender: female; genetic background: FVB/N; tissue: ErbB2 KI tumor from whole murine mammary gland; genotype: ErbB2 knock-in; ' GSE69813 Homo sapiens 16 Expression profiling by array GPL20321 Expresssion data from reovirus treated breast cancer cell lines 2015-06-12 Reovirus mediated cell death of breast cancer is orchestrated via apoptotic cell death pathways We used inhouse microarrays to detail the global programme of gene expression following reovirus treatment https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE69813 PUMA and NF-kB Are Cell Signaling Predictors of Reovirus Oncolysis of Breast Cancer. PloS one 2.776 https://doi.org/10.1371/journal.pone.0168233 {PloS one (2.776): 10.1371/journal.pone.0168233} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA286858 https://www.ebi.ac.uk/ena/browser/view/PRJNA286858 None [Overal design]Breast cancer cell lines were treated with reovirus for 12 and 24 hours and RNA was extracted. Microarray was performed in inhouse (University of Calgary miroarray facility) chips.; [Treatment]'Cells were infected with reovirus for 12 or 24 hours.'; [Growth]'MCF7 and HTB133 cells were grown in 6 well plates until 75% confluent.'; [Extraction]"Total RNA extracted using Trizol following manufacturer's instructions and quantified. RNA was then subjected to DNase treatment and the intergrity of the purified RNA was confirmed following gel analysis"; [Cell type]'breast cancer''cell line: MCF7; cell type: breast cancer; ', 'cell line: HTB133; cell type: breast cancer; ' GSE151317 Homo sapiens 15 Expression profiling by high throughput sequencing GPL24676 Gene Expression Profiling of TNBC and OVCA in response to Azacitidine and Talazoparib (RNA-Seq) 2020-05-27 Triple negative breast cancer and ovarian cancer cells were treated with Azacitidine, Talazoparib, or combination for a period of 10 days to assess global transcriptional response. The focus of these transcriptional studies were on the assessment of DNA repair and immune pathway alteration. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE151317 Pharmacologic induction of innate immune signaling directly drives homologous recombination deficiency. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.2003499117 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.2003499117} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA635430 https://www.ebi.ac.uk/ena/browser/view/PRJNA635430 https://www.ncbi.nlm.nih.gov/sra?term=SRP264996 [Overal design]Therapeutic induced gene expression was assayed in human cell lines after 10 days of continous exposure to doses of Azacitidine, Talazoparib, or combination treatment.; [Treatment]'Cell lines detailed above were treated with the agents indicated above for a period of 10 days'; [Growth]'Cell lines were cultured in RPMI 1640 medium supplemented with 10% heat-inactivated fetal bovine serum. The cultures were incubated for 10 days at 37 ºC in a humidified incubator with 5% CO2.'; [Extraction]'Total RNA was isolated from cell pellets using Takara NucleoSpin RNA extraction kit. RNA was quantified with NanoDrop ND-1000 followed by quality assessment with 2100 Bioanalyzer (Agilent Technologies) according to manufacturer’s protocol.\nRNA-seq libraries were prepared using SMARTer® Stranded Total RNA Sample Prep Kit - HI Mammalian without significant modification of standard protocol\nTotal Transcriptome RNA-seq, ribosomal RNA depletion'; [Cell type]'Source: ''source: in-vitro cultured cell lines; Sex: Female; ' GSE118774 Homo sapiens 6 Expression profiling by high throughput sequencing GPL20301 Genome wide expression change in LCC2 and MCF-7 cells 2018-08-20 We aim to the investigate the role of tamoxifen in breast cancer progression. LCC2 and MCF-7 cells were used as the resistant and sensitive model. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE118774 STAT1 facilitates oestrogen receptor α transcription and stimulates breast cancer cell proliferation. Journal of cellular and molecular medicine 4.658 https://doi.org/10.1111/jcmm.13882 {Journal of cellular and molecular medicine (4.658): 10.1111/jcmm.13882} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA486779 https://www.ebi.ac.uk/ena/browser/view/PRJNA486779 https://www.ncbi.nlm.nih.gov/sra?term=SRP158393 [Overal design]The MCF-7 and LCC2 cells were lysed and the total RNA was extracted.; [Treatment]'None'; [Growth]'cells were cultured in DMEM with 10% FBS.'; [Extraction]"The total RNA was extracted from cells by the qiagen RNA exaction kit\nLibraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit (Part# 0801-0303)."; [Cell type]'Source: ''cell line: LCC2; passage: 15-18 passage; ', 'cell line: MCF-7; passage: 15-18 passage; ' GSE126037 Homo sapiens 13 Expression profiling by array GPL20311 FGFR4 is a key regulator of tumor subtype differentiation in luminal breast cancer and metastatic disease [set 2] 2019-02-04 Mechanisms driving tumor progression from less aggressive subtypes to more aggressive states represent key targets for breast cancer therapy. We observed that a subset of Luminal A primary breast tumors give rise to HER2-enriched (HER2E) subtype metastases, but remain clinically HER2 negative (cHER2-). By testing the unique genetic and transcriptomic features of these cases, we developed the hypothesis that FGFR4 drives this subtype switching. To evaluate this, we developed two FGFR4 signatures using a PDX model treated with a FGFR4 inhibitor (BLU9931), which inhibited PDX growth in vivo. Examining patient outcomes in the METABRIC breast cancer cohort showed that the FGFR4-induced and FGFR4-repressed signatures each predicted overall survival (OS) (HR=6.30, P<0.0001; HR=0.33; P<0.0001, respectively). Multivariate analysis showed that the FGFR4-induced signature was also an independent prognostic factor beyond subtype and stage for OS (HR=2.34, P=0.014). Supervised analysis of 77 primary tumors with paired metastasis revealed that the FGFR4-induced signature was significantly higher in luminal/ER+ tumor metastases compared with their primaries. Finally, multivariate analysis demonstrated that the FGFR4-induced signature also predicted site-specific metastasis for lung, liver and brain, but not for bone or lymph nodes. These data identify a link between FGFR4-regulated genes and metastasis, suggesting a treatment options for FGFR4-positive patients, whose high expression is non-genetically determined. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE126037 FGFR4 regulates tumor subtype differentiation in luminal breast cancer and metastatic disease. The Journal of clinical investigation 12.282 https://doi.org/10.1172/JCI130323 {The Journal of clinical investigation (12.282): 10.1172/JCI130323} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA520842 https://www.ebi.ac.uk/ena/browser/view/PRJNA520842 None [Overal design]There are 13 samples in this set. We analyzed 5 replicates of the untreated tumors (control) plus 4 replicates of the BLU9931 treated and Lapatinib treated PDX tumors. [set1]; [Treatment]'Tumors treated with BLU9931 (0.6g/Kg/day) or Lapatinib (0.22g/kg/day) for 18 days'; [Growth]'PDX WHIM11 tumors were engrafted in the mammary fat pad of NSG mice by subcutaneous injection of 1.0 × 10^6 cells in RPMI:Matrigel (1:1) in a total volume of 200 μl'; [Extraction]'Tumor tissue was disrupted using roto-stator homogenization. RNA was isolated using the RNeasy Mini Kit (QUIAGEN) according to manufacturer protocol. Isolated RNA was quantified using a NanoDrop® Spectrophotometer.'; [Cell type]'Source: ''reference: High-quality total RNA. Comprised of 10 different cell lines for broad gene coverage on human microarrays; ', 'tissue: WHIM11 tumor; agent: Untreated; ', 'tissue: WHIM11 tumor; agent: Lapatinib treated for 18 days; ', 'tissue: WHIM11 tumor; agent: BLU9931 treated for 18 days; ' GSE71926 Mus musculus 4 Expression profiling by array GPL4134 Identification of a Highly Immunogenic Mouse Breast Cancer Sub Cell Line, 4T1-S 2015-08-11 Recently, cancer immunotherapy has been paid much attention because of its improved efficacy and low frequency of adverse effects. A mouse breast cancer cell line, 4T1, has been known as poorly immunogeneic and highly metastatic cell line. In this study, we have identified a sub cell line of 4T1, designated as 4T1-Sapporo (4T1-S), which could induce a strong immune response against the same line. When 4T1-S was subcutaneously injected, striking enlargement of draining lymph nodes and increase of activated T cells were observed. The strong immune responses could not be observed when 4T1-S was injected to nude mice, indicating that this phenomenon is mediated by T cell response. Identification of 4T1-S characteristics may help to improve immunotherapy against breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE71926 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA292490 https://www.ebi.ac.uk/ena/browser/view/PRJNA292490 None [Overal design]4T1-A1, 4T1-A2, 4T1-S1, 4T1-S2; [Treatment]'None'; [Growth]'None'; [Extraction]"RNA was prepared using the RNeasy Plus Mini kit (QIAGEN) following the manufacturer's recommendations. RNA was quantified using spectrophotometer and quality was monitored with the Agilent 2100 Bioanalyzer (Agilent Technologies)."; [Cell type]'Source: ''parental cell line: 4T1; ' GSE117930 Mus musculus 12 Expression profiling by high throughput sequencing GPL17021 Signature of CD45- metastatic niche cells at different stages of the metastatic disease 2018-07-31 We analysed the signature of the non-immune cells from the metastatic niche and the distal lung using the breast tumour 4T1 cell line as a model of lung metastasis from breast cancer https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE117930 Metastatic-niche labelling reveals parenchymal cells with stem features. Nature 43.070 https://doi.org/10.1038/s41586-019-1487-6 {Nature (43.070): 10.1038/s41586-019-1487-6} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA483753 https://www.ebi.ac.uk/ena/browser/view/PRJNA483753 https://www.ncbi.nlm.nih.gov/sra?term=SRP155859 [Overal design]Syngenic Balb/c female mice were injected intravenously with 4T1 tumour cells and lung tissue were collected at day 5 and day 10. post-injection. RNA was isolated from CD45-Ter119- FACS sorted cells.; [Treatment]'Balb/c female mice 6-10 weeks old were injected intravenously with 4T1-labelling tumour cells and lungs were isolated at day 5 and day 10 after injection'; [Growth]'None'; [Extraction]'Lungs were minced manually and then digested for 30 min at 37 degrees in a HBSS digestion solution containing DNase I (Sigma-Aldrich) and Liberase TM and TH (Roche Diagnostics). Samples were then washed, passed through a 100 um filter and incubated with Red Blood Cell Lysis buffer (Miltenyi Biotec) for 3-5 min. After a wash with MACS buffer (0.5% BSA and 250 mM EDTA in PBS), samples were passed through a 40 um filter and a 20 um strainer-capped flow cytometry tube to generate a single cell suspension to use for flow cytometric analysis or further purification. Samples were stained with a CD45 and a Ter119 antibody. Murine CD45-Ter119- cells were isolated via FACS.\nTotal RNA from sorted cell samples was isolated using the MagMax-96 Total RNA Isolation Kit (ThermoFIsher Scientific). The quality and concentration of total RNA for each sample was determined on Agilent 2100 Bioanalyzer using the Total RNA 6000 Pico Kit. RNA was amplified and libraries were prepared for sequencing using Illumina protocols.'; [Cell type]'Source: ''tissue: Lung; treatment: CD45-Ter119- cells; ' GSE48565 Mus musculus 133 Expression profiling by array GPL6246 Expression data from mammary tumors from a Diversity Outcross x PyMT mouse cross 2013-07-05 Mouse genetic crosses were established between the PyMT model of metastatic breast cancer and the G5 generation of the Diversity Outcross (DO). Tumors were harvested from the animals for gene expression analysis to identify genes associated with progression to distant metastatic disease. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48565 Aicardi-Goutières syndrome gene Rnaseh2c is a metastasis susceptibility gene in breast cancer. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1008020 {PloS one (2.776) doi:10.1371/journal.pone.0072287}; {PLoS genetics (5.224) doi:10.1371/journal.pgen.1008020}; {PLoS genetics (5.224) doi:10.1371/journal.pgen.1005989}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA210666 https://www.ebi.ac.uk/ena/browser/view/PRJNA210666 None [Overal design]Gene expression of 133 samples from the Diversity Outcross were assayed on Affymetrix chips.; [Treatment]'No treatment was performed.'; [Growth]'Tumors were permitted to grow until animal neared humane endpoints. Tumors were harvested, snap frozen and stored at -80oC until RNA extraction.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14087; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14264; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14227; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14176; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14273; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14056; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13955; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14267; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14095; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14249; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14266; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14247; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14233; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14015; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14091; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14149; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14061; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14141; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14064; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14121; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14078; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13960; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14089; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14103; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14127; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14182; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14051; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14048; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14024; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14118; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14271; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14098; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14086; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14199; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14090; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14052; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14128; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14125; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14110; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13953; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14261; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14028; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14198; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13976; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14150; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14077; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14185; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14021; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13948; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13950; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13951; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13956; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13958; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13973; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13974; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13975; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13981; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13983; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13986; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13987; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13998; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 13999; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14000; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14001; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14002; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14005; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14018r; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14022r; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14026; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14027; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14032; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14033; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14037; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14043; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14044; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14050; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14050r; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14055; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14058; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14072; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14083; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14085; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14094; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14099; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14106; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14122; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14124; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14126; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14148; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14151; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14170; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14187; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14189; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14190; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14195; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14200; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14201; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14223; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14224; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14231; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14248; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14250; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14251; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14252r; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14253r; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14260; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14262; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14272; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14275; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14280; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14281; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14282; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14286; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14287; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14289; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14290; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14291; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14295; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14306; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14308; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14309; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14311; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14312; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14320; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14322; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14327; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14328; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14329; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14352; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14352r; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14354; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14356; ', 'strain/background: Diversity Outcross x PyMT; tissue: mammary tumor; mouse id: 14358; ' GSE75333 Homo sapiens 9 Expression profiling by array GPL570 Aging reduces the pro-tumorigenic potential of bone marrow cells and influences triple-negative breast cancer progression 2015-11-24 To examine the effects of recombinant granulin on human mammary stromal fibroblasts, we cultured immortalized GFP+ normal human mammary fibroblasts in the presence of recombinant human granulin (1ug/ml) or PBS every 24h for 6 days. To generate GRN-independent CAFs, we injected immortalized GFP+ human mammary fibroblasts, MCF7Ras human breast carcinoma cells, and 20% Matrigel subcutaneously into nude mice. Tumors were allowed to form for a period of 45 days. GFP+ fibroblasts were isolated from tumors by mincing the tumors, dissociating, and culturing in the presence of 1 ug/ml puromycin for ~3-4 weeks. CAF purity was confirmed by ensuring that 100% of the population was GFP-positive. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE75333 Hematopoietic Age at Onset of Triple-Negative Breast Cancer Dictates Disease Aggressiveness and Progression. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-15-3332 {Cancer research (8.378): 10.1158/0008-5472.CAN-15-3332} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA304091 https://www.ebi.ac.uk/ena/browser/view/PRJNA304091 None [Overal design]We cultured normal human mammary fibroblasts in the presence human granulin (1ug/ml) or PBS control every 24h for 6 days. The analysis showen are for 3 control (control) and 3 granulin-treated (PGRN) fibrobast cultures.; [Treatment]'Cells were cultured for 6 days in presence of 1ug/ml recombinant human granulin protein or PBS control'; [Growth]'Normal human mamary fibroblasts were cultured with DMEM medium containing 10% calf serum and 10% fetal bovine serum'; [Extraction]'Total RNA was extracted from fibroblasts using RNA extraction kits according to the manufacturer’s instructions (Qiagen)'; [Cell type]'Source: ''clinical status: Normal mammary human; ', 'clinical status: Granulin-stimulated fibroblasts; ', 'clinical status: Cancer-associated fibroblasts; ' GSE37965 Homo sapiens 30 Methylation profiling by genome tiling array GPL13534 DNA methylation profiling in breast cancer discordant identical twins 2012-05-14 We obtained a comprehensive DNA methylation profile of 15 breast cancer discordant twins, using the high resolution Infinium HumanMethylation450 BeadChip platform (450K, Illumina), previously established to reliably detect methylation changes of more than 450,000 CpG sites. To provide insight into the temporal and causal relationships and predictive potential, samples from breast cancer patients before (7) and after diagnosis (8) were also analyzed. Using whole blood from 15 twin pairs discordant for breast cancer and high-resolution (450k) DNA methylation analysis we identified 403 differentially methylated CpG sites including known and novel potential breast cancer genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37965 DNA methylation profiling in breast cancer discordant identical twins identifies DOK7 as novel epigenetic biomarker. Carcinogenesis 4.004 https://doi.org/10.1093/carcin/bgs321 {Carcinogenesis (4.004): 10.1093/carcin/bgs321} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA165843 https://www.ebi.ac.uk/ena/browser/view/PRJNA165843 None [Overal design]30 Samples; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA samples from blood were extracted from thawed frozen whole blood collected in EDTA using the Nucleon Genomic DNA Extraction Kit BACC3'; [Cell type]'Source: ''gender: Female; tissue: Whole blood; twin pair: Pair_1; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_2; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_3; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_1; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_4; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_4; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_5; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_6; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_6; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_7; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_8; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_8; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_9; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_9; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_3; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_10; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_10; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_11; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_11; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_12; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_12; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_13; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_13; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_14; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_15; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_15; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_14; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_5; disease status: breast cancer sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_7; disease status: healthy sample; ', 'gender: Female; tissue: Whole blood; twin pair: Pair_2; disease status: breast cancer sample; ' GSE129858 Mus musculus 16 Expression profiling by high throughput sequencing GPL19057 Transcriptomic profiling of 4T1 cells depleted for Id1/3 and Robo1 2019-04-16 Id1 and its closely related family member Id3 are expressed by a diversity of stem and progenitor cells. We show that Id1/3 are required for the self-renewal and proliferation of triple negative breast cancer (TNBC) cells both in vitro and in vivo. Furthermore, we identified that Id1/3 negatively regulates the tumour suppressor gene Robo1. Depletion of Robo1 could rescue the proliferative defect induced by Id1/3 knockdown. To understand the mechanisms by which Robo1 rescues cell proliferation in Id1/3 depleted cells, we performed RNA-Sequencing on 4T1 cells with Dox-inducible Id1/3 KD and/or Robo1 depletion using siRNA. We conclude that following Id1/3 knockdown, Robo1 is induced and exerts anti-proliferative effects via suppression of a Myc transcriptional program. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE129858 Targeting the Id1-Kif11 Axis in Triple-Negative Breast Cancer Using Combination Therapy. Biomolecules 4.694 https://doi.org/10.3390/biom10091295 {Biomolecules (4.694): 10.3390/biom10091295} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA533191 https://www.ebi.ac.uk/ena/browser/view/PRJNA533191 https://www.ncbi.nlm.nih.gov/sra?term=SRP193147 [Overal design]mRNA sequencing of 4T1 cells with 4 treatment groups: Control (Non-targeting siRNA [NT]), Id1/3 knockdown (NT+Dox), Robo1 knockdown (siRobo1), and Id1/3 + Robo1 knockdown (siRobo1+Dox). Experiments were performed in quadruplicate.; [Treatment]'Dox (1 µg/mL) was added to the wells as indicated in the Characteristics section above at the time of seeding. siRNA (Non-targeting or Robo1) (Dharmacon) were transfected into the cells at the time of seeding according the Characteristics section above following the Dharmacon standard protocol for siRNA transfection. Following treatment cells were grown for 48 hours and then cells pellets were frozen for RNA extraction.'; [Growth]'3.5x10e4 4T1 K1 cells were seeded in 6-well plates in 4T1 media (RPMI 1640 (Gibco) supplemented with 10% (v/v) FBS (Thermo Fisher Scientific), 20mM HEPES (Gibco), 1mM sodium pyruvate (Gibco), and 0.25% (v/v) glucose (Gibco).'; [Extraction]'Total RNA was extracted from 1-3 million fresh frozen cells using the automated QiaSymphony magetic bead extraction.\nLibraries were constructed according to Illumina’s instructions using the TruSeq Stranded mRNA library prep kit.'; [Cell type]'4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3''cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: -; sirna treatment: Non-targeting siRNA; genotype: Control; replicate: 1; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: -; sirna treatment: Non-targeting siRNA; genotype: Control; replicate: 2; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: -; sirna treatment: Non-targeting siRNA; genotype: Control; replicate: 3; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: -; sirna treatment: Non-targeting siRNA; genotype: Control; replicate: 4; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: +; sirna treatment: Non-targeting siRNA; genotype: Id1/3 knockdown; replicate: 1; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: +; sirna treatment: Non-targeting siRNA; genotype: Id1/3 knockdown; replicate: 2; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: +; sirna treatment: Non-targeting siRNA; genotype: Id1/3 knockdown; replicate: 3; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: +; sirna treatment: Non-targeting siRNA; genotype: Id1/3 knockdown; replicate: 4; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: -; sirna treatment: Robo1 siRNA; genotype: Robo1 knockdown; replicate: 1; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: -; sirna treatment: Robo1 siRNA; genotype: Robo1 knockdown; replicate: 2; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: -; sirna treatment: Robo1 siRNA; genotype: Robo1 knockdown; replicate: 3; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: -; sirna treatment: Robo1 siRNA; genotype: Robo1 knockdown; replicate: 4; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: +; sirna treatment: Robo1 siRNA; genotype: Id1/3 + Robo1 knockdwon; replicate: 1; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: +; sirna treatment: Robo1 siRNA; genotype: Id1/3 + Robo1 knockdwon; replicate: 2; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: +; sirna treatment: Robo1 siRNA; genotype: Id1/3 + Robo1 knockdwon; replicate: 3; ', 'cell line: 4T1; cell type: 4T1 K1 cell line with dox-inducible shRNA targeting Id1 and Id3; dox treatment: +; sirna treatment: Robo1 siRNA; genotype: Id1/3 + Robo1 knockdwon; replicate: 4; ' GSE99941 Homo sapiens 6 Expression profiling by array GPL6244 Effects of PPARgamma-inactive Delta-2-TGZ on breast cancer cells MCF-7 2017-06-12 TGZ is an agonist of the nuclear receptor PPARgamma. This synthetic compound displays anticancer effects on breast cancer cells but some of them are PPARgamma independent. Delta-2-TGZ (delta-2-troglotazone) is a PPARgamma inactive TGZ derivative possessing a double bond adjoining the thiazolidinedione ring. This compound still displays anticancer efefcts. It is an interesting tool to study the PPARgamma-independent mechanisms. We used microarrays to examine the global programme of gene expression in response to Delta-2-TGZ treatment in MCF7 cell line. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99941 Pro-apoptotic effect of Δ2-TGZ in "claudin-1-low" triple-negative breast cancer cells: involvement of claudin-1. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-017-4378-2 {Breast cancer research and treatment (3.471): 10.1007/s10549-017-4378-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA390157 https://www.ebi.ac.uk/ena/browser/view/PRJNA390157 None [Overal design]We compare global gene expression levels between untreated and delta-2-troglitazone treated MCF7 cells at 12H. Each data point was realized in triplicate; [Treatment]'MCF-7 cells were culture in 6 well-plated for 12h in presence of DMSO or Delta-2-TGZ'; [Growth]'MCF-7 cells were cultured at 37°C under 5% CO2 in DMEM media'; [Extraction]"Total RNA were extracted using Rneasy Mini Kit from Qiagen according to manufacturer's intructions"; [Cell type]'Source: ''cell line: MCF7; ' GSE20342 Homo sapiens 32 Expression profiling by array GPL5175; GPL5188 Estrogen regulation and physiopathologic significance of alternative promoters in breast cancer 2010-02-16 Alternative promoters (APs) occur in >30% protein-coding genes and contribute to proteome diversity. However, large-scale analyses of AP regulation are lacking, and little is known about their potential physiopathologic significance. To better understand the transcriptomic impact of estrogens, which play a major role in breast cancer, we analyzed gene and AP regulation by estradiol in MCF7 cells using pan-genomic exon arrays. We thereby identified novel estrogen-regulated genes, and determined the regulation of AP-encoded transcripts in 150 regulated genes. In <30% cases, APs were regulated in a similar manner by estradiol, while in >70% cases, they were regulated differentially. The patterns of AP regulation correlated with the patterns of estrogen receptor (ERα) and CCCTC-binding factor (CTCF) binding sites at regulated gene loci. Interestingly, among genes with differentially regulated APs, we identified cases where estradiol regulated APs in an opposite manner, sometimes without affecting global gene expression levels. This promoter switch was mediated by the DDX5/DDX17 family of ERα coregulators. Finally, genes with differentially regulated promoters were preferentially involved in specific processes (e.g., cell structure and motility, and cell cycle). We show in particular that isoforms encoded by the NET1 gene APs, which are inversely regulated by estradiol, play distinct roles in cell adhesion and cell cycle regulation, and that their expression is differentially associated with prognosis in ER+ breast cancer. Altogether, this study identifies the patterns of AP regulation in estrogen-regulated genes, demonstrates the contribution of AP-encoded isoforms to the estradiol-regulated transcriptome, as well as their physiopathologic significance in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE20342 Estrogen regulation and physiopathologic significance of alternative promoters in breast cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-09-3988 {Cancer research (8.378): 10.1158/0008-5472.CAN-09-3988} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA125419 https://www.ebi.ac.uk/ena/browser/view/PRJNA125419 None [Overal design]16 samples of MCF7 cells exposed to different treatments were analyzed: 4 x control_6 hours; 4 x estradiol_6 hours; 4 x control_24 hours; 4 x estradiol_24 hours.; [Treatment]'Cells were treated with 17β-estradiol (Sigma, 10 nM) or 0.1% ethanol as a control.'; [Growth]'MCF7 cells were maintained in DMEM with 10% fetal bovine serum in a CO2 humidified chamber at 37 °C, then grown for 3 days in phenol red-free medium supplemented with 2% charcoal-stripped serum before treatment.'; [Extraction]"Total RNA was isolated using Trizol total RNA isolation reagent (Invitrogen) according to the manufacturer's protocol."; [Cell type]'Source: ''disease state: ER+ breast cancer; cell line: MCF7; agent: 0.1% ethanol (control); time point: 6 hours; ', 'disease state: ER+ breast cancer; cell line: MCF7; agent: estradiol; time point: 6 hours; ', 'disease state: ER+ breast cancer; cell line: MCF7; agent: 0.1% ethanol (control); time point: 24 hours; ', 'disease state: ER+ breast cancer; cell line: MCF7; agent: estradiol; time point: 24 hours; ' GSE55529 Homo sapiens 14 Expression profiling by array GPL570 EcadEGFP expression in MDA-MB-134 and IPH-926 2014-03-03 This experiment aims to study transcriptional alterations induced by reconstitution of wild type E-cadherin expression in human lobular breast cancer cells harbouring deleterious, somatic CDH-1 mutations https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55529 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA239879 https://www.ebi.ac.uk/ena/browser/view/PRJNA239879 None [Overal design]Two cell lines (IPH-926 and MDA-MB-134) expressing synthetic Ecad (EcadEGFP) or not (EGFP) were compared against each other. Analysis were conducted in triplicates (IPH-926) and quadruplicates (MDA-MB-134), respectively.; [Treatment]'None'; [Growth]'None'; [Extraction]"Qiagen RNAeasy extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'lobular breast cancer''cell line: IPH-926; cell type: lobular breast cancer; genotype: EGFP; ', 'cell line: IPH-926; cell type: lobular breast cancer; genotype: EcadEGFP; ', 'cell line: MDA-MB-134; cell type: lobular breast cancer; genotype: EGFP; ', 'cell line: MDA-MB-134; cell type: lobular breast cancer; genotype: EcadEGFP; ' GSE169716 Homo sapiens 5 Genome binding/occupancy profiling by high throughput sequencing GPL18573 CBFB cooperates with p53 to maintain TAp73 expression and suppress breast cancer 2021-03-26 The goal of this study is to use H3K4me3 signal to mark the promoter regions of the p73 gene. The p73 gene expresses TAp73 and DNp73 isoforms, which use two different promoters. H3K4me3 is generally associated with the promoter of a gene and, therefore, can be used to mark the promoters for TAp73 and DNp73. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE169716 CBFB cooperates with p53 to maintain TAp73 expression and suppress breast cancer. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1009553 {PLoS genetics (5.224): 10.1371/journal.pgen.1009553} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA717752 https://www.ebi.ac.uk/ena/browser/view/PRJNA717752 https://www.ncbi.nlm.nih.gov/sra?term=SRP312331 [Overal design]For wild type MCF10A cells, H3K4me3 were repeated twice. Other conditions were repeated once.; [Treatment]'No treatment'; [Growth]'DMEM/F12 media supplemented with 5% horse serum, 10 µg/ml human recombinant insulin (Sigma, Cat# 910077C), 20 ng/ml human EGF (PeproTech, Cat# AF100-15), 500 ng/ml hydrocortisone (Sigma, Cat# H0888g), 100 ng/ml cholera toxin (Sigma, Cat# C8052-5MG) and antibiotics.'; [Extraction]'ChIP DNA was extracted by standard phenol approach.\nTruSeq ChIP Library Prep Kit (IP-202-1012)'; [Cell type]'Source: ''treatment: untreated; repeat: repeat1; genotype: wild type; chip antibody: H3K4me3 (Abcam, ab8580, 5ug); ', 'treatment: untreated; repeat: repeat1; genotype: CBFB knockout; chip antibody: H3K4me3 (Abcam, ab8580, 5ug); ', 'treatment: untreated; repeat: repeat1; genotype: RUNX1 knockout; chip antibody: H3K4me3 (Abcam, ab8580, 5ug); ', 'treatment: untreated; repeat: repeat2; genotype: wild type; chip antibody: H3K4me3 (Abcam, ab8580, 5ug); ', 'treatment: untreated; repeat: repeat1; genotype: p53 knockout; chip antibody: H3K4me3 (Abcam, ab8580, 5ug); ' GSE156873 Homo sapiens 28 Expression profiling by array GPL17586 Hsa-miR-375/RASD1 signaling predicts local control in early breast cancer 2020-08-25 The current analysis was a two phase study. The first step of the pilot phase comprised an in-silico search for potential target molecules in five different databases. The second step was a screen for potential targets in 28 patients (14 with local relapse and 14 matched controls) by means of microarray technology. The combined results formed the basis for the validation phase in an independent set of 53 patients performed with droplet digital PCR (ddPCR). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE156873 Hsa-miR-375/RASD1 Signaling May Predict Local Control in Early Breast Cancer. Genes 3.331 https://doi.org/10.3390/genes11121404 {Genes (3.331): 10.3390/genes11121404} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA659262 https://www.ebi.ac.uk/ena/browser/view/PRJNA659262 None [Overal design]28 patients (14 with local relapse and 14 matched controls); [Treatment]'The tissue was retrieved during breast conserving surgery.'; [Growth]'FFPE fresh frozen paraffin embedded breast cancer tissue from surgical excision'; [Extraction]'none provided by the submitter'; [Cell type]'Source: ''tissue: surgical breast tumor sample; gender: female; tumor stage: early breast cancer; ' GSE22610 Homo sapiens 26 Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing GPL96; GPL9052 Genome-Wide Analysis of Estrogen Receptor-α DNA Binding and Tethering Mechanisms 2010-06-29 The nuclear receptor, estrogen receptor alpha (ERα), controls the expression of hundreds of genes responsible for target cell phenotypic properties, but the relative importance of direct vs. tethering mechanisms of DNA binding has not been established. In this first report, we examine the genome-wide chromatin localization of an altered-specificity mutant ER with a DNA-binding domain deficient in binding to estrogen response element (ERE)-containing DNA (DBDmut ER) vs. wild type ERα. Using high-throughput sequencing of ER chromatin immunoprecipitations (ChIP-Seq) and mRNA transcriptional profiling, we show that direct ERE binding is required for most (75%) estrogen-dependent gene regulation and 90% of hormone-dependent recruitment of ER to genomic binding sites. De novo motif analysis of the chromatin binding regions in MDA-MB-231 human breast cancer cells defined unique transcription factor profiles responsible for genes regulated through tethering vs. direct DNA (ERE) binding, with Runx motifs enriched in ER-tethered sites. We confirmed a role for Runx1 in mediating ERa genomic recruitment and regulation of tethering genes. Our findings delineate the contributions of ERE binding vs. binding through response elements for other transcription factors in chromatin localization and ER-dependent gene regulation, paradigms likely to underlie the gene regulatory actions of other nuclear receptors as well. This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22610 Genome-wide analysis of estrogen receptor alpha DNA binding and tethering mechanisms identifies Runx1 as a novel tethering factor in receptor-mediated transcriptional activation. Molecular and cellular biology 3.735 https://doi.org/10.1128/MCB.00118-10 {Molecular and cellular biology (3.735): 10.1128/MCB.00118-10} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA128349 https://www.ebi.ac.uk/ena/browser/view/PRJNA128349 None [Overal design]Refer to individual Series; [Treatment]'Cells were treated with 10 nM E2 for 1-24 hours.', 'Cells were treated with 10 nM E2 for 45 minutes, fixed with 1% formaldehyde for 10 minutes and sonicated to shear chromatin.'; [Growth]"Cells were grown in phenol-red free DMEM-Ham's F-12 media with 10 mM HEPES, 10% Charcoal-dextran stripped media, 6 ng/ml bovine insulin, 3.75 ng/ml Hydrocortisone and 16 ug/ml glutathione."; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions.", 'Chromatin was sonicated and precipitated using an specific antibody for ERa (HC20,Santa Cruz)'; [Cell type]'Source: ', 'MDA-MB 231 cells stably expressing ER''genotype/variation: WT-ER; time point: 0 Hr E2; ', 'genotype/variation: WT-ER; time point: 1 Hr E2; ', 'genotype/variation: WT-ER; time point: 2 Hr E2; ', 'genotype/variation: WT-ER; time point: 4 Hr E2; ', 'genotype/variation: WT-ER; time point: 8 Hr E2; ', 'genotype/variation: WT-ER; time point: 24 Hr E2; ', 'genotype/variation: DBDmut-ER; time point: 0 Hr E2; ', 'genotype/variation: DBDmut-ER; time point: 1 Hr E2; ', 'genotype/variation: DBDmut-ER; time point: 2 Hr E2; ', 'genotype/variation: DBDmut-ER; time point: 4 Hr E2; ', 'genotype/variation: DBDmut-ER; time point: 8 Hr E2; ', 'genotype/variation: DBDmut-ER; time point: 24 Hr E2; ', 'cell type: MDA-MB 231 cells stably expressing ER; genotype/variation: WT-ER; antibody: ERa; antibody manufacturer: HC20 Santa Cruz; cell amount: 20 million Cells; ', 'cell type: MDA-MB 231 cells stably expressing ER; genotype/variation: DBDmut-ER; antibody: ERa; antibody manufacturer: HC20 Santa Cruz; cell amount: 20 million Cells; ' GSE76714 Homo sapiens 71 Expression profiling by array GPL14951 Brain Metastasis Prediction by DASL Transcriptomic Profiling in Triple Negative Breast Cancer based on FFPE samples 2016-01-11 Triple negative breast cancer (TNBC) lacks expression of steroid hormone receptors (estrogen alpha and progesterone) and epidermal growth factor receptor type 2. This phenotype shows high metastatic potential, with particular predilection to lungs and brain. Determination of transcriptomic profiles specific for brain metastasis (BM)-prone TNBC might identify high-risk patients requiring the use of alternative, more aggressive or specific preventive and therapeutic approaches. The aim of the study was to compare the gene expression profile in the primary tumor of patients who developed brain metastases in comparison to these who were metastatic to other organs (excluding central nervous system) in an attempt to verify, whether there exist a significant difference in the transcriptome of these two subgroups. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76714 Brain Metastasis Prediction by Transcriptomic Profiling in Triple-Negative Breast Cancer. Clinical breast cancer 2.762 https://doi.org/10.1016/j.clbc.2016.08.008 {Clinical breast cancer (2.762): 10.1016/j.clbc.2016.08.008} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA308446 https://www.ebi.ac.uk/ena/browser/view/PRJNA308446 None [Overal design]Gene expression profiles of primary tumors in 71 TNBC patients (23 patients with BM and 48 patients without BM, discovery cohort), derived from a consecutive series of 324 advanced TNBC treated in 17 oncology centers in Poland and Italy between 1997 and 2013. Analysis was carried out in mRNA samples isolated from formalin-fixed paraffin embedded (FFPE) specimens, using Illumina cDNA-mediated Annealing, Selection, Extension and Ligation (DASL) method and Illumina HumanHT-12 oligonucleotide microarrays. The expression of 29,369 gene transcripts was compared between patients with and without BM, no reliable differences were identified. The results were validated in independent cohort of 48 samples, the top transcripts selected in discovery cohort showed no significant differences in the test set.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA isolation was performed using the QIAGEN RNeasy FFPE Kit (Qiagen, Hilden, Germany), in accordance with the manufacturer’s protocol. The RNeasy FFPE kit includes traditional RNeasy MinElute series columns for RNA purification, and additionally gDNA Eliminator columns, which allow for the removal from the sample of genomic DNA that contaminates the isolated RNA. The blocks were cut into 5 μm-thick sections. In RNA isolation, 5 sections were used per one examination. The material was deparaffinized using xylene and, after supernatant removal, rinsed in alcohol. RNA concentration was evaluated using the Nanodrop ND-1000 microspectrophotometer. No routine RNA quality analysis was carried out.'; [Cell type]'Source: ''patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 52.27; disease stage at diagnosis: 4-IV; tumor grade: 3; patient age at metastatic disease: 52.45; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 41.11; disease stage at diagnosis: 2-IIB; tumor grade: 3; patient age at metastatic disease: 42.25; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 60.85; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: NA; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 77.41; disease stage at diagnosis: 4-IV; tumor grade: 3; patient age at metastatic disease: 77.62; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 58.98; disease stage at diagnosis: 4-IV; patient age at metastatic disease: 59.14; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 67.75; disease stage at diagnosis: 3-IIIA; tumor grade: 3; patient age at metastatic disease: 69.09; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 52.66; disease stage at diagnosis: 4-IV; tumor grade: 3; patient age at metastatic disease: 52.66; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 68.03; disease stage at diagnosis: 2-IIB; tumor grade: 2; patient age at metastatic disease: 72.18; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 47.96; disease stage at diagnosis: 2-IIA; tumor grade: 3; patient age at metastatic disease: 49.22; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 51.96; disease stage at diagnosis: 2-IIA; tumor grade: 2; patient age at metastatic disease: 54.86; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 72.89; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: 73.80; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 50.33; disease stage at diagnosis: 4-IV; patient age at metastatic disease: 50.33; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 69.12; patient age at metastatic disease: 69.80; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 59.81; tumor grade: 3; patient age at metastatic disease: NA; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 68.94; disease stage at diagnosis: 4-IV; tumor grade: 3; patient age at metastatic disease: 68.96; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 57.23; disease stage at diagnosis: 2-IIA; patient age at metastatic disease: 61.64; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 33.12; patient age at metastatic disease: 49.15; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 43.96; disease stage at diagnosis: 3-IIIA; tumor grade: 3; patient age at metastatic disease: 45.31; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 59.88; tumor grade: 2; patient age at metastatic disease: NA; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 46.05; disease stage at diagnosis: 1-IA; tumor grade: 2; patient age at metastatic disease: 49.66; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 59.02; disease stage at diagnosis: 2-IIB; tumor grade: 3; patient age at metastatic disease: 62.28; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 71.72; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: 72.77; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 61.50; disease stage at diagnosis: 3-IIIB; tumor grade: 2; patient age at metastatic disease: 68.15; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 59.77; disease stage at diagnosis: 3-IIIC; tumor grade: 2; patient age at metastatic disease: 60.48; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 55.52; disease stage at diagnosis: 2-IIA; tumor grade: 3; patient age at metastatic disease: 59.56; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 81.59; disease stage at diagnosis: 4-IV; tumor grade: 3; patient age at metastatic disease: 81.65; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 66.35; disease stage at diagnosis: 3-IIIA; tumor grade: 3; patient age at metastatic disease: 68.33; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 55.39; disease stage at diagnosis: 3-IIIA; tumor grade: 2; patient age at metastatic disease: 56.85; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 55.71; tumor grade: 3; patient age at metastatic disease: 56.09; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 48.34; disease stage at diagnosis: 2-IIA; tumor grade: 3; patient age at metastatic disease: 49.22; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 41.44; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: 45.48; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 47.73; disease stage at diagnosis: 2-IIB; tumor grade: 3; patient age at metastatic disease: 49.81; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 49.67; disease stage at diagnosis: 2-IIB; tumor grade: 3; patient age at metastatic disease: 51.67; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 60.61; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: 61.63; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 71.84; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: 73.06; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 54.05; disease stage at diagnosis: 4-IV; tumor grade: 2; patient age at metastatic disease: 54.18; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 46.84; disease stage at diagnosis: 2-IIB; tumor grade: 2; patient age at metastatic disease: 50.19; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 65.61; disease stage at diagnosis: 3-IIIA; tumor grade: 2; patient age at metastatic disease: 66.27; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 53.31; disease stage at diagnosis: 1-IA; tumor grade: 2; patient age at metastatic disease: 55.71; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 56.07; disease stage at diagnosis: 3-IIIB; tumor grade: 3; patient age at metastatic disease: 56.41; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 47.83; disease stage at diagnosis: 2-IIB; patient age at metastatic disease: 49.16; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 79.30; disease stage at diagnosis: 4-IV; patient age at metastatic disease: 79.53; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 59.96; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: 60.79; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 44.90; disease stage at diagnosis: 3-IIIB; tumor grade: 2; patient age at metastatic disease: 46.07; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 63.46; disease stage at diagnosis: 3-IIIA; tumor grade: 3; patient age at metastatic disease: 67.81; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 50.43; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: 51.41; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 64.06; disease stage at diagnosis: 2-IIB; tumor grade: 3; patient age at metastatic disease: 65.70; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 71.12; disease stage at diagnosis: 3-IIIA; tumor grade: 2; patient age at metastatic disease: 74.23; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 64.55; tumor grade: 3; patient age at metastatic disease: 66.84; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 50.14; disease stage at diagnosis: 4-IV; tumor grade: 3; patient age at metastatic disease: 50.14; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 74.61; disease stage at diagnosis: 1-IA; tumor grade: 2; patient age at metastatic disease: 75.88; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 79.82; disease stage at diagnosis: 4-IV; tumor grade: 3; patient age at metastatic disease: 79.82; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 30.84; tumor grade: 2; patient age at metastatic disease: NA; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 71.94; disease stage at diagnosis: 4-IV; tumor grade: 3; patient age at metastatic disease: 72.07; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 36.65; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: 37.84; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 43.42; disease stage at diagnosis: 3-IIIA; tumor grade: 3; patient age at metastatic disease: 49.54; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 65.16; disease stage at diagnosis: 4-IV; tumor grade: 3; patient age at metastatic disease: 65.16; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 54.60; disease stage at diagnosis: 3-IIIA; tumor grade: 2; patient age at metastatic disease: 57.14; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 28.51; disease stage at diagnosis: 2-IIA; tumor grade: 3; patient age at metastatic disease: NA; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 65.01; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: 67.11; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 69.50; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: NA; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 70.99; disease stage at diagnosis: 2-IIB; tumor grade: 3; patient age at metastatic disease: 73.02; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 70.62; disease stage at diagnosis: 2-IIB; tumor grade: 3; patient age at metastatic disease: 71.49; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 52.38; disease stage at diagnosis: 2-IIA; tumor grade: 3; patient age at metastatic disease: 53.73; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 64.37; disease stage at diagnosis: 3-IIIA; tumor grade: 2; patient age at metastatic disease: 65.65; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient with brain metastasis (BM); patient age at breast cancer diagnosis: 36.52; disease stage at diagnosis: 3-IIIA; tumor grade: 2; patient age at metastatic disease: 37.90; location of metastatic disease: with brain metastases; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 76.53; disease stage at diagnosis: 3-IIIC; tumor grade: 2; patient age at metastatic disease: 77.47; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 46.31; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: 47.67; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 50.14; disease stage at diagnosis: 2-IIA; tumor grade: 3; patient age at metastatic disease: 52.71; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 57.76; disease stage at diagnosis: 4-IV; tumor grade: 2; patient age at metastatic disease: 57.76; location of metastatic disease: other than central nervous system; ', 'patient group: TNBC patient without brain metastasis (BM); patient age at breast cancer diagnosis: 67.78; disease stage at diagnosis: 3-IIIC; tumor grade: 3; patient age at metastatic disease: 73.44; location of metastatic disease: other than central nervous system; ' GSE145316 Homo sapiens 8 Expression profiling by high throughput sequencing GPL18573 Pan-cancer molecular analysis of the RB-pathway 2020-02-14 The retinoblastoma tumor suppressor (RB1) plays a critical role in coordinating multiple pathways that impact on tumor initiation, disease progression, and therapeutic responses. Here we interrogated the TCGA pan-cancer data collection to probe fundamental molecular features associated with the RB-pathway across 31 tumor-types. While the RB-pathway has been purported to exhibit multiple mutually exclusive events, only RB1 is mutually exclusive with multiple genetic events that deregulate CDK4/6 activity. Using an isogenic ER+ breast cancer model with targeted RB1 deletion, we identified gene expression features that link CDK4/6 activity and RB-dependency (CDK4/6-RB integrated signature). This gene expression signature is associated with prognosis across a spectrum of tumors that exhibit average lower signature value indicative of more indolent diseases. Single copy loss on chromosome 13q encompassing the RB1 locus is prevalent in many cancers, and is associated with reduced expression of multiple genes on 13q including RB1, and inversely related to the CDK4/6-RB integrated signature supporting a genetic cause/effect relationship. To probe the broader implications on tumor biology, we investigated genes that are positively and inversely correlated with the CDK4/6-RB integrated signature. This approach defined tumor-specific pathways that could represent new therapeutic vulnerabilities associated with RB-pathway activity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE145316 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA606752 https://www.ebi.ac.uk/ena/browser/view/PRJNA606752 https://www.ncbi.nlm.nih.gov/sra?term=SRP249539 [Overal design]MCF7 wild type and RB knockout cells were exposed to DMSO and Palbociclib (250 nM). Following 48 hours exposure, RNA was extracted from these cells using RNeasy plus kit (Quiagen) according to manufacturer's protocol and then subjected to RNA sequence analysis.; [Treatment]'Cells were treated with DMSO(0.1%) and Palbociclib(250nM+0.1% DMSO) upto 48 hrs'; [Growth]'Cells were grown in DMEM medium supplemented with 10% FBS'; [Extraction]'Total RNA was extracted using the RNeasy kit from Quiagen\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''cell line: MCF7; tissue: mammary gland, breast; genotype: RB Knockout; agent: DMSO; ', 'cell line: MCF7; tissue: mammary gland, breast; genotype: RB Knockout; agent: Palbociclib; ', 'cell line: MCF7; tissue: mammary gland, breast; genotype: wild type; agent: DMSO; ', 'cell line: MCF7; tissue: mammary gland, breast; genotype: wild type; agent: Palbociclib; ' GSE52099 Mus musculus; Homo sapiens 36 Expression profiling by array GPL1261; GPL17889 cMET 2013-11-05 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE52099 SPSB1 promotes breast cancer recurrence by potentiating c-MET signaling. Cancer discovery 26.370 https://doi.org/10.1158/2159-8290.CD-13-0548 {Cancer discovery (26.370): 10.1158/2159-8290.CD-13-0548} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA226671 https://www.ebi.ac.uk/ena/browser/view/PRJNA226671 None [Overal design]Refer to individual Series; [Treatment]'Cells were seeded on 100mm plate with 10% FBS for 24 h and then starved in serum-free media overnight. Increasing concentrations of HGF were then added to cells cultured with serum-free media and RNAs were harvested 4h after HGF addition.', 'Vehicle ( 2% HPMC 1% Tween ) or 100mg/kg AMG was gavaged into the animals, and tumors were harvested 12 hours after the gavage.'; [Growth]'MCF10A is maintained in DMEM+10%FBS+5ug/ml insulin+10ug/ml EGF+1ug/ml hydrocortisone. Cells are passaged 1:3 every 2-3 days.', 'MTB-TAN recurrent cells were injected into the number four mammary glands of nude mice. Tumors with sizes of 5mm in diameters were formed around two weeks after injection, at which point the mice received one dose of vehicle or 100mg/kg MET inhibitor (AMG2100517).'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions"; [Cell type]'Source: ''cell line: MCF10A; treatment: 0ng HGF; ', 'cell line: MCF10A; treatment: 1ng HGF; ', 'cell line: MCF10A; treatment: 3ng HGF; ', 'cell line: MCF10A; treatment: 7.5ng HGF; ', 'cell line: MCF10A; treatment: 15ng HGF; ', 'cell line: MCF10A; treatment: 30ng HGF; ', 'strain: FVB; gender: F; tissue: xenograft mammary tumor; genotype: MTB-TAN; treatment: vehicle; ', 'strain: FVB; gender: F; tissue: xenograft mammary tumor; genotype: MTB-TAN; treatment: 100mg/kg AMG2100517; ' GSE130989 Homo sapiens 8 Genome binding/occupancy profiling by high throughput sequencing GPL20301 ChIP-seq analysis of HIF-1b binding in hypoxic cancer cell lines 2019-05-09 Pan-genomic analysis of hypoxic HIF-1b binding by ChIP-seq in cancer cell lines https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130989 Co-incidence of RCC-susceptibility polymorphisms with HIF cis-acting sequences supports a pathway tuning model of cancer. Scientific reports 4.011 https://doi.org/10.1038/s41598-019-55098-7 {Scientific reports (4.011): 10.1038/s41598-019-55098-7} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA542174 https://www.ebi.ac.uk/ena/browser/view/PRJNA542174 https://www.ncbi.nlm.nih.gov/sra?term=SRP197386 [Overal design]ChIP_seq analysi of HIF-1b binding in 4 cancer cell lines incubated in 0.5% hypoxia for 16 hours; [Treatment]'Hypoxic incubations were performed for the specified duration and ambient oxygen concentration in an In Vivo2 400 Hypoxia Work Station (Ruskinn Technology).'; [Growth]'Cell lines were grown in Dulbecco’s modified Eagle’s Medium, 100 U/ml penicillin, 100 μg/ml streptomycin and 10% fetal bovine serum (Sigma Aldrich) and regularly tested for mycoplasma infection.'; [Extraction]'Chromatin immunoprecipitation (ChIP) experiments were performed using antibodies directed against HIF-1a (rabbit polyclonal, PM14), HIF-2a (rabbit polyclonal, PM9), or HIF-1b (rabbit polyclonal, Novus Biologicals, NB100-110).\nLibraries were prepared from immunoprecipitated chromatin using the Illumina ChIP-Seq kit; All ChIP-seq experiments were performed in duplicate in accordance with ENCODE consortium guidelines.'; [Cell type]'Lung cancer cell line', 'Colorectal cancer cell line', 'Prostate cancer cell line', 'Breast cancer cell line''cell line: A549; cell type: Lung cancer cell line; ambient o2 concentration: 0.50%; duration of hypoxia: 16 hours; tchip antibody: HIF1b (Novus NB100-110); ', 'cell line: HCT-116; cell type: Colorectal cancer cell line; ambient o2 concentration: 0.50%; duration of hypoxia: 16 hours; tchip antibody: HIF1b (Novus NB100-110); ', 'cell line: PC-3; cell type: Prostate cancer cell line; ambient o2 concentration: 0.50%; duration of hypoxia: 16 hours; tchip antibody: HIF1b (Novus NB100-110); ', 'cell line: T47D; cell type: Breast cancer cell line; ambient o2 concentration: 0.50%; duration of hypoxia: 16 hours; tchip antibody: HIF1b (Novus NB100-110); ' GSE27574 Homo sapiens 79 Genome variation profiling by array GPL8841; GPL9128 High-resolution analysis of copy number changes in circulating and disseminated tumor cells in breast cancer patients 2011-02-28 The aim of this study was to establish a single-cell array comparative genomic hybridization (SCaCGH) method providing in-depth genomic analysis of circulating tumor cells (CTCs) and disseminated tumor cells (DTCs). The robustness and resolution limits of the method were estimated with different cell amounts of the breast cancer cell line SKBR3 using 44k and 244k arrays. Subsequent adjustments of the method were conducted analyzing the copy number profiles of 28 CTCs in combination with four hematopoietic cell (HC) controls from eight metastatic patients and of 24 DTCs, three probable HCs, and five HC controls from seven breast cancer patients and one healthy donor. The frequency of the major genomic gains and losses of the analyzed DTC revealed similarities to primary breast tumor samples with some evident differences. Three of the patients had available profiles for DTC and the corresponding primary tumor. In 2/3 of the examined DTCs, equivalent genomic changes and common aberration breakpoints were disclosed, both to each other and to the corresponding primary tumors. Interestingly, similar copy number changes were found in DTCs taken at time of diagnosis or in DTCs collected at 3-years relapse-free follow up. Residual immunomorphological characterized tumor cells showed balanced profiles with only minor aberrations. Three cells with unclear morphological identification showed either balanced profiles (n=2) or aberrations comparable to the primary tumor and DTC (n=1). SCaCGH may be a powerful tool for molecular characterisation of immunostained and morphological identified CTCs and DTCs to explore the malignant potential, therapeutic targets and tumor heterogeneity of single tumor cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE27574 High-resolution analyses of copy number changes in disseminated tumor cells of patients with breast cancer. International journal of cancer 4.982 https://doi.org/10.1002/ijc.26444 {International journal of cancer (4.982): 10.1002/ijc.26444} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA181273 https://www.ebi.ac.uk/ena/browser/view/PRJNA181273 None [Overal design]24 DTCs, 3 probable HCs, and 5 HCs from 7 early-stage breast cancer patients, 28 CTCs and 4 HCs from 8 metastatic breast cancer patients, and 1 healthy donor were analysed. Comparison with the primary tumor was done in 3 patients. The reference for the patients was DNA from multiple anonymous female donors. This submission does not include the SKBR3 data obtained from the 44k array.; [Treatment]'None'; [Growth]'None'; [Extraction]"For the single cells: All samples were amplified using the GenomePlex® Single Cell Whole Genome Amplification Kit (Sigma-Aldrich, Missouri, USA) according to the manufacturer's instructions with some modifications. Clean up was performed according to the manufacturer's instructions with the Gen elute™ PCR clean up kit (Sigma-Aldrich, Missouri, USA). DNA concentrations were measured using the NanoDrop® ND-1000 (Thermo Fisher Scientific, Delaware, USA). For the 3 primary tumors: Primary tumor DNA was extracted using an ABI 341 Nucleic Acid Purification System (Applied Biosystems, Carlsbad, CA, USA) according to the manufacturer's protocol."; [Cell type]'Source: ', 'breast cancer''tissue: bone marrow; type of isolated tumor cells: disseminated tumor cell (DTC); disease state: metastatic breast cancer; patient identifier: Mm2002; ', 'gender: female; donor: multiple anonymous donors; sample type: reference; vendor; catalog#: Promega (Madison, WI, USA); cat.# G1521; ', 'tissue: bone marrow; type of isolated tumor cells: disseminated tumor cell (DTC); disease state: metastatic breast cancer; patient identifier: Mm2031; ', 'tissue: bone marrow; type of isolated tumor cells: disseminated tumor cell (DTC); disease state: metastatic breast cancer; patient identifier: Mm2141; ', 'tissue: bone marrow; type of isolated tumor cells: disseminated tumor cell (DTC); disease state: metastatic breast cancer; patient identifier: Mm2471; ', 'tissue: bone marrow; type of isolated tumor cells: disseminated tumor cell (DTC); disease state: early-stage breast cancer; patient identifier: MicMa003; ', 'tissue: bone marrow; type of isolated tumor cells: normal hematopoietic cell (HC); disease state: early-stage breast cancer; patient identifier: MicMa003; ', 'tissue: breast cancer tumor; type of isolated tumor cells: breast cancer tumor; disease state: early-stage breast cancer; patient identifier: MicMa003; ', 'tissue: bone marrow; type of isolated tumor cells: disseminated tumor cell (DTC); disease state: early-stage breast cancer; patient identifier: MicMa083; ', 'tissue: bone marrow; type of isolated tumor cells: normal hematopoietic cell (HC); disease state: early-stage breast cancer; patient identifier: MicMa083; ', 'tissue: breast cancer tumor; type of isolated tumor cells: breast cancer tumor; disease state: early-stage breast cancer; patient identifier: MicMa083; ', 'tissue: bone marrow; type of isolated tumor cells: disseminated tumor cell (DTC); disease state: early-stage breast cancer; patient identifier: MicMa107; ', 'tissue: bone marrow; type of isolated tumor cells: normal hematopoietic cell (HC)?; disease state: early-stage breast cancer; patient identifier: MicMa107; ', 'tissue: bone marrow; type of isolated tumor cells: normal hematopoietic cell (HC); disease state: early-stage breast cancer; patient identifier: MicMa107; ', 'tissue: breast cancer tumor; type of isolated tumor cells: breast cancer tumor; disease state: early-stage breast cancer; patient identifier: MicMa107; ', 'tissue: bone marrow; type of isolated tumor cells: normal hematopoietic cell (HC); disease state: healthy; patient identifier: NBM031; ', 'tissue: bone marrow; type of isolated tumor cells: normal hematopoietic cell (HC); disease state: early-stage breast cancer; patient identifier: MicMa009; ', 'tissue: bone marrow; type of isolated tumor cells: normal hematopoietic cell (HC); disease state: early-stage breast cancer; patient identifier: MicMa017; ', 'tissue: peripheral blood; type of isolated tumor cells: circulating tumor cell (CTC); disease state: metastatic breast cancer; patient identifier: Mm2235; ', 'tissue: peripheral blood; type of isolated tumor cells: circulating tumor cell (CTC); disease state: metastatic breast cancer; patient identifier: Mm4100; ', 'tissue: peripheral blood; type of isolated tumor cells: circulating tumor cell (CTC); disease state: metastatic breast cancer; patient identifier: Mm4236; ', 'tissue: peripheral blood; type of isolated tumor cells: circulating tumor cell (CTC); disease state: metastatic breast cancer; patient identifier: Mm4319; ', 'tissue: peripheral blood; type of isolated tumor cells: circulating tumor cell (CTC); disease state: metastatic breast cancer; patient identifier: Mm4329; ', 'tissue: peripheral blood; type of isolated tumor cells: circulating tumor cell (CTC); disease state: metastatic breast cancer; patient identifier: Mm4355; ', 'cell line: SKBR3; cell type: breast cancer; ', 'cell line: SKBR3; cell type: breast cancer; sample type: reference; vendor; catalog#: LGC Standards (Middlesex, United Kingdom); ' GSE101691 Homo sapiens 4 Expression profiling by high throughput sequencing GPL16791 BRCA1-mimetic compound NSC35446.HCl inhits IKKB expression by reducing estrogen receptor alpha occupancy in the IKKB promoter and inhibts NF-κB activity in anti-estrogen resitant human breast cells 2017-07-20 We previously identified small molecules that fit into a BRCA1-binding pocket within estrogen receptor-alpha (ER), mimic the ability of BRCA1 to inhibit ER activity (“BRCA1-mimetics”), and overcome antiestrogen resistance. One such compound, the hydrochloride salt of NSC35446 (“NSC35446.HCl”), also inhibited growth of antiestrogen-resistant LCC9 tumor xenografts. The purpose of this study was to investigate the down-stream effects of NSC35446.HCl and its mechanism of action. Methods: Here, we studied antiestrogen-resistant (LCC9, T47DCO, MCF-7/RR, LY2), ER-negative (MDA-MB-231, HCC1806, MDA-MB-468), and antiestrogen-sensitive (MCF-7) cell lines. Techniques utilized include RNA-seq, qRT-PCR, cell growth analysis, cell-cycle analysis, Western blotting, luciferase reporter assays, TUNEL assays, in-silico analysis of the IKKB gene, and ChIP assays. Results: NSC35446.HCl inhibited proliferation and induced apoptosis in antiestrogen resistant LCC9, T47DCO, MCF-7/RR, and LY2 cells but not in ER-negative breast cancer cell lines. IKKB (IKKβ, IKBKB), an upstream activator of NF-B, was identified as a BRCA1-mimetic-regulated gene, based on an RNA-seq analysis; and NSC35446.HCl inhibited IKKB mRNA and protein expression in LCC9 cells. NSC35446.HCl also inhibited NF-B activity and expression of NF-B target genes. In-silico analysis of the IKKB promoter identified nine estrogen response element (ERE) half-sites and one ERE-like full-site. ChIP assays revealed that ER was recruited to the ERE-like full-site and five of the nine half-sites and that ER recruitment was inhibited by NSC35446.HCl in LCC9 and T47DCO cells. Conclusions: These studies identify functional EREs in the IKKB promoter and identify IKKB as an NSC35446.HCl-regulated gene; and they suggest that NF-B and IKKB, which were previously linked to antiestrogen resistance, are targets for NSC35446.HCl in reversing antiestrogen resistance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE101691 BRCA1-mimetic compound NSC35446.HCl inhibits IKKB expression by reducing estrogen receptor-α occupancy in the IKKB promoter and inhibits NF-κB activity in antiestrogen-resistant human breast cancer cells. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-017-4442-y {Breast cancer research and treatment (3.471): 10.1007/s10549-017-4442-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA395214 https://www.ebi.ac.uk/ena/browser/view/PRJNA395214 https://www.ncbi.nlm.nih.gov/sra?term=SRP113228 [Overal design]Examination of mRNA profiles of BRCA1 mimetic treated LCC9 cells: 4 samples Total: 2 Vehicle(DMSO) Control and 2 BRCA1 mimetic (A7) treated LCC9 cells; [Treatment]'Subconfluent proliferating cells were seeded into 6-well dishes at 1 x 105 cells/well on Day 0 and allowed to attach for 24-hr. The cells were treated with vehicle or BRCA1 mimetic compound A7 for 24 hrs before harvesting'; [Growth]'LCC9 were grown in phenol red-free IMEM (Corning Cellgro, Manassas, VA) plus 5% charcoal-stripped serum (CSS).'; [Extraction]"Total RNA was extracted from Control and A7 treated LCC9 cells using miRNeasy Mini Kit (Qiagen), and submitted to Otogenetics Corporation (Norcross, GA USA) for RNA-Seq assays. Briefly, the integrity and purity of total RNA were assessed using Agilent Bioanalyzer or Tapestation and OD260/280. cDNA was generated from high quality total RNA using SMARTer PCR cDNA Synthesis kit (Clontech Laboratories, Inc., Mountain View, CA USA, catalog# 634926).\nThe resulting cDNA was fragmented using Bioruptor (Diagenode, Inc., Denville, NJ USA), profiled using Agilent Tapestation, and subjected to Beckman Biomek FXp (Biomek 6000, Beckman Coulter) fully automatic workstation and a Beckman HT library kit (SPRIworks HT, Beckman Coulter, Inc. CA USA; PN B09855AA) to generate fragment libraries. The instructions were strictly followed to perform library construction. Briefly, after fragmentation the ends were repaired and 'A' bases were added to the 3' end of the fragments. Adapters were then ligated to both ends. The adaptor-ligated templates were further purified using Agencourt AMPure SPRI beads (Beckman Coulter, Inc. CA USA). The adaptor-ligated library was amplified by ligation-mediated PCR which consisted of 11 cycles of amplification, and the PCR product was purified using Agencourt AMPure SPRI beads again. After the library construction procedure was completed, QC was performed using Nanodrop 2000 (Thermo Scientific, USA) and an Agilent TapeStation (Agilent, USA) to ensure the library quality and quantity."; [Cell type]'Source: ''cell line: LCC9 Tam resistant; tissue: Breast Lumen; hormone status: Eralpha positive wt; ' GSE143948 Homo sapiens 6 Expression profiling by high throughput sequencing GPL20301 Genome wide expression change by ZNF213 knockdown in MCF-7 cells 2020-01-20 We aim to the investigate the role of ZNF213 in breast cancer progression. MCF-7 cells were used as the model , ZNF213 was silenced by siRNA. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE143948 ZNF213 Facilitates ER Alpha Signaling in Breast Cancer Cells. Frontiers in oncology 4.137 https://doi.org/10.3389/fonc.2021.638751 {Frontiers in oncology (4.137): 10.3389/fonc.2021.638751} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA602309 https://www.ebi.ac.uk/ena/browser/view/PRJNA602309 https://www.ncbi.nlm.nih.gov/sra?term=SRP243455 [Overal design]The MCF-7 cells were treated with 50nM stramble siRNA and siZNF213. After 48 hours, cells were harvested and the total RNA was extacted by Qiagen kit. The RNA sample was sent to BGI for RNA expression anaylsis.; [Treatment]'cells were treated with 50nM siZNF213 or sicontrol'; [Growth]'cells were cultured in DMEM with 10% FBS.'; [Extraction]"The total RNA was extracted from cells by the qiagen RNA exaction kit\nLibraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit (Part# 0801-0303)."; [Cell type]'Source: ''passages: 15-18 passage; cell line: MCF-7; treatment: control; ', 'passages: 15-18 passage; cell line: MCF-7; treatment: siZNF213; ' GSE144044 Homo sapiens 6 Expression profiling by array GPL13915 Gene expression profiles in maspin-overexpressing MDA-MB-231 breast cancer cells 2020-01-22 A comparison of gene expression profiles between control- and mascpin-overexpressing MDA-MB-231 cells was performed to investigate the role of cytoplasmic maspin in breast cancer progression. The data provides insight into the importance of cytoplasmic maspin in breast cancer progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144044 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA602620 https://www.ebi.ac.uk/ena/browser/view/PRJNA602620 None [Overal design]MB-231-control and MB-231-maspin cells were established by stable transduction with lentivirus-based vector. Total RNA from these cells were recovered using Rneasy Mini Kit. Isolated RNA was labeled by Cy5 and hybridized onto the 3D-Gene human mRNA oligo chip 25k (Ver 2.1). Oligo chip was scanned by a 3D-Gene Scanner 3000.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted with RNeasy Mini Kit.'; [Cell type]'breast cancer cells''cell line: MDA-MB-231; cell type: breast cancer cells; genotype/variation: stably expressing ZsGreen; ', 'cell line: MDA-MB-231; cell type: breast cancer cells; genotype/variation: stably expressing maspin and ZsGreen (Maspin-P2A-ZsGreen); ' GSE29127 Homo sapiens 2 Methylation profiling by high throughput sequencing GPL10999; GPL11154 Genome-wide DNA methylation mapping in breast cancer cells (HCC1954) and normal breast cells (HMEC) 2011-05-06 While genetic mutation is a hallmark of cancer, many cancers also acquire epigenetic alterations during tumorigenesis including aberrant DNA hypermethylation of tumor suppressors as well as changes in chromatin modifications as caused by genetic mutations of the chromatin-modifying machinery. However, the extent of epigenetic alterations in cancer cells has not been fully characterized. Here, we describe the first complete methylome maps at single nucleotide resolution of a low-passage breast cancer cell line and primary human mammary epithelial cells. We find widespread DNA hypomethylation in the cancer cell, primarily at partially methylated domains (PMDs) in normal breast cells. Unexpectedly, genes within these regions are largely silenced in cancer cells. The loss of DNA methylation in these regions is accompanied by formation of repressive chromatin, with a significant fraction displaying allelic DNA methylation where one allele is DNA methylated while the other allele is occupied by histone modifications H3K9me3 or H3K27me3. Our results show a mutually exclusive and complementary relationship between DNA methylation and H3K9me3 or H3K27me3. These results suggest that global DNA hypomethylation in breast cancer is tightly linked to the formation of repressive chromatin domains and gene silencing, thus identifying a potential epigenetic pathway for gene regulation in cancer cells and suggesting a possible new approach toward the development of cancer therapeutics. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE29127 Global DNA hypomethylation coupled to repressive chromatin domain formation and gene silencing in breast cancer. Genome research 9.944 https://doi.org/10.1101/gr.125872.111 {Genome research (9.944): 10.1101/gr.125872.111} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA142895 https://www.ebi.ac.uk/ena/browser/view/PRJNA142895 https://www.ncbi.nlm.nih.gov/sra?term=SRP006728 [Overal design]methylC-Seq on breast cancer HCC1954 and normal breast HMEC. 100 cycles of sequencing on Illumina platform.; [Treatment]'None'; [Growth]'None'; [Extraction]"5.5 µg of genomic DNA was extracted from frozen cell pellets using the DNeasy Mini Kit (Qiagen, Valencia, CA) and spiked with 25 ng unmethylated cl857 Sam7 Lambda DNA (Promega, Madison, WI). The DNA was fragmented with a Biorupter (Diagenode, Woburn, MA) to 100-300 bp, followed by end repair and addition of a 3' A base. Single-end cytosine-methylated adapters were ligated to the sonicated DNA and 150-350bp fragments were purified from a 2% agarose gel. Adapter-ligated DNA (~450 ng) was subjected to sodium bisulfite conversion using the MethylCode kit (Life Technologies, Carlsbad, CA) as per manufacturer's instructions. The bisulfite-converted, adapter-ligated DNA molecules were enriched by 5 cycles of PCR with PfuTurboCx Hotstart DNA polymerase (Stratagene). The reaction products were purified with a 2% agarose gel."; [Cell type]'breast cancer cells', 'primary human mammary epithelial cells''cell line: HCC1954; cell type: breast cancer cells; ', 'cell line: HMEC; cell type: primary human mammary epithelial cells; ' GSE99626 Homo sapiens 62 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL16791; GPL18573; GPL20301 Combinatorial Reprogramming of Estrogen Signaling by the Nuclear Receptor Family 3C 2017-06-02 Estrogen receptor (ER) positive breast cancers exist in a complex environment of steroid hormones and their cognate receptors. Receptors for estrogens, progestogens (PR), androgens (AR), glucocorticoids (GR) and mineralocorticoids (MR) are variably expressed in these hormone- sensitive breast cancers. Clinical translation of crosstalk among these receptors has been limited by an incomplete understanding of ER reprogramming by PR, GR, AR and MR (NR3C receptors). This study reports that each of the NR3C receptors reprograms ER chromatin binding to sites enriched for NR3C binding motifs and that hormonal co-treatment increases the likelihood of ER binding to estrogen response elements. A major overlap is observed among ER conserved sites, but not among ER sites that are lost or gained due to reprogramming by each of the NR3C receptors. This stability of ER genomic binding is reflected in the resulting transcriptomes, as there is significant overlap among genes whose expression is unaltered in response to joint hormonal interventions but not among genes whose expression is enhanced or opposed by an individual NR3C receptor. The addition of NR3C ligands can enhance or oppose estrogen-mediated induction and repression of gene transcription, resulting in net agonism or antagonism of ER-mediated actions at gene loci and of cellular pathways of interest. In addition to differential modulation of chromatin binding, differences in cofactor associations for ER, PR and GR likely contribute to the divergent functions of these receptors in breast cancer. Among the NR3C receptors, MR activation differentially reprograms ER chromatin binding and, in contrast to ligands for PR, GR or AR, the MR ligand aldosterone does not inhibit estrogen-induced cell proliferation or potentiate the anti-proliferative effect of tamoxifen in ER+ MCF7 cells. PR, GR, AR and MR may be functionally relevant in ER+ breast cancer because higher expression of these NR3C receptors; or genes whose estrogen-regulated expression is altered by each of these receptors is significantly associated with better overall and relapse-free survival. In summary, this study highlights the diverse yet overlapping activities of NR3C receptors in reprogramming ER signaling. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99626 None None None None None 'genomic DNA', 'polyA RNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA389107 https://www.ebi.ac.uk/ena/browser/view/PRJNA389107 https://www.ncbi.nlm.nih.gov/sra?term=SRP108515 [Overal design]Model systems were deprived of steroids by culturing them in phenol red free RPMI 1640 media that is supplemented with 10% charcoal-stripped fetal bovine serum and 1% penicillin/streptomycin. Subsequently, these steroid-deprived models were treated with either vehicle, 10 nM estradiol, 10 nM of NR3C ligand (Progesterone, Dexamethasone, DHT or Aldosterone) or 10 nM of both estradiol and NR3C ligand for the time duration mentioned in the paper. Subsequently anti-ER ChIP-seq and polyA-selected mRNA-seq was performed on the treated cells.; [Treatment]'Steroid-deprived cell models were treated with 10 nM estradiol, 10 nM NR3C ligand (progesterone (PR), dexamethasone (GR), DHT (AR) or aldosterone (MR)) or 10 nM of both the hormones for the above-mentioned time.', 'Steroid-deprived cell models were treated with 10 nM estradiol, 10 nM NR3C ligand (progesterone, dexamethasone, DHT or aldosterone) or 10 nM of both the hormones for 45 minutes or 4 hours.', 'Cells were stripped (using RPMI complete medium with 10% Charcoal Stripped FBS for 48 hours, then treated with compound for 24 hours'; [Growth]'Cells were cultured for 48 hours in charcoal-stripped serum media to deprive them of steroids.', 'Cells maintained in RPMI+10%FBS+L-Glutamine+Penn/Strep'; [Extraction]'Hormone-treated were harvested and ChIP was performed as per the directions provided in materials and method (ChIP and ChIP-sequencing).\nChIP-seq libraries were prepared using Kapa ChIP-seq kits.\nDetails of library preparation strategy are provided in the materials and methods section (ChIP and ChIP-seq) of the paper.', 'Hormone-treated cells were homogenized and total RNA was extracted using Qiagen RNAeasy kit\nPolyA tail selection was performed on 250 ng of total RNA. RNA-seq libraries were prepared using NEBNext kit. Details of library preparation strategy are provided in the materials and methods section (RNA expression and RNA-sequencing) of the paper.', 'Hormone-treated were harvested and ChIP was performed as per the directions provided in materials and method (ChIP and ChIP-sequencing)\nChIP-seq libraries were prepared using Kapa ChIP-seq kits. Details of library preparation strategy are provided in the materials and methods section (ChIP and ChIP-seq) of the paper.', 'Cells were scraped after 24 hour treatment, spun down, snap frozen. RNA extraction was performed using Quiagen Rneasy plus mini kit\nKAPA stranded mRNA-Seq kit (KR0960-v3.15) was used'; [Cell type]'Source: ''tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: Vehicle; hormone exposure time: 45 minutes; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# F0515); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10 nM Estradiol; hormone exposure time: 45 minutes; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# F0515); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10 nM DHT; hormone exposure time: 45 minutes; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# F0515); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10nM Estradiol + 10 nM DHT; hormone exposure time: 45 minutes; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# F0515); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: Vehicle; hormone exposure time: 60 minutes; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# F0515); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10 nM Estradiol; hormone exposure time: 75 minutes; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# F0515); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10 nM Dexamethasone; hormone exposure time: 60 minutes; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# F0515); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10nM Estradiol + 10 nM Dexamethasone; hormone exposure time: 75 minutes (15 min E2 and 60 min E2+Dexamethasone); chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# F0515); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10 nM Aldosterone; hormone exposure time: 45 minutes; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# F0515); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10nM Estradiol + 10 nM Aldosterone; hormone exposure time: 45 minutes; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# F0515); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: Vehicle; hormone exposure time: 45 minutes; chip antibody: none (INPUT); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10 nM Estradiol; hormone exposure time: 45 minutes; chip antibody: none (INPUT); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10 nM DHT; hormone exposure time: 45 minutes; chip antibody: none (INPUT); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10nM Estradiol + 10 nM DHT; hormone exposure time: 45 minutes; chip antibody: none (INPUT); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: Vehicle; hormone exposure time: 60 minutes; chip antibody: none (INPUT); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10 nM Estradiol; hormone exposure time: 75 minutes; chip antibody: none (INPUT); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10 nM Dexamethasone; hormone exposure time: 60 minutes; chip antibody: none (INPUT); ', 'tissue type: ER+/PR+ MCF7 cell models; er/pr status: ER+/PR+; drug treatment: 10nM Estradiol + 10 nM Dexamethasone; hormone exposure time: 75 minutes (15 min E2 and 60 min E2+Dexamethasone); chip antibody: none (INPUT); ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: Vehicle; hormone exposure time: 24 hours; protocol: Cell models RNA-seq; ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM E2; hormone exposure time: 24 hours; protocol: Cell models RNA-seq; ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM Progesterone; hormone exposure time: 24 hours; protocol: Cell models RNA-seq; ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM Dexamethasone; hormone exposure time: 24 hours; protocol: Cell models RNA-seq; ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM DHT; hormone exposure time: 24 hours; protocol: Cell models RNA-seq; ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM Aldosterone; hormone exposure time: 24 hours; protocol: Cell models RNA-seq; ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM E2+10 nM Progesterone; hormone exposure time: 24 hours; protocol: Cell models RNA-seq; ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM E2+10 nM Dexamethasone; hormone exposure time: 24 hours; protocol: Cell models RNA-seq; ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM E2+10 nM DHT; hormone exposure time: 24 hours; protocol: Cell models RNA-seq; ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM E2+10 nM Aldosterone; hormone exposure time: 24 hours; protocol: Cell models RNA-seq; ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: Vehicle; hormone exposure time: 4 hours; protocol: Cell models ChIP-seq; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# L1911); ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM E2; hormone exposure time: 4 hours; protocol: Cell models ChIP-seq; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# L1911); ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM E2+10 nM Progesterone; hormone exposure time: 4 hours; protocol: Cell models ChIP-seq; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# L1911); ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM E2+10 nM Dexamethasone; hormone exposure time: 4 hours; protocol: Cell models ChIP-seq; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# L1911); ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM E2+10 nM DHT; hormone exposure time: 4 hours; protocol: Cell models ChIP-seq; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# L1911); ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM E2+10 nM Aldosterone; hormone exposure time: 4 hours; protocol: Cell models ChIP-seq; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# L1911); ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: INPUT; hormone exposure time: 4 hours; protocol: Cell models ChIP-seq; chip antibody: none; ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: Vehicle; hormone exposure time: 45 minutes; protocol: Cell models ChIP-seq; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# L1911); ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM E2; hormone exposure time: 45 minutes; protocol: Cell models ChIP-seq; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# L1911); ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM R5020; hormone exposure time: 45 minutes; protocol: Cell models ChIP-seq; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# L1911); ', 'cell line: MCF7; er/pr status: ER+/PR+; drug treatment: 10 nM E2 + 10 nM R5020; hormone exposure time: 45 minutes; protocol: Cell models ChIP-seq; chip antibody: anti-ER (SC biotech HC-20, cat# SC-543, lot# L1911); ', 'treatment: Vehicle; time: 24h; replicate: rep1; ', 'treatment: 10nM E2; time: 24h; replicate: rep1; ', 'treatment: 10nM E2 + 10nM Progesterone; time: 24h; replicate: rep1; ', 'treatment: 10nM E2 + 10nM Dexamethasone; time: 24h; replicate: rep1; ', 'treatment: 10nM E2 + 10nM DHT; time: 24h; replicate: rep1; ', 'treatment: 10nM E2 + 10nM Aldosterone; time: 24h; replicate: rep1; ', 'treatment: Vehicle; time: 24h; replicate: rep2; ', 'treatment: 10nM E2; time: 24h; replicate: rep2; ', 'treatment: 10nM E2 + 10nM Progesterone; time: 24h; replicate: rep2; ', 'treatment: 10nM E2 + 10nM Dexamethasone; time: 24h; replicate: rep2; ', 'treatment: 10nM E2 + 10nM DHT; time: 24h; replicate: rep2; ', 'treatment: 10nM E2 + 10nM Aldosterone; time: 24h; replicate: rep2; ', 'treatment: Vehicle; time: 24h; replicate: rep3; ', 'treatment: 10nM E2; time: 24h; replicate: rep3; ', 'treatment: 10nM E2 + 10nM Progesterone; time: 24h; replicate: rep3; ', 'treatment: 10nM E2 + 10nM Dexamethasone; time: 24h; replicate: rep3; ', 'treatment: 10nM E2 + 10nM DHT; time: 24h; replicate: rep3; ', 'treatment: 10nM E2 + 10nM Aldosterone; time: 24h; replicate: rep3; ' GSE57677 Homo sapiens 8 Expression profiling by array GPL6244 Targeting IL13Ralpha2 activates STAT6-TP63 pathway to suppress breast cancer lung metastasis 2014-05-14 IL13Rα2 overexpression promotes metastasis of basal-like breast cancers IL13Rα2 depletion in highly metastatic breast cancer cells suppresses lung metastases formation by upregulating TP63 and decreasing their migratory potential https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE57677 Targeting IL13Ralpha2 activates STAT6-TP63 pathway to suppress breast cancer lung metastasis. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-015-0607-y {Breast cancer research : BCR (5.676): 10.1186/s13058-015-0607-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA247609 https://www.ebi.ac.uk/ena/browser/view/PRJNA247609 None [Overal design]MCF10CA1a (MIV) cells expressing the luciferase gene (MIV-Luc), were stably transduced with lentiviral constructs expressing either scrambled shRNA or shRNA against IL13Rα2. The two cell lines were then either mock treated or treated with 20ng/ml IL13 for 16h followed by RNA isolation. Gene expression analysis was performed using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by Affymetrix Exon Array Computational Tool.; [Treatment]'None'; [Growth]'MCF10CA1a cells were maintained in DMEM F/12 medium containing 5% heat inactivated horse serum, 10 μg/ml insulin, 20 ng/ml EGF, 0.1 ng/ml cholera enterotoxin, 0.5 μg/ml hydrocortisone and 1% penicillin/streptomycin.'; [Extraction]'Total RNA was isolated from 1 million cells using the RNeasy Mini Kit (Qiagen), according to the manufacturer’s instructions.'; [Cell type]'breast cancer''cell line: MCF10CA1a; cell type: breast cancer; construct: pLKO-shSCR; treatment: Mock; ', 'cell line: MCF10CA1a; cell type: breast cancer; construct: pLKO-shSCR; treatment: IL13; ', 'cell line: MCF10CA1a; cell type: breast cancer; construct: pLKO-shIL13RA2; treatment: Mock; ', 'cell line: MCF10CA1a; cell type: breast cancer; construct: pLKO-shIL13RA2; treatment: IL13; ' GSE87590 Homo sapiens 18 Expression profiling by array GPL16686 Restoring miR-150-5p to breast cancer cell lines 2016-10-04 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE87590 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA345308 https://www.ebi.ac.uk/ena/browser/view/PRJNA345308 None [Overal design]Refer to individual Series; [Treatment]"Mature miR-150-5p (miRNA mimic) or non-specific negative control (NC) (Ambion, Austin, TX, USA) at a concentration of 50 nM were incubated with Lipofectamine RNAiMAX (Invitrogen, Carlsbad, CA, USA) in culture medium per the manufacturer's instructions before addition to cells. Mock transfection using just lipofectamine without added RNA was also used as a negative control. Cells were incubated at 37°C for 24 hrs before replacement of medium. Transfected cells were then harvested for RNA and protein at 48 hours.", "Mature miR-150-5p (miRNA mimic) or non-specific negative control (NC) (Ambion, Austin, TX, USA) at a concentration of 50 nM were incubated with Lipofectamine RNAiMAX (Invitrogen, Carlsbad, CA, USA) in culture medium per the manufacturer's instructions before addition to cells. Mock transfection using just lipofectamine without added RNA was also used as a negative control. Cells were incubated at 37°C for 24 hrs before replacement of medium. Transfected cells were then harvested for RNA and protein at 72 hours."; [Growth]'ZR-75-1 cell were grown in RPMI-1640 supplemented with 10% FBS.', 'BT-549 cell were grown in RPMI-1640 supplemented with 10% FBS.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'breast cancer cell line''cell line: ZR-75-1; cell type: breast cancer cell line; transfected with: mock; time point: 48 hours post transfection; ', 'cell line: ZR-75-1; cell type: breast cancer cell line; transfected with: negative control; time point: 48 hours post transfection; ', 'cell line: ZR-75-1; cell type: breast cancer cell line; transfected with: miR-150-5p mimic; time point: 48 hours post transfection; ', 'cell line: BT-549; cell type: breast cancer cell line; transfected with: mock; time point: 72 hours post transfection; ', 'cell line: BT-549; cell type: breast cancer cell line; transfected with: negative control; time point: 72 hours post transfection; ', 'cell line: BT-549; cell type: breast cancer cell line; transfected with: miR-150-5p mimic; time point: 72 hours post transfection; ' GSE40622 Homo sapiens 275 Expression profiling by RT-PCR; Genome variation profiling by genome tiling array GPL6359; GPL16020 Expanded Genomic Profiling of Circulating Tumor Cells in Metastatic Breast Cancer Patients to Assess Biomarker Status and Biology Over Time (CALGB 40502 and CALGB 40503, Alliance). 2012-09-05 We developed a novel approach to isolate tumor cells with high purity from blood which was subjected to immunomagnetic enrichment using EpCAM beads followed by fluorescence activated cell sorting (IE/FACS) to isolate EpCAM-positive cells away from leukocytes (CD45+). Duplicate samples of 20 cells were isolated from the same enriched blood from MBC patients and then subjected to DNA and RNA profiling in parallel. For DNA profiling, sorted cells were subjected to BAC array comparative genomic hybridization analysis following whole genome amplification. For RNA profiling, QPCR analysis was performed on sixty four (64) cancer-related genes using Taqman® low density arrays. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE40622 Genomic and expression profiling reveal molecular heterogeneity of disseminated tumor cells in bone marrow of early breast cancer. NPJ breast cancer 32.43 https://doi.org/10.1038/s41523-018-0083-5 {Clinical cancer research : an official journal of the American Association for Cancer Research (None) doi:10.1158/1078-0432.CCR-17-2312}; {NPJ breast cancer (32.43) doi:10.1038/s41523-018-0083-5}; 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA174414 https://www.ebi.ac.uk/ena/browser/view/PRJNA174414 None [Overal design]Differential gene expression analysis between EpCAM-positive cells and matched leukocytes confirmed the up-regulation of EPCAM and other genes including MUC1 and KRT19 (adjusted p <0.05). In addition, EpCAM-positive cells showed a significant down-regulation of the leukocyte-specific marker PTPRC (encodes CD45) as well as CD44 and VIM, markers associated with stem cellness and epithelial to mesenchymal transition, respectively. Unsupervised hierarchical clustering analysis of RNA profiles showed that EpCAM-positive cells clustered away from the leukocytes. Genome-wide copy number analysis of EpCAM-expressing cells revealed gains (e.g. 1q and 8q), losses (e.g. 8p and 16q), and focal amplifications (e.g. on 8q and 11q including CCND1) frequently seen in primary breast cancers.; [Treatment]'Array CGH experiments of Circulating Tumor, Primary Tumor, or cell line genomic DNA as test samples and normal human genomic DNA as reference sample.', 'Cell isolation via IE/FACS: If a patient had ≥1 CTC/mL the remaining volume of blood was subjected to immunomagnetic enrichment and fluorescence activated cell sorting (IE/FACS) within 24-32 hr after blood draw. In the initial step, magnetic beads coated with EpCAM mAb are used to enrich for tumor cells. Enriched samples are then subjected to FACS analysis using differentially labeled mAbs to distinguish tumor cells (EpCAM+/CD45-) from leukocytes (CD45+/EpCAM-) during sorting. This procedure allows for the isolation of small pools cells, which can be subjected to downstream molecular analyses.'; [Growth]'None'; [Extraction]'Magnetic beads coated with EpCAM mAb are used to enrich for tumor cells and then subjected to FACS analysis using differentially labeled mAbs to distinguish tumor cells (EpCAM+) from leukocytes (CD45+) during sorting. Using this protocol, we isolated small pools of highly purified CTCs from breast cancer patients. DNA from Tumor cells sorted in 10uL of TE was amplified using the GenomePlex Single Cell Whole Genome Amplification Kit (Sigma-Aldrich) according to manufacturer’s protocol. The approach was evaluated using breast tumor cell model systems, BT474 and MCF7, and CTCs metastatic breast cancer (MBC) patients. Microdissection and DNA extraction of archival formalin-fixed paraffin-embedded (FFPE) primary tumor were done as previously described in Waldman FM, DeVries S, Chew KL, Moore DH, 2nd, Kerlikowske K, Ljung BM. Chromosomal alterations in ductal carcinomas in situ and their in situ recurrences. J Natl Cancer Inst 2000;92(4):313-20.', 'Magnetic beads coated with EpCAM mAb are used to enrich for tumor cells and then subjected to FACS analysis using differentially labeled mAbs to distinguish tumor cells (EpCAM+) from leukocytes (CD45+) during sorting. Using this protocol, we isolated small pools of highly purified CTCs from breast cancer patients. DNA from Tumor cells sorted in 10µL of TE was amplified using the GenomePlex® Single Cell Whole Genome Amplification Kit (Sigma-Aldrich) according to manufacturer’s protocol. The approach was evaluated using breast tumor cell model systems, BT474 and MCF7, and CTCs metastatic breast cancer (MBC) patients. Microdissection and DNA extraction of archival formalin-fixed paraffin-embedded (FFPE) primary tumor were done as previously described in Waldman FM, DeVries S, Chew KL, Moore DH, 2nd, Kerlikowske K, Ljung BM. Chromosomal alterations in ductal carcinomas in situ and their in situ recurrences. J Natl Cancer Inst 2000;92(4):313-20.', 'Cells were sorted into reaction tubes containing 9.5µL of lysis buffer and 0.5 µL of DNAse. Lysis reaction was carried out for 5 min at room temperature and 1µL of Stop solution was added and incubated for 2 min and immediately placed on ice. Whole cell lysates were then stored in -80°C until further use.'; [Cell type]'Circulating tumor cells Isolated from peripheral blood of metastatic breast cancer patient', 'Source: ', 'Circulating Tumor Cells', 'Blood Leukocytes''cell type: Circulating tumor cells Isolated from peripheral blood of metastatic breast cancer patient; assayed molecule: Whole genome amplified genomic DNA; ', 'assayed molecule: Whole genome amplified reference male genomic DNA; ', 'diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; ', 'reference: Promega Human Genomic DNA cat#G147A; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 116285.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 116285.20CD45; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: no pair; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 117494.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 117494.20CD45; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 118273.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 118273.20CTC.1; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 119982.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 119982.20CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 120153.40CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 120153.20CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 120447.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 120447.20CD45; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 120660.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 120660.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 120670.20CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 120670.10CTC; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 120850.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 120850.20CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 121059.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 121059.20CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 121276.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 121276.20CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 121295.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 121295.20CD45; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 121304.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 121304.20CTC; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 121975.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 121975.20CD45; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 122025.50CD45.T2; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 122025.20CTC.1.T2; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 122030.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 122030.20CD45; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 122306.50CD45.A1; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 122306.20CTC.1.A1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 122413.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 122413.20CTC; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 122478.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 122478.20CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 122504.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 122504.20CD45; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 123024.50CD45.T2; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 123024.20CTC.1.T2; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 123036.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 123036.15CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 123328.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 123328.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 123490.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 123490.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 123544.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 123544.15CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 123547.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 123547.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 123680.50CD45.T2; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 123680.20CTC.1.T2; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 123781.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 123781.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 124088.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 124088.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 124437.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 124437.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 124504.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 124504.18CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 124523.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 124523.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 124551.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 124551.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 124759.50CD45.T2.A1; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 124759.13CTC.T2.A1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 125051.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 125051.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 125054.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 125054.15CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 125122.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 125122.19CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 125183.50CD45.A1; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 125183.20CTC.A1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 125233.50CD45.A1; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 125233.20CTC.A1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 125263.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 125263.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 125301.50CD45.A2; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 125301.14CTC.A2; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 125323.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 125323.10CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 125796.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 125796.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 125904.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 125904.16CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126149.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126149.20CTC.2; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126320.50CD45.T2; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126320.19CTC.T2; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126358.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126358.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126423.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126423.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126563.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126563.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126608.50CD45.1; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126608.20CTC.1.A1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126624.50CD45.1; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126624.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126632.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126632.18CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126703.50CD45.1; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126703.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126746.50CD45.1; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126746.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126750.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126750.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126850.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126850.14CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126958.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126958.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 126976.24CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 126976.16CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 127055.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 127055.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 127201.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 127201.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 127268.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 127268.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 128026.50CD45.T3; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 128026.20CTC.T3; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 128099.50CD45.1; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 128099.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 128311.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 128311.15CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 128449.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 128449.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 128619.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 128619.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 128914.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 128914.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 129063.6CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 129063.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 129093.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 129093.20CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 129195.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 129195.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 4024.20CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 4024.12CTC; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 4037.50CD45.1; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 4037.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 4042.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 4042.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 4043.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 4043.20CTC.1; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 81.50CD45.T2; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 81.20CTC.1.T2; ', 'sample type: Test; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Circulating Tumor Cells; matched leukocyte sample: 83.50CD45; ', 'sample type: Control; diagnosis: Breast cancer; tumor stage: Metastatic; gender: Female; tissue: Peripheral Blood; cell type: Blood Leukocytes; matched leukocyte sample: 83.20CTC.1; ' GSE95087 Homo sapiens 6 Expression profiling by array; Non-coding RNA profiling by array GPL16956 TSA induced gene expression variation on breast cancer cell SKBR3 2017-02-20 To explore TSA influence on human breast cancer cells, we attempt to analyze genes differentially expressed between TSA treated and untreated SKBR3 cells, which will hopefully provide clues for TSA target genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95087 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA376012 https://www.ebi.ac.uk/ena/browser/view/PRJNA376012 None [Overal design]Gene expression in human breast cancer cell SKBR3 was measured at 24 hours after treated with 330nM TSA. Three independent experiments were performed at each time using different donors for each experiment.; [Treatment]'Gene expression in human breast cancer cell SKBR3 was measured at 24 hours after treated with 330nM TSA. Three independent experiments were performed at each time using different donors for each experiment.'; [Growth]'None'; [Extraction]'Three cases of TSA treated and untreated SKBR3 cells were prepared for the extraction of total RNA.RNA quantity and quality were measured by NanoDrop ND-1000. RNA integrity was assessed by standard denaturing agarose gel electrophoresis.'; [Cell type]'Source: ''tissue: Breast cancer; cell line: SKBR3; treatment: pbs; ', 'tissue: Breast cancer; cell line: SKBR3; treatment: 330nM TSA treated for 24 hours.; ' GSE21422 Homo sapiens 19 Expression profiling by array GPL570 Expression profiling of human DCIS and invasive ductal breast carcinoma 2010-04-21 Human healthy tissue samples, DCIS and invasive mammary tumors were analyzed in order to identify marker genes which show enhanced expresssion in DCIS and invasive ductal carcinomas. Using this approach, we were able to identify a set of genes which might allow a better detection of DCIS and invasive carcinomas in the future. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE21422 Identification of early molecular markers for breast cancer. Molecular cancer 10.679 https://doi.org/10.1186/1476-4598-10-15 {Molecular cancer (10.679) doi:10.1186/1476-4598-10-15}; {Cellular oncology (Dordrecht) (None) doi:10.1007/s13402-011-0023-y}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA126373 https://www.ebi.ac.uk/ena/browser/view/PRJNA126373 None [Overal design]5 healthy tissue samples, 9 DCIS and 5 invasive ductal carcinomas were analysed.; [Treatment]'None'; [Growth]'Fresh frozen samples were optaint from the Robert-Rössle-Biobank at the ECRC (Experimental and Clinical Research Center).'; [Extraction]"Rneasy lipip tissue Kit (Qiagen) was used according to the manufacturer's instructions."; [Cell type]'Source: ''tissue: tumor; disease state: DCIS; ', 'tissue: breast; disease state: healthy; ', 'tissue: tumor; disease state: IDC; ' GSE63957 Homo sapiens 6 Expression profiling by array GPL10904 TRPM7 maintains mesenchymal phenotype of breast cancer cells by tensional regulation of SOX4 (SOX4 shRNA) 2014-12-08 Analysis of the effect of shRNA-mediated knockdown of SOX4 on global gene expression levels in MDA-MB-231 human breast cancer cells. Results were used for the identification of overlapping up- and downregulated genes in TRPM7 + SOX4 shRNA MDA-MB-231 cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE63957 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA269599 https://www.ebi.ac.uk/ena/browser/view/PRJNA269599 None [Overal design]Total RNA isolated from MDA-MB-231 breast cancer cells transduced with a scrambled shRNA (shCntrl) or SOX4 shRNA (shSOX4#1); [Treatment]'Transduced with scrambled or SOX4 shRNA'; [Growth]'Cultured in DMEM supplemented with Glutamax, 10% fetal bovine serum and 1% pen/strep'; [Extraction]'RNA was extracted with RNeasy Minikit (Qiagen), followed by clean-up and DNase I treatment in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'breast cancer''cell line: MDA-231; cell type: breast cancer; transduced with: scrambled shRNA; ', 'cell line: MDA-231; cell type: breast cancer; transduced with: SOX4 shRNA; ' GSE138957 Mus musculus 6 Expression profiling by array GPL1261 Genn expression influenced by Akt1 knock out in mouse ErbB2 mammary tumor cells 2019-10-16 Analysis of ErbB2 mammary tumor cells derived from Akt1 wild type and knockout MMTV-ErbB2 transgenic mice using Affymetrix Mouse 430A v2.0 GeneChip arrays. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE138957 Endogenous Cyclin D1 Promotes the Rate of Onset and Magnitude of Mitogenic Signaling via Akt1 Ser473 Phosphorylation. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2020.108151 {Cell reports (7.815): 10.1016/j.celrep.2020.108151} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA577885 https://www.ebi.ac.uk/ena/browser/view/PRJNA577885 None [Overal design]Three akt1(+/+) erbb2 mammary tumor cell lines were compared to three akt1(-/-) erbb2 mammary tumor cell lines.; [Treatment]'None'; [Growth]"ErbB2 mammary tumor cells isolated from spontaneously formed MMTV-ErbB2 induced mammary tumor. The mammary tumors were dissociated by chopping and then digested with 0.4 mg/ml collagenase in MEC culture media (Ham's F12 with 10% FBS, 1× MEM nonessential amino acids, 100 μg/ml penicillin and streptomycin, 50 μg/ml gentamicin, 4 μg/ml insulin, 1 μg/ml hydrocortisone, 10 ng/ml EGF, 10 ng/ml cholera toxin) in 5% CO2 at 37°C for 18 h. The digested material was homogenized by pipetting up and down and then was washed with PBS with 50 μg/ml gentamicin three times. The pellet was resuspended in MEC culture media in a 10-cm plate and then cultured for 4 h to remove fibroblasts. The suspension was keeping culture for 25 passages."; [Extraction]'Total RNA was extracted with Trizol from Invitrogen. DNA was removed by Dnase I digestion and then purified with Qiagen RNAeasy kit.'; [Cell type]'Source: ''cell line: akt(+/+) 31; ', 'cell line: akt(+/+) 101; ', 'cell line: akt(+/+) 102; ', 'cell line: akt(-/-) 72; ', 'cell line: akt(-/-) 75; ', 'cell line: akt(-/-) 116; ' GSE77348 Homo sapiens 85 Methylation profiling by genome tiling array GPL13534 Genome-wide methylation analysis of DNMT3B gene isoforms revealed specific methylation profiles in breast cell lines 2016-01-28 Both DNA methylation and alternative splicing represent mechanisms closely involved in regulation of gene expression and are well known to be involved in cancer susceptibility and development. Human DNA methylation is introduced into DNA by enzymes of the DNA cytosine methyltransferases family, which includes DNMT3B. The DNMT3B protein allows a de novo DNA methylation activity, which is a key mechanism involved in the transformation of normal cell into cancer cell. The DNMT3B3 isoform is overexpressed in cancerous tissues and tumor cell lines, and could act as a dominant negative factor. This isoform was found to be highly expressed in our cohort of non-BRCA1/2 families. Using Infinium Human Methylation 450 BeadChips, we undertook the characterization of the specific methylation profile associated with this DNMT3B3 isoform and its DNMT3B2 wild type counterpart in ER/PR-positive and –negative breast cancer cell lines. A large spectrum of DNMT3B3/DNMT3B2 expression ratio values was observed in cancer and non-cancerous cell lines. Based on their methylation profiles, hierarchical clustering of parental cell lines revealed clustering of cells based on their ER/PR status. Overexpression of DNMT3B3 triggered methylation changes of thousands of CpG sites in MCF7, T-47D, MDA-MB-231 and MCF10A cells. These methylated loci were distributed in similar proportion over the 22 autosomal chromosomes and genomic locations such as promoter, gene body or intergenic regions. Pathways associated with genes containing these differentially methylated CpG sites were also determined regarding their enrichment. Moreover, based on the trend of methylation changes, the results suggest an anti-proliferative effect of the DNMT3B3 isoform through negative effect on its wild-type isoform counterpart DNMT3B2. To our knowledge, this study represents the first exhaustive analysis describing specific methylation profile triggered by modulated expression of DNMT3B isoforms and revealed specific genes and pathways, which could significantly regulate cell growth and proliferation as well as other biological and molecular mechanisms. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE77348 Genome-wide methylation analysis of DNMT3B gene isoforms revealed specific methylation profiles in breast cell lines. Epigenomics 4.404 https://doi.org/10.2217/epi-2016-0013 {Epigenomics (4.404): 10.2217/epi-2016-0013} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA310106 https://www.ebi.ac.uk/ena/browser/view/PRJNA310106 None [Overal design]For each cell line treatment, between 3 and 6 replicates have been performed. Cell line treatments include negative controls such as untreated, scramble shRNA-transduced+empty vector-transfected as well as empty vector-transfected only. A total of 94 samples have been analyzed which include all appropriate treatments in 7 different cell lines namely MCF7, T-47D, CAMA1, ZR-75-1, MDA-231, BT549 and MCF10A. The main goal was to generate extreme (low and high) gene expression ratios of DNMT3B3/DNMT3B2 in each cell line.; [Treatment]'MCF7, T-47D, ZR-75-1 and CAMA-1 cell lines were untreated (negative control), either transduced with scramble shRNA/transfected with empty pcDNA3 vector (B2-overexpressing), transduced with DNMT3B2 shRNA or transduced with DNMT3B2 shRNA/transfected with DNMT3B3 pcDNA3 vector. MDA-MB-231, BT-549 and MCF10A cell lines were untreated, transfected with empty pcDNA3 vector (B3-overexpressing) or transfected with DNMT3B2 pcDNA3 vector (B2-overexpressing). MDA-MB-231, BT-549 and MCF10A cell lines were untreated, transfected with empty pcDNA3 vector (B3-overexpressing) or transfected with DNMT3B2 pcDNA3 vector (B2-overexpressing)'; [Growth]'The human breast cancer cell lines MCF7, CAMA-1, ZR-75-1, T-47D, MDA-MB-231, BT549 as well as the human MCF10A cell line are all routinely cultured in our laboratory, and the conditions have been optimized as recommended by the American Type Culture Collection (ATCC, Manassas, VA).'; [Extraction]'Genomic DNA was isolated using the QIAamp DNA mini kit (QIAGEN Inc., Mississauga, ON) as described by the manufacturer. kit, as recommended by the manufacturer'; [Cell type]'Source: ''cell line: MCF7; ', 'cell line: CAMA; ', 'cell line: ZR-75-1; ', 'cell line: T-47D; ', 'cell line: BT-549; ', 'cell line: MDA-MB-231; ', 'cell line: MCF10A; ' GSE73296 Mus musculus 14 Expression profiling by array GPL6246 Effect of Cnot7 expression on 4T1 mammary tumor cell line transcriptome 2015-09-22 The goal of this study was to determine what the effect of modulating Cnot7 expression levels would have on the steady state transcription program of the 4T1 mammary tumor cell line. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE73296 Post-transcriptional Control of Tumor Cell Autonomous Metastatic Potential by CCR4-NOT Deadenylase CNOT7. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1005820 {PLoS genetics (5.224): 10.1371/journal.pgen.1005820} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA296556 https://www.ebi.ac.uk/ena/browser/view/PRJNA296556 None [Overal design]Three biological replicates for over expression compared to vector control. Three biological replicates for two different shRNAs versus shScramble control; [Treatment]'None'; [Growth]'DMEM + 10% FBS + PS'; [Extraction]'Trizol, following manufacturers protocol'; [Cell type]'Source: ''cell line: 4T1 mammary tumor cell line; treatment: control; ', 'cell line: 4T1 mammary tumor cell line; treatment: Cnot over-expression; ', 'cell line: 4T1 mammary tumor cell line; treatment: Cnot shRNA74; ', 'cell line: 4T1 mammary tumor cell line; treatment: Cnot shRNA75; ', 'cell line: 4T1 mammary tumor cell line; treatment: shScramble control; ' GSE64728 Homo sapiens 100 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL13135 Post-zygotic structural variants in histologically normal breast tissue may predispose to sporadic breast cancer [SET 10] 2015-01-07 Sporadic breast cancer (SBC) is a common and heterogeneous disease. There is no reliable way of early prediction of risk for SBC in the general population. We studied 282 females with SBC concentrating on copy number aberrations in tumor-free breast tissue (uninvolved margin, UM) outside the area of primary tumor (PT). Totally 1162 UMs (1-14 per breast) were studied. PT and blood/skin as control was also analyzed. Comparative analysis between genetic profiles for UM(s), PT(s) and blood/skin from the same patient is the core of study design. We identified 108 patients with at least one aberrant UM specimen, representing 38.3% of all cases. Gains were the dominating mutations in microscopically normal breast cells and gain of ERBB2, with overexpression of HER2 protein, was the most common aberration in normal cells. Five additional receptor genes (EGFR, FGFR1, IGF1R, LIFR and NGFR) also showed gains, and these were occasionally present in combination with the gain of ERBB2. Up to 67.6% of patients showed gain of one or more of these genes in normal cells. The aberrations found in normal cells from UMs were previously described in cancer literature, which suggest their causative, driving role in this disease. We demonstrate that analysis of normal cells from cancer-bearing patients leads to identification of genetic signatures that may predispose to SBC. Early detection of signals suggesting a predisposition towards development of SBC, long before detectable tumors are formed, is a key to the anticipated shift into a preventive paradigm of personalized medicine of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64728 Signatures of post-zygotic structural genetic aberrations in the cells of histologically normal breast tissue that can predispose to sporadic breast cancer. Genome research 9.944 https://doi.org/10.1101/gr.187823.114 {Genome research (9.944): 10.1101/gr.187823.114} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA271751 https://www.ebi.ac.uk/ena/browser/view/PRJNA271751 None [Overal design]We studied 282 female breast cancer patients that were assessed as affected by sporadic disease at the time of diagnosis and all underwent mastectomy. In total, 1162 UMs (uninvolved margin tissues), ranging from 1 to 14 UMs per patient, taken outside the location of clinically characterized index primary tumor, were analyzed on Illumina arrays. For each subject, DNA from at least one control tissue was also analyzed, which was predominantly blood DNA, alternatively skin-derived DNA. We also studied primary tumor (PT), or up to 3 primary tumor foci from patients with diagnosis of multifocal disease. This GEO project contains the genotyping profiles (processed and normalized data including Log R Ratio and B allele frequency) for these 1162 UMs used in the study. Information on phenotypes (age at diagnosis, tumor focality, tumor grade, tumor molecular phenotype) is also provided, whenever available. The experiements 1-100 out of 238 experiments runned on platform GPL13135 (HumanOmniExpress BeadChip); [Treatment]'None'; [Growth]'None'; [Extraction]'The tissues were stored at -70 degrees C prior to DNA extraction. The solid tissues were homogenized with a Tissuerupter (Qiagen). Proteinase K and Sarcosine was then added and the sample was incubated at 50oC over-night. The samples were transferred to PhaseLock Gel tubes and the DNA was purified with phenol/chloroform extraction. Due to very rich content of fat in UMs, phenol/chloroform extraction was repeated 6 times for all UMs, and 3 times for PTs and control samples from skin. The purified DNA was precipitated with sodium acetate, pH 5.4 and 95% ethanol. The DNA precipitate was dried before dissolving in water. Control samples of blood were extracted with QIAmp DNA Blood Maxi Kit (Qiagen).'; [Cell type]'Source: ''subject_code: 001GZ; gender: female; age at cancer diagnosis (yrs): 57; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 002MP; gender: female; age at cancer diagnosis (yrs): 58; molecular_phenotype: Triple negative; tumor focality: multifocal; ', 'subject_code: 003MC; gender: female; age at cancer diagnosis (yrs): 65; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 005ZW; gender: female; age at cancer diagnosis (yrs): 57; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 007ETP; gender: female; age at cancer diagnosis (yrs): 55; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: 008AG; gender: female; age at cancer diagnosis (yrs): 46; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 009SO; gender: female; age at cancer diagnosis (yrs): 74; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: unifocal; ', 'subject_code: 010LG; gender: female; age at cancer diagnosis (yrs): 73; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 011BM; gender: female; age at cancer diagnosis (yrs): 53; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 012MC; gender: female; age at cancer diagnosis (yrs): 84; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ', 'subject_code: 013WS; gender: female; age at cancer diagnosis (yrs): 65; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: multifocal; ', 'subject_code: 014ZR; gender: female; age at cancer diagnosis (yrs): 83; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 016JS; gender: female; age at cancer diagnosis (yrs): 72; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: 018MS; gender: female; age at cancer diagnosis (yrs): 51; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: multifocal; ', 'subject_code: 019ZB; gender: female; age at cancer diagnosis (yrs): 63; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: unifocal; ', 'subject_code: 020HK; gender: female; age at cancer diagnosis (yrs): 68; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 021MB; gender: female; age at cancer diagnosis (yrs): 64; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ', 'subject_code: 022ZT; gender: female; age at cancer diagnosis (yrs): 45; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ', 'subject_code: 023GC; gender: female; age at cancer diagnosis (yrs): 56; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: multifocal; ', 'subject_code: 024MZ; gender: female; age at cancer diagnosis (yrs): 35; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 025JT; gender: female; age at cancer diagnosis (yrs): 56; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 026MS; gender: female; age at cancer diagnosis (yrs): 48; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: 027MW; gender: female; age at cancer diagnosis (yrs): 41; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 028BM; gender: female; age at cancer diagnosis (yrs): 66; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: 030SK; gender: female; age at cancer diagnosis (yrs): 61; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; ' GSE27883 Mus musculus 10 Expression profiling by array GPL4134 MAP3K4/CBP Regulated H2B acetylation Controls Epithelial-Mesenchymal Transition in Trophoblast Stem Cells 2011-03-10 Epithelial stem cells self-renew while maintaining multipotency, but the dependence of stem cell properties on maintenance of the epithelial phenotype is unclear. We previously showed that trophoblast stem (TS) cells lacking the protein kinase MAP3K4 maintain properties of both stemness and epithelial-mesenchymal transition (EMT). Here, we show that MAP3K4 controls the activity of the histone acetyltransferase CBP, and that acetylation of histone H2B by CBP is specifically required to maintain the epithelial phenotype. Combined loss of MAP3K4/CBP activity represses expression of epithelial genes and causes TS cells to undergo EMT while maintaining their self-renewal and multipotency properties. The expression profile of MAP3K4 deficient TS cells defines an H2B acetylation regulated gene signature that closely overlaps with that of human breast cancer cells. Taken together, our data define an epigenetic switch that maintains the epithelial phenotype in TS cells and reveal previously unrecognized genes potentially contributing to breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE27883 MAP3K4/CBP-regulated H2B acetylation controls epithelial-mesenchymal transition in trophoblast stem cells. Cell stem cell 21.464 https://doi.org/10.1016/j.stem.2011.03.008 {Cell stem cell (21.464): 10.1016/j.stem.2011.03.008} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA137993 https://www.ebi.ac.uk/ena/browser/view/PRJNA137993 None [Overal design]Three separate trophoblast stem (TS) cell conditions were compared to define the gene expression changes that occur with the induction of epithelial-mesenchymal transition (EMT) in TS cells. These conditions were TS cells differentiated for 4 days (T^Diff), TS cells differentiated for 4-days and isolated following invasion through Matrigel (T^Inv), and TS cells with an inactive MAP3K4 (TS^KI4). All conditions were normalized to wild-type control TS cells (TS^WT). T^Diff and T^Inv were analyzed in triplicate. TS^KI4 was analyzed in duplicate in two independent biological replicates.; [Treatment]'None'; [Growth]'None'; [Extraction]'total RNA', 'Qiagen Rneasy Kit'; [Cell type]'trophoblast stem (TS) cells''cell type: trophoblast stem (TS) cells; protocol: wild-type control (TS^WT); ', 'cell type: trophoblast stem (TS) cells; protocol: differentiated for 4 days (T^Diff); ', 'cell type: trophoblast stem (TS) cells; protocol: differentiated for 4-days and isolated following invasion through Matrigel (T^Inv); ', 'cell type: trophoblast stem (TS) cells; protocol: inactive MAP3K4 (TS^KI4); ' GSE93636 Homo sapiens 3 Expression profiling by high throughput sequencing GPL11154 WT1 expression in breast cancer disrupts the epithelial/mesenchymal balance of tumour cells and correlates with the metabolic response to docetaxel 2017-01-15 The Wilms' Tumour gene 1 (WT1), encodes for a complex protein with transcription factor activity which is essential in mammals throughout life. We provide a complete study of WT1 expression across different breast cancer subtypes as well as isoform specific expression analysis. Using in vitro cell lines, clinical samples and publicly available gene expression datasets, we demonstrate that WT1 plays a role in regulating the epithelial-mesenchymal balance of breast cancer cells and that WT1-expressing tumours are mainly associated with a mesenchymal phenotype. WT1 gene expression also correlates with CYP3A4 levels and is associated with poorer response to taxane treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93636 WT1 expression in breast cancer disrupts the epithelial/mesenchymal balance of tumour cells and correlates with the metabolic response to docetaxel. Scientific reports 4.011 https://doi.org/10.1038/srep45255 {Scientific reports (4.011): 10.1038/srep45255} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA361398 https://www.ebi.ac.uk/ena/browser/view/PRJNA361398 https://www.ncbi.nlm.nih.gov/sra?term=SRP096784 [Overal design]RNA profiles of breast cancer cells (MDA-MB-157) were generated by deep sequencing on the Illumina HiSeq 2000 platform. Untreated MDA-MB-157 cells, MDA-MB-157 cells transduced with a lacZ control vector, and MDA-MB-157 cells transduced with a lentiviral vector carrying a Wt1 shRNA were sequenced (titled untreated, lacZ and Wt1 respectively).; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted using RNeasy Mini Kit (Qiagen) with on-column DNase digestion as per manufacturer’s instructions.\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'breast cancer cell line''cell line: MDA-MB-157; cell type: breast cancer cell line; treatment: untreated; ', 'cell line: MDA-MB-157; cell type: breast cancer cell line; treatment: lacZ; ', 'cell line: MDA-MB-157; cell type: breast cancer cell line; treatment: Wt1 KO; ' GSE110204 Homo sapiens 4 Non-coding RNA profiling by array GPL16770 miRNAs expression in four breast cancer cells 2018-02-06 To determine the miRNAs’ roles in the tumorigenesis behavior of TNBC, we profiled the global miRNA expression in 2 highly aggressive TNBC cell lines (MDA-MB-231 and CAL-51) in comparison with that in 2 non-aggressive luminal-type breast cancer cell lines (ZR-75-1 and MCF-7). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE110204 Transcriptional Downregulation of miR-4306 serves as a New Therapeutic Target for Triple Negative Breast Cancer. Theranostics 8.063 https://doi.org/10.7150/thno.30701 {Theranostics (8.063) doi:10.7150/thno.30701}; {Aging (None) doi:10.18632/aging.202414}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA433165 https://www.ebi.ac.uk/ena/browser/view/PRJNA433165 None [Overal design]miRNA expression in 2 highly aggressive TNBC cell lines (MDA-MB-231 and CAL-51) in comparison with that in 2 non-aggressive luminal-type breast cancer cell lines (ZR-75-1 and MCF-7); [Treatment]"Primary cultured breast cancer cells completely adhered to the wall at 24 hours, entered the logarithmic phase,at 37 ºC in a humidified incubator with 5% CO2. RNA was prepared using the TRIzol reagent following the manufacturer's recommendations."; [Growth]'MCF-7, MDA-MB-231 and CAL-51 were cultured in DMEM medium supplemented with 10 % fetal bovine serum (FBS) and antibiotics. ZR-75-1 was cultured in RPMI-1640 medium supplemented with 10 % fetal bovine serum (FBS) and antibiotics.'; [Extraction]"RNA was prepared using the TRIzol reagent following the manufacturer's recommendations. RNA was quantified using a NanoDrop-1000 spectrophotometer and RNA integrity was determined by 1% formaldehyde denaturing gel electrophoresis."; [Cell type]'Source: ''cell line: luminal type breast cancer cell line; ', 'cell line: triple negative breast cancer cell line; ' GSE77215 Homo sapiens 6 Expression profiling by array GPL18756 Assessing the mutagenic and estrogenic effect potential of pharmaceuticals and of their transformation products. Implications in the gene expression profiling 2016-01-26 Mixtures of diclofenac, sulfamethoxazole and ofloxacin and their photolysed mixtures were evaluated for their mutagenicity and estrogenicity. Implications in the gene expression profiling were evaluated as well Microarrays were used to understand the effects of exposure to mixtures of pharmaceuticals as contaminants of emerging concern https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE77215 Assessing the potential of pharmaceuticals and their transformation products to cause mutagenic effects: Implications for gene expression profiling. Environmental toxicology and chemistry 3.421 https://doi.org/10.1002/etc.3444 {Environmental toxicology and chemistry (3.421): 10.1002/etc.3444} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA309760 https://www.ebi.ac.uk/ena/browser/view/PRJNA309760 None [Overal design]For a better understanding of photolabile pharmaceuticals, human breast cancer cells T47D-KBluc were exposed to a mixture of diclofenac (50uM), sulfamethoxazole (50uM) and ofloxacin (50uM). A part of the setup was irradiated with UV-Light for 15 minutes to test the reaction of possible created products.; [Treatment]'Cells were grown for 24 h in growth medium and then for 40 h in assay medium (lacking antibiotics) in the presence of the different types of mixtures'; [Growth]'Cells were grown in RPMI 1640, supplemented with sodium pyruvate (1%), Fetal Bovine Serum (FBS) (10%) and 50 U/mL mixture of penicillin and streptomycin (1%)'; [Extraction]"The NucleoSpin RNA II kit was used for extraction as per manufacturer's instructions"; [Cell type]'Source: ''concentration: 50µM; uv-irradiation: control; ', 'concentration: 50µM; uv-irradiation: irradiated; ', 'concentration: 0µM; uv-irradiation: control; ' GSE29616 Mus musculus 16 Expression profiling by array GPL6885 Gene expression of primary MMTV-Neu tumors compared to secondary tumors generated from lin- and single tumor initiating cell (TIC) transplantation 2011-05-29 Most solid tumors seem to be organized in a hierarchy in which only a fraction of cells, termed tumor-initiating cells (TICs), is capable of disseminating new tumors after transplantation into recipient mice. However, whether a single TIC can induce a tumor or whether it requires additional TICs or non-TICs for tumor initiation is not known. Here we show that injections of single CD24+:Jag1- cells from Her2/Neu+ mammary tumors into recipient mammary glands induced tumors at a frequency of 1/22. Single cell-derived secondary tumors exhibited histology, flow cytometry and global expression profiles that were indistinguishable from primary tumors. Thus, a single TIC can act cell autonomously to induce a tumor and therefore complete eradication of all TICs would be required to cure cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE29616 Seventeen-gene signature from enriched Her2/Neu mammary tumor-initiating cells predicts clinical outcome for human HER2+:ERα- breast cancer. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1201105109 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1201105109} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA141361 https://www.ebi.ac.uk/ena/browser/view/PRJNA141361 None [Overal design]Total RNA obtained from primary MMTV-Neu tumors, secondary tumors generated by lin- cell transplantation, and secondary tumors generated by a single TIC, were used for microarray analysis to determine differentially regulated genes in the secondary tumors. Cluster analysis based on gene expression were then performed to assess tumor similarity; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted with Trizol reagent. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''strain: FvB; size: Mammary Tumor less than 1.0 cm diameter; tissue: Primary MMTV-Neu Mammary Tumor; ', 'strain: FvB; size: Mammary Tumor less than 1.0 cm diameter; tissue: Secondary MMTV-Neu Mammary Tumor; ' GSE58881 Homo sapiens 24 Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing GPL10999; GPL11154 Coordinated epigenetic remodelling occurs during early breast carcinogenesis [ChIP-seq & MBD-Seq] 2014-06-27 Dysregulation of the epigenome is a common event in malignancy. However, deciphering the earliest cancer associated epigenetic events remains a challenge. Cancer epigenome studies to date have primarily utilised cancer cell lines or clinical samples, where it is difficult to identify the initial epigenetic lesions from those that occur over time. Here, we analysed the epigenome of normal Human Mammary Epithelial Cells (HMEC) and a matched variant cell population (vHMEC) that has escaped senescence and undergone partial carcinogenic transformation. Using this model system we sought to identify the earliest epigenetic changes that potentially occur during carcinogenesis. First we show that the transcriptome of vHMEC resembles that of basal-like breast cancer. Moreover, in vHMEC there is significant deregulation of MYC, p53, EZH2/polycomb, the Aryl Hydrocarbon Receptor (AHR) and miRNAs-143, 145, 199a and 519a at the transcriptional level. Second, we find that vHMEC exhibit genome-wide changes in DNA methylation affecting key cancer-associated pathways. Hypermethylation predominately impacted gene promoters (particularly those targeted by AHR and TP53) and polycomb associated loci, whereas hypomethylation frequently affected enhancers. Next we show that long range epigenetic deregulation occurred in vHMEC involving concordant change in chromatin modification and gene expression across ~0.5-1Mb regions. Finally, we demonstrate that the DNA methylation changes we observe in vHMECs, occur in basal-like breast cancer (notably FOXA1 hypermethylation).. Overall our results suggest that the first steps of carcinogenesis are associated with a co-ordinated deregulation of DNA methylation and chromatin modification spanning a range of genomic loci potentially targeted by key transcription factors and a corresponding deregulation of transcriptional networks. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58881 Coordinated epigenetic remodelling of transcriptional networks occurs during early breast carcinogenesis. Clinical epigenetics 5.496 https://doi.org/10.1186/s13148-015-0086-0 {Clinical epigenetics (5.496): 10.1186/s13148-015-0086-0} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA253805 https://www.ebi.ac.uk/ena/browser/view/PRJNA253805 https://www.ncbi.nlm.nih.gov/sra?term=SRP043626 [Overal design]We sought to study the chromatin modification profile of human mammary epithelial cells (HMEC) and a matched isogenic variant population (vHMEC) utilising ChIP-seq. ChIP was performed against H3K27ac, H3K36me3 and H3K27me3 for a HMEC and vHMEC timpoint in one donor. H3K4me3 CHIP was performed in two donors, which were treated as biological replicates.; [Treatment]'None'; [Growth]'HMEC lines were generated from tissue taken from healthy women with informed donor consent as part of breast reduction mammoplasty (institutional ethics approval provided by the Sydney Adventist Hospital Ethics Committee, Project ID 06/03). At the time of surgery, all donors were aged between 23 and 43 years of age. Breast tissue was diced and then digested with collagenase to generate organoids. To establish HMEC lines, organoids were allowed to expand in MBD170 serum free basal medium (Life Technologies, Carlsbad CA, USA) until large colonies (1-2 cm) were observed (5-10 days). Organoid colonies were partially trypsinised to remove stromal cells and the remaining epithelial cells were transferred into a new tissue culture flask to generate passage 1 HMEC. vHMEC lines were then generated by serial passage of HMEC until proliferation slowed and the cells entered the selection phase. Selection phase HMEC were maintained with twice-weekly media changes until large, actively growing colonies (1-2 cm) were observed. Growing cells were trypsinised and transferred to a new culture vessel, generating the vHMEC lines.'; [Extraction]'ChIP experiments utilised ~2x10^6 cells (per immunoprecipitation) fixed for 10 minutes at 37°C in culture media containing 2.7% (w/v) formaldehyde (Sigma-Aldrich, St Louis MO, USA). Immunoprecipitation was performed using the Chromatin Immunoprecipitation Assay Kit (Merck Millipore, Billerica MA, USA) according to the manufacturers protocol withthe included salmon sperm DNA blocked agarose beads substituted with Protein A/G PLUS-Agarose Immunoprecipitation Reagent (Santa Cruz Biotechnology). Illumina 36 bp single end sequencing was performed on 5-12 ng of ChIP DNA.\n10ng DNA of MBDCap enriched DNA was prepared for Ilumina sequencing using the Illumina ChIP-Seq DNA sample prep kit (IP-102-1001) according to the manufacturer’s instructions. The library preparation was analyzed on Agilent High Sensitivity DNA 1000 Chip.', 'Each capture utilised 1 μg genomic DNA sonicated to mean fragment size of ~500 bp using a Bioruptor® water bath sonicator. Methylated DNA was captured using the Methylminer® Methylated DNA Enrichment Kit (Life Technologies, Carlsbad CA, USA) according to the manufacturer’s protocol with a single high salt elution. Next generation sequencing was performed on 10 ng of MBD captured DNA at two commercial sequencing centres on the Illumina GAIIX sequencing platform.\n10ng DNA of MBDCap enriched DNA was prepared for Ilumina sequencing using the Illumina ChIP-Seq DNA sample prep kit (IP-102-1001) according to the manufacturer’s instructions. The library preparation was analyzed on Agilent High Sensitivity DNA 1000 Chip.'; [Cell type]'Source: ''tissue: Breast; passage: 2; growth phase: HMEC; chip antibody: ChIPAb+ Trimethyl-Histone H3 (Lys4), Millipore, #17-614; ', 'tissue: Breast; passage: 7; growth phase: vHMEC; chip antibody: ChIPAb+ Trimethyl-Histone H3 (Lys4), Millipore, #17-614; ', 'tissue: Breast; passage: 4; growth phase: HMEC; chip antibody: Anti-trimethyl-Histone H3 (Lys27), Millipore, #07-449; ', 'tissue: Breast; passage: 4; growth phase: HMEC; chip antibody: Anti-Histone H3 (tri methyl K36), abcam, #ab9050-100; ', 'tissue: Breast; passage: 5; growth phase: HMEC; chip antibody: Anti-Histone H3 (acetyl K27), abcam, ab4729; ', 'tissue: Breast; passage: 5; growth phase: HMEC; chip antibody: none (input); ', 'tissue: Breast; passage: 8; growth phase: vHMEC; chip antibody: ChIPAb+ Trimethyl-Histone H3 (Lys4), Millipore, #17-614; ', 'tissue: Breast; passage: 9; growth phase: vHMEC; chip antibody: Anti-Histone H3 (acetyl K27), abcam, ab4729; ', 'tissue: Breast; passage: 9; growth phase: vHMEC; chip antibody: Anti-trimethyl-Histone H3 (Lys27), Millipore, #07-449; ', 'tissue: Breast; passage: 9; growth phase: vHMEC; chip antibody: Anti-Histone H3 (tri methyl K36), abcam, #ab9050-100; ', 'tissue: Breast; passage: 9; growth phase: vHMEC; chip antibody: none (input); ', 'tissue: Breast; passage: 14; growth phase: vHMEC; chip antibody: Methylminer DNA enrichment Kit (Life Technologies); ', 'tissue: Breast; passage: 3; growth phase: HMEC; chip antibody: Methylminer DNA enrichment Kit (Life Technologies); ', 'tissue: Breast; passage: 7; growth phase: vHMEC; chip antibody: Methylminer DNA enrichment Kit (Life Technologies); ', 'tissue: Breast; passage: 26; growth phase: vHMEC; chip antibody: Methylminer DNA enrichment Kit (Life Technologies); ', 'tissue: Breast; passage: 2; growth phase: HMEC; chip antibody: Methylminer DNA enrichment Kit (Life Technologies); ' GSE157383 Homo sapiens 22 Expression profiling by high throughput sequencing GPL20301 RNA-seq analysis of human breast cancer cell lines treated with abemaciclib 2020-09-02 We measured changes in gene expression after treatment of human breast cancer cell lines with abemaciclib. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE157383 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA661088 https://www.ebi.ac.uk/ena/browser/view/PRJNA661088 https://www.ncbi.nlm.nih.gov/sra?term=SRP279854 [Overal design]Examination of changes in gene expression in breast cancer cell lines after treatment with abemaciclib.; [Treatment]'Abemaciclib (500 nM) or DMSO for 7 days for all cell lines.'; [Growth]'Cells were cultured in sterile dishes in media as described. Cells were plated at densities such that final density at time of RNA-seq was between 60-70%.'; [Extraction]'Total RNA was isolated from cell lines using a Nucleospin RNA Plus kit (Macherey-Nagel).\nNEBNext® Ultra™ RNA Library Prep Kit for Illumina'; [Cell type]'Source: ''cell line: MDA-MB-453 breast carcinoma cell line; treamtent: DMSO; treatment length: 7 days; ', 'cell line: MDA-MB-453 breast carcinoma cell line; treamtent: abemaciclib; treatment length: 7 days; ', 'cell line: MCF7 breast carcinoma cell line; treamtent: DMSO; treatment length: 7 days; ', 'cell line: MCF7 breast carcinoma cell line; treamtent: abemaciclib; treatment length: 7 days; ', 'cell line: MDA-MB-468 breast carcinoma cell line; treamtent: DMSO; treatment length: 7 days; ', 'cell line: MDA-MB-468 breast carcinoma cell line; treamtent: abemaciclib; treatment length: 7 days; ' GSE60182 Homo sapiens 6 Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing GPL16791 Integrative transcriptome-wide analyses reveal critical HER2-regulated mRNAs and lincRNAs in HER2+ breast cancer 2014-08-07 Breast cancer is a major health problem affecting millions of women worldwide. Over 200,000 new cases are diagnosed annually in the USA, with approximately 40,000 of these cases resulting in death. HER2-positive (HER2+) breast tumors, representing 20–30 % of early-stage breast cancer diagnoses, are characterized by the amplification of the HER2 gene. However, the critical genes and pathways that become affected by HER2 amplification in humans are yet to be specifically identified. Furthermore, it is yet to be determined if HER2 amplification also affects the expression of long intervening non-coding (linc)RNAs, which are involved in the epigenetic regulation of gene expression. We examined changes in gene expression by next generation RNA sequencing in human tumors pre- and post- HER2 inhibition by trastuzumab in vivo, and changes in gene expression in response to HER2 knock down in cell culture models. We integrated our results with gene expression analysis of HER2+ tumors vs matched normal tissue from The Cancer Genome Atlas. The integrative analyses of these datasets led to the identification of a small set of mRNAs, and the associated biological pathways that become deregulated by HER2 amplification. Furthermore, our analyses identified three lincRNAs that become deregulated in response to HER2 amplification both in vitro and in vivo. Our results should provide the foundation for functional studies of these candidate mRNAs and lincRNAs to further our understanding of how HER2 amplification results in tumorigenesis. Also, the identified lincRNAs could potentially open the door for future RNA-based biomarkers and therapeutics in HER2+ breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60182 Integrative transcriptome-wide analyses reveal critical HER2-regulated mRNAs and lincRNAs in HER2+ breast cancer. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-015-3327-1 {Breast cancer research and treatment (3.471): 10.1007/s10549-015-3327-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA257691 https://www.ebi.ac.uk/ena/browser/view/PRJNA257691 https://www.ncbi.nlm.nih.gov/sra?term=SRP045322 [Overal design]We compared changes in gene expression of both mRNAs and lincRNAs in BT474 cells that are treated with HER2 siRNAs vs cells treated with negative control siRNAs by RNA-seq.; [Treatment]'siRNA knockdown of HER2 was achieved through the transfection of HER2-specific siRNAs (Life Technologies, Cat # 4390824, s611 and s613\xa0) at a final concentration of 15 nM with Lipofectamine RNAiMax at 7.5 μL/well of 6-well plate. Negative control siRNA #1 and #2 (Ambion Cat. # AM4611 and AM4613) were used as negative controls for the HER2 knockdown.'; [Growth]'BT474 cells were grown in Hybri-Care Medium (ATCC® 46-X™) supplemented with 10% fetal bovine serum, 100 units/ml of Penicillin, and 100 μg/ml Streptomycin at 37°C with 5% CO2.'; [Extraction]'RNA was isolated using RNeasy® Mini Kit (Qiagen) according to the manufacturer’s protocol. An added DNase (Qiagen) treatment step was included after the first wash.\nLibrary prepartion as per Illumina Scriptseq Complete Gold (Human/Mouse/Rat) instructions including Ribo-Zero Gold rRNA Removal Reagents.'; [Cell type]'breast cancer cell line''cell line: BT-474; cell line origin: female caucasian with ductal carcinoma; cell type: breast cancer cell line; transfected with: negative control siRNAs; ', 'cell line: BT-474; cell line origin: female caucasian with ductal carcinoma; cell type: breast cancer cell line; transfected with: HER2-specific siRNAs; ' GSE132083 Homo sapiens 15 Expression profiling by high throughput sequencing GPL16791 A transcriptome dataset revealing the molecular features of breast cancer stem cells 2019-06-03 Triple negative breast cancers lack targeted therapies with little side effects and contain higher percentage of cancer stem cells than the other breast cancer subtypes. Genes capturing the features of cancer stem cells of such diseases may serve as potential subtyping marker or therapeutic targets for triple negative breast cancer management. This data descriptor presents a set of transcriptome data from 3 cohorts of cancer stem cells as represented as CD44+/CD24-/low and 2 cohorts of non-cancer stem cells isolated from triple negative breast cancer cells, each having 3 replicates. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132083 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA545898 https://www.ebi.ac.uk/ena/browser/view/PRJNA545898 https://www.ncbi.nlm.nih.gov/sra?term=SRP200157 [Overal design]3 cohorts of cancer stem cells as represented as CD44+/CD24-/low and 2 cohorts of non-cancer stem cells isolated from triple negative breast cancer cells, each having 3 replicates are sequenced; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was harvested using Trizol reagent and DNase. mRNA was extracted using Oligo(dT) attached beads.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''cell line: SUM149; stemness: non-cancer stem cells; subtype: Triple Negative; ', 'cell line: SUM149; stemness: cancer stem cells; subtype: Triple Negative; ', 'cell line: HCC1937; stemness: non-cancer stem cells; subtype: Triple Negative; ', 'cell line: HCC1937; stemness: cancer stem cells; subtype: Triple Negative; ', 'cell line: SUM159; stemness: cancer stem cells; subtype: Triple Negative; ' GSE112723 Mus musculus 9 Expression profiling by array GPL6246 A Syngeneic ErbB2 Mammary Cancer Model for Preclinical Immunotherapy Trials [microarray] 2018-04-05 A cell line was derived from a mammary carcinoma in the transgenic FVB/N-Tg(MMTV-ErbB2)NDL2-5Mul mouse. The line, referred to as “NDL(UCD)” is adapted to standard cell culture and can be transplanted into syngeneic FVB/N mouse. The line maintains stable phenotype over multiple in vitro passages and rounds of in vivo transplantation. The cell line exhibits high expression of ErbB2 and ErbB3 and signaling molecules downstream ErbB2. The line was previously shown to be reactive to anti-immune checkpoint therapy with responses conducive to immunotherapy studies. Here, using both histology/immunophenotyping and gene expression/microarray analysis, we show that the syngeneic transplant tumors elicit an immune reaction in the adjacent stroma, with additional tumor infiltrating lymphocytes. We also show that this immune activating effect is greater in the syngeneic transplants than in the tumors arising in the transgenic mouse. We further analyzed the PD-1 and PD-L-1 expression in the model and found strong PD-L1 expression in the tumors and in vitro. Three distinct transplantable syngenic mouse models of mammary carcinoma were compared to identify differentially expressed genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112723 A Syngeneic ErbB2 Mammary Cancer Model for Preclinical Immunotherapy Trials. Journal of mammary gland biology and neoplasia 2.758 https://doi.org/10.1007/s10911-019-09425-3 {Journal of mammary gland biology and neoplasia (2.758): 10.1007/s10911-019-09425-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA448828 https://www.ebi.ac.uk/ena/browser/view/PRJNA448828 None [Overal design]For evaluating differential gene expression of the tumors arose from the NDL(UCD), Met1(UCD) and SSM2(UCD) cell lines grown in the FVB mouse we collected snap-frozen tumor samples, and three samples per model were processed in Mouse Gene 1.0 ST Array.; [Treatment]'None'; [Growth]'The NDL(UCD) SSM2(UCD) and Met1(UCD) transplantable mouse mammary tumor cell line was propagated in vitro and then injected as a bolus (0.1 – 2.0 x 10^6 cells) bilaterally into the uncleared #2, #3, and #4 mammary fat pads of 6- to 8-week-old female FVB/NJ mice. Tumors were harvested when they reached a maximum width of 5-10 mm, cut into 1-2mm sections, and then immediately snap-frozen.'; [Extraction]'RNA was isolated from frozen samples using the miRNeasy FFPE Kit (Qiagen) according to the manufacturer’s protocols specific for each type of specimen.'; [Cell type]'Source: ''gender: female; strain: FVB/N; tissue: mammary tumor; cell line: SSM2; ', 'gender: female; strain: FVB/N; tissue: mammary tumor; cell line: Met1; ', 'gender: female; strain: FVB/N; tissue: mammary tumor; cell line: NDL; ' GSE106100 Homo sapiens 6 Expression profiling by array GPL10558 Genome-wide analysis of differential gene expression in MDA-MB-231 cells after GRMI silencing 2017-10-24 MDA-MB-231 cells were used to determine genes differentially regulated by metabotropic glutamate receptor-1 (GRM1) https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE106100 Metabotropic glutamate receptor-1 regulates inflammation in triple negative breast cancer. Scientific reports 4.011 https://doi.org/10.1038/s41598-018-34502-8 {Scientific reports (4.011): 10.1038/s41598-018-34502-8} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA415602 https://www.ebi.ac.uk/ena/browser/view/PRJNA415602 None [Overal design]MDA-MB-231 cells were transduced with GIPZ Lentiviral vectors expressing either GRM1 shRNA or a control non-silencing vector and differientially expressed genes were determined by microarray analysis after stable transduction; [Treatment]'Cells were transduced with GIPZ Lentiviral vectors expressing either GRM1 shRNA or a non-silencing vector and a stable cell culture established using puromycin (10 ug/ml) for two weeks prior to RNA extraction'; [Growth]'Cells were cultured in RPMI media supplemented with 5% FBS, 50 U/ml penicillin, 50 mg/ml streptomycin and 250 ng/ml amphotericin B'; [Extraction]"RNA was extracted with the QIAGEN Rneasy Plus kit according to manufacturer's instructions and quality assessed using the Agilent 2100 Bioanalyzer"; [Cell type]'triple-negative breast cancer cell line''cell line: MDA-MB-231; cell type: triple-negative breast cancer cell line; tranduced with: GIPZ Lentiviral vectors expressing control non-silencing vector; ', 'cell line: MDA-MB-231; cell type: triple-negative breast cancer cell line; tranduced with: GIPZ Lentiviral vectors expressing GRM1 shRNA; ' GSE39543 Homo sapiens 51 Non-coding RNA profiling by array GPL15834 miRNA profiling of breast cancer patients 2012-07-20 Chemotherapy resistance frequently drives tumor progression. However, the underlying molecular mechanisms are poorly characterized. Epithelial-to-mesenchymal transition (EMT) has been shown to correlate with therapy resistance, but the functional link and signaling pathways remain to be elucidated. We report here that miR-30c, a human breast tumor prognostic marker, plays a pivotal role in chemo-resistance by a direct targeting of the actintransporter TWF1, which promotes EMT. An IL-6 family member, IL-11 was identified as a secondary target of TWF1 in the miR-30c signaling pathway. Expression of miR-30c inversely correlated with IL-11 expression in clinical tumors and IL-11 correlated with relapse-free survival in breast cancer patients. Identification of a novel miRNA-mediated pathway that regulates chemo-resistance in breast cancer will facilitate the development of new management strategies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39543 MicroRNA-30c inhibits human breast tumour chemotherapy resistance by regulating TWF1 and IL-11. Nature communications 11.878 https://doi.org/10.1038/ncomms2393 {Nature communications (11.878): 10.1038/ncomms2393} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA171094 https://www.ebi.ac.uk/ena/browser/view/PRJNA171094 None [Overal design]For the primary breast tumor and normal breast samples, both mRNAs (Agilent array data deposited in GSE22049) and miRNAs (Exiqon array data deposited here) profiles have been examined. Patient information include age, tumor subtype and outcome etc. When clustering samples and genes 152 of 757 miRNA passed the filtering criteria on variation across samples; standard deviation > 0.50. Hence, the upper 152 miRNAs in the expression matrix were used in the two-way hierarchical clustering of genes. The matrix numbers are all log2(Hy3/Hy5) ratios, meaning sample/pool. The percentages above the matrix indicates the present call in each sample/slide. When calling of a particular miRNA failed on an array this is indicated as a blank in the row containing this miRNA and in the column corresponding to this array. The criteria for deciding that the calling of a miRNA had failed on a particular array, was that 2 or more of the 4 replicated measures of this miRNA were flagged 1 or 2 (i.e. the signal is below background) by the image analysis software. Further in the expression matrix all capture probes with Hy3 and Hy5 signals lower than 1.5x of the median signal intensity of the given slide is indicated as a blank.; [Treatment]'None'; [Growth]'None'; [Extraction]'The Qiagen miRNA easy kit with total RNA extraction.'; [Cell type]'Source: ''tissue: Breast Tumor; OS time: 49.0666666666667; age_dx: 55.441095890411; race: Black; ajcc_stage: 4; pathological stage_t: 4; grade: 9; tumor size: 1.8; tnm: T1cN3M1; er: pos; pr: pos; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): u; tumor subtype ihc: LumA; subtypes_by_dna_microarray: NA; ', 'sample type: referene pool; ', 'tissue: Breast Tumor; OS time: 61; age_dx: 57; race: Black; ajcc_stage: 3A; pathological stage_t: 3; grade: 2; tumor size: 4; tnm: T2N3MX; er: pos; pr: neg; her-2: pos; triple_negative: Non_Triple; subtypes_by_dna_microarray: HER2; ', 'tissue: Breast Tumor; OS time: 15.9; age_dx: 23.6958904109589; race: Black; ajcc_stage: 2A; pathological stage_t: 2; grade: 3; tumor size: 3; tnm: T2N0M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): M; tumor subtype ihc: unclassified; subtypes_by_dna_microarray: Basal_like; ', 'tissue: Breast Tumor; OS time: 44.9; age_dx: 43.4465753424658; race: Black; ajcc_stage: 3C; pathological stage_t: 3; grade: 2; tumor size: 0.5; tnm: T4dN3M0; er: pos; pr: pos; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: N/A; subtypes_by_dna_microarray: Lum A; ', 'tissue: Breast Tumor; OS time: 45.3; age_dx: 61.3178082191781; race: Black; ajcc_stage: 3B; pathological stage_t: 3; grade: 2; tumor size: 1.4; tnm: T4bN1M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Basal; subtypes_by_dna_microarray: Basal_like; ', 'tissue: Breast Tumor; OS time: 13.4333333333333; age_dx: 26.9068493150685; race: Black; ajcc_stage: 3C; pathological stage_t: 3; grade: 3; tumor size: 1; tnm: T4dN3M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: unclassified; subtypes_by_dna_microarray: Basal_like; ', 'tissue: Breast Tumor; OS time: 39.1666666666667; age_dx: 45.1178082191781; race: Black; ajcc_stage: 1; pathological stage_t: 1; grade: 2; tumor size: 1.8; tnm: T1cN0M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): u; tumor subtype ihc: unclassified; subtypes_by_dna_microarray: NA; ', 'tissue: Breast Tumor; OS time: 58.8; age_dx: 34.5232876712329; race: Black; ajcc_stage: 2B; pathological stage_t: 2; grade: 3; tumor size: 2.8; tnm: T2N1M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): M; tumor subtype ihc: Basal; subtypes_by_dna_microarray: Basal_like; ', 'tissue: Breast Tumor; OS time: 16.9666666666667; age_dx: 47.4547945205479; race: White; ajcc_stage: 3C; pathological stage_t: 3; grade: 2; tumor size: 2; tnm: T1cN3M0; er: neg; pr: neg; her-2: pos; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: unclassified; subtypes_by_dna_microarray: HER2; ', 'tissue: Breast Tumor; OS time: 137.766666666667; age_dx: 55.7972602739726; race: Black; ajcc_stage: 1; pathological stage_t: 1; grade: 1; tumor size: 0.3; tnm: T1aN0M0; er: pos; pr: neg; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: unclassified; subtypes_by_dna_microarray: LumA; ', 'tissue: Normal Breast Tissue; subtypes_by_dna_microarray: NA; ', 'tissue: Breast Tumor; OS time: 10.2333333333333; age_dx: 40.986301369863; race: White; ajcc_stage: 4; pathological stage_t: 4; grade: 3; tumor size: 7; tnm: T3N3M1; er: pos; pr: pos; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: LumA; subtypes_by_dna_microarray: LumB; ', 'tissue: Breast Tumor; OS time: 33.9; age_dx: 58.9041095890411; race: Black; ajcc_stage: 2B; pathological stage_t: 2; grade: 2; tumor size: 3; tnm: T2N1M0; er: neg; pr: neg; her-2: pos; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: unclassified; subtypes_by_dna_microarray: HER2; ', 'tissue: Normal; subtypes_by_dna_microarray: NA; ', 'tissue: Breast Tumor; OS time: 46.9666666666667; age_dx: 66.6821917808219; race: Black; ajcc_stage: 2B; pathological stage_t: 2; grade: 3; tumor size: 3; tnm: T2N1M0; er: pos; pr: pos; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: LumA; subtypes_by_dna_microarray: LumB; ', 'tissue: Breast Tumor; OS time: 174.633333333333; age_dx: 55.3150684931507; race: Black; ajcc_stage: 2B; pathological stage_t: 2; grade: 3; tumor size: 4; tnm: T2N1M0; er: neg; pr: neg; her-2: pos; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Her2; subtypes_by_dna_microarray: HER2; ', 'tissue: Breast Tumor; OS time: 69.2; age_dx: 74.2630136986301; race: White; ajcc_stage: unknown; pathological stage_t: 9; grade: 2; tumor size: 3; tnm: T2NxM0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: N/A; subtypes_by_dna_microarray: LumA; ', 'tissue: Breast Tumor; OS time: 53.2333333333333; age_dx: 77.5972602739726; race: Black; ajcc_stage: 3A; pathological stage_t: 3; grade: 2; tumor size: 3.5; tnm: T2N2M0; er: pos; pr: pos; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: LumA; subtypes_by_dna_microarray: LumA; ', 'tissue: Breast Tumor; OS time: 117.766666666667; age_dx: 43.0602739726027; race: White; ajcc_stage: 2A; pathological stage_t: 2; grade: 3; tumor size: 3.5; tnm: T2N0M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): M; tumor subtype ihc: Basal; subtypes_by_dna_microarray: Basal_like; ', 'tissue: Breast Tumor; OS time: 10.6333333333333; age_dx: 77.3890410958904; race: White; ajcc_stage: 4; pathological stage_t: 4; grade: 2; tumor size: 6; tnm: T3N1M1; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Basal; subtypes_by_dna_microarray: Normal; ', 'tissue: Breast Tumor; OS time: 78.0666666666667; age_dx: 43.5506849315069; race: White; ajcc_stage: 2B; pathological stage_t: 2; grade: 3; tumor size: 3.5; tnm: T2N1M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Basal; subtypes_by_dna_microarray: Basal_like; ', 'tissue: Breast Tumor; OS time: 151.9; age_dx: 51.6986301369863; race: White; ajcc_stage: 2A; pathological stage_t: 2; grade: 2; tumor size: 2.5; tnm: T2N0M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Basal; subtypes_by_dna_microarray: HER2; ', 'tissue: Breast Tumor; OS time: 28.4; age_dx: 71.7780821917808; race: Black; ajcc_stage: 3A; pathological stage_t: 3; grade: 3; tumor size: 4.5; tnm: T2N2M0; er: neg; pr: neg; her-2: pos; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Unclassified; subtypes_by_dna_microarray: Normal; ', 'tissue: Breast Tumor; OS time: 30.2666666666667; age_dx: 56.2219178082192; race: Black; ajcc_stage: 3A; pathological stage_t: 3; grade: 2; tumor size: 5; tnm: T2N2M0; er: neg; pr: neg; her-2: pos; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Unclassified; subtypes_by_dna_microarray: HER2; ', 'tissue: Breast Tumor; OS time: 12.2666666666667; age_dx: 52.0191780821918; race: Black; ajcc_stage: 3A; pathological stage_t: 3; grade: 3; tumor size: 3; tnm: T2N2M0; er: neg; pr: neg; her-2: pos; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Unclassified; subtypes_by_dna_microarray: HER2; ', 'tissue: Breast Tumor; OS time: 63.8333333333333; age_dx: 39.2849315068493; race: Black; ajcc_stage: 3A; pathological stage_t: 3; grade: 3; tumor size: 11; tnm: T3N2M0; er: pos; pr: pos; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: LumA; subtypes_by_dna_microarray: LumB; ', 'tissue: Breast Tumor; OS time: 9.1; age_dx: 36.3534246575342; race: Black; ajcc_stage: 4; pathological stage_t: 4; grade: 3; tumor size: 6; tnm: T3N3M1; er: neg; pr: neg; her-2: pos; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Unclassified; subtypes_by_dna_microarray: HER2; ', 'tissue: Breast Tumor; OS time: 48.1666666666667; age_dx: 33.3753424657534; race: White; ajcc_stage: 3A; pathological stage_t: 3; grade: 2; tumor size: 2.9; tnm: T2N2M0; er: neg; pr: neg; her-2: pos; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Unclassified; subtypes_by_dna_microarray: HER2; ', 'tissue: Breast Tumor; OS time: 76.1333333333333; age_dx: 51.5260273972603; race: Black; ajcc_stage: 2A; pathological stage_t: 2; grade: 3; tumor size: 4.3; tnm: T2N0M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Unclassified; subtypes_by_dna_microarray: Basal_like; ', 'tissue: Breast Tumor; OS time: 91.8; age_dx: 40.5890410958904; race: White; ajcc_stage: 3A; pathological stage_t: 3; grade: 3; tumor size: 3.5; tnm: T2N2M0; er: neg; pr: neg; her-2: pos; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Unclassified; subtypes_by_dna_microarray: HER2; ', 'tissue: Breast Tumor; OS time: 21.0666666666667; age_dx: 60.2849315068493; race: Black; ajcc_stage: 2A; pathological stage_t: 2; grade: 3; tumor size: 3.2; tnm: T2N0M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): M; tumor subtype ihc: Basal; subtypes_by_dna_microarray: Basal_like; ', 'tissue: Breast Tumor; OS time: 61; age_dx: 59.6931506849315; race: Black; ajcc_stage: 2B; pathological stage_t: 2; grade: 2; tumor size: 2.6; tnm: T2N1M0; er: pos; pr: pos; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: LumA; subtypes_by_dna_microarray: LumA; ', 'tissue: Breast Tumor; OS time: 47.1666666666667; age_dx: 52.0657534246575; race: White; ajcc_stage: 2A; pathological stage_t: 2; grade: 3; tumor size: 4; tnm: T2N0M0; er: pos; pr: pos; her-2: pos; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: N/A; subtypes_by_dna_microarray: LumB; ', 'tissue: Breast Tumor; OS time: 51.6666666666667; age_dx: 49.5945205479452; race: Black; ajcc_stage: 2B; pathological stage_t: 2; grade: 3; tumor size: 2.5; tnm: T2N1M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Basal; subtypes_by_dna_microarray: LumB; ', 'tissue: Breast Tumor; OS time: 32.7333333333333; age_dx: 28.3780821917808; race: Black; ajcc_stage: 3A; pathological stage_t: 3; grade: 3; tumor size: 3; tnm: T2N2M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Unclassified; subtypes_by_dna_microarray: Normal; ', 'tissue: Breast Tumor; OS time: 43.2333333333333; age_dx: 33.0712328767123; race: Black; ajcc_stage: 3A; pathological stage_t: 3; grade: 3; tumor size: 0.5; tnm: T1aN2M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Basal; subtypes_by_dna_microarray: Basal_like; ', 'tissue: Breast Tumor; OS time: 32.0333333333333; age_dx: 44.7671232876712; race: Black; ajcc_stage: 0; pathological stage_t: 5; grade: 3; tumor size: Tis; tnm: TisN0M0; er: neg; pr: neg; her-2: pos; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Her2; subtypes_by_dna_microarray: LumA; ', 'tissue: Breast Tumor; OS time: 50.8; age_dx: 43.0739726027397; race: Black; ajcc_stage: 3A; pathological stage_t: 3; grade: 3; tumor size: 4.5; tnm: T2N2M0; er: pos; pr: pos; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: LumA; subtypes_by_dna_microarray: LumB; ', 'tissue: Breast Tumor; OS time: 30.5666666666667; age_dx: 40.9753424657534; race: Black; ajcc_stage: 2B; pathological stage_t: 2; grade: 2; tumor size: 2.8; tnm: T2N1M0; er: pos; pr: pos; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: LumA; subtypes_by_dna_microarray: LumA; ', 'tissue: Breast Tumor; OS time: 52.0333333333333; age_dx: 37.8328767123288; race: Black; ajcc_stage: 2A; pathological stage_t: 2; grade: 3; tumor size: 3.2; tnm: T2N0M0; er: pos; pr: pos; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: n/a; subtypes_by_dna_microarray: LumA; ', 'tissue: Normal; ', 'tissue: Breast Tumor; OS time: 44.6; age_dx: 57.7534246575342; race: Black; ajcc_stage: 3A; pathological stage_t: 3; grade: 3; tumor size: 6.5; tnm: T3N1miMX; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: N/A; subtypes_by_dna_microarray: Basal_like; ', 'tissue: Breast Tumor; OS time: 31.3; age_dx: 50.8438356164384; race: Black; ajcc_stage: 3A; pathological stage_t: 3; grade: 3; tumor size: 4; tnm: T2N2M0; er: neg; pr: neg; her-2: pos; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: N/A; subtypes_by_dna_microarray: LumA; ', 'tissue: Breast Tumor; OS time: 37.5666666666667; age_dx: 54.7780821917808; race: Black; ajcc_stage: 1; pathological stage_t: 1; grade: 2; tumor size: 1.8; tnm: T1cN0M0; er: pos; pr: pos; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Unclassified; subtypes_by_dna_microarray: LumA; ', 'tissue: Breast Tumor; OS time: 24; age_dx: 69; race: Black; ajcc_stage: 3c; pathological stage_t: 3; tumor size: 4; tnm: T2N3M0; er: Pos; pr: neg; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): NA; tumor subtype ihc: LUM A; subtypes_by_dna_microarray: LumA; ', 'tissue: Breast Tumor; OS time: 3; age_dx: 68; race: Black; ajcc_stage: 3c; pathological stage_t: 3; tumor size: 3; tnm: T2N3M0; er: Neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): NA; tumor subtype ihc: BASAL; subtypes_by_dna_microarray: Basal_Like; ', 'tissue: Breast Tumor; OS time: 154; age_dx: 68; race: Black; ajcc_stage: 1; pathological stage_t: 1; tumor size: 1; tnm: T1cN0M0; er: Pos; pr: neg; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): NA; tumor subtype ihc: LUM A; subtypes_by_dna_microarray: LumB; ', 'tissue: Breast Tumor; OS time: 113; age_dx: 62; race: Black; er: pos; pr: neg; her-2: neg; triple_negative: Non_Triple; methylation (m-methylation, u-unmethylated): NA; tumor subtype ihc: LUM A; subtypes_by_dna_microarray: Lum_A; ', 'tissue: Breast Tumor; OS time: 29.3666666666667; age_dx: 46.5698630136986; race: Black; ajcc_stage: 2A; pathological stage_t: 2; grade: 3; tumor size: 2.5; tnm: T2N0M0; er: neg; pr: neg; her-2: neg; triple_negative: Triple_negative; methylation (m-methylation, u-unmethylated): U; tumor subtype ihc: Basal; subtypes_by_dna_microarray: Basal_like; ' GSE46925 Homo sapiens 6 Expression profiling by array GPL570 Aerobic training modulation of the host systemic milieu directly alters breast cancer cell phenotype in vitro. 2013-05-14 Aberrant production and/or function of multiple host systemic factors (e.g., metabolic and immune-inflammatory mediators) act in concert to promote a ‘tumorigenic’ host milieu that directly promotes an aggressive malignant phenotype as well as drug resistance. Hence, strategies with the capacity to simultaneously act across multiple host systemic pathways may be required to optimize therapeutic outcomes in solid tumors. We hypothesized that chronic aerobic training, a pleiotropic whole-body intervention, modulates multiple systemic host pathways that, in turn, effectively alters cancer cell phenotype in vitro. Plasma samples from patients with solid tumors exposed to chronic aerobic training or sedentary control were comprehensively characterized for changes in immune, inflammatory, and metabolic pathways. Compared with sedentary control, aerobic training caused significant reductions in interleukin (IL)-4, macrophage inflammatory protein-1 beta (MIP1-β), vascular endothelial growth factor (VEGF), tumor necrosis factor-alpha (TNF-α), and hepatocyte growth factor (HGF). There were no significant changes in leukocyte phenotype or any plasma metabolite signatures. Exposure of estrogen receptor (ER) distinct human breast cancer cell lines (MCF-7 and MDA-MB-231) to post-intervention serum from breast cancer patients exposed to aerobic training caused marked increases in proliferation, migration, and apoptosis, compared to control patient serum. Only the combination of cytokines significantly reduced in plasma following aerobic training recapitulated the phenotype observed with patient serum in MCF-7 cells whereas only the single addition of MIP-1β or HGF significantly increased apoptosis in MDA-MB-231 cells. Co-culturing of MDA-MB-231 cells with patient exercise serum and a HGF neutralizing antibody increased proliferation and completely abrogated exercise serum-induced apoptosis. Finally, whole-genome microarray of MDA-MB-231 cells exposed to exercise or control patient serum revealed differential modulation of 310 genes including PTEN, CDK3, and IGFBP1. Our findings indicate the widespread potential of chronic aerobic training to modulate host immune-inflammatory systemic factors in patients with solid tumors. Modulation of such pathways directly alters breast cancer phenotypes providing novel insight into the molecular pathways by which exercise may inhibit malignant progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE46925 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA203043 https://www.ebi.ac.uk/ena/browser/view/PRJNA203043 None [Overal design]MDA-MB-231 cells were plated at 250,000 cells/well in triplicate with 10% FBS in 6-well plates and left overnight to adhere. Media was suctioned off and replaced with serum free media. Patient serum was then added to the wells at a 10% final concentration and RNA was harvested using Qiagen RNeasy kit after 4 days.; [Treatment]'Patient serum was then added to the wells at a 10% final concentration and RNA was harvested using Qiagen RNeasy kit after 4 days.'; [Growth]'MDA-MB-231 cells were plated at 250,000 cells/well with 10% FBS in 6-well plates and left overnight to adhere. Media was suctioned off and replaced with serum free media. Patient serum was then added to the wells at a 10% final concentration and RNA was harvested using Qiagen RNeasy kit after 4 days.'; [Extraction]'Total RNA were assessed for quality with Agilent 2100 Bioanalyzer G2939A (Agilent Technologies,Santa Clara, CA)) and Nanodrop 8000 spectrophotometer (Thermo Scientific/Nanodrop, Wilmington, DE).'; [Cell type]'human breast adenocarcinoma cells''cell line: MDA-MB-231; cell type: human breast adenocarcinoma cells; treated with: serum from sedentary control breast cancer patient; ', 'cell line: MDA-MB-231; cell type: human breast adenocarcinoma cells; treated with: serum from breast cancer patients exposed to aerobic training; ' GSE26517 Mus musculus 6 Expression profiling by array GPL6887 Detecting transcription profile associated to mammosphere medium 2011-01-10 Mammosphere medium (Grange et al. Neoplasia 2008;10(12):1433-43) contains epidermal growth factor (EGF), insulin and basic fibroblast growth factor (bFGF) that may influence transcript expression in a way not necessarily related to the assembly of mammspheres. To identify the set of genes associated mammosphere cell growth medium we analyzed two prototypic situations in triplicate experiments: TUBO cells (a mouse breast cancer cell line derived by Balb-neuT mice) grown in DMEM under adherent conditions (TDA), TUBO cells grown in Mammosphere medium under adherent conditions (TMA). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26517 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA136705 https://www.ebi.ac.uk/ena/browser/view/PRJNA136705 None [Overal design]Two prototypic situations in triplicate experiments were analysed: TUBO cells (Rovero et al. Gene Ther 2001;8(6):447-52) grown in DMEM under adherent conditions (TDA), TUBO cells grown in Mammosphere medium under adherent conditions (TMA).; [Treatment]'None'; [Growth]"TUBO cells grown in adherent conditions as epithelial monolayer (TDA), were generated from a mammary carcinoma arising in a BALB-neuT female mouse, and cultured in epithelial medium, Dulbecco's Modified Eagle Medium supplemented with 20% fetal calf serum. TUBO cells grown in adherent conditions in mammosphere medium (TMA). Mammosphere medium, serum-free DMEM-F12 medium supplemented with 20 ng/ml basic-fibroblast growth factor (bFGF), 20 ng/ml epidermal growth factor (EGF), 5 μg/ml insulin, and 0.4% bovine serum albumin (BSA)."; [Extraction]'Trizol total RNA extraction'; [Cell type]'Source: ''cell line: TUBO; origin tissue: breast cancer; ' GSE156331 Homo sapiens 9 Non-coding RNA profiling by array GPL19065 IRE1 modulates expression of a set of tumor suppressor miRNAs in luminal breast cancer cells. 2020-08-17 To explore the regulatory mechanism by which inositol-requiring enzyme 1 (IRE1) regulates oncogenic factors, particularly RAB3B, in luminal breast cancer cells, we blocked IRE1 activity in breast cancer cell lines by using the IRE1 inhibitor 4μ8C or expressing IRE1 dominant-negative for miRNA microarray analysis. SUM52 and SUM225 lines with high-level IRE1 expression were treated with 4μ8C for 2 days. The IRE1 kinase dominant-negative mutant K599A or K907A was also used to suppress IRE1 kinase or RNase activity in SUM52 cells. The miRNA microarray analysis revealed a landscape change in miRNA expression profiling in IRE1-inhibited luminal breast cancer cells. Using a criterion of p < 0.05 in miRNA analysis, we identified 41 miRNAs in both SUM52 and SUM225 cells that were altered after inhibiting IRE1 activity. Additionally, we exogenously overexpressed wild-type IRE1 in human nontumorigenic mammary epithelial MCF10A cells and then performed miRNA array assays. When we combined miRNA data from both IRE1 inhibition models in breast cancer cells and exogenous overexpression of IRE1 in MCF10A cells (p<0.05), we identified 5 miRNAs (3607-3p, 374a-5p, 4764-3p, 516a-3p, and 6073) that were upregulated in IRE1-inhibited breast cancer cells and downregulated in MCF10A-IRE1 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE156331 The UPR Transducer IRE1 Promotes Breast Cancer Malignancy by Degrading Tumor Suppressor microRNAs. iScience None https://doi.org/10.1016/j.isci.2020.101503 {iScience (None): 10.1016/j.isci.2020.101503} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA657550 https://www.ebi.ac.uk/ena/browser/view/PRJNA657550 None [Overal design]Total RNAs from SUM52, SUM225, or MCF10A cells that were treated with IRE1 inhibitor 4μ8C or transducted with the IRE1 dominant-negative K599A, K907A, or wild-type IRE1 were harvested, frozen, and sent to the LC Sciences (Houston, TX, USA) for miRNA analysis.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted with miRNeasy Mini kits (Qiagen, Hilden, Germany), and miRNA microarray analysis was performed by LC Sciences (Houston,TX).'; [Cell type]'Source: ''tissue: Breast; ' GSE95299 Homo sapiens 9 Expression profiling by high throughput sequencing GPL20301 Overexpression of NFIB and YBX1 in MCF-7 cells 2017-02-23 Studying transcription factor (TF) interactions and gene regulatory networks in breast cancer, we have recently identified two distinct and opposing clusters of TFs associated with estrogen receptor-positive and -negative breast cancer and breast cancer risk. The relative activity of these two groups of TFs has a dramatic effect on patient outcomes and is likely to influence the phenotypic plasticity observed in breast cancer. We have identified two novel interactors (NFIB and YBX1) of the estrogen receptor (ESR1) using Rapid Immunoprecipitation Mass Spectrometry of Endogenous Proteins (RIME), co-immunoprecipitation and microscopy experiments. Both NFIB and YBX1 are members of the group of risk TFs that oppose the activity of the risk TFs associated with estrogen receptor-positive disease, and we have demonstrated that they both repress the transcriptional activity of ESR1. Here, we examine the effect of NFIB and YBX1 overexpression on the transcriptome of an estrogen receptor-positive breast cancer cell line to see if these risk TFs are able to repress the ESR1 regulon and drive cells towards a less estrogen-dependent phenotype. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95299 ERα Binding by Transcription Factors NFIB and YBX1 Enables FGFR2 Signaling to Modulate Estrogen Responsiveness in Breast Cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-17-1153 {Cancer research (8.378): 10.1158/0008-5472.CAN-17-1153} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA376585 https://www.ebi.ac.uk/ena/browser/view/PRJNA376585 https://www.ncbi.nlm.nih.gov/sra?term=SRP100638 [Overal design]Data consists of three different cell lines (MCF-7 parental, MCF-7 stably overexpressing FLAG-tagged NFIB, and MCF-7 stably overexpressing FLAG-tagged YBX1), analysed to detect gene expression differences. Each cell line was tested in triplicate (biological replicates consisting of three separate clones of stable cells).; [Treatment]'None'; [Growth]'MCF-7 human breast cancer cells were cultured in DMEM (Invitrogen) supplemented with 10% FBS and antibiotics. Cells stably overexpressing NFIB/YBX1 were grown in the presence of geneticin (G418; Invitrogen). All cells were maintained at 37°C, 5% CO2.'; [Extraction]'RNA was extracted using the miRNeasy spin column kit (QIAGEN) and quality checked using an RNA 6000 Nano chip on a 2100 Bioanalyser (Agilent).\nmRNA-seq libraries were prepared from three biological replicates of each stable overexpression system using the TruSeq Stranded mRNA Library Prep Kit (Illumina).'; [Cell type]'Source: ''cell line: MCF-7; genotype/variation: Parental MCF7; ', 'cell line: MCF-7; genotype/variation: MCF-7 stably overexpressing FLAG-tagged NFIB; ', 'cell line: MCF-7; genotype/variation: MCF-7 stably overexpressing FLAG-tagged YBX1; ' GSE83608 Homo sapiens 4 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL16104 SNP arrays of BT474 Latpatinib and/or Trastuzumab resistant cell lines for copy number analysis. 2016-06-22 Targeting HER2 with lapatinib (L), trastuzumab (T), or the LT combination, is effective in HER2+ breast cancer (BC), but de novo and acquired resistance commonly occur. The purpose of this experiment was to investigate the somatic alterations found in Lapatinib and/or Trastuzumab resistant cells lines. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE83608 HER2 Reactivation through Acquisition of the HER2 L755S Mutation as a Mechanism of Acquired Resistance to HER2-targeted Therapy in HER2+ Breast Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-16-2191 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-16-2191} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA326958 https://www.ebi.ac.uk/ena/browser/view/PRJNA326958 None [Overal design]SNP arrays of BT474 cell derivative genomic DNA was performed using HumanOmni2.5-8 BeadChip Kit.; [Treatment]'Resistant derivatives of both BT474 P lines to HER-targeted therapies were derived independently: cells were treated with gradually increasing doses until cells resume growth in the presence of 1 μM L, 50 μg/ml T, or the combination.'; [Growth]'Source, culture media and conditions of the BT474/AZ parental (P) line were described previously (Wang et al., Breast Cancer Research 2011).'; [Extraction]'Cell line genomic DNA (gDNA) was isolated using the Wizard Genomic DNA Kit (Promega).'; [Cell type]'Source: ''strain: BT474; phenotype: parental line; ', 'strain: BT474; phenotype: resistant to the combination of Lapatinib and Trastuzumab treatment; ', 'strain: BT474; phenotype: resistant to Lapatinib treatment; ' GSE66085 Mus musculus 8 Expression profiling by array GPL13912 RANK-Fc treatment in MMTV-PyMT late carcinoma 2015-02-19 Transcriptional profile of MMTV-PyMT late carcinomas after adjuvant or neoadjuvant treatment with RANK-Fc (receptor activator of NF-kB) cells isolated from one single MMTV-PyMT carcinoma were orthotopically injected in syngeneic WT mice, which were randomized 1:1 for neoadjuvant RANK-Fc or mock treatment (passage 1) for 4 weeks. Cells isolated from both treatment arms were pooled and injected into the fat pad of FvB recipients (passage 2) in limiting dilutions (mimicking occult disease) and again randomized 1:1 for additional RANK-Fc (adjuvant) or mock treatment https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE66085 RANK Signaling Blockade Reduces Breast Cancer Recurrence by Inducing Tumor Cell Differentiation. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-15-2745 {Cancer research (8.378): 10.1158/0008-5472.CAN-15-2745} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA275855 https://www.ebi.ac.uk/ena/browser/view/PRJNA275855 None [Overal design]passage 1: 2 control tumor samples (CT), 3 RANK-Fc treated tumor samples (Fc); passage 2: 2 control tumor samples (CT_CT), 3 neoadjuvant RANK-Fc treated tumor samples (Fc_CT, pre-RANK-Fc), 3 adjuvant RANK-Fc treated tumor samples (CT_Fc, post-RANK-Fc); 3 neoadjuvant and adjuvant RANK-Fc treated tumor samples (FC_FC, pre&post-RANK-Fc); [Treatment]'RANK-Fc (10 mg/Kg) was injected intraperitoenally, 3 times per week into WT FVB mice with an orthotopic PyMT tumor'; [Growth]'RNA was collected from tumor fragments'; [Extraction]'Tripure (Roche)'; [Cell type]'Source: ''strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: FC c558: RANK-Fc adjuvant treatment, passage 1; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: CT-FC c633: adjuvant treatment RANK-Fc, passage 2; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: FC_CT c608: RANK-Fc neoadjuvant treatment, passage 2; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: FC c567: RANK-Fc adjuvant treatment, passage 1; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: CT c566: control passage 1; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: Fc c559: RANK-Fc adjuvant treatment, passage 1; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: CT_CT c642: control passage 2; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: Fc_CT c603: RANK-Fc neoadjuvant treatment, passage 2; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: FC_FC c607: RANK-Fc neoadjuvant & adjuvant treatment , passage 2; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: CT c564: control passage 1; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: CT_Fc c635: RANK-Fc adjuvant treatment, passage 2; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: CT_CT c641: control passage 2; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: Fc_Fc c606: RANK-Fc neoadjuvant & adjuvant treatment , passage 2; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: CT_FC c646: adjuvant treatment RANK-Fc, passage 2; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: Fc_CT c609: RANK-Fc neoadjuvant treatment, passage 2; ', 'strain: FVB; tissue: MMTV-PyMT (FVB) orthotopic mammary tumor piece; treatment: Fc_FC c626: neoadjuvant & adjuvant treatment RANK-Fc, passage 2; ' GSE12093 Homo sapiens 136 Expression profiling by array GPL96 The 76-gene Signature Defines High-Risk Patients that Benefit from Adjuvant Tamoxifen Therapy 2008-07-11 Classification of tamixifen-treated breast cancer patients into high and low risk groups using the 76-gene signature https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE12093 The 76-gene signature defines high-risk patients that benefit from adjuvant tamoxifen therapy. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-008-0183-2 {Breast cancer research and treatment (3.471): 10.1007/s10549-008-0183-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA113529 https://www.ebi.ac.uk/ena/browser/view/PRJNA113529 None [Overal design]136 breast cancer samples that were treated with tamoxifen were classified using the 76-gene signature; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted from cell samples using the Trizol Kit.'; [Cell type]'Source: ''' GSE114329 Homo sapiens 18 Non-coding RNA profiling by high throughput sequencing GPL20301 small RNA profiling of extracellular RNA from breast cancer cell lines [EV] 2018-05-10 We performed small RNA sequencing of exosomes and extracellular vesicles collected from breast cancer cells as well as human mammary epithelial cells (HUMEC) in biological replicates (using Norgen's cell culture media exosme purification and RNA isoaltion kits). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE114329 Cancer cells exploit an orphan RNA to drive metastatic progression. Nature medicine 30.641 https://doi.org/10.1038/s41591-018-0230-4 {Nature medicine (30.641): 10.1038/s41591-018-0230-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA471078 https://www.ebi.ac.uk/ena/browser/view/PRJNA471078 https://www.ncbi.nlm.nih.gov/sra?term=SRP145491 [Overal design]BRCA-lines_EV_smRNA: Eight breast cancer lines and human mammary epithelial cells were cultured in biological replicates. Exosomes/small extracellular vesicles (EV) were then collected from the conditioned media using the Cell Culture Media Exosome Purification Mini Kit (Norgen). Samples were then subjected to small RNA sequencing. The number of unique orphan non-coding RNAs were then recorded for each sample.; [Treatment]'Preparation of conditioned media for isolation of RNA from extracellular vesicle and total conditioned media was carried out by seeding cells at 7x105. Twenty-four hours later, cells were washed twice with PBS and 10mL exosome-depleted media was added. Forty-eight hours later, media was harvested by spinning at 200xg for 15 minutes and taking the supernatant. Exosome-depleted media was prepared by substituting exosome-depleted FBS (Thermo Fisher Scientific cat. no. A2720803) for FBS. Exosome-depleted HuMEC media was prepared by centrifuging the bovine pituitary extract at 100,000xg, 4°C for 16 hours.'; [Growth]'All cells were cultured in a 37°C, 5% CO2 humidified incubator. Cell lines MDA-MB-231, MDA-LM2, CN34-par, CN34-Lm1a, MCF7 and MDA-MB-453 were propagated in DMEM base media supplemented with 4.5 g/L glucose, 10% FBS, 4mM L-glutamine, 1mM sodium pyruvate, penicillin (100 units/mL), streptomycin (100 μg/mL) and amphotericin (1μg/mL). Cell lines HCC1395, ZR-75-1 and HCC38 were propagated in RPMI 1640 base media supplemented with 10% FBS, 2mM L-glutamine, penicillin (100 units/mL), streptomycin (100 μg/mL) and amphotericin (1μg/mL). SK-BR-3 cell line was propagated in McCoy’s 5a modified media supplemented with 10% FBS, penicillin (100 units/mL), streptomycin (100 μg/mL) and amphotericin (1μg/mL). HMECs were propagated in HuMEC media (Thermo Fisher Scientific cat. no. 175010).'; [Extraction]'Extracellular vesicle RNA was isolated from 5mL conditioned media using the Cell Culture Media Exosome Purification Mini Kit (Norgen, cat. no. 60400).\nThe libraries were constructed using the NEXTflex small RNA sequencing kit v3 for Illumina platforms (Bioo Scientific NOVA-5132-06). 15 ng of extracellular vesicle RNA and 10 ng of conditioned media RNA were used as starting material, and gel extraction was performed for all libraries.'; [Cell type]'Source: ''cell line: CN34; rep: 1; compartment: Evs; ', 'cell line: CN34; rep: 2; compartment: Evs; ', 'cell line: HCC1395; rep: 1; compartment: Evs; ', 'cell line: HCC1395; rep: 2; compartment: Evs; ', 'cell line: HCC38; rep: 1; compartment: Evs; ', 'cell line: HCC38; rep: 2; compartment: Evs; ', 'cell line: HuMEC; rep: 1; compartment: Evs; ', 'cell line: HuMEC; rep: 2; compartment: Evs; ', 'cell line: MCF7; rep: 1; compartment: Evs; ', 'cell line: MCF7; rep: 2; compartment: Evs; ', 'cell line: MDA231; rep: 1; compartment: Evs; ', 'cell line: MDA231; rep: 2; compartment: Evs; ', 'cell line: MDA453; rep: 1; compartment: Evs; ', 'cell line: MDA453; rep: 2; compartment: Evs; ', 'cell line: SKBR3; rep: 1; compartment: Evs; ', 'cell line: SKBR3; rep: 2; compartment: Evs; ', 'cell line: ZR75; rep: 1; compartment: Evs; ', 'cell line: ZR75; rep: 2; compartment: Evs; ' GSE62598 Mus musculus 15 Expression profiling by array GPL7202 Granulocytic immune infiltrates are essential for the efficient formation of breast cancer liver metastases 2014-10-22 Breast cancer cells display preferences for specific metastatic sites including the bone, lung and liver. Metastasis is a complex process that relies, in part, on interactions between disseminated cancer cells and resident/infiltrating stromal cells that constitute the metastatic microenvironment. Distinct immune infiltrates can either impair the metastatic process or conversely, assist in the seeding, colonization and growth of disseminated cancer cells. Using in vivo selection approaches, we previously isolated 4T1-derived breast cancer cells that preferentially metastasize to these organs and tissues. In this study, we examined whether the propensity of breast cancer cells to metastasize to the lung, liver or bone is associated with and dependent on distinct patterns of immune cell infiltration. Immunohistocytochemistry and immunohistofluorescence approaches were used to quantify granulocytic infiltrates within distinct metastases and depletion of Gr1+ cells was performed to functionally interrogate the role of myeloid/granulocytic infiltrates in promoting metastasis to these organs. We show that T lymphocytes (CD3+), myeloid-derived/granulocytic cells (Gr-1+) cells and neutrophils (NE+) exhibit the most pronounced recruitment in lung and liver metastases, with markedly less recruitment within bone metastatic lesions. Interestingly, these infiltrating cell populations display different patterns of localization within soft tissue metastases. T lymphocytes and neutrophils are localized around the periphery of liver metastases whereas they were dispersed throughout the lung metastases. Furthermore, Gr-1+ cell-depletion studies demonstrate that infiltrating myeloid-derived/granulocytic cells, including neutrophils, are essential for the formation of breast cancer liver metastases but dispensable for metastasis to the lung and bone. Finally, we demonstrate that neutrophils that infiltrate and surround the liver metastases are polarized towards an N2 phenotype, which have previously been shown to enhance tumor growth and metastasis. Our results demonstrate that the liver metastatic potential of breast cancer cells is heavily reliant on interactions with infiltrating myeloid/granulocytic cells in the liver microenvironment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE62598 Granulocytic immune infiltrates are essential for the efficient formation of breast cancer liver metastases. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-015-0558-3 {Breast cancer research : BCR (5.676): 10.1186/s13058-015-0558-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA264523 https://www.ebi.ac.uk/ena/browser/view/PRJNA264523 None [Overal design]Gene expression profile comparison from 4T1 parental and individual in vivo selected metastatic sub-populations.; [Treatment]'None'; [Growth]'All cell lines were grown in DMEM supplemented with 10% fetal bovine serum, 10 mmol/L HEPES, 1 mmol/L sodium pyruvate, 1.5 g/L sodium bicarbonate, penicillin/streptomycin, and fungizone.'; [Extraction]'RNA was extracted from 4T1 parental and individual in vivo selected metastatic sub-populations using RNeasy Mini Kits and QIAshredder columns (Qiagen, Mississauga, ON, Canada).'; [Cell type]'Source: ', 'primary tumor explant', 'lung-aggressive explant', 'bone-aggressive explant', 'liver-aggressive explant''cell line: 4T1 parental; ', 'cell type: primary tumor explant; ', 'cell type: lung-aggressive explant; ', 'cell type: bone-aggressive explant; ', 'cell type: liver-aggressive explant; ' GSE149406 Homo sapiens 9 Expression profiling by array GPL6244 Intermittent treatment on exemestane acquired resistance 2020-04-27 MCF7aro cells were cultured in hormone-stripped medium and treated with EXE continuously or intermittently (2 weeks on and 1 week off) in the presence of 1nM testosterone. At week 14, EXE-treated cells as well as MCF7aro cells were hormone-stripped for 48h were harvested and RNA was extracted.Gene expression profiles in each cell line were analyzed by the Affymetrix GeneChip Human Genome U133 Plus 2.0 arrays. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE149406 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA628626 https://www.ebi.ac.uk/ena/browser/view/PRJNA628626 None [Overal design]Microarray analysis of gene expression in exemestane intermittently or continuously-treated ER+ breast cancer MCF7aro cells; [Treatment]'MCF7aro cells were cultured in hormone-stripped medium and treated with 1μM exemestane continuously or intermittently (2 weeks on and 1 week off) in the presence of 1nM testosterone. At week 14, EXE-treated cells as well as MCF7aro cells were hormone-stripped for 48h were harvested and RNA was extracted.Gene expression profiles in each cell line were analyzed by the Affymetrix GeneChip Human Genome U133 Plus 2.0 arrays.'; [Growth]'MCF7aro cells were cultured in MEM medium with 10% CD FBS.'; [Extraction]"Qiagen RNA extraction kit was used according to manufacturer's guide"; [Cell type]'Source: ''cell line: MCF7aro; treatment: MCF7aro cells were cultured in MEM medium with 10% CD FBS for 48h; ', 'cell line: MCF7aro; treatment: MCF7aro cells was cultured in MEM medium with 10% CD FBS in the presence of 1nM testesterone, and treated with 1μM exemestane with 2 weeks ON, 1 week OFF for 14 weeks; ', 'cell line: MCF7aro; treatment: MCF7aro cells was cultured in MEM medium with 10% CD FBS in the presence of 1nM testesterone, and treated with 1μM exemestane continuously for 14 weeks; ' GSE130564 Homo sapiens 4 Expression profiling by high throughput sequencing GPL11154 Overexpression of poly(rC) binding protein 2 by alternative cleavage and polyadenylation promotes breast cancer progression via regulating UFD1 and NT5E 2019-05-01 Alternative cleavage and polyadenylation (APA) is an important post-transcriptional regulatory mechanism, which could lead many diseases. PCBP2 plays critical roles in mRNA stabilization, translational enhancement and contributes to human cancer development and progression even though the molecular mechanism is not completely understood. Herein, we report that increased expression of PCBP2 is observed in human breast cancer tissues compared to benign or normal breast tissues, and high expression of PCBP2 is significantly associated with disease progression and poor outcome in patients with breast cancer. Knockdown of PCBP2 expression significantly decreased breast cancer cell proliferation, migration and invasion in vitro and in vivo. Molecularly, UFD1 and NT5E were identified as the downstream genes of PCBP2, which were scanned and verified based on RNA sequencing. Moreover, PCBP2 promotes oncogenic behaviors of breast cancer cells via upregulating the expression of UFD1 and NT5E by directly binding to their 3' untranslated regions (UTRs). Furthermore, we determine that the APA process is involved in regulating the overexpression PCBP2 in breast cancer cells. Therefore, our findings reveal that APA of PCBP2 3' UTR contributes to its overexpression and then promotes breast cancer progression by regulating the expression of UFD1 and NT5E. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130564 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA540620 https://www.ebi.ac.uk/ena/browser/view/PRJNA540620 https://www.ncbi.nlm.nih.gov/sra?term=SRP194383 [Overal design]The expression of PCBP2 in human benign breast disease tissues and breast cancer tissues was evaluated by immunohistochemistry and western blot. Second, the association of PCBP2 expression with clinicopathological parameters and survival of breast cancer patients were analyzed. Third, the role of PCBP2 in breast cancer cell proliferation, migration and invasion was determined in vitro and in vivo. In the following stage, the downstream genes of PCBP2 was scanned by RNA sequencing and verified by western blotting, immunohistochemistry as well as qRT-PCR. Meanwhile, Biotin pull-down assay was carried out to examine the binding site of PCBP2 protein in UFD1 or NT5E mRNA. Finally, 3'RACE was performed to detect the APA status of PCBP2 mRNA.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted using TRIzol (Invitrogen), then the purity and quality of the total RNA were checked using UVmini-1240 (SHIMADZU, Japan). The total RNA was sent to Kangcheng Biotechnology Co. (Shanghai, China) for RNA-Seq analysis.\nA total amount of 2 μg RNA per sample was used as input material for the RNA sample preparations. Sequencing libraries were generated using mRNA-seq V2 Library Prep Kit for Illumina® following manufacturer’s recommendations and index codes were added to attribute sequences to each sample. Briefly, mRNA was purified from total RNA using poly-T oligo-attached magnetic beads. Fragmentation was carried out using divalent cations under elevated temperature in First Strand Synthesis Reaction Buffer (5X). First strand cDNA was synthesized using random hexamer primer and M-MuLV Reverse Transcriptase (RNase H-). Second strand cDNA synthesis was subsequently performed using DNA polymerase I and RNase H. Remaining overhangs were converted into blunt ends via exonuclease/polymerase activities. After adenylation of 3’ ends of DNA fragments, adaptor was ligated to prepare for library. In order to select cDNA fragments of preferentially 150~200 bp in length, the library fragments were purified with AMPure XP system (Beckman Coulter, Beverly, USA). Then 3 μL USER Enzyme (NEB, USA) was used with size-selected, adaptor-ligated cDNA at 37°C for 15 min followed by 5 min at 95°C before PCR. Then PCR was performed with Phusion High-Fidelity DNA polymerase, Universal PCR primers and Index (X) Primer. At last, PCR products were purified (AMPure XP system) and library quality was assessed on the Agilent Bioanalyzer 2100 system. The libraries were then quantified and pooled. Paired- end sequencing of the library was performed on the HiSeq XTen sequencers (Illumina, San Diego, CA).'; [Cell type]'breast cancer cells''cell line: MDA-MB-231; cell type: breast cancer cells; treatment: untreated; ', 'cell line: MDA-MB-231; cell type: breast cancer cells; treatment: cells were transfected with PCBP2; ' GSE89206 Homo sapiens 12 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL17303 ZEB1-regulated inflammatory phenotype in breast cancer cells 2016-10-26 This SuperSeries is composed of the SubSeries listed below. Zinc finger E-box binding protein 1 (ZEB1) and ZEB2 induce epithelial-mesenchymal transition (EMT) and cancer progression. However, little is known about global picture of transcriptional regulation by ZEB1 and ZEB2. Here we identified an inflammatory phenotype regulated by ZEB1 using chromatin immunoprecipitation-sequencing (ChIP-seq) and RNA-sequencing (RNA-seq) in basal type breast cancer cells, followed by gene set enrichment analysis (GSEA) of ZEB1-bound genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE89206 ZEB1-regulated inflammatory phenotype in breast cancer cells. Molecular oncology 5.962 https://doi.org/10.1002/1878-0261.12098 {Molecular oncology (5.962): 10.1002/1878-0261.12098} 'genomic DNA', 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA350678 https://www.ebi.ac.uk/ena/browser/view/PRJNA350678 None [Overal design]Refer to individual Series; [Treatment]'Cells were treated with 1 ng/ml of TGF-beta3 for 1.5 h.', 'MDA-231-D cells were transfected with siRNAs and treated with/without 1 ng/mL TGF-beta for 24 hours.', 'MDA-231-D cells were transfected with siRNAs.'; [Growth]'MDA-231-D human mammary gland triple-negative cancer cell line, a highly bone metastatic clone of MDA-MB-231, was established as described (Ehata et al., Cancer Sci 98: 127-133, 2007) and cultured in Dulbecco’s modified Eagle’s medium (DMEM: #11965, Thermo Fisher Scientific, Waltham, MA, USA). Hs578T human triple-negative breast cancer cells were obtained from American Type Culture Collection (ATCC) (Manassas, VA, USA) for this research and cultured in RPMI1640 (#11875, Thermo Fisher Scientific) with 0.01 mg/mL of insulin (12585-014, Thermo Fisher Scientific).', 'MDA-231-D human mammary gland triple-negative cancer cell line, a highly bone metastatic clone of MDA-MB-231, was established as described (Ehata et al., Cancer Sci 98: 127-133, 2007) and cultured in Dulbecco’s modified Eagle’s medium (DMEM: #11965, Thermo Fisher Scientific, Waltham, MA, USA).', 'MCF7 human luminal type breast cancer cells were obtained from Japanese Collection of Research Bioresources (JCRB) Cell Bank (Ibaragi, Osaka, Japan) and cultured in DMEM (#11965, Thermo Fisher Scientific) with 0.01 mg/mL of insulin (12585-014, Thermo Fisher Scientific) and 10% fetal bovine serum (FBS), 100 units/ml penicillin G, and 100 μg/ml streptomycin. Cells were maintained in a 5% CO2 atmosphere at 37°C.'; [Extraction]'ChIP were performed as described (Koinuma et al, Mol Cell Biol 29: 172-186, 2009). ZEB1-DNA complexes were isolated with anti-ZEB1 antibody (NBP1-05987, Novus Biologicals, Minneapolis, MN, USA, lot number not available).\nLibraries were prepared as described (Murai et al, Cell Discovery 1: 15026, 2015), using IonXpress Plus Fragment Library Kit (Thermo Fisher Scientific). Adaptor-ligated samples were amplified by 15 cycles of PCR and purified by E-Gel SizeSelect (Thermo Fisher Scientific).', 'Total RNAs were extracted as described previously (Mizutani et al., 2011, J Biol Chem).\nLibraries were prepared using Dynabeads mRNA DIRECT Purification Kit (Life Technologies) and Ion Total RNA-seq kit v2 (Thermo Scientific). Sequencing was performed as described (Sakurai et al., 2016, Oncogene).'; [Cell type]'human mammary gland triple-negative cancer cell line', 'human triple-negative breast cancer cells', 'basal type breast cancer cell line', 'Source: ''cell line: MDA-231-D; cell type: human mammary gland triple-negative cancer cell line; histology: basal type breast cancer; zeb1 expression: positive; histology: basal type breast cancer; treated with: 1 ng/ml of TGF-beta3 for 1.5 h; ChIP: ZEB1; ', 'cell line: Hs578T; cell type: human triple-negative breast cancer cells; histology: basal type breast cancer; zeb1 expression: positive; histology: basal type breast cancer; treated with: 1 ng/ml of TGF-beta3 for 1.5 h; ChIP: ZEB1; ', 'cell line: MDA-231-D; cell type: basal type breast cancer cell line; sirna: Negative control siRNA (12935-112, Thermo Fisher Scientific); tgf-beta treatment: no; ', 'cell line: MDA-231-D; cell type: basal type breast cancer cell line; sirna: Negative control siRNA (12935-112, Thermo Fisher Scientific); tgf-beta treatment: 1 ng/ml for 24 h; ', 'cell line: MDA-231-D; cell type: basal type breast cancer cell line; sirna: ZEB1, ZEB2 siRNAs (HSS110548 and HSS114854, Thermo Fisher Scientific); tgf-beta treatment: no; ', 'cell line: MDA-231-D; cell type: basal type breast cancer cell line; sirna: ZEB1, ZEB2 siRNAs (HSS110548 and HSS114854, Thermo Fisher Scientific); tgf-beta treatment: 1 ng/ml for 24 h; ', 'zeb1 expression: negative; histology: luminal type breast cancer; ChIP: ZEB1; ', 'sirna: Negative control siRNA (12935-112, Thermo Fisher Scientific); tgf-beta treatment: no; histology: basal type breast cancer; ', 'sirna: ZEB1 siRNA (HSS110548, Thermo Fisher Scientific); tgf-beta treatment: no; histology: basal type breast cancer; ', 'sirna: ZEB1 siRNA (HSS186235, Thermo Fisher Scientific); tgf-beta treatment: no; histology: basal type breast cancer; ', 'sirna: ZEB1 siRNA (HSS114854, Thermo Fisher Scientific); tgf-beta treatment: no; histology: basal type breast cancer; ', 'sirna: ZEB1 siRNA (HSS190654, Thermo Fisher Scientific); tgf-beta treatment: no; histology: basal type breast cancer; ' GSE118960 Homo sapiens 1 Protein profiling by protein array GPL25484 Establishment and characterization of a chemoresistant glioblastoma cell line from an Iraqi patient 2018-08-23 Glioblastoma multiforme is a highly aggressive malignant primary brain tumor in humans, with poor prognosis. ANGM5 has been established from a cerebral glioblastoma multiforme in a 72-years-old Iraqi man who underwent surgery for an intracranial tumor in 2005. The morphology, growth kinetics, karyotype, immunocytochemistry and angiogenesis factors expression profile were studied. ANGM5 has been grown continuously for more than 200 serial passages in culture for the last 13 years. The cultured cells are elongated or multipolar in shape and the population doubling time is 28 hours. The karyotype is complex, and the chromosomal number varied between 39-114. ANGM5 is resistant to Temozolomide, cisplatin, vincristine and etoposide. This chemoresistance could be explained by the overexpression of the breast cancer resistance protein (BCRP) and MGMT. Immunocytochemistry analysis of glial markers demonstrated that cells are positive for glial fibrillary acidic protein (GFAP), and negative for nestin and calbindin. Protein microarray analysis showed high production of tissue inhibitor of metalloproteinase 2 (TIMP2) as well as other factors that are important for the invasiveness and aggressiveness of glioblastoma. ANGM5 is a useful addition to the cell lines currently available for study of the pathobiology and chemoresistance properties of glioblastoma multiforme and antitumor drug discovery. Angiogenesis signaling is being evaluated in new human Iraqi glioblastoma multiforme cell line. Here, we measured angiogenesis factors released by cancer cells in vitro. We find that glioblastoma up-regulates many proteins and metabolites during the logarithmic phase, suggesting initiation of their endo-vesiculo-membrane system. Importantly, GM-CSF and G-CSF as they increase angiogenesis through promoting endothelial cell function. Also, b-FGF which promote tumor growth and proliferation. Moreover, it showed up-regulation to inflammatory, and extracellular matrix proteins. These factors will help proliferating glioblastoma cells to overcome stress conditions, such as cytotoxic chemotherapy, serum deprivation, hypoxia in vitro and in vivo. These findings support other evidence of chemoresistance ability of this cell line named AMGN5 as it found to resist several types of conventional chemotherapies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE118960 None None None None None 'protein' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA487540 https://www.ebi.ac.uk/ena/browser/view/PRJNA487540 None [Overal design]Secreted Angiogenesis protein profile of ANGM5 glioblastoma multiforme cells during the logarithmic phase of cell proliferation was generated using antibody arrays. This is part of full characterization to the new established cell line.; [Treatment]'To determine the angiogenesis factors profile of the ANGM5 glioblastoma cell line in exponential growth phase, a protein microarray assay was conducted. Glioblastoma tumor cells were plated in tissue culture flasks (Nunc, Denmark). Two flasks were seeded with 1×10^6 cells in growth medium and incubated at 37°C. Cells collected after 24h.'; [Growth]'ANGM5 was maintained in RPMI-1640, 10% FCS, with L-glutamine, 100 U/mL penicillin, and 100µg/mL streptomycin and grown at 37°C and 5% CO2.'; [Extraction]'ANGM5 cells were freeze and thawed for three times and the cell lysate collected using centrifugation for 3000RPM/min for 10 minutes to form them into pellets. The supernatant was collected for the study and the pellets were removed. Supernatant protein concentration was determined using bio-drop spectrophotometer (Biochrom, UK). The resulting supernatant was stored in a -86℃ deep freeze until used.'; [Cell type]'Source: ''age of patient when tumor sample obtained: 72; tissue: Primary Glioblastoma multiforme tumor; ' GSE176536 Homo sapiens 4 Genome binding/occupancy profiling by high throughput sequencing GPL16791 SNP rs4971059 Predisposes to Breast Carcinogenesis and Chemoresistance by Powering DNA Replication [ChIP-seq] 2021-06-10 Identification of the driving force behind malignant transformation holds the promise to combat the relapse and therapeutic resistance of cancer. We report here that the single-nucleotide polymorphism (SNP) rs4971059, one of the 65 new breast cancer risk loci identified in a recent genome-wide association analysis, locates at the 6th intron of TRIM46 that functions as an active enhancer. We find that G to A polymorphic switch of the rs4971059 allele augments its chromosomal interaction with the promoter and boosts its enhancer activity. Accordingly, cells carry SNP[A] rs4971059 display an elevated TRIM46 expression. We find that TRIM46 is a ubiquitin ligase that targets HDAC1 for ubiquitination and degradation. Integrative genomic and transcriptomic studies reveal that the TRIM46-HDAC1 axis regulates a panel of genes including ones that are critically involved in DNA replication and repair. Consistently, depletion of TRIM46 impedes S phase progression and sensitizes cells to DNA-damaging reagents. We demonstrate that TRIM46 promotes breast cancer cell proliferation and chemoresistance in vitro and accelerates breast cancer growth in vivo. Importantly, TRIM46 is frequently overexpressed in breast carcinomas, and its level of expression is negatively correlated with that of HDAC1 as well as with higher histological grades and worse prognosis of breast cancer patients. Together, our study links SNP rs4971059 to replication and to breast carcinogenesis and chemoresistance, supporting the pursuit of TRIM46 as a potential target for breast cancer intervention. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE176536 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA736668 https://www.ebi.ac.uk/ena/browser/view/PRJNA736668 https://www.ncbi.nlm.nih.gov/sra?term=SRP323543 [Overal design]Examination of the targetgenes regulated by TRIM46-HDAC1 axis; [Treatment]'MCF-7 cells stably expressing vector and FLAG-TRIM46 were maintained in DMEM supplemented with 10% fetal bovine serum. Approximately 5×10^7 cells were used for each ChIP-seq assay. The chromatin DNA precipitated by either normal rabbit IgG (control) or polyclonal antibodies against HDAC1.'; [Growth]"MCF-7 cells were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% fetal bovine serum (FBS)."; [Extraction]"Lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody.\nLibraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit (Part# 0801-0303). Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation DNA was PCR amplified with Illumina primers for 15 cycles and library fragments of ~250 bp (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the Illumina HiSeq 2500 following the manufacturer's protocols."; [Cell type]'breast cancer cells''cell line: MCF-7; cell type: breast cancer cells; genotype/variation: stably expressing FLAG-TRIM46; chip antibody: rabbit IgG (control); ', 'cell line: MCF-7; cell type: breast cancer cells; genotype/variation: stably expressing FLAG-TRIM46; chip antibody: Anti-HDAC1 antibody (Abcam, ab7028, GR225006-11); ', 'cell line: MCF-7; cell type: breast cancer cells; genotype/variation: stably expressing vector; chip antibody: rabbit IgG (control); ', 'cell line: MCF-7; cell type: breast cancer cells; genotype/variation: stably expressing vector; chip antibody: Anti-HDAC1 antibody (Abcam, ab7028, GR225006-11); ' GSE73383 Homo sapiens 38 Expression profiling by array GPL11010 Identification of novel biomarkers associated with poor patient outcome in invasive breast carcinoma 2015-09-23 Breast carcinoma (BC) is the leading cause of death in women worldwide, making up 23% of all cancers in women, with 1.38 million new cases worldwide annually and responsible for 460,000 deaths. Despite the significant advances in the identification of molecular markers and different modalities of treatment in primary BC, the ability to predict the metastatic behavior in breast cancer is still limited. The purpose of this study was to help identify novel molecular markers associated with clinical outcome in a cohort of Brazilian BC patients. We generated global gene expression profiles from 24 patients with invasive ductal BC followed for ≥ 5-years, including 15 samples from patients classified as presenting good prognosis based on traditional markers and clinical criteria and 9 patients that developed metastasis. We identified a set of 58 differentially expressed genes (p ≤0.01) between groups of patients with good and poor prognosis. Up-regulation of B3GNT7, PPM1D, TNKS2, PHB and GTSE1 in patients with poor prognosis was confirmed by quantitative RT-PCR in an independent sample set from patients with BC (47 with good prognosis and 8 that presented metastasis). Expression of BAD protein was investigated by immunohistochemistry in 1276 BC samples and confirmed the reduced expression levels in metastatic cases observed in the oligoarray data. These findings point to novel prognostic markers that can distinguish breast carcinoma samples according to clinical course and progression of the disease. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE73383 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA296844 https://www.ebi.ac.uk/ena/browser/view/PRJNA296844 None [Overal design]Global expression profiles from 38 ductal breast tumor patient samples were used to search for molecular signatures correlated with current prognostic markers. A subset of 24 cases comprising 15 patients that remained free of disease after surgery and 9 patients that developed metastasis was used to identify candidate biomarkers associated with metastatic progression. Candidates were subsequently validated in additional independent samples by RT-qPCR or immunohistochemistry.; [Treatment]'None'; [Growth]'None'; [Extraction]'Snap-frozen breast tumor tissue samples were macro-dissected (>80% of tumor cells) prior to RNA isolation. Total RNA was extracted using the RNeasy mini Kit.'; [Cell type]'Source: ''tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: negative; her2 status: negative; ki67 status: positive; metastatic progression: no; prognostic: undetermined; population: Brazilian; ', 'tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: positive; her2 status: negative; ki67 status: negative; metastatic progression: no; prognostic: good; population: Brazilian; ', 'tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: positive; her2 status: negative; ki67 status: positive; metastatic progression: no; prognostic: good; population: Brazilian; ', 'tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: positive; her2 status: negative; ki67 status: negative; metastatic progression: yes; prognostic: poor; population: Brazilian; ', 'tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: negative; her2 status: negative; ki67 status: negative; metastatic progression: no; prognostic: undetermined; population: Brazilian; ', 'tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: negative; her2 status: positive; ki67 status: positive; metastatic progression: no; prognostic: undetermined; population: Brazilian; ', 'tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: negative; her2 status: negative; ki67 status: positive; metastatic progression: yes; prognostic: undetermined; population: Brazilian; ', 'tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: positive; her2 status: positive; ki67 status: negative; metastatic progression: no; prognostic: good; population: Brazilian; ', 'tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: positive; her2 status: positive; ki67 status: positive; metastatic progression: yes; prognostic: undetermined; population: Brazilian; ', 'tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: positive; her2 status: positive; ki67 status: positive; metastatic progression: yes; prognostic: poor; population: Brazilian; ', 'tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: negative; her2 status: positive; ki67 status: negative; metastatic progression: no; prognostic: undetermined; population: Brazilian; ', 'tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: positive; her2 status: negative; ki67 status: positive; metastatic progression: no; prognostic: undetermined; population: Brazilian; ', 'tissue: breast tumor; disease status: invasive ductal breast adenocarcinoma; estrogen/progesterone receptor status: positive; her2 status: positive; ki67 status: negative; metastatic progression: no; prognostic: poor; population: Brazilian; ' GSE107693 Homo sapiens 12 Expression profiling by high throughput sequencing GPL18573 Comparing oestrogen-responsive genes in endometrial and breast cancer cell lines 2017-12-05 Up to 80% of endometrial and breast cancers express the oestrogen receptor ERa. Unlike breast cancer, anti-oestrogen therapy has had limited success in endometrial cancer, raising the possibility that oestrogen has different effects in the two cancer types. We investigated the role of oestrogen in endometrial and breast cancers using cell lines and found that oestrogen-responsive genes were predominantly unique between the two cancer types. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE107693 Molecular basis of distinct oestrogen responses in endometrial and breast cancer. Endocrine-related cancer 4.774 https://doi.org/10.1530/ERC-17-0563 {Endocrine-related cancer (4.774): 10.1530/ERC-17-0563} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA421096 https://www.ebi.ac.uk/ena/browser/view/PRJNA421096 https://www.ncbi.nlm.nih.gov/sra?term=SRP126145 [Overal design]Endometrial and breast cancer cell lines were treated with oestradiol or vehicle for three hours and RNA sequenced in duplicate.; [Treatment]'Cells were treated with 10nM oestradiol or vehicle (ethanol) for three hours.'; [Growth]'Cells were grown in phenol-red free DMEM for 72 hours prior to treatment.'; [Extraction]"RNA was harvested using Trizol reagent according to the manufacturer's instructions.\nRNA libraries were prepared for sequencing using standard Illumina protocols."; [Cell type]'Source: ''tissue: Endometrium; cell line: Ishikawa; treatment: Vehicle; ', 'tissue: Endometrium; cell line: Ishikawa; treatment: Oestradiol; ', 'tissue: Endometrium; cell line: JHUEM14; treatment: Vehicle; ', 'tissue: Endometrium; cell line: JHUEM14; treatment: Oestradiol; ', 'tissue: Breast; cell line: MCF7; treatment: Vehicle; ', 'tissue: Breast; cell line: MCF7; treatment: Oestradiol; ' GSE5945 Mus musculus 10 Expression profiling by array GPL4371 Mouse Stromal Response to Tumor Invasion 2006-09-30 Primary and metastatic tumor growth induce host tissue responses that are believed to support tumor progression. Understanding the molecular changes within the tumor microenvironment during tumor progression may therefore be relevant not only for discovering potential therapeutic targets but also for identifying putative molecular signatures that may improve tumor classification and predict clinical outcome. To selectively address stromal gene expression changes during cancer progression we performed cDNA microarray analysis of laser-microdissected stromal cells derived from prostate intraepithelial neoplasia (PIN) and invasive cancer in a multistage model of prostate carcinogenesis. Human orthologs of genes identified in the stromal reaction to tumor progression in this mouse model were observed to be expressed in several human cancers and to cluster prostate and breast cancer patients into groups with statistically different clinical outcomes. Univariate Cox analysis showed that overexpression of these genes is associated with shorter survival and recurrence free periods. Taken together our observations provide evidence that the expression signature of the stromal response to tumor invasion in a mouse tumor model can be used to probe human cancer and provide a powerful prognostic indicator for some of the most frequent human malignancies. Keywords: disease state analysis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE5945 A mouse stromal response to tumor invasion predicts prostate and breast cancer patient survival. PloS one 2.776 https://doi.org/10.1371/journal.pone.0000032 {PloS one (2.776): 10.1371/journal.pone.0000032} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA97397 https://www.ebi.ac.uk/ena/browser/view/PRJNA97397 None [Overal design]Samples from 10 mice, 6 with invasive cancer and 4 with prostate intraepithelial neoplasia (PIN), were analyzed. The common reference (control) for all 10 samples was provided by pooled mRNA from the 4 PIN samples. In each of the 10 microarrays the control RNA (pooled from 4 PIN samples) was labeled with Cy3 and the test RNA (derived from each PIN lesion and invasive carcinoma) with Cy5.; [Treatment]'LCM slides were prepared from serial 8-μm-thick frozen tissues sections placed on a polyvinyl nuclease free membrane (Molecular Machines&Industries, Glattbrugg, CH). Tissue sections were fixed in ethanol 70% (30 sec), stained with haematoxylin and eosin (15 sec each), dehydrated in graded ethanol, treated with xylene and air-dried in a sterile laminar flow hood. Slides were microdissected immediately following staining using a μCut Laser Microdissection system (Nikon Eclipse TE200). All steps and solutions were performed under RNase free conditions.'; [Growth]'standard mice maintenance in a specific pathogen-free facility according to Swiss guidelines for animal experimentation (authorization #1477)', 'standard mice maintenance in a specific pathogen-free facility according to Swiss guidelines for animal experimentation (authorization #1477).'; [Extraction]'PicoPure RNA isolation kit (Arcturus, Mountain View, CA, www.arctur.com).'; [Cell type]'Source: ''Strain: FVB.; Gender: male.; Age: 10-weeks old.; Tissue: prostate.; Tumor stage: prostate intraepithelial neoplasia (PIN).; ', 'Strain: FVB.; Gender: male.; Age: 24-weeks old.; Tissue: prostate.; Tumor stage: invasive cancer stage (PT).; ', 'Strain: FVB.; Gender: male.; Age: PIN = 10-weeks old.; Tissue: prostate.; Tumor stage: prostate intraepithelial neoplasia (PIN).; ', 'Strain: FVB.; Gender: male.; Age: 24-weeks old; Tissue: prostate; Tumor stage: invasive cancer stage (PT); ', 'Strain: FVB.; Gender: male.; Age: 10-weeks old; Tissue: prostate; Tumor stage: prostate intraepithelial neoplasia (PIN); ', 'Strain: FVB; Gender: male; Age: 10-weeks old; Tissue: prostate; Tumor stage: prostate intraepithelial neoplasia (PIN); ', 'Strain: FVB; Gender: male; Age: 24-weeks old; Tissue: prostate; Tumor stage: invasive cancer stage (PT); ' GSE113571 Homo sapiens 15 Expression profiling by array GPL570 Microarray: Discovery of a glucocorticoid receptor (GR) activity signature using selective GR antagonism in ER-negative breast cancer 2018-04-24 HGU133+2.0 Microarray on TNBC cells (MDA-MB-231) treated for 4, 8, or 12h with vehicle, 100nM dexamethasone, 100nM Dex/100nM Mifepristone, or 100nM Dex/100nM CORT108297 Purpose: Although high glucocorticoid receptor (GR) expression in early-stage estrogen receptor (ER)-negative breast cancer (BC) is associated with shortened relapse-free survival (RFS), how associated GR transcriptional activity contributes to aggressive BC behavior is not well understood. Using potent GR antagonists and primary tumor gene expression data, we sought to identify a tumor-relevant gene signature based on GR activity that would be more predictive than GR expression alone. Design: Global gene expression and GR ChIP-sequencing were performed to identify GR-regulated genes inhibited by two chemically distinct GR antagonists, mifepristone and CORT108297. Differentially expressed genes from MDA-MB-231 cells were cross-evaluated with significantly expressed genes in GR-high versus GR-low ER-negative primary BCs. The resulting subset of GR targeted genes was analyzed in two independent ER-negative BC cohorts to derive and then validate the GR activity signature (GRsig). Results: Gene expression pathway analysis of glucocorticoid-regulated genes (inhibited by GR antagonism) revealed cell survival and invasion functions. GR ChIP-seq analysis demonstrated that GR antagonists decreased GR chromatin association for a subset of genes. A GRsig comprised of n=74 GR activation-associated genes (also reversed by GR antagonists) was derived from an adjuvant chemotherapy-treated Discovery cohort and found to predicted probability of relapse in a separate Validation cohort (HR=1.9; p= 0.012). Conclusions: The GRsig discovered herein identifies high-risk ER-negative/GR-positive BCs most likely to relapse despite administration of adjuvant chemotherapy. Because GR antagonism can reverse expression of these genes, we propose that addition of a GR antagonist to chemotherapy may improve outcome of these high-risk patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113571 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA453420 https://www.ebi.ac.uk/ena/browser/view/PRJNA453420 None [Overal design]MDA-MB-231 cells were treated with either Vehicle, 100 nM Dex +/- 100 nM C297 or 100 nM Mif for 4, 8, and 12h. Duplicate microarray experiments (n=2) for 4h treatments of Vehicle, Dex, and Dex/Mif conditions were performed along with a single experiment for the Dex/C297 treatment condition. 8h and 12h treatments for all samples were performed n=1 time.; [Treatment]'Treatments include either Vehicle, 100 nM Dex +/- 100 nM C297 or 100 nM Mif for 4, 8, and 12h. )'; [Growth]'MDA-MB-231 cells were grown to 80% confluence in 15-cm dishes in DMEM with 10% FBS. After culturing cells for 48h in DMEM with 2.5% charcoal-stripped FBS, 2 x 10^7 cells (per condition) were treated.'; [Extraction]'Following compound exposure, cells were washed in PBS, and lysed in RNA lysis buffer (Qiagen overnight at -80°C. RNA extraction, with accompanying DNase treatment, was performed using the RNeasy kit (Qiagen) following the manufacturer’s protocol'; [Cell type]'Source: ''cell line: MDA-MB-231; ' GSE60124 Homo sapiens 5 Expression profiling by array GPL570 Examination of gene expression in human breast cancer cells exposed to the HDAC inhibitor SAHA 2014-08-05 The identification of proteins that change in response to a drug perturbation can shed light on the molecular mechanisms of the drug and its potential use in therapies. Histone deacetylases (HDACs) are targets for cancer therapy. Suberoylanilide hydroxamic acid (SAHA) is an FDA approved HDAC inhibitor used for the treatment of cutaneous T-cell lymphoma. ING2 is a non-catalytic component of the Sin3/HDAC complex. To obtain a better mechanistic understanding of the Sin3/HDAC complex in cancer, we extended its protein-protein interaction network and identified a mutually exclusive pair within the complex. We then assessed the effects of SAHA on the disruption of the complex network through six homologous baits. SAHA perturbs multiple protein interactions and therefore compromises the composition of large parts of the Sin3/HDAC network. A comparison of the effect of SAHA treatment on gene expression in breast cancer cells to a knockdown of the ING2 subunit indicated that a portion of the anticancer effects of SAHA may be attributed to the disruption of ING2's association with the complex. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60124 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA257522 https://www.ebi.ac.uk/ena/browser/view/PRJNA257522 None [Overal design]Cells from human breast cancer cell line MDA-MB-231 were treated with the HDAC inhibitor drug SAHA in duplicate and compared to a DMSO vehicle control in triplicate, for a total of 5 samples.; [Treatment]'SAHA or DMSO was added directly to the culture media for a final concentration of 2 uM, and cells were collected after 30 hrs of incubation.'; [Growth]'MDA-MB-231 cells were obtained from the American Type Culture Collection. All cell lines were maintained in DMEM (GIBCO) supplemented with 10% FBS, Pen/Strep, and Glutamax (GIBCO) in a humidified atmosphere at 370C with 5% CO2.'; [Extraction]'Cells were lysed in Trizol (Invitrogen) three days after transfection, RNA was extracted and then processed through an RNeasy column (QIAGEN) using the RNA clean-up protocol.'; [Cell type]'human breast cancer cell line''cell line: MDA-MB-231; cell type: human breast cancer cell line; drug: DMSO; ', 'cell line: MDA-MB-231; cell type: human breast cancer cell line; drug: suberoylanilide hydroxamic acid (SAHA); ' GSE58464 Homo sapiens 5 Expression profiling by high throughput sequencing GPL17303 Rapid isolation of extracellular vesicles from cell culture and biological fluids using a synthetic peptide with specific affinity for heat shock proteins 2014-06-13 Background: Exosomes and extracellular vesicles (EVs) are increasingly recognized as important sources of biomarkers for disease study and diagnosis. Results: A synthetic peptide, Vn96, allows for capture of EVs from biological fluids using basic laboratory equipment. Conclusion: The Vn96-captured EVs are qualitatively equivalent or superior to exosomes isolated by ultracentrifugation. Significance: The Vn96 peptide provides an effective affinity-capture method for the isolation of EVs from biological fluids. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58464 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA252722 https://www.ebi.ac.uk/ena/browser/view/PRJNA252722 https://www.ncbi.nlm.nih.gov/sra?term=SRP043204 [Overal design]In order to compare different methods of exosome purification, we compared RNA content of exosomes purified with each method. We used two different breast cancer cell lines MCF7 and MDA-MB-231. We processed data in order to identify large RNAs as well as small RNA by using different methods for the alignment; [Treatment]'None'; [Growth]'None'; [Extraction]'The conditioned cell culture media (from MCF-7 and MDA-MB-231 cells) were used to isolate EVs using the Vn96 peptide, ExoQuick and ultracentrifugation methods described above. RNA from the isolated EVs was harvested with TRIZOL reagent (Life Technologies)\nBarcoded cDNA libraries were prepared using RNA-Seq Version 2 kit from Life Technologies following their recommended protocol. Library preparations were assayed for both quality control and quantity using Experion DNA 1K chip (Life Technologies) and diluted to 16 pM concentration. Samples were sequenced using a Proton Sequencer from Life Technologies on a PI chip following the manufacturer recommended protocol. Each chip was loaded with ten samples.'; [Cell type]'Source: ''cell line: MCF7; exosome purification: Exoquick; ', 'cell line: MCF7; exosome purification: VN96 method; ', 'cell line: MCF7; exosome purification: ultracentrifugation method; ', 'cell line: MDA-MB-231; exosome purification: VN96 method; ', 'cell line: MDA-MB-231; exosome purification: ultracentrifugation method; ' GSE79446 Homo sapiens 16 Genome variation profiling by genome tiling array GPL21613 Analysis of Paired Primary-Metastatic Hormone-Receptor Positive Breast Tumors (HRPBC) Uncovers Potential Novel Drivers of Hormonal Resistance 2016-03-21 We sought to identify genetic variants associated with disease relapse and failure to hormonal treatment in hormone-receptor positive breast cancer (HRPBC). We analyzed a series of HRPBC with distant relapse, by sequencing pairs (n=11) of tumors (primary and metastases) at >800X. Comparative genomic hybridization was performed as well. Top hits, based on the frequency of alteration and severity of the changes, were tested in the TCGA series. Genes determining the most parsimonious prognostic signature were studied for their functional role in vitro, by performing cell growth assays in hormonal-deprivation conditions, a setting that mimics treatment with aromatase inhibitors. Severe alterations were recurrently found in 18 genes in the pairs. However, only MYC, DNAH5, CSFR1, EPHA7, ARID1B, and KMT2C preserved an independent prognosis impact and/or showed a significantly different incidence of alterations between relapsed and non-relapsed cases in the TCGA series. The signature composed of MYC, KMT2C, and EPHA7 best discriminated the clinical course, (overall survival 90,7 vs. 144,5 months; p=0.0001). Having an alteration in any of the genes of the signature implied a hazard ratio of death of 3.25 (p<0.0001), and early relapse during the adjuvant hormonal treatment. The presence of the D348N mutation in KMT2C and/or the T666I mutation in the kinase domain of EPHA7 conferred hormonal resistance in vitro. Novel inactivating mutations in KMT2C and EPHA7, which confer hormonal resistance, are linked to adverse clinical course in HRPBC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE79446 Analysis of Paired Primary-Metastatic Hormone-Receptor Positive Breast Tumors (HRPBC) Uncovers Potential Novel Drivers of Hormonal Resistance. PloS one 2.776 https://doi.org/10.1371/journal.pone.0155840 {PloS one (2.776): 10.1371/journal.pone.0155840} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA315859 https://www.ebi.ac.uk/ena/browser/view/PRJNA315859 None [Overal design]Pairs of tumors (primary and metastases); [Treatment]'None'; [Growth]'None'; [Extraction]'10um tissue sections were deparaffined using heated Xylol and rehidratation was conducted with subsequent lowered EtOH (00%,80%, 50%, H20). Tissue was then treated with sodium thiocyanate. DNA then was extracted with DNA was extracted a tissue protocol from Qiagen Dneasy blood and tissue kit, using EtOH 80% instead of Wash Buffer 2 (according to ULS protocols)'; [Cell type]'Source: ''disease state: HRPBC; tumor pair: A; tumor state: Metastasis; age: 45.6; Sex: Female; ', 'reference: PROMEGA CONTROL DNA; Sex: Male; ', 'disease state: HRPBC; tumor pair: A; tumor state: Primary Tumor; age: 45.6; Sex: Female; ', 'disease state: HRPBC; tumor pair: C; tumor state: Metastasis; age: 69.1; Sex: Female; ', 'disease state: HRPBC; tumor pair: C; tumor state: Primary Tumor; age: 69.1; Sex: Female; ', 'disease state: HRPBC; tumor pair: E; tumor state: Metastasis; age: 68.4; Sex: Female; ', 'disease state: HRPBC; tumor pair: E; tumor state: Primary Tumor; age: 68.4; Sex: Female; ', 'disease state: HRPBC; tumor pair: J; tumor state: Metastasis; age: 43.8; Sex: Female; ', 'disease state: HRPBC; tumor pair: J; tumor state: Primary Tumor; age: 43.8; Sex: Female; ', 'disease state: HRPBC; tumor pair: K; tumor state: Metastasis; age: 65.6; Sex: Female; ', 'disease state: HRPBC; tumor pair: K; tumor state: Primary Tumor; age: 65.6; Sex: Female; ', 'disease state: HRPBC; tumor pair: L; tumor state: Metastasis; age: 47; Sex: Female; ', 'disease state: HRPBC; tumor pair: L; tumor state: Primary Tumor; age: 47; Sex: Female; ', 'disease state: HRPBC; tumor pair: M; tumor state: Metastasis; age: 54.2; Sex: Female; ', 'disease state: HRPBC; tumor pair: M; tumor state: Primary Tumor; age: 54.2; Sex: Female; ', 'disease state: HRPBC; tumor pair: O; tumor state: Metastasis; age: 61.2; Sex: Female; ', 'disease state: HRPBC; tumor pair: O; tumor state: Primary Tumor; age: 61.2; Sex: Female; ' GSE36351 Homo sapiens 4 Genome binding/occupancy profiling by high throughput sequencing GPL9052 Transcriptional Regulation of the GPX1 Gene by TFAP2C and Aberrant CpG Methylation in Human Breast Cancer 2012-03-07 The complexity of gene regulation has created obstacles to defining mechanisms that establish the patterns of gene expression characteristic of the different clinical phenotypes of breast cancer. Transcription factor TFAP2C plays a critical role in the regulation of both estrogen receptor-alpha (ERα) and c-ErbB2/HER2 (Her2). Herein, we performed chromatin immunoprecipitation and direct sequencing (ChIP-seq) for TFAP2C in four breast cancer cell lines representing different clinical phenotypes. Comparing the genomic binding sites for TFAP2C in the various cell lines, we identified that glutathione peroxidase (GPX1) is regulated by TFAP2C through an AP-2 regulatory region in the promoter of the GPX1 gene. Knock-down of TFAP2C, but not the related factor TFAP2A, resulted in an abrogation of GPX1 expression. Selenium-dependent GPX activity correlated with endogenous GPX1 expression, and overexpression of exogenous GPX1 induced GPX activity and significantly increased resistance to tert-butyl hydroperoxide. Methylation of the CpG island encompassing the AP-2 regulatory region was identified in cell lines where TFAP2C failed to bind the GPX1 promoter and GPX1 expression was unresponsive to TFAP2C. Furthermore, in cell lines where GPX1 promoter methylation was associated with gene silencing, treatment with 5-aza-dC (an inhibitor of DNA methylation) resulted in activation of GPX1 RNA and protein expression. Methylation of the GPX1 promoter was identified in approximately 20% of primary breast cancers and a highly significant correlation between TFAP2C and GPX1 expression was confirmed when considering only those tumors with an unmethylated promoter, whereas the related factor, TFAP2A, failed to demonstrate a correlation. The results demonstrate that TFAP2C regulates the expression of GPX1, which influences the redox state and sensitivity to oxidative stress induced by peroxides. Given the established role of GPX1 in breast cancer, the results provide an important mechanism for TFAP2C to further influence oncogenesis and progression of breast carcinoma cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36351 Transcriptional regulation of the GPX1 gene by TFAP2C and aberrant CpG methylation in human breast cancer. Oncogene 6.634 https://doi.org/10.1038/onc.2012.400 {Oncogene (6.634) doi:10.1038/onc.2012.400}; {Oncogene (6.634) doi:10.1038/onc.2015.59}; 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA153311 https://www.ebi.ac.uk/ena/browser/view/PRJNA153311 https://www.ncbi.nlm.nih.gov/sra?term=SRP011377 [Overal design]4 ChIP-Seq data for TFAP2C in human breast carcinoma cell lines MCF-7, BT-474, MDA-MB-453 and SKBR-3.; [Treatment]'None'; [Growth]'The human breast cancer cell lines MCF-7, BT-474, MDA-MB-453 and SKBR-3 were obtained from the American Type Culture Collection (ATCC). All cell lines were grown in appropriate medium at 37°C in a humidified 5% CO2 incubator.'; [Extraction]"One hundred million cells were cross-linked for 10 min at 37°C using 0.7% formaldehyde, 0.125 M glycine. Cells were washed twice with PBS, re-suspended in lysis buffer and incubated for 5 minutes. Cells were collected by centrifugation and cell pellets were frozen in liquid nitrogen and stored at minus 80°C. Cell pellets were thawed in lysis buffer, collected by centrifugation and cell nuclei were re-suspended in RIPA buffer. Chromatin was sonicated using conditions determined empirically for MCF-7 cells to achieve an optimal fragment length between 100 to 400 bp. After sonication, samples were centrifuged at 20,000 × g for 10 min at 4°C. The supernatant containing cross-linked DNA/histones was diluted with IP dilution buffer to 2 mg/ml. Half of the sample was immunoprecipitated with 10 μg of TFAP2C monoclonal antibody SC-12762 (Santa Cruz Biotechnology, Santa Cruz, CA), which was previously shown to be specific for TFAP2C without cross-reactivity to TFAP2A, and half with control nonspecific IgG (Upstate, Waltham, MA) with the addition of Dynal sheep anti-mouse Dynabeads and allowed to recognize their antigens overnight at 4°C with rotation. Protein/antibody/DNA complexes were collected magnetically, followed by washing and elution. Protein/DNA cross-links were reversed using 200 mmol/L NaCl at 65°C overnight. DNA was treated with Proteinase K and RNase A and was recovered with the QIAquick PCR Kit (Qiagen) according to the manufacturer's suggested protocol. Purified DNA was quantified by using a NanoDrop ND-1000 (NanoDrop, Wilmington, DE)."; [Cell type]'Source: ''cell line: MCF-7; chip antibody: TFAP2C monoclonal antibody; antibody vendor: Santa Cruz; antibody catalog #: sc-12762; ', 'cell line: BT-474; chip antibody: TFAP2C monoclonal antibody; antibody vendor: Santa Cruz; antibody catalog #: sc-12762; ', 'cell line: MDA-MB-453; chip antibody: TFAP2C monoclonal antibody; antibody vendor: Santa Cruz; antibody catalog #: sc-12762; ', 'cell line: SKBR-3; chip antibody: TFAP2C monoclonal antibody; antibody vendor: Santa Cruz; antibody catalog #: sc-12762; ' GSE36526 Homo sapiens 63 Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing GPL6947; GPL9052; GPL10558; GPL11154 Hes6 drives a network with therapeutic potential in castrate-resistant prostate cancer 2012-03-15 Castrate-resistant prostate cancer (CRPC) is poorly characterized and heterogeneous and while the androgen receptor (AR) is of singular importance in early prostate cancer, other factors such as c-Myc and the E2F family also play a role in later stage disease. Hes6 is a transcription co-factor that has been associated with neurogenesis during gastrulation, a neuroendocrine phenotype in the prostate and metastasis in breast cancer but its role in prostate cancer remains uncertain. Here we show that Hes6 is controlled by c-Myc and AR and drives castration resistance in prostate cancer. Hes6 activates a cell-cycle enhancing transcriptional network that maintains tumour growth and nuclear AR localization in castrate conditions. We show aphysical interaction between E2F1 and both Hes6 and AR, and suggest a co-dependency of these transcription factors in castration-resistance. In the clinical setting, we have uncovered a Hes6-associated signature that predicts poor outcome in prostate cancer, which can be pharmacologically targeted. We have therefore shown for the first time the critical role of Hes6 in the development of CRPC and identified its potential in patient specific therapeutic strategies. This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36526 HES6 drives a critical AR transcriptional programme to induce castration-resistant prostate cancer through activation of an E2F1-mediated cell cycle network. EMBO molecular medicine 10.624 https://doi.org/10.1002/emmm.201303581 {EMBO molecular medicine (10.624): 10.1002/emmm.201303581} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA153483 https://www.ebi.ac.uk/ena/browser/view/PRJNA153483 None [Overal design]Refer to individual Series; [Treatment]'Castration of host mice at 100mm3', 'No treatment', 'Bicalutamide 1uM or Vehicle (Ethanol)', 'nil', 'Bicalutamide 1µM or Vehicle (Ethanol)'; [Growth]'LNCaP-LM xenografts were grown subcutaneously in NSG mice', 'LNCaP cells grown in RPMI & 10% FBS', 'RPMI & 10% Foetal Bovine Serum & Puromycin', 'RPMI & 10% Foetal Bovine Serum'; [Extraction]'Total RNA was extracted using the QIAGEN AllPrep kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.', "Lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody. Libraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit (Part# 0801-0303). Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation DNA was PCR amplified with Illumina primers for 15 cycles and library fragments of ~250 bp (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the Genome Analyzer following the manufacturer's protocols."; [Cell type]'Source: ''tissue: LNCaP-LM NSG xenografts; expression: Hes6 overexpression; ', 'tissue: LNCaP-LM NSG xenografts; expression: vector control; ', 'cell line: LNCaP; expression: Hes6 overexpression; ', 'cell line: LNCaP; expression: vector control; ', 'cell line: LNCaP; antibody: none; sample type: INPUT; condition: Hes6-Cast; ', 'cell line: LNCaP; antibody: none; sample type: INPUT; condition: EV-Full; ', 'cell line: LNCaP; antibody: E2F1(C-20); vendor: SantaCruz; catalog#: sc-193; condition: empty vector and vehicle treated; ', 'cell line: LNCaP; antibody: E2F1(C-20); vendor: SantaCruz; catalog#: sc-193; condition: empty vector and Bicalutamide treated; ', 'cell line: LNCaP; antibody: E2F1(C-20); vendor: SantaCruz; catalog#: sc-193; condition: overexpressing Hes6 and vehicle treated; ', 'cell line: LNCaP; antibody: E2F1(C-20); vendor: SantaCruz; catalog#: sc-193; condition: overexpressing Hes6 and Bicalutamide treated; ', 'cell line: LNCaP; chip anitbody: IgG; ', 'cell line: LNCaP; chip antibody: c-Myc; chip vendor: SantaCruz; chip catalog#: sc-764; ', 'cell line: LNCaP; sample type: Input; antibody: none; ', 'factor: Input; condition: N/A; antibody: N/A; ', 'factor: AR; condition: Vehicle; antibody: ARN20, sc816X, LOT#E0712; ', 'factor: E2F1; condition: Vehicle; antibody: E2F1, sc193, LOT#1611; ', 'factor: AR; condition: BICALUTAMIDE; antibody: ARN20, sc816X, LOT#E0712; ', 'factor: E2F1; condition: BICALUTAMIDE; antibody: E2F1, sc193, LOT#1611; ' GSE85150 Mus musculus 4 Expression profiling by array GPL4134 The truncated somatostatin receptor sst5TMD4 stimulates the angiogenic process and is associated with lymphatic metastasis and poor prognosis in breast cancer patients 2016-08-03 The presence of the truncated somatostatin receptor sst5TMD4 is associated with poor prognosis in breast cancers and increases malignancy in breast cancer cell lines. The objective of this study was to examine the cellular and molecular mechanisms underlying this association in order to identify new molecular targets for diagnosis, prognosis or therapy of these tumors. Therefore, a gene expression array was implemented using sst5TMD4 stably-transfected MCF-7 cells and their respective controls (empty plasmid); which revealed the existence of a profound alteration in the expression of genes involved in several tumoral processes such as cell survival or angiogenesis. Further characterization of sst5TMD4-overexpressing MCF-7 cells demonstrated increased expression/production of key pro-angiogenic factors and enhanced capacity to form mammospheres. These data were confirmed in a xenograft model of in vivo tumoral growth, where inoculation of sst5TMD4 transfected MCF-7 cells induced tumors with higher levels of VEGF and elevated number of blood vessels. Finally, sst5TMD4 was found to be expressed in a subset of human breast cancer samples where it correlated with angiogenic markers (VEGF, Angiopoietin-1 and CD34), the presence of lymphatic metastasis and disease-free survival of the breast cancer patients. Altogether, these data demonstrate a key role of the truncated sst5TMD4 receptor in the control of the angiogenic process during breast cancer progression. Therefore, these results support the role of sst5TMD4 in tumor malignancy and metastatic potential in breast cancers and may help to identifying new lines of actions for future drug therapies for these tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE85150 The truncated somatostatin receptor sst5TMD4 stimulates the angiogenic process and is associated to lymphatic metastasis and disease-free survival in breast cancer patients. Oncotarget None https://doi.org/10.18632/oncotarget.11076 {Oncotarget (None): 10.18632/oncotarget.11076} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA336346 https://www.ebi.ac.uk/ena/browser/view/PRJNA336346 None [Overal design]Four independent passages from stably-transfected sst5TMD4-pCDNA3.1 and empty-pCDNA3.1 vector, used as control (mock), MFC7 cells were used.; [Treatment]'None'; [Growth]'MCF-7 cells were maintained in Dulbecco’s Modified Eagle Medium (Sigma, San Louis, MO) supplemented with 10% fetal bovine serum, 1% antibiotic-antimycotic and 2mM L-glutamine, in a constant atmosphere with 37ºC and 5% CO2.'; [Extraction]'Total RNA was extracted from paraffin-embedded breast cancer samples, frozen xenografted tumors and MCF-7 cell lines using Trizol (Life Technologies, Barcelona, Spain) following the manufacturer’s protocol and subsequently treated with DNase (Promega, Barcelona, Spain). Total RNA concentration and purity was assessed using Nanodrop 2000 spectrophotometer (Thermo Scientific, Wilmington, NC, USA), and subsequently retro-transcribed using random hexamer primers and cDNA First Strand Synthesis kit (MRI Fermentas, Hanover, MD, USA)'; [Cell type]'Epithelial''cell line: MCF-7; cell type: Epithelial; ' GSE35189 Homo sapiens 124 Genome variation profiling by genome tiling array GPL9128 Paradigm Test Set aCGH Array 2012-01-18 aCGH data was used in Paradigm analysis for exploration of networks affected by copy number and gene expression changes based on mutation spectra of recurrently mutated genes in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE35189 Whole-genome analysis informs breast cancer response to aromatase inhibition. Nature 43.070 https://doi.org/10.1038/nature11143 {Nature (43.070): 10.1038/nature11143} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA155959 https://www.ebi.ac.uk/ena/browser/view/PRJNA155959 None [Overal design]124 patients including 3 Pre-Operative Letrozole and 43 Z1031 patients were arrayed and analyzed; [Treatment]'None'; [Growth]'patient biopsies were frozen and stored in oct compound'; [Extraction]'DNA was isolated using Qiagen DNA Isolation kits.'; [Cell type]'Source: ''comment: patient germline DNA isolated from whole blood or cell pellets; tissue: blood; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.423; er bl: 6; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0; er bl: 7; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.088; er bl: 8; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.204; er bl: 7; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.016; er bl: 8; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.09; er bl: 7; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.155; er bl: 6; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.286; er bl: 4; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.017; er bl: 8; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.094; er bl: 6; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.19; er bl: 7; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.02; er bl: 5; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.025; er bl: 8; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.013; er bl: 8; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.145; er bl: 4; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0; er bl: 5; study id: pol; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; 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', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.092; er bl: 7; study id: z1031; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.051; er bl: 7; study id: z1031; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.01; er bl: 5; study id: z1031; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.017; er bl: 8; study id: z1031; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.038; er bl: 8; study id: z1031; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.03; er bl: 7; study id: z1031; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; 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', 'sample type: patient germline DNA isolated from whole blood or cell pellets; tissue: whole blood or cell pellets; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.115; er bl: 5; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.432; er bl: 5; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.007; er bl: 6; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.005; er bl: 7; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.15; er bl: 0; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.005; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; 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', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0; er bl: 6; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.097; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.013; er bl: 6; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.106; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.032; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.014; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.027; er bl: 5; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.06; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.011; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.006; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.112; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.007; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.025; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.003; er bl: 7; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.004; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.018; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: <1%; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.003; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: triaged to chemo; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.059; er bl: y; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.133; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.008; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.013; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.11; er bl: 8; tissue: breast cancer tumor; ', 'sample type: Genomic DNA isolated from pre-treatment human breast biospsies.; ki67 surg: 0.02; er bl: 8; tissue: breast cancer tumor; ' GSE133683 Mus musculus 40 Expression profiling by high throughput sequencing GPL13112 RNA-seq performed on either wild-type, p53 null, or p21 null MMTV-Wnt1 mouse mammary tumors treated with or without doxorubicin. 2019-07-02 The effects of doxorubicin on mammary tumors https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE133683 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA552227 https://www.ebi.ac.uk/ena/browser/view/PRJNA552227 https://www.ncbi.nlm.nih.gov/sra?term=SRP212753 [Overal design]MMTV-Wnt1 transgenic mice formed spontaneous mammary tumors, and then were treated or not with doxorubicin. Genotypes of MMTV-Wnt1 mice were Trp53 wild-type (untreated n=6, doxorubicin n=6), Trp53 null (untreated n=6, doxorubicin n=6), Cdkn1a (p21) null (untreated n=6, doxorubicin n=10). Tumors were harvested 24hr following final doxorubicin treatment.; [Treatment]'Untreated or 4mg/kg Doxorubicin IP daily for 5 consecutive days, harvested 24 hours after final injection'; [Growth]'In vivo spontaneous mouse mammary tumors in MMTV-Wnt1 mice, either p53 null, p21 null, or wild type for Trp53 and Cdkn1a'; [Extraction]'Rna was extracted from snap frozen, pulverized tumor tissue using Trizol reagent\nTrp53 WT tumors: Illumina TruSeq® Stranded Total RNA; Trp53null tumors: Illumina TruSeq RNA Library Preparation Kit v2; Cdkn1a null tumors: Illumina TruSeq RNA Library Preparation Kit v2'; [Cell type]'Source: ''tissue: mammary tumor; strain: MMTV-Wnt1; genotype: wild-type; treatment: untreated; ', 'tissue: mammary tumor; strain: MMTV-Wnt1; genotype: wild-type; treatment: doxorubicin; ', 'tissue: mammary tumor; strain: MMTV-Wnt1; genotype: p53 null; treatment: untreated; ', 'tissue: mammary tumor; strain: MMTV-Wnt1; genotype: p53 null; treatment: doxorubicin; ', 'tissue: mammary tumor; strain: MMTV-Wnt1; genotype: p21 null; treatment: untreated; ', 'tissue: mammary tumor; strain: MMTV-Wnt1; genotype: p21 null; treatment: doxorubicin; ' GSE80365 Homo sapiens 48 Expression profiling by high throughput sequencing GPL16791 Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. [tumor samples RNA-seq] 2016-04-18 Transcriptomic changes and estrogen and progesterone receptor binding in multiple ER+/PR+ models (eight ER+/PR+ patient tumors, various T47Ds, ZR75) and multiple ER+/PR-negative models (four ER+/PR- patient tuumors, PR-deficient T47D and MCF7 cells) treated with various hormone combinations. Results: In isolation, estrogen and progestin act as genomic agonists by regulating the expression of common target genes in similar directions, but at different levels. Similarly, in isolation, progestin is also a weak phenotypic agonist of estrogen action. However, in the presence of both hormones, progestin behaves as a phenotypic estrogen antagonist. PR remodels nucleosomes to noncompetitively redirect ER genomic binding to distal enhancers enriched for BRCA1 binding motifs and sites that link PR and ER/PR complexes. Importantly, when both hormones are present, progestin modulates estrogen action such that responsive transcriptomes, cellular processes and ER/PR recruitment to genomic sites correlate with those observed with PR alone, but not ER alone. Conclusions: Genomic Agonism and Phenotypic Antagonism between Estrogen and Progesterone Receptors in Breast Cancer. Individual and concerted actions of ER and PR highlight the prognostic and therapeutic value of PR in ER+/PR+ breast cancers. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80365 Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. Science advances 12.804 https://doi.org/10.1126/sciadv.1501924 {Science advances (12.804): 10.1126/sciadv.1501924} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA318946 https://www.ebi.ac.uk/ena/browser/view/PRJNA318946 None [Overal design]ER+/PR+ and ER+/PR-deficient model systems were deprived of steroids by culturing them in phenol red free RPMI 1640 media that is supplemented with 10% charcoal-stripped fetal bovine serum and 1% penicillin/streptomycin. Subsequently, these steroid-deprived models were treated with either vehicle, 10 nM estradiol, 10 nM progestin R5020 or 10 nM of both the hormones and genomics (ChIP-seq and RNA-seq) was performed. ChIP-seq was done after 45 minutes of hormone treatments. For cell models, RNA-seq was done after 12 hours of hormone treatments. Tumor explants were treated with either 24 or 48 hours.; [Treatment]'Steroid-deprived tumor explants were treated with 10 nM estradiol, 10 nM R5020 or 10 nM of both the hormones for 24 or 48 hours. Finer details are provided in materials and methods section (Patient tumor explants)'; [Growth]'Tumor explants: Within one hour of surgery, sliced pieces of tumors were incubated on gelatin sponges for 36 hours in charcoal-stripped serum media. Representative pieces of tumors were in parallel fixed in 4% formalin and subsequently immunohistochemistry for ER and PR protein was performed to assess the status of tumors for these receptors.'; [Extraction]'Hormone-treated explant was homogenized and total RNA was extracted using Qiagen RNAeasy kit\nPolyA tail selection was performed on 250 ng of total RNA. RNA-seq libraries were prepared using NEBNext kit.\nDetails of library preparation strategy are provided in the materials and methods section (RNA expression and RNA-sequencing) of the paper.'; [Cell type]'Source: ''tissue type: ER+/PR+ Human tumor explants; er/pr status: ER+/PR+; drug treatment: Vehicle; hormone exposure time: 24 Hours; ', 'tissue type: ER+/PR+ Human tumor explants; er/pr status: ER+/PR+; drug treatment: 10 nM Estradiol; hormone exposure time: 24 Hours; ', 'tissue type: ER+/PR+ Human tumor explants; er/pr status: ER+/PR+; drug treatment: 10 nM R5020; hormone exposure time: 24 Hours; ', 'tissue type: ER+/PR+ Human tumor explants; er/pr status: ER+/PR+; drug treatment: 10nM Estradiol + 10 nM R5020; hormone exposure time: 24 Hours; ', 'tissue type: ER+/PR+ Human tumor explants; er/pr status: ER+/PR+; drug treatment: Vehicle; hormone exposure time: 48 Hours; ', 'tissue type: ER+/PR+ Human tumor explants; er/pr status: ER+/PR+; drug treatment: 10 nM Estradiol; hormone exposure time: 48 Hours; ', 'tissue type: ER+/PR+ Human tumor explants; er/pr status: ER+/PR+; drug treatment: 10 nM R5020; hormone exposure time: 48 Hours; ', 'tissue type: ER+/PR+ Human tumor explants; er/pr status: ER+/PR+; drug treatment: 10nM Estradiol + 10 nM R5020; hormone exposure time: 48 Hours; ', 'tissue type: ER+/PR- Human tumor explants; er/pr status: ER+/PR-; drug treatment: Vehicle; hormone exposure time: 24 Hours; ', 'tissue type: ER+/PR- Human tumor explants; er/pr status: ER+/PR-; drug treatment: 10 nM Estradiol; hormone exposure time: 24 Hours; ', 'tissue type: ER+/PR- Human tumor explants; er/pr status: ER+/PR-; drug treatment: 10 nM R5020; hormone exposure time: 24 Hours; ', 'tissue type: ER+/PR- Human tumor explants; er/pr status: ER+/PR-; drug treatment: 10nM Estradiol + 10 nM R5020; hormone exposure time: 24 Hours; ', 'tissue type: ER+/PR- Human tumor explants; er/pr status: ER+/PR-; drug treatment: Vehicle; hormone exposure time: 48 Hours; ', 'tissue type: ER+/PR- Human tumor explants; er/pr status: ER+/PR-; drug treatment: 10 nM Estradiol; hormone exposure time: 48 Hours; ', 'tissue type: ER+/PR- Human tumor explants; er/pr status: ER+/PR-; drug treatment: 10 nM R5020; hormone exposure time: 48 Hours; ', 'tissue type: ER+/PR- Human tumor explants; er/pr status: ER+/PR-; drug treatment: 10nM Estradiol + 10 nM R5020; hormone exposure time: 48 Hours; ' GSE30775 Homo sapiens 6 Expression profiling by array GPL570 Gene expression change after LSD1 siRNA treatment in ER-negative breast cancer cells MDA-MB-231 2011-07-19 Knock-down of LSD1 using siRNA approach induced regulation of several proliferation-associated genes in ER-negative breast cancer cells MDA-MB-231. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE30775 Lysine-specific demethylase 1 (LSD1) and histone deacetylase 1 (HDAC1) synergistically repress proinflammatory cytokines and classical complement pathway components. Biochemical and biophysical research communications 2.705 https://doi.org/10.1016/j.bbrc.2012.04.057 {Biochemical and biophysical research communications (2.705): 10.1016/j.bbrc.2012.04.057} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA144327 https://www.ebi.ac.uk/ena/browser/view/PRJNA144327 None [Overal design]To identify changes on gene expression caused by treatment with siRNA directed against LSD1 (si) or control siRNA (control) in MDA-MB-231 cells, total RNA was purified from the cells after treatment for 6 days (2 rounds of transfection). Three biological replicates were used.; [Treatment]'None'; [Growth]'None'; [Extraction]'total RNA extraction using RNeasyMini Kit (Qiagen)'; [Cell type]'Source: ''cell line: MDA-MB-231; tumor cell type: ER-negative breaset cancer cells; genotype/variation: transfected with control siRNA; ', 'cell line: MDA-MB-231; tumor cell type: ER-negative breaset cancer cells; genotype/variation: transfected with LSD1 siRNA; ' GSE114839 synthetic construct 18 Non-coding RNA profiling by array GPL8786 mirRNA Expression data from Human Mammary Epithelial Cells (HMECs) transduced with shp53, HRASV12, WNT1 and CCNE1 [miRNA expression] 2018-05-23 Gene expression differences, combined with distinct patterns of genomic rearrangements and epigenetic modifications constitute the bases of molecular classification of breast cancer. Molecular subtypes may originate from different cell lineages in the mammary gland, but also from the early activation of oncogenes that may drive the establishment of these molecular subtypes. However, in the natural history of human cancer, it is difficult to discriminate between these two factors : cell lineage and initial oncogenic alterations. In this work, we designed an experimental strategy aiming at determining whether activation of distinct oncogenic pathways in human mammary epithelial cells (HMEC) could lead to different patterns of genetic and epigenetic changes. This work suggests that the early activation of oncogenes is an important determinant of the establishment of breast cancer molecular subtypes along with cell lineage origin. In this work, we overexpressed by retroviral transduction three oncogenes WNT1, CCNE1 and RASv12, known to activate different oncogenic pathways, in shp53 immortalized human HMECs and monitored epigenetic and genetic changes at different steps of cell progression.Submitted publication : Distinct Oncogenic events induces different DNA methylation and copy number changes in human mammary epithelial cells.Claire Fonti, Anne Saumet, Amanda Abi-Khalil, Béatrice Orsetti,..., J. Colinge, Michael Weber, Claude Sardet, Stanislas du Manoir, Charles Theillet. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE114839 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA472792 https://www.ebi.ac.uk/ena/browser/view/PRJNA472792 None [Overal design]For miR profiling total RNA were extracted uzing Trizol (Invitrogen/Thermo-Fisher, Illkirch-Graffenstaden, France ) according to manufacturer’s instructions from 18 samples. All samples are in duplicates. samples corresponding to HMEC cell just after cell culture establishement are named R2. Two samples correspond to HMEC samples shortly after shP53 transduction (R2shP53early) and several weeks after shP53 transduction(R2shP53late). HMEC was then transduced with oncogene construct (either HRASV12, WNT1 or CCNE1), samples are called R2shp53-ONCOGENE.Late. Finaly,R2shp53-ONCOGENE samples were grown in soft agar. Samples are named R2shp53-ONCOGENE.SA after selection in soft agar. For exact timing see the associated publication.; [Treatment]'Primary HMEC cultures were transduced with amphotropic retroviral supernatants produced by 293T cells transfected with one of the following retroviral constructs: pSUPER.retro.hygro-shp53, pBABE.neo-CCNE1, pLNC-WNT1, pBABE.puro-HRASV12. Transduction was followed by a 3 weeks period of antibiotic selection.'; [Growth]'MEBM medium supplemented with antibiotics (Gibco/Thermo-Fisher, Illkirch-Graffenstaden, France), 1M HEPES, hydrocortisone, insulin, EGF, BPE and Gentamycine (MEGM single Quots, Lonza, Levallois-Perret, France)'; [Extraction]'For miR profiling total RNA were extracted uzing Trizol (Invitrogen/Thermo-Fisher, Illkirch-Graffenstaden, France ) according to manufacturer’s instructions.'; [Cell type]'primary human mammary epithelial cells (HMECs)''gender: female; cell type: primary human mammary epithelial cells (HMECs); ', 'gender: female; cell type: primary human mammary epithelial cells (HMECs); transduced with: shP53; ', 'gender: female; cell type: primary human mammary epithelial cells (HMECs); transduced with: shP53; transduced with: CCNE1; ', 'gender: female; cell type: primary human mammary epithelial cells (HMECs); transduced with: shP53; transduced with: RASV12; ', 'gender: female; cell type: primary human mammary epithelial cells (HMECs); transduced with: shP53; transduced with: WNT1; ' GSE23384 Homo sapiens 25 Expression profiling by array GPL8432 Gene profiling using archival formalin-fixed paraffin-embedded breast cancer specimens can generate informative microarray data: A comparison with matched fresh fine needle aspiration biopsy samples (FFPE samples) 2010-08-02 The Formalin-Fixed Paraffin-Embedded (FFPE) samples on selected breast cancer subtypes (ER+/Her2-, ER+/Her2+, ER-/Her2+, and ER-/Her2-) and their paired fresh fine needle aspirated biopsies (FNA) were investigated. The cases represented different subtypes of breast cancers based on their clinical receptors ER (E) and Her2 (H) status to demonstrate the ability of gene profiles to differentiate these tumors. Compared to FNA specimens, FFPE samples yielded relatively more degraded RNA, and 80% of the samples deemed suitable for cDNA-mediated annealing, selection, extension and ligation (DASL) assay. It is able to demonstrate that gene profiles from FFPE microarrays were reproducible and correlated well with the corresponding gene profiles from FNA microarrays. The gene profiles from both FNA and FFPE could differentiate the four breast cancer subtypes, and the expression levels of corresponding gene set were consistent with qRT-PCR and correlated to the clinical outcomes on published microarray data. It supports the use of FFPE specimens to develop a prognostic tool for breast cancers which can obviate the need for fresh specimens. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23384 Clinical relevance of DNA microarray analyses using archival formalin-fixed paraffin-embedded breast cancer specimens. BMC cancer 2.933 https://doi.org/10.1186/1471-2407-11-253 {BMC cancer (2.933): 10.1186/1471-2407-11-253} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA133317 https://www.ebi.ac.uk/ena/browser/view/PRJNA133317 None [Overal design]25 FFPE specimens were processed for whole genome DASL assays using Illumina Human-Ref8 version 3 BeadChips. Invasive ductal carcinoma (IDC)-type subtypes ER+/Her2-, ER+/Her2+, ER-/Her2+, and ER-/Her2- (ER: estrogen receptor, HER2: human epidermal growth factor receptor 2) were analyzed.; [Treatment]'Breast cancer specimens were formalin fixed and paraffin embedded.'; [Growth]'None'; [Extraction]'RNA was extracted with the RecoverAll Total Nucleic acid kit followed by DNase I treatment. Quality control was performed with the Agilent Bioanalyser.'; [Cell type]'Source: ''tissue: breast cancer; age: 56; type: IDC; size: 1.2; grade: 2; positive node: 0(1); er: +; pr: +; her2: -; rin: 1.7; ', 'tissue: breast cancer; age: 47; type: IDC; size: 2.2; grade: 2; positive node: 1(12); er: +; pr: +; her2: -; rin: 2.3; ', 'tissue: breast cancer; age: 63; type: IDC; size: 2.4; grade: 2; positive node: 0(1); er: +; pr: +; her2: -; rin: 2.5; ', 'tissue: breast cancer; age: 76; type: IDC; size: 2.8; grade: 3; positive node: 0(3); er: +; pr: +; her2: -; rin: 2.5; ', 'tissue: breast cancer; age: 58; type: IDC; size: 10.6; grade: 2; positive node: 6(24); er: +; pr: +; her2: -; rin: 2.5; ', 'tissue: breast cancer; age: 50; type: IDC; size: 3.7; grade: 2; positive node: 0(2); er: +; pr: +; her2: -; rin: 2.4; ', 'tissue: breast cancer; age: 55; type: IDC; size: 1.9; grade: 2; positive node: 2(15); er: +; pr: +; her2: -; rin: 1.5; ', 'tissue: breast cancer; age: 68; type: IDC; size: 2; grade: 2; positive node: 4(17); er: +; pr: +; her2: -; rin: 2.7; ', 'tissue: breast cancer; age: 42; type: IDC; size: 2.6; grade: 2; positive node: 0(3); er: +; pr: +; her2: -; rin: 2.3; ', 'tissue: breast cancer; age: 64; type: IDC; size: 1.5; grade: 2; positive node: 0(4); er: +; pr: +; her2: -; rin: 2.1; ', 'tissue: breast cancer; age: 41; type: IDC; size: 1.6; grade: 3; positive node: 0(3); er: +; pr: +; her2: +; rin: 2.2; ', 'tissue: breast cancer; age: 37; type: IDC; size: 1.5; grade: 3; positive node: 0(18); er: +; pr: +; her2: +; rin: 2.1; ', 'tissue: breast cancer; age: 61; type: IDC; size: 2.2; grade: 3; positive node: 2(18); er: +; pr: -; her2: +; rin: 2.4; ', 'tissue: breast cancer; age: 43; type: IDC; size: 2.5; grade: 3; positive node: 0(5); er: +; pr: -; her2: +; rin: 2.4; ', 'tissue: breast cancer; age: 51; type: IDC; size: 1.6; grade: 3; positive node: 1(23); er: -; pr: -; her2: -; rin: 1.7; ', 'tissue: breast cancer; age: 54; type: IDC; size: 3.6; grade: 2; positive node: 0(11); er: -; pr: -; her2: -; rin: 2.4; ', 'tissue: breast cancer; age: 62; type: IDC; size: 1.6; grade: 3; positive node: 1(21); er: -; pr: -; her2: -; rin: 2.4; ', 'tissue: breast cancer; age: 47; type: IDC; size: 1.5; grade: 3; positive node: 0(4); er: -; pr: -; her2: -; rin: 2.3; ', 'tissue: breast cancer; age: 57; type: IDC; size: 2.9; grade: 2; positive node: 0(4); er: -; pr: -; her2: -; rin: 2.2; ', 'tissue: breast cancer; age: 44; type: IDC; size: 3.2; grade: 3; positive node: 0(1); er: -; pr: -; her2: +; rin: 2.7; ', 'tissue: breast cancer; age: 56; type: IDC; size: 1.4; grade: 3; positive node: 0(3); er: -; pr: -; her2: +; rin: 1.9; ', 'tissue: breast cancer; age: 76; type: IDC; size: 2.3; grade: 3; positive node: 2(20); er: -; pr: -; her2: +; rin: 2.3; ', 'tissue: breast cancer; age: 64; type: IDC; size: 2.3; grade: 3; positive node: 5(21); er: -; pr: -; her2: +; rin: 2.2; ', 'tissue: breast cancer; age: 73; type: IDC; size: 1.6; grade: 3; positive node: 0(2); er: -; pr: -; her2: +; rin: 2.4; ', 'tissue: breast cancer; age: 54; type: IDC; size: 2.9; grade: 3; positive node: 0(12); er: -; pr: -; her2: +; rin: 2.5; ' GSE107754 Homo sapiens 84 Expression profiling by array GPL6480 A novel genomic signature predicting FDG uptake in diverse metastatic tumors 2017-12-06 Purpose: Building a universal genomic signature predicting the intensity of FDG uptake in diverse metastatic tumors may allow us to understand better the biological processes underlying this phenomenon and their requirements of glucose uptake. Methods: A balanced training set (n=71) of metastatic tumors including some of the most frequent histologies, with matched PET/CT quantification measurements and whole human genome gene expression microarrays, was used to build the signature. Selection of microarray features was carried out exclusively on the basis of their strong association with FDG uptake (as measured by SUVmean35) by means of univariate linear regression. A thorough bioinformatics study of these genes was performed and multivariable models were built by fitting several state of the art regression techniques to the training set for comparison. Results: The 909 probes with the strongest association with the SUVmean35 (comprising 742 identifiable genes and 62 probes not matched to a symbol) were used to build the signature. Partial Least Squares using 3 components (PLS-3) was the best performing model in the training dataset cross-validation (Root Mean Square Error, RMSE=0.443) and was validated further in an independent validation dataset (n=13) obtaining a performance within the 95% CI of that obtained in the training dataset (RMSE=0.645). Significantly overrepresented biological processes correlating with the SUVmean35 were identified beyond glycolysis, such as ribosome biogenesis and DNA replication (correlating with a higher SUVmean35), and cytoskeleton reorganization and autophagy (correlating with a lower SUVmean35), among others. Conclusions: PLS-3 is a signature predicting accurately the intensity of FDG uptake in diverse metastatic tumors. FDG-PET might help in the design of specific targeted therapies directed to counteract the identified malignant biological processes more likely activated in a tumor as inferred from the SUVmean35 and also from its variations in response to antineoplastic treatments. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE107754 A novel genomic signature predicting FDG uptake in diverse metastatic tumors. EJNMMI research 3.000 https://doi.org/10.1186/s13550-017-0355-3 {EJNMMI research (3.000): 10.1186/s13550-017-0355-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA421282 https://www.ebi.ac.uk/ena/browser/view/PRJNA421282 None [Overal design]Whole human genome microarrays from biopsies of human metastatic tumors (71 patients) with matched SUVmean35 measurements, this submission includes the 71 patients of the training set used to build the genomic signature predicting FDG uptake in diverse metastatic tumors. This dataset is complemented with a validation set comprised of 13 patients.; [Treatment]'None'; [Growth]'None'; [Extraction]'QIAGEN Rneasy kit'; [Cell type]'Source: ''gender: Male; dataset: Validation set; biopsy location: Lung; suvmean35: 4.09; ', 'tissue: Normal lung; ', 'gender: Female; dataset: Validation set; biopsy location: Lymph node; suvmean35: 8.36; ', 'tissue: Normal kidney; ', 'gender: Male; dataset: Validation set; biopsy location: Primary; suvmean35: 5.18; ', 'tissue: Normal pancreas; ', 'gender: Male; dataset: Validation set; biopsy location: Primary; suvmean35: 10.74; ', 'tissue: Universal normal tissue; ', 'gender: Female; dataset: Validation set; biopsy location: Lymph node; suvmean35: 8.62; ', 'tissue: Normal breast; ', 'gender: Male; dataset: Validation set; biopsy location: Liver; suvmean35: 8.02; ', 'gender: Female; dataset: Validation set; biopsy location: Retroperitoneal implant; suvmean35: 6.87; ', 'tissue: Normal ovary; ', 'gender: Female; dataset: Validation set; biopsy location: Lymph node; suvmean35: 4.93; ', 'gender: Female; dataset: Validation set; biopsy location: Lymph node; suvmean35: 1.96; ', 'tissue: Normal cervix; ', 'gender: Female; dataset: Validation set; biopsy location: Retroperitoneal implant; suvmean35: 8.83; ', 'gender: Female; dataset: Validation set; biopsy location: Retroperitoneal implant; suvmean35: 3.96; ', 'tissue: Normal esofagus; ', 'gender: Female; dataset: Validation set; biopsy location: Retroperitoneal implant; suvmean35: 3.38; ', 'gender: Female; dataset: Validation set; biopsy location: Retroperitoneal implant; suvmean35: 9.95; ', 'gender: Male; dataset: Training set; tissue: Pancreatic cancer; suvmean35: 5.19; ', 'gender: Male; dataset: Training set; tissue: Esophagus cancer; suvmean35: 7.22; ', 'tissue: Normal esophagus; ', 'gender: Female; dataset: Training set; tissue: Esophagus cancer; suvmean35: 5.02; ', 'gender: Female; dataset: Training set; tissue: Breast cancer; suvmean35: 4.92; ', 'gender: Female; dataset: Training set; tissue: Colorectal cancer; suvmean35: 4.99; ', 'tissue: Normal colon; ', 'gender: Female; dataset: Training set; tissue: Ovarian cancer; suvmean35: 4.01; ', 'gender: Female; dataset: Training set; tissue: Head&neck cancer; suvmean35: 2.52; ', 'tissue: Universal normal; ', 'gender: Male; dataset: Training set; tissue: Lung cancer; suvmean35: 5.52; ', 'gender: Male; dataset: Training set; tissue: Malignant Melanoma; suvmean35: 8.02; ', 'tissue: Normal fat; ', 'gender: Female; dataset: Training set; tissue: Endometrial cancer; suvmean35: 8.38; ', 'gender: Female; dataset: Training set; tissue: Cervix cancer; suvmean35: 3.46; ', 'gender: Male; dataset: Training set; tissue: Colorectal cancer; suvmean35: 4.07; ', 'gender: Female; dataset: Training set; tissue: Breast cancer; suvmean35: 4.67; ', 'gender: Female; dataset: Training set; tissue: Ovarian cancer; suvmean35: 7.09; ', 'gender: Male; dataset: Training set; tissue: Colorectal cancer; suvmean35: 4.83; ', 'gender: Male; dataset: Training set; tissue: Pancreatic cancer; suvmean35: 6.7; ', 'gender: Female; dataset: Training set; tissue: Soft tissue sarcoma; suvmean35: 3.95; ', 'tissue: Normal skeletal muscle; ', 'gender: Female; dataset: Training set; tissue: Soft tissue sarcoma; suvmean35: 5.03; ', 'gender: Female; dataset: Training set; tissue: Head&neck cancer; suvmean35: 12.61; ', 'gender: Female; dataset: Training set; tissue: Gastric cancer; suvmean35: 6.12; ', 'tissue: Normal stomach; ', 'gender: Female; dataset: Training set; tissue: Unknown primary; suvmean35: 11.72; ', 'gender: Male; dataset: Training set; tissue: Head&neck cancer; suvmean35: 3.39; ', 'gender: Female; dataset: Training set; tissue: Ovarian cancer; suvmean35: 4.17; ', 'gender: Male; dataset: Training set; tissue: Malignant Mesothelioma; suvmean35: 12.08; ', 'gender: Female; dataset: Training set; tissue: Head&neck cancer; suvmean35: 3.36; ', 'gender: Female; dataset: Training set; tissue: Ovarian cancer; suvmean35: 8.86; ', 'gender: Male; dataset: Training set; tissue: Thyroid cancer; suvmean35: 5.92; ', 'tissue: Normal thyroid; ', 'gender: Female; dataset: Training set; tissue: Breast cancer; suvmean35: 7.73; ', 'gender: Male; dataset: Training set; tissue: Testes cancer; suvmean35: 3.62; ', 'gender: Female; dataset: Training set; tissue: Non Hodgkin lymphoma; suvmean35: 13.63; ', 'tissue: Normal spleen; ', 'gender: Male; dataset: Training set; tissue: Esophagus cancer; suvmean35: 6.59; ', 'gender: Male; dataset: Training set; tissue: Merkel cell carcinoma; suvmean35: 6.98; ', 'gender: Female; dataset: Training set; tissue: Breast cancer; suvmean35: 5.06; ', 'gender: Male; dataset: Training set; tissue: Colorectal cancer; suvmean35: 9.16; ', 'gender: Female; dataset: Training set; tissue: Soft tissue sarcoma; suvmean35: 2.35; ', 'gender: Female; dataset: Training set; tissue: Breast cancer; suvmean35: 7.4; ', 'gender: Male; dataset: Training set; tissue: Lung cancer; suvmean35: 12.14; ', 'gender: Male; dataset: Training set; tissue: Esophagus cancer; suvmean35: 8.29; ', 'gender: Male; dataset: Training set; tissue: Soft tissue sarcoma; suvmean35: 6.3; ', 'gender: Male; dataset: Training set; tissue: Soft tissue sarcoma; suvmean35: 3.78; ', 'gender: Female; dataset: Training set; tissue: Lung cancer; suvmean35: 7.81; ', 'gender: Female; dataset: Training set; tissue: Breast cancer; suvmean35: 6.45; ', 'gender: Male; dataset: Training set; tissue: Testes cancer; suvmean35: 5.09; ', 'tissue: Normal universal tissue; ', 'gender: Female; dataset: Training set; tissue: Vaginal cancer; suvmean35: 4.7; ', 'gender: Female; dataset: Training set; tissue: Colorectal cancer; suvmean35: 7.48; ', 'gender: Female; dataset: Training set; tissue: Pancreatic cancer; suvmean35: 4.38; ', 'gender: Male; dataset: Training set; tissue: Pancreatic cancer; suvmean35: 4.87; ', 'gender: Male; dataset: Training set; tissue: Colorectal cancer; suvmean35: 3.41; ', 'gender: Male; dataset: Training set; tissue: Lung cancer; suvmean35: 8.38; ', 'gender: Female; dataset: Training set; tissue: Breast cancer; suvmean35: 2.62; ', 'gender: Female; dataset: Training set; tissue: Soft tissue sarcoma; suvmean35: 2.61; ', 'gender: Female; dataset: Training set; tissue: Thyroid cancer; suvmean35: 9.12; ', 'gender: Female; dataset: Training set; tissue: Ovarian cancer; suvmean35: 9.05; ', 'gender: Male; dataset: Training set; tissue: Kidney cancer; suvmean35: 7.53; ', 'tissue: Normal renal; ', 'gender: Female; dataset: Training set; tissue: Breast cancer; suvmean35: 9.64; ', 'gender: Female; dataset: Training set; tissue: Pancreatic cancer; suvmean35: 5.8; ', 'gender: Female; dataset: Training set; tissue: Head&neck cancer; suvmean35: 5.96; ', 'gender: Female; dataset: Training set; tissue: Cervical cancer; suvmean35: 5.18; ', 'gender: Female; dataset: Training set; tissue: Soft tissue sarcoma; suvmean35: 8.25; ', 'gender: Female; dataset: Training set; tissue: Ovarian cancer; suvmean35: 7.5; ', 'gender: Female; dataset: Training set; tissue: Lung cancer; suvmean35: 8.62; ', 'gender: Male; dataset: Training set; tissue: Lung cancer; suvmean35: 11.23; ', 'gender: Male; dataset: Training set; tissue: Bile duct cancer; suvmean35: 10.9; ', 'gender: Male; dataset: Training set; tissue: Pancreatic cancer; suvmean35: 12.2; ', 'gender: Male; dataset: Training set; tissue: Colorectal cancer; suvmean35: 4.65; ', 'gender: Female; dataset: Training set; tissue: Colorectal cancer; suvmean35: 6.99; ', 'gender: Male; dataset: Training set; tissue: Bile duct cancer; suvmean35: 5.27; ', 'gender: Female; dataset: Training set; tissue: Ovarian cancer; suvmean35: 8.52; ', 'gender: Male; dataset: Training set; tissue: Colorectal cancer; suvmean35: 5.75; ', 'gender: Male; dataset: Training set; tissue: Lung cancer; suvmean35: 16.69; ', 'gender: Male; dataset: Training set; tissue: Urothelial cancer; suvmean35: 3.22; ' GSE133473 Homo sapiens 11 Expression profiling by high throughput sequencing GPL18460 Requirement for Cleavage Factor IIm in the Control of Alternative Polyadenylation in Breast Cancer Cells 2019-06-27 This experimental series concerns the position bias and extent of 3'-end choice in MCF7 cells after knock-down of the CFII subunits PCF11 and CLP1 in MCF7. Loss of either subunit results in 3'-lengthening by APA. Importantly this lengthening is toward a more 'normal-like' distribution. MCF7 cells show a native 3'-end distribution favoring short internal adenylation sites compared to MDAMD231 cells. The difference between the two cell lines might be driven by a higher expression of the exosome in MDAMD231 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE133473 Requirement for cleavage factor IIm in the control of alternative polyadenylation in breast cancer cells. RNA (New York, N.Y.) 3.949 https://doi.org/10.1261/rna.075226.120 {RNA (New York, N.Y.) (3.949): 10.1261/rna.075226.120} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA551515 https://www.ebi.ac.uk/ena/browser/view/PRJNA551515 https://www.ncbi.nlm.nih.gov/sra?term=SRP212229 [Overal design]Analysis of 3'-focused PAT-seq data in human breast cancer cell-lines (MCF7 vs MDAMB231) and after siRNA depletion of the CFII subunits (CLP1 and PCF11); [Treatment]'MDAMB231 cells were seeded at 100,000 cells/well (with RPMI + 10% FBS and 0.25% insulin) into 6 well plates and incubated at 37ºC for 48 hours to ~80% confluence. Cells were at passage 4 from thawing. MCF7 cells were seeded at 250,000 cells/well (with DMEM + 10% FBS media to 2.5 ml) into 6 well plates and incubated at 37ºC for 6 hrs. Media was removed and replaced with 2 ml of fresh media in each well. RNA interference (RNAi) was prepared for each well from 5 µM small interfering RNA (siRNA) stocks in total of 250 µl of opti-MEM (Gibco); positive control was LAMIN 6 µl/well, negative control scramble 6 µl/well, mock negative control 0 µl/well, hPCF11 1 and 2 siRNA 15 µl each/well, hCLP1 1 and 2 siRNA 15 µl each of each/well, hCLP1 3 and 4 siRNA 15 µl each/well. 5 µl in 245 µl of Lipofectamine RNAiMAX (Invitrogen) was added to each siRNA preparation and incubated at 10 - 20 mins at room temperature (RT). 500 µl of siRNA preparation was then added to the appropriate well.'; [Growth]"MDAMB231 cells were grown in RPMI (Gibco) containing 10% Fetal Bovine Serum (FBS) and 0.25% insulin. MCF7 breast cancer cells were grown in T75 flasks with Dulbecco's Modified Eagle's Medium (DMEM; Gibco) containing 10% FBS. Cells were kept in 5% carbon dioxide (CO2) incubator at 37ºC. Culture media was removed from flask at 70 - 90% confluent cells, cells were washed with 5 ml phosphate bufferer saline (PBS), and 2 ml of TrypLE for 2 mins at 37ºC was used to dissociate cells from flask. When 90% of cells dissociated, 4 ml of DMEM + 10% FBS added to flask, centrifuged for 5 min at 200 g. Cell pellet resuspended in 10 ml DMEM + 10% FBS. Cell counts and viability determined using the Countess Automated cell counter; 20 µl of Trypan blue mixed with 20 µl of cell suspension, 10 µl added to cell counter plate, repeated twice. Cells were seeded between 1:6 to 1:10 in new flask and DMEM + 10% FBS added to total 15 ml."; [Extraction]'Medium was removed and wells were washed with 1 ml 1% PBS. For MDAMB231 cells, 600 µl of TRIzol was added to each well and incubated at RT for 10 mins before transfer to 2ml tubes and storage at -80ºC prior to RNA extraction. For MCF7 cells, 750 µl of TRIzol was added to each well and incubated at RT for 2 mins. Cells and TRIzol were transferred to a tube and 200 µl chloroform was added, vortexed for 15 sec, incubated at RT for 3 mins, and centrifuged at 4ºC for 5 mins at 13000 rpm. The aqueous phase was transferred to a fresh tube and an equal amount of 70% EtOH was added. RNA was then purified over Qiagen RNeasy spin columns according to manufacturer’s instructions. RNA was eluted in 40 µl RNase free H2O. One microgram of total RNA was used for library preparation by the PAT-seq method (Harrison et al., 2015).\nLibrary construction was by the PAT-seq approach (Harrison et al RNA 2015)\nCluster Generation: 9pM of libraries per lane using Illumina c-bot. Illumina protocol 15006165 Rev J, July 2012\nSequencing chemistry: 1 x 150bp sequencing using Illumina protocol 15035788 Rev A, Oct 2012'; [Cell type]'Breast cancer cell line''cell line: MCF7; cell type: Breast cancer cell line; treatment: Cells growing in culture; genotype/variation: Independent control for cell line dependent APA; ', 'cell line: MDAMD231; cell type: Breast cancer cell line; treatment: Cells growing in culture; genotype/variation: Independent control for cell line dependent APA; ', 'cell line: MCF7; cell type: Breast cancer cell line; treatment: Transfected with siRNA; genotype/variation: Control Non-targeting siRNA; ', 'cell line: MCF7; cell type: Breast cancer cell line; treatment: Transfected with siRNA; genotype/variation: PCF11 knockdown; ', 'cell line: MCF7; cell type: Breast cancer cell line; treatment: Transfected with siRNA; genotype/variation: CLIP1 knockdown; ' GSE63284 Homo sapiens 2 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Response and resistance to BET bromodomain inhibitors in triple negative breast cancer [Chem-Seq] 2014-11-14 Triple negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. Here we report the preferential and high sensitivity of TNBCs to BET bromodomain inhibitors such as JQ1 manifested by cell cycle arrest in early G1, apoptosis, and induction of markers of luminal epithelial differentiation in vitro and in vivo. The sensitivity of TNBC and other tumor types to BET inhibition establishes a rationale for clinical investigation, and a motivation to understand mechanisms of resistance. After engendering acquired resistance to BET inhibition in previously sensitive TNBCs, we utilized integrative approaches to identify a unique mechanism of epigenomic resistance to this epigenetic therapy. Resistant cells remain dependent on BRD4, confirmed by RNA interference. However, TNBC cells adapt to BET bromodomain inhibition by re-recruitment of unmutated BRD4 to super-enhancers, now in a bromodomain-independent manner. Proteomic studies of resistant TNBC identify hyper-phosphorylation of BRD4 and strong association with MED1. Together, these studies provide a rationale for BET inhibition in TNBC and argue for combination strategies to anticipate clinical drug resistance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE63284 Response and resistance to BET bromodomain inhibitors in triple-negative breast cancer. Nature 43.070 https://doi.org/10.1038/nature16508 {Nature (43.070): 10.1038/nature16508} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA267196 https://www.ebi.ac.uk/ena/browser/view/PRJNA267196 https://www.ncbi.nlm.nih.gov/sra?term=SRP049808 [Overal design]Chem-Seq in parental and JQ1 resistant triple negative breast cancer (TNBC); [Treatment]'Sonicated nuclear lysates were incubated with Biotin-JQ1 for 6 hour'; [Growth]'Cells were growed with SUM medium'; [Extraction]'Whole cell extracts were sonicated to solubilize the chromatin. The chromatin extracts containing DNA fragments with an average size of 500 bp were precipitated using streptavidin conjugated beads. Purified precipitated DNA were prepared for sequencing according to a modified version of the Solexa Genomic DNA protocol. Fragmented DNA was end repaired and subjected to 18 cycles of LM-PCR using oligos provided by Illumina. Amplified fragments between 150 and 300bp (representing shear fragments between 50 and 200nt in length and ~100bp of primer sequence) were isolated by agarose gel electrophoresis and purified.'; [Cell type]'Source: ''cell line: SUM159R; sonicated nuclear lysates incubated with: Biotin-JQ1; dna fragments precipitated using: Streptavidin; barcode (already removed): TAGCTT; ', 'cell line: SUM159; sonicated nuclear lysates incubated with: Biotin-JQ1; dna fragments precipitated using: Streptavidin; barcode (already removed): GATCAG; ' GSE80647 Homo sapiens 3 Expression profiling by RT-PCR GPL21770 Baseline Expression of Inflammatory Cytokines and Receptors in the T47D Human Breast Cancer Cell Line 2016-04-25 Immortalized human breast cancer cell line, T47D, was analyzed via RT-qPCR for transcript expression of selected inflammatory cytokines and cytokine receptors associated with promotion of tumor vasculature and breast cancer metastasis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80647 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA319563 https://www.ebi.ac.uk/ena/browser/view/PRJNA319563 None [Overal design]An array of inflammatory cytokines and matching receptors that have been associated with the promotion of tumor vasculature and breast cancer metastasis were identified based on literature and clinical data. Using this array, we screened normal breast tissue and seven breast cancer cell lines (T47D, MCF7, ZR-75, HCC1806, MDA-MB-231, HCC1954, SUM149), representing a range of breast cancer types. These results can be analyzed individually or used to compare the expression differences in normal breast tissue to breast cancer cell lines to identify potential mediators of autocrine or paracrine promotion of tumor angiogenesis, lymphangiogenesis and metastasis. Each cell line is published separately in GEO.; [Treatment]'n/a'; [Growth]'T47D cell line was cultured in 5% FBS in DMEM at 37ºC in a 10% CO2 incubator.'; [Extraction]'Total RNA was isolated by TRI-Reagent.'; [Cell type]'Source: ''disease: Ductal carcinoma; er: Positive; pr: Positive; her2: Negative; ' GSE78113 Homo sapiens 26 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Capture-C reveals preformed chromatin interactions between HIF-binding sites and distant promoters. [ChIP-Seq] 2016-02-19 Hypoxia inducible factor (HIF) directs an extensive transcriptional cascade that transduces numerous adaptive responses to hypoxia. Pan-genomic analyses, using chromatin immunoprecipitation and transcript profiling, have revealed large numbers of HIF-binding sites that are generally associated with hypoxia-inducible transcripts, even over long chromosomal distances. However, these studies do not define the specific targets of HIF-binding sites and do not reveal how induction of HIF affects chromatin conformation over distantly connected functional elements. To address these questions we deployed a recently developed chromosome conformation assay that enables simultaneous high-resolution analyses from multiple viewpoints. These assays defined specific long-range interactions between intergenic HIF-binding regions and one or more promoters of hypoxia-inducible genes, revealing the existence of multiple enhancer-promoter, promoter-enhancer and enhancer-enhancer interactions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE78113 Capture-C reveals preformed chromatin interactions between HIF-binding sites and distant promoters. EMBO reports 8.383 https://doi.org/10.15252/embr.201642198 {EMBO reports (8.383) doi:10.15252/embr.201642198}; {The Journal of biological chemistry (None) doi:10.1074/jbc.RA119.009827}; 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA312626 https://www.ebi.ac.uk/ena/browser/view/PRJNA312626 https://www.ncbi.nlm.nih.gov/sra?term=SRP070572 [Overal design]We utilised ChIP-seq to study the histone marks and CTCF binding in MCF7 cells in normoxia and hypoxia; [Treatment]'For hypoxia treatment cells, were incubated for 16 hr in an In Vivo2 Hypoxia Work station (Ruskinn Technology) at 0.5% oxygen.'; [Growth]'Dulbecco Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum, 2 mM L-glutamine, 100U/ml penicillin and 100 μg/ml streptomycin.'; [Extraction]'ChIP-seq: Cells were fixed with 1% formaldehyde and quenched with glycine (125mM). After washing, cells were lysed (0.5%SDS, 10mM EDTA, 50mM Tris-HCl pH 8.1) and sonicated (Diagenode Biorupter, Belgium). Chromatin was immunoprecipitated using antibodies indicated. Eluted chromatin was heated to reverse cross-linking, treated with proteinase-K, RNaseA and purified on a qiagen PCR pufircation column.\nLibraries were prepared using PrepX Complete ILMN DNA library kit (#400076, Wafergen) by the High-Throughput Genomics Group at the Wellcome Trust Centre for Human Genetics, Oxford, UK.'; [Cell type]'Source: ''cell line: MCF-7; treatment: Normoxia; repeat: 1; chip antibody: H3K4me1 (Millipore, #07-436); ', 'cell line: MCF-7; treatment: Normoxia; repeat: 2; chip antibody: H3K4me1 (Millipore, #07-436); ', 'cell line: MCF-7; treatment: Hypoxia; repeat: 1; chip antibody: H3K4me1 (Millipore, #07-436); ', 'cell line: MCF-7; treatment: Hypoxia; repeat: 2; chip antibody: H3K4me1 (Millipore, #07-436); ', 'cell line: MCF-7; treatment: Normoxia; repeat: 1; chip antibody: H3K27ac (#ab4729, Abcam); ', 'cell line: MCF-7; treatment: Normoxia; repeat: 2; chip antibody: H3K27ac (#ab4729, Abcam); ', 'cell line: MCF-7; treatment: Hypoxia; repeat: 1; chip antibody: H3K27ac (#ab4729, Abcam); ', 'cell line: MCF-7; treatment: Hypoxia; repeat: 2; chip antibody: H3K27ac (#ab4729, Abcam); ', 'cell line: MCF-7; treatment: Normoxia; repeat: 1; chip antibody: CTCF (#07-729, Millipore); ', 'cell line: MCF-7; treatment: Normoxia; repeat: 2; chip antibody: CTCF (#07-729, Millipore); ', 'cell line: MCF-7; treatment: Hypoxia; repeat: 1; chip antibody: CTCF (#07-729, Millipore); ', 'cell line: MCF-7; treatment: Hypoxia; repeat: 2; chip antibody: CTCF (#07-729, Millipore); ', 'cell line: MCF-7; treatment: Normoxia; repeat: 1; chip antibody: INPUT DNA; ', 'cell line: MCF-7; treatment: Hypoxia; repeat: 1; chip antibody: INPUT DNA; ', 'cell line: 786-O; treatment: Normoxia; repeat: 1; chip antibody: H3K4me1 (Millipore, #07-436); ', 'cell line: 786-O; treatment: Normoxia; repeat: 2; chip antibody: H3K4me1 (Millipore, #07-436); ', 'cell line: 786-O; treatment: Normoxia; repeat: 1; chip antibody: H3K4me3 (#9751, Cell Signaling Technology); ', 'cell line: 786-O; treatment: Normoxia; repeat: 2; chip antibody: H3K4me3 (#9751, Cell Signaling Technology); ', 'cell line: 786-O; treatment: Normoxia; repeat: 1; chip antibody: H3K27ac (#ab4729, Abcam); ', 'cell line: 786-O; treatment: Normoxia; repeat: 2; chip antibody: H3K27ac (#ab4729, Abcam); ', 'cell line: 786-O; treatment: Normoxia; repeat: 1; chip antibody: CTCF (#07-729, Millipore); ', 'cell line: 786-O; treatment: Normoxia; repeat: 2; chip antibody: CTCF (#07-729, Millipore); ', 'cell line: 786-O; treatment: Normoxia; repeat: 1; chip antibody: RNApol2 (#sc-899, Santa Cruz ); ', 'cell line: 786-O; treatment: Normoxia; repeat: 2; chip antibody: RNApol2 (#sc-899, Santa Cruz ); ', 'cell line: 786-O; treatment: Normoxia; repeat: 1; chip antibody: INPUT DNA; ', 'cell line: 786-O; treatment: Normoxia; repeat: 2; chip antibody: INPUT DNA; ' GSE133068 Mus musculus 32 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL19057 Pygopus2-Histone interaction is important for de-differentiation and breast cancer progression 2019-06-20 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE133068 A Pygopus 2-Histone Interaction Is Critical for Cancer Cell Dedifferentiation and Progression in Malignant Breast Cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-19-2910 {Cancer research (8.378): 10.1158/0008-5472.CAN-19-2910} 'polyA RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA549869 https://www.ebi.ac.uk/ena/browser/view/PRJNA549869 None [Overal design]Refer to individual Series; [Treatment]'For Wnt3a treatment, Pygo2 WT (+/+) and mutant (AE/AE) cell lines were treated with 100 ng/ml Wnt3a for 3 days. Medium was changed and fresh Wnt3a was added daily. Untreated cells served as control. For TGFb treatment, Pygo2 WT (+/+) and mutant (AE/AE) cell lines were treated with 2 ng/ml TGFb for 4 days. Medium was changed every second day with fresh addition of TGFb. Untreated cells served as control.'; [Growth]'Pygo2 WT (+/+) and mutant (AE/AE) cell lines were cultured in Dulbecco’s modified Eagle’s medium (DMEM) (Sigma-Aldrich, D5671) supplemented with 10% Fetal Bovine Serum (FBS, 10%; Sigma-Aldrich), 2 mM glutamine (Sigma-Aldrich, G7513), 100 U penicillin (Sigma-Aldrich) and 0.1 mg/ml streptomycin (Sigma-Aldrich). All cell lines were grown at 37°C, 5% CO2, 95% humidity.'; [Extraction]'Total RNA was isolated from the samples above using the miRNeasy Mini Kit (Qiagen, 217004) with on-column DNAse digestion according to the manufacturer’s instructions.\n200 ng of RNA was processed with the TruSeq Stranded mRNA LT Sample Prep Kit (Illumina). Library QC was performed with a Fragment Analyzer (AATI) using the Standard Sensitivity NGS Fragment Analysis Kit (DNF-473). RNA-Seq libraries were sequenced with the SR75 with NextSeq (Illumina).', '75x10^3 cells were subjected to lysis and transposition reaction according to the protocol described previously (Buenrostro et al., 2015).\nBarcoded libraries were prepared according to the protocol described previously (Buenrostro et al., 2015). 75x10^3 cells were used in each transposition reaction using the Nextera Tn5 Transposase kit (Illumina, FC-121-1030) followed by purification using Qiagen MinElute PCR purification kit (Qiagen, 28004). Transposed DNA fragments were PCR amplified over 13 cycles using barcoded PCR primers and NEB High Fidelity PCR Master Mix (NEB, M0541). Libraries were purified using QIAquick PCR purification kit (Qiagen, 28104) and sequenced with Illumina Illumina NextSeq 500.'; [Cell type]'Source: ', 'Breast cancer cells''strain: MMTV-PyMT (FVB/N); tissue: Breast cancer cells; transgene: PyMT; mutation: Pygo2 +/+ (WT); treatment: UT (4 days); ', 'strain: MMTV-PyMT (FVB/N); tissue: Breast cancer cells; transgene: PyMT; mutation: Pygo2 +/+ (WT); treatment: TGFb treated (4 days); ', 'strain: MMTV-PyMT (FVB/N); tissue: Breast cancer cells; transgene: PyMT; mutation: Pygo2 A342E/A342E knockin; treatment: UT (4 days); ', 'strain: MMTV-PyMT (FVB/N); tissue: Breast cancer cells; transgene: PyMT; mutation: Pygo2 A342E/A342E knockin; treatment: TGFb treated (4 days); ', 'strain: MMTV-PyMT (FVB/N); tissue: Breast cancer cells; transgene: PyMT; mutation: Pygo2 +/+ (WT); treatment: UT (3 days); ', 'strain: MMTV-PyMT (FVB/N); tissue: Breast cancer cells; transgene: PyMT; mutation: Pygo2 +/+ (WT); treatment: Wnt3a treated (3 days); ', 'strain: MMTV-PyMT (FVB/N); tissue: Breast cancer cells; transgene: PyMT; mutation: Pygo2 A342E/A342E knockin; treatment: UT (3 days); ', 'strain: MMTV-PyMT (FVB/N); tissue: Breast cancer cells; transgene: PyMT; mutation: Pygo2 A342E/A342E knockin; treatment: Wnt3a treated (3 days); ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; cell type: Breast cancer cells; transgene: PyMT; genotype: Pygo2 +/+ (WT); treatment: UT; time: 4 days; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; cell type: Breast cancer cells; transgene: PyMT; genotype: Pygo2 +/+ (WT); treatment: TGFb treated; time: 4 days; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; cell type: Breast cancer cells; transgene: PyMT; genotype: Pygo2 A342E/A342E knockin; treatment: UT; time: 4 days; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; cell type: Breast cancer cells; transgene: PyMT; genotype: Pygo2 A342E/A342E knockin; treatment: TGFb treated; time: 4 days; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; cell type: Breast cancer cells; transgene: PyMT; genotype: Pygo2 +/+ (WT); treatment: UT; time: 3 days; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; cell type: Breast cancer cells; transgene: PyMT; genotype: Pygo2 +/+ (WT); treatment: Wnt3a treated; time: 3 days; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; cell type: Breast cancer cells; transgene: PyMT; genotype: Pygo2 A342E/A342E knockin; treatment: UT; time: 3 days; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; cell type: Breast cancer cells; transgene: PyMT; genotype: Pygo2 A342E/A342E knockin; treatment: Wnt3a treated; time: 3 days; ' GSE150131 Homo sapiens 12 Genome binding/occupancy profiling by high throughput sequencing GPL24676 IL6/STAT3 co-opts ER/FOXA1 regulatory elements to drive metastasis in breast cancer [ATAC-Seq] 2020-05-08 Interleukin 6 (IL6) signaling has been associated with an aggressive and metastatic phenotype in multiple solid tumors including breast cancer, but its mechanism of action in mediating tumor progression and treatment response is not clear. By exploiting a clinically relevant intraductal xenograft model of estrogen receptor positive (ER+) breast cancer, we demonstrate that IL6 increases both primary tumor growth and distant metastases. By integrating pre-clinical models and clinical specimens, we show that signal transducer and activator of transcription 3 (STAT3) mediates IL6-induced activation of a metastatic gene program from enhancer-elements shared with ER and its pioneer factor FOXA1. Although IL6 activated STAT3 and ER/FOXA1 share cis-regulatory regions, STAT3 drives transcription independent of ER and FOXA1 function, and the IL6/STAT3 gene program is not influenced by ER-targeted therapies, decoupling these two important pathways. This demonstrates that ER/FOXA1 and IL6/STAT3 are two parallel, but independent actionable pathways controlling breast cancer progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE150131 IL6/STAT3 Signaling Hijacks Estrogen Receptor α Enhancers to Drive Breast Cancer Metastasis. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2020.06.007 {Cancer cell (23.916): 10.1016/j.ccell.2020.06.007} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA631243 https://www.ebi.ac.uk/ena/browser/view/PRJNA631243 https://www.ncbi.nlm.nih.gov/sra?term=SRP260801 [Overal design]ATAC-sequencing on T47D cells with FOXA1 siRNA with or without IL6; [Treatment]'Cells were treated with human recombinant IL6 (206-IL-200, R&D systems) for 30 min.'; [Growth]'T47D cells were grown in RPMI supplemented with 10% FBS, 2mM L-glutamine and 50 U/ml penicillin and 50 ug/ml streptomycin. On target plus siRNAs were used for the knockdown.'; [Extraction]'Omni ATAC-seq protocol was performed from Corces et al., 2017, Nature Methods. Transposase and buffers were purchased from Illumina Nextera kits.\nDNA was prepared for Illumina sequencing using Nextera indices on the Novaseq 6000 with paired end 50 bp.'; [Cell type]'ER+ Breast Cancer Cell Line''cell line: T47D cells; cell type: ER+ Breast Cancer Cell Line; passages: 27-30; ' GSE101122 Homo sapiens 4 Non-coding RNA profiling by array GPL19978 circRNA expression in breast cancer cell lines 2017-07-11 Use of circRNA array to examine the circRNA expression profile in breast cancer cell lines https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE101122 circTADA2As suppress breast cancer progression and metastasis via targeting miR-203a-3p/SOCS3 axis. Cell death & disease 5.959 https://doi.org/10.1038/s41419-019-1382-y {Cell death & disease (5.959): 10.1038/s41419-019-1382-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA393779 https://www.ebi.ac.uk/ena/browser/view/PRJNA393779 None [Overal design]Arraystar Human circRNAs chip (Arraystar) were used to determine the circRNA expression in four breast cancer cell lines.; [Treatment]'Treated with Trizol for extraction'; [Growth]'Cells are cultured in EMEM containing 2 mM L-glutamine, 0.01 mg/mL bovine insulin (90%), fetal bovine serum (10%) and Earle’s BSS containing 1.5 g/L sodium bicarbonate, 0.1 mM non-essential amino acids and 1 mM sodium pyruvate.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: breast cancer; subtype: MCF-7; ', 'cell line: breast cancer; subtype: MDA-MB-231; ', 'cell line: breast cancer; subtype: Primary cells isolated from breast ductal carcinoma; ', 'cell line: breast cancer; subtype: Tamoxifen-Resistant MCF-7 cell; ' GSE165459 Mus musculus 3 Expression profiling by high throughput sequencing GPL21626 scRNAseq of MMTV-Neu lung cancer cells in early and late stage 2021-01-25 Cancer cells can disseminate from early-evolved primary lesions. It is thought that a state of early disseminated cancer cell (early DCC) dormancy would precede genetic maturation of DCCs and metastasis initiation. Here we reveal at single cell resolution a previously unrecognized role of mesenchymal- and pluripotency-like programs in coordinating early cancer cell spread and a long-lived dormancy program in early DCCs. We identify in early lesions and early DCCs, the transcription factor ZFP281 as an inducer of mesenchymal- and primed pluripotency-like programs, which is absent in advanced primary tumors and overt metastasis. ZFP281 not only controls the early spread of cancer cells but also locks early DCCs in a prolonged dormancy state by preventing the acquisition of an epithelial-like proliferative program. Thus, ZFP281-driven dormancy of early DCCs may be a rate-limiting step in metastatic progression functioning as a first barrier that DCCs must overcome to then undergo genetic maturation. This data set aims to characterize MMTV-Neu early and late lung disseminated cancer cells (DCCs). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE165459 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA694650 https://www.ebi.ac.uk/ena/browser/view/PRJNA694650 https://www.ncbi.nlm.nih.gov/sra?term=SRP303164 [Overal design]RNA profile of MMTV-Neu early and late lung disseminated cancer cells (DCCs); [Treatment]'None'; [Growth]'MMTV-HER2/Neu mice were maintained on FvB background and bred and crossed in our facilities. All experimental procedures were approved by the Institutional Animal Care and Use Committee (IACUC) of Icahn School of Medicine at Mount Sinai.'; [Extraction]'Lungs from ‘early’ and ‘late stage’ mice (eL and LL) were dissected and digested. Cancer cells (CD45- HER2+) and non-cancer lung cells (CD45-HER2-) were sorted. Cells were encapsulated using the 10X Chromium 3’ v3 and chemistry kit according to manufacturer instructions.\nSequencing, libraries were prepared according to manufacturer instructions. QC of cDNA and final libraries was performed by CyberGreen qPCR library quantification assay (KAPA). Samples were sequenced on an Illumina Nextseq 550 using the 75-cycle kit to a depth of 100 million reads per library.'; [Cell type]'Source: ''strain: FvB; age: 14-18 wk; tumor stage: No palpable tumor; tissue: lungs; cell tyoe: non-cancer lung cells; ', 'strain: FvB; age: 14-18 wk; tumor stage: No palpable tumor; tissue: lungs; cell tyoe: breast cancer cells; ', 'strain: FvB; age: >20 wk; tumor stage: With primary tumor(s); tissue: lungs; cell tyoe: breast cancer cells; ' GSE85356 Mus musculus; Homo sapiens 285 Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL11154; GPL13112; GPL16791; GPL17021; GPL20301; GPL21103 DNA methylation repels binding of hypoxia-inducible transcription factors to maintain tumour immunotolerance 2016-08-09 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE85356 DNA methylation repels binding of hypoxia-inducible transcription factors to maintain tumor immunotolerance. Genome biology 14.028 https://doi.org/10.1186/s13059-020-02087-z {Genome biology (14.028): 10.1186/s13059-020-02087-z} 'genomic DNA', 'polyA RNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA338248 https://www.ebi.ac.uk/ena/browser/view/PRJNA338248 None [Overal design]Refer to individual Series; [Treatment]'None', 'Cells were incubated in hypoxic conditions (0.5% oxygen) for 16 hours.'; [Growth]'None', 'cultured feeder-free in fibroblast-conditioned medium', 'cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.', 'cultured in 0.1% Gelatin Solution in DMEM 4,500\u2009mg\u2009/L glucose, 1% sodium pyruvate, 15% FBS, 1% Pen Strep, 0.1\u2009mM of non-essential amino acids (EmbryoMax), 50\u2009μM β-mercaptoethanol, 103\u2009U LIF ESGRO (Millipore).', 'cultured at 37 °C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5 mL of 100 U/mL Penicillin-Streptomycin (Pen Strep, Life Technologies), 10 µg/mL of blasticidin (ant-bl-05, Invivogen), puromycin (P9620, Sigma-Aldrich) 1.5 µg/mL medium and 5 mL of L-Glutamine 200 mM, 1 µM DMSO', 'cultured at 37°C in Roswell Park Memorial Institut 1640 Medium (RPMI) 10% FBS 1% Pen Strep and 1% L-Glutamine.'; [Extraction]'cultured cells were washed on ice with ice-cold phosphate-buffer saline (PBS), detached using cell scrapers and collected by centrifugation (400 ×G, 4°C). Nucleic acids were subsequently extracted using the Wizard Genomic DNA Purification (Promega, Leiden, The Netherlands) kit according to instructions, dissolved in 80 µL PBS with RNAse A (200 units, NEB, Ipswich, MA, USA), incubated for 10 minutes at 37°C. After proteinase K addition (200 units) and incubation for 30 minutes at 56°C, DNA was purified using the QIAQuick blood and tissue kit, eluted in 100 µL of a 10 mM Tris, 1mM EDTA solution (pH 8) and stored at -80°C until further processing.\nDNA libraries were prepared using methylated adapters and the NEBNext DNA library prep master mix set following manufacturer recommendations. Libraries were bisulfite-converted using the Imprint DNA modification kit (Sigma) as recommended, and PCR amplified for 12 cycles using barcoded primers (NEB) and the KAPA HiFi HS Uracil+ ready mix (Sopachem, Eke, Belgium) according to manufacturers instructions. Fragments were selected from these libraries using the SeqCap Epi CpGiant Enrichment Kit (Roche) following the manufacturers instructions, sequenced from both ends for 100 bases on a HiSeq 2000.', 'cultured cells were washed on ice with ice-cold phosphate-buffer saline (PBS), detached using cell scrapers and collected by centrifugation (400 ×G, 4°C). Nucleic acids were subsequently extracted using the Wizard Genomic DNA Purification (Promega, Leiden, The Netherlands) kit according to instructions, dissolved in 80 µL PBS with RNAse A (200 units, NEB, Ipswich, MA, USA), incubated for 10 minutes at 37°C. After proteinase K addition (200 units) and incubation for 30 minutes at 56°C, DNA was purified using the QIAQuick blood and tissue kit, eluted in 100 µL of a 10 mM Tris, 1mM EDTA solution (pH 8) and stored at -80°C until further processing.\nDNA libraries were prepared using methylated adapters and the NEBNext DNA library prep master mix set following manufacturer recommendations. Libraries were bisulfite-converted using the Imprint DNA modification kit (Sigma) as recommended, and PCR amplified for 12 cycles using barcoded primers (NEB) and the KAPA HiFi HS Uracil+ ready mix (Sopachem, Eke, Belgium) according to manufacturers instructions.', "Cells were incubated in hypoxic conditions for 16 hours. Cultured cells were subsequently immediately fixed by adding 1% Formaldehyde (16% Formaldehyde (w/v), Methanol-free, Thermo Scientific) directly in the medium and incubating for 8 minutes. Fixed cells were incubated with 150 mM of glycine for 5 min to revert the cross-links, washed twice with ice-cold PBS 0.5% Triton-X100, scraped and collected by centrifugation (1000 ×G 5min at 4°C). The pellet was resuspended in 1400 µL of RIPA buffer (50 mM Tris-HCl pH 8, 150 mM NaCl, 2 mM EDTA pH 8, 1% Triton-X100, 0.5% Sodium deoxycholate, 1% SDS, 1% protease inhibitors) and transferred in a new eppendorf tube. The chromatin was sonicated for 3 min by using a Branson 250 Digital Sonifier with 0.7 s 'On' and 1.3 s 'Off' pulses at 40% power amplitude, yielding a size of 100 to 500 bp. The sample was kept ice-cold at all times during the sonication. The samples were centrifuged (10 min at 16000 ×G at 4°C) and the supernatant were transferred in a new eppendorf tube. The protein concentration was assessed using a BCA assay. Fifty µL of shared chromatin was used as “input” and 1.4 µg of primary ARNT/HIF-1β monoclonal antibody (NB100-124, Novus) per 1 mg of protein was added to the remainder of the chromatin, and incubated overnight at 4°C in a rotator. Pierce Protein A/G Magnetic Beads (Life Technologies) were added to the samples in a volume that is 4X the volume of the primary Ab and incubated at 4°C for at least 5 hours. A/G Magnetic Beads were collected and the samples were washed 5 times with the washing buffer (50 mM Tris-HCl, 200 mM LiCl, 2 mM EDTA, pH 8, 1% Triton, 0.5% Sodium deoxycholate, 0.1% SDS, 1% protease inhibitors), and twice with TE buffer. The A/G magnetic beads were resuspended in 50 µL of TE buffer, and 1.5 µL of RNAse A (200 units, NEB, Ipswich, MA, USA) were added to the A/G beads samples and to the input, incubated for 10 minutes at 37°C. After addition of 1.5 µL of proteinase K (200 units) and overnight incubation at 65°C, the DNA was purified using 1.8´ volume of Agencourt AMPure XP (Beckman Coulter) according to the manufactory instructions\nOne µg of input and all of the immunoprecipitated DNA were converted into sequencing libraries using the NEBNext Ultra DNA library prep kit.", 'cultured cells were washed on ice with ice-cold phosphate-buffer saline (PBS), detached using cell scrapers and collected by centrifugation (400 ×G, 4°C). Nucleic acids were subsequently extracted using the Wizard Genomic DNA Purification (Promega, Leiden, The Netherlands) kit according to instructions, dissolved in 80 µL PBS with RNAse A (200 units, NEB, Ipswich, MA, USA), incubated for 10 minutes at 37°C. After proteinase K addition (200 units) and incubation for 30 minutes at 56°C, DNA was purified using the QIAQuick blood and tissue kit, eluted in 100 µL of a 10 mM Tris, 1mM EDTA solution (pH 8) and stored at -80°C until further processing.\nDNA libraries were prepared using methylated adapters and the NEBNext DNA library prep master mix set following manufacturer recommendations. Libraries were bisulfite-converted using the EZ DNA Methylation-Lightning™ kit (Zymo) as recommended, and PCR amplified for 12 cycles using barcoded primers (NEB) and the KAPA HiFi HS Uracil+ ready mix (Sopachem, Eke, Belgium) according to manufacturers instructions. Fragments were selected from these libraries using the SeqCap Epi CpGiant Enrichment Kit (Roche) following the manufacturers instructions, sequenced from both ends for 100 bases on a HiSeq 2000.', 'PolyA mRNA capture by using KAPA Stranded mRNA-Seq Kit (Illumina)\nStrand specific library preparation', 'For PolyA mRNA capture system, RNA was extracted using TRIzol (Invitrogen) according to manufacture instructions. RNA was subsiquently used for PolyA capture.\nStrand specific library preparation (KAPA stranded mRNA seq kit)', "Cells were incubated in hypoxic conditions for 16 hours. Cultured cells were subsequently immediately fixed by adding 1% Formaldehyde (16% Formaldehyde (w/v), Methanol-free, Thermo Scientific) directly in the medium and incubating for 8 minutes. Fixed cells were incubated with 150 µM of glycine for 5 min to revert the cross-links, washed twice with ice-cold PBS 0.5% Triton-X100, scraped and collected by centrifugation (1000 ×G 5min at 4°C). The pellet was resuspended in 1400 µL of RIPA buffer (50 mM Tris-HCl pH 8, 150 mM NaCl, 2 mM EDTA pH 8, 1% Triton-X100, 0.5% Sodium deoxycholate, 1% SDS, 1% protease inhibitors) and transferred in a new eppendorf tube. The chromatin was sonicated for 3 min by using a Branson 250 Digital Sonifier with 0.7 s 'On' and 1.3 s 'Off' pulses at 40% power amplitude, yielding a size of 100 to 500 bp. The sample was kept ice-cold at all times during the sonication. The samples were centrifuged (10 min at 16000 ×G at 4°C) and the supernatant were transferred in a new eppendorf tube. The protein concentration was assessed using a BCA assay. Fifty µL of shared chromatin was used as “input” and 1.4 µg of primary ARNT/HIF-1β monoclonal antibody (NB100-124, Novus) per 1 mg of protein was added to the remainder of the chromatin, and incubated overnight at 4°C in a rotator. Pierce Protein A/G Magnetic Beads (Life Technologies) were added to the samples in a volume that is 4X the volume of the primary Ab and incubated at 4°C for at least 5 hours. A/G Magnetic Beads were collected and the samples were washed 5 times with the washing buffer (50 mM Tris-HCl, 200 mM LiCl, 2 mM EDTA, pH 8, 1% Triton, 0.5% Sodium deoxycholate, 0.1% SDS, 1% protease inhibitors), and twice with TE buffer. The A/G magnetic beads were resuspended in 50 µL of TE buffer, and 1.5 µL of RNAse A (200 units, NEB, Ipswich, MA, USA) were added to the A/G beads samples and to the input, incubated for 10 minutes at 37°C. After addition of 1.5 µL of proteinase K (200 units) and overnight incubation at 65°C, the DNA was purified using 1.8´ volume of Agencourt AMPure XP (Beckman Coulter) according to the manufactory instructions\nDNA libraries were prepared using methylated adapters and the NEBNext DNA library prep master mix set following manufacturer recommendations. DNA libraries were bisulfite converted using the EZ DNA Methylation-Lightning™ kit (Zymo) prior to library amplification using HiFi Uracil+ (KAPA).", "Cells were incubated in hypoxic conditions for 16 hours. Cultured cells were subsequently immediately fixed by adding 1% Formaldehyde (16% Formaldehyde (w/v), Methanol-free, Thermo Scientific) directly in the medium and incubating for 8 minutes. Fixed cells were incubated with 150 µM of glycine for 5 min to revert the cross-links, washed twice with ice-cold PBS 0.5% Triton-X100, scraped and collected by centrifugation (1000 ×G 5min at 4°C). The pellet was resuspended in 1400 µL of RIPA buffer (50 mM Tris-HCl pH 8, 150 mM NaCl, 2 mM EDTA pH 8, 1% Triton-X100, 0.5% Sodium deoxycholate, 1% SDS, 1% protease inhibitors) and transferred in a new eppendorf tube. The chromatin was sonicated for 3 min by using a Branson 250 Digital Sonifier with 0.7 s 'On' and 1.3 s 'Off' pulses at 40% power amplitude, yielding a size of 100 to 500 bp. The sample was kept ice-cold at all times during the sonication. The samples were centrifuged (10 min at 16000 ×G at 4°C) and the supernatant were transferred in a new eppendorf tube. The protein concentration was assessed using a BCA assay. Fifty µL of shared chromatin was used as “input” and 1.4 µg of primary ARNT/HIF-1β monoclonal antibody (NB100-124, Novus) per 1 mg of protein was added to the remainder of the chromatin, and incubated overnight at 4°C in a rotator. Pierce Protein A/G Magnetic Beads (Life Technologies) were added to the samples in a volume that is 4X the volume of the primary Ab and incubated at 4°C for at least 5 hours. A/G Magnetic Beads were collected and the samples were washed 5 times with the washing buffer (50 mM Tris-HCl, 200 mM LiCl, 2 mM EDTA, pH 8, 1% Triton, 0.5% Sodium deoxycholate, 0.1% SDS, 1% protease inhibitors), and twice with TE buffer. The A/G magnetic beads were resuspended in 50 µL of TE buffer, and 1.5 µL of RNAse A (200 units, NEB, Ipswich, MA, USA) were added to the A/G beads samples and to the input, incubated for 10 minutes at 37°C. After addition of 1.5 µL of proteinase K (200 units) and overnight incubation at 65°C, the DNA was purified using 1.8´ volume of Agencourt AMPure XP (Beckman Coulter) according to the manufactory instructions\nFive µg of input and all of the immunoprecipitated DNA were converted into sequencing libraries using the NEBNext Ultra DNA library prep kit.", 'RiboMinus Eukaryote System (Life technologies)\nBriefly, total RNA was extracted using TRIzol (Invitrogen), and remaining DNA contaminants in 17-20ug of RNA was removed using Turbo DNase (Ambion) according to the manufacturers instruction. RNA was repurified using RNeasy Mini Kit (Qiagen).\nStrand specific library preparation', "Cultured cells were subsequently immediately fixed by adding 1% Formaldehyde (16% Formaldehyde (w/v), Methanol-free, Thermo Scientific) directly in the medium and incubating for 8 minutes. Fixed cells were incubated with 150 µM of glycine for 5 min to revert the cross-links, washed twice with ice-cold PBS 0.5% Triton-X100, scraped and collected by centrifugation (1000 ×G 5min at 4°C). The pellet was resuspended in 1400 µL of RIPA buffer (50 mM Tris-HCl pH 8, 150 mM NaCl, 2 mM EDTA pH 8, 1% Triton-X100, 0.5% Sodium deoxycholate, 1% SDS, 1% protease inhibitors) and transferred in a new eppendorf tube. The chromatin was sonicated for 3 min by using a Branson 250 Digital Sonifier with 0.7 s 'On' and 1.3 s 'Off' pulses at 40% power amplitude, yielding a size of 100 to 500 bp. The sample was kept ice-cold at all times during the sonication. The samples were centrifuged (10 min at 16000 ×G at 4°C) and the supernatant were transferred in a new eppendorf tube. The protein concentration was assessed using a BCA assay. Fifty µL of shared chromatin was used as “input” and 1.4 µg of primary ARNT/HIF-1β monoclonal antibody (NB100-124, Novus) per 1 mg of protein was added to the remainder of the chromatin, and incubated overnight at 4°C in a rotator. Pierce Protein A/G Magnetic Beads (Life Technologies) were added to the samples in a volume that is 4X the volume of the primary Ab and incubated at 4°C for at least 5 hours. A/G Magnetic Beads were collected and the samples were washed 5 times with the washing buffer (50 mM Tris-HCl, 200 mM LiCl, 2 mM EDTA, pH 8, 1% Triton, 0.5% Sodium deoxycholate, 0.1% SDS, 1% protease inhibitors), and twice with TE buffer. The A/G magnetic beads were resuspended in 50 µL of TE buffer, and 1.5 µL of RNAse A (200 units, NEB, Ipswich, MA, USA) were added to the A/G beads samples and to the input, incubated for 10 minutes at 37°C. After addition of 1.5 µL of proteinase K (200 units) and overnight incubation at 65°C, the DNA was purified using 1.8´ volume of Agencourt AMPure XP (Beckman Coulter) according to the manufactory instructions\nDNA libraries were prepared using methylated adapters and the NEBNext DNA library prep master mix set following manufacturer recommendations. DNA libraries were bisulfite converted using the EZ DNA Methylation-Lightning™ kit (Zymo) prior to library amplification using HiFi Uracil+ (KAPA)."; [Cell type]'Source: ', 'Beast cancer cell line', 'Embryonic Stem Cells', 'Breast cancer cell line', 'Renal cell carcinoma cell line', 'Melanoma cell line', 'Embryonic Stem cells', 'Renal cell carcinoma''tissue: kidney; treatment: none; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: skin; treatment: none; growth protocol: cultured at 37°C in Roswell Park Memorial Institut 1640 Medium (RPMI) 10% FBS 1% Pen Strep and 1% L-Glutamine.; ', 'tissue: inner cell mass; treatment: none; ', 'tissue: lung; treatment: 0.5% O2 16h; type of sample: Input; chip antibody: none; ', 'tissue: lung; treatment: 0.5% O2 16h; type of sample: ChIP; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); ', 'tissue: breast; treatment: 0.5% O2 16h; type of sample: ChIP; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); ', 'tissue: breast; treatment: 0.5% O2 16h; type of sample: Input; chip antibody: none; ', 'tissue: breast; treatment: none; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: 1uM 5-Aza-2′-deoxycytidine (aza) for 72h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: PBS 0.8mg/kg BW; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: aza 0.8mg/kg BW; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: skin; treatment: IgG 40mg/kg BW; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: DMSO 72h, 21% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: DMSO 72h, 0.5% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: 1 µM aza 72h, 21% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: 1 µM aza 72h, 0.5% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: DMSO 24h, DMSO 72h, 21% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: 2mM DMOG 24h, DMSO 72h, 21% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: DMSO 24h, 1 µM aza 72h, 21% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: 2mM DMOG 24h, 1 µM aza 72h, 21% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: aza 0.8mg/kg BW, 40mg/kg BW IgG; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: aza 0.8mg/kg BW, IgG 40mg/kg BW; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; treatment: aza 0.8mg/kg BW, DC101 40mg/kg BW; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: skin; ', 'tissue: inner cell mass; treatment: 0.5% O2 16h; type of sample: ChIP; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); genotype/variation: mES-Dnmt-WT; ', 'tissue: inner cell mass; treatment: 0.5% O2 16h; type of sample: ChIP; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); genotype/variation: mES-Dnmt-TKO; ', 'tissue: murine breast tumour; treatment: 0.5% O2 16h; 1 µM DMSO; type of sample: ChIP; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); genotype/variation: 4T1-HIF1b-WT; ', 'cell line: MCF7; cell type: Beast cancer cell line; treatment: 0.5% O2 16h; type of sample: ChIP-BS; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); ', 'cell type: Embryonic Stem Cells; treatment: 0.5% O2 16h; type of sample: ChIP-BS; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); ', 'tissue source: breast; cell line: MCF7; cell type: Breast cancer cell line; treatment: DMSO 72h, 0.5% O2 16h; type of sample: Input; chip antibody: none; ', 'tissue source: breast; cell line: MCF7; cell type: Breast cancer cell line; treatment: DMSO 72h, 0.5% O2 16h; type of sample: ChIP; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); ', 'tissue source: breast; cell line: MCF7; cell type: Breast cancer cell line; treatment: 1 µM aza 72h, 0.5% O2 16h; type of sample: ChIP; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); ', 'tissue source: breast; cell line: MCF7; cell type: Breast cancer cell line; treatment: 1 µM aza 72h, 0.5% O2 16h; type of sample: Input; chip antibody: none; ', 'tissue source: kidney; cell line: RCC4; cell type: Renal cell carcinoma cell line; treatment: 0.5% O2 16h; type of sample: ChIP; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); ', 'tissue source: skin; cell line: SK-MEL-28; cell type: Melanoma cell line; treatment: 0.5% O2 16h; type of sample: ChIP; chip antibody: ARNT/HIF-1β monoclonal antibody (NB100-124, Novus); ', 'tissue source: kidney; cell line: RCC4; cell type: Renal cell carcinoma cell line; treatment: 0.5% O2 16h; type of sample: Input; chip antibody: none; ', 'tissue source: skin; cell line: SK-MEL-28; cell type: Melanoma cell line; treatment: 0.5% O2 16h; type of sample: Input; chip antibody: none; ', 'tissue: skin; cell line: SK-MEL-28; cell type: Melanoma cell line; treatment: 21% O2 24h; growth protocol: cultured at 37°C in Roswell Park Memorial Institut 1640 Medium (RPMI) 10% FBS 1% Pen Strep and 1% L-Glutamine.; ', 'tissue: skin; cell line: SK-MEL-28; cell type: Melanoma cell line; treatment: 0.5% O2 24h; growth protocol: cultured at 37°C in Roswell Park Memorial Institut 1640 Medium (RPMI) 10% FBS 1% Pen Strep and 1% L-Glutamine.; ', 'tissue: inner cell mass; cell line: mES Dnmt-WT; cell type: Embryonic Stem cells; treatment: 21% O2 24h; growth protocol: cultured feeder-free in fibroblast-conditioned medium; ', 'tissue: inner cell mass; cell line: mES Dnmt-WT; cell type: Embryonic Stem cells; treatment: 0.5% O2 24h; growth protocol: cultured feeder-free in fibroblast-conditioned medium; ', 'tissue: inner cell mass; cell line: mES Dnmt-TKO; cell type: Embryonic Stem cells; treatment: 21% O2 24h; growth protocol: cultured in 0.1% Gelatin Solution in DMEM 4,500\u2009mg\u2009/L glucose, 1% sodium pyruvate, 15% FBS, 1% Pen Strep, 0.1\u2009mM of non-essential amino acids (EmbryoMax), 50\u2009μM β-mercaptoethanol, 103\u2009U LIF ESGRO (Millipore).; ', 'tissue: inner cell mass; cell line: mES Dnmt-TKO; cell type: Embryonic Stem cells; treatment: 0.5% O2 24h; growth protocol: cultured in 0.1% Gelatin Solution in DMEM 4,500\u2009mg\u2009/L glucose, 1% sodium pyruvate, 15% FBS, 1% Pen Strep, 0.1\u2009mM of non-essential amino acids (EmbryoMax), 50\u2009μM β-mercaptoethanol, 103\u2009U LIF ESGRO (Millipore).; ', 'tissue: kidney; cell line: RCC4; cell type: Renal cell carcinoma; treatment: 21% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: kidney; cell line: RCC4; cell type: Renal cell carcinoma; treatment: 0.5% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: skin; cell line: SK-MEL-28; cell type: Melanoma cell line; treatment: 21% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: skin; cell line: SK-MEL-28; cell type: Melanoma cell line; treatment: 0.5% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; cell line: MCF7; cell type: Breast cancer cell line; treatment: 1 µM aza 72h, 21% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'tissue: breast; cell line: MCF7; cell type: Breast cancer cell line; treatment: 1 µM aza 72h, 0.5% O2 24h; growth protocol: cultured at 37°C in Dulbecco’s modified Eagle medium (DMEM) with 10% fetal bovine serum (FBS), 5ml of 100 U/ml Penicillin-Streptomycin (Pen Strep, Life Technologies) and 5ml of L-Glutamine 200mM.; ', 'oxygen status: 16 hours of 0.5% oxygen (hypoxia); cell line: SK-MEL-28; ', 'oxygen status: 16 hours of 0.5% oxygen (hypoxia); cell line: RCC4; ', 'oxygen status: 16 hours of 0.5% oxygen (hypoxia); cell line: MCF7; ' GSE72823 Mus musculus 20 Expression profiling by high throughput sequencing GPL13112 Mammary Tumor Associated RNAs impact tumor cell proliferation, invasion and migration 2015-09-09 Recent genome-wide studies revealed that only 2% of the human genome encodes for mRNAs that are translated into proteins while as much as 80% of the genome can be transcribed. Of these non-coding transcripts, long non-coding RNAs (lncRNAs) represent the largest and most diverse class, comprising almost 16,000 currently annotated transcripts in human and 10,000 in mouse. Here, we investigated the role of lncRNAs in mammary tumors by performing RNA-Seq on tumor sections and organoids derived from MMTV-PyMT and MMTV-Neu-NDL mice. We identified several hundred long non-coding transcripts that were over-expressed compared to the normal mammary epithelium. Among these potentially oncogenic lncRNAs we prioritized a subset as Mammary Tumor Associated RNAs (MaTARs) and determined their human counterparts, hMaTARs. To functionally validate the role of MaTARs, we performed antisense knockdown and observed reduced cell proliferation, invasion and/or organoid branching in a cancer-specific context. Assessing the expression of hMaTARs in human breast tumors revealed that 19 hMaTARs are significantly up-regulated and many of these correlate with breast cancer subtype and/or hormone receptor status, indicating potential clinical relevance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72823 Mammary Tumor-Associated RNAs Impact Tumor Cell Proliferation, Invasion, and Migration. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2016.08.081 {Cell reports (7.815): 10.1016/j.celrep.2016.08.081} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA295152 https://www.ebi.ac.uk/ena/browser/view/PRJNA295152 https://www.ncbi.nlm.nih.gov/sra?term=SRP063501 [Overal design]20 RNA-Seq-datasets. Mammary tumors and organoids derived from MMTV-PyMT, MMTV-Neu-NDL and MMTV-Cre;Flox-Neo-Neu-NT were compared to normal wild type mammary gland organoids.; [Treatment]'None'; [Growth]'Organoids from MMTV-PyMT tumors were prepared as described previously (Ewald AJ et al, Cold Spring Harbor Protocols, 2013) and cultured in matrigel in the presence of FGF2 for 6 days. For day 0 datasets, RNA was extratced directly after organoid preparation. For tumor sections, RNA was extratced from a homogenous, 30 µm cryo-section.'; [Extraction]'Total RNA was extracted using TRIzol reagent from both organoids and homogenized tumor tissue.\nLibraries for polyA+ RNA-Sequencing were prepared from 1 μg RNA per sample using TruSeq chemistry (Illumina)'; [Cell type]'Source: ''strain: FVB; genotype: wild type; processing: organoids; culture time: 6 days; ', 'strain: FVB; genotype: MMTV-PyMT; processing: tumor section; culture time: -; ', 'strain: FVB; genotype: MMTV-PyMT; processing: organoids; culture time: 0 days; ', 'strain: FVB; genotype: MMTV-PyMT; processing: organoids; culture time: 6 days; ', 'strain: FVB; genotype: MMTV-Neu-NDL; processing: organoids; culture time: 6 days; ', 'strain: FVB; genotype: MMTV-Cre;Flox-Neo-Neu-NT; processing: tumor section; culture time: -; ' GSE67071 Mus musculus 10 Expression profiling by high throughput sequencing GPL13112 A model of breast cancer heterogeneity reveals vascular mimicry as a driver of metastasis 2015-03-19 Cancer metastasis requires that primary tumour cells evolve the capacity to intravasate into the lymphatic system or vasculature, and extravasate into and colonize secondary sites1. Others have demonstrated that individual cells within complex populations show heterogeneity in their capacity to form secondary lesions2 5. Here we develop a polyclonal mouse model of breast tumour heterogeneity, and show that distinct clones within a mixed population display specialization, for example, dominating the primary tumour, contributing to metastatic populations, or showing tropism for entering the lymphatic or vasculature systems. We correlate these stable properties to distinct gene expression profiles. Those clones that efficiently enter the vasculature express two secreted proteins, Serpine2 and Slpi, which were necessary and sufficient to program these cells for vascular mimicry. Our data indicate that these proteins not only drive the formation of extravascular networks but also ensure their perfusion by acting as anticoagulants. We propose that vascular mimicry drives the ability of some breast tumour cells to contribute to distant metastases while simultaneously satisfying a critical need of the primary tumour to be fed by the vasculature. Enforced expression of SERPINE2 and SLPI in human breast cancer cell lines also programmed them for vascular mimicry, and SERPINE2 and SLPI were overexpressed preferentially in human patients that had lung-metastatic relapse. Thus, these two secreted proteins, and the phenotype they promote, may be broadly relevant as drivers of metastatic progression in human cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE67071 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA278860 https://www.ebi.ac.uk/ena/browser/view/PRJNA278860 https://www.ncbi.nlm.nih.gov/sra?term=SRP056340 [Overal design]RNAseq of Individual 4T1 Clonal Populations_10samples; [Treatment]'None'; [Growth]'DMEM high glucose (Life Technologies) supplemented with 5% fetal bovine serum (Thermo Scientific), 5% fetal calf serum (Thermo Scientific), non-essential amino acids (Life Technologies) and penicillin streptomycin (Life Technologies)'; [Extraction]'RNA was purified and DNAse treated using the Qiagen RNeasy Mini Kit\nThe NuGEN Ovation RNA-Seq V2 protocol was carried out on 100 ng of total RNA. cDNA was fragmented using the Covaris LE220 sonicator according to the manufacturer’s instruction to yield a target fragment size of 200 bp. The fragmented cDNA was subsequently processed using the NuGEN Ovation Ultralow DR Multiplex System.\nLibraries were analyzed on an Illumina Hiseq-2.0 using 76bp reads.'; [Cell type]'Source: ''clone: Clone 4T1-T (derived From Single Cell); treatment: shRNA Infected (shRenilla); ', 'clone: Clone 4T1-T (derived From Single Cell); treatment: shRNA Infected (shSerpine2-1); ', 'clone: Clone 4T1-T (derived From Single Cell); treatment: shRNA Infected (shSerpine2-2); ', 'clone: Clone 4T1-T (derived From Single Cell); treatment: shRNA Infected (shSlpi-1); ', 'clone: Clone 4T1-T (derived From Single Cell); treatment: shRNA Infected (shSlpi-2); ' GSE33146 Homo sapiens 6 Expression profiling by array GPL570 Expression data from DKAT breast cancer cell line pre- and post-EMT 2011-10-21 The DKAT cell line is a novel model of triple-negative breast cancer that was isolated from the pleural effusion of a 35 year-old caucasian woman with triple-negative breast cancer. When cultured in serum-free media (MEGM, Lonza) this cell line exhibits an epithelial morphology and gene expression pattern. However, when cultured in the presence of serum (SCGM, Lonza) it undergoes a reversible EMT. We used microarrays to look at gene expression changes in the DKAT cell line when cultured in Mammary Epithelial Growth Media (MEGM, where DKAT cells have an epithelial morphology) vs Stromal Cell Growth Media (SCGM, where DKAT cells have a mesenchymal morphology). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE33146 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA156601 https://www.ebi.ac.uk/ena/browser/view/PRJNA156601 None [Overal design]DKAT breast cancer cells (passage 10) grown in MEGM (Lonza) were split and cultured in T75 flasks in either in MEGM or SCGM for 14 days. RNA was isolated using Qiagen RNeasy kit and hybridization on Affymetrix microarrays was performed. Three separate cDNA reactions were performed and these were run as technical replicates.; [Treatment]'DKAT cells (passage 10) in MEGM were split and grown for 14 days either in MEGM (Lonza) or SCGM (Lonza) in adherent culture.'; [Growth]'DKAT cells (passage 10) in MEGM were split and grown for 14 days either in MEGM (Lonza) or SCGM (Lonza) in adherent culture.'; [Extraction]"Extraction of total RNA was performed using the Qiagen RNeasy kit according to the manufacturer's instructions with option DNAse step."; [Cell type]'Source: ''cell line: Human breast cancer-derived cell line DKAT; culture medium: MEGM; ', 'cell line: Human breast cancer-derived cell line DKAT; culture medium: SCGM; ' GSE81941 Mus musculus 4 Expression profiling by high throughput sequencing GPL17021 Impact of HGFL-Ron signaling on breast cancer stem cell transcriptomic profiles. 2016-05-26 Introduction: HGFL-Ron signaling is augmented in human breast cancer and is associated with poor overall prognosis. Here, we investigate the role of HGFL-Ron signaling in murine breast cancer stem cells (BCSC) through characterization of BCSC transcriptomes through RNA-sequencing, focusing on the impact of Ron knockdown through a short hairpin construct. Methods:R7 breas cancer cell lines were drived from mammary tumors in transgenic MMTV_Ron mice. They were sorted based on expression of cell surface markers indicative of lineage negative, CD29hi and CD24+ cells. Bulk R7, sorted cells, and sorted cells treated with shRon were submitted for transcriptomic characterization on the Illumina HiSeq 2500. High quality reads were aligned to the mm9 genome and quantified to generate RPKM. Results: Approximately 30 million reads were aligned to the mouse genome in each sample which corresponded to over 36000 transcripts. Of these, ~16000 were included in analysis. Conclusions: Differential expression analysis indicated that depletion of Ron markely reduces mammosphere formation and self-renewal, and highlighted by the decrease in B-catenin and NFKB pathways. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE81941 HGFL-mediated RON signaling supports breast cancer stem cell phenotypes via activation of non-canonical β-catenin signaling. Oncotarget None https://doi.org/10.18632/oncotarget.19441 {Oncotarget (None): 10.18632/oncotarget.19441} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA323477 https://www.ebi.ac.uk/ena/browser/view/PRJNA323477 https://www.ncbi.nlm.nih.gov/sra?term=SRP075767 [Overal design]Transcriptome profiles of bulk and sorted R7 BCSCs with Ron knockdown through RNA-sequencing.; [Treatment]'R7 cells were sorted based on the following: Lin-CD29HiCD24+. Experimental conditions included bulk R7 parental BCSCs, sorted BCSCs, and sorted BCSCs treated with a short hairpin construct targeting and knocking down Ron.'; [Growth]'R7 murine breast cancer cell lines were derived from a mammary tumor from a transgenic MMTV_Ron mouse.'; [Extraction]'Total RNA was extracted from BCSCs using the TRIZOL method\nIllumina HiSeq2500', 'Total RNA was extracted from BCSCs using the TRIZOL method'; [Cell type]'Bulk', 'Lin-CD29HiCD24+ sorted''cell type: Bulk; cell line: R7; ', 'cell type: Lin-CD29HiCD24+ sorted; cell line: R7; ', 'cell type: Lin-CD29HiCD24+ sorted; genotype/variation: shRon knockdown; cell line: R7; ', 'cell type: Lin-CD29HiCD24+ sorted; treatment: shHGFL; source: Breast cancer stem cells; ' GSE95165 Homo sapiens 12 Expression profiling by array GPL10558 LSD1 maintains mammary luminal cell differentiation and suppresses luminal breast cancer cell invasion 2017-02-22 LSD1 (KDM1A) is a histone demethylase that plays both oncogenic and tumor suppressor roles in breast cancer. However, the exact contexts under which it plays these opposite roles remain largely elusive. By characterizing its role in normal and cancerous luminal mammary epithelial cells (MECs), here we show that LSD1 is essential for maintaining differentiation and survival of luminal cells. LSD1-inhibition by both genetic and pharmacological approaches increases invasion of luminal breast cancer cells. Mechanistically, we find LSD1 interacts with GATA3 and their common target genes are highly related to breast cancer. LSD1 positively regulates GATA3 expression and represses that of TRIM37, a histone H2A ubiquitin ligase and breast cancer oncoprotein. LSD1-loss leads to reduced expression of several cell junction genes (e.g., CDH1, VCL, CTNNA1), possibly via TRIM37-mediated repression. Collectively, our data suggest LSD1 largely plays a tumor suppressor role in luminal breast cancer and the increased MEC invasiveness associated with LSD1-inhibition can be blocked via TRIM37-inhibition. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95165 LSD1 suppresses invasion, migration and metastasis of luminal breast cancer cells via activation of GATA3 and repression of TRIM37 expression. Oncogene 6.634 https://doi.org/10.1038/s41388-019-0923-2 {Oncogene (6.634): 10.1038/s41388-019-0923-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA376261 https://www.ebi.ac.uk/ena/browser/view/PRJNA376261 None [Overal design]Total RNA obtained from MCF7 cells treated with either LSD1 siRNA, or GATA3 siRNA, or ESR1 siRNA compared to that from MCF7 cells treated with nonspecific control siRNA.; [Treatment]'Small interfering RNA (siRNA) (Human GATA3 or LSD1 or ESR1 SMARTpool, Dharmacon) and nonspecific control siRNA were obtained from Invitrogen (California, USA) and transfected into MCF7 cells using Lipofectamine RNAiMAX (Invitrogen)'; [Growth]'MCF7 cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) (Gibco) supplemented with 10% fetal bovine serum (FBS), 100 IU/ml penicillin/streptomycin'; [Extraction]'Total RNA samples from three independent biological replicates were extracted using RNA Extraction kit (Invitrogen)'; [Cell type]'ER+ luminal breast cancer cell''sirna: control siRNA; cell type: ER+ luminal breast cancer cell; cell line: MCF7; ', 'sirna: LSD1 siRNA; cell type: ER+ luminal breast cancer cell; cell line: MCF7; ', 'sirna: GATA3 siRNA; cell type: ER+ luminal breast cancer cell; cell line: MCF7; ', 'sirna: ESR1 siRNA; cell type: ER+ luminal breast cancer cell; cell line: MCF7; ' GSE96637 Homo sapiens 6 Expression profiling by high throughput sequencing GPL11154 Knock-down of Ror1 in MDA-MB-231 cell line decreases cell invasiveness 2017-03-15 RNA-Seq profiling of triple-negative MDA-MB-231 cell line with know-down of non-canonical WNT signaling receptor Ror1. The MDA-MB231 cells were either transfected with a non-sense control shRNA (shCTL) or with a ROR1 shRNA (shROR1) construct. The objective was to find expression-responsive targets of these perturbations as potential drivers of MDA-MB231 cell invasiveness. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE96637 Ror2 Signaling and Its Relevance in Breast Cancer Progression. Frontiers in oncology 4.137 https://doi.org/10.3389/fonc.2017.00135 {Frontiers in oncology (4.137): 10.3389/fonc.2017.00135} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA379273 https://www.ebi.ac.uk/ena/browser/view/PRJNA379273 https://www.ncbi.nlm.nih.gov/sra?term=SRP101934 [Overal design]Two conditions of MDA-MB-231 cells each in 3 replicates: 1. non-sense control shRNA (shCTL), 2. ROR1 shRNA (shROR1); [Treatment]'For ROR1 knockdown, MDA-MB231 cells were co-transfected with the packaging plasmids pMD2.G (Addgene plasmid 12259) and pCMVΔR8.2 (Addgene plasmid 12263, both provided by Didier Trono, École Polytechnique Fédéral de Lausanne, Lausanne, Switzerland) and either the pGIPZ shCTL or shROR1 vector (Thermo Scientific, Schwerte, Germany) through calcium phosphate precipitation. Virus-containing supernatants were concentrated using the lentiviral enrichment reagent (MoBiTech, Göttingen, Germany) and cells transfected with a MOI of 5.0. Stable expression was achieved by selecting for puromycin (2 µg/ml) resistance.'; [Growth]'The human breast cancer cell line MDA-MB231 was purchased from ATCC (Rockville, USA) and was cultured in RPMI-1640 media (PAA, Coelbe, Germany) supplemented with 10% heat-inactivated fetal bovine serum (FCS; Sigma, Munich, Germany).'; [Extraction]'RNA was isolated using Trizol reagent including a DNase I (Roche, Mannheim, Germany) digestion step.\nLibrary preparation for RNA-Seq was performed using the TruSeq Stranded Sample Preparation Kit (Illumina, RS-122-2201) starting from 1000 ng of total RNA. Accurate quantitation of cDNA libraries was performed using the QuantiFluor TM dsDNA System (Promega). The size range of nal cDNA libraries was determined applying the SS-NGS-Fragment 1-6000 bp Kit on the Fragment Analyzer from Advanced Analytical (320 bp). cDNA libraries were amplied and sequenced by using the cBot and the HiSeq2000 from Illumina (SR; 50 bp; 35 million reads per sample).'; [Cell type]'breast cancer''cell line: MDA-MB-231; cell type: breast cancer; ' GSE31892 Homo sapiens 42 Genome variation profiling by SNP array GPL13270 Identification of copy number alterations associated with the progression of DCIS to Invasive Ductal Carcinoma 2011-09-06 Ductal carcinoma in situ (DCIS) is a non-obligate precursor to invasive ductal carcinoma (IDC). Annotation of the genetic differences between the two lesions may assist in the identification of genes that promote the invasive phenotype. Matched IDC and DCIS showed highly similar copy number profiles (average of 83% of the genome shared) indicating a common clonal orgin although there is evidence that the DCIS continues to evolve in parallel with the co-existing IDC. Four chromosomal regions of loss (3q, 6q, 8p and 11q) and four regions of gain (5q, 16p, 19q and 20) were recurrently affected in IDC but not in DCIS. CCND1 and MYC showed increased amplitude of gain in IDC. One region of loss (17p11.2) was specific to DCIS. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE31892 Identification of copy number alterations associated with the progression of DCIS to invasive ductal carcinoma. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-011-1835-1 {Breast cancer research and treatment (3.471): 10.1007/s10549-011-1835-1} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA145225 https://www.ebi.ac.uk/ena/browser/view/PRJNA145225 None [Overal design]21 cases of synchronous DCIS and IDC were microdissected from FFPE tissue and analysed by molecular inversion probe (MIP) copy number arrays. The arrays were early release OncoScan arrays and the data in this submission are CN values for the ~300,000 probes common to two batches performed. Raw data is retained by Affymetrix.; [Treatment]'retrospective cases received standard care'; [Growth]'None'; [Extraction]'up to 20x 10 micron FFPE sections were needle microdissected for epithelial cells. Total genomic DNA was isolated using the DNeasy Blood and Tissue Kit (Qiagen) using a modified protocol: Wu L, Patten N, Yamashiro CT, Chui B (2002) Extraction and amplification of DNA from formalin-fixed, paraffin-embedded tissues. Appl Immunohistochem Mol Morphol 10 (3):269-274'; [Cell type]'Source: ''grade: High; er status: Negative; ', 'grade: Intermediate; er status: Negative; ', 'grade: Intermediate; er status: Positive; ', 'grade: Low; er status: Positive; ', 'grade: Low; er status: Negative; ', 'grade: High; er status: Positive; ' GSE159680 Homo sapiens 12 SNP genotyping by SNP array GPL29257 Spontaneous Cell Fusions as a Mechanism of Parasexual Recombination in Tumor Cell Populations. [2] 2020-10-20 Initiation and progression of cancers reflect the underlying process of somatic evolution, which follows a Darwinian logic, i.e., diversification of heritable phenotypes provides a substrate for natural selection, resulting in the outgrowth of the most fit subpopulations. Although somatic evolution can tap into multiple sources of diversification, it is assumed to lack access to (para)sexual recombination – a key diversification mechanism throughout all strata of life. Based on observations of spontaneous fusions involving cancer cells, reported genetic instability of polypoid cells, and precedence of fusion-mediated parasexual recombination in fungi, we asked whether cell fusions could serve as a source of parasexual recombination in cancer cell populations. Using differentially labelled tumor cells, we found evidence of low-frequency, spontaneous cell fusions between carcinoma cells in multiple cell line models of breast cancer both in vitro and in vivo. While some hybrids remained polyploid, many displayed partial ploidy reduction, generating diverse progeny with heterogeneous inheritance of parental alleles, indicative of partial recombination. Hybrid cells also displayed elevated levels of phenotypic plasticity, which may further amplify the impact of cell fusions on the diversification of phenotypic traits. Using mathematical modeling, we demonstrated that the observed rates of spontaneous somatic cell fusions may enable populations of tumor cells to amplify clonal heterogeneity, thus facilitating the exploration of larger areas of the adaptive landscape, relative to strictly asexual populations, which may substantially accelerate a tumor’s ability to adapt to new selective pressures. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE159680 Spontaneous cell fusions as a mechanism of parasexual recombination in tumour cell populations. Nature ecology & evolution 10.965 https://doi.org/10.1038/s41559-020-01367-y {Nature ecology & evolution (10.965): 10.1038/s41559-020-01367-y} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA670185 https://www.ebi.ac.uk/ena/browser/view/PRJNA670185 None [Overal design]Illumina CytoNP arrays were performed according to the manufacturer's protocol. DNA was extracted from frosen cell pellet using Quiagen DNAeasy kit. 12 samples were analysed: 8 subclones of hybrid between SUM159 and MDA231 cell lines, 2 bulk samples from passage 3 ans passage 8 of hybrid SUM159-MDA231 cells. Parental cell lines: MDA231, SUM159. Cell were grown in correcponding media before collecting the samples, no treatment was applied.; [Treatment]'None'; [Growth]'Cell were grown in the corresponding media in standard conditions'; [Extraction]'Quiagen DNAeasy'; [Cell type]'cell line''cell line: SUM159PT; cell type: cell line; sample group: G1; ', 'cell line: SUM159PT; cell type: cell line; sample group: G2; ', 'cell line: MDA-MB-231; cell type: cell line; sample group: G3; ', 'cell line: MDA-MB-231; cell type: cell line; sample group: G4; ', 'cell line: hybrid between SUM159PT and MDA-MB-231; cell type: cell line; sample group: G5; ', 'cell line: hybrid between SUM159PT and MDA-MB-231; cell type: cell line; sample group: G6; ', 'cell line: hybrid between SUM159PT and MDA-MB-231; cell type: cell line; sample group: G7; ', 'cell line: hybrid between MDA-MB-231 and SUM159PT; cell type: cell line; sample group: G8; ', 'cell line: hybrid between MDA-MB-231 and SUM159PT; cell type: cell line; sample group: G9; ', 'cell line: hybrid between MDA-MB-231 and SUM159PT; cell type: cell line; sample group: G10; ', 'cell line: MCFDCIS; cell type: cell line; sample group: G11; ', 'cell line: hybrid between MCFDCIS and SUM159; cell type: cell line; sample group: G12; ' GSE66082 Homo sapiens 12 Expression profiling by array; Third-party reanalysis GPL17811 Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth [gene expression] 2015-02-19 The goal of this study was to identify YAP/TAZ direct transcriptional targets and transcriptional partners, through ChIP-sequencing and gene expression profiling. Keywords: Expression profiling by array https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE66082 Genome-wide association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth. Nature cell biology 17.728 https://doi.org/10.1038/ncb3216 {Nature cell biology (17.728): 10.1038/ncb3216} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA275843 https://www.ebi.ac.uk/ena/browser/view/PRJNA275843 None [Overal design]MDA-MB-231 cells growing at low confluence in standard growth conditions were transfected with the indicated siRNAs (Dupont et al., Nature 2011). The following day, growth medium was renewed and cells were incubated for 24 more hours, and then harvested for total RNA extraction. 4 independent biological replicates were plated, transfected and harvested in parallel for each siRNA. Raw .CEL files are the same as in GSE59230 (Enzo et al., EMBO J 2015), but gene expression levels have been quantified using Brainarray HGU133Plus2_Hs_ENTREZG_v17 custom chip definition files.; [Treatment]"Cells were transfected on day 2 with siRNA oligonucleotides (final concentration 33nM) by using RNAi MAX (Life Technologies), following a direct transfection protocol as indicated by manifacturer's instructions. On day 3, medium was renewed. On day 4, cells were washed with 1XHBSS and harvested for RNA extraction."; [Growth]'Cells were seeded at low confluence on day 1 in standard growth medium (DMEM/F12 with 2mM Glutamine, 17.5mM D-glucose, without antibiotics, 10% Fetal Bovine Serum).'; [Extraction]"Trizol extraction of total RNA, followed by DNAseI digestion to reduce genomic DNA contaminations, was performed according to the manufacturer's instructions."; [Cell type]'breast cancer''cell line: MDA-MB-231; cell type: breast cancer; transfection construct: Control siRNA; ', 'cell line: MDA-MB-231; cell type: breast cancer; transfection construct: YAP/TAZ siRNA #1; ', 'cell line: MDA-MB-231; cell type: breast cancer; transfection construct: YAP/TAZ siRNA #2; ' GSE40617 Homo sapiens 6 Non-coding RNA profiling by high throughput sequencing GPL10999 iMir: An integrated pipeline for high-throughput miRNA-Seq data analysis 2012-09-05 We report a novel modular pipeline (iMir) for comprehensive analysis of miRNA-Seq data, from linker removal and sequence quality check to differential expression and biological target prediction, integrating multiple open source modules and resources linker together in an automated flow. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE40617 iMir: an integrated pipeline for high-throughput analysis of small non-coding RNA data obtained by smallRNA-Seq. BMC bioinformatics 2.511 https://doi.org/10.1186/1471-2105-14-362 {BMC bioinformatics (2.511): 10.1186/1471-2105-14-362} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA174404 https://www.ebi.ac.uk/ena/browser/view/PRJNA174404 https://www.ncbi.nlm.nih.gov/sra?term=SRP015409 [Overal design]Development of an integrated pipeline (iMir) for comprehensive analysis of miRNA-Seq experiment.; [Treatment]'None'; [Growth]'MCF-7 cells were either maintained in Dulbecco’s modified Eagle medium (DMEM) supplemented with 10% FBS, antibiotics (100U/ml penicillin, 100mg/ml streptomycin, 250ng/ml Amfotericin-B), 50µg/ml G418 (standard growth conditions) or hormone deprived (starvation). Starvation was performed by culturing in DMEM w/o phenol red and 5% Dextran Coated Charcoal stripped serum (DCC-FBS) for 5 days, as described earlier.'; [Extraction]'Total RNA was extracted from MCF-7 wt using the standard RNA Extraction method with TRI Reagent (Sigma) method. 7.5μg of total RNA was used in a library preparation according to the Illumina TruSeq small RNA sample preparation protocol.'; [Cell type]'breast cancer''cell line: MCF-7; cell type: breast cancer; ' GSE29137 Homo sapiens 24 Expression profiling by array GPL570 Numb variant specific transcriptome analysis 2011-05-09 Numb has 4 known variants and we are reporting two novel Numb variants, Numb5 and Numb6 in this study. The metastaticability variations between the numb variants were evaulated through the transcriptome. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE29137 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA140339 https://www.ebi.ac.uk/ena/browser/view/PRJNA140339 None [Overal design]breast cancer cells were transfected with GFP-Numb4, GFP-Numb5, GFP-Numb6 or GFP-only vectors and their transcriptome were assessed on Affymetrix platform; [Treatment]'cells were transfected with CMV-GFP vector inserted with null, Numb4, Numb5 or Numb6 plasmid.'; [Growth]'MCF7 cells were cultured withDMEM/F12, plus 10% FBS and 0.01 mg/ml bovine insulin. MDA-MB-231 cells were cultured with alpha modified MEM medium plus 10% FBS. Both cells were add 1% penicollin/streptomycin. Both cells with stably transfections were added 0.5 mg/ml of G418. Atmosphere: air, 95%; carbon dioxide (CO2), 5% Temperature: 37.0°C'; [Extraction]'Total RNA was isolated with Trizol. RNA quality was checked on Agilent Bioanalyzer. All samples used for microarray analysis have high quality score (RIN >9).'; [Cell type]'Source: ''cell line: MCF7; transfection: GFP vector control; ', 'cell line: MCF7; transfection: GFP-Numb4 Transfected; ', 'cell line: MCF7; transfection: GFP-Numb5 Transfected; ', 'cell line: MCF7; transfection: GFP-Numb6 Transfected; ', 'cell line: MDA-MB-231; transfection: GFP vector control; ', 'cell line: MDA-MB-231; transfection: GFP-Numb4 Transfected; ', 'cell line: MDA-MB-231; transfection: GFP-Numb5 Transfected; ', 'cell line: MDA-MB-231; transfection: GFP-Numb6 Transfected; ' GSE107692 Homo sapiens 12 Expression profiling by high throughput sequencing GPL18573 siRNA-mediated silencing of ORAI3 in MDA-MB-468 breast cancer cells exposed to hypoxia 2017-12-05 Analysis of the effect of siRNA-mediated silencing of ORAI3 in MDA-MB-468 basal-like breast cancer cells exposed to 48 and 72 h hypoxia https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE107692 ORAI1 and ORAI3 in Breast Cancer Molecular Subtypes and the Identification of ORAI3 as a Hypoxia Sensitive Gene and a Regulator of Hypoxia Responses. Cancers 6.162 https://doi.org/10.3390/cancers11020208 {Cancers (6.162): 10.3390/cancers11020208} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA421090 https://www.ebi.ac.uk/ena/browser/view/PRJNA421090 https://www.ncbi.nlm.nih.gov/sra?term=SRP126141 [Overal design]MDA-MB-468 cells were seeded in 96-well plates. Post plating (24 h), cells were transfected with siRNA for 48 h. Cells were then serum starved (0.5% FBS) for 24 h and exposed to hypoxic conditions (1% O2) for the indicated time-points. Total RNA was isolated and purified using an RNeasy Plus Mini Kit. Three independent biological replicates were collected for each treatment.; [Treatment]'Cells were seeded at 6000 (for 48 h hypoxia) and 3500 (for 72 h hypoxia) per well in 96-well plates. Post seeding (24 h), cells were transfected with siRNA for 48 h. DharmaFECT4 Transfection Reagent (0.1 µL per well) and Dharmacon ON-TARGETplus SMARTpool siRNAs (Thermo Scientific, Waltham, MA, USA) were used for silencing ORAI3 (L-015896-00). Non-targeting siRNA (siNT; D-001810-10) was used as control treatment. Cells were then serum starved (0.5% FBS) for 24 h and exposed to hypoxic conditions (1% O2) for 48 h or 72 h.'; [Growth]'The MDA-MB-468 cell line was obtained from The Brisbane Breast Bank, UQCCR, Brisbane, QLD, Australia and maintained in Dulbecco’s Modified Eagle’s Medium (DMEM) with high glucose (Sigma-Aldrich, St Louise, MO, USA), supplemented with 4 mM L-glutamine 10% fetal bovine serum (FBS).'; [Extraction]'Total RNA was isolated and purified using an RNeasy Plus Mini Kit (74134; Qiagen). mRNA integrity was assessed on a Agilent 2100 Bioanalyzer, and were of high quality (RNA integrity numbers [RIN] of 8.7-9.2).\nTruSEQ Stranded Total RNA'; [Cell type]'basal-like breast cancer cells''cell line: MDA-MB-468; cell type: basal-like breast cancer cells; transfected with: Non-targeting siRNA (siNT); exposed to: hypoxic conditions (1% O2) for 48hrs; ', 'cell line: MDA-MB-468; cell type: basal-like breast cancer cells; transfected with: siRNAs silencing ORAI3 (siORAI3); exposed to: hypoxic conditions (1% O2) for 48hrs; ', 'cell line: MDA-MB-468; cell type: basal-like breast cancer cells; transfected with: Non-targeting siRNA (siNT); exposed to: hypoxic conditions (1% O2) for 72hrs; ', 'cell line: MDA-MB-468; cell type: basal-like breast cancer cells; transfected with: siRNAs silencing ORAI3 (siORAI3); exposed to: hypoxic conditions (1% O2) for 72hrs; ' GSE113255 Homo sapiens 140 Expression profiling by high throughput sequencing GPL18573 Gene expression profiling study to identify distinct subtypes in diffuse type gastric cancer 2018-04-17 Although recent advances in high-throughput technology have provided many insights into gastric cancer (GC), few reliable biomarkers for handling diffuse type GC are identified. Here, we aim to identify a signature classifying high risk diffuse type GC. To identify molecular subtypes of diffuse type GC, we generated RNA-seq based transcriptome data, which were generated using normal mucosa and tumor cells from 140 fresh frozen tissues including diffuse type GCs (n = 107). Unsupervised hierarchical cluster analysis of the RNA-seq data revealed three distinct subgroups of GC. Based on these subtypes, we generated a signature reflecting the best characteristics of aggressive diffuse type GC. When estimating prognostic value, the signature showed a strong prediction ability and an independent clinical utility in diffuse type GC patients. Our signature represents a promising diagnostic tool for the identification of diffuse type GC patients that have a high risk of poor clinical behavior. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113255 Identification of a molecular signature of prognostic subtypes in diffuse-type gastric cancer. Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association 5.554 https://doi.org/10.1007/s10120-019-01029-4 {Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association (5.554): 10.1007/s10120-019-01029-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA450596 https://www.ebi.ac.uk/ena/browser/view/PRJNA450596 https://www.ncbi.nlm.nih.gov/sra?term=SRP140636 [Overal design]RNA-seq data of 140 fresh frozen tissues including diffuse type gastric cancer tissues (n = 107), intestinal type gastric cancer tissue (n = 23) and normal gastric tissues (n = 10) were generated. Total RNA was isolated by RNeasy Mini Kit (Qiagen, CA, USA), according to the manufacturer's protocol. The quality and integrity of the RNA were confirmed by agarose gel electrophoresis and ethidium bromide staining, followed by visual examination under ultraviolet light. Sequencing library was prepared using TruSeq RNA Sample Preparation kit v2 (Illumina, CA, USA) according to the manufacturer’s protocols. Briefly, mRNA was purified from total RNA using poly-T oligo-attached magnetic beads, fragmented, and converted into cDNAs. Then, adapters were ligated and the fragments were amplified on a PCR. Sequencing was performed in paired end reads (2x75 bp) using NextSeq 500 platform (Illumina).; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was isolated by RNeasy Mini Kit (Qiagen, CA, USA), according to the manufacturer's protocol. The quality and integrity of the RNA were confirmed by agarose gel electrophoresis and ethidium bromide staining, followed by visual examination under ultraviolet light.\nSequencing library was prepared using TruSeq RNA Sample Preparation kit v2 (Illumina, CA, USA) according to the manufacturer’s protocols. Briefly, mRNA was purified from total RNA using poly-T oligo-attached magnetic beads, fragmented, and converted into cDNAs. Then, adapters were ligated and the fragments were amplified on a PCR."; [Cell type]'Source: ''tissue: gastric cancer; cancer type: intestinal type; age: 53; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 81; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 89; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 44; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 81; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 86; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 48; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: normal intestinal mucosae; cancer type: n/a; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 74; gender: M; histologic type: papillary; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 70; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 58; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 65; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 78; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 79; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 73; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 56; gender: M; histologic type: mucinous adenocarcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 52; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 71; gender: M; histologic type: papillary adenocarcinoma; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 61; gender: M; histologic type: Medullary carcinoma; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 52; gender: M; histologic type: Medullary carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 46; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 74; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 52; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 80; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 55; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 65; gender: F; histologic type: adenocarcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 57; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 54; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 63; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 51; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 68; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 55; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 72; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 65; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 64; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 44; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 67; gender: M; histologic type: mucinous adenocarcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 46; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 34; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 56; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 75; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 42; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 75; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 55; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 68; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 56; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 48; gender: F; histologic type: mucinous adenocarcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 67; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 25; gender: F; histologic type: mucinous adenocarcinoma; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 66; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 80; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 60; gender: M; histologic type: papillary adenocarcinoma; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 60; gender: M; histologic type: invasive ductal carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 66; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 70; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 59; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 59; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 77; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 60; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 52; gender: M; histologic type: papillary adenocarcinoma; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 44; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 72; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 35; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: intestinal type; age: 77; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 59; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 80; gender: M; histologic type: mucinous adenocarcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 75; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 66; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 45; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 62; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 71; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 40; gender: M; histologic type: mucinous adenocarcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 43; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 57; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 63; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 48; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 84; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 51; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 49; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 78; gender: M; histologic type: mucinous adenocarcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 77; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 72; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 59; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 72; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 50; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 53; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 66; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 56; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 78; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 61; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 51; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 52; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 73; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 53; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 51; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 69; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 69; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 81; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 82; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 36; gender: F; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 85; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 36; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 76; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 48; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 71; gender: M; histologic type: poorly cohesive carcinoma; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 83; gender: F; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 67; gender: M; histologic type: poorly differentiated; ', 'tissue: gastric cancer; cancer type: diffuse type; age: 46; gender: M; histologic type: poorly differentiated; ' GSE35206 Mus musculus 14 Expression profiling by array GPL1261 Specific transcriptional response of four blockers of estrogen receptors on estradiol-modulated genes in the mouse mammary gland 2012-01-19 The efficacy and exceptionally good tolerance of estrogen blockade in the treatment of breast cancer is well recognized but novel agents are required, especially to take advantage of the multiple consecutive responses obtained in breast cancer progressing following previous hormone therapy, thus delaying the use of cytotoxic chemotherapy with its usually serious side effects. Acolbifene (ACOL) is a novel and unique antiestrogen completely free of estrogen-like activity in both the mammary gland and uterus while preventing bone loss. From the preclinical and clinical data so-far available, this new antiestrogen represents a unique opportunity for a highly potent and specific blockade of estrogen action in the mammary gland and uterus while exerting estrogen-like beneficial effects in other tissues (selective estrogen receptor modulator or SERM activity). In order to better understand the specificity of action of acolbifene, we have used Affymetrix GeneChips containing 45,000 probe sets to analyze 34,000 genes to determine the specificity of this compound compared to the pure antiestrogen fulvestrant, as well as the mixed antagonists/agonists tamoxifen and raloxifene to block the effect of estradiol (E2) and to induce effects of their own on gene expression in the mouse mammary gland. The genes modulated by E2 were those identified in two separate experiments and validated by quantitative real-time PCR (Q_RT-PCR). Three hours after the single subcutaneous injection of E2 (0.05 ug), the simultaneous administration of acolbifene, fulvestrant, tamoxifen and raloxifene blocked by 98%, 62%, 43% and 92% the number of E2-upregulated genes, respectively. On the other hand, 70%, 10%, 25% and 55% of the genes down-regulated by E2 were blocked by the same compounds. Acolbifene was also the compound which, when used alone, modulated the smallest number of genes also influenced by E2, namely 4%, thus possibly explaining the potent tumoricidal action of this compound in human breast cancer xenografts where 61% of tumors disappeared, thus bringing a new paradigm in the hormonal therapy of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE35206 Specific transcriptional response of four blockers of estrogen receptors on estradiol-modulated genes in the mouse mammary gland. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-012-2104-7 {Breast cancer research and treatment (3.471): 10.1007/s10549-012-2104-7} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA150697 https://www.ebi.ac.uk/ena/browser/view/PRJNA150697 None [Overal design]Female C57BL6 mice were ovariectomized (OVX). One week after OVX, mice were treated with EM-652.HCl (acolbifene), tamoxifen citrate, raloxifene or ICI 182780 (fulvestrant). Compounds were administered to OVX mice or to OVX mice simultaneously treated with 17b-estradiol (E2). Control groups received an injection of the vehicle alone. All animals were sacrificed after 3h of treatment.Mammary glands from all mice of the same group were collected and pooled. Total mRNA was isolated and converted to biotinylated cRNA.A microarray analysis was performed using Murine U74Av2 Affymetrix microarrays.; [Treatment]'EM-652.HCl (acolbifene), tamoxifen citrate, raloxifene or ICI\xa0182780 (fulvestrant), were administered to ovariectomized (OVX) mice or to OVX mice simultaneously treated with 17b-estradiol (E2; 0.05\xa0mg/mouse; single sc injection). Mice from the OVX control group received an injection of the vehicle alone. All animals were sacrificed 3h after treatment.'; [Growth]'Eleven to twelve week-old female C57BL6 mice obtained from Harlan Sprague Dawley (Indianapolis, IN) were allowed to acclimatate for 1 week after their arrival. Animals weighing between 17 to 23 g (average of 20g) were randomized according to their body weights and were assigned to experimental groups of 8 animals each. Ovariectomy was performed under isoflurane-induced anesthesia 7\xa0days prior to treatment.'; [Extraction]'Mammary glands from all mice of the same group were collected, rapidly trimmed, snap-frozen in liquid nitrogen and stored at -80°C until mRNA extraction. Total mRNA was isolated with TRIzol (Invitrogen, Burlington, Ontario) following the manufacturer’s protocol.'; [Cell type]'Source: ''strain: C57BL/6; treatment: vehicle; tissue: Mammary gland; ', 'strain: C57BL/6; treatment: estradiol; tissue: Mammary gland; ', 'strain: C57BL/6; treatment: acolbifene; tissue: Mammary gland; ', 'strain: C57BL/6; treatment: estradiol plus acolbifene; tissue: Mammary gland; ', 'strain: C57BL/6; treatment: tamoxifen; tissue: Mammary gland; ', 'strain: C57BL/6; treatment: raloxifen; tissue: Mammary gland; ', 'strain: C57BL/6; treatment: estradiol plus fulvestrant; tissue: Mammary gland; ', 'strain: C57BL/6; treatment: estradiol plus raloxifen; tissue: Mammary gland; ', 'strain: C57BL/6; treatment: estradiol plus tamoxifen; tissue: Mammary gland; ', 'strain: C57BL/6; treatment: fulvestrant; tissue: Mammary gland; ' GSE97481 Homo sapiens 12 Genome binding/occupancy profiling by high throughput sequencing GPL11154 ChIP-seq analysis of H3K4me3 and H3K27ac localization in breast cancer cells treated with a novel KDM5 inhibitor, , 5-aza-2' Deoxycytidine, or both 2017-04-06 Recently, the H3K4 demethylase, KDM5B, was shown to be amplified and overexpressed in luminal breast cancer, suggesting it might constitute a potential cancer therapy target. Here, we characterize, in breast cancer cells, the molecular effects of a recently developed small-molecule inhibitor of the KDM5 family of proteins, either alone, or in combination with the DNA demethylating agent 5-aza-2’ deoxycytidine (DAC). Alone, the KDM5 inhibitor (KDM5i) increased expression of a small number of genes, but when combined with DAC, the drug enhanced the effects of the latter for increasing expression of hundreds of DAC responsive genes. ChIP-seq studies revealed that KDM5i resulted in the broadening of existing, and creation of thousands of new H3K4me3 domains. When compared to DAC alone, increased promoter and gene body H3K4me3 occupancy at DAC responsive genes was observed in cells treated with the drug combination. Importantly, treatment with either DAC or DAC+KDM5i induced a dramatic increase in H3K27ac at enhancers with an associated significant increase in target gene expression, suggesting a previously unappreciated effect of DAC on transcriptional regulation. Finally, we found that KDM5i could synergize with DAC to reduce the viability of luminal breast cancer cells in in-vitro assays. Our study provides the first look into the molecular effects of novel KDM5i compounds and suggests that combining these with DAC may represent an exciting new approach to epigenetic therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE97481 A KDM5 Inhibitor Increases Global H3K4 Trimethylation Occupancy and Enhances the Biological Efficacy of 5-Aza-2'-Deoxycytidine. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-17-1453 {Cancer research (8.378): 10.1158/0008-5472.CAN-17-1453} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA381955 https://www.ebi.ac.uk/ena/browser/view/PRJNA381955 https://www.ncbi.nlm.nih.gov/sra?term=SRP103237 [Overal design]MCF-7 cells were treated with either a mock treatment, KDM5 inhibitor (CPI-455), DAC, or both. Cells were treated with either DAC or treament mock for 3 days, followed by 3 days of KDM5i or treatment mock. Cells were fixed and chromatin was isolated immediately following this treatment. H3K4me3 and H3K27ac localization was determined by ChIP-seq; [Treatment]'MCF-7 cells were treated with either 62.5 nM DAC or treament mock for 3 days, followed by 3 days of 9.375 uM KDM5i or treatment mock. Cells were fixed and chromatin was isolated immediately following this treatment. H3K4me3 and H3K27ac localization was determined by ChIP-seq'; [Growth]'standard as recommended by ATCC'; [Extraction]'ChIP DNA was prepared as described previously by our group (O’Hagan et al. 2011). Briefly, following drug treatment, cells were crosslinked with 37% formaldehyde and nuclei were subsequently extracted. Nuclear lysate was sonicated on Diagenode Bioruptor until majority of chromatin fragments were in the 100-300 bp range. Antibodies were incubated with sonicated chromatin overnight at 4°C, followed by capturing primary antibodies by adding ProteinA/G magnetic beads (DynaBeads) and incubating at room temperature for 3 hrs. Captured antibody complexes were then washed with low and hi-salt buffers. Chromatin was eluted off of the beads in elution buffer and cross-linking was reversed with an overnight incubation at 65°C. Chromatin fragments were then incubated with Rnase A for 1 hr at 37°C, and then Proteinase-K for 2 hrs at 55°C.\nLibraries were constructed according to the protocol provided by Illumina’s TruSeq DNA Sample Preparation v2 Kit'; [Cell type]'Source: ''cell line: MCF-7 Breast adenocarcinoma cell line; chip antibody: Input; ', 'cell line: MCF-7 Breast adenocarcinoma cell line; chip antibody: anti-trimethyl Histone H3K4 (Millipore #07-473); ', 'cell line: MCF-7 Breast adenocarcinoma cell line; chip antibody: anti-acetyl H3K27 (abcam #ab4729).; ' GSE41998 Homo sapiens 279 Expression profiling by array GPL571 Biomarker analysis of neoadjuvant Doxorubicin/Cyclophosphamide followed by Ixabepilone or Paclitaxel in early-stage breast cancer 2012-11-02 A randomized, open-label, multicenter, phase II trial (NCT00455533) enrolled previously untreated women with histologically-confirmed primary invasive breast adenocarcinoma (T2–3, N0–3, M0, tumor size ≥2.0 cm), regardless of hormone receptor or HER2 expression status. Patients received sequential neoadjuvant therapy starting with 4 cycles of AC (doxorubicin 60 mg/m2 intravenously and cyclophosphamide 600 mg/m2 intravenously) given every 3 weeks, followed by 1:1 randomization to either ixabepilone (40 mg/m2 3-hour infusion) every 3 weeks for 4 cycles, or paclitaxel (80 mg/m2 1-hour infusion) weekly for 12 weeks. Fresh tumor biopsies at screening were a mandatory prerequisite for study entry for biomarker analyses. Gene expression profiling was performed by Affymetrix GeneChip to determine if pre-specified gene models could distinguish between the clinical activity of two microtubule stabilizing agents, ixabepilone and paclitaxel. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41998 Biomarker analysis of neoadjuvant doxorubicin/cyclophosphamide followed by ixabepilone or Paclitaxel in early-stage breast cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-12-1359 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-12-1359} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA178709 https://www.ebi.ac.uk/ena/browser/view/PRJNA178709 None [Overal design]Three core needle tumor tissue biopsies were obtained from all subjects before neoadjuvant therapy with AC and immediately combined in RNAlater® solution for subsequent RNA extraction, cRNA labeling and gene expression profiling. Pre-specified gene models were tested for their capacity to distinguish pathologic complete response rates between the AC followed by ixabepilone versus the AC followed by paclitaxel treatment regimens. All samples were collected prior to treatment. All subject received cyclophosphamide/doxorubicin (AC) prior to randomization to either Ixabepilone or Paclitaxel.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted from RNAlater samples using standard procedures.'; [Cell type]'Source: ''specimen name: S1178752-1; gender: female; age: 41; treatment arm: none; ac response: progressive disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: pre-menopausal; ', 'specimen name: E3837722-1; gender: female; age: 72; treatment arm: none; ac response: 0; basetms: not reported; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; ', 'specimen name: A6263061-1; gender: female; age: 72; treatment arm: none; ac response: 0; basetms: not reported; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; ', 'specimen name: A6263065-1; gender: female; age: 72; treatment arm: none; ac response: 0; basetms: not reported; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; ', 'specimen name: S1038589-1; gender: female; age: 28; treatment arm: none; ac response: progressive disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; ', 'specimen name: A6999197-1; gender: female; age: 34; treatment arm: none; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; ', 'specimen name: E3800109-1; gender: female; age: 34; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: positive; her2stat: negative; her2: other; mnssl: not reported; pcr: No; pcrrcb1: No; ', 'specimen name: S1116462-1; gender: female; age: 50; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6997531-1; gender: female; age: 45; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4340702-1; gender: female; age: 49; treatment arm: Ixabepilone; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4639353-1; gender: female; age: 52; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1297269-1; gender: female; age: 31; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1032217-1; gender: female; age: 52; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1089746-1; gender: female; age: 56; treatment arm: Ixabepilone; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: S1032225-1; gender: female; age: 40; treatment arm: Ixabepilone; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4343481-1; gender: female; age: 27; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1126096-1; gender: female; age: 56; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A7082100-1; gender: female; age: 65; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3800101-1; gender: female; age: 61; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4343479-1; gender: female; age: 40; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3916680-1; gender: female; age: 67; treatment arm: Ixabepilone; ac response: complete response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6952000-1; gender: female; age: 45; treatment arm: Ixabepilone; ac response: complete response; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: not reported; pcr: No; pcrrcb1: No; ', 'specimen name: E4222992-1; gender: female; age: 48; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4332196-1; gender: female; age: 46; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: positive; her2: positive; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7295220-1; gender: female; age: 41; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1076366-1; gender: female; age: 60; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7330542-1; gender: female; age: 47; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4606438-1; gender: female; age: 65; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4606440-1; gender: female; age: 51; treatment arm: Ixabepilone; ac response: stable disease; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4340700-1; gender: female; age: 50; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7241236-1; gender: female; age: 45; treatment arm: Ixabepilone; ac response: complete response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4477306-1; gender: female; age: 48; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1123419-1; gender: female; age: 47; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1032221-1; gender: female; age: 66; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7082102-1; gender: female; age: 42; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4708763-1; gender: female; age: 46; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4710305-1; gender: female; age: 56; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: L0628963-1; gender: female; age: 59; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7573397-1; gender: female; age: 41; treatment arm: Ixabepilone; ac response: stable disease; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4534819-1; gender: female; age: 44; treatment arm: Ixabepilone; ac response: partial response; basetms: < 2 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4690595-1; gender: female; age: 47; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: E4751070-1; gender: female; age: 37; treatment arm: Ixabepilone; ac response: stable disease; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4751072-1; gender: female; age: 48; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6736485-1; gender: female; age: 54; treatment arm: Ixabepilone; ac response: complete response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: not reported; pcr: 0; pcrrcb1: 0; ', 'specimen name: S1076360-1; gender: female; age: 55; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3648192-1; gender: female; age: 54; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: L0488310-1; gender: female; age: 50; treatment arm: Ixabepilone; ac response: stable disease; basetms: > 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1121949-1; gender: female; age: 56; treatment arm: Ixabepilone; ac response: complete response; basetms: > 5 cm; er: positive; pr: positive; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1141087-1; gender: female; age: 40; treatment arm: none; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: S1141089-1; gender: female; age: 47; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: S1038597-1; gender: female; age: 42; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: positive; her2: positive; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1148765-1; gender: female; age: 40; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4343389-4; gender: female; age: 68; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4343389-3; gender: female; age: 68; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1123405-1; gender: female; age: 29; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6999199-1; gender: female; age: 60; treatment arm: Ixabepilone; ac response: stable disease; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3837732-1; gender: female; age: 56; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1189555-1; gender: female; age: 67; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: positive; pr: positive; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1134718-1; gender: female; age: 46; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4690599-1; gender: female; age: 54; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7330534-1; gender: female; age: 79; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1148757-1; gender: female; age: 47; treatment arm: Ixabepilone; ac response: complete response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1189563-1; gender: female; age: 46; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4708767-1; gender: female; age: 46; treatment arm: Ixabepilone; ac response: unable to determine; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1178750-1; gender: female; age: 43; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: positive; her2stat: positive; her2: positive; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4764497-1; gender: female; age: 48; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: UNKNOWN; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: A6657371-1; gender: female; age: 44; treatment arm: Ixabepilone; ac response: complete response; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: E4751060-1; gender: female; age: 56; treatment arm: Ixabepilone; ac response: complete response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: E4719356-1; gender: female; age: 63; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4999453-1; gender: female; age: 41; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4343389-2; gender: female; age: 68; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4597713-1; gender: female; age: 47; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: L0638228-4; gender: female; age: 70; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4751058-1; gender: female; age: 48; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4669580-1; gender: female; age: 56; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: positive; pr: negative; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4534823-1; gender: female; age: 70; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4830792-1; gender: female; age: 62; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3385598-1; gender: female; age: 31; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3730747-1; gender: female; age: 59; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S0895769-1; gender: female; age: 40; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S0895765-1; gender: female; age: 62; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S0898012-1; gender: female; age: 45; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S0895767-1; gender: female; age: 57; treatment arm: Ixabepilone; ac response: progressive disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: S0960945-1; gender: female; age: 54; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3569360-1; gender: female; age: 50; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S0895756-1; gender: female; age: 44; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3663949-1; gender: female; age: 52; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3569362-1; gender: female; age: 54; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: A6718068-1; gender: female; age: 39; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1183157-1; gender: female; age: 43; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1089744-1; gender: female; age: 47; treatment arm: Ixabepilone; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1005949-1; gender: female; age: 65; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6926680-1; gender: female; age: 49; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1005935-1; gender: female; age: 32; treatment arm: Ixabepilone; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: A6719819-1; gender: female; age: 46; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1121959-1; gender: female; age: 35; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1123415-1; gender: female; age: 48; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4242182-1; gender: female; age: 61; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1121945-1; gender: female; age: 32; treatment arm: Ixabepilone; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1038593-1; gender: female; age: 30; treatment arm: Ixabepilone; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4376531-1; gender: female; age: 49; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1121963-1; gender: female; age: 36; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3648194-1; gender: female; age: 61; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1172325-1; gender: female; age: 38; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7181969-1; gender: female; age: 40; treatment arm: Ixabepilone; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4332194-1; gender: female; age: 62; treatment arm: Ixabepilone; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: A6914216-1; gender: female; age: 56; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1230596-1; gender: female; age: 47; treatment arm: Ixabepilone; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1212000-1; gender: female; age: 29; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4597723-1; gender: female; age: 35; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3416700-1; gender: female; age: 59; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A7347583-1; gender: female; age: 43; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A7347583-2; gender: female; age: 43; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4555791-1; gender: female; age: 53; treatment arm: none; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: E4555791-2; gender: female; age: 53; treatment arm: none; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: E4555791-3; gender: female; age: 53; treatment arm: none; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: A6997527-1; gender: female; age: 63; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3416702-1; gender: female; age: 42; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3385596-1; gender: female; age: 58; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7342589-1; gender: female; age: 50; treatment arm: none; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: E4343543-1; gender: female; age: 41; treatment arm: Ixabepilone; ac response: unable to determine; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1121941-4; gender: female; age: 45; treatment arm: Ixabepilone; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1038591-1; gender: female; age: 43; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7082075-1; gender: female; age: 63; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1172333-1; gender: female; age: 35; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3837740-1; gender: female; age: 49; treatment arm: Ixabepilone; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3800099-1; gender: female; age: 31; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7181973-1; gender: female; age: 60; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: not reported; pcr: No; pcrrcb1: No; ', 'specimen name: E4791654-1; gender: female; age: 66; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A7585250-1; gender: female; age: 51; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4751082-1; gender: female; age: 36; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: L0638222-4; gender: female; age: 62; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: L0638218-4; gender: female; age: 55; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: L0638232-4; gender: female; age: 40; treatment arm: Ixabepilone; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1037482-1; gender: female; age: 55; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S0898799-1; gender: female; age: 67; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1005937-1; gender: female; age: 25; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: S1005933-1; gender: female; age: 63; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1172331-1; gender: female; age: 43; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4532900-1; gender: female; age: 72; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4639355-1; gender: female; age: 38; treatment arm: Ixabepilone; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3569373-1; gender: female; age: 42; treatment arm: Ixabepilone; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3665685-1; gender: female; age: 37; treatment arm: Ixabepilone; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S0922645-1; gender: female; age: 56; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: S0869886-1; gender: female; age: 44; treatment arm: Ixabepilone; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: A6719815-1; gender: female; age: 36; treatment arm: Ixabepilone; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A7347583-3; gender: female; age: 43; treatment arm: Ixabepilone; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4343539-1; gender: female; age: 35; treatment arm: Ixabepilone; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4343515-1; gender: female; age: 58; treatment arm: Ixabepilone; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S0953607-1; gender: female; age: 28; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: negative; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S0953605-1; gender: female; age: 40; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: A6952002-1; gender: female; age: 56; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4606442-1; gender: female; age: 45; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: pre-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: S1178754-1; gender: female; age: 39; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1230600-1; gender: female; age: 57; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: A7013456-1; gender: female; age: 67; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7013465-1; gender: female; age: 73; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: positive; pr: positive; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1091332-1; gender: female; age: 33; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: pre-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: S1005927-1; gender: female; age: 53; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1032219-1; gender: female; age: 55; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: positive; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4555795-1; gender: female; age: 56; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1089750-1; gender: female; age: 63; treatment arm: Paclitaxel; ac response: complete response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: E4343391-4; gender: female; age: 33; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4343391-3; gender: female; age: 33; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4343391-2; gender: female; age: 33; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1148763-1; gender: female; age: 60; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7241230-1; gender: female; age: 55; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1148753-1; gender: female; age: 42; treatment arm: Paclitaxel; ac response: stable disease; basetms: < 2 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1189561-1; gender: female; age: 41; treatment arm: Paclitaxel; ac response: complete response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1230608-1; gender: female; age: 55; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: positive; her2stat: positive; her2: positive; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4597719-1; gender: female; age: 44; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4597721-1; gender: female; age: 54; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: L0506122-1; gender: female; age: 39; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4597711-1; gender: female; age: 43; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4597717-1; gender: female; age: 41; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3837750-1; gender: female; age: 45; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4534882-1; gender: female; age: 57; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6997529-1; gender: female; age: 55; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4830790-1; gender: female; age: 45; treatment arm: Paclitaxel; ac response: complete response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4751064-1; gender: female; age: 58; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S0869900-2; gender: female; age: 39; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: negative; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6926682-1; gender: female; age: 50; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: not reported; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4242180-1; gender: female; age: 58; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: negative; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1089752-1; gender: female; age: 39; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: positive; her2stat: positive; her2: positive; mnssl: pre-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: E3837744-1; gender: female; age: 56; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1184746-1; gender: female; age: 48; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1076358-1; gender: female; age: 46; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1032223-1; gender: female; age: 43; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4597705-1; gender: female; age: 42; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3837736-1; gender: female; age: 36; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1126094-4; gender: female; age: 44; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4597715-1; gender: female; age: 58; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: S1178760-1; gender: female; age: 59; treatment arm: Paclitaxel; ac response: complete response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1189557-4; gender: female; age: 57; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4343519-1; gender: female; age: 38; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4477302-1; gender: female; age: 43; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4477304-1; gender: female; age: 58; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1121939-4; gender: female; age: 34; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1230610-1; gender: female; age: 65; treatment arm: Paclitaxel; ac response: complete response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3837746-1; gender: female; age: 50; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: L0638234-4; gender: female; age: 40; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7082104-1; gender: female; age: 70; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: E4708765-1; gender: female; age: 50; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4751084-1; gender: female; age: 60; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: L0506126-1; gender: female; age: 74; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: L0661244-4; gender: female; age: 39; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6779099-4; gender: female; age: 64; treatme nt arm: Paclitaxel; ac response: unable to determine; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1141081-1; gender: female; age: 37; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: E4690597-1; gender: female; age: 54; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4682893-1; gender: female; age: 42; treatment arm: none; ac response: partial response; basetms: 2 - 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: E4669578-1; gender: female; age: 40; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: positive; pr: positive; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4830786-1; gender: female; age: 35; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: positive; her2: positive; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4669582-1; gender: female; age: 47; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: positive; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3385594-1; gender: female; age: 50; treatment arm: Paclitaxel; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3730745-1; gender: female; age: 33; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S0898797-1; gender: female; age: 54; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: S0898016-1; gender: female; age: 54; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3569371-1; gender: female; age: 42; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S0900086-1; gender: female; age: 38; treatment arm: none; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: E3569369-1; gender: female; age: 53; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S0895758-1; gender: female; age: 32; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: E3569364-1; gender: female; age: 36; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S0960943-1; gender: female; age: 48; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A6263046-1; gender: female; age: 48; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S0922647-1; gender: female; age: 37; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S0900095-1; gender: female; age: 46; treatment arm: Paclitaxel; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S0922641-1; gender: female; age: 44; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S0952246-1; gender: female; age: 52; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A6432766-3; gender: female; age: 52; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6432766-2; gender: female; age: 52; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6432766-4; gender: female; age: 52; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3665687-1; gender: female; age: 34; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6719817-1; gender: female; age: 54; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3665683-2; gender: female; age: 50; treatment arm: none; ac response: unable to determine; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: E3800107-1; gender: female; age: 37; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6926678-1; gender: female; age: 65; treatment arm: Paclitaxel; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1123417-1; gender: female; age: 41; treatment arm: Paclitaxel; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1089748-1; gender: female; age: 30; treatment arm: Paclitaxel; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6719813-1; gender: female; age: 44; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1121955-1; gender: female; age: 52; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3916682-1; gender: female; age: 54; treatment arm: Paclitaxel; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A6718367-1; gender: female; age: 57; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4376535-1; gender: female; age: 57; treatment arm: Paclitaxel; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7013452-1; gender: female; age: 42; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1087426-1; gender: female; age: 38; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7014562-1; gender: female; age: 50; treatment arm: Paclitaxel; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: peri-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A6779101-1; gender: female; age: 42; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1083021-1; gender: female; age: 40; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6914218-1; gender: female; age: 37; treatment arm: Paclitaxel; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: Yes; ', 'specimen name: E4332198-1; gender: female; age: 52; treatment arm: Paclitaxel; ac response: progressive disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: not reported; pcr: No; pcrrcb1: No; ', 'specimen name: A7181967-1; gender: female; age: 41; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3837738-1; gender: female; age: 60; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6765383-1; gender: female; age: 51; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1134710-1; gender: female; age: 40; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: E3800093-1; gender: female; age: 48; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A7241234-1; gender: female; age: 45; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4340698-1; gender: female; age: 69; treatment arm: Paclitaxel; ac response: stable disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1172335-1; gender: female; age: 26; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A6999201-1; gender: female; age: 41; treatment arm: Paclitaxel; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E3800095-1; gender: female; age: 50; treatment arm: Paclitaxel; ac response: unable to determine; basetms: < 2 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3837748-1; gender: female; age: 45; treatment arm: Paclitaxel; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: S1148759-1; gender: female; age: 50; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A7274132-1; gender: female; age: 32; treatment arm: Paclitaxel; ac response: complete response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A7341588-1; gender: female; age: 31; treatment arm: Paclitaxel; ac response: unable to determine; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3800097-1; gender: female; age: 48; treatment arm: Paclitaxel; ac response: complete response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4534827-1; gender: female; age: 46; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: E4785455-1; gender: female; age: 46; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A6999299-1; gender: female; age: 34; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: A7241232-1; gender: female; age: 59; treatment arm: Paclitaxel; ac response: progressive disease; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1121937-4; gender: female; age: 53; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: 0; pcrrcb1: 0; ', 'specimen name: E4376533-1; gender: female; age: 73; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1172323-1; gender: female; age: 46; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E4534878-1; gender: female; age: 61; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S0869902-1; gender: female; age: 35; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: pre-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1005947-1; gender: female; age: 56; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: E3416698-4; gender: female; age: 62; treatment arm: Paclitaxel; ac response: stable disease; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ', 'specimen name: S1172329-1; gender: female; age: 44; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: S1172337-1; gender: female; age: 44; treatment arm: Paclitaxel; ac response: partial response; basetms: 2 - 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: Yes; pcrrcb1: Yes; ', 'specimen name: A7585244-1; gender: female; age: 41; treatment arm: Paclitaxel; ac response: partial response; basetms: > 5 cm; er: negative; pr: negative; her2stat: negative; her2: other; mnssl: post-menopausal; pcr: No; pcrrcb1: No; ' GSE132207 Homo sapiens 15 Expression profiling by high throughput sequencing GPL16791 Epigenetic remodelling of enhancers in response to estrogen deprivation and re-stimulation [RNA-Seq] 2019-06-05 Estrogen hormones are implicated in a majority of breast cancers and estrogen receptor alpha (ER) orchestrates a complex molecular circuitry that is not yet fully elucidated. Here we investigated genome-wide DNA methylation, histone acetylation and transcription after estradiol (E2) deprivation and re-stimulation to better characterise the ability of ER to coordinate gene regulation. We found that E2 deprivation mostly resulted in DNA hypermethylation and histone deacetylation in enhancers. Transcriptome analysis revealed that E2 deprivation leads to a global down-regulation in gene expression. Enrichment analysis of transcription factor (TF) binding and motif occurrence in the proximity of E2 deprivation-mediated differentially methylated and acetylated sites reinforces the importance of AP-1 and FOX proteins, Finally, most deprivation-dependent epigenetic changes were reversed following E2 re-stimulation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132207 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA546515 https://www.ebi.ac.uk/ena/browser/view/PRJNA546515 https://www.ncbi.nlm.nih.gov/sra?term=SRP200463 [Overal design]Control MCF-7 HTB-22 breast cancer cells (CTR) were cultured continuously for 14 days in E2-containing medium, while E2-deprived cells (E2D) were cultured in the same conditions as CTR only lacking E2. The re-stimulated cells (ReSt) were E2-deprived for 4 days and re-stimulated for the 10 following. Each treatment (CTR, E2D and ReSt) and timepoint (d0, d4, d14) is available in triplicates. See publication for schematic design; [Treatment]'10nM 17β-estradiol in 0.1% DMSO (CTR and ReSt) or only 0.1% DMSO (E2D)'; [Growth]'For maintainance, cells were cultured in DMEM/F-12 supplemented with 10% (v/v) charcoal-stripped fetal bovine serum, 1% nonessential amino acids, sodium pyruvate and penicillin/streptomycin and with a daily addition of 10nM E2 in 0.1% DMSO'; [Extraction]'AllPrep DNA/RNA Mini kit (Qiagen)\n1 µg of RNA was processed with a TruSeq RNA library preparation kit and sequenced on HiSeq 2500 (Illumina)'; [Cell type]'Source: ''cell line: MCF-7 HTB22 (ATCC); treatment: CTR; time point: d4; ', 'cell line: MCF-7 HTB22 (ATCC); treatment: CTR; time point: d14; ', 'cell line: MCF-7 HTB22 (ATCC); treatment: E2D; time point: d4; ', 'cell line: MCF-7 HTB22 (ATCC); treatment: E2D; time point: d14; ', 'cell line: MCF-7 HTB22 (ATCC); treatment: ReSt; time point: d14; ' GSE37172 Homo sapiens 6 Expression profiling by array GPL15424 EpCAM overexpression prolongs proliferative capacity of primary human breast epithelial cells and supports hyperplastic growth 2012-04-11 Background: The Epithelial Cell Adhesion Molecule (EpCAM) has been shown to be strongly expressed in human breast cancer and cancer stem cells and its overexpression has been supposed to support tumor progression and metastasis. However, effects of EpCAM overexpression on normal breast epithelial cells have never been studied before. Therefore, we analyzed effects of transient adenoviral overexpression of EpCAM on proliferation, migration and differentiation of primary human mammary epithelial cells (HMECs). METHODS: HMECs were transfected by an adenoviral system for transient overexpression of EpCAM. Thereafter, changes in cell proliferation and migration were studied using a real time measurement system. Target gene expression was evaluated by transcriptome analysis in proliferating and polarized HMEC cultures. A Chicken Chorioallantoic Membrane (CAM) xenograft model was used to study effects on in vivo growth of HMECs. RESULTS: EpCAM overexpression in HMECs did not significantly alter gene expression profile of proliferating or growth arrested cells. Proliferating HMECs displayed predominantly glycosylated EpCAM isoforms and were inhibited in cell proliferation and migration by upregulation of p27KIP1 and p53. HMECs with overexpression of EpCAM showed a down regulation of E-cadherin. Moreover, cells were more resistant to TGF-beta1 induced growth arrest and maintained longer capacities to proliferate in vitro. EpCAM overexpressing HMECs xenografts in chicken embryos showed hyperplastic growth, lack of lumen formation and increased infiltrates of the chicken leukocytes. CONCLUSIONS: EpCAM revealed oncogenic features in normal human breast cells by, inducing resistance to TGF-beta1-mediated growth arrest and supporting a cell phenotype with longer proliferative capacities in vitro. EpCAM overexpression resulted in hyperplastic growth in vivo. Thus, we suggest that EpCAM acts as a prosurvival factor counteracting terminal differentiation processes in normal mammary glands. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37172 EpCAM overexpression prolongs proliferative capacity of primary human breast epithelial cells and supports hyperplastic growth. Molecular cancer 10.679 https://doi.org/10.1186/1476-4598-12-56 {Molecular cancer (10.679): 10.1186/1476-4598-12-56} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA158607 https://www.ebi.ac.uk/ena/browser/view/PRJNA158607 None [Overal design]For each gene a representative transcript probe set was selected based on a score that combines average expression and variation of expression across all samples. Transcript probe sets with more than 4 probes were preferred. Differential expression analysis between EPCAM over-expressing and control cells (expressing GFP) was performed using a paired moderated t-test employing functions provided by Bioconductor's limma package. p-values were subsequently adjusted for multiple hypothesis testing using the method from Benjamini and Hochberg for a strong control of the false discovery rate.; [Treatment]'HMECs were cultured on a transwells for 10 days until we polarized culture was obtained, medium was chcnged daily. On day 10 of culture cells were transfected for 32 hours with EpCAM adenoviruses (or GFP control adenoviruses) to obtain overexpression of this antigen. After 32 h of transfection, RNA was extracted.'; [Growth]'HMECs of 3 independent donors were seeded on a Transwell 0.4 µm Polyester Membrane (Costar) coated with Growth Factor Reduced Matrigel (BD Biosciences) diluted 1:40 in a serum free RPMI1640. Cell culture medium was exchanged daily. Until day 4-5 cells cells formed confluent monolayer and until day 12 they polarized. The polarization status of the culture was confirmed by transepithelial resistance measurement.'; [Extraction]"RNA of HMECs (3 independent donors) with EpCAM/GFP adenoviruses was extracted using TRI-reagent (Sigma) acording to manufacture's protocol. After extraction, DNA was digested using Dnase I (Qisgen), RNA was purified using RNeasy kit (Qiagen)."; [Cell type]'human mammary epithelial cells''cell type: human mammary epithelial cells; genotype/variation: EpCAM overexpression; transfected with: EpCAM adenoviruses; sample/donor pairing: II; ', 'cell type: human mammary epithelial cells; genotype/variation: GFP control overexpression; transfected with: GFP control adenoviruses; sample/donor pairing: II; ', 'cell type: human mammary epithelial cells; genotype/variation: EpCAM overexpression; transfected with: EpCAM adenoviruses; sample/donor pairing: III; ', 'cell type: human mammary epithelial cells; genotype/variation: GFP control overexpression; transfected with: GFP control adenoviruses; sample/donor pairing: III; ', 'cell type: human mammary epithelial cells; genotype/variation: EpCAM overexpression; transfected with: EpCAM adenoviruses; sample/donor pairing: IV; ', 'cell type: human mammary epithelial cells; genotype/variation: GFP control overexpression; transfected with: GFP control adenoviruses; sample/donor pairing: IV; ' GSE37181 Homo sapiens 123 Expression profiling by array GPL6884 Subtype-dependent prognostic relevance of an interferon-induced pathway metagene in human node negative breast cancer 2012-04-11 We identified and validated the pivotal role for a metagene containing IFN-induced genes in association to higher metastatic potential as a function of the specific molecular subtype https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37181 Subtype-dependent prognostic relevance of an interferon-induced pathway metagene in node-negative breast cancer. Molecular oncology 5.962 https://doi.org/10.1016/j.molonc.2014.04.010 {Molecular oncology (5.962): 10.1016/j.molonc.2014.04.010} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA158617 https://www.ebi.ac.uk/ena/browser/view/PRJNA158617 None [Overal design]Fresh frozen primary tumors were collected at the time of diagnosis from 123 patients with operable breast cancer previously untreated and undergoing radical or conservative surgery at the Istituto Nazionale Tumori of Milano (INTM) between1990 and 1998. All patients were pathologically defined as axillary node negative and were not submitted to any type of adjuvant systemic treatment until relapse. Patients were selected in order to have a comparable pattern of classical risk factors (age, tumor size).; [Treatment]'None'; [Growth]'Tissue samples collected at time of surgery were stored at -80°C until RNA extraction'; [Extraction]'Tissue was pulverized using a Mikrodismembrator (Braun Biotech International , Germany). Total RNA was extracted with the Trizol reagent (Invitrogen, Carlsbad, CA) according to manufacture instructions and an additional DNase digestion was performed using the RNeasy kit (Qiagen, Valencia, CA).'; [Cell type]'Source: ''distant metastasis (0-none): 0; dfs (months): 122; age (y): 68; tumor size: 4.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 52; age (y): 51; tumor size: 1.8; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 102; age (y): 69; tumor size: 2; histotype: other; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 117; age (y): 47; tumor size: 2; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 39; age (y): 43; tumor size: 2; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 21; age (y): 61; tumor size: 2.7; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 111; age (y): 68; tumor size: 1.1; histotype: CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 33; age (y): 39; tumor size: 2.4; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 66; age (y): 37; tumor size: 2.4; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 12; age (y): 32; tumor size: 2.5; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 15; age (y): 44; tumor size: 2.2; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 30; age (y): 30; tumor size: 9; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 168; age (y): 50; tumor size: 2.3; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 50; age (y): 46; tumor size: 2.8; histotype: CDI+CLI; esr1 status (0-negative): 0; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 124; age (y): 49; tumor size: 2.6; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 91; age (y): 50; tumor size: 0.6; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 173; age (y): 61; tumor size: 3.5; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 19; age (y): 55; tumor size: 3.8; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 122; age (y): 48; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 136; age (y): 45; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 9; age (y): 69; tumor size: 1.8; histotype: CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 56; age (y): 50; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 33; age (y): 37; tumor size: 2.1; histotype: CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 82; age (y): 78; tumor size: 2.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 12; age (y): 37; tumor size: 3.6; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 91; age (y): 45; tumor size: 2.5; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 26; age (y): 40; tumor size: 1.3; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 9; age (y): 69; tumor size: 3.9; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 54; age (y): 52; tumor size: 4; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 159; age (y): 62; tumor size: 2.8; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 89; age (y): 65; tumor size: 2.3; histotype: other; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 159; age (y): 50; tumor size: 2.3; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 83; age (y): 61; tumor size: 2.5; histotype: other; esr1 status (0-negative): 1; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 50; age (y): 85; tumor size: 2.3; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 77; age (y): 41; tumor size: 1.6; histotype: CDI+CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 52; age (y): 58; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 159; age (y): 45; tumor size: 3; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 11; age (y): 67; tumor size: 2.3; histotype: CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 53; age (y): 51; tumor size: 1.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 32; age (y): 78; tumor size: 2.3; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 90; age (y): 57; tumor size: 2.2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 30; age (y): 70; tumor size: 3; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 111; age (y): 40; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 152; age (y): 47; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 16; age (y): 60; tumor size: 1.3; histotype: CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 11; age (y): 61; tumor size: 3.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 36; age (y): 59; tumor size: 2.4; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 83; age (y): 59; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 31; age (y): 67; tumor size: 2.4; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 72; age (y): 76; tumor size: 2.2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 25; age (y): 70; tumor size: 2.3; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 11; age (y): 65; tumor size: 2.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 16; age (y): 53; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 98; age (y): 75; tumor size: 1.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 87; age (y): 47; tumor size: 4; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 22; age (y): 39; tumor size: 2.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 41; age (y): 52; tumor size: 1.6; histotype: CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 172; age (y): 45; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 10; age (y): 62; tumor size: 2.1; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 120; age (y): 49; tumor size: 1; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 152; age (y): 51; tumor size: 3; histotype: CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 165; age (y): 59; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 93; age (y): 62; tumor size: 1.6; histotype: CDI+CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 13; age (y): 50; tumor size: 1.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 49; age (y): 42; tumor size: 1.5; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 163; age (y): 43; tumor size: 1.8; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 82; age (y): 57; tumor size: 1.7; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 8; age (y): 56; tumor size: 1.5; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 10; age (y): 66; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 131; age (y): 48; tumor size: 1.7; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 20; age (y): 58; tumor size: 1.8; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 30; age (y): 69; tumor size: 1.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 60; age (y): 77; tumor size: 2; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 118; age (y): 63; tumor size: 1.2; histotype: CDI+CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 11; age (y): 53; tumor size: 0.7; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 114; age (y): 63; tumor size: 1.7; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 28; age (y): 67; tumor size: 3; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 58; age (y): 67; tumor size: 2.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 72; age (y): 60; tumor size: 3.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 148; age (y): 44; tumor size: 1.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 114; age (y): 42; tumor size: 1.3; histotype: CDI+CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 135; age (y): 82; tumor size: 4; histotype: other; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 71; age (y): 58; tumor size: 1.4; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 26; age (y): 70; tumor size: 1.8; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 160; age (y): 51; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 19; age (y): 60; tumor size: 1.7; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 16; age (y): 61; tumor size: 2.6; histotype: CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 180; age (y): 44; tumor size: 3; histotype: other; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 52; age (y): 71; tumor size: 3.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 24; age (y): 41; tumor size: NA; histotype: CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 93; age (y): 68; tumor size: 4; histotype: other; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 71; age (y): 76; tumor size: 4; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 57; age (y): 62; tumor size: 0.8; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 52; age (y): 38; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 124; age (y): 41; tumor size: 1.4; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 112; age (y): 55; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 89; age (y): 45; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 158; age (y): 57; tumor size: 1.8; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 90; age (y): 71; tumor size: 1.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 137; age (y): 49; tumor size: 1; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 95; age (y): 67; tumor size: 2.8; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 170; age (y): 65; tumor size: 2.5; histotype: CDI+CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 116; age (y): 74; tumor size: 2; histotype: other; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 117; age (y): 53; tumor size: 1.7; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 55; age (y): 65; tumor size: 1.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 57; age (y): 62; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 20; age (y): 56; tumor size: 1.8; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 112; age (y): 52; tumor size: 1.4; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 53; age (y): 51; tumor size: 2; histotype: CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 145; age (y): 52; tumor size: 1.8; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 185; age (y): 43; tumor size: 2.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 22; age (y): 48; tumor size: 3.2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 13; age (y): 45; tumor size: 2.5; histotype: CDI+CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 45; age (y): 38; tumor size: 1.8; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 140; age (y): 49; tumor size: 1.6; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 132; age (y): 52; tumor size: 1.8; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 24; age (y): 71; tumor size: 3; histotype: CDI; esr1 status (0-negative): 0; erbb2 status (0-negative): 1; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 127; age (y): 37; tumor size: 2.7; histotype: CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 91; age (y): 57; tumor size: 2.2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 35; age (y): 78; tumor size: 3.5; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 41; age (y): 64; tumor size: 2.2; histotype: CLI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 1; dfs (months): 45; age (y): 56; tumor size: 2.2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ', 'distant metastasis (0-none): 0; dfs (months): 79; age (y): 65; tumor size: 2; histotype: CDI; esr1 status (0-negative): 1; erbb2 status (0-negative): 0; tissue: breast cancer specimen; ' GSE126003 Homo sapiens 84 Expression profiling by high throughput sequencing GPL20301 IL6/STAT3 co-opts ER/FOXA1 regulatory elements to drive metastasis in breast cancer (RNA-Seq) 2019-02-01 Interleukin 6 (IL6) signaling has been associated with an aggressive and metastatic phenotype in multiple solid tumors including breast cancer, but its mechanism of action in mediating tumor progression and treatment response is not clear. By exploiting a clinically relevant intraductal xenograft model of estrogen receptor a positive (ER+) breast cancer, we demonstrate that IL6 increases both primary tumor growth and distant metastases. In pre-clinical models and clinical specimens, signal transducer and activator of transcription 3 (STAT3) mediates IL6-induced activation of a metastatic gene program from enhancers shared with ER and its pioneer factor FOXA1. However, STAT3 drives transcription independent of ER and FOXA1 function from these enhancers, and the IL6/STAT3 pathway is therefore resistant to ER-targeted therapies, decoupling these two important oncogenic pathways. This demonstrates that ER/FOXA1 and IL6/STAT3 are two parallel, but functionally independent and actionable pathways controlling breast cancer progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE126003 IL6/STAT3 Signaling Hijacks Estrogen Receptor α Enhancers to Drive Breast Cancer Metastasis. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2020.06.007 {Cancer cell (23.916): 10.1016/j.ccell.2020.06.007} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA518886 https://www.ebi.ac.uk/ena/browser/view/PRJNA518886 https://www.ncbi.nlm.nih.gov/sra?term=SRP183162 [Overal design]RNA-seq in human breast cancer cell lines in response to short-term interleukin 6 (IL6) treatment; [Treatment]'Cells were treated with human recombinant IL6 (206-IL-200, R&D systems) for 1 hour. For the siRNA-mediated knock down experiments, T47D cells were transfected with ON-TARGETplus SMARTPools (Dharmacon) targeting STAT3, FOXA1, or ER. Non-targeting pool was used as a control. Media was changed 24 hours after transfection, and cells were treated with IL6 for 1 hour 48 hours after transfection.'; [Growth]'MCF7 cell were grown in DMEM supplemented with 10% FBS, 2mM L-glutamine, 50 U/ml penicillin, 50 ug/ml streptomycin. T47D cells were grown in RPMI supplemented with 10% FBS, 2mM L-glutamine and 50 U/ml penicillin and 50 ug/ml streptomycin.'; [Extraction]"RNA was extracted using the Qiagen RNeasy kit according to the manufacturer's instructions.\nLibraries were prepared using the TruSeq mRNA Stranded Sample prep kit from Illumina."; [Cell type]'Source: ''tissue: Breast cancer cell line; replicate: 1; ', 'tissue: Breast cancer cell line; replicate: 2; ', 'tissue: Breast cancer cell line; replicate: 3; ', 'tissue: Breast cancer cell line; replicate: 4; ', 'tissue: Breast cancer cell line; replicate: 5; ', 'tissue: Breast cancer cell line; replicate: 6; ' GSE166609 Homo sapiens 4 Expression profiling by high throughput sequencing GPL24676 The AXL-PYK2-PKCα axis as a nexus of stemness circuits in TNBC 2021-02-11 Cancer stem cells (CSCs) are implicated in tumor initiation, metastasis and drug resistance, and are considered as attractive targets for cancer therapy. We identified a clinically relevant signaling nexus mediated by PYK2 and its impact on stemness in triple negative breast cancer (TNBC). PYK2 depletion in multiple mesenchymal TNBC cell lines markedly reduced the expression of PKCα and AXL proteins and reduced the number of mammosphere-forming cells and cells harboring CSCs characteristic markers. PYK2 and PKCα cooperate at a convergence point of multiple stemness-inducing pathways to regulate AXL levels and concomitantly the levels/activation of key transcription factors implicated in stemness including STAT3, TAZ, FRA1 and SMAD3 as well as the pluripotent transcription factors Nanog and Oct4, and in-turn affect their target genes. Targeting the AXL-PYK2-PKCα circuit could be a promising strategy to eliminate CSCs in TNBC and possibly overcome drug resistance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE166609 The AXL-PYK2-PKCα axis as a nexus of stemness circuits in TNBC. Life science alliance 3.448 https://doi.org/10.26508/lsa.202000985 {Life science alliance (3.448): 10.26508/lsa.202000985} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA701409 https://www.ebi.ac.uk/ena/browser/view/PRJNA701409 https://www.ncbi.nlm.nih.gov/sra?term=SRP305833 [Overal design]PYK2 (PTK2B) was knocked-down in the triple negative breast cancer cell line MDA-MB-231 using shRNA. The empty lentiviral vector (PLKO) was used as control. Experiment was done in duplicates.; [Treatment]'None'; [Growth]'MDA-MB-231 cells were transduced with PLKO (control) or shPYK2 KD lentivirus and grown in selection medium (RPMI supplemented with 10% FBS, 1% Penicillin-Streptomycin solution and 1.5µg/ ml Puromycine) for 2 passages before RNA extraction.'; [Extraction]'RNA was extracted from 4 - 6 million cells per samples using TRI reagent (Sigma), following standard extraction protocol.\nRNAseq libraries were constructed by applying a bulk adaptation of the MARS‐seq protocol (Jaitin et al. 2014 Science.343:776-9).'; [Cell type]'Source: ''cell line: MDA-MB-231; shRNA: PLKO; ', 'cell line: MDA-MB-231; shRNA: shPYK2; ' GSE22262 Homo sapiens 2 Expression profiling by array GPL6102 Gene expression profiles upon a microarray-based NSD3L-directed siRNA knockdown in human breast cancer cell line MDA-MB-231. 2010-06-09 No genes have been described to be regulated by NSD3L. To identify genes regulated by NSD3L we inverstigated the effect of NSD3L depletion on gene regulation in the human breast cancel cell line MDA-MB-231 by a Illumina expression microarray (Human WG-6 v3.0) screening. We identified 113 different potential target genes out of 25.400 probe sets which have a more than 2-fold changed expression. Of these genes 44 were up-regulated and 69 down-regulated. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22262 The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells. Biochemical and biophysical research communications 2.705 https://doi.org/10.1016/j.bbrc.2010.06.119 {Biochemical and biophysical research communications (2.705): 10.1016/j.bbrc.2010.06.119} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA128737 https://www.ebi.ac.uk/ena/browser/view/PRJNA128737 None [Overal design]To deplete NSD3L we used siRNA directed specifically against this isoform. RNA isolated from NSD3L siRNA transfected cells was together with RNA from control siRNA transfected cells used to screen an Illumina expression microarray (HumanWG-6 v3.0). We identified 113 different potential target genes out of 25.400 probe sets which have a more than 2-fold changed expression. Of these genes 44 were up-regulated and 69 down-regulated.; [Treatment]'MDA-MB-231 cells were transfected with TransIT-siQUEST® Transfection Reagent (MIR2110) according to the protocol provided by the manufacturer. Cells were seeded into a 6-well plate to obtain 25% confluence on the following day. 4 μl of the TransIT-siQUEST Transfection Reagent was diluted into 250 μl serum-free media, mixed thoroughly by pipetting. Then 20 nM NSD3L directed siRNA 5’-AUUAGUUACACUGUUCUCGUG (dTdT)-3’ was added to the diluted TransIT-siQUEST Reagent, using nonspecifically targeted siRNA 5’-AGGUAGUGUAAUCGCCUUG (dTdT)-3’ as negative control. The complex was mixed by gentle pipetting and incubated at room temperature for 20 min. The TransIT-siQUEST Reagent/siRNA complex mixture was then added to cultured cells containing 1250 μl complete medium. After 48 h incubation, the siRNA was transfected again and incubated for another 48 h. Cells were collected and RNA was purified.'; [Growth]'the cell lines were grown in Dulbecco’s modified Eagle medium (Invitrogen) supplemented with 10% fetal calf serum (FCS) and penicillin and streptomycin.'; [Extraction]'RNA extraction was performed with TRI-reagent (Sigma) according to the manufacturer’s instructions.'; [Cell type]'High-invasive human breast cancer cell line''cell type: High-invasive human breast cancer cell line; cell line: MDA-MB-231; sirna: NSD3L-directed siRNA; ', 'cell type: High-invasive human breast cancer cell line; cell line: MDA-MB-231; sirna: non-specific targeted control siRNA; ' GSE72110 Homo sapiens 80 Methylation profiling by array GPL9183 DNA methylation and hormone receptor status in breast cancer, the BCCC study 2015-08-16 Genome wide DNA methylation profiling of invasive breast cancer samples isolated from an ethnically diverse group of 80 patients in the Breast Cancer Care in Chicago (BCCC) study. DNA was extracted from formalin fixed, paraffin-embedded samples on 80 patients (21 White, 31 African-American, 23 Hispanic and 5 not reported) (training dataset) enrolled in the BCCC. Hormone receptor status was defined as negative if tumors were negative for both estrogen and progesterone (ER/PR) receptors (N=22/75). Formalin-fixed, paraffin-embedded (FFPE) tumor samples came from the Breast Cancer Care in Chicago (BCCC) study (Dookeran KA, Silva A, Warnecke RB, Rauscher GH: Race/ethnicity and disparities in mastectomy practice in the Breast Cancer Care in Chicago study. Ann Surg Oncol 2015, 22:66–74). Copies of pathology reports and the corresponding set of Hematoxylin and Eosin (H&E) stained slides were requested from the pathology department at each diagnosing institution, and a single pathologist selected tumor blocks representative of the tumor. Two recuts (at 4 µm each) were made from each selected block for H&E staining. The recuts were then examined in order to identify invasive components of the sample, and areas were marked according to tissue component. Cores of invasive tissue (2 mm in diameter) were obtained from the marked areas and DNA was extracted for the DNA methylation study. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72110 DNA methylation and hormone receptor status in breast cancer. Clinical epigenetics 5.496 https://doi.org/10.1186/s13148-016-0184-7 {Clinical epigenetics (5.496): 10.1186/s13148-016-0184-7} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA292997 https://www.ebi.ac.uk/ena/browser/view/PRJNA292997 None [Overal design]Bisulphite converted DNA from the 80 samples were hybridised to the Illumina GoldenGate Methylation Cancer Panel I; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA extraction was performed by adding to each core 100 µl Xylene. After the incubation with gentle shaking for 5 minutes, supernatant was removed by centrifugation at 14,000 g to remove the paraffin. The process was repeated two more times. The tissue was then weighted and 2-4 mg tissue was used for DNA extraction using Gentra Puregene kit (QIAGEN). All tissues were homogenized after adding Cell Lysis solution, Proteinase K and overnight incubation. The extracted DNA was measured by NanoDrop and normalized at 50 ng/µl concentration.'; [Cell type]'Source: ''gender: Female; tissue: invasive breast cancer; hormone receptor status (presence or absence of er and pr) # 1 means either er+ or pr+ (er+pr+, er+pr- or er-pr+) 0 means negative for both (er-pr-): 0; ', 'gender: Female; tissue: invasive breast cancer; hormone receptor status (presence or absence of er and pr) # 1 means either er+ or pr+ (er+pr+, er+pr- or er-pr+) 0 means negative for both (er-pr-): 1; ', 'gender: Female; tissue: invasive breast cancer; hormone receptor status (presence or absence of er and pr) # 1 means either er+ or pr+ (er+pr+, er+pr- or er-pr+) 0 means negative for both (er-pr-): unknown; ' GSE143222 Homo sapiens 55 Expression profiling by array GPL18649 Prediction of prognostic signatures in triple-negative breast cancer based on the differential expression analysis via NanoString nCounter immune panel 2020-01-07 Triple Negative Breast Cancer (TNBC) has been considered an aggressive and complex subtype of breast cancer. Current biomarkers used in breast cancer treatment are highly dependent on targeting ER, PR, or HER2 in clinical practice, which results in ttreatment failure and disease recurrence continue to be clinically challenging. In this regards, there is still a crucial need for improvement of TNBC treatment by discovery of effective biomarkers that can be easily translated to the clinics and possible targets as prognosis and novel therapies. This study reports an approach for biomarker discovery, which predicts tumour relapse and pathologic complete response (pCR) in TNBC on the basis of mRNA expression quantified using NanoString nCounter Immunology Panel. We identify nine and 13 differentially expressed genes (DEGs), respectively, that are strongly associated with pCR and relapse from 579 immune genes over a small number of samples (n=55) using edgeR. To overcome a small sample size limitation, prediction models based on the random forest are constructed on the DEGs as selected features extracted from the DEG analysis. Comprehensive analysis indicated that our prediction models outperform those constructed on features extracted from the existing feature selection model such as, Elastic Net in terms of accuracy. The prediction models are assessed by randomization test to validate the robustness (empirical P for the model of pCR= 0.022 and empirical P for the model of relapse= 0.025). Furthermore, three DEGs (IL17B, EDNRB, and TGFBI) in the model of relapse show prognostic significance to predict cancer patient survival through Cox proportional hazards regression model based survival analysis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE143222 Prediction of prognostic signatures in triple-negative breast cancer based on the differential expression analysis via NanoString nCounter immune panel. BMC cancer 2.933 https://doi.org/10.1186/s12885-020-07399-8 {BMC cancer (2.933): 10.1186/s12885-020-07399-8} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA599342 https://www.ebi.ac.uk/ena/browser/view/PRJNA599342 None [Overal design]Paraffin-embedded tissue biopsy samples from 55 Among 108 TNBC patients diagnosed and treated with anthracycline and taxane-based NAC and by surgery from 2010 to 2012 at Asan Medical Centre, paraffin-embedded tissue samples from 55 patients were processed using GX Human Immunology V2kit for NanoString nCounter Gene expression for a total of 579 immunology-related human genes. Among 55 cases, operation specimens from 14 patients, including 6 cases of pCR, were also analysed. Tthe patient's clinical data including survival time, survival parameters, and chemotherapeutic responsiveness (pCR, residual cancer burden, RCB, Miller Payne grade), relapse and pCR under PRE and POST conditions, were collected; [Treatment]'None'; [Growth]'None'; [Extraction]'On average, 10 5 um-thick FFPE sections were prepared for the extraction of total RNA from tumor cell-rich areas, which were identified by a surgical pathologist (HJL) using section stained by H & E.'; [Cell type]'Source: ''tissue: Triple Negative Breast cancer; status after 5 years: Alive; relapse: non reccurence; pcr: complete remission; pre/post: Post; ', 'tissue: Triple Negative Breast cancer; status after 5 years: Alive; relapse: non reccurence; pcr: complete remission; pre/post: Pre; ', 'tissue: Triple Negative Breast cancer; status after 5 years: Alive; relapse: non reccurence; pcr: non complete remission; pre/post: Post; ', 'tissue: Triple Negative Breast cancer; status after 5 years: Dead; relapse: reccurence; pcr: non complete remission; pre/post: Post; ', 'tissue: Triple Negative Breast cancer; status after 5 years: Alive; relapse: non reccurence; pcr: non complete remission; pre/post: Pre; ', 'tissue: Triple Negative Breast cancer; status after 5 years: Dead; relapse: reccurence; pcr: non complete remission; pre/post: Pre; ', 'tissue: Triple Negative Breast cancer; status after 5 years: Dead; relapse: reccurence; pcr: complete remission; pre/post: Post; ', 'tissue: Triple Negative Breast cancer; status after 5 years: Dead; relapse: non reccurence; pcr: non complete remission; pre/post: Pre; ' GSE69926 Mus musculus 71 Expression profiling by high throughput sequencing GPL16417 Single-cell RNA-seq reveals activation of unique gene groups as a consequence of stem cell-parenchymal cell fusion 2015-06-16 Fusion of donor mesenchymal stem cells with parenchymal cells of the recipient can occur in the brain, liver, intestine and heart following transplantation. The therapeutic benefit or detriment of resultant hybrids is unknown. Here we sought a global view of phenotypic diversification of mesenchymal stem cell-cardiomyocyte hybrids and associated time course. Using single-cell RNA-seq, we found hybrids consistently increase ribosome components and decrease genes associated with the cell cycle suggesting an increase in protein production and decrease in proliferation to accommodate the fused state. But in the case of most other gene groups, hybrids were individually distinct. In fact, though hybrids can express a transcriptome similar to individual fusion partners, approximately one-third acquired distinct expression profiles in a single day. Some hybrids underwent reprogramming, expressing pluripotency and cardiac precursor genes latent in parental cells and associated with developmental and morphogenic gene groups. Other hybrids expressed genes associated with ontologic cancer sets and two hybrids of separate experimental replicates clustered with breast cancer cells, expressing critical oncogenes and lacking tumor suppressor genes. Rapid transcriptional diversification of this type garners consideration in the context of cellular transplantation to damaged tissues, those with viral infection or other microenvironmental conditions that might promote fusion. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE69926 Single-cell RNA-seq reveals activation of unique gene groups as a consequence of stem cell-parenchymal cell fusion. Scientific reports 4.011 https://doi.org/10.1038/srep23270 {Scientific reports (4.011): 10.1038/srep23270} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA287141 https://www.ebi.ac.uk/ena/browser/view/PRJNA287141 https://www.ncbi.nlm.nih.gov/sra?term=SRP059549 [Overal design]Examination was performed using single-cell RNA-seq of five fusion products (BiFC_D1_F1-5, 24 hours) identified using BiFC, twenty-three fusion products (DC_D1_F1-16, 24 hours; DC_D3_F1-7, 72 hours) identified using dual expression of GFP and mCherry, the parental controls, and the population controls (mMSC_PC and HL1cm_PC). Parental controls included 15 cells of each parental type isolated prior to co-culture (mMSC_1-15 and HL1cm_1-15) and 5 cells of each parental cell type isolated 24 hours after co-culture (mMSC_D1_1-5 and HL1cm_D1_1-5). In addition, a population containing a mixture of both parental cells and fusion products obtained 24 hours after co-culture was included (Mix_D1).; [Treatment]'To induce “accidental cell fusion” between MSCs (hMSCs or mMSCs) and HL1cms, we utilized the measles virus to create a recombinant DNA fusion system. The recombinant DNA system contains three components and enables fusion only when the hemagglutinin (H) protein of the virus binds to the human signaling lymphocytic activation molecule (hSLAM) of the human cell, which then forms a trimeric complex with the fusion protein (F) of the virus to initiate fusion. HL1cms are transfected with the receptor component, hSLAM, while MSCs are transfected with the hemagglutinin (H) and fusion (F) proteins (viral fusogens provided by Yoshihiro Kawaoka of the University of Wisconsin-Madison). Fusion only occurs when all three proteins are present and we utilized this ability to induce fusion between MSCs and HL1cms. Transfection was accomplished using the Neon Transfection System (Invitrogen, Carlsbad, CA), according to the manufacturer’s protocol. Briefly, 5 x 105 HL1cms were transfected with 2 μg of hSLAM and 2 μg of the detection system plasmid with one 1,300 V pulse for 30 msec and plated into 6-well plates (Falcon, Fisher Scientific, Forest Lawn, NJ) containing Claycomb-complete medium without penicillin-streptomycin as per Neon Transfection System protocol. The HL1cm electroporation was repeated and added to the same well to obtain approximately 1 x 106 total cells transfected. Eighteen hours later, fresh Claycomb-complete medium without penicillin-streptomycin was added to the transfected HL1cm and 5 x 105 MSCs were transfected with 2 μg of F-H and 2 μg of the detection system plasmid with one 1,500 V pulse for 20 msec and plated directly onto the previously electroporated HL1cms in the 6-well plate. The co-culture was allowed to incubate overnight and the fusion products were analyzed on the following day and identified using flow cytometry for GFP.'; [Growth]'MSCs were cultured on a 0.1% gelatin (Sigma Aldrich, St. Louis, MO) pretreated flask containing a-minimum essential medium (MEM) complete. Alpha-MEM-complete consisted of a-MEM (Invitrogen, Carlsbad, CA), 10% fetal bovine serum (Hyclone, Logan, UT), 0.1 mM nonessential amino acids (Invitrogen), and 2 mM L-glutamine (Invitrogren). MSC cultures were allowed to grow to 60-70% confluence and were replated at a concentration of 1,500 cells/cm\xad2. HL1cms were cultured on fibronectin/gelatin (1.25 mg fibronectin/100 mL 0.02% gelatin) (Sigma Aldrich) pretreated flasks containing Claycomb-complete. Claycomb-complete medium was comprised of Claycomb medium (SAFC Biosciences, St. Louis, MO, USA), 10% fetal bovine serum qualified for CMs (SAFC Biosciences), 100 U/mL: 100 μg/mL penicillin-streptomycin (Lonza, Walkersville, MD, USA), 0.1 mM norepinephrine (Sigma-Aldrich), and 2 mM L-glutamine (Invitrogen). HL1cms were passaged at 100% confluence and split 1:3. HL1cm coating and HL1cm medium was used when the two cell types were co-cultured.'; [Extraction]'Fluorescent fusion products were sorted via flow activated cell sorting and placed into the Fluidigm C1 chip (17-25 micron) for capture. Controls were captured in a similar manner.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Fusion Product', 'Mixture of HL-1 cardiomyocytes, MSCs and fusion products', 'HL-1 cardiomyocyte', 'HL-1 cardiomyocyte, population control', 'Bone marrow MSC', 'Bone marrow MSC, population control''cell type: Fusion Product; passages: Fused within 24 hours of capture; ', 'cell type: Fusion Product; passages: Fused within 72 hours of capture; ', 'cell type: Mixture of HL-1 cardiomyocytes, MSCs and fusion products; passages: Mixture of 70-85 HL1cm, 6-11 mMSC, and newly formed fusion products; ', 'cell type: HL-1 cardiomyocyte; passages: 70-85; ', 'cell type: HL-1 cardiomyocyte, population control; passages: 70-85; ', 'cell type: Bone marrow MSC; passages: 6-11; ', 'cell type: Bone marrow MSC, population control; passages: 6-11; ' GSE144580 Homo sapiens 15 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL18573; GPL20301 Non-linear relationship between chromatin accessibility and estradiol-regulated gene expression 2020-01-30 Chromatin accessibility is central to basal and inducible gene expression. Through ATAC-seq experiments in Estrogen Receptor-positive (ER+) breast cancer cell line MCF-7 and integrationvwith multi-omics data, we found that estradiol (E2) induced chromatin accessibility changes in the widely studied E2-regulated genes. As expected, open chromatin regions associated with E2-inducible gene expression showed enrichment of estrogen response element and those associated with E2-repressible gene expression were enriched for PBX1, PBX3, and ERE. Surprisingly, a significant number of E2-inducible genes displayed closed promoters/enhancers and these were enriched for binding for transcription factors such as NF-Y, FOXA1, GRHL2, and BATF, which are known to interact with nucleosomes. While a significant number of open chromatin regions showed FOXA1 occupancy in the absence of E2, E2-treatment further enhanced FOXA1 occupancy suggesting that ER-E2 enhances chromatin occupancy of FOXA1 to a subset of E2-regulated genes. In summation, our results reveal complex mechanisms of ER-E2 interaction with nucleosomes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144580 Nonlinear relationship between chromatin accessibility and estradiol-regulated gene expression. Oncogene 6.634 https://doi.org/10.1038/s41388-020-01607-2 {Oncogene (6.634): 10.1038/s41388-020-01607-2} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA604072 https://www.ebi.ac.uk/ena/browser/view/PRJNA604072 https://www.ncbi.nlm.nih.gov/sra?term=SRP246235 [Overal design]We conducted both ATAC-seq and RNA-seq for MCF7 cells. Total RNA from MCF-7 cells treated with vehicle ethanol or E2 for three hours in biologic triplicates was used for sequencing. MCF-7 cells treated with vehicle (ethanol) control, E2 (10-10 M) for one or three hours were were done in biologic triplicates with ~50,000 cells.; [Treatment]'Ethanol or estradiol (0.1 nM) were added for indicated time'; [Growth]'MCF-7 cells maintained in phenol red free MEM plus 5% charcoal-dextran treated fetal bovine serum for three days were treated with either ethanol or 0.1 nM E2 for indicated time'; [Extraction]'Total RNA was prepared using RNAeasy kit from Qiagen'; [Cell type]'estrogen receptor-positive (ER+) breast cancer cell line''cell line: MCF-7; cell type: estrogen receptor-positive (ER+) breast cancer cell line; treatment: E2 (10-10 M) for 1hr; ', 'cell line: MCF-7; cell type: estrogen receptor-positive (ER+) breast cancer cell line; treatment: E2 (10-10 M) for 3hr; ', 'cell line: MCF-7; cell type: estrogen receptor-positive (ER+) breast cancer cell line; treatment: vehicle (ethanol); ' GSE104264 Mus musculus 12 Expression profiling by high throughput sequencing GPL17021 Transcriptome determinants of lung seeding by mammary tumor cells 2017-09-26 Metastasis accounts for most of cancer-related deaths. Paracrine signaling between tumor cells and the stroma induces changes in the tumor microenvironment required for metastasis. Transcription factor c-Myb was associated with breast cancer (BC) progression but its role in metastasis remains unclear. Here we show that increased c-Myb expression in BC cells inhibits spontaneous lung metastasis through impaired tumor cell extravasation. On contrary, BC cells with increased lung metastatic capacity exhibited low c-Myb levels. We identified a specific inflammatory signature, including Ccl2 chemokine; that was expressed in lung metastatic cells but was suppressed in tumor cells with higher c-Myb levels. Tumor cell-derived Ccl2 expression facilitated lung metastasis and rescued trans-endothelial migration of c-Myb overexpressing cells. Clinical data show that the identified inflammatory signature, together with a MYB expression, predicts lung metastasis relapse in BC patients. These results demonstrate that the c-Myb-regulated transcriptional program in BCs results in a blunted inflammatory response and consequently suppresses lung metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE104264 Transcription factor c-Myb inhibits breast cancer lung metastasis by suppression of tumor cell seeding. Oncogene 6.634 https://doi.org/10.1038/onc.2017.392 {Oncogene (6.634) doi:10.1038/onc.2017.392}; {Scientific reports (4.011) doi:10.1038/s41598-019-48051-1}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA412197 https://www.ebi.ac.uk/ena/browser/view/PRJNA412197 https://www.ncbi.nlm.nih.gov/sra?term=SRP118895 [Overal design]The study objective was to compare the transcriptomes of two independent variants of 4T1 cells with altered capacity to colonize lungs: (1) genetically modified 4T1 with Myb oncogene overexpression (MYBup), (2) 4T1 cells selected in vivo for high efficiency in lung seeding (lung3). Myb overexpression reduces the capacity of 4T1 cells to seed in lungs in experimental setting and to produce overt pulmonary metastases in orthotopic setting, whereas in vivo passaging rendered cells with enhanced metastatic ability. We tested the hypothesis that c-Myb drives transcriptional program preventing lung colonization by breast cancer cells, which is blunted in highly metastatic cells. To identify components of the program, we performed RNAseq and searched for genes that are either down-regulated in MYBup (compared to mock-transfected) and up-regulated in lung3 (compared to wt) or vice versa. All samples (mock, MYBup, wt, and lung3) were analysed in triplicates.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was isolated using RNeasy Plus Mini kit (Qiagen). Illumina TruSeq RNA Sample Prep Kit was used for the construction of sequencing libraries.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'mammary tumor cells''cell line: 4T1; cell type: mammary tumor cells; transfected with: pcDNA3.1; in vivo passaging: no; lung metastatic activity: normal; ', 'cell line: 4T1; cell type: mammary tumor cells; transfected with: pcDNA3-mMyb; in vivo passaging: no; lung metastatic activity: low; ', 'cell line: 4T1; cell type: mammary tumor cells; transfected with: none; in vivo passaging: no; lung metastatic activity: normal; ', 'cell line: 4T1; cell type: mammary tumor cells; transfected with: none; in vivo passaging: 3x lung; lung metastatic activity: high; ' GSE26081 Homo sapiens 47 Genome binding/occupancy profiling by genome tiling array; Expression profiling by array GPL4910; GPL4911; GPL4912; GPL4913; GPL4914; GPL4915; GPL4916; GPL11364 Growth Factor Stimulation Induces a Distinct ERα Cistrome Underlying Breast Cancer Endocrine Resistance 2010-12-15 Estrogen receptor alpha (ERα) expression in breast cancer is predictive of response to endocrine therapy, however resistance is common in ERα-positive tumors that over-express the growth factor receptor ERBB2. Even in the absence of estrogen, ERα can be activated by growth factors including the epidermal growth factor (EGF). EGF induces a transcriptional program distinct from estrogen, however the mechanism of the stimulus-specific response is unknown. Here we show that the EGF-induced ERα genomic targets, its cistrome, are distinct from those induced by estrogen in a process dependent on the transcription factor AP-1. The EGF-induced ERα cistrome specifically regulates genes found over-expressed in ERBB2-positive human breast cancers. This provides a potential molecular explanation for the endocrine therapy resistance seen in ERα-positive breast cancers that over-express ERBB2. These results suggest a central role for ERα in hormone-refractory breast tumors dependent on growth factor pathway activation and favors the development of therapeutic strategies completely antagonizing ERα as opposed to blocking its estrogen responsiveness alone. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26081 Growth factor stimulation induces a distinct ER(alpha) cistrome underlying breast cancer endocrine resistance. Genes & development 8.990 https://doi.org/10.1101/gad.1944810 {Genes & development (8.990): 10.1101/gad.1944810} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA135217 https://www.ebi.ac.uk/ena/browser/view/PRJNA135217 None [Overal design]ChIP-Chip against ERa in MCF7 breast cancer cells treated with Epidermal Growth Factor (EGF) for 90 min and expression profile analysis (mRNA) in MCF7 cells treated with EGF (3h or 12h) or pre-treated with ICI182,780 and then with EGF from 3h.; [Treatment]'Described in method section: http://www.ncbi.nlm.nih.gov/pubmed/20889718'; [Growth]'Described in method section: http://www.ncbi.nlm.nih.gov/pubmed/20889718'; [Extraction]'Described in method section: http://www.ncbi.nlm.nih.gov/pubmed/20889718'; [Cell type]'Source: ', 'breast cancer cells''agent: EGF treated MCF7 breast cancer cells; fraction: ChIP; ', 'reference: Input DNA from same sample used for ChIP against ERa; ', 'agent: EGF treated MCF7 breast cancer cells; fraction: control Input DNA; ', 'stimulation: control; cell type: breast cancer cells; cell line: MCF7; ', 'stimulation: 3h EGF stimulation; cell type: breast cancer cells; cell line: MCF7; ', 'stimulation: 12h EGF stimulation; cell type: breast cancer cells; cell line: MCF7; ', 'stimulation: 3h ICI pre-treatment 3hEGF treatment stimulation; cell type: breast cancer cells; cell line: MCF7; ' GSE126894 Homo sapiens 24 Expression profiling by high throughput sequencing GPL16791 A TFAP2C Gene Signature is Predictive of Outcome in HER2 Breast Cancer (RNA-Seq) 2019-02-21 Abstract: A subset of HER2 breast cancers with amplification of the TFAP2C gene locus becomes addicted to AP-2g. We sought to define AP-2g-regulated genes that control growth and invasiveness by comparing HER2 cell lines with differential response to TFAP2C knockdown. A set of 68 differentially expressed genes was identified, which included CDH5 and CDKN1A. Pathway analysis implicated the MAPK13/p38δ and retinoic acid regulatory nodes, which were confirmed to display divergent responses. The AP-2g gene signature was highly predictive of outcome in HER2-positive breast cancer patients. We conclude that AP-2g regulates a set of genes in HER2 breast cancer that drive cancer growth and invasiveness and that the AP-2g gene signature can predict outcome of patients with HER2 breast cancer. Results: Using an optimized data analysis workflow, we mapped about 50-75 million sequence reads per sample to the human genome Human Feb.2009 (GRCh37/hg19) (hg19). By RNA-seq analysis, knockdown of TFAP2C in HCC1954 with siRNA (compared to NT siRNA) identified 364 genes with significantly altered expression. To further create specificity for AP-2gamma-regulated genes, RNA-seq analysis was performed comparing expression in shHCC1954 with shTFAP2C cells vs. shNT; this analysis identified 8,986 genes with significantly altered expression. The two data sets were subsequently compared to identify a set of genes that were consistently altered with knockdown of TFAP2C by siRNA and shRNA. This comparison confirmed the identification of 152 AP-2gamma target genes in HCC1954 cells. Because HCC1954 demonstrated opposite growth regulation and invasiveness with knockdown of TFAP2C compared to SKBR3, we hypothesized that the AP-2gamma target genes responsible for growth and invasion would be differentially regulated with knockdown of TFAP2C in HCC1954 versus SKBR3. Hence, RNA-seq analysis was performed in SKBR3 after knockdown of TFAP2C with siRNA; in this analysis, a total of 3814 genes were significantly altered. The pattern of expression for the 152 AP-2gamma target genes identified in HCC1954 was subsequently compared to expression changes in SKBR3. Of note, only 79 of the 152 TFAP2C target genes in HCC1954 were found to change expression significantly in the RNA-seq data set from SKBR-3. Conclusions: Knockdown of TFAP2C with co-knockdown of CDH5 in SKBR-3 confirmed no significant effect on invasion, though there was a slight reduction in invasiveness with knockdown of CDH5 that failed to reach statistical significance (p=0.12). These findings support the conclusion that regulation of CDH5 and CDKN1A contribute to alterations of proliferation and invasiveness induced by knockdown of TFAP2C. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE126894 A TFAP2C Gene Signature Is Predictive of Outcome in HER2-Positive Breast Cancer. Molecular cancer research : MCR 4.484 https://doi.org/10.1158/1541-7786.MCR-19-0359 {Molecular cancer research : MCR (4.484): 10.1158/1541-7786.MCR-19-0359} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA523613 https://www.ebi.ac.uk/ena/browser/view/PRJNA523613 https://www.ncbi.nlm.nih.gov/sra?term=SRP186504 [Overal design]To identify the key AP-2gamma target genes mediating cell growth and invasiveness, RNA-seq was used to characterize significant changes in gene expression with knockdown of TFAP2C in HER2 positive cell lines, in triplicate.; [Treatment]'Cells were transfected using small interfering RNA (siRNA) directed towards non-targeting #2 (NT Thermo Fisher Scientific ID:4390843), TFAP2C (TFS ID:10.7041) with lipofectamine RNAiMAX reagent (Cat# 13778150, Thermo Fisher Scientific, USA), accordingly a manufacturer’s instruction. After 72 to 96 hours of incubation, cell were immediately analyzed or used in consequent experiments. Cell clones of HCC1954 lines with stable knockdown of TFAP2C (Cat#TRCN0000019745, Sigma, USA) and negative control (Cat#SHC002, Sigma, USA) were generated using lentivirus-mediated shRNA cassette.'; [Growth]'Cell lines HCC1954 and SKBR3 were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA) and propagated in the appropriate medium as recommended by manufacturer. Additionally, all media were supplemented with 10% FBS (LS26140079, Gibco, USA), 1% 100X Pen/Strep antibiotics (10378016, Gibco, USA), and 0.2% Plasmocin (Cat# ant-mpp, InvivoGen, USA). The cell lines were cultured in a standard humidified incubator at 37° C and 5% CO2 (16). The cells were not tested and authenticated by the authors. Only early passages of cell lines (less than 10) were used for experiments.', 'Cell lines HCC1954, HCC1569 and SKBR3 were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA) and propagated in the appropriate medium as recommended by manufacturer. Additionally, all media were supplemented with 10% FBS (LS26140079, Gibco, USA), 1% 100X Pen/Strep antibiotics (10378016, Gibco, USA), and 0.2% Plasmocin (Cat# ant-mpp, InvivoGen, USA). The cell lines were cultured in a standard humidified incubator at 37° C and 5% CO2 (16). The cells were not tested and authenticated by the authors. Only early passages of cell lines (less than 10) were used for experiments.'; [Extraction]'mRNA from cell lysates were obtained from cell lines using the Rneasy Mini Kit (Qiagen, Valencia, CA, USA). Illumina TruSeq RNA Sample Prep Kit (Cat#FC-122-1001) was used with 1 ug of total RNA for the construction of sequencing libraries.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''passage: between 5 and 10; cell line: SKBR3; transfection reagent: Lipofectamine RNAi_Max; sirna/shrna: Negative control siRNA#2; ', 'passage: between 5 and 10; cell line: SKBR3; transfection reagent: Lipofectamine RNAi_Max; sirna/shrna: TFAP2C siRNA ID:107041; ', 'passage: between 5 and 10; cell line: HCC1954; transfection reagent: Lipofectamine RNAi_Max; sirna/shrna: Negative control siRNA#2; ', 'passage: between 5 and 10; cell line: HCC1954; transfection reagent: Lipofectamine RNAi_Max; sirna/shrna: TFAP2C siRNA ID:107041; ', 'passage: between 5 and 10; cell line: HCC1954; transfection reagent: Lentiviral particles; sirna/shrna: Cat#SHC002, Sigma, USA; ', 'passage: between 5 and 10; cell line: HCC1954; transfection reagent: Lentiviral particles; sirna/shrna: Cat#TRCN0000019745, Sigma, USA; ', 'passage: between 5 and 10; cell line: HCC1569; transfection reagent: Lipofectamine RNAi_Max; sirna/shrna: Negative control siRNA#2; ', 'passage: between 5 and 10; cell line: HCC1569; transfection reagent: Lipofectamine RNAi_Max; sirna/shrna: TFAP2C siRNA ID:107041; ' GSE37038 Homo sapiens 12 Non-coding RNA profiling by array GPL10850 Evaluation of microRNA expression in vehicle and metformin-treated breast cancer cells and evaluation of the dicer relevance 2012-04-04 We have evaluated the microRNA expression profile of SUM159 cells stably infected with a control shRNA or a dicer-targeting shRNA treated with vehicle or metformin for 24 hrs at non cytotoxic doses. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37038 Metformin elicits anticancer effects through the sequential modulation of DICER and c-MYC. Nature communications 11.878 https://doi.org/10.1038/ncomms1859 {Nature communications (11.878): 10.1038/ncomms1859} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA157853 https://www.ebi.ac.uk/ena/browser/view/PRJNA157853 None [Overal design]microRNA expression was evaluated from total RNA extracted from logaritmically growing SUM159 cells stably expressing a control shRNA or a dicer-targeting shRNA and treated with vehicle (PBS) or metformin (0.5mM) for 24 hrs.; [Treatment]'logaritmically growing SUM159 cells stably expressing a control shRNA or a dicer-targeting shRNA treated with vehicle (PBS) or metformin (0.5mM) for 24 hrs.'; [Growth]'SUM159 were grown in DMEM/F-12 supplemented with 5% FBS, Insulin 5ug/ml (SIGMA) and Hydrocortisone 0.5 ug/mL (SIGMA). The cells were stably infected with PLKO1-based lentiviral vectors. PLKO.1-shdicer was a gift of Dr. Stefano Piccolo (Padua, ITALY)(Martello et al, 2010). The CONTROL scrambled-shRNA consisted of an shRNA insert that contains 4 base pair mismatches to any known human or mouse gene in the same backbone vector (PLKO.1) (SIGMA- SHC002).'; [Extraction]"Total RNA from breast cancer cell lines was extracted by TRI Reagent lysis reagent (Ambion) according to manufacturer's instructions."; [Cell type]'Source: ''cell line: SUM159; knockdown: control shRNA; treatment: PBS; ', 'cell line: SUM159; knockdown: Dicer shRNA; treatment: PBS; ', 'cell line: SUM159; knockdown: control shRNA; treatment: 0.5 mM metformin; ', 'cell line: SUM159; knockdown: Dicer shRNA; treatment: 0.5 mM metformin; ' GSE20361 Homo sapiens 8 Expression profiling by array GPL570 Dynamic changes during adaptation to estrogen deprivation in MCF7 cell line 2010-02-16 Endocrine therapies targeting the proliferative effect of 17β-estradiol (17βE2) through estrogen receptor α (ERα) are the most effective systemic treatment of ERα-positive breast cancer. However, most breast tumors initially responsive to these therapies develop resistance through a molecular mechanism that is not yet fully understood. The long-term estrogen-deprived (LTED) MCF7 cell model has been proposed to recapitulate acquired resistance to aromatase inhibitors (AIs) in postmenopausal women. To elucidate this resistance, genomic, transcriptomic and molecular data were integrated into the time course of MCF7-LTED adaptation. Dynamic and widespread genomic changes were observed, including amplification of the ESR1 locus consequently linked to an increase in ERα. Dynamic transcriptomic profiles were also observed that correlated significantly with genomic changes and were influenced by transcription factors known to be involved in acquired resistance or cell proliferation (e.g. IRF1 and E2F1, respectively) but, notably, not by canonical ERα transcriptional function. Consistently, at the molecular level, activation of growth factor signaling pathways by EGFR/ERBB/AKT and a switch from phospho-Ser118 (pS118)- to pS167-ERα were observed during MCF7-LTED adaptation. Evaluation of relevant clinical settings identified significant associations between MCF7-LTED and breast tumor transcriptome profiles that characterize ERα-negative status, early response to letrozole and recurrence after tamoxifen treatment. This study proposes a mechanism for acquired resistance to estrogen deprivation that is coordinated across biological levels and independent of canonical ERα function. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE20361 Biological reprogramming in acquired resistance to endocrine therapy of breast cancer. Oncogene 6.634 https://doi.org/10.1038/onc.2010.333 {Oncogene (6.634): 10.1038/onc.2010.333} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA125453 https://www.ebi.ac.uk/ena/browser/view/PRJNA125453 None [Overal design]LTED (long term estrogen deprived) cell line was generated from MCF-7 cells by long-term culture under estrogen deprivated conditions. And RNA samples were obtained after 3, 15, 30, 90, 120, 150 and 180 days.; [Treatment]'None'; [Growth]'MCF7 cells were grown in phenol red-free RPMI medium containing 10% dextran-coated charcoal-stripped FBS (DCC-FBS) during 6 months'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''tissue: breast cancer; cell line: MCF7; ' GSE65886 Homo sapiens 8 Genome binding/occupancy profiling by high throughput sequencing GPL18573 H4K12ac is regulated by estrogen receptor-alpha and is associated with BRD4 function and inducible transcription 2015-02-12 Hormone-dependent gene expression requires dynamic and coordinated epigenetic changes. Estrogen receptor-positive (ER+) breast cancer is particularly dependent upon extensive chromatin remodeling and changes in histone modifications for the induction of hormone-responsive gene expression. Our previous studies established an important role of bromodomain-containing protein-4 (BRD4) in promoting estrogen-regulated transcription and proliferation of ER+ breast cancer cells. Here, we investigated the association between genome-wide occupancy of histone H4 acetylation at lysine 12 (H4K12ac) and BRD4 in the context of estrogen-induced transcription. Similar to BRD4, we observed that H4K12ac occupancy increases near the transcription start sites (TSS) of estrogen-induced genes as well as at distal ERα binding sites in an estrogen-dependent manner. Interestingly, H4K12ac occupancy highly correlates with BRD4 binding and enhancer RNA production on ERα-positive enhancers. Consistent with an importance in estrogen-induced gene transcription, H4K12ac occupancy globally increased in ER-positive cells relative to ER-negative cells and these levels were further increased by estrogen treatment in an ERα-dependent manner. Together, these findings reveal a strong correlation between H4K12ac and BRD4 occupancy with estrogen-dependent gene transcription and further suggest that modulators of H4K12ac and BRD4 may serve as new therapeutic targets for hormone-dependent cancers. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE65886 H4K12ac is regulated by estrogen receptor-alpha and is associated with BRD4 function and inducible transcription. Oncotarget None https://doi.org/10.18632/oncotarget.3439 {Oncotarget (None): 10.18632/oncotarget.3439} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA275306 https://www.ebi.ac.uk/ena/browser/view/PRJNA275306 https://www.ncbi.nlm.nih.gov/sra?term=SRP054970 [Overal design]ChIP-seq profiles of H4K12ac in MCF7 cells treated with +/- estrogen treatment and MCF10A cells.; [Treatment]'After 2 days of hormone deprivation, vehicle (ethanol - Veh) was added as negative control.', 'After 2 days of hormone deprivation, vehicle (ethanol - Veh) was added as negative control for 2 hours.', 'After 2 days of hormone deprivation, MCF7 cells were treated with 10 nmol/L 17-β-estradiol (E2) (Sigma-Aldrich) treatment for 2 hours.', 'No special treatment.'; [Growth]"MCF7 cells were grown in phenol red- free high-glucose Dulbecco's Modified Eagle's Media (DMEM; Invitrogen) with 10% bovine growth serum (Thermo Scientific) and 1% penicillin/streptomycin. After one day of cell-splitting, the media was changed to DMEM containing 5% charcoal-dextran treated FBS (Biochrome).", 'MCF10A cells were grown in phenol-red free DMEM/F12 medium supplemented with 5% horse serum, 20 ng/mL epidermal growth factor, 0.1 µg/mL Cholera toxin, 10 µg/mL insulin, 0.5 µg/mL hydrocortisone, 1% penicillin/streptomycin at 37°C.'; [Extraction]'Cells were crosslinked with 1% Formaldehyde for 10 minutes and quenched with 1.25 M Glycine. The nuclear pellets were sonicated to the fragment range of 200-400 bp. Sonicated extracts were incubated with specific antibodies at 4˚C overnight and ChIP-immune complexes were pulled down using Protein A sepharose.\nLibrary preparations were done using NEBnext Ultra DNA library preparation kit according to the manufacturer’s instructions.'; [Cell type]'Human breast adenocarcinoma cell line', 'Breast epithelial cells''cell type: Human breast adenocarcinoma cell line; passages: 20-30; chip-seq antibody: Anti-acetyl-histone H4 (Lys12) (07-595; EMD Millipore) (1 µg used); cell line: MCF7; ', 'cell type: Breast epithelial cells; chip-seq antibody: Anti-acetyl-histone H4 (Lys12) (07-595; EMD Millipore) (1 µg used); cell line: MCF10A; ', 'cell type: Breast epithelial cells; cell line: MCF10A; ' GSE39693 Homo sapiens 4 Expression profiling by array GPL15207 Expression data from MCF7 and HCC1937 cells long-term treated with everolimus 2012-07-27 Inhibitors of the mechanistic target of rapamycin (mTOR) are currently used to treat advanced metastatic breast cancer. However, whether an aggressive phenotype is sustained through adaptation or resistance to mTOR inhibition remains unknown. Here, complementary studies in human tumors, cancer models and cell lines reveal transcriptional reprogramming that supports metastasis in response to mTOR inhibition. This cancer feature is driven by EVI1 and SOX9. EVI1 functionally cooperates with and positively regulates SOX9, and promotes the transcriptional upregulation of key mTOR pathway components (REHB and RAPTOR) and of lung metastasis mediators (FSCN1 and SPARC). The expression of EVI1 and SOX9 is associated with stem cell-like and metastasis signatures, and their depletion impairs the metastatic potential of breast cancer cells. These results establish the mechanistic link between resistance to mTOR inhibition and cancer metastatic potential, thus enhancing our understanding of mTOR targeting failure. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39693 Stem cell-like transcriptional reprogramming mediates metastatic resistance to mTOR inhibition. Oncogene 6.634 https://doi.org/10.1038/onc.2016.427 {Oncogene (6.634): 10.1038/onc.2016.427} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA171490 https://www.ebi.ac.uk/ena/browser/view/PRJNA171490 None [Overal design]MCF7 and HCC1937 cell cultures were treated with everolimus for approximately 120 days and subsequently RNA extracted, processed and hybridized on Affymetrix microarrays.; [Treatment]'MCF7 cells were treated with everolimus (100 nM) and HCC1937 cells were treated with everolimus (150 nM) or vehicle (DMSO) for 120 days.'; [Growth]'MCF7 and HCC1937 cells were cultured and maintained in RPMI medium containing 10% FBS and 2 mM glutamine.'; [Extraction]"Trizol extraction of total RNA was performed according to manufacturer's instructions"; [Cell type]'Source: ''cell line: MCF7; cell line orgin: Breast cancer; agent: vehicle (DMSO); ', 'cell line: MCF7; cell line orgin: Breast cancer; agent: Everolimus (100 nM); ', 'cell line: HCC1937; cell line orgin: Breast cancer; agent: vehicle (DMSO); ', 'cell line: HCC1937; cell line orgin: Breast cancer; agent: Everolimus (150 nM); ' GSE118923 Homo sapiens 6 Expression profiling by high throughput sequencing GPL19415 ATO treatment on mesenchymal stem cells (MSCs) interacting breast cancer cells 2018-08-22 Based on next generation RNA-seq, we examed Arsenic trioxide treatment (ATO) effect on MSCs-interacting MCF7 cells in 3D cultures. We found gap junction protein Cx43 is dramatically downregulated after ATO treatment.. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE118923 The Osteogenic Niche Is a Calcium Reservoir of Bone Micrometastases and Confers Unexpected Therapeutic Vulnerability. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2018.10.002 {Cancer cell (23.916): 10.1016/j.ccell.2018.10.002} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA487341 https://www.ebi.ac.uk/ena/browser/view/PRJNA487341 https://www.ncbi.nlm.nih.gov/sra?term=SRP158607 [Overal design]human breast cancer cell line MCF-7 cells cocultured with mouse MSCs in 3D culture, with or without ATO treatment, are subject to NGS and then analyzed.; [Treatment]'None'; [Growth]'2E5/well MCF-7 cells are cultured in DMEM with 10% FBS and then cocultured with 2E5/well mouse MSC in serum-free DMEM/F12 media in 6-well low attachment plates, treated with 5uM Arsenic trioxide or PBS (Vehicle) for <48h'; [Extraction]'After centrifuge, total RNA were extracted by Direct-zol RNA miniprep kit. . The first and second strand cDNA were prepared by SuperScript III First-Strand Synthesis System and NEBNext mRNA Second Strand Synthesis Module from at least 200ng total RNA for each sample. Illumina Nextera XT DNA Sample Prep Kit was used with 1 ng of dsDNA for the construction of sequencing libraries.\nRNA libraries were prepared for sequencing using nextera Illumina protocols'; [Cell type]'mouse MSC cells''cell line: human breast cancer cell line MCF-7; cell type: mouse MSC cells; growth protocol: MCF-7 cells cocultured with MSCs in 3D culture; passage: P140-P142; reporter gene: Firefly Luciferase (MCF-7); treatment: control; ', 'cell line: human breast cancer cell line MCF-7; cell type: mouse MSC cells; growth protocol: MCF-7 cells cocultured with MSCs in 3D culture; passage: P140-P142; reporter gene: Firefly Luciferase (MCF-7); treatment: ATO; ' GSE70508 Homo sapiens 36 Expression profiling by array GPL16686 Effect of ruxolitinib treatment on gene expression in triple-negative breast cancer cell lines 2015-07-06 HCC1143, HCC70, HCC38, and SUM159PT cells were treated for 4 or 24 hrs with 1uM ruxolitinib. Control cells were treated for 24 hrs with DMSO (0.1%). The purpose was to determine changes in gene expresison patterns following inhibition of JAK1/2 in the cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE70508 Triple-negative breast cancers with amplification of JAK2 at the 9p24 locus demonstrate JAK2-specific dependence. Science translational medicine 17.161 https://doi.org/10.1126/scitranslmed.aad3001 {Science translational medicine (17.161): 10.1126/scitranslmed.aad3001} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA288929 https://www.ebi.ac.uk/ena/browser/view/PRJNA288929 None [Overal design]Three independent experiments were conducted for three biological replicates at each time point, for each cell line; [Treatment]'ruxolitinib 1uM in DMSO for 4 or 24 hrs, or DMSO at 0.1% for 24 hrs'; [Growth]'ATCC-defined media + 10% fetal bovine serum'; [Extraction]'Qiagen RNEasy'; [Cell type]'Source: ''cell line: HCC1143; treatment: DMSO 0.1% 24 hrs; replicate: 1; ', 'cell line: HCC1143; treatment: DMSO 0.1% 24 hrs; replicate: 2; ', 'cell line: HCC1143; treatment: ruxolitinib 1uM 4 hrs; replicate: 1; ', 'cell line: HCC1143; treatment: ruxolitinib 1uM 4 hrs; replicate: 2; ', 'cell line: HCC1143; treatment: ruxolitinib 1uM 4 hrs; replicate: 3; ', 'cell line: HCC1143; treatment: ruxolitinib 1uM 24 hrs; replicate: 1; ', 'cell line: HCC1143; treatment: ruxolitinib 1uM 24 hrs; replicate: 2; ', 'cell line: HCC1143; treatment: ruxolitinib 1uM 24 hrs; replicate: 3; ', 'cell line: SUM159PT; treatment: DMSO 0.1% 24 hrs; replicate: 1; ', 'cell line: SUM159PT; treatment: DMSO 0.1% 24 hrs; replicate: 2; ', 'cell line: SUM159PT; treatment: ruxolitinib 1uM 4 hrs; replicate: 1; ', 'cell line: SUM159PT; treatment: ruxolitinib 1uM 4 hrs; replicate: 2; ', 'cell line: SUM159PT; treatment: ruxolitinib 1uM 4 hrs; replicate: 3; ', 'cell line: SUM159PT; treatment: ruxolitinib 1uM 24 hrs; replicate: 1; ', 'cell line: SUM159PT; treatment: ruxolitinib 1uM 24 hrs; replicate: 2; ', 'cell line: SUM159PT; treatment: ruxolitinib 1uM 24 hrs; replicate: 3; ', 'cell line: HCC38; treatment: DMSO 0.1% 24 hrs; replicate: 1; ', 'cell line: HCC38; treatment: DMSO 0.1% 24 hrs; replicate: 2; ', 'cell line: HCC38; treatment: DMSO 0.1% 24 hrs; replicate: 3; ', 'cell line: HCC38; treatment: ruxolitinib 1uM 4 hrs; replicate: 1; ', 'cell line: HCC38; treatment: ruxolitinib 1uM 4 hrs; replicate: 2; ', 'cell line: HCC38; treatment: ruxolitinib 1uM 4 hrs; replicate: 3; ', 'cell line: HCC38; treatment: ruxolitinib 1uM 24 hrs; replicate: 1; ', 'cell line: HCC38; treatment: ruxolitinib 1uM 24 hrs; replicate: 2; ', 'cell line: HCC38; treatment: ruxolitinib 1uM 24 hrs; replicate: 3; ', 'cell line: HCC70; treatment: DMSO 0.1% 24 hrs; replicate: 1; ', 'cell line: HCC70; treatment: DMSO 0.1% 24 hrs; replicate: 2; ', 'cell line: HCC70; treatment: ruxolitinib 1uM 4 hrs; replicate: 1; ', 'cell line: HCC70; treatment: ruxolitinib 1uM 24 hrs; replicate: 1; ', 'cell line: HCC70; treatment: ruxolitinib 1uM 24 hrs; replicate: 2; ', 'cell line: HCC70; treatment: ruxolitinib 1uM 24 hrs; replicate: 3; ', 'cell line: HCC1143; treatment: DMSO 0.1% 24 hrs; replicate: 3; ', 'cell line: SUM159PT; treatment: DMSO 0.1% 24 hrs; replicate: 3; ', 'cell line: HCC70; treatment: DMSO 0.1% 24 hrs; replicate: 3; ', 'cell line: HCC70; treatment: ruxolitinib 1uM 4 hrs; replicate: 2; ', 'cell line: HCC70; treatment: ruxolitinib 1uM 4 hrs; replicate: 3; ' GSE129558 Homo sapiens 120 Expression profiling by array GPL96 Study to evaluate the effect of technical repetition on gene expression measurements 2019-04-09 To evaluate the effect of technical repetition on gene expression measurements, we repeated the laboratory protocol at 6 different steps. Information was used to select probesets with a high technical reproducibility for the development of gene signatures. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE129558 SETER/PR: a robust 18-gene predictor for sensitivity to endocrine therapy for metastatic breast cancer. NPJ breast cancer 32.43 https://doi.org/10.1038/s41523-019-0111-0 {NPJ breast cancer (32.43): 10.1038/s41523-019-0111-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA531726 https://www.ebi.ac.uk/ena/browser/view/PRJNA531726 None [Overal design]20 breast cancer samples were profiled on Affymetrix U133A microarrays. The samples were chopped in pieces, mixed and 80% were used to repeat the laboratory protocol at five different levels: RNA extraction, cDNA synthesis, cRNA synthesis and re-scan of the same chip. The remaining 20% of the sample mix were used to repeat all steps, resulting in a total of six technical replicates.; [Treatment]'Patients prospectively consented to a surgical tissue sample'; [Growth]'N/A'; [Extraction]'Total RNA was extracted from tissue using Qiagen RNeasy columns.'; [Cell type]'Source: ''tissue: Breast cancer; sample number: 2; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 2; level of repetition: Full replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 2; level of repetition: Original; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 2; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 2; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 2; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 3; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR+/HER2+; ', 'tissue: Breast cancer; sample number: 3; level of repetition: Full replicate; immunohistochemistry subtype: HR+/HER2+; ', 'tissue: Breast cancer; sample number: 4; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 4; level of repetition: Full replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 4; level of repetition: Original; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 4; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 4; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 4; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 3; level of repetition: Original; immunohistochemistry subtype: HR+/HER2+; ', 'tissue: Breast cancer; sample number: 3; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR+/HER2+; ', 'tissue: Breast cancer; sample number: 3; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR+/HER2+; ', 'tissue: Breast cancer; sample number: 3; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR+/HER2+; ', 'tissue: Breast cancer; sample number: 5; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 5; level of repetition: Full replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 6; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 6; level of repetition: Full replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 5; level of repetition: Original; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 5; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 5; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 5; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 6; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 6; level of repetition: Original; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 6; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 6; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 7; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR-/HER2+; ', 'tissue: Breast cancer; sample number: 7; level of repetition: Full replicate; immunohistochemistry subtype: HR-/HER2+; ', 'tissue: Breast cancer; sample number: 8; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 8; level of repetition: Full replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 7; level of repetition: Original; immunohistochemistry subtype: HR-/HER2+; ', 'tissue: Breast cancer; sample number: 7; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR-/HER2+; ', 'tissue: Breast cancer; sample number: 7; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR-/HER2+; ', 'tissue: Breast cancer; sample number: 7; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR-/HER2+; ', 'tissue: Breast cancer; sample number: 8; level of repetition: Original; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 8; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 8; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 8; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 9; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 9; level of repetition: Full replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 10; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 10; level of repetition: Full replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 9; level of repetition: Original; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 9; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 9; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 9; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 10; level of repetition: Original; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 10; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 10; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 10; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 11; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 11; level of repetition: Full replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 12; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 12; level of repetition: Full replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 13; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR-/HER2+; ', 'tissue: Breast cancer; sample number: 13; level of repetition: Full replicate; immunohistochemistry subtype: HR-/HER2+; ', 'tissue: Breast cancer; sample number: 14; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 14; level of repetition: Full replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 11; level of repetition: Original; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 11; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 11; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 11; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 12; level of repetition: Original; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 12; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 12; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 12; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 13; level of repetition: Original; immunohistochemistry subtype: HR-/HER2+; ', 'tissue: Breast cancer; sample number: 13; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR-/HER2+; ', 'tissue: Breast cancer; sample number: 13; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR-/HER2+; ', 'tissue: Breast cancer; sample number: 13; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR-/HER2+; ', 'tissue: Breast cancer; sample number: 14; level of repetition: Original; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 14; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 14; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 14; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 15; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 15; level of repetition: Full replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 16; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR+/HER2+; ', 'tissue: Breast cancer; sample number: 16; level of repetition: Full replicate; immunohistochemistry subtype: HR+/HER2+; ', 'tissue: Breast cancer; sample number: 17; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 17; level of repetition: Full replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 18; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 18; level of repetition: Full replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 19; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 19; level of repetition: Full replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 20; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 20; level of repetition: Full replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 15; level of repetition: Original; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 15; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 15; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 15; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 16; level of repetition: Original; immunohistochemistry subtype: HR+/HER2+; ', 'tissue: Breast cancer; sample number: 16; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR+/HER2+; ', 'tissue: Breast cancer; sample number: 16; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR+/HER2+; ', 'tissue: Breast cancer; sample number: 16; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR+/HER2+; ', 'tissue: Breast cancer; sample number: 17; level of repetition: Original; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 17; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 17; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 17; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 18; level of repetition: Original; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 18; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 18; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 18; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 19; level of repetition: Original; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 19; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 19; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 19; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 20; level of repetition: Original; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 20; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 20; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 20; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR+/HER2-; ', 'tissue: Breast cancer; sample number: 1; level of repetition: Full replicate re-scan; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 1; level of repetition: Full replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 1; level of repetition: Original; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 1; level of repetition: RNA extraction replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 1; level of repetition: cDNA synthesis replicate; immunohistochemistry subtype: HR-/HER2-; ', 'tissue: Breast cancer; sample number: 1; level of repetition: cRNA synthesis replicate; immunohistochemistry subtype: HR-/HER2-; ' GSE82171 Homo sapiens 20 Expression profiling by array GPL570 Expression data from primary breast tumors 2016-06-02 Expression data were used to predict the activity status of diverse pathways, which were compared to Tamoxifen response 20 M1 breast cancer patients were evaluated for the activity of transcriptomic pathways. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE82171 Phosphoserine aminotransferase 1 is associated to poor outcome on tamoxifen therapy in recurrent breast cancer. Scientific reports 4.011 https://doi.org/10.1038/s41598-017-02296-w {Scientific reports (4.011): 10.1038/s41598-017-02296-w} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA324254 https://www.ebi.ac.uk/ena/browser/view/PRJNA324254 None [Overal design]Comparison of response to Tamoxifen; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted with RNABee (Campro, Veenendaal, the Netherlands) according to the manufacturer procedure'; [Cell type]'Source: ''response: SD; ', 'response: PD; ', 'response: PR; ' GSE111665 Homo sapiens 3 Expression profiling by high throughput sequencing GPL20301 Next Generation Sequencing Facilitates Quantitative Analysis of a circRNA, hsa_circ_0005505 regulated Transcriptomes in breast cancer cells (MDA-MB-231 lung metastatic cells LM2) 2018-03-11 Purpose: hsa_circ_0005505 stably knockdown cells (circ-sh1 and circ-sh2) and its corresponing control cells (con-sh) were constructed using its specific shRNAs. Next-generation sequencing (NGS) has used to examine hsa_circ_0005505 regulated transcripts. Methods: mRNA profiles of circsh1, circsh2 and con-sh were generated by deep sequencing using IlluminaI HiSeq 4000. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using SYBR Green assays Results: We found 816 and 909 transcripts downregulated in circ-sh1 and circ-sh2 cells compared with con-sh cells, respectively. But 712 and 723 transcripts upregulated in circ-sh1 and circ-sh2 cells compared with con-sh cells, respectively. The differential expression with a fold change ≥1.5 and p value <0.05. Conclusions: Our study represents the first detailed analysis of hsa_circ_0005505-regulated transcripts in breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE111665 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA437772 https://www.ebi.ac.uk/ena/browser/view/PRJNA437772 https://www.ncbi.nlm.nih.gov/sra?term=SRP134738 [Overal design]Next Generation Sequencing Facilitates Quantitative Analysis of a circRNA, hsa_circ_0005505 regulated Transcriptomes in breast cancer cells; [Treatment]'N/A'; [Growth]'The cells cultured in DMEM medium. The media were supplemented with 10% fetal bovine serum (FBS). Cultures were incubated at 37°C in a humidified chamber with 5% CO2.'; [Extraction]"Total RNA extracted using RNeasy Plus Mini Kit with QIAshredder columns (Qiagen) following manufacturer's instructions\nRNA libraries were prepared for sequencing using standard Illumina protocols"; [Cell type]'Source: ''cell line: MDA-MB-231 lung metastatic cells LM2; ' GSE42640 Mus musculus 110 Expression profiling by array GPL2881; GPL4134; GPL10732; GPL11383 Transcriptomic Classification of Genetically Engineered Mouse Models of Breast Carcinoma Identifies Human Subtype Counterparts 2012-11-29 Background: Human breast cancer is a heterogeneous disease consisting of multiple molecular subtypes. Genetically engineered mouse models (GEMMs) are useful resources for studying breast cancers in vivo under genetically controlled and immune competent conditions. Identifying murine models with conserved human tumor features will facilitate etiology determinations, highlight the effects of mutations on pathway activation, and improve preclinical drug validation. Results: Transcriptomic profiles of 27 murine models of mammary carcinoma and normal mammary tissue were determined using gene expression microarrays. Hierarchical clustering analysis identified 17 distinct murine subtypes (classes). Across species analyses using three independent human breast cancer datasets identified eight murine classes that represent specific human breast cancer subtypes. Multiple models were associated with human basal-like tumors including TgC3(1)-Tag, TgWap-Myc, and Trp53-/-. Interestingly, the TgWAPCre-Etv6 model mimicked the HER2-enriched subtype, a group of human tumors without a murine counterpart in previous comparative studies. Gene signature analysis identified hundreds of commonly expressed pathways between linked mouse and human subtypes, highlighting potentially common genetic drivers of tumorigenesis and candidate pathways for therapeutic intervention. Conclusion: This study consolidates murine models of breast carcinoma into the largest comprehensive transcriptomic dataset to date to identify human-mouse disease subtype counterparts. This approach illustrates the value of comparisons between species to identify murine models that faithfully mimic the human condition and indicates that multiple GEMMs are needed to represent the diversity of human breast cancers. These trans-species associations should guide model selection during preclinical study design to ensure appropriate representatives of the human disease subtypes are used. Keywords: breast cancer, comparative genomics, genetically engineered mouse models, and molecular pathway signatures https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE42640 Transcriptomic classification of genetically engineered mouse models of breast cancer identifies human subtype counterparts. Genome biology 14.028 https://doi.org/10.1186/gb-2013-14-11-r125 {Genome biology (14.028): 10.1186/gb-2013-14-11-r125} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA182516 https://www.ebi.ac.uk/ena/browser/view/PRJNA182516 None [Overal design]reference x sample; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA isolated using Qiagen RNeasy Kit', 'Total RNA isolated using Qiagen Rneasy Kit'; [Cell type]'Source: ''reference: common reference RNA sample for these experiments consisted of total RNA harvested from equal numbers of C57Bl6/J and 129 male and female Day1 pups; ', 'sample: p53null; ', 'sample: p18null; ', 'sample: p53het, Irradiated; ', 'sample: Normal Mammary; ', 'sample: C3 Tag; ', 'sample: MMTV Aib1; ', 'sample: MMTV FGF3; ', 'sample: MMTV HRAS; ', 'sample: MMTV Myc; ', 'sample: MMTV Neu; ', 'sample: MMTV PyMT; ', 'sample: MMTV Wnt1; ', 'sample: Mammary Normal Lactating; ', 'sample: Wap Myc; ', 'sample: Rbnull; ', 'sample: Pik3ca with H1047R mutation; ', 'sample: STAT1null; ' GSE23905 Homo sapiens 8 Expression profiling by array GPL570; GPL6947 miR-126 over-expression in highly metastatic LM2 breast cancer cells. 2010-08-31 miR-126 were over-expressed using the miR-Vec system in highly metastatic LM2 cells. The LM2 cell line are described in detail in Minn et al. Nature 2005 This approach was used to conduct an unbiased search for specific miR-126 target genes in breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23905 A microRNA regulon that mediates endothelial recruitment and metastasis by cancer cells. Nature 43.070 https://doi.org/10.1038/nature10661 {Nature (43.070): 10.1038/nature10661} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA133187 https://www.ebi.ac.uk/ena/browser/view/PRJNA133187 None [Overal design]4 Samples; [Treatment]'None'; [Growth]'Cells were grown in DMEM supplemented with 10% FBS.'; [Extraction]'Total RNA was extracted using the Mirvana kit from Ambion. Quality control was performed with Agilent Bioanalyser', 'Total RNA was extraced using the miRVana Kit (Ambion)'; [Cell type]'Source: ''tumor type: Poorly Metastatic; cell line: MDA-MB-231; ', 'tumor type: Highly Metastatic; cell line: LM2; ', 'cell line: LM2; expression: Control; ', 'cell line: LM2; expression: miR-126 Over-expression; ' GSE141142 Homo sapiens 24 Expression profiling by high throughput sequencing GPL18573 An immune-centric exploration of BRCA1 and BRCA2 germline mutation related breast and ovarian cancers 2019-11-27 Background:This study was a hypothesis generating exploration of genomic data collected at diagnosis for 19 patients, who later participated in a clinical trial. BRCA1/2 germline mutation related hereditary cancers are candidates for new immune therapeutic interventions. However, contrary to what is expected of tumors with compromised DNA repair, a prominent tumor mutation burden (TMB) in hereditary breast and ovarian cancers in this cohort, was not correlated with high global immune activity in their microenvironments. More information is needed about the relationship between genomic instability, phenotypes and immune microenvironments of BRCA1/2 related hereditary tumors in order to find appropriate markers of immune activity and the most effective anticancer immune strategies. Methods:Mining and statistical analyses of the original DNA and RNA sequencing data and data available from The Cancer Genome Atlas (TCGA) were performed using the R computing environment. To interpret the data, we have used published literature and web available resources such as Gene Ontology Tools, The Cancer immunome Atlas (TCIA) and the Cancer Research Institute iAtlas. Results: We found that BRCA1/2 germline related breast and ovarian cancers do not represent a unique phenotypic identity, but that they express a range of phenotypes similar to sporadic cancers. Importantly, BRCA2 germline mutation related breast tumors have a different profile of genomic instability compared to those related to BRCA1. However, all breast and ovarian BRCA1/2 related tumors are characterized by high homologous recombination deficiency (HRD) and low aneuploidy. Interestingly, all sporadic high grade serous ovarian cancers (HGSOC) and most of the subtypes of triple negative breast cancers (TNBC), but not other types of breast cancer, also express a high degree of HRD. Conclusion: : Tumor mutation burdon (TMB) is not associated with the magnitude of the immune response in hereditary BRCA1/2 related breast and ovarian cancers or in sporadic TNBC and sporadic HGSOC. Hereditary tumors express phenotypes as heterogenous as sporadic tumors with various degree of “BRCAness” and various characteristics of the immune microenvironments. The subtyping criteria developed for sporadic tumors can be applied for the classification of hereditary tumors and possibly also characterization of their immune microenvironment. A high HRD score may be a good candidate biomarker for response to platinum, and potentially PARP-inhibition. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE141142 An immune-centric exploration of BRCA1 and BRCA2 germline mutation related breast and ovarian cancers. BMC cancer 2.933 https://doi.org/10.1186/s12885-020-6605-1 {BMC cancer (2.933): 10.1186/s12885-020-6605-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA592199 https://www.ebi.ac.uk/ena/browser/view/PRJNA592199 https://www.ncbi.nlm.nih.gov/sra?term=SRP233583 [Overal design]RNA sequencing data from FFPE samples of 19 patients with recurrent Triple Negative Breast Cancer (TNBC) or High Grade Serous Ovarian Cancer (HGSOC) from a Phase I clinical trial study (9 TNBC and 10 HGSOC) and 5 normal tissues are generated.; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen RNeasy FFPE kit is used for FFPE sample extraction.\nIllumina library preparation for RNA-Seq is done using the TruSeq RNA Access library prep kit. The samples were sequenced on Illumina Nextseq 500 high output v2 platform (2x75).'; [Cell type]'Source: ''cancer type: BRCA; tissue: Breast; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: PR; brca.status: Neg; brca.study.entry: Non-Carrier; Sex: Female; ', 'cancer type: BRCA; tissue: Breast; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: SD; brca.status: BRCA2; brca.study.entry: Carrier; Sex: Female; ', 'cancer type: BRCA; tissue: Breast; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: PR; brca.status: BRCA1; brca.study.entry: Carrier; Sex: Female; ', 'cancer type: BRCA; tissue: Breast; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: PR; brca.status: BRCA2; brca.study.entry: Carrier; Sex: Female; ', 'cancer type: BRCA; tissue: Breast; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: SD; brca.status: Neg; brca.study.entry: Carrier; Sex: Female; ', 'cancer type: BRCA; tissue: Breast; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: SD; brca.status: Neg; brca.study.entry: Non-Carrier; Sex: Female; ', 'cancer type: BRCA; tissue: Breast; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: SD; brca.status: NA; brca.study.entry: Unknown; Sex: Female; ', 'cancer type: BRCA; tissue: Ovary; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: SD; brca.status: BRCA1; brca.study.entry: Non-Carrier; Sex: Female; ', 'cancer type: BRCA; tissue: Ovary; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: PR; brca.status: BRCA1; brca.study.entry: Carrier; Sex: Female; ', 'cancer type: BRCA; tissue: Ovary; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: PR; brca.status: NA; brca.study.entry: Unknown; Sex: Female; ', 'cancer type: BRCA; tissue: Ovary; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: SD; brca.status: BRCA1; brca.study.entry: Carrier; Sex: Female; ', 'cancer type: BRCA; tissue: Ovary; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: NA; brca.status: BRCA2; brca.study.entry: Carrier; Sex: Female; ', 'cancer type: BRCA; tissue: Ovary; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: SD; brca.status: Neg; brca.study.entry: Non-Carrier; Sex: Female; ', 'cancer type: BRCA; tissue: Ovary; race: White; ethnicity: Non_Hispanic; sample.type: Tumor; reservation.type: FFPE; treatment.best.response: SD; brca.status: BRCA2; brca.study.entry: Carrier; Sex: Female; ', 'cancer type: NA; tissue: Breast; race: NA; ethnicity: NA; sample.type: Normal; reservation.type: FFPE; treatment.best.response: NA; brca.status: NA; brca.study.entry: NA; Sex: Female; ' GSE124934 Homo sapiens 4 Expression profiling by high throughput sequencing GPL16791 Gene expression altered by HOTAIR knockdown in MCF-7-TNR 2019-01-10 The human HOTAIR-specific siRNA and control siRNA were transfected into MCF-7-TNR cells. RNA was collected at 72 hrs after transfection. RNA-SEQ was carried out to profile the gene expression altered by HOTAIR knockdown. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124934 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA514345 https://www.ebi.ac.uk/ena/browser/view/PRJNA514345 https://www.ncbi.nlm.nih.gov/sra?term=SRP178255 [Overal design]The goal of this experiment was to profile the genes that are regulated by HOTAIR in a human breast cancer cell line. HOTAIR was knockdown by siRNA. Gene expression was probed globally using RNA-SEQ.; [Treatment]'HOTAIR-specific siRNA or control siRNA was transfected into MCF-7-TNR cells using RNAiMAX.'; [Growth]'MCF-7-TNR cells were cultured in DMEM with 10% FBS.'; [Extraction]'Total cell RNA was extracted when cells were ~80% confluent using TRIZOL.\nLibraries were constructed using the Illumina TruSeq Stranded Total RNA Library Prep Kit/Ribo-Zero Gold kit.'; [Cell type]'Breast cancer cell line''cell line: MCF-7-TNR; cell type: Breast cancer cell line; sirna: CTLsi; ', 'cell line: MCF-7-TNR; cell type: Breast cancer cell line; sirna: HOTAIRsi; ' GSE79761 Homo sapiens 12 Expression profiling by array GPL570 GR and ER co-activation alters the expression of differentiation genes and associates with improved ER+ breast cancer outcome 2016-03-31 Analysis of MCF-7 cells treated for 4h with Ethanol, Estradiol (E2), Dexamethasone (Dex), or Estradiol + Dexamethasone (E2 + Dex) In estrogen receptor (ER)-negative breast cancer (BC), high tumor glucocorticoid receptor (GR) expression has been associated with a relatively poor outcome. In contrast, using a meta-analysis of several genomic datasets, here we find that tumor GR mRNA expression is associated with improved ER+ relapse-free survival (RFS) (independently of progesterone receptor (PR) expression). To understand the mechanism by which GR expression is associated with a better ER+ BC outcome, the global effect of GR-mediated transcriptional activation in ER+ BC cells was studied. Analysis of GR chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq) in ER+/GR+ MCF-7 cells revealed that upon co-activation of GR and ER, GR chromatin association became enriched at proximal promoter regions. Furthermore, following ER activation, increased association of GR was observed at ER, FOXO, and AP1 response elements. In addition, it was determined that ER associated with GR response elements, suggesting that ER and GR interact in a complex. Co-activation of GR and ER resulted in increased expression (relative to ER activation alone) of transcripts that encode proteins promoting cellular differentiation (e.g. KDM4B, VDR) and inhibiting Wnt-signaling (IGFBP4). Finally, expression of these individual pro-differentiation genes was associated with significantly improved RFS in ER+ BC patients. Together, these data demonstrate that the co-expression and subsequent activity of tumor cell GR and ER contribute to the less aggressive natural history of early-stage BC by coordinating the altered expression of genes favoring differentiation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE79761 GR and ER Coactivation Alters the Expression of Differentiation Genes and Associates with Improved ER+ Breast Cancer Outcome. Molecular cancer research : MCR 4.484 https://doi.org/10.1158/1541-7786.MCR-15-0433 {Molecular cancer research : MCR (4.484): 10.1158/1541-7786.MCR-15-0433} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA316961 https://www.ebi.ac.uk/ena/browser/view/PRJNA316961 None [Overal design]Four treatment samples (Vehicle V, Dex D, E2, or Dex+E2). Three biological replicate experiments per sample. Vehicle sample is Ethanol control.; [Treatment]'MCF-7 cells were incubated in phenol red-free DMEM containing 2.5% charcoal-stripped serum for 4 days total (with a media change after 48h), MCF-7 cells were treated with either vehicle, Dex (100 nM), E2 (10 nM) or Dex/E2 for 4 h'; [Growth]'MCF-7 cells were grown at 37°C in 5% CO2 in Dulbecco’s Modified Eagle’s Medium (DMEM, Lonza) supplemented with 10% fetal bovine serum (FBS, Gemini Bio-Products), and 1% penicillin/streptomycin (Lonza).'; [Extraction]'Cells were lysed in a RNA lysis buffer (Ambion, Invitrogen) and total RNA was isolated using an PureLink ® RNA extraction kit (Ambion, Invitrogen)'; [Cell type]'Source: ''condition: Vehicle; cell line: MCF7; ', 'condition: Estradiol; cell line: MCF7; ', 'condition: Dexamethasone; cell line: MCF7; ', 'condition: Dexamethasone and Estradiol; cell line: MCF7; ' GSE19300 Mus musculus 8 Expression profiling by array GPL6096 Activation of ER-alpha network in MMTV-Wnt/ILK mammary tumors 2009-12-03 A transgenic mouse model, MMTV-Wnt/ILK, with mammary specific expression of both Wnt-1 and ILK, was generated by crossing the two mouse lines MMTV-Wnt-1 and MMTV-ILK. Affymetrix Mouse Exon chips were hybridized with material from four independent mammary tumors from each MMTV-Wnt-1 and MMTV-Wnt/ILK transgenic model, in order to identify possible signaling differences involved during increased tumor incidence. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE19300 Cooperative signaling between Wnt1 and integrin-linked kinase induces accelerated breast tumor development. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr2592 {Breast cancer research : BCR (5.676): 10.1186/bcr2592} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA120887 https://www.ebi.ac.uk/ena/browser/view/PRJNA120887 None [Overal design]One-way ANOVA: MMTV-Wnt vs. MMTV-Wnt/ILK; [Treatment]'None'; [Growth]'Nulliparous females were monitored bi-weekly for the appearance of a small palpable tumor nodule in the mammary fat pads.'; [Extraction]'1 μg of RNA was used as starting material and rRNA reduced using the RiboMinus Transcriptome Isolation Kit (Invitrogen) as per Affymetrix recommendations.'; [Cell type]'Source: ''tissue: mammary fat pad; gender: female; parity: nulliparous; transgenic strain: MMTV-Wnt-1; ', 'tissue: mammary fat pad; gender: female; parity: nulliparous; transgenic strain: MMTV-Wnt/ILK; ' GSE79787 Homo sapiens 4 Non-coding RNA profiling by high throughput sequencing GPL18573 small RNA sequencing for identifying hypoxic responsive miRNAs 2016-03-31 we identify certain hypoxia responsive miRNAs that associate with hypoxia-induced tumor malignancy https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE79787 miR-25/93 mediates hypoxia-induced immunosuppression by repressing cGAS. Nature cell biology 17.728 https://doi.org/10.1038/ncb3615 {Nature cell biology (17.728): 10.1038/ncb3615} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA317000 https://www.ebi.ac.uk/ena/browser/view/PRJNA317000 https://www.ncbi.nlm.nih.gov/sra?term=SRP072699 [Overal design]examination of global changes in small RNAs in four different lines; [Treatment]'1% hypoxia treatment for 18 hrs'; [Growth]'culture in DMEM medium'; [Extraction]'Trizol based RNA extraction method\nSmall RNA libraries were constructed using the NEBNext Small RNA Library prep kit.'; [Cell type]'epithelial''cell line: MCF7; cell type: epithelial; ' GSE126365 Homo sapiens 18 Expression profiling by high throughput sequencing GPL16791 ZRANB2 and SYF2 mediated splicing programs converging on ECT2 are involved in breast cancer cell resistance to doxorubicin 2019-02-11 We explored the regulation of alternative splicing in a cell model of breast cancer resistance to doxorubicin, and the impact of the depletion of two splicing factors (ZRANB2 and SYF2) in this context. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE126365 ZRANB2 and SYF2-mediated splicing programs converging on ECT2 are involved in breast cancer cell resistance to doxorubicin. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkz1213 {Nucleic acids research (11.147): 10.1093/nar/gkz1213} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA521712 https://www.ebi.ac.uk/ena/browser/view/PRJNA521712 https://www.ncbi.nlm.nih.gov/sra?term=SRP185438 [Overal design]We analyzed by RNA-seq, alternative splicing regulation between doxorubicin-resistant and sensitive cells, and between resistant cells with ot without depletion of either ZRANB2 or SYF2 (2 independent siRNAs for each, all conditions in triplicate).; [Treatment]'Cells were transfected with siRNAs at a final concentration of 100 nM with lipofectamine RNAimax from ThermoFischer Scientific.'; [Growth]'Cells were cultured in 4,5 g/L Glucose DMEM (Eurobio) supplemented with 10% (v/v) fetal bovine serum (Dutscher), and 2 mM L-Glutamine (Eurobio) in 5% CO2 at 37°C.'; [Extraction]'RNA was extracted from total cells using TRIzol Reagent (ThermoFiscer Scientific).\nLibraries were made using one µg of total RNA and the TruSeq Stranded mRNA Library Preparation Kit (Illumina) involving polyA+ RNA selection. Equimolar pool of libraries were sequenced on a Illumina HiSeq 2500 machine using paired-ends reads (PE, 2x101bp) and High Output run mode allowing to get 200 millions of raw reads per sample.'; [Cell type]'Breast cancer cell line''cell line: MCF7; cell type: Breast cancer cell line; transfected sirna: Negative Control siRNA; extract: Total cells; ', 'cell line: MCF7-DoxoR; cell type: Breast cancer cell line; transfected sirna: Negative Control siRNA; extract: Total cells; ', 'cell line: MCF7-DoxoR; cell type: Breast cancer cell line; transfected sirna: ZRANB2 #1 siRNA; extract: Total cells; ', 'cell line: MCF7-DoxoR; cell type: Breast cancer cell line; transfected sirna: ZRANB2 #2 siRNA; extract: Total cells; ', 'cell line: MCF7-DoxoR; cell type: Breast cancer cell line; transfected sirna: SYF2 #1 siRNA; extract: Total cells; ', 'cell line: MCF7-DoxoR; cell type: Breast cancer cell line; transfected sirna: SYF2 #2 siRNA; extract: Total cells; ' GSE111204 Homo sapiens 6 Expression profiling by array GPL6244 Effect of restricted glycolysis on gene expression in MDA-MB-231 cells 2018-02-27 Cultured breast cancer cells in standard media are highly glycolytic To determine the effect of glycolysis on gene expression in MDA-MB-231 we adapted cells to cuture in mediae containing 10 mM fructose, and compared the gene expression to cells cutured in standard high glucse (25 mM) DMEM https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE111204 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA436155 https://www.ebi.ac.uk/ena/browser/view/PRJNA436155 None [Overal design]Cells were adapted to growth in the different sugars for 25 days prior to analysis. Biological replicates represent separately adpated batches of cells.; [Treatment]'mRNA was prepared from cells at circa 70% confluency, circa 24 hours after replenishment of media'; [Growth]'Cells were cultured in DMEM media containing either 25 mM glucose or 10 mM fructose for 25 days, with regular passage and media changes'; [Extraction]'Qiagen RNAeasy with on column DNAse digestion'; [Cell type]'Source: ''cell line: MDA-MB-231; growth media: 25 mM glucose; ', 'cell line: MDA-MB-231; growth media: 10 mM fructose; ' GSE54275 Homo sapiens 486 Expression profiling by array GPL15931; GPL15932 Microarray gene expression analysis: Batch effect removal improves the cross-platform consistency 2014-01-22 Microarray is a powerful technique that has been used extensively for genome-wide gene expression analysis. Several different microarray technologies are available, but lack of standardization makes it challenging to compare and integrate data from different platforms. Furthermore, batch related biases within datasets are common, but are often not tackled prior to the data analysis, potentially affecting the end results. In the current study, a set of 234 breast cancer samples were analyzed on two different microarray platforms. The aim was to compare and evaluate the reproducibility and accuracy of gene expression measurements obtained from our in-house 29K array platform with data from Agilent SurePrint G3 microarray platform. The 29K dataset contained known batch-effects associated with the fabrication procedure. We here demonstrate how the use of ComBat batch adjustments method can unmask true biological signals by successfully overcoming systematic technical variations caused by differences between fabrication batches and microarray platforms. Paired correlation analysis revealed a high level of consistency between data obtained from the 29K gene expression platform and Agilent SurePrint G3 platform, which could be further improved by ComBat batch adjustment. Particularly high-variance genes were found to be highly reproducibly expressed across platforms. Furthermore, high concordance rates were observed both for prediction of estrogen receptor status and intrinsic molecular breast cancer subtype classification, two clinical important parameters. In conclusion, the current study emphasizes the importance of utilizing proper batch adjustment methods to reduce systematically technical bias when comparing and integrating data from different fabrication batches and microarray platforms. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54275 Microarray-based RNA profiling of breast cancer: batch effect removal improves cross-platform consistency. BioMed research international 2.197 https://doi.org/10.1155/2014/651751 {BioMed research international (2.197): 10.1155/2014/651751} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA236097 https://www.ebi.ac.uk/ena/browser/view/PRJNA236097 None [Overal design]This study was performed on a series of 243 frozen primary breast tumors obtained from the bio-banks of the Dept. of Pathology, Odense University Hospital and the Danish Breast Cancer Cooperative Group (DBCG). The tumor samples comprise a subset of a larger series of 253 tumor samples previously reported. Breast tumor tissues from 120 patients with germline mutations in BRCA1 (n = 33) or BRCA2 (n = 22) or familial non-BRCA1/2 cases with no detectable germline mutation in BRCA1 or BRCA2 (n = 65) were included in the study.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted from freshly frozen tumor tissue using Trizol Reagent (Invitrogen) and RNeasy Micro Kit (Qiagen).'; [Cell type]'Source: ''menopause_status: Postmenopausal; age: 64; tumor_size: 6; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'reference: Universal Human Reference RNA (Stratagene); ', 'menopause_status: Premenopausal; age: 49; tumor_size: 20; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 36; tumor_size: 51; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.3319G>T, Exon11, p.(Glu1107*); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Postmenopausal; age: 68; tumor_size: 7; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 55; tumor_size: 30; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5143A>C, Exon18, p.(Ser1715Arg); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Premenopausal; age: 45; tumor_size: 42; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: Normal; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 46; tumor_size: 21; who: Medullary carcinoma; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; her2_dbcg: 0; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5213G>A, Exon20, p.(Gly1738Glu); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Postmenopausal; age: 75; tumor_size: 32; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 71; tumor_size: 46; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 41; tumor_size: 11; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: BRCA1; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA1 c.1082_1092del, Exon11, p.(Ser361*); general_brca1_pred_agilent: BRCA1; ', 'menopause_status: Premenopausal; age: 41; tumor_size: 12; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 57; tumor_size: 21; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: BRCA1; pam50agilent: LumB; er: 1; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5266dupC, Exon20, p.(Gln1756Profs*74); general_brca1_pred_agilent: BRCA1; ', 'menopause_status: Postmenopausal; age: 85; tumor_size: 13; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Perimenopausal; age: 60; tumor_size: 23; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 46; tumor_size: 30; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 38; tumor_size: 16; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; her2_dbcg: 0; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5266dupC, Exon20, p.(Gln1756Profs*74); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Postmenopausal; age: 45; tumor_size: 17; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 69; tumor_size: 11; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Perimenopausal; age: 82; tumor_size: 27; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 53; tumor_size: 7; who: Tubular carcinoma; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 69; tumor_size: 15; who: Invasive lobular carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 69; tumor_size: 25; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Basal; er: 0; pr: 0; her2: 0; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; basal_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 67; tumor_size: 30; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 36; tumor_size: 14; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; group: BRCA1; pam50agilent: Her2; er: 1; pr: 1; her2: 1; mutation_hgvs: BRCA1 c.3400G>T, Exon11, p.(Glu1134*); general_brca1_pred_agilent: Sporadic; ', 'age: 76; who: Invasive ductal carcinoma; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Basal; er: 0; pr: 0; her2: 0; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; basal_brca1_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 52; tumor_size: 23; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5089T>C, Exon18, p.(Cys1697Arg); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Premenopausal; age: 39; tumor_size: 15; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 0; group: BRCA1; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.2476delA, Exon11, p.(Thr826Glnfs*20); general_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 72; tumor_size: 28; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: BRCA2; pam50agilent: LumB; er: 1; pr: 0; her2: 0; mutation_hgvs: BRCA2 c.2808_2811delACAA, Exon11, p.(Ala938Profs*21); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Premenopausal; age: 41; tumor_size: 15; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5089T>C, Exon18, p.(Cys1697Arg); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Postmenopausal; age: 64; tumor_size: 32; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Her2; er: 0; pr: 0; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 38; tumor_size: 14; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: BRCA2; pam50agilent: LumB; her2_dbcg: 1; er: 1; pr: 1; her2: 1; mutation_hgvs: BRCA2 c.6373delA, Exon11, p.(Thr2125Profs*12); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 58; tumor_size: 15; who: Invasive lobular carcinoma; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Perimenopausal; age: 51; tumor_size: 50; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 47; tumor_size: 19; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Her2; her2_dbcg: 1; er: 0; pr: 0; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 86; who: Invasive ductal carcinoma; group: Sporadic; pam50agilent: LumA; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 74; tumor_size: 11; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 0; group: BRCA1; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.4987-?_5193+?del, Exon17-19, p.(Met1663_Glu1731del); general_brca1_pred_agilent: BRCA1; ', 'menopause_status: Postmenopausal; age: 65; tumor_size: 15; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Perimenopausal; age: 75; tumor_size: 22; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Basal; er: 0; pr: 0; her2: 0; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; basal_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 51; tumor_size: 31; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 46; tumor_size: 14; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: BRCA2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.6486_6489delACAA, Exon11, p.(Lys2162Asnfs*5); general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 72; tumor_size: 35; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 76; tumor_size: 25; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Basal; er: 0; pr: 0; her2: 0; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; basal_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 78; tumor_size: 46; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 61; tumor_size: 20; who: Invasive lobular carcinoma; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 45; tumor_size: 28; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: BRCA2; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.6601delT, Exon11, p.(Ser2201Leufs*5); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 65; tumor_size: 40; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 62; tumor_size: 22; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; group: BRCA1; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.2475delC, Exon11, p.(Asp825Glufs*21); general_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 56; tumor_size: 20; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; her2_dbcg: 0; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5213G>A, Exon20, p.(Gly1738Glu); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Premenopausal; age: 50; tumor_size: 13; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 39; tumor_size: 15; who: Invasive lobular carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: BRCA2; pam50agilent: Normal; her2_dbcg: 0; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.145G>T, Exon3, p.(Glu49*); general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Premenopausal; age: 50; tumor_size: 32; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Perimenopausal; age: 87; tumor_size: 47; who: Mucinous carcinoma; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 65; tumor_size: 50; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 76; tumor_size: 28; who: Other; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 48; tumor_size: 25; who: Invasive lobular carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 32; tumor_size: 25; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.181T>G, Exon5, p.(Cys61Gly); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Perimenopausal; age: 95; tumor_size: 24; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumA; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 42; tumor_size: 18; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: BRCA2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.7617+1G>A, Splice mut, Exon15 skipping; general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Perimenopausal; age: 85; tumor_size: 18; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 50; tumor_size: 20; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Other; age: 55; tumor_size: 16; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 52; tumor_size: 26; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 86; tumor_size: 20; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 42; tumor_size: 15; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 0; pr_dbcg: 1; group: BRCA2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.1310_1313delAAGA, Exon10, p.(Lys437Ilefs*22); general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 28; tumor_size: 27; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: BRCA2; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.2830A>T, Exon11, p.(Lys944*); general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 56; tumor_size: 26; who: Invasive lobular carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 53; tumor_size: 9; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 32; tumor_size: 52; who: Invasive lobular carcinoma; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.1505delT, Exon11, p.(Leu502*); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Postmenopausal; age: 66; tumor_size: 61; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumA; er: 1; pr: 0; her2: 1; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 45; tumor_size: 26; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; er: 1; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.3319G>T, Exon11, p.(Glu1107*); general_brca1_pred_agilent: Sporadic; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Premenopausal; age: 36; tumor_size: 19; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Perimenopausal; age: 61; tumor_size: 9; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: Her2; er: 0; pr: 0; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 54; tumor_size: 12; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 56; tumor_size: 31; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 46; tumor_size: 14; who: Invasive ductal carcinoma; grade: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 59; tumor_size: 10; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 61; tumor_size: 25; who: Medullary carcinoma; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; her2_dbcg: 0; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.3400G>T, Exon11, p.(Glu1134*); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Premenopausal; age: 51; tumor_size: 14; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 32; tumor_size: 25; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 0; pr_dbcg: 0; group: BRCA2; pam50agilent: Basal; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA2 c.5754delT, Exon11, p.(His1918Glnfs*45); general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 57; tumor_size: 23; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: BRCA1; pam50agilent: LumB; er: 1; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5503C>T, Exon24, p.(Arg1835*); general_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 70; tumor_size: 36; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 72; tumor_size: 25; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 46; tumor_size: 30; group: BRCA1; pam50agilent: LumB; er: 1; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.2475delC, Exon11, p.(Asp825Glufs*21); general_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 66; tumor_size: 11; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 44; tumor_size: 26; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Premenopausal; age: 43; tumor_size: 30; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 46; tumor_size: 30; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 0; pr_dbcg: 1; group: BRCA1; pam50agilent: Normal; er: 0; pr: 1; her2: 0; mutation_hgvs: BRCA1 c.181T>G, Exon5, p.(Cys61Gly); general_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 70; tumor_size: 14; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'age: 74; group: Sporadic; pam50agilent: Her2; er: 1; pr: 0; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Premenopausal; age: 49; tumor_size: 22; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Her2; er: 0; pr: 0; her2: 1; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 54; tumor_size: 13; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 84; tumor_size: 13; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'age: 74; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 50; tumor_size: 27; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 54; tumor_size: 8; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 60; tumor_size: 19; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 52; tumor_size: 15; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; group: BRCA1; pam50agilent: LumB; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA1 c.115T>G, Exon3, p.(Cys39Gly); general_brca1_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 45; tumor_size: 28; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: BRCA2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.6486_6489delACAA, Exon11, p.(Lys2162Asnfs*5); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Premenopausal; age: 48; tumor_size: 25; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 60; tumor_size: 47; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 36; tumor_size: 15; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: BRCA2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.6486_6489delACAA, Exon11, p.(Lys2162Asnfs*5); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 60; tumor_size: 10; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5153-?_5193+?del, Exon19, p.(Trp1718Serfs*2); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Postmenopausal; age: 55; tumor_size: 27; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; her2_dbcg: 0; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.2475delC, Exon11, p.(Asp825Glufs*21); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Premenopausal; age: 27; tumor_size: 14; who: Tubular carcinoma; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Other; age: 51; tumor_size: 12; who: Invasive lobular carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 66; tumor_size: 18; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 60; tumor_size: 18; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA2; pam50agilent: LumB; er: 1; pr: 0; her2: 0; mutation_hgvs: BRCA2 c.9015delA, Exon23, p.(Arg3005Serfs*23); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Premenopausal; age: 41; tumor_size: 19; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: BRCA2; pam50agilent: LumB; er: 1; pr: 0; her2: 0; mutation_hgvs: BRCA2 c.2830A>T, Exon11, p.(Lys944*); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Premenopausal; age: 53; tumor_size: 18; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: Basal; er: 0; pr: 0; her2: 1; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; basal_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 61; tumor_size: 25; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Her2; er: 0; pr: 0; her2: 1; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; ', 'age: 63; group: BRCA2; pam50agilent: LumB; er: 1; pr: 0; her2: 0; mutation_hgvs: BRCA2 c.8575delC, Exon20, p.(Gln2859Lysfs*4); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Perimenopausal; age: 87; tumor_size: 16; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: Basal; er: 0; pr: 0; her2: 0; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; basal_brca1_pred_agilent: Sporadic; ', 'menopause_status: Perimenopausal; age: 66; tumor_size: 19; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: BRCA2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.3530_3533delACAG, Exon11, p.(Asp1177Alafs*19); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Premenopausal; age: 37; tumor_size: 25; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.6490_6492delinsGACT, Exon11, p.(Gln2164Aspfs*12); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Premenopausal; age: 25; tumor_size: 8; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; her2_dbcg: 0; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.181T>G, Exon5, p.(Cys61Gly); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Postmenopausal; age: 51; tumor_size: 15; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 28; tumor_size: 30; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: BRCA1; pam50agilent: LumB; er: 1; pr: 1; her2: 1; mutation_hgvs: BRCA1 c.2475delC, Exon11, p.(Asp825Glufs*21); general_brca1_pred_agilent: BRCA1; ', 'menopause_status: Postmenopausal; age: 54; tumor_size: 24; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 43; tumor_size: 15; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 64; tumor_size: 9; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 68; tumor_size: 18; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 66; tumor_size: 26; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Her2; her2_dbcg: 1; er: 0; pr: 0; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 40; tumor_size: 18; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5266dupC, Exon20, p.(Gln1756Profs*74); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 50; tumor_size: 14; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 0; pr_dbcg: 0; group: BRCA2; pam50agilent: Basal; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA2 c.1813delA, Exon10, p.(Ile605Tyrfs*9); general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 83; tumor_size: 16; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 75; tumor_size: 14; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 74; tumor_size: 12; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; her2_dbcg: 1; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Premenopausal; age: 39; tumor_size: 21; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: Her2; her2_dbcg: 1; er: 1; pr: 1; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 42; tumor_size: 40; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; er: 1; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5213G>A, Exon20, p.(Gly1738Glu); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 85; tumor_size: 15; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 43; tumor_size: 10; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 88; tumor_size: 130; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 1; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 48; tumor_size: 8; who: Invasive lobular carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 69; tumor_size: 35; who: Other; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'age: 37; group: BRCA1; pam50agilent: Basal; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.2476delA, Exon11, p.(Thr826Glnfs*20); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Postmenopausal; age: 57; tumor_size: 8; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 52; tumor_size: 18; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 54; tumor_size: 22; who: Medullary carcinoma; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 79; tumor_size: 12; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: Her2; er: 0; pr: 0; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 57; tumor_size: 34; who: Invasive ductal carcinoma; grade: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 69; tumor_size: 25; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumA; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 77; tumor_size: 30; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: Her2; er: 0; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 34; tumor_size: 60; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: BRCA2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.2808_2811delACAA, Exon11, p.(Ala938Profs*21); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 58; tumor_size: 35; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 31; tumor_size: 29; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; her2_dbcg: 0; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5266dupC, Exon20, p.(Gln1756Profs*74); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Postmenopausal; age: 78; tumor_size: 15; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumA; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 52; tumor_size: 19; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: Her2; er: 1; pr: 0; her2: 1; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 60; tumor_size: 60; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Basal; er: 0; pr: 0; her2: 0; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: BRCA2; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Premenopausal; age: 31; tumor_size: 60; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 0; pr_dbcg: 0; group: BRCA2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.1310_1313delAAGA, Exon10, p.(Lys437Ilefs*22); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 53; tumor_size: 35; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: BRCA2; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.8575delC, Exon20, p.(Gln2859Lysfs*4); general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 36; tumor_size: 28; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: BRCA1; pam50agilent: Basal; her2_dbcg: 0; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.1556delA, Exon11, p.(Lys519Argfs*13); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Premenopausal; age: 38; tumor_size: 23; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; group: BRCA1; pam50agilent: Her2; her2_dbcg: 1; er: 1; pr: 1; her2: 1; mutation_hgvs: BRCA1 c.4389C>A, Exon14, p.(Tyr1463*); general_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 59; tumor_size: 15; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 66; tumor_size: 34; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Basal; her2_dbcg: 0; er: 0; pr: 0; her2: 0; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; basal_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 55; tumor_size: 24; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Basal; her2_dbcg: 0; er: 0; pr: 0; her2: 0; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; basal_brca1_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 54; tumor_size: 22; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 42; tumor_size: 28; who: Invasive lobular carcinoma; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 68; tumor_size: 29; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Her2; er: 0; pr: 0; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 61; tumor_size: 45; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 86; tumor_size: 20; who: Tubular carcinoma; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Perimenopausal; age: 64; tumor_size: 80; who: Invasive lobular carcinoma; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 56; tumor_size: 12; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 55; tumor_size: 26; who: Invasive ductal carcinoma; grade: 3; group: Sporadic; pam50agilent: Her2; er: 0; pr: 0; her2: 1; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Premenopausal; age: 41; tumor_size: 22; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 0; group: BRCA1; pam50agilent: Basal; er: 0; pr: 0; her2: 0; mutation_hgvs: BRCA1 c.5089T>C, Exon18, p.(Cys1697Arg); general_brca1_pred_agilent: BRCA1; basal_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 75; tumor_size: 20; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 72; tumor_size: 17; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: BRCA1; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA1 c.4987-?_5193+?del, Exon17-19, p.(Met1663_Glu1731del); general_brca1_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 63; tumor_size: 30; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 81; tumor_size: 38; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Perimenopausal; age: 85; tumor_size: 28; who: Invasive lobular carcinoma; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 0; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Perimenopausal; age: 69; tumor_size: 42; who: Mucinous carcinoma; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Premenopausal; age: 50; tumor_size: 25; who: Invasive lobular carcinoma; er_dbcg: 1; group: BRCA2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.5576_5579delTTAA, Exon11, p.(Ile1859Lysfs*3); general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 48; tumor_size: 28; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: BRCA2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; mutation_hgvs: BRCA2 c.2830A>T, Exon11, p.(Lys944*); general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Perimenopausal; age: 75; tumor_size: 18; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; ge neral_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 53; tumor_size: 30; who: Invasive lobular carcinoma; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; ', 'menopause_status: Postmenopausal; age: 75; tumor_size: 37; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: Sporadic; pam50agilent: Basal; er: 0; pr: 0; her2: 0; general_brca1_pred_agilent: BRCA1; general_brca2_pred_agilent: Sporadic; basal_brca1_pred_agilent: BRCA1; ', 'menopause_status: Premenopausal; age: 44; tumor_size: 45; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 0; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: BRCA2; lumb_brca2_pred_agilent: Sporadic; ', 'menopause_status: Postmenopausal; age: 80; tumor_size: 20; who: Invasive lobular carcinoma; grade: 1; er_dbcg: 1; group: Sporadic; pam50agilent: LumA; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; ', 'menopause_status: Premenopausal; age: 47; tumor_size: 19; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: Sporadic; pam50agilent: LumB; er: 1; pr: 1; her2: 0; general_brca1_pred_agilent: Sporadic; general_brca2_pred_agilent: Sporadic; lumb_brca2_pred_agilent: Sporadic; ', 'group: Sporadic; pam50agilent: LumB; ', 'group: BRCA2; pam50agilent: LumB; ', 'group: BRCA1; pam50agilent: Basal; ', 'group: Sporadic; pam50agilent: Basal; ', 'age: 50; er_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; family_id: 054; lumb_brca2-like_pred: BRCA2-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 41; tumor_size: 17; who: Invasive lobular carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; family_id: 029; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 36; tumor_size: 30; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Her2; er: 0; pr: 0; her2: 1; family_id: 028; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 47; tumor_size: 20; who: Medullary carcinoma; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Basal; er: 0; pr: 0; her2: 0; family_id: 051; basal_brca1-like_pred: BRCA1-like; meth_brca1: TRUE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 57; tumor_size: 27; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 052; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 53; tumor_size: 17; who: Invasive ductal carcinoma; grade: 3; group: non-BRCA1/2; pam50agilent: Basal; er: 0; pr: 0; her2: 0; family_id: 035; basal_brca1-like_pred: BRCA1-like; ', 'menopause_status: Postmenopausal; age: 76; tumor_size: 24; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 017; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 81; tumor_size: 34; who: Invasive ductal carcinoma; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Her2; er: 0; pr: 0; her2: 0; family_id: 018; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 50; tumor_size: 30; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; family_id: 058; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 45; tumor_size: 16; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; family_id: 030; lumb_brca2-like_pred: Sporadic-like; ', 'menopause_status: Premenopausal; age: 32; tumor_size: 35; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Basal; her2_dbcg: 1; er: 0; pr: 0; her2: 0; family_id: 008; basal_brca1-like_pred: Sporadic-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 66; tumor_size: 11; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 0; her2: 0; family_id: 025; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 61; tumor_size: 9; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 0; her2: 0; family_id: 041; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 64; tumor_size: 14; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; family_id: 053; lumb_brca2-like_pred: Sporadic-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 65; tumor_size: 40; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Her2; er: 0; pr: 0; her2: 0; family_id: 055; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 42; tumor_size: 13; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Basal; er: 0; pr: 0; her2: 0; family_id: 023; basal_brca1-like_pred: BRCA1-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 43; tumor_size: 10; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 013; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 41; tumor_size: 62; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; family_id: 034; lumb_brca2-like_pred: BRCA2-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 33; tumor_size: 20; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; family_id: 024; lumb_brca2-like_pred: Sporadic-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 68; tumor_size: 37; who: Invasive lobular carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; family_id: 044; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Perimenopausal; age: 61; tumor_size: 17; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Her2; er: 0; pr: 0; her2: 1; family_id: 022; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 39; tumor_size: 8; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Basal; er: 0; pr: 0; her2: 0; family_id: 026; basal_brca1-like_pred: BRCA1-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 54; tumor_size: 14; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 0; her2: 1; family_id: 009; lumb_brca2-like_pred: BRCA2-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 64; tumor_size: 25; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 042; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 57; tumor_size: 15; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 014; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 47; tumor_size: 32; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Basal; her2_dbcg: 0; er: 0; pr: 0; her2: 0; family_id: 027; basal_brca1-like_pred: BRCA1-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 46; tumor_size: 22; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 017; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 48; tumor_size: 19; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 1; family_id: 005; ', 'menopause_status: Premenopausal; age: 29; tumor_size: 22; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: Her2; er: 1; pr: 1; her2: 1; family_id: 018; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 70; tumor_size: 11; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 0; her2: 0; family_id: 048; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 45; tumor_size: 22; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 1; family_id: 029; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 54; tumor_size: 12; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; family_id: 024; lumb_brca2-like_pred: Sporadic-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 37; tumor_size: 45; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; family_id: 045; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 38; tumor_size: 23; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; family_id: 039; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 43; tumor_size: 24; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: Normal; er: 0; pr: 1; her2: 1; family_id: 011; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 86; tumor_size: 32; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 0; her2: 0; family_id: 006; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 37; tumor_size: 8; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Basal; er: 0; pr: 0; her2: 0; family_id: 031; basal_brca1-like_pred: BRCA1-like; meth_brca1: TRUE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 45; tumor_size: 16; who: Invasive lobular carcinoma; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 015; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 66; tumor_size: 11; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 050; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 62; tumor_size: 18; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; family_id: 030; lumb_brca2-like_pred: Sporadic-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 72; tumor_size: 21; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 0; her2: 0; family_id: 043; lumb_brca2-like_pred: Sporadic-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'age: 73; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 042; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 63; tumor_size: 23; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; family_id: 036; lumb_brca2-like_pred: Sporadic-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 59; tumor_size: 45; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 0; her2: 0; family_id: 014; lumb_brca2-like_pred: Sporadic-like; ', 'menopause_status: Postmenopausal; age: 59; tumor_size: 16; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 029; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 47; tumor_size: 15; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; family_id: 032; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 36; tumor_size: 15; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Normal; er: 0; pr: 0; her2: 0; family_id: 007; meth_brca1: TRUE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 76; tumor_size: 8; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 021; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Perimenopausal; age: 71; tumor_size: 15; who: Invasive lobular carcinoma; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 046; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 50; tumor_size: 30; who: Invasive lobular carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; family_id: 019; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 55; tumor_size: 12; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 004; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 63; tumor_size: 12; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; family_id: 027; lumb_brca2-like_pred: Sporadic-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 35; group: non-BRCA1/2; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 0; her2: 0; family_id: 057; lumb_brca2-like_pred: BRCA2-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 45; tumor_size: 120; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumB; er: 1; pr: 1; her2: 0; family_id: 034; lumb_brca2-like_pred: BRCA2-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 46; tumor_size: 10; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 003; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Other; age: 48; tumor_size: 51; who: Invasive lobular carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; family_id: 010; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 42; tumor_size: 16; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 016; ', 'menopause_status: Premenopausal; age: 45; tumor_size: 27; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 0; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Basal; her2_dbcg: 0; er: 0; pr: 0; her2: 0; family_id: 031; basal_brca1-like_pred: BRCA1-like; meth_brca1: TRUE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 29; tumor_size: 35; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 0; group: non-BRCA1/2; pam50agilent: Her2; her2_dbcg: 1; er: 1; pr: 0; her2: 1; family_id: 047; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Postmenopausal; age: 54; tumor_size: 51; who: Invasive lobular carcinoma; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 038; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Other; age: 70; tumor_size: 18; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: Her2; er: 1; pr: 1; her2: 1; family_id: 056; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 52; tumor_size: 80; who: Invasive ductal carcinoma; grade: 2; er_dbcg: 0; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 1; family_id: 002; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 45; tumor_size: 20; who: Invasive ductal carcinoma; grade: 3; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumB; her2_dbcg: 0; er: 1; pr: 1; her2: 0; family_id: 012; lumb_brca2-like_pred: BRCA2-like; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 34; tumor_size: 61; who: Invasive lobular carcinoma; grade: 2; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; her2_dbcg: 0; er: 1; pr: 1; her2: 0; family_id: 037; meth_brca1: FALSE; meth_brca2: FALSE; ', 'menopause_status: Premenopausal; age: 51; tumor_size: 7; who: Invasive ductal carcinoma; grade: 1; er_dbcg: 1; pr_dbcg: 1; group: non-BRCA1/2; pam50agilent: LumA; er: 1; pr: 1; her2: 0; family_id: 020; meth_brca1: FALSE; meth_brca2: FALSE; ', 'group: BRCA2; pam50agilent: Basal; ', 'group: BRCA1; pam50agilent: LumB; ', 'group: BRCA2; pam50agilent: LumA; ', 'group: BRCAx; pam50agilent: LumB; ', 'group: BRCAx; pam50agilent: Her2; ', 'group: BRCAx; pam50agilent: LumA; ', 'group: BRCAx; pam50agilent: Basal; ', 'group: BRCAx; pam50agilent: Normal; ', 'group: BRCA1; pam50agilent: LumA; ', 'group: BRCA1; pam50agilent: Her2; ', 'group: BRCA2; pam50agilent: Normal; ', 'group: BRCA1; pam50agilent: Normal; ', 'group: Sporadic; pam50agilent: Her2; ', 'group: Sporadic; pam50agilent: LumA; ', 'group: Sporadic; pam50agilent: Normal; ' GSE125743 Homo sapiens 54 Expression profiling by high throughput sequencing GPL20795 Fractional Deletion of Compound Kushen Injection Indicates Cytokine Signaling Pathways are Critical for its Perturbation of the Cell Cycle 2019-01-28 We have used computational and experimental biology approaches to identify candidate mechanisms of action of a traditional Chinese medicine; Compound Kushen Injection (CKI), in a breast cancer cell line in which CKI has been shown to cause apoptosis. Because CKI is a complex mixture of plant secondary metabolites, we used a high-performance liquid chromatography (HPLC) fractionation and reconstitution approach to define chemical fractions required for CKI to induce apoptosis in MDA-MB-231 cells. Our initial fractionation separated major from minor compounds, and showed that the major compounds accounted for little of the activity of CKI. By systematically perturbing the major compounds in CKI we found that removal of no single major compound could alter the effect of CKI on cell viability and apoptosis. However, simultaneous removal of two major compounds identified oxymatrine and oxysophocarpine as critical compounds with respect to CKI activity. We then used RNA sequencing and transcriptome analysis to correlate compound removal with gene expression and phenotype data. We determined that many compounds in CKI are required for its effectiveness in triggering apoptosis but that significant modulation of its activity is conferred by a small number of compounds. In conclusion, CKI may be typical of many plant based extracts that contain many compounds in that no single compound is responsible for all of the bioactivity of the mixture and that many compounds interact in a complex fashion to influence a network containing many targets. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE125743 Effect of Compound Kushen Injection, a Natural Compound Mixture, and Its Identified Chemical Components on Migration and Invasion of Colon, Brain, and Breast Cancer Cell Lines. Frontiers in oncology 4.137 https://doi.org/10.3389/fonc.2019.00314 {Frontiers in oncology (4.137) doi:10.3389/fonc.2019.00314}; {Scientific reports (4.011) doi:10.1038/s41598-019-50271-4}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA517432 https://www.ebi.ac.uk/ena/browser/view/PRJNA517432 https://www.ncbi.nlm.nih.gov/sra?term=SRP182663 [Overal design]High-depth paired-end RNA-seq from MDA-MB-231 cell line. Each sample contains 3 biological replicates. N_2(where N represents the total number of compounds in CKI, N_2 represents removal of Omt and Ospc from CKI which is N-OmtOspc), N_3 represents removal of Mac, Omt and Ospc from CKI (hence N-MacOmtOspc), OO represents two compounds only: Omt and Ospc, MOO represents three compounds only: Mac, Omt and Ospc, N_Mac represents removal of Mac from CKI (hence N-Mac), N_Nme represents removal of Nme from CKI, N_Omt represents removal of Omt from CKI, and N_Tri represents removal of Tri from CKI. See the manuscript doi: https://doi.org/10.1101/462135 for more details.; [Treatment]'Drug treatments were as follows: CKI (2.0 mg/m) or fractionated and reconstituted mixtures (2 mg/ml equivalent) for 24 and 48 hours'; [Growth]"MDA-MB-231 cells were purchased from the American Type Culture Collection (ATCC, VA, USA). HEK-293 and HFF were kindly provided by Prof. Andrea Yool (Medical School, University of Adelaide). Cells were cultured in Dulbecco's Modified Eagle's Medium (Thermo Fisher Scientific) with 10 % Fetal bovine serum (Thermo Fisher Scientific) at 370C with 5 % CO2."; [Extraction]'Total RNA was isolated by using an RNA extraction kit (Thermo Fisher Scientific) according to the manufacturer’s instructions and RNA samples were quantified and quality determined using a Bioanalyzer at the Cancer Genome Facility of the Australian Cancer Research Foundatin (Australia).\nRNA samples with RNA integrity number (RINs) > 7.0 were sent to be sequenced at Novogene (China). Briefly, after QC procedures were performed, mRNA was isolated using oligo(dT) beads and randomly fragmented by adding fragmentation buffer, followed by cDNA synthesis primed with random hexamers. Next, a custom second-strand synthesis buffer (Illumina) , dNTPs, RNase H and DNA polymerase I were added for second-strand synthesis. After end repair, barcode ligation and sequencing adaptor ligation, the double-stranded cDNA library was size selected and PCR amplified. Sequencing was carried out on an Illumina HiSeq platform PE150 with paired-end 150 bp reads.'; [Cell type]'Source: ''cell line: MDA-MB-231; tumor type: breast cancer; treatment: UT; time: 24h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: CKI; time: 24h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: N_2; time: 24h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: N_3; time: 24h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: OO; time: 24h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: MOO; time: 24h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: UT; time: 48h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: CKI; time: 48h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: N_2; time: 48h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: N_3; time: 48h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: OO; time: 48h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: MOO; time: 48h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: N_Mac; time: 48h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: N_Nme; time: 48h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: N_Omt; time: 48h; ', 'cell line: MDA-MB-231; tumor type: breast cancer; treatment: N_Tri; time: 48h; ' GSE87479 Homo sapiens 8 Expression profiling by array GPL17077 Global surveillance of somatic alterations in triple negative breast cancers by whole exon sequencing analyses 2016-09-29 Triple negative breast cancers (TNBC), defined by lacking the expression of oestrogen receptor-alpha (ERa), progesterone receptor, and HER2, is considered to be one of the most aggressive subtypes of all breast cancers. To elucidate the genomic and molecular aberrations in TNBC, we performed whole exon sequencing (WES) analysis on 36 TNBC, and identified 117 genes that significantly mutated (q < 0.05) in TNBC including MUC4, MUC6, TP53, and PIK3CA. Interestingly, genes associated with chromatin regulators including the subunits of SWI/SNF complex were frequently mutated in 44.7% of the cases. Furthermore, from the aspect of the possible association of epigenetic dysregulation and TNBC carcinogenesis, we focused on epigenome and genetic alterations of SALL3, an intrinsic inhibitor of DNMT3A, and identified the role of its dysfunction on cancer cell growth. Our study suggests that epigenetic aberrations caused by somatic alterations including DNA methylation might be a potential pathogenesis of TNBC in a certain number of cases. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE87479 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA344888 https://www.ebi.ac.uk/ena/browser/view/PRJNA344888 None [Overal design]Human TNBC cell line, BT-20, was seeded at a density of 2.5x10^5 cells per 3.5 cm dish. Cells were transfected with 50nM siRNA (siEGFP or siSALL3) by Lipofectamine RNAiMAX reagent. Total RNA was extracted 48h and 96h after transfection. 100 ng of total RNA from each sample was amplified using T7 RNA polymerase with simultaneous Cy3-labeled CTP incorporation. Then, 2 μg of Cy3-labeled cRNA was fragmented, and hybridized onto the Agilent Whole Human Genome Microarray 8x60K slide. Then, a slide was scanned by the Agilent Microarray scanner system. The data were analyzed using GeneSpring. We identified up- and down-regulated genes common to siSALL3_48h and siSALL3_96h compared with siEGFP_48h. The fold change was >2.0.; [Treatment]"BT-20 was seeded at a density of 2.5 x 10^5 cells per 3.5 cm dish in MEM with 10% FBS, Penicillin G 100 units/ml, Streptomycin 100 ug/ml and amphotericin B 0.025 ug/ml. Cells were transfected with 50nM siRNA (siEGFP or siSALL3) treatment by Lipofectamine RNAiMAX reagent (Life Technologies, Carlsbad, CA) according to manufacturer's protocol."; [Growth]'None'; [Extraction]'Total RNA was extracted 48h and 96h after transfection by NucleoSpin RNA II (TaKaRa Bio, Shiga, Japan).'; [Cell type]'triple negative breast cancer cell line''cell line: BT-20; cell type: triple negative breast cancer cell line; sirna: siEGFP; time: 48h; ', 'cell line: BT-20; cell type: triple negative breast cancer cell line; sirna: siSALL3; time: 48h; ', 'cell line: BT-20; cell type: triple negative breast cancer cell line; sirna: siEGFP; time: 96h; ', 'cell line: BT-20; cell type: triple negative breast cancer cell line; sirna: siSALL3; time: 96h; ' GSE117747 Homo sapiens 45 Non-coding RNA profiling by high throughput sequencing GPL18573 MicroRNA-mediated suppression of the TGF-β pathway confers transmissible and reversible CDK4/6 inhibitor resistance (miRNA-Seq) 2018-07-26 CDK4/6 inhibition is now part of the standard armamentarium for patients with estrogen receptor (ER)-positive breast cancer, so that defining mechanisms of resistance is a pressing issue. Here, we identify increased CDK6 expression as a key determinant of acquired resistance after exposure to palbociclib in ER-positive breast cancer cells. Increased CDK6 in resistant cells was dependent on TGF-β pathway suppression via miR-432-5p expression. Exosomal miR-432-5p expression mediated transfer of the resistance phenotype between neighboring cell populations. We confirmed these data in pre-treatment and post-progression biopsies from a parotid cancer patient who had responded to ribociclib, demonstrating clinical relevance of this mechanism. Additionally, the CDK4/6 inhibitor resistance phenotype can be reversed in vitro and in vivo by a prolonged drug holiday. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE117747 MicroRNA-Mediated Suppression of the TGF-β Pathway Confers Transmissible and Reversible CDK4/6 Inhibitor Resistance. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2019.02.023 {Cell reports (7.815): 10.1016/j.celrep.2019.02.023} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA483061 https://www.ebi.ac.uk/ena/browser/view/PRJNA483061 https://www.ncbi.nlm.nih.gov/sra?term=SRP155416 [Overal design]We performed miRNAseq in 44 tumor biopsies taken from patients who received CDK4/6 inhibitor treatment. Samples were grouped based on the patients response into sensitive (S), inherent (IR) or aquired (AR) CDK4/6 inhibitor resistance.; [Treatment]'All patients were treated with a CDK4/6'; [Growth]'None'; [Extraction]"Qiagen's AllPrep DNA/RNA/miRNA Universal\nNEBNext® Small RNA Library Prep Set for Illumina, as per manufacturers instructions"; [Cell type]'Source: ''sample type: Tissue; cdk4/6 inhibitor phenotype: Sensitive; ', 'sample type: Tissue; cdk4/6 inhibitor phenotype: Intrinsic Resistance; ', 'sample type: Tissue; cdk4/6 inhibitor phenotype: Aquired Resistance; ', 'sample type: Tissue; cdk4/6 inhibitor phenotype: NA; ' GSE140396 Homo sapiens 4 Expression profiling by high throughput sequencing GPL24676 Next Generation Sequencing Quantitative Analysis of TEAD Palmitoylation Inhibitor MGH-CP1 in Breast Cancer Cell Line 2019-11-14 Purpose: The goal of this study is to understand the signaling pathway alteration in cancer cell line treated with TEAD palmitoylation inhibitor MGH-CP1, and to further validate TEAD inhibitor for specifity in TEAD-YAP interuption. Methods:Breast cancer cell line MDA-MB-231 was chosen to be treated with TEAD palmitoylation inhibitor MGH-CP1 at 10μM for 24 hours. Total RNA was isolated for the analysis. RNA samples were sent to Novogen for library construction, RNA sequencing and raw data process. Results: MGH-CP1 specifically blocks TEAD transcriptional activity compared with YAP/TAZ siRNA in MDA-MB-231 cells. Conclusions: Our study privides gene expression profiling evidence to validate our TEAD palmitoylation inhibitor MGH-CP1 as specific small molecule to block TEAD transcriptional activity. We report the application of next generation sequencing technology for high-throughput profiling of TEAD palmitoylation inhibitor MGH-CP1 in breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE140396 Lats1/2 Sustain Intestinal Stem Cells and Wnt Activation through TEAD-Dependent and Independent Transcription. Cell stem cell 21.464 https://doi.org/10.1016/j.stem.2020.03.002 {Cell stem cell (21.464): 10.1016/j.stem.2020.03.002} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA589597 https://www.ebi.ac.uk/ena/browser/view/PRJNA589597 None [Overal design]Examination of vehicle control and MGH-CP1 in one breast cancer cell line. *** Submitter has indicated raw files are no longer available.; [Treatment]'Cells were treated with vehicle control or MGH-CP1 for 24 hours'; [Growth]'MDA-MB-231 cells were culture in DMEM supplied with 10% FBS and Penicillin-Streptomycin'; [Extraction]"RNA was harvested using RNeasy Mini Kit (Qiagen 74104)\nmRNA from Eukaryote organisms is purified from total RNA using poly-T oligo-attached magnetic beads (For prokaryotes, mRNA was purified through the removal of rRNA by using kit). The mRNA is first fragmented randomly by addition of fragmentation buffer.Then first strand cDNA is synthesized using random hexamer primer and M-MuLV Reverse Transcriptase (RNase H-). Second strand cDNA synthesis is subsequently performed using DNA Polymerase I and RNase H. Double-stranded cDNA is purified using AMPure XP beads. Remaining overhangs of the purified double-stranded cDNA are converted into blunt ends via exonuclease/polymerase activities. After adenylation of 3' ends of DNA fragments, NEBNext Adaptor with hairpin loop structure is ligated to prepare for hybridization(1). In order to select cDNA fragments of preferentially 150~200 bp in length, the library fragments are purified with AMPure XP system (Beckman Coulter, Beverly, USA). Finally, the final library is gotten by PCR amplification and purification of PCR products by AMPure XP beads."; [Cell type]'breast cancer cells''cell type: breast cancer cells; cell line: MDA-MB-231; treatment: vehicle control; ', 'cell type: breast cancer cells; cell line: MDA-MB-231; treatment: MGH-CP1 10μM 24 hours; ' GSE60882 Homo sapiens 6 Expression profiling by array GPL570 Effect of tamoxifen on early gene expression in T47D and MDA-MB-231 cells 2014-08-28 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60882 Tamoxifen induces a pluripotency signature in breast cancer cells and human tumors. Molecular oncology 5.962 https://doi.org/10.1016/j.molonc.2015.05.008 {Molecular oncology (5.962): 10.1016/j.molonc.2015.05.008} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA259734 https://www.ebi.ac.uk/ena/browser/view/PRJNA259734 None [Overal design]Refer to individual Series; [Treatment]'T47D cells were incubated with vehicle, E2 (10-6M) or tamoxifen (10-6M) for 3 hours after preincubation for 4 hours with medium containing 10% charcoal stripped FBS', 'MDA-MB-231 cells were incubated with vehicle, E2 (10-6M) or tamoxifen (10-6M) for 3 hours after preincubation for 4 hours with medium containing 10% charcoal stripped FBS'; [Growth]'The human breast cancer cell line T47D was obtained from DSMZ (Braunschweig, Germany) and cultured in RPMI 1640 supplemented with 10% fetal bovine serum, at 37 °C, 5% CO2.', 'The human breast cancer cell line MDA-MB-231 was obtained from DSMZ (Braunschweig, Germany) and cultured in RPMI 1640 supplemented with 10% fetal bovine serum, at 37 °C, 5% CO2.'; [Extraction]'Total RNA was isolated using Nucleospin II columns (Macheray-Nagel, Dttren, Germany), according to the manufacturer’s instructions.'; [Cell type]'Source: ''cell line: T47D; treatment: 3 hours with 0.1% Ethanol; ', 'cell line: T47D; treatment: 3 hours with 10-6M estradiol; ', 'cell line: T47D; treatment: 3 hours with 10-6M tamoxifen; ', 'cell line: MDA-MB-231; treatment: 3 hours with 0.1% Ethanol; ', 'cell line: MDA-MB-231; treatment: 3 hours with 10-6M estradiol; ', 'cell line: MDA-MB-231; treatment: 3 hours with 10-6M tamoxifen; ' GSE10466 Homo sapiens 27 Expression profiling by array GPL2746 Genomics of signalling crosstalk of estrogen receptor alpha in breast cancer cells 2008-02-11 The estrogen receptor a (ERa) is a ligand-regulated transcription factor. However, a wide variety of other extracellular signals can activate ERa in the absence of estrogen. The impact of these alternate modes of activation on gene expression profiles has not been characterized. We show that estrogen, growth factors and cAMP elicit surprisingly distinct ERa-dependent transcriptional responses in human MCF7 breast cancer cells. In response to growth factors and cAMP, ERa primarily activates and represses genes, respectively. The combined treatments with the antiestrogen tamoxifen and cAMP or growth factors regulate yet other sets of genes. In many cases, tamoxifen is perverted to an agonist, potentially mimicking what is happening in certain tamoxifen-resistant breast tumors and emphasizing the importance of the cellular signaling environment. Using a computational analysis, we predicted that a Hox protein might be involved in mediating such combinatorial effects, and then confirmed it experimentally. Although both tamoxifen and cAMP block the proliferation of MCF7 cells, their combined application stimulates it, and this can be blocked with a dominant-negative Hox mutant. Thus, the activating signal dictates both target gene selection and regulation by ERa, and this has consequences on global gene expression patterns that may be relevant to understanding the progression of ERa-dependent carcinomas. Keywords: treatment response https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE10466 Genomics of signaling crosstalk of estrogen receptor alpha in breast cancer cells. PloS one 2.776 https://doi.org/10.1371/journal.pone.0001859 {PloS one (2.776): 10.1371/journal.pone.0001859} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA108025 https://www.ebi.ac.uk/ena/browser/view/PRJNA108025 None [Overal design]10 treatment conditions (3 biological replicates for each, totalling 30 individual samples), of which 3 were untreated controls. Each replicate was hybridized to a separate chip, totalling 27 cDNA slides representing 9 unique conditions.; [Treatment]'Cells were treated for 4 hours with 100 nM 17β-estradiol (E2). 24 hours prior to treatment, cells were starved of serum. 30 min prior to induction, 50 µg/ml cycloheximide was added to all cultures.', 'Cells were treated for 4 hours with 100 nM ICI182,780 (ICI). 24 hours prior to treatment, cells were starved of serum. 30 min prior to induction, 50 µg/ml cycloheximide was added to all cultures.', 'Cells were treated for 4 hours with 100 nM 4-hydroxytamoxifen (OHT). 24 hours prior to treatment, cells were starved of serum. 30 min prior to induction, 50 µg/ml cycloheximide was added to all cultures.', 'Cells were treated for 4 hours with 1mM 8-Br-cAMP (cAMP). 24 hours prior to treatment, cells were starved of serum. 30 min prior to induction, 50 µg/ml cycloheximide was added to all cultures.', 'Cells were treated for 4 hours with 1mM 8-Br-cAMP (cAMP) + 100 nM ICI182,780 (ICI). 24 hours prior to treatment, cells were starved of serum. 30 min prior to induction, 50 µg/ml cycloheximide was added to all cultures.', 'Cells were treated for 4 hours with 1mM 8-Br-cAMP (cAMP) + 100 nM 4-hydroxytamoxifen (OHT). 24 hours prior to treatment, cells were starved of serum. 30 min prior to induction, 50 µg/ml cycloheximide was added to all cultures.', 'Cells were treated for 4 hours with 50 μg/ml EGF and 50 μg/ml IGF-I. 24 hours prior to treatment, cells were starved of serum. 30 min prior to induction, 50 µg/ml cycloheximide was added to all cultures.', 'Cells were treated for 4 hours with 50 μg/ml EGF and 50 μg/ml IGF-I + 100 nM ICI182,780 (ICI). 24 hours prior to treatment, cells were starved of serum. 30 min prior to induction, 50 µg/ml cycloheximide was added to all cultures.', 'Cells were treated for 4 hours with 50 μg/ml EGF and 50 μg/ml IGF-I + 100 nM 4-hydroxytamoxifen (OHT). 24 hours prior to treatment, cells were starved of serum. 30 min prior to induction, 50 µg/ml cycloheximide was added to all cultures.'; [Growth]"Cells were grown in phenol red-free Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% (v/v) charcoal-treated fetal calf serum (FCS), 1 mM sodium pyruvate, 2 mM L-glutamine, 100 U/ml penicillin, 100 µg/ml streptomycin."; [Extraction]"Total RNA extracted using Trizol following manufacturer's instructions"; [Cell type]'Source: ''Cell line: MCF7.SH; ' GSE18431 Homo sapiens 12 Expression profiling by array GPL6947 Gene expression profile of NR2E3 in MCF7 cells 2009-10-06 While the roles of individual nuclear receptor (NR) in human diseases have been well characterized, interplays among NRs have not been extensively characterized due, in part, to technical difficulties in simultaneously monitoring molecular activities of all 48 NR genes. Using systems-level analysis of publically available gene expression data from NCI-60 cell lines, we uncovered novel interaction between ESR1 and orphan receptor NR2E3. Expression of NR2E3 is significantly associated with expression of ESR1 in NCI-60 cell lines as well as in breast cancer patients. To investigate how NR2E3 gene signatures are globally correlated with ESR1 signaling pathway, we performed microarray after knocking down NR2E3 or ESR1 in MCF-7 cells. Keywords: DNA microarray (Illumina human Ht12 V3) https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE18431 Reconstruction of nuclear receptor network reveals that NR2E3 is a novel upstream regulator of ESR1 in breast cancer. EMBO molecular medicine 10.624 https://doi.org/10.1002/emmm.201100187 {EMBO molecular medicine (10.624): 10.1002/emmm.201100187} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA118229 https://www.ebi.ac.uk/ena/browser/view/PRJNA118229 None [Overal design]3 shControl, 3 shNR2E3, 3 siLuc, 3 siESR1; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was isolated from tissues with mirVanaTM RNA Isolation labeling kit (Ambion Inc) according to the manufacturer's protocol. RNA quality and integrity were confirmed by ExperionTM Automated Electrophoresis System (BIO-RAD)"; [Cell type]'Source: ''cell line: MCF7; ' GSE16380 Mus musculus 8 Expression profiling by array GPL1261 Gene expression analyses of C/EBPb knockout in stem/progenitor cell populations 2009-06-02 CCAAT/enhancer binding protein beta (C/EBPb) is a member of a family of highly conserved transcription factors that regulates numerous genes involved in proliferation and differentiation in a variety of tissues. C/EBPb is deregulated in human breast cancer and germline deletion of this gene results in multiple defects in mammary gland development. We hypothesized that C/EBPb regulates mammary stem cell self-renewal, maintenance and/or differentiation through the regulation of multiple target genes that coordinate mammary gland development. Utilizing both a germline knockout mouse model and a conditional knockout strategy, we demonstrated that mammosphere formation was significantly decreased in C/EBPb-deficient mammary epithelial cells (MECs). The ability of C/EBPb-deleted MECs to regenerate the mammary gland in vivo was severely impaired when transplanted at limiting dilution. Furthermore, serial transplantation of C/EBPb-null mammary tissue resulted in decreased outgrowth potential when compared to wildtype, and an early senescence phenotype. Flow cytometric analysis revealed that C/EBPb-null MECs contain a lower frequency of repopulating stem cells accompanied by an increase in committed, differentiated luminal cells as compared to wildtype. Microarray analysis of stem/progenitor cell populations was performed and revealed an alteration in cell fate specification in C/EBPb-null glands, exemplified by the aberrant expression of basal markers in the luminal cell compartment. Collectively, our studies demonstrate that C/EBPb is a critical regulator of mammary stem cell differentiation, and an important determinant of luminal cell fate specification. Keywords: multiple group comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE16380 CCAAT/enhancer binding protein beta regulates stem cell activity and specifies luminal cell fate in the mammary gland. Stem cells (Dayton, Ohio) 5.614 https://doi.org/10.1002/stem.297 {Stem cells (Dayton, Ohio) (5.614): 10.1002/stem.297} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA115291 https://www.ebi.ac.uk/ena/browser/view/PRJNA115291 None [Overal design]To identify potential signaling pathways regulated by C/EBPb in stem/progenitor cells, microarray analysis was performed on two stem/progenitor cell subpopulations. For this analysis, subpopulations defined by LIN-CD24+CD29hi and LIN-CD24hiCD29lo were FACS sorted from wildtype and germline C/EBPb-/- glands, and RNA was isolated from each group.; [Treatment]'None'; [Growth]'Mammary epithlial cells (MECs) were isolated from two paired sets of wildtype and germline C/EBPb-/- glands (10 mice per group). Cells were FACS sorted based on CD24, CD29 and LIN expression.'; [Extraction]'Total RNA was isolated using the Arcturus Pico Pure RNA isolation kit (Molecular Devices, Sunnyvale, CA). The mRNA was then amplified using a NuGEN FFPE amplification kit (NuGEN, San Carlos, CA).'; [Cell type]'Mammary epithlial cells (MECs)''genotype/variation: CEBPb knockout; cell type: Mammary epithlial cells (MECs); stem/progenitor cell subpopulation: CD24+CD29hi cells; ', 'genotype/variation: CEBPb knockout; cell type: Mammary epithlial cells (MECs); stem/progenitor cell subpopulation: CD24hiCD29lo cells; ', 'genotype/variation: CEBPb wildtype; cell type: Mammary epithlial cells (MECs); stem/progenitor cell subpopulation: CD24+CD29hi cells; ', 'genotype/variation: CEBPb wildtype; cell type: Mammary epithlial cells (MECs); stem/progenitor cell subpopulation: CD24hiCD29lo cells; ' GSE124224 Homo sapiens 20 Genome binding/occupancy profiling by high throughput sequencing GPL11154 ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer (ATAC-Seq) 2018-12-20 Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. ARID1A knockout cells were found to be less responsive to endocrine therapy compared to intact ARID1A cells in vitro and in vivo. This set of observations in patients’ tumours and in unbiased CRISPR screens led us to explore the epigenetic mechanisms whereby loss of ARID1A may influence breast cancer progression and/or endocrine therapy resistance. ARID1A disruption in ER+ breast cancer cells led to widespread changes in chromatin accessibility converging on loss of the master transcription factors (TFs) that regulate gene expression programs critical for luminal lineage identity. Global transcriptome profiling of ARID1A knockout cell lines and patient samples harbouring ARID1A inactivating mutations revealed an enrichment for basal-like gene expression signatures. The state of increased cellular plasticity of luminal cells that acquire a basal-like phenotype upon ARID1A inactivation is enabled by loss of ARID1A-dependent SWI/SNF complex targeting to genomic sites of the major luminal-lineage determining transcription factors including ER, FOXA1, and GATA3. We also show that ARID1A regulates genome-wide ER-chromatin interactions and ER-dependent transcription. Altogether, we uncover a critical role for ARID1A in the determination of breast luminal cell identity and endocrine therapeutic response in ER+ breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124224 ARID1A determines luminal identity and therapeutic response in estrogen-receptor-positive breast cancer. Nature genetics 25.455 https://doi.org/10.1038/s41588-019-0554-0 {Nature genetics (25.455): 10.1038/s41588-019-0554-0} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA511016 https://www.ebi.ac.uk/ena/browser/view/PRJNA511016 https://www.ncbi.nlm.nih.gov/sra?term=SRP174127 [Overal design]ATAC-seq assay was performed on MCF7 breast cancer cells expressing three distinct sgARID1As or two control sgRNAs in DMSO or fulvestrant treated cells; [Treatment]'MCF7 cells were treated with DMSO of Fulvestrant (100nM) for 24 hours.'; [Growth]'MCF7 cells were obtained from ATCC and were cultured in DMEM/F-12 (Corning) and supplemented with 10% FBS, MEM non-essential amino acids (Corning), 50U/ml penicillin, and 50ng/ml streptomycin under normal oxygen conditions (5% CO2, 37 °C)'; [Extraction]"ATAC-seq was performed as described by Buenrostro et al, 2013 with the exception that 0.2% NP40 was used for cell lysis.\nATAC-seq libraries were prepared using Illumina's TruSeq ChIP sample prep.Libraries were validated using the Agient Technologies 2100 Bioanalyzer and Qubit high sensitivity assay."; [Cell type]'Source: ''cell line: MCF-7; treatment: DMSO; sgguide: sgNT-1; genotype: Control; ', 'cell line: MCF-7; treatment: DMSO; sgguide: sgNT-2; genotype: Control; ', 'cell line: MCF-7; treatment: DMSO; sgguide: sgARID1A-1; genotype: ARID1A KO; ', 'cell line: MCF-7; treatment: DMSO; sgguide: sgARID1A-2; genotype: ARID1A KO; ', 'cell line: MCF-7; treatment: DMSO; sgguide: sgARID1A-3; genotype: ARID1A KO; ', 'cell line: MCF-7; treatment: Fulvestrant; sgguide: sgNT-1; genotype: Control; ', 'cell line: MCF-7; treatment: Fulvestrant; sgguide: sgNT-2; genotype: Control; ', 'cell line: MCF-7; treatment: Fulvestrant; sgguide: sgARID1A-1; genotype: ARID1A KO; ', 'cell line: MCF-7; treatment: Fulvestrant; sgguide: sgARID1A-2; genotype: ARID1A KO; ', 'cell line: MCF-7; treatment: Fulvestrant; sgguide: sgARID1A-3; genotype: ARID1A KO; ' GSE109879 Homo sapiens 1 Non-coding RNA profiling by high throughput sequencing GPL15520 High-throughput sequencing identify miRNAs involved in exosomes of MDA-MB-231 cocultivated with or without mature 3T3-L1 2018-01-30 To identify miRNAs involved in exosomes from MDA-MB-231 cultivated with mature 3T3-L1, small RNA libraries from exosomes stored at 20 °C for 0 and 24 h were constructed. A total of 432 small RNA sequences were generated, and 88 known and 1224 new candidate miRNAs were obtained. Among them, 85 miRNAs were up-regulated and 300 were down-regulated in exosomes from MDA-MB-231 cultivated with mature 3T3-L1. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE109879 Breast cancer-released exosomes trigger cancer-associated cachexia to promote tumor progression. Adipocyte 3.533 https://doi.org/10.1080/21623945.2018.1551688 {Journal of experimental & clinical cancer research : CR (None) doi:10.1186/s13046-019-1210-3}; {Adipocyte (3.533) doi:10.1080/21623945.2018.1551688}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA432230 https://www.ebi.ac.uk/ena/browser/view/PRJNA432230 https://www.ncbi.nlm.nih.gov/sra?term=SRP131793 [Overal design]exosomes from MDA-MB-231 cultivated with mature 3T3-L1; [Treatment]'Breast cancer cells and mature adipocytes were co-cultured using Transwell culture plates (0.4-m pore size; Millipore). A total of 3 x 105 (MCF-7, MDA-MB-231) cells were seeded in the top chamber of the Transwell system in the culture medium of adipocytes and cultivated with or without mature adipocytes in the bottom chamber for the indicated times. Mature adipocytes were cultivated 4 hours with serum-free medium containing 1% of bovine serum albumin (Sigma). The cancer-conditioned mediums were collected from cells cultivated alone in similar conditions for 3 days served as controls, while cancer-associated adipocytes conditioned medium (CA-CM) was collected from adipocytes cultivated with tumor cells for 3 days.'; [Growth]'The breast cancer cell line MDA-MB-231 and mouse preadipocytes line 3T3-L1 were obtained from the American Type Culture Collection (Manassas, VA). MDA-MB-231 cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% free-exosome fetal bovine serum (FBS, Shin Chin Industrial, SCI) and 1 % penicillin–streptomycin (Hyclone, Logan, UT, USA) in a humidified 37 ℃ incubator supplemented with 5% CO2. Preadipocytes 3T3-L1, obtained from ATCC (Shanghai), were cultured in DMEM supplemented with 10% fetal calf serum (FCS, Gibico) and 1 % penicillin–streptomycin (Hyclone, Logan, UT, USA) in a humidified 37 ℃ incubator supplemented with 5% CO2 and were differentiated as previously report.'; [Extraction]'To isolate exosomes, cells were cultured with exosome-depleted serum (Shin Chin Industrial, SCI). We collected the conditioned medium to isolate exosomes according to the instructions83. The medium from cell culture was centrifuged at 500 g for five minutes followed by 2,000 g for thirty minutes at 4 °C to remove cellular debris and large apoptotic bodies. Once centrifuged, the media was added to an equal volume of a 2× polyethylene glycol (PEG, MW 6000, Sigma, 81260) solution (final concentration 8%) at 4 °C. Before incubated at 4 °C overnight, samples were mixed thoroughly by inversion. Samples were further centrifuged in a tabletop centrifuge at maximum speed (15,000 rpm) for 1 hour at 4 °C. After the practice, the tubes were allowed to tap occasionally and drain for five minutes to remove excess PEG. The resulting pellets were further purified for a second time using a 5 % concentration of PEG and were then stored at – 80 ℃ after suspended in 50–500 μl of particle-free PBS (pH 7.4). The average yield of approximately 300 \uf06dg exosome protein which was produced from 5 ml of supernatant. One was subjected to RNA extraction using Trizol reagent (Life Technologies) followed by miRNA assessment by microarrays and RT-PCR described as follow. The characteristics of exosomes were analyzed by electron microscopy to verify the presence, nanoparticle characterization system to measure the size and determine concentration of exosomes, and western bolt to detect the proteins (HSP70, TSG101, CD63 and CD81) of exosomes.\nIsolation of miRNA from exosomes was conducted with the miRNeasy Kit (Qiagen, USA), following the manufacturer’s instructions. miRNA levels were performed using TruSeq Small RNA Sample Prep Kits (Illumina, San Diego, USA), according to the manufacturer’s instructions. Each library was indexed in order to multiplex samples per sequencing run on the Illumina MiSeq platform using MiSeq 50 cycle Reagent Kits v2. A minimum of 17 million 50bp sequencing reads were collected from each sample and data were analyzed using Genesifter software (formerly Geospiza) (PerkinElmer, Santa Clara CA). Raw data for each sample were aligned to the most recent mirBASE database (mirBase.org [17]) with remaining reads aligned to the most recent human genome (hg18 build [18]) build in order to identify previously unknown regions that may encode for unique miRNAs. Pairwise comparison of the alignment results was done using Genesifter for identification of miRNAs that are differentially expressed at a significant level, i.e. up- or down-regulated.'; [Cell type]'Source: ''treatment: MDA-MB-231 cultivated with mature 3T3-L1 for 3 days; ' GSE19154 Homo sapiens 6 Expression profiling by array GPL5188 Exon level integration of proteomics and microarray data 2009-11-23 Background: Previous studies comparing quantitative proteomics and microarray data have generally found poor correspondence between the two. We hypothesised that this might in part be because the different assays were targeting different parts of the expressed genome and might therefore be subjected to confounding effects from processes such as alternative splicing. Results: Using a genome database as a platform for integration, we combined quantitative protein mass spectrometry with Affymetrix Exon array data at the level of individual exons. We found significantly higher degrees of correlation than have been previously observed (r=0.808). The study was performed using cell lines in equilibrium in order to reduce a major potential source of biological variation, thus allowing the analysis to focus on the data integration methods in order to establish their performance. Conclusion: We conclude that much of the variation observed when integrating microarray and proteomics data may occur as a consequence both of the data analysis and of the high granularity to which studies have until recently been limited. The approach opens up the possibility for the first time of considering combined microarray and proteomics datasets at the level of individual exons and isoforms, important given the high proportion of alternative splicing observed in the human genome. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE19154 An integrated mass-spectrometry pipeline identifies novel protein coding-regions in the human genome. PloS one 2.776 https://doi.org/10.1371/journal.pone.0008949 {BMC bioinformatics (2.511) doi:10.1186/1471-2105-9-118}; {PloS one (2.776) doi:10.1371/journal.pone.0008949}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA120707 https://www.ebi.ac.uk/ena/browser/view/PRJNA120707 None [Overal design]This data set contains three technical replicates of the cell lines MCF7 and MCF10A; [Treatment]'None'; [Growth]'None'; [Extraction]'Rneasy Midi (QIAGEN)'; [Cell type]'Source: ''cell line: MCF7; ', 'cell line: MCF10; ' GSE165431 Mus musculus 6 Expression profiling by high throughput sequencing GPL17021 RNA sequencing of MMTV-Neu early lesion (EL) and primary tumor (PT) spheres 2021-01-25 Cancer cells can disseminate from early-evolved primary lesions. It is thought that a state of early disseminated cancer cell (early DCC) dormancy would precede genetic maturation of DCCs and metastasis initiation. Here we reveal at single cell resolution a previously unrecognized role of mesenchymal- and pluripotency-like programs in coordinating early cancer cell spread and a long-lived dormancy program in early DCCs. We identify in early lesions and early DCCs, the transcription factor ZFP281 as an inducer of mesenchymal- and primed pluripotency-like programs, which is absent in advanced primary tumors and overt metastasis. ZFP281 not only controls the early spread of cancer cells but also locks early DCCs in a prolonged dormancy state by preventing the acquisition of an epithelial-like proliferative program. Thus, ZFP281-driven dormancy of early DCCs may be a rate-limiting step in metastatic progression functioning as a first barrier that DCCs must overcome to then undergo genetic maturation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE165431 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA694615 https://www.ebi.ac.uk/ena/browser/view/PRJNA694615 https://www.ncbi.nlm.nih.gov/sra?term=SRP303137 [Overal design]RNA sequencing of MMTV-Neu early lesion (EL) and primary tumor (PT) spheres, which recapitulate the in vivo behavior of EL and PT lesions; [Treatment]'None'; [Growth]'MMTV-HER2/Neu mice were maintained on FvB background and bred and crossed in our facilities. All experimental procedures were approved by the Institutional Animal Care and Use Committee (IACUC) of Icahn School of Medicine at Mount Sinai. Mammary glands and primary tumors were digested and cells were cultured for 7-days in ultra-low adhesion plates in mammosphere media.'; [Extraction]'RNA was extracted using RNeasy protocol (Qiagen) following manufacturer instructions.\nSequencing libraries were prepared according to manufacturer instructions. Samples were sequenced on Illumina MiSeq.'; [Cell type]'Source: ''strain: FvB; age: 14-18 wk; tumor stage: No palpable tumor; tissue: mammary lung; cell tyoe: breast cancer cells; ', 'strain: FvB; age: >20 wk; tumor stage: With primary tumor(s); tissue: breast tumor; cell tyoe: breast cancer cells; ' GSE80413 Mus musculus 12 Expression profiling by array GPL18752 Effect of sphingosine kinase 1 deletion on HER/neu-induced mammary tumor development 2016-04-18 Analysis of gene expression of mouse mammary tumors with different SphK1 expressions. The hypothesis tested in this study is that SphK1 deletion in mice influence the cancer promoting/inhibiting genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80413 Genetic deletion of sphingosine kinase 1 suppresses mouse breast tumor development in an HER2 transgenic model. Carcinogenesis 4.004 https://doi.org/10.1093/carcin/bgx097 {Carcinogenesis (4.004): 10.1093/carcin/bgx097} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA318821 https://www.ebi.ac.uk/ena/browser/view/PRJNA318821 None [Overal design]MMTV-neu Tg and SphK1 KO mice wre intercrossed and tumors from MMTV-neu Tg mice with homozygous KO, heterozygous KO and wild-type SphK1 were analyzed. Please note that WT are SphK1 +/+ from the intercross and control MMTV-neu single Tg mice (SphK1+/+).; [Treatment]'MMTV-neu Tg mice and SPhK1 KO mice were intercrosserd and MMTV-neu Tg mice with homozygous KO, heterozygous KO and wildtype SphK1 were generated.'; [Growth]'All animals were maintained under controlled conditions of humidity (50±10%), light (12/12 hour light/dark cycle) and temperature (23 ± 2˚C) with free access to feeds and water.'; [Extraction]'RNA was extracted using Rneasy Plus kit (QIAGEN) in accordance with prescribed protocol provided with the kit.'; [Cell type]'Source: ''strain background: FVB; genotype/variation: MMTV-neu Tg mice with wildtype SphK1; gender: female; age: 35 weeks; tissue: Mammary tumor; ', 'strain background: FVB; gender: female; age: 35 weeks; tissue: Mammary tumor; ', 'strain background: FVB; genotype/variation: MMTV-neu Tg mice with homozygous KO; gender: female; age: 35 weeks; tissue: Mammary tumor; ', 'strain background: FVB; genotype/variation: MMTV-neu Tg mice with heterozygous KO; gender: female; age: 35 weeks; tissue: Mammary tumor; ' GSE93601 Homo sapiens 1110 Expression profiling by array GPL22920 Alcohol Consumption and Breast Tumor Gene Expression 2017-01-13 Investigating the association of alcohol and gene expression of breast tumors and tumor-adjacent tissues. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93601 Alcohol Consumption and Risk of Breast Cancer by Tumor Receptor Expression. Hormones & cancer 2.74 https://doi.org/10.1007/s12672-015-0235-0 {Hormones & cancer (2.74): 10.1007/s12672-015-0235-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA361267 https://www.ebi.ac.uk/ena/browser/view/PRJNA361267 None [Overal design]Total of 1110 samples which includes 602 tumor and 508 tumor-adjacent tissues from participants of the Nurses' Heath Study I and II diagnosed with invasive breast cancer. Limma analyses compared how alcohol intake at 0, >0-<10 and 10+ grams/day influenced gene expression in breast tumor and tumor-adjacent tissues.; [Treatment]'Formalin-fixed paraffin-embedded tissue blocks.'; [Growth]'None'; [Extraction]'Qiagen AllPrep RNA isolation kit was used to isolate total RNA.'; [Cell type]'Source: ''tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X115976993; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.45598082; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X115976993; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.45598082; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 76; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X116437722; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 40.03369237; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 5; patient id: X110614116; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.11215161; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 5; patient id: X110614116; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.11215161; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52; year of diagnosis: 1985; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X121988357; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.86251522; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 52; year of diagnosis: 1985; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X121988357; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.86251522; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X110110241; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.97092436; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X110110241; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.97092436; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 76; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X113368486; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.2873845; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 76; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X113368486; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.2873845; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X111565982; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.91393128; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X111565982; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.91393128; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X119206089; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.96416615; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X119206089; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.96416615; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X120253833; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.43507725; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X120253833; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.43507725; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 63; year of diagnosis: 2003; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X112570050; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 36.17980404; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 63; year of diagnosis: 2003; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X112570050; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 36.17980404; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68.25; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X110725860; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.17858497; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X112782507; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.91576334; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X112782507; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.91576334; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X110726041; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.59515834; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 56; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X110726041; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.59515834; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X113194053; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.30165413; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X112634362; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.8594748; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X112634362; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.8594748; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 65; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X121510527; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.38438371; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X112049534; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.41213818; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X112049534; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.41213818; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 56; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X114390892; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.5133774; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X121510630; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.82441064; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X121510630; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.82441064; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X121205615; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.80087828; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X121205615; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.80087828; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 69; year of diagnosis: 2003; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 8; patient id: X121954110; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.02823012; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 2003; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 8; patient id: X121954110; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.02823012; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 74; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 11; patient id: X112319958; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.08752613; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 41.66666667; year of diagnosis: 1987; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X115881758; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.50776492; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 41.66666667; year of diagnosis: 1987; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X115881758; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.50776492; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X119823572; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.20537035; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 73; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X121009716; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.43507725; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 74.58333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X113368801; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.57552914; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X113752287; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.04546489; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 55; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X113752287; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.04546489; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 75.08333333; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X114679447; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.52646913; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 64; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X115449211; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.59416643; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X119048111; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.8949004; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 78; year of diagnosis: 2004; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X120215294; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.58226077; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X110602614; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.1298721; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 56.16666667; year of diagnosis: 1998; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X112230607; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.80243313; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X117320161; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.63291014; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X115025436; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.17245929; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X115025436; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.17245929; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 73; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X117741745; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.38251059; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 73; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 3; patient id: X117741745; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.38251059; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1992; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 5; patient id: X118353834; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.98233364; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1992; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 5; patient id: X118353834; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.98233364; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 64; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X117790157; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.40337214; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 64; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X117790157; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.40337214; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X114767029; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.62823616; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X114767029; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.62823616; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 68.08333333; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X111653152; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.21675429; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X114619508; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 36.79978516; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X114619508; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 36.79978516; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X115096078; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.98815661; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X119484575; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.43280339; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X119484575; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.43280339; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X119579192; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.6060721; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X119579192; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.6060721; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X121511223; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.27355418; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X121511223; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.27355418; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.16666667; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X113134938; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.17245929; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 52.16666667; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X113134938; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.17245929; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 6; patient id: X117802424; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.61830085; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 64; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X113973746; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.57103476; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 64; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X113973746; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.57103476; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X118065091; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.43495674; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X118065091; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.43495674; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X117790672; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.4166624; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 74; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X117039695; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.09107151; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X119762275; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.36510924; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X119762275; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.36510924; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 65.91666667; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X121583803; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.12122519; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 57; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X116568759; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.52342961; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X118708559; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.82441064; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X118708559; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.82441064; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 74; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X110123057; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.94871192; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X119413109; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 36.3137475; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 69; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X114901906; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.67479197; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 74.08333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X117902744; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.96105017; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 69.33333333; year of diagnosis: 2001; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X121716270; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.72617727; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X119353950; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.83683823; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 64; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X112073731; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.08279805; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 64; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X112073731; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.08279805; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 70; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X118127187; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 45.34713763; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X118127187; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 45.34713763; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1992; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X112085645; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.28433298; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1992; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X112085645; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.28433298; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 53; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X114031822; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.78373721; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X121791822; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.80695115; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X121791822; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.80695115; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X110882280; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 43.16452154; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 66.58333333; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X112622551; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.38251059; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X115904625; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.96728214; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 70; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X118998753; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.46494515; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X118998753; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.46494515; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 44; year of diagnosis: 1989; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X111041372; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.57103476; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 69; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X117502179; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.53096124; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X117502179; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.53096124; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 3; patient id: X113035623; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.12745717; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 2002; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 4; patient id: X113422027; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.97859899; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 2002; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 3; patient id: X113422027; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.97859899; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X116428102; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.21038497; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X116428102; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.21038497; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 64; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X119738805; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.37399422; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 64; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X119738805; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.37399422; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 3; patient id: X112171526; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.05928553; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 1997; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X117634536; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.96884013; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 1997; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X117634536; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.96884013; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 53.83333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X119256542; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.88893776; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1996; estrogen receptor status: NA; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X119801960; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.61363377; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 77; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 6; patient id: X110858604; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.69507746; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 74; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 11; patient id: X111593272; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.32766712; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X120857204; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.30861834; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X120857204; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.30861834; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 53.66666667; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X121573481; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.47842001; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.58333333; year of diagnosis: 1989; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X113568411; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.24011591; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 48.58333333; year of diagnosis: 1989; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X113568411; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.24011591; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X110245716; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.02823012; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X116005023; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.04546489; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 70; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X115695351; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.14721577; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X115695351; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.14721577; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X117707644; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.51575498; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X117707644; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.51575498; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 66.5; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X118720842; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.43376838; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 59.16666667; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X120987030; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.89661239; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 56.83333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X114645921; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.96416615; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 65; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X110246000; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.79963244; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X110246000; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.79963244; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 68.75; year of diagnosis: 1999; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X119874103; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.03837315; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 7; patient id: X119813462; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.31422006; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 78; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X110196127; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.89828137; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X111763994; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.66648763; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 56; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X111763994; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.66648763; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 74; year of diagnosis: 2000; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X115476217; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.90254734; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 74; year of diagnosis: 2000; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X115476217; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.90254734; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X113371870; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.24753687; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X119448670; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.11128376; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X119448670; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.11128376; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X115816528; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.98815661; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X112384364; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.96105017; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X112384364; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.96105017; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X117372006; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.22813823; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X117372006; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.22813823; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X121957022; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.74717699; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X121957022; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.74717699; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X113110074; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.71985383; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X113110074; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.71985383; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 2; patient id: X116958178; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.45871318; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 2; patient id: X116958178; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.45871318; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X111495065; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.60541622; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 2; patient id: X117635438; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.20455407; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 56; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 7; patient id: X112396896; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.19398641; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 81; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 7; patient id: X118757589; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.47079424; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 81; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 7; patient id: X118757589; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.47079424; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X119073725; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.08349537; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 66.08333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X117941355; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.99954055; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 65; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X113321835; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.71367973; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X113321835; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.71367973; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X116620284; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.57103476; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X116620284; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.57103476; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 65; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X120941790; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.55965082; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X120941790; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.55965082; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 73; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X118794711; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.76288477; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 73; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X118794711; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.76288477; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1992; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X112348253; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.67356881; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1992; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X112348253; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.67356881; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X113767943; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.31944386; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X113767943; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.31944386; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X120156425; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.54564206; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X120156425; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.54564206; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 80; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 2; patient id: X112610946; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.86247383; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 80; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 2; patient id: X112610946; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.86247383; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X113436878; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.73126108; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X110776700; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.14286798; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 52; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X110776700; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.14286798; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X111802340; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.79931714; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X114782430; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.61110827; avg_bo dysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X114782430; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.61110827; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 65.25; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X115315565; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.47350047; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 76.66666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X120532229; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.77706695; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 6; patient id: X113001988; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.06927622; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 6; patient id: X113001988; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.06927622; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 65.83333333; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X111386052; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.12589917; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 72.58333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X111594901; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.73218898; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 63; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 3; patient id: X118475251; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.63446814; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 63; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X118475251; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.63446814; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 57; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 2; patient id: X120568486; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.65952851; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 57; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 2; patient id: X120568486; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.65952851; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 55; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X118298258; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.4879873; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 70.5; year of diagnosis: 1992; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 10; patient id: X114069471; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.82441064; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X116983071; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 38.61657051; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X116983071; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 38.61657051; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X121048430; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.64970072; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X121048430; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.64970072; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X113472989; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.19899624; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 54; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X113472989; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.19899624; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X117128179; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.85353227; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X110284224; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.45598082; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 55.5; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X120988756; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.01739781; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X119899554; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.99954055; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 6; patient id: X119899554; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.99954055; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 68.58333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X121946422; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.95637618; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.25; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X114208858; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.4038813; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 53.25; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X114208858; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.4038813; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.25; year of diagnosis: 1977; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X115863445; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.6853336; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 52.25; year of diagnosis: 1977; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X115863445; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.6853336; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X119814776; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.78232681; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X119814776; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.78232681; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X121807279; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.39722898; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 12; patient id: X112749823; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.78934648; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 55; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 12; patient id: X112749823; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.78934648; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 70; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X121744178; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.14338031; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X121744178; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.14338031; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 63; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X116743845; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.8949004; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 63; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X116743845; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.8949004; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X117077513; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.79617056; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X117077513; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.79617056; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 53; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 2; patient id: X121820155; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.36862551; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68.75; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 10; patient id: X111853277; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.08790671; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X113817507; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.40958389; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X113817507; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.40958389; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X117624735; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 43.93077746; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X117624735; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 43.93077746; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 65; year of diagnosis: 1995; estrogen receptor status: NA; alcohol intake: >10 g/day; microarray batch: 1; patient id: X122150833; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.26821174; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1995; estrogen receptor status: NA; alcohol intake: >10 g/day; microarray batch: 1; patient id: X122150833; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.26821174; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X114610457; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.03069852; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 65.75; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X121085752; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.34957982; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 63; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X114968983; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.91393128; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 76; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X121611852; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.24544914; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 79; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 7; patient id: X111546149; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.62512018; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 79; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 7; patient id: X111546149; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.62512018; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 2001; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 1; patient id: X120592374; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.21675429; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58; year of diagnosis: 1997; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 7; patient id: X121014486; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.59635931; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 1997; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 7; patient id: X121014486; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.59635931; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X122151014; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.71538085; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X122151014; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.71538085; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X110705743; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.12122519; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X110705743; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.12122519; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48; year of diagnosis: 1990; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 1; patient id: X111879121; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.15090043; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 48; year of diagnosis: 1990; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 1; patient id: X111879121; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.15090043; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X117423708; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.4524812; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X117423708; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.4524812; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 64; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X117553637; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.08349537; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 64; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X117553637; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.08349537; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 58.83333333; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X119644672; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.62549088; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 78; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X121859639; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.17532081; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 78; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X121859639; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.17532081; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.58333333; year of diagnosis: 1985; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X118381227; nhs_cohort: NHS1; bmi_2yrs_bef_dx: NA; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 52.58333333; year of diagnosis: 1985; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X118381227; nhs_cohort: NHS1; bmi_2yrs_bef_dx: NA; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X116275409; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.01092449; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 65; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 6; patient id: X117650633; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.50776492; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 6; patient id: X117650633; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.50776492; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 2; patient id: X111448869; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.17699346; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 53; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 2; patient id: X111448869; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.17699346; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 66.08333333; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X118191315; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.54446372; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X118452840; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.65751575; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 51; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X118452840; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.65751575; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 79; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X121198682; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.33645965; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 79; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X121198682; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.33645965; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 75.91666667; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X120714865; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.80991372; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 57.83333333; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 17; patient id: X113906815; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.16748638; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 57.83333333; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 17; patient id: X113906815; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.16748638; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 73; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X118393141; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.31422006; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 73; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X118393141; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.31422006; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 6; patient id: X116419615; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.89031226; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 6; patient id: X116419615; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.89031226; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X119645059; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.17245929; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X115444077; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.74717699; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X115444077; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.74717699; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X112714874; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.40337214; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X112714874; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.40337214; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 74; year of diagnosis: 2004; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X116732318; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.59635931; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 74; year of diagnosis: 2004; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X116732318; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.59635931; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 69; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X119222501; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.88893776; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X119222501; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.88893776; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 63; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X120978852; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.09047268; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 63; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X120978852; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.09047268; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 62.16666667; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X113941818; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.95074904; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 74; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X119063615; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.17858497; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 74; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X119063615; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.17858497; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 54.33333333; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X121099161; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.82476926; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X113708694; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.17532081; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X113708694; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.17532081; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 57; year of diagnosis: 1997; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 2; patient id: X114148257; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.50121717; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 57; year of diagnosis: 1997; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 2; patient id: X114148257; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.50121717; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 1999; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 7; patient id: X120777310; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.04898241; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 1999; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 2; patient id: X120777310; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.04898241; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 61.83333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X111486166; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 36.60954024; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X121236435; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.77750524; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X121236435; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.77750524; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X117447124; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.74717699; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X117447124; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.74717699; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X118846485; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.23995463; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X118846485; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.23995463; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X119730450; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 41.09653376; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X119730450; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 41.09653376; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X114466815; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.65952851; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 6; patient id: X114466815; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.65952851; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X120777516; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 17.35974271; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 57; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X113721982; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.72617727; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 57; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X113721982; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.72617727; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 69; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X115875874; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.12589917; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X115875874; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.12589917; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X116924652; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.69671754; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X116924652; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.69671754; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.91666667; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 17; patient id: X113549190; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.39722898; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 53.91666667; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 17; patient id: X113549190; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.39722898; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 73; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X116337505; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.37112665; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 73; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X116337505; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.37112665; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 69; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X111571866; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.11563117; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X111571866; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.11563117; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 6; patient id: X112588309; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 17.6797282; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 6; patient id: X112588309; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 17.6797282; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 77; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X117674770; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.57921316; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X111412612; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.21645974; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X111412612; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.21645974; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 71.58333333; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X120363336; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.28140022; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X117020128; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.79963244; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X117020128; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.79963244; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X116338092; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.61733021; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 56; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X116338092; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.61733021; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 73; year of diagnosis: 2002; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 12; patient id: X112186764; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.26333168; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 73; year of diagnosis: 2002; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 12; patient id: X112186764; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.26333168; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 4; patient id: X119513223; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.54826688; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 4; patient id: X119513223; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.54826688; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X110520710; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.03069852; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X110520710; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.03069852; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X110249942; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.05928553; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 75; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X116082579; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.55335698; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 75; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X116082579; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.55335698; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 69.58333333; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X110558668; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.45249695; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 76; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 12; patient id: X116128681; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.68740283; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 76; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 12; patient id: X116128681; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.68740283; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X117845364; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.62979416; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X111255530; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.32189469; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X119550236; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.40337214; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 56; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X119550236; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.40337214; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 60.91666667; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X119719584; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.47350047; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 75; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X113027729; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.75485162; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 75; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X113027729; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.75485162; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X115008334; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.89981729; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X115008334; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.89981729; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X116840223; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.39722898; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X116840223; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.39722898; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X118325617; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.74717699; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X118325617; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.74717699; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X110558977; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.75109785; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X110558977; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.75109785; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 12; patient id: X116239401; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.03355922; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 12; patient id: X116239401; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.03355922; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 56; year of diagnosis: 1998; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X121861400; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.9220927; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 47.83333333; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X111741661; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.12901516; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 47.83333333; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X111741661; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.12901516; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 72.58333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X121861503; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.52342961; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 2002; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 1; patient id: X120679103; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.46654134; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 2002; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 1; patient id: X120679103; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.46654134; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 65.66666667; year of diagnosis: 1994; estrogen receptor status: NA; alcohol intake: >10 g/day; microarray batch: 10; patient id: X119890406; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.39673644; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 6; patient id: X120050378; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.9532602; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 7; patient id: X120050378; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.9532602; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X115354176; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.2640824; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 57; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X116879392; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.77706407; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 57; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X116879392; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.77706407; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X120002456; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.38251059; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X120002456; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.38251059; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X112861808; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.34243707; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 70; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X115796058; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.22813823; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X115796058; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.22813823; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 63; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X119371851; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.41126592; avg_bodysize_ age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 63; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X119371851; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.41126592; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X110359033; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.52057467; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X110359033; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.52057467; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 4; patient id: X113846214; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.76043383; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 52; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 4; patient id: X113846214; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.76043383; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 12; patient id: X118071908; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.17858497; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 7; patient id: X118071908; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.17858497; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X112187769; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.91393128; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 60.25; year of diagnosis: 1994; estrogen receptor status: NA; alcohol intake: 0 g/day; microarray batch: 10; patient id: X115736840; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.66648763; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X118691370; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.02823012; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X118691370; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.02823012; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 57.16666667; year of diagnosis: 1998; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 10; patient id: X121924083; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.12901516; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X110768079; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.02823012; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 51; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X110768079; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.02823012; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 57; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X114921508; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.91916444; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 57; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X114921508; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.91916444; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X118488994; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.45871318; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X118488994; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.45871318; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X111718572; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.46365546; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 53; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X111718572; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.46365546; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 4; patient id: X117243076; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.03961406; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X121937111; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.2283654; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X121937111; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.2283654; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51.25; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 17; patient id: X111952180; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.92297246; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X113128848; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.0605856; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X113128848; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.0605856; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55.5; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 17; patient id: X113326139; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.27618286; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 55.5; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 17; patient id: X113326139; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.27618286; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X113613150; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.51575498; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X113613150; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.51575498; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X116829357; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.9640682; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 53; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X116829357; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.9640682; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 82; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 9; patient id: X118799221; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.53666967; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 82; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 9; patient id: X118799221; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.53666967; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X110850867; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.40958389; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X110850867; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.40958389; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X112564784; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.61733021; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X112564784; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.61733021; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 64; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X121004273; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.79963244; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 3; patient id: X121051814; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.61363377; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 56; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 3; patient id: X121051814; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.61363377; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 64; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X112528158; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.26821174; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 64; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X112528158; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.26821174; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 12; patient id: X113626069; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.65514; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 12; patient id: X113626069; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.65514; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 62.66666667; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X117290411; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.98627363; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 64; year of diagnosis: 1999; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 1; patient id: X110446640; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.45715518; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 64; year of diagnosis: 1999; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 1; patient id: X110446640; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.45715518; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 76; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X117507931; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.82441064; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 76; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X117507931; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.82441064; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 70; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X112654994; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.28451621; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X112654994; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.28451621; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X111882505; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.79775915; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X111882505; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.79775915; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X117472223; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.35094397; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X117472223; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.35094397; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 48.83333333; year of diagnosis: 1977; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 17; patient id: X117958609; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.92687484; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 63; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X115456100; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.80718792; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 63; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X115456100; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.80718792; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 7; patient id: X119372444; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.79963244; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 55; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 2; patient id: X119372444; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.79963244; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 80; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X120300273; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.20050793; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 80; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X120300273; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.20050793; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 64; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 4; patient id: X113649928; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.55335698; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X116782353; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.6060721; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X116782353; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.6060721; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 69.25; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X113079156; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.63446814; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X117822232; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.87845515; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 62.33333333; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X118326622; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.30009614; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 73.08333333; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X119756809; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.14252896; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X115258288; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.50866901; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X115258288; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.50866901; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 67.83333333; year of diagnosis: 1998; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X115307259; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.15562927; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 70.5; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X120087028; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.33645965; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 64.83333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X110459353; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.1539129; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X114785754; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.57173383; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X114785754; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.57173383; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 63.91666667; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X115761012; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.95481819; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 63.91666667; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X115761012; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.95481819; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1992; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 1; patient id: X116868380; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.42804634; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1992; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 1; patient id: X116868380; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.42804634; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X120680471; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.24544914; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X110509638; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.20455407; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X110509638; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.20455407; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 63; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X116503480; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 40.60998412; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 63; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X116503480; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 40.60998412; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 76; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X117302775; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.45715518; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 76; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X117302775; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.45715518; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X121481776; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.66648763; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 70; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X116673237; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.64297793; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X116673237; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.64297793; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 74; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X119879849; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.31422006; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 74; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X119879849; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.31422006; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 69; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X116340059; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.77706695; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X116340059; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.77706695; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X120389071; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.28670873; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 78; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 4; patient id: X111905572; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.48485768; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 50.58333333; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X119891205; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.45054228; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X115653622; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.95074904; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 54; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X115653622; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.95074904; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X113416040; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.75790157; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X113416040; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.75790157; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X111905778; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.56303288; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 1; patient id: X117522296; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 40.72133899; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 55; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 1; patient id: X117522296; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 40.72133899; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X120560652; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.88757984; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 63.58333333; year of diagnosis: 1992; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 10; patient id: X111023471; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.46365546; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X112579616; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.58500886; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X115457105; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.82704578; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X115457105; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.82704578; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 6; patient id: X118022769; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.12901516; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 6; patient id: X118022769; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.12901516; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 73; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X118121981; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.65514; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 73; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X118121981; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.65514; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 4; patient id: X115270056; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.50866901; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 4; patient id: X115270056; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.50866901; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 4; patient id: X120439768; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.72540711; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 51; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 4; patient id: X120439768; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.72540711; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 4; patient id: X112068955; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.62549088; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1997; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X118501496; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.9517022; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1997; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X118501496; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.9517022; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X120063200; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.63142347; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X120063200; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.63142347; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 62.41666667; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X112022376; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.36520495; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X120187554; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.61577222; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X120187554; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.61577222; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 77; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 4; patient id: X121962622; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.69156952; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 77; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 4; patient id: X121962622; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.69156952; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 77; year of diagnosis: 2004; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 5; patient id: X117340587; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.01035322; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 77; year of diagnosis: 2004; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 5; patient id: X117340587; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.01035322; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X110722330; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.29200761; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X110722330; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.29200761; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 79; year of diagnosis: 2003; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 12; patient id: X111365239; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.45673591; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X113340432; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.60541622; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 54; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X113340432; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.60541622; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X119709268; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 40.35064162; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X119709268; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 40.35064162; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 9; patient id: X121875221; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.79152718; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 9; patient id: X121875221; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.79152718; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 65; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X110227403; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.17615712; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X110227403; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.17615712; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 75; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X114138250; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.46365546; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 75; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X114138250; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.46365546; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X114873439; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 36.49088773; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X114873439; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 36.49088773; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X120655784; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.25682781; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X120655784; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.25682781; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X110537340; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.89661239; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X110537340; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.89661239; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 69; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X117885501; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.78373721; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 6; patient id: X117885501; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.78373721; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 65; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X118850462; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.29698015; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X118850462; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.29698015; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 12; patient id: X119153928; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.39673644; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 12; patient id: X119153928; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.39673644; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X113614876; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.83937271; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X113614876; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.83937271; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 70.08333333; year of diagnosis: 1997; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 10; patient id: X118837277; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.98581321; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X115022421; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 43.08360949; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 57; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X118571963; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.79152718; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X121252738; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.94547023; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X121252738; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.94547023; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 52; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X122083446; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.53319011; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X116328085; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.5824187; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X116328085; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.5824187; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X119276041; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.85353227; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X119276041; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.85353227; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 69; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X119420095; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.18013392; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X119420095; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.18013392; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X119807990; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.92687484; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58; year of diagnosis: 2001; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 12; patient id: X112303303; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.78410475; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 2001; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 12; patient id: X112303303; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.78410475; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X114251549; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.63176295; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X114251549; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.63176295; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X118219928; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 18.88126313; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X118219928; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 18.88126313; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 63.58333333; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X122008518; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.47133009; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X113042821; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.21038497; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X113042821; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.21038497; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 3; patient id: X115320753; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.52057467; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 3; patient id: X115320753; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.52057467; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 77; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X117120860; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.4038813; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 73; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X118643448; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.45559719; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 61.41666667; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X119903775; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.6060721; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X119154006; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.07460414; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X119154006; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.07460414; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X111111568; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.83003547; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 56; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X111111568; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.83003547; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 65.58333333; year of diagnosis: 1992; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 10; patient id: X117714430; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.56742752; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 56; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X119844488; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.01739781; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X121724576; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.75570345; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 55; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X121724576; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.75570345; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 63; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X113131196; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.28433298; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 63; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X113131196; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.28433298; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X117935059; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.46654134; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 56; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X117935059; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.46654134; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 65; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X118011242; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.89679028; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X118011242; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.89679028; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 64.66666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X114640272; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.88893776; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1998; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X119722041; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.03069852; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1998; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X119722041; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.03069852; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 74; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X121876123; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.05928553; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 46; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X115703283; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.40621193; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 46; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X115703283; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.40621193; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 66.66666667; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X110901127; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.11689888; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X117303883; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.79963244; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 3; patient id: X117303883; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.79963244; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X117897827; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.42094629; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X113982439; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.81897356; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X113982439; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.81897356; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X118445436; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.13911634; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X118445436; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.13911634; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X122133319; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.11689888; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 73; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X112994958; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.80087514; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 73; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X112994958; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.80087514; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 4; patient id: X116132143; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.7852952; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 9; patient id: X110511502; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 48.55236571; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 9; patient id: X110511502; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 48.55236571; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 76; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X115545093; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.34243707; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X119611945; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.43376838; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X119611945; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.43376838; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 79; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 4; patient id: X122133422; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.08279805; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 66.66666667; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 10; patient id: X116881874; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.79963244; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X110841350; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.10435382; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X110841350; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.10435382; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 74.25; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X117094615; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.6188882; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 81; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X117170689; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.42094629; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 81; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X117170689; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.42094629; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 65; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X118159636; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.47133009; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1995; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 5; patient id: X118159636; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.47133009; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X113316235; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.59140326; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X113316235; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.59140326; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 64.33333333; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X119758716; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.96416615; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 63; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X119696311; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.26821174; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 63; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 8; patient id: X119696311; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.26821174; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 57; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 4; patient id: X116725017; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.13680513; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 57; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 4; patient id: X116725017; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.13680513; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 45.08333333; year of diagnosis: 1982; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X114716292; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.45598082; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 45.08333333; year of diagnosis: 1982; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X114716292; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.45598082; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 11; patient id: X117404796; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.45249695; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 11; patient id: X117404796; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.45249695; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 56.58333333; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X121375366; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.05737055; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X114152955; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.32189469; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X114152955; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.32189469; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 76; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X116905746; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.96471399; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 76; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X116905746; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.96471399; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 38.25; year of diagnosis: 1980; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 17; patient id: X120757811; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 17.2282588; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 38.25; year of diagnosis: 1980; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 17; patient id: X120757811; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 17.2282588; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 64.66666667; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X121963936; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.46654134; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X117630413; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.63291014; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X117630413; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.63291014; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X112592280; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.77921792; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X112592280; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.77921792; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 58; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X111797217; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.44698291; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 1; patient id: X111954608; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.63291014; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 54; year of diagnosis: 1995; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 1; patient id: X111954608; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.63291014; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 11; patient id: X114402438; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.59391844; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 11; patient id: X114402438; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.59391844; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 73; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 12; patient id: X119350832; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.23681401; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 73; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 12; patient id: X119350832; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.23681401; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 77.66666667; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X115608406; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.13155341; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 2; patient id: X119106181; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.61733021; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 2; patient id: X121117518; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.8291636; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 2; patient id: X121117518; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.8291636; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 60.33333333; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X121712971; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.18013392; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 60; year of diagnosis: 1993; estrogen receptor status: NA; alcohol intake: 0 g/day; microarray batch: 7; patient id: X121890622; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.2640824; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 60; year of diagnosis: 1993; estrogen receptor status: NA; alcohol intake: 0 g/day; microarray batch: 7; patient id: X121890622; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.2640824; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 63; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X111785091; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.91393128; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 63; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X111785091; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.91393128; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 76; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X117972902; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.40958389; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 76; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X117972902; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.40958389; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.66666667; year of diagnosis: 1988; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 17; patient id: X120077536; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.26212053; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 53.66666667; year of diagnosis: 1988; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 17; patient id: X120077536; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.26212053; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X111514839; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.96884013; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X111514839; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.96884013; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 1999; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X111990616; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.28451621; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 1999; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X111990616; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.28451621; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X113688539; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.0605856; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X113688539; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.0605856; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 70; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X121019826; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.9532602; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 65; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 2; patient id: X112518769; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.65751575; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 2; patient id: X112518769; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.65751575; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 58.83333333; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X114099601; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.65751575; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 76; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X115655941; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.68740283; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 76; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X115655941; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.68740283; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 70.66666667; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 10; patient id: X116155481; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.75325562; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 74; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X115546104; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.96416615; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 74; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X115546104; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.96416615; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 2; patient id: X115988913; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.69156952; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 54; year of diagnosis: 1994; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 2; patient id: X115988913; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.69156952; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 74; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 11; patient id: X119612847; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.17858497; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 74; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 11; patient id: X119612847; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.17858497; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 2; patient id: X112228228; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.82441064; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 75.08333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 10; patient id: X120657279; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.64526009; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 80; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X110439133; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.46494515; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 80; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X110439133; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.46494515; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X111847708; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 26.62549088; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 6; patient id: X115764336; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.57552914; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X115764336; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.57552914; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 70; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X116458741; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.77706695; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 70; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 8; patient id: X116458741; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.77706695; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 77; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X111343009; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.85555509; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 77; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X111343009; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.85555509; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 62.5; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X116193814; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 38.73401339; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 72; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X111872601; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.69243154; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X121291967; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.77750524; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X121291967; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.77750524; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 9; patient id: X110327002; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.00598993; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 11; patient id: X110327002; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.00598993; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 1998; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 11; patient id: X118717561; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.36066949; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 69; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X111076939; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.9220927; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 1991; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 2; patient id: X111076939; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.9220927; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 69; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X113922912; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.57552914; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 1; patient id: X113922912; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.57552914; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X111576376; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.50493729; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X111576376; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.50493729; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1998; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 9; patient id: X117084608; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 38.27361025; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1998; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 9; patient id: X117084608; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 38.27361025; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X113786334; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.14377217; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X113786334; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.14377217; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 62; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X117171694; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.49308018; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 1; patient id: X117171694; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.49308018; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 4; patient id: X113799356; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.8891047; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 4; patient id: X113799356; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.8891047; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X114215850; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.80718792; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 1; patient id: X114215850; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.80718792; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 7; patient id: X119482668; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.36830798; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X117463633; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.02357128; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 12; patient id: X117463633; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.02357128; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 69; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X110313902; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.7852952; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 69; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X110313902; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.7852952; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 63; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X114141222; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.26821174; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 63; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X114141222; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.26821174; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 75; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X119968230; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.56521408; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 75; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X119968230; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 27.56521408; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X110954801; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.31422006; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X110954801; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.31422006; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 7; patient id: X116305983; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.55335698; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 67; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X112481051; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.31422006; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 67; year of diagnosis: 1990; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X112481051; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.31422006; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 77; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X118622738; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.79963244; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 77; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X118622738; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 24.79963244; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 65; year of diagnosis: 1991; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X116750322; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.1539129; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 76; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X117356733; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.46494515; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 76; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X117356733; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.46494515; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 64; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X121534561; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.69030269; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 64; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 9; patient id: X121534561; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.69030269; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 74; year of diagnosis: 1997; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X121593810; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.62762867; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 72; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X113217950; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.91916444; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X118305500; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.11215161; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X118305500; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.11215161; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X118670866; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.11383939; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X118670866; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.11383939; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 73; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 9; patient id: X112544770; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.24544914; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 73; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 9; patient id: X112544770; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.24544914; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X121280337; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.79617056; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 73; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X112481257; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 19.37028434; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 64; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 11; patient id: X112168348; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 18.09370242; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 11; patient id: X114141737; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 30.13155341; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 66; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 9; patient id: X116156486; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.8305311; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 66; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 9; patient id: X116156486; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.8305311; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 64; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X111565570; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.79617056; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 64; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X111565570; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 28.79617056; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 9; patient id: X112013374; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.59635931; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 59; year of diagnosis: 1992; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 9; patient id: X112013374; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.59635931; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 73; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X115118558; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.47133009; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 73; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 9; patient id: X115118558; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 33.47133009; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 9; patient id: X112217628; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.76613885; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 53; year of diagnosis: 1993; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 9; patient id: X112217628; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 34.76613885; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 80; year of diagnosis: 2004; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 8; patient id: X114938138; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.3120979; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 80; year of diagnosis: 2004; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 8; patient id: X114938138; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 31.3120979; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 64; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 10; patient id: X112949536; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 23.08056701; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X118575056; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.67356881; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 74; year of diagnosis: 1996; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 5; patient id: X119242412; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.74717699; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 62; year of diagnosis: 2000; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X121305523; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 32.09814731; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 68; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X117776482; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.18013392; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68; year of diagnosis: 1993; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 11; patient id: X117776482; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.18013392; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 2002; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X116207673; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.70997751; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 2002; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 4; patient id: X116207673; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 22.70997751; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 71; year of diagnosis: 2000; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X111137206; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.50160551; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 71; year of diagnosis: 2000; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 12; patient id: X111137206; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.50160551; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 63.75; year of diagnosis: 1990; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 10; patient id: X111686291; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 20.08279805; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 72.91666667; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X119542857; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.18013392; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 61; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X117344407; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.30009614; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 61; year of diagnosis: 1994; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 5; patient id: X117344407; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.30009614; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 80; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X117381832; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.45598082; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 80; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 8; patient id: X117381832; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 21.45598082; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 73; year of diagnosis: 1997; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 11; patient id: X119555879; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 29.9532602; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 68.58333333; year of diagnosis: 1996; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 10; patient id: X110576878; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 35.14403166; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 79; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 3; patient id: X110772983; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.74717699; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 79; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 4; patient id: X110772983; nhs_cohort: NHS1; bmi_2yrs_bef_dx: 25.74717699; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54.75; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X220356035; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.57; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 54.75; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X220356035; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.57; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 42; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X218694694; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.03; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 42; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X218694694; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.03; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51.08333333; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X211644253; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.21; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 51.08333333; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X211644253; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.21; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 42.08333333; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X218287658; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.71; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 42.08333333; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X218287658; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.71; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56.66666667; year of diagnosis: 2004; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 13; patient id: X215524692; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.61; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 56.66666667; year of diagnosis: 2004; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 13; patient id: X215524692; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.61; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.33333333; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X219138424; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.77; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 49.33333333; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X219138424; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.77; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51.58333333; year of diagnosis: 2005; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 13; patient id: X210545749; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.28; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 51.58333333; year of diagnosis: 2005; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 13; patient id: X210545749; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.28; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 42.91666667; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X220769210; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 42.29; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 42.91666667; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X220769210; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 42.29; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51.83333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X213975550; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 35.44; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 51.83333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X213975550; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 35.44; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 46.91666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X212564887; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 18.33; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 46.91666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X212564887; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 18.33; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 58.33333333; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X211762886; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.22; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.66666667; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X219271119; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 34.22; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 53.66666667; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X219271119; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 34.22; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 51.08333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X217632526; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.17; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 42.33333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X214858553; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.24; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.83333333; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X215215245; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.95; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 49.83333333; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X215215245; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.95; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.66666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X215166377; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.93; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 48.66666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X215166377; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.93; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.08333333; year of diagnosis: 2006; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 16; patient id: X217979525; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.21; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 50.08333333; year of diagnosis: 2006; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 16; patient id: X217979525; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.21; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.16666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X212311300; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 19.16; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 52.16666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X212311300; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 19.16; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 57.08333333; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X221219745; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.4; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 57.08333333; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X221219745; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.4; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.33333333; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: NA; microarray batch: 15; patient id: X214564816; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.25; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 42.75; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X217841344; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.21; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 42.75; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X217841344; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.21; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54.25; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X212333736; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.63; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 54.25; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X212333736; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.63; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 42.5; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: NA; microarray batch: 15; patient id: X213645702; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.5; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 42.5; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: NA; microarray batch: 15; patient id: X213645702; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.5; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 41.41666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X215167176; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.2; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 41.41666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X215167176; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.2; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.33333333; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X220368773; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.06; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 50.33333333; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X220368773; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.06; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54.5; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X217553637; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.9; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 54.5; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X217553637; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.9; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.75; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X210650433; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.7; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 50.75; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X210650433; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.7; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 43.58333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 17; patient id: X214193576; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.31; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 43.58333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 17; patient id: X214193576; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.31; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58.91666667; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X211478890; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.63; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 58.91666667; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X211478890; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.63; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X212811767; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 35.51; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 51; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X212811767; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 35.51; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.41666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X221613038; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.32; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 52.41666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X221613038; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.32; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 47.58333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 13; patient id: X210417212; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 19.57; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.08333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X219033382; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 31.62; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 48.08333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X219033382; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 31.62; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 44.83333333; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X220876934; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.21; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 44.83333333; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X220876934; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.21; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.41666667; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X212139538; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.28; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 53.41666667; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X212139538; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.28; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.66666667; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X210467247; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.29; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 50.66666667; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X210467247; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.29; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.83333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X212836709; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 27.44; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 53.83333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X212836709; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 27.44; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 45.66666667; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X215349612; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.79; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 45.66666667; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X215349612; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.79; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54.41666667; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X217703933; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.25; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 54.41666667; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X217703933; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.25; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51.41666667; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X213857226; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.57; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 51.41666667; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X213857226; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.57; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51.16666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X214757743; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 33.45; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 51.16666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X214757743; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 33.45; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.75; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X218966722; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.09; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.5; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X215666026; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.05; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 49.5; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X215666026; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.05; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.25; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X216822219; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 31.28; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.83333333; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X216457839; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.03; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 49.83333333; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X216457839; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.03; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.58333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X213752390; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.84; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 45.08333333; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X212462763; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.81; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 45.08333333; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X212462763; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.81; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.83333333; year of diagnosis: 1997; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X212706053; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.32; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 41.25; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 13; patient id: X216458020; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 29.65; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56.83333333; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 13; patient id: X214108538; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.37; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.5; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: NA; microarray batch: 16; patient id: X219506334; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 34.22; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 50.5; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: NA; microarray batch: 16; patient id: X219506334; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 34.22; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 38.83333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X215326680; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.58; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 38.83333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X215326680; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.58; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51.58333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 13; patient id: X219298374; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.6; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51.91666667; year of diagnosis: 2005; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X210255826; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.3; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 51.91666667; year of diagnosis: 2005; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X210255826; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.3; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 53.66666667; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X213952521; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 29.76; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.16666667; year of diagnosis: 2004; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 13; patient id: X210186429; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.19; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 52.16666667; year of diagnosis: 2004; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 13; patient id: X210186429; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.19; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.83333333; year of diagnosis: 2006; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 17; patient id: X211362224; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 41.81; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 50.83333333; year of diagnosis: 2006; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 17; patient id: X211362224; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 41.81; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51.5; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 13; patient id: X220336433; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.04; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 51.5; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 13; patient id: X220336433; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.04; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.08333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X213978359; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.28; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 46; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X212101986; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.84; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 46; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X212101986; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.84; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55.58333333; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 17; patient id: X211042583; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 29.5; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 55.58333333; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 17; patient id: X211042583; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 29.5; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.08333333; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X213385279; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.54; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 52.08333333; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X213385279; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.54; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.41666667; year of diagnosis: 2008; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X221615254; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.04; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 50.41666667; year of diagnosis: 2008; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X221615254; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.04; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 54.75; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X211019912; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.17; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 42.83333333; year of diagnosis: 1999; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X216697168; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.13; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 42.83333333; year of diagnosis: 1999; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X216697168; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.13; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 50.16666667; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X212580057; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 18.6; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 46.16666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X216435191; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.61; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.58333333; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X211092212; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.68; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 48.58333333; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X211092212; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.68; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 42.25; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X218935072; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.57; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 42.25; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X218935072; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.57; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.16666667; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X221541965; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 34.96; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 49.16666667; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X221541965; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 34.96; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X219129319; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.67; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 54; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X219129319; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.67; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58.41666667; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X218540525; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.3; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 44.66666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X218119917; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 30.79; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 44.66666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X218119917; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 30.79; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.25; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X215716517; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.49; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 48.25; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 13; patient id: X215716517; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.49; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 49.66666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 17; patient id: X220183431; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.63; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 44.33333333; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X213222829; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.67; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.75; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X215243359; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.92; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 48.75; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 13; patient id: X215243359; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.92; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.91666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 17; patient id: X210244814; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.91; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 50.91666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 17; patient id: X210244814; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.91; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51.91666667; year of diagnosis: 1999; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 14; patient id: X217785175; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.34; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 41.83333333; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X220120677; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.34; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 41.83333333; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X220120677; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.34; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 42.91666667; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X219853078; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 19.31; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58.66666667; year of diagnosis: 2006; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 15; patient id: X215043337; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.59; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 58.66666667; year of diagnosis: 2006; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 15; patient id: X215043337; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.59; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.41666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 14; patient id: X213337254; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.17; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 50.41666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 14; patient id: X213337254; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.17; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.08333333; year of diagnosis: 2000; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 14; patient id: X219656792; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.49; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 48.08333333; year of diagnosis: 2000; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 14; patient id: X219656792; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.49; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.08333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 17; patient id: X210691260; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 19.3; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 49.08333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 17; patient id: X210691260; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 19.3; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.91666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 14; patient id: X213310102; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.1; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 50.91666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 14; patient id: X213310102; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.1; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 39.5; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X221148853; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.41; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.5; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X213754818; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.46; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 48.5; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X213754818; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.46; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.66666667; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X214487937; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.9; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 49.66666667; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X214487937; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.9; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 56.5; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X219086438; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 34.72; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 39.91666667; year of diagnosis: 2004; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 15; patient id: X211142079; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.37; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.08333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 14; patient id: X213023291; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.63; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 52.08333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 14; patient id: X213023291; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.63; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55.25; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X216118880; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.46; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 55.25; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X216118880; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.46; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.33333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X210458039; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 18.97; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 53.33333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X210458039; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 18.97; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.33333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X216353602; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 40.35; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 53.33333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X216353602; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 40.35; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55.91666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 17; patient id: X212452447; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.54; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 55.91666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 17; patient id: X212452447; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.54; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 54.33333333; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X210665568; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.03; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 46.08333333; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X212130796; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.83; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 46.08333333; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X212130796; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.83; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54.91666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X211269042; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.73; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 54.91666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X211269042; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.73; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56.91666667; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X213708700; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.4; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 56.91666667; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X213708700; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.4; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 46.25; year of diagnosis: 2000; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X215767351; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 36.02; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54.33333333; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X217808763; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.96; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 54.33333333; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X217808763; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.96; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 58.75; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X218212887; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.29; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 58.75; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X218212887; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.29; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 47.75; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 17; patient id: X213092238; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 19.97; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 47.75; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 17; patien t id: X213092238; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 19.97; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 57.75; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X214371471; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.74; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 57.75; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X214371471; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.74; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.08333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 17; patient id: X217695068; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 33; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 49.08333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 17; patient id: X217695068; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 33; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.08333333; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X213023915; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.13; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 50.08333333; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X213023915; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.13; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 47.41666667; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X212179669; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.8; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 47.41666667; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X212179669; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.8; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.66666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 14; patient id: X214077983; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.15; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 48.66666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 14; patient id: X214077983; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.15; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.66666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X217485760; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 44.43; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 49.66666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X217485760; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 44.43; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.41666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X213188375; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.85; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 50.41666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X213188375; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.85; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 44.08333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 14; patient id: X217403482; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.26; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 44.08333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 14; patient id: X217403482; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.26; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 45; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X214478523; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.61; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 45; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X214478523; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.61; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.25; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X215976375; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.58; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 53.25; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X215976375; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.58; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.58333333; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X212867323; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.27; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 52.58333333; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X212867323; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.27; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 40.83333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 16; patient id: X217194214; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.4; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 40.83333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 16; patient id: X217194214; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.4; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55.75; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X214558520; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.37; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 55.75; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X214558520; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.37; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 46.91666667; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X211023368; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.35; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 46.91666667; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X211023368; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.35; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54.5; year of diagnosis: 2003; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 15; patient id: X215439095; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 27.67; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 54.5; year of diagnosis: 2003; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 15; patient id: X215439095; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 27.67; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.16666667; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X221081526; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.25; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 48.16666667; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X221081526; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.25; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: NA; microarray batch: 14; patient id: X211592576; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 31.01; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 55; year of diagnosis: 2007; estrogen receptor status: Positive; alcohol intake: NA; microarray batch: 14; patient id: X211592576; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 31.01; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.5; year of diagnosis: 2005; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 14; patient id: X211967836; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.95; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 52.5; year of diagnosis: 2005; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 14; patient id: X211967836; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.95; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 41.5; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X216518312; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 18.25; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 41.5; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X216518312; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 18.25; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.33333333; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X217638453; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 19.94; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 52.33333333; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X217638453; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 19.94; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 47.25; year of diagnosis: 2002; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X216664750; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.58; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 47.25; year of diagnosis: 2002; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X216664750; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.58; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 40.91666667; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X211034174; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.75; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 40.91666667; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X211034174; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.75; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 52.33333333; year of diagnosis: 1999; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X216652424; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.63; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 53.33333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X213851608; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.31; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.5; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 16; patient id: X214514157; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.92; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 52.5; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 16; patient id: X214514157; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.92; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.33333333; year of diagnosis: 2000; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 16; patient id: X211177955; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.3; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.41666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X213721982; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 29.23; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 50.41666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X213721982; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 29.23; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 55.58333333; year of diagnosis: 2007; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X213782211; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 36.05; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 55.58333333; year of diagnosis: 2007; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X213782211; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 36.05; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.5; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 17; patient id: X216307272; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.17; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 48.5; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 17; patient id: X216307272; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.17; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.25; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X213165037; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.7; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 50.25; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X213165037; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.7; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.83333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X218111665; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 31.95; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 52.83333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X218111665; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 31.95; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.5; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X215343473; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.56; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 52.5; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X215343473; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.56; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 53.16666667; year of diagnosis: 2006; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X210355940; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 31.58; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54.41666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X219499195; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.96; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 54.41666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 15; patient id: X219499195; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.96; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 57.16666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X217512289; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 35.43; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 57.16666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X217512289; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 35.43; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.08333333; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X218193943; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 29.12; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 52.08333333; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X218193943; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 29.12; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.91666667; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X219546259; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.67; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.66666667; year of diagnosis: 2001; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X210609134; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.43; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 48.66666667; year of diagnosis: 2001; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X210609134; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.43; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.75; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X212890618; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.24; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 46.16666667; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X215747028; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.42; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 46.16666667; year of diagnosis: 2005; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X215747028; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.42; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56.41666667; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X218320380; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 19.77; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 56.41666667; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X218320380; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 19.77; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.83333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X212432124; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.19; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 52.83333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X212432124; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.19; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 56.83333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X211191939; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.8; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 56.83333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X211191939; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.8; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.75; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X211192120; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 31.78; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 53.75; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X211192120; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 31.78; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 59.41666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X211663571; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.09; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 59.41666667; year of diagnosis: 2006; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X211663571; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.09; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.91666667; year of diagnosis: 2000; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 15; patient id: X213676522; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 30.55; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 50.91666667; year of diagnosis: 2000; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 15; patient id: X213676522; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 30.55; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.25; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X218972291; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 17.94; avg_bodysize_age1020: NA; ', 'tissue: breast tumor; age at diagnosis: 49.25; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X218972291; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 17.94; avg_bodysize_age1020: NA; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51.75; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 15; patient id: X214436891; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.02; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.91666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 16; patient id: X216192809; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 17.72; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 50.91666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X216192809; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 17.72; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 51.16666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 16; patient id: X221261843; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.4; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 51.16666667; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 16; patient id: X221261843; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.4; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.08333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 16; patient id: X219786521; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 30.55; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 50.08333333; year of diagnosis: 2000; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 16; patient id: X219786521; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 30.55; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 45.91666667; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 16; patient id: X212832168; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 27.98; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 45.91666667; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 16; patient id: X212832168; nhs_cohort: NHS2; 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microarray batch: 14; patient id: X213464477; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.3; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 38.08333333; year of diagnosis: 1997; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 14; patient id: X213464477; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.3; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 46.25; year of diagnosis: 2002; estrogen receptor status: Negative; alcohol intake: >10 g/day; microarray batch: 14; patient id: X216440173; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.24; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 41; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X214459411; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 30.67; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 41; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 15; patient id: X214459411; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 30.67; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 44.91666667; year of diagnosis: 2006; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 14; patient id: X210368035; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.85; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 44.91666667; year of diagnosis: 2006; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 14; patient id: X210368035; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 25.85; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 39.58333333; year of diagnosis: 2003; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X213984655; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.8; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 39.58333333; year of diagnosis: 2003; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X213984655; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.8; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 47.5; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X221004582; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.3; avg_bodysize_age1020: 3; ', 'tissue: breast tumor; age at diagnosis: 47.5; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X221004582; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.3; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 47.91666667; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X216497867; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 27.44; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 47.91666667; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X216497867; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 27.44; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 42.41666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X211841672; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 18.8; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 42.41666667; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X211841672; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 18.8; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.41666667; year of diagnosis: 2001; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 16; patient id: X212551453; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.2; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 53.41666667; year of diagnosis: 2001; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 16; patient id: X212551453; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.2; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54.83333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X214653506; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.19; avg_bodysize_age1020: 5; ', 'tissue: breast tumor; age at diagnosis: 54.83333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X214653506; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 32.19; avg_bodysize_age1020: 5; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 49.75; year of diagnosis: 1998; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X220286354; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 30.9; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 54.75; year of diagnosis: 2003; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X212943609; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.56; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 54.75; year of diagnosis: 2003; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X212943609; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 26.56; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 52.75; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 16; patient id: X214437793; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 24.96; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 52.75; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 16; patient id: X214437793; 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estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X219721345; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.17; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 51; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X219721345; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 23.17; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.91666667; year of diagnosis: 2007; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 17; patient id: X213579114; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 29.76; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 53.58333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 16; patient id: X217999436; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 30.18; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 53.58333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 16; patient id: X217999436; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 30.18; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 45.33333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 16; patient id: X216760020; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.08; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 45.33333333; year of diagnosis: 1999; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 16; patient id: X216760020; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.08; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 44.91666667; year of diagnosis: 1998; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 14; patient id: X219016692; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 29.95; avg_bodysize_age1020: 3; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 44.75; year of diagnosis: 1999; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 14; patient id: X210720732; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.05; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.08333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 16; patient id: X216299546; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.46; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 50.08333333; year of diagnosis: 2004; estrogen receptor status: Positive; alcohol intake: >10 g/day; microarray batch: 16; patient id: X216299546; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 22.46; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 48.75; year of diagnosis: 2005; estrogen receptor status: Negative; alcohol intake: 0-10 g/day; microarray batch: 16; 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estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 16; patient id: X221428357; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 29.62; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 43.66666667; year of diagnosis: 2000; estrogen receptor status: Negative; alcohol intake: 0 g/day; microarray batch: 16; patient id: X221428357; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 29.62; avg_bodysize_age1020: 4; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.83333333; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X215547418; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.55; avg_bodysize_age1020: 2; ', 'tissue: breast tumor; age at diagnosis: 50.83333333; year of diagnosis: 2003; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X215547418; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 20.55; avg_bodysize_age1020: 2; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 50.83333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 17; patient id: X216819144; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.89; avg_bodysize_age1020: 1; ', 'tissue: breast tumor; age at diagnosis: 50.83333333; year of diagnosis: 2002; estrogen receptor status: Positive; alcohol intake: 0 g/day; microarray batch: 17; patient id: X216819144; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 28.89; avg_bodysize_age1020: 1; ', 'tissue: breast tumor-adjacent normal; age at diagnosis: 44.83333333; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X216547328; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.4; avg_bodysize_age1020: 4; ', 'tissue: breast tumor; age at diagnosis: 44.83333333; year of diagnosis: 2001; estrogen receptor status: Positive; alcohol intake: 0-10 g/day; microarray batch: 16; patient id: X216547328; nhs_cohort: NHS2; bmi_2yrs_bef_dx: 21.4; avg_bodysize_age1020: 4; ' GSE9204 Homo sapiens 8 Expression profiling by array GPL5620 Role of CSN5 in breast cancer (siRNA transfections) 2007-10-01 CSN5 has been implicated as a candidate oncogene in human breast cancers by genetic linkage with activation of the poor-prognosis, wound response gene expression signature. CSN5 is a subunit of the eight-protein COP9 signalosome, a signaling complex with multiple biochemical activities; the mechanism of CSN5 action in cancer development remains poorly understood. Here we show that CSN5 isopeptidase activity is essential for breast epithelial transformation and progression. Amplification of CSN5 is required for transformation of primary human breast epithelial cells by defined oncogenes. The transforming effects of CSN5 require CSN subunits for assembly of the full COP9 signalosome and the isopeptidase activity of CSN5, which potentiates the transcriptional activity of MYC. Transgenic inhibition of CSN5 isopeptidase activity blocks breast cancer progression evoked by MYC and RAS in vivo. These results highlight CSN5 isopeptidase activity in breast cancer progression, suggesting it as a therapeutic target in aggressive human breast cancers. A genetic modification design type is where an organism(s) has had genetic material removed, rearranged, mutagenized or added, such as knock out. Keywords: genetic_modification_design https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE9204 CSN5 isopeptidase activity links COP9 signalosome activation to breast cancer progression. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-07-3060 {Cancer research (8.378): 10.1158/0008-5472.CAN-07-3060} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA105247 https://www.ebi.ac.uk/ena/browser/view/PRJNA105247 None [Overal design]Computed; [Treatment]'None', 'siRNAs against the indicated genes were transfected 48 hours before harvesting RNA'; [Growth]'None'; [Extraction]'not provided'; [Cell type]'Source: ''' GSE148344 Homo sapiens 20 Expression profiling by high throughput sequencing GPL16791 EXP. 229_AC_RNAseq data of human cancer cell lines 94T778, SKBR3, AU565, SKMEL28 and A375 exposed to the selective MTOR inhibitor torkinib (PP242, Selleckchem, TX, USA) for 72 hours. 2020-04-08 Drug concentrations were selected to halt cell cycle progression without affecting cell viability: 94T778 10 µM, A375, SKMEL28 and AU565 4 µM, SKBR3 0.8 µM. The pharmacologic inhibition of MTOR repressed expression of the homologous recombination (HR) and Fanconi Anemia (FA) pathways, and selectively high-fidelity but not error-prone DNA polymerases in all cancer cell lines sequenced https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148344 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA623939 https://www.ebi.ac.uk/ena/browser/view/PRJNA623939 https://www.ncbi.nlm.nih.gov/sra?term=SRP255761 [Overal design]The experiment has been designed to understand the impact of MTOR inhibition on the expression profile of different genes involved in DNA repair.; [Treatment]'Drug concentrations were selected to halt cell cycle progression without affecting cell viability: 94T778 10 µM, A375, SKMEL28 and AU565 4 µM, SKBR3 0.8 µM. The pharmacologic inhibition of MTOR repressed expression of the homologous recombination (HR) and Fanconi Anemia (FA) pathways, and selectively high-fidelity but not error-prone DNA polymerases in all cancer cell lines sequenced'; [Growth]'Untreated controls were cultured as follows: 94T778 cells and SKBR3 were grown in RPMI 1640 Gibco supplemented with penicillin, streptomycin, L-glutamine and 10% fetal bovine serum (FBS). AU565 were grown in RPMI complete media supplemented with 1mM sodium pyruvate and 1.5g/L sodium bicarbonate. A375 cells were grown in DMEM Gibco media supplemented with penicillin, streptomycin, L-glutamine and 10% fetal bovine serum (FBS). SKMEL28 were grown in MEM Gibco supplemented with penicillin, streptomycin, L-glutamine and 10% fetal bovine serum (FBS).'; [Extraction]'Qiagen RNeasy midi kit'; [Cell type]'Source: ''cell line: 94T778; treatment: untreated; sample name: FD02699707; ', 'cell line: 94T778; treatment: untreated; sample name: FD02699715; ', 'cell line: A375; treatment: untreated; sample name: FD02699773; ', 'cell line: A375; treatment: untreated; sample name: FD02699928; ', 'cell line: SKMEL28; treatment: untreated; sample name: FD02699936; ', 'cell line: SKMEL28; treatment: untreated; sample name: FD02699975; ', 'cell line: SKBR3; treatment: untreated; sample name: FD02699976; ', 'cell line: SKBR3; treatment: untreated; sample name: FD02700010; ', 'cell line: AU565; treatment: untreated; sample name: FD02700052; ', 'cell line: AU565; treatment: untreated; sample name: FD02700062; ', 'cell line: 94T778; treatment: 10 uM Torkinib; sample name: FD02700076; ', 'cell line: 94T778; treatment: 10 uM Torkinib; sample name: FD02700082; ', 'cell line: A375; treatment: 4 uM Torkinib; sample name: FD02700103; ', 'cell line: A375; treatment: 4 uM Torkinib; sample name: FD02700122; ', 'cell line: SKMEL28; treatment: 4 uM Torkinib; sample name: FD02700149; ', 'cell line: SKMEL28; treatment: 4 uM Torkinib; sample name: FD02700235; ', 'cell line: SKBR3; treatment: 0.8 uM Torkinib; sample name: FD02700276; ', 'cell line: SKBR3; treatment: 0.8 uM Torkinib; sample name: FD02700328; ', 'cell line: AU565; treatment: 4 uM Torkinib; sample name: FD02700330; ', 'cell line: AU565; treatment: 4 uM Torkinib; sample name: FD02700332; ' GSE56822 Homo sapiens 16 Expression profiling by array GPL6883 IL-17 mediates susceptibility to breast cancer growth by promoting the recruitment of tumorigenic neutrophils 2014-04-15 The aggressiveness of invasive ductal carcinoma (IDC) of the breast is associated with increased IL-17 levels. In this study, we investigated the role of IL-17 in invasive breast tumor pathogenesis. We found that metastatic tumor-infiltrating T lymphocytes produced elevated levels of IL-17, whereas IL-17 neutralization inhibited tumor growth and prevented the migration of neutrophils and tumor cells to secondary disease sites. Tumorigenic neutrophils promote disease progression, and their depletion suppressed tumor growth. Moreover, IL-17 induced IL-6 and CXCL1 production in tumor cells, and IL-6 depletion reduced metastatic tumor growth and infiltration by Th17 cells and neutrophils. In addition, inoculation of a non-metastatic mammary tumor cell line pre-incubated with IL-17 promoted tumor growth, confirming the pro-tumor role of IL-17. Furthermore, high IL-17 expression was associated with lower disease-free survival (DFS) and worse prognosis in IDC patients. Thus, IL-17 blockade represents an attractive approach for the control of invasive breast tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE56822 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA244683 https://www.ebi.ac.uk/ena/browser/view/PRJNA244683 None [Overal design]Biopsies of patients with breast tumors; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''il17 status: high; tissue: breast cancer biopsy; ', 'il17 status: low; tissue: breast cancer biopsy; ' GSE101410 Homo sapiens 12 Non-coding RNA profiling by high throughput sequencing GPL11154 Luminal subtype-specific circRNAs in breast cancer cells by a novel tool for external data analysis. 2017-07-13 Circular RNAs are molecules present in all eukaryotes that are generated from a large number of genes by a particular processing of transcripts. We have exploited poly(A-) RNA-Seq data generated in our lab in MCF-7 breast cancer cells to define a compilation of exonic circRNAs more comprehensive than previously existing lists. Development of novel computational algorithms allowed us to quantitatively evaluate expression of these circRNA also in publicly available data. We report here novel findings with important implications both for circRNA biogenesis and as specific markers for breast cancer. We observed and confirmed by ChIP analysis that exons involved in circularization events display significantly higher levels of the histone post-transcriptional modification H3K36me3 than non-circularizing exons. This suggests a clear link with a published alternative splicing mechanism in the circRNA biogenesis mechanism. We also found that circRNAs contain an unexpectedly elevated number of Ago binding sites, revamping the hypothesis of circRNAs acting as miRNA sponges in some cases. Finally, we report that a subset of MCF-7 circRNAs are specific to tumor versus normal tissue, while others can differentiate the Luminal tumor subtype, thus suggesting that circRNAs can be exploited as novel biomarkers and drug targets for breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE101410 Luminal breast cancer-specific circular RNAs uncovered by a novel tool for data analysis. Oncotarget None https://doi.org/10.18632/oncotarget.24522 {Oncotarget (None): 10.18632/oncotarget.24522} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA394133 https://www.ebi.ac.uk/ena/browser/view/PRJNA394133 https://www.ncbi.nlm.nih.gov/sra?term=SRP111855 [Overal design]The RNA-seq datasets were obtained from libraries generated with the TruSeq stranded library preparation kit (Illumina) using as input material RNA depleted of both poly(A+) and ribosomal RNAs fractions. Pool of 12 libraries (pooled at equimolar concentration) was generated, quantified and run on the HiSeq2000 (Illumina) sequencer in 50 nts paired-end sequencing mode following manufacturer instruction. A total of 12 datasets, with an average depth from 30.7 to 116.1 million paired-end reads, were obtained, composed of triplicates of four MCF-7 culture conditions: i) hormone-deprived (HD) media ii) HD+ 17b-estradiol (6h) iii) medium added of FSC 5% iv) double-stranded RNA complementary to ESR1 mRNA (siRNA) (48h).; [Treatment]'None'; [Growth]'MCF-7 were growth separately in four culture conditions: i) hormone-deprived (HD) media ii) HD+ 17b-estradiol (6h) iii) medium added of FSC 5% iv) double-stranded RNA complementary to ESR1 mRNA (siRNA) (48h)'; [Extraction]'The starting RNA-seq datasets were obtained from libraries generated with the TruSeq stranded library preparation kit (Illumina) using as input material RNA depleted of both poly(A+) and ribosomal RNAs fractions.'; [Cell type]'breast cancer cell line''cell type: breast cancer cell line; ' GSE160363 Homo sapiens 2 Expression profiling by high throughput sequencing GPL18573 RNA-sequencing results of MDA-MB-231 with/without OGFOD1 2020-10-28 Recently, high levels of OGFOD1 has been reported in variety of cancers. Despite of the significances, the precise mechanism is poor understood. In order to find how OGFOD1 affects the cancer development, we conducted RNA-sequencing in MDA-MB-231. OGFOD1 was knocked out using CRISPR/Cas9 system. Total mRNA was isolated from parental and OGFOD1-knockout (OGFOD1Δ/Δ) MDA-MB-231 cells. Isolated RNA was used to prepare an mRNA sequencing library using TruSeq Stranded mRNA sample preparation kit. All the samples were sequenced on Illumina NextSeq 500 Sequencer with a 75 bp paired-end High Output kit. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE160363 Phosphorylation of OGFOD1 by Cell Cycle-Dependent Kinase 7/9 Enhances the Transcriptional Activity of RNA Polymerase II in Breast Cancer Cells. Cancers 6.162 https://doi.org/10.3390/cancers13143418 {Cancers (6.162): 10.3390/cancers13143418} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA672999 https://www.ebi.ac.uk/ena/browser/view/PRJNA672999 https://www.ncbi.nlm.nih.gov/sra?term=SRP289578 [Overal design]mRNA profiles of parantel and OGFOD1 KO MDA-MB-231 cells.; [Treatment]'None'; [Growth]'Human breast carcinoma cell line MDA-MB-231 were cultured in Dulbecco’s modified eagle medium (DMEM) with 10% (v/v) fetal bovine serum (FBS) and penicillin–streptomycin at 37°C in a humidified atmosphere of 5% CO2.'; [Extraction]'Using TRIzol RNA isolation reagent (Life Technologies, Carlsbad, CA), total mRNA was isolated. RNA integrity was confirmed using an Agilent RNA 6000 Pico kit (Agilent, Santa Clara, CA).\nIsolated RNA was used to prepare an mRNA sequencing library using TruSeq Stranded mRNA sample preparation kit (Illumina, San Diego, CA).'; [Cell type]'Source: ''cell line: MDA-MB-231; genotype: wild type; ', 'cell line: MDA-MB-231; genotype: OGFOD1-/-; ' GSE82161 Homo sapiens 4 Expression profiling by array GPL6480 Preclinical and phase I clinical studies of KW-2450, a dual IGF-1R/IR tyrosine kinase inhibitor, in combination with lapatinib and letrozole. 2016-06-02 KW-2450 is an oral dual insulin-like growth factor-1 receptor/insulin receptor tyrosine kinase inhibitor. We investigated the in vitro and in vivo preclinical activity of KW-2450 plus lapatinib and letrozole and conducted a phase I trial of the triple-drug combination in one male and 10 postmenopausal female patients with advanced/metastatic hormone receptorpositive, human epidermal growth factor receptor 2 (HER2)-positive breast cancer. A series of in vitro and in vivo animal studies was undertaken of KW-2450 in combination with lapatinib and hormonal agents. The phase I trial was conducted to establish the safety, tolerability, and recommended phase II dose (RP2D) of KW-2450 administered in combination with lapatinib and letrozole. Preclinical studies showed KW-2450 and lapatinib act synergistically to induce in vitro apoptosis and inhibit growth of HER2-positive MDA-MB-361 and BT-474 breast cancer cell lines. This combined effect was confirmed in vivo using the MDA-MB-361 xenograft model. KW-2450 showed synergistic in vitro growth inhibition with letrozole and 4-hydroxytamoxifen in ER-positive MCF-7 breast cancer cells and MCF-7-Ac1 aromatase-transfected MCF-7 cells. In the phase I study, dose-limiting toxicity (DLT; grade 3 rash and grade 3 hyperglycemia, respectively) occurred in two of three patients at the dose of KW-2450 25 mg/day plus lapatinib 1500 mg/day and letrozole 2.5 mg/day. The RP2D of the triple-drug combination was established as KW-2450 25 mg/day, lapatinib 1250 mg/day, and letrozole 2.5 mg/day with no DLT at this dose level. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE82161 Preclinical and phase I clinical studies of KW-2450, a dual IGF-1R/IR tyrosine kinase inhibitor, in combination with lapatinib and letrozole. Therapeutic advances in medical oncology 5.670 https://doi.org/10.1177/1758835918786858 {Therapeutic advances in medical oncology (5.670): 10.1177/1758835918786858} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA324235 https://www.ebi.ac.uk/ena/browser/view/PRJNA324235 None [Overal design]Breast cancer cell line MDA-MB-361 was treated with DMSO, 100 nM KW-2450, 100 nM Lapatinib or 100 nM KW-2450 + 100 nM Lapatinib for 48 hours.; [Treatment]'Cells were treated with 100 nmol/L KW-2450 and/or 100 nmol/L lapatinib for 48 hours.'; [Growth]'Breast cancer cell line MDA-MB-361 were seeded into 15 cm dishes by 2 x 10^5 cells/mL with assay medium [Leibovit’s L-15 medium supplemented with 10% heat inactivated FBS].'; [Extraction]'Total RNA was extracted using TRIzol reagents (Invitrogen, Carlsbad, CA, USA) according to the manufacturer’s instruction. All RNA samples were quantitated using NanoDrop ND-1000 spectrophotometer (Nanodrop, Wilmington, DE, USA), and RNA quality was analyzed using Bioanalyser 2100 (Agilent Technologies, Santa Clara, CA, USA).'; [Cell type]'Source: ''tissue: cancer cell line; cell line: MDA-MB-361; treatment: DMSO; time: 48hr; ', 'tissue: cancer cell line; cell line: MDA-MB-361; treatment: KW-2450; time: 48hr; ', 'tissue: cancer cell line; cell line: MDA-MB-361; treatment: Lapatinib; time: 48hr; ', 'tissue: cancer cell line; cell line: MDA-MB-361; treatment: KW-2450+Lapatinib; time: 48hr; ' GSE54892 Homo sapiens 16 Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing GPL10558; GPL11154 LRH-1 governs vital transcriptional programs in endocrine sensitive and resistant breast cancer cells 2014-02-11 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54892 LRH-1 governs vital transcriptional programs in endocrine-sensitive and -resistant breast cancer cells. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-13-2351 {Cancer research (8.378): 10.1158/0008-5472.CAN-13-2351} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA237974 https://www.ebi.ac.uk/ena/browser/view/PRJNA237974 None [Overal design]Refer to individual Series; [Treatment]'None', 'MCF7 cells were maintained in DMEM without phenol red and supplemented with 5% charcoal–dextran-treated FBS for 4 days prior to their use in estradiol (E2) treatment (10-7M, 30 min).', 'Cells were transduced with shLRH-1 or shCTL lentiviruses for 4 days before mRNA extraction.'; [Growth]'MCF7 cells were grown to 70% of confluence in DMEM with 10% FBS.', 'MCF7 are growth in DMEM containing 10% fetal bovine serum (FBS), glutamine and antibiotics.', 'LCC2 are maintained in DMEM without phenol red containing 5% charcoal-dextran treated FBS, glutamine and antibiotics.', 'LCC9 are maintained in DMEM without phenol red containing 5% charcoal-dextran treated FBS, glutamine and antibiotics.'; [Extraction]"For ChIP and FAIRE assays, DNA was extracted according to Svotelis et al. (Methods Mol Biol., 2009) and to Eeckhoute et al. (Genome Res., 2009) with few modifications. In brief, ~20-30.106 cells were cross-linked using 1.1% formaldehyde for 10 or 30 min at RT in 20ml of PBS 1X, reaction was quenched with 1ml of 2.5M Glycine. Cells were lysed with SDS lysis buffer (1% SDS, 10 mM EDTA, 50 mM Tris–HCI of pH 8.1) during 30 min at 4°C and sonicated to have DNA fragment size between 200 and 300 bp. For ChIP, lysate was incubated overnight at 4°C on a rotator with 5µg of antibody. 35 µl of protein-A magnetic beads (Invitrogen) were added during 2h before washing with TSE-150 (0.1% SDS, 1% Triton, 2 mM EDTA, 20 mM Tris–HCl of pH 8.1, 150 mM NaCl), TSE-500 (0.1% SDS, 1% Triton, 2 mM EDTA, 20 mM Tris of pH 8.1, 500 mM NaCl), LiCl detergent (0.25 M LiCl, 1% NP40, 1% sodium deoxycholate, 1 mM EDTA, 10 mM Tris of pH 8.1) and three times with TE 1X. For FAIRE, soluble chromatin was subjected to three consecutive phenol-chloroform extractions. DNA was then reverse-crosslinked overnight at 65ºC and treated with RNAse A for 30 min at 37°C, followed by Proteinase K for 2 h at 37°C. After purification, DNA was quantified with Picogreen (Invitrogen) before library preparation.\nLibraries were prepared according to Illumina's instructions. Briefly, 10 ng (ChIP-seq) or 50 ng (FAIRE-seq) of DNA were end-repaired using a combination of T4 DNA polymerase and T4 polynucleotide kinase (Enzymatics). DNA fractions of ~300 bp were selectively isolated with solid-phase reversible immobilization (SPRI) beads (Agencourt AMPure, Beckman Coulter). After adapter ligation, DNA was PCR amplified with Illumina primers, the quality and quantity of each DNA library was analyzed using Agilent Bioanalyser before sequencing on HiSeq (Illumina) following the manufacturer's protocols.", 'Total RNA was isolated using the GenElute mammalian total RNA miniprep kit (Sigma).'; [Cell type]'breast adenocarcinoma cells', 'Source: ''cell line: MCF-7; cell type: breast adenocarcinoma cells; chip antibody: LRH-1; chip antibody vendor: R&D; chip antibody cat. #: PP-H2325-00; chip antibody lot #: A-2; ', 'cell line: MCF-7; cell type: breast adenocarcinoma cells; chip antibody: Med12; chip antibody vendor: Bethyl; chip antibody cat. #: A300-774A; chip antibody lot #: A300-774A-1; ', 'cell line: MCF-7; cell type: breast adenocarcinoma cells; ', 'cell line: MCF-7; cell type: breast adenocarcinoma cells; chip antibody: RNAPII; chip antibody vendor: Covance; chip antibody cat. #: MMS-126R; chip antibody lot #: E12CF00481; ', 'tissue: breast cancer; cell line: MCF7; endocrine sensitivity: endocrine sensitive; ', 'tissue: breast cancer; cell line: LCC2; endocrine sensitivity: endocrine resistant (Tamoxifen); ', 'tissue: breast cancer; cell line: LCC9; endocrine sensitivity: endocrine resistant (Tamoxifen and Fulvestrant); ' GSE61208 Mus musculus 12 Expression profiling by array GPL1261 Gene expression data from 4T1 irradiated tumors treated with TGFbeta blockade 2014-09-08 Accumulating data support the concept that ionizing radiation therapy (RT) has the potential to convert the tumor into an in situ, individualized vaccine; however this potential is rarely realized by RT alone. Transforming growth factor β (TGFβ) is an immunosuppressive cytokine that is activated by RT and inhibits the antigen-presenting function of dendritic cells and the differentiation of effector CD8+ T cells. Here we tested the hypothesis that TGFβ hinders the ability of RT to promote anti-tumor immunity. Development of tumor-specific immunity was examined in a pre-clinical model of metastatic breast cancer. Mice bearing established 4T1 mouse mammary carcinoma treated with pan-isoform specific TGFβ neutralizing antibody, 1D11, showed significantly improved control of the irradiated tumor and non-irradiated metastases, but no effect in the absence of RT. Notably, whole tumor transcriptional analysis demonstrated the selective upregulation of genes associated with immune-mediated rejection only in tumors of mice treated with RT+TGFβ blockade. Mice treated with RT+TGFβ blockade exhibited cross-priming of CD8+ T cells producing IFNγ in response to three tumor-specific antigens in tumor-draining lymph nodes, which was not evident for single modality treatment. Analysis of the immune infiltrate in mouse tumors showed a significant increase in CD4+ and CD8+ T cells only in mice treated with the combination of RT+TGFβ blockade. Depletion of CD4+ or CD8+ T cells abrogated the therapeutic benefit of RT+TGFβ blockade. These data identify TGFβ as a master inhibitor of the ability of RT to generate an in situ tumor vaccine, which supports testing inhibition of TGFβ during radiotherapy to promote therapeutically effective anti-tumor immunity. We used genome-wide microarray to depict main biological processes responsibles for the therapeutic benefit of the combination ofTGF-beta blockade and local radiotherapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE61208 TGFβ Is a Master Regulator of Radiation Therapy-Induced Antitumor Immunity. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-14-3511 {Cancer research (8.378): 10.1158/0008-5472.CAN-14-3511} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA260508 https://www.ebi.ac.uk/ena/browser/view/PRJNA260508 None [Overal design]To gain a more comprehensice protrait of the effects of RT and TGFbeta blockade on gene expressionin tumors, we collected 4T1 tumors 4 days after completion of RT. Three tumors from each group were then subjected to RNA extraction and hybridization on affymetrix array.; [Treatment]'4T1-tumor bearing mice received i.p. injections of 1D11, a pan-isoform neutralizing TGFbeta monoclonal antobody (mAb) or its isotype control starting at day 12 post-tumor cells injection. In half of the mice of each group, tumors were treated with local RT given in 5 fractions of 6Gy starting on day 13. On day 22, tumors were harvested and kept in RNAlater at -80C until RNA extraction.'; [Growth]'50,000 4T1 tumor cells were injected to the right flank of a Balb/C mice'; [Extraction]'RNA was extracted and purified with Qiagen Rneasy Mini kit as described by the manufacturer.'; [Cell type]'Source: ''gender: Female; strain: Balb/C; tissue: 4T1 tumor; ' GSE47462 Homo sapiens 72 Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing GPL10999 A shared transcriptional program in early breast neoplasias despite genetic and clinical distinctions 2013-05-29 The earliest recognizable stages of breast neoplasia are lesions that represent a heterogeneous collection of epithelial proliferations currently classified based on morphology. Their role in the development of breast cancer is not well understood but insight into the critical events at this early stage will improve efforts in breast cancer detection and prevention. These microscopic lesions are technically difficult to study so very little is known about their molecular alterations. To characterize the transcriptional changes of early breast neoplasia, we sequenced 3'- end enriched RNAseq libraries from formalin-fixed paraffin-embedded tissue of early neoplasia samples and matched normal breast and carcinoma samples from 25 patients. We find that gene expression patterns within early neoplasias are distinct from both normal and breast cancer patterns and identify a pattern of pro-oncogenic changes, including elevated transcription of ERBB2, FOXA1, and GATA3 at this early stage. We validate these findings on a second independent gene expression profile data set generated by whole transcriptome sequencing. Measurements of protein expression by immunohistochemistry on an independent set of early neoplasias confirms that ER pathway regulators FOXA1 and GATA3, as well as ER itself, are consistently upregulated at this early stage. The early neoplasia samples also demonstrate coordinated changes in long non-coding RNA expression and microenvironment stromal gene expression patterns. This study is the first examination of global gene expression in early breast neoplasia, and the genes identified here represent candidate participants in the earliest molecular events in the development of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47462 A shared transcriptional program in early breast neoplasias despite genetic and clinical distinctions. Genome biology 14.028 https://doi.org/10.1186/gb-2014-15-5-r71 {Genome biology (14.028): 10.1186/gb-2014-15-5-r71} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA205694 https://www.ebi.ac.uk/ena/browser/view/PRJNA205694 https://www.ncbi.nlm.nih.gov/sra?term=SRP023262 [Overal design]3SEQ was performed on 72 FFPE human breast samples from 25 patients: 24 normal, 25 early neoplasia, 9 carcinoma in situ, and 14 invasive cancer; [Treatment]'Clinical tissue samples were formalin-fixed and paraffin-embedded (FFPE).'; [Growth]'None'; [Extraction]"Multiple 2 mm-diameter core punches were taken from FFPE tissue blocks to collect dense areas of neoplasia and adjacent normal breast epithelial content separately. When ductal carcinoma in situ (DCIS) and/or invasive ductal carcinoma (IDC) were present, these were also cored. Three to ten tissue cores were pooled for each diagnosis per patient, and tissue cores were re-embedded in paraffin and re-evaluated histologically for lesion purity by sectioning length-wise along the core. Only samples which possessed >90% of luminal cells with the appropriate diagnosis within the epithelial compartment were included among our samples. Adjacent normal cores contained no identifiable pathologies, and cancer cores possessed less than 5% early neoplasia or normal epithelial cells. In all cases stromal cells were present in the core samples. DNA and total RNA were purified from paraffin slices of the embedded tissue cores following deparaffination with a xylene incubation, ethanol wash, and a protease digestion, using the RecoverAll Total Nucleic Acid Isolation Kit (Ambion/Life Technologies; catalog #1975).\n3SEQ libraries were prepared from as little as 5 ug total RNA. RNA was enriched for 3’ ends by using the Oligotex mRNA mini Kit (QIAgen). The 3’- poly(A)-enriched RNA pools were made into directional 3SEQ Illumina sequencing libraries as follows. RNA that was not sufficiently fragmented was heat-sheared to a size of approximately 100-200 bases by incubation with First Strand Buffer (Invitrogen/Life Technologies) and oligo-dT-P7 primer (5’- CAA GCA GAA GAC GGC ATA CGA GCT CTT CCG ATC TTT TTT TTT TTT TTT TTT TTT TTT TVN -3’) at 85oC for 3-5 minutes, depending on the extent of fragmentation required. The mixture was cooled to 50oC and first strand cDNA synthesis was performed in a 20 ul reaction using Superscript III Reverse Transcriptase (Invitrogen/Life Technologies) for 1 hour at 50oC. Second strand cDNA was synthesized using Second Strand Buffer (Invitrogen/Life Technologies), DNA ligase (Invitrogen/Life Technologies), DNA polymerase I (New England Biolabs), and RNaseH (Epicentre Biotechnologies/Illumina), and purified using the QIAquick PCR Purification Kit (QIAgen). 3’ end repair and modification used dATP, Klenow exo (New England Biolabs) and Klenow Buffer, and was purified using the QIAgen MinElute PCR Purification Kit (QIAgen). cDNA was then ligated to the double-stranded P5 Linker (Adapter Oligo Mix; Illumina) for 15 minutes at 22oC. SPRI bead purification (Agencourt Biosciences/Beckman Coulter) was performed both prior to and following PCR amplification of the linker-ligated cDNA using 5' - AAT GAT ACG GCG ACC ACC GAG ATC TAC ACT CTT TCC CTA CAC GAC GCT CTT CCG ATC T - 3' and 5' - CAA GCA GAA GAC GGC ATA CGA GCT CTT CCG ATC - 3' primers and the Phusion PCR Master Mix (New England Biolabs) using a 15 cycle program (98oC for 30 sec; 15 cycles of 98oC for 10 sec, 65oC for 30 sec, 72oC for 30 sec; 72oC for 5 min). The libraries were then size selected for 200–300 bp fragments by agarose gel fractionation (3% Nusieve GTG; Lonza/Fisher Scientific) and purified using the QIAquick Gel Extraction Kit (QIAgen). The libraries contain P7 sequence at the 3’ end downstream of poly(A) and P5 at the 5’ end."; [Cell type]'Source: ''tissue id: STT5424; patient number: 1; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5425; patient number: 1; disease state: normal breast; tissue: breast; ', 'tissue id: STT5426; patient number: 23; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5427; patient number: 23; disease state: normal breast; tissue: breast; ', 'tissue id: STT5430; patient number: 2; disease state: normal breast; tissue: breast; ', 'tissue id: STT5431; patient number: 2; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5437; patient number: 3; disease state: ductal carcinoma in situ; tissue: breast; ', 'tissue id: STT5439; patient number: 3; disease state: normal breast; tissue: breast; ', 'tissue id: STT5440; patient number: 3; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5441; patient number: 4; disease state: normal breast; tissue: breast; ', 'tissue id: STT5442; patient number: 4; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5445; patient number: 5; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5446; patient number: 5; disease state: normal breast; tissue: breast; ', 'tissue id: STT5449; patient number: 6; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5450; patient number: 6; disease state: ductal carcinoma in situ; tissue: breast; ', 'tissue id: STT5451; patient number: 6; disease state: normal breast; tissue: breast; ', 'tissue id: STT5462; patient number: 7; disease state: ductal carcinoma in situ; tissue: breast; ', 'tissue id: STT5463; patient number: 7; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5465; patient number: 7; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5466; patient number: 7; disease state: normal breast; tissue: breast; ', 'tissue id: STT5472; patient number: 8; disease state: normal breast; tissue: breast; ', 'tissue id: STT5474; patient number: 8; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5475; patient number: 9; disease state: normal breast; tissue: breast; ', 'tissue id: STT5476; patient number: 9; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5477; patient number: 9; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5502; patient number: 10; disease state: normal breast; tissue: breast; ', 'tissue id: STT5503; patient number: 10; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5504; patient number: 10; disease state: ductal carcinoma in situ; tissue: breast; ', 'tissue id: STT5510; patient number: 11; disease state: normal breast; tissue: breast; ', 'tissue id: STT5511; patient number: 11; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5567; patient number: 12; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5568; patient number: 12; disease state: ductal carcinoma in situ; tissue: breast; ', 'tissue id: STT5570; patient number: 13; disease state: normal breast; tissue: breast; ', 'tissue id: STT5571; patient number: 13; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5572; patient number: 13; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5573; patient number: 14; disease state: normal breast; tissue: breast; ', 'tissue id: STT5574; patient number: 14; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5575; patient number: 14; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5576; patient number: 15; disease state: normal breast; tissue: breast; ', 'tissue id: STT5577; patient number: 15; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5578; patient number: 15; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5580; patient number: 16; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5581; patient number: 16; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5611; patient number: 17; disease state: normal breast; tissue: breast; ', 'tissue id: STT5612; patient number: 17; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5613; patient number: 17; disease state: ductal carcinoma in situ; tissue: breast; ', 'tissue id: STT5614; patient number: 19; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5616; patient number: 19; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5617; patient number: 19; disease state: normal breast; tissue: breast; ', 'tissue id: STT5618; patient number: 18; disease state: ductal carcinoma in situ; tissue: breast; ', 'tissue id: STT5619; patient number: 18; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5620; patient number: 18; disease state: normal breast; tissue: breast; ', 'tissue id: STT5667; patient number: 20; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5668; patient number: 20; disease state: normal breast; tissue: breast; ', 'tissue id: STT5669; patient number: 20; disease state: ductal carcinoma in situ; tissue: breast; ', 'tissue id: STT5670; patient number: 20; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5706; patient number: 25; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5747; patient number: 21; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5749; patient number: 21; disease state: normal breast; tissue: breast; ', 'tissue id: STT5750; patient number: 21; disease state: ductal carcinoma in situ; tissue: breast; ', 'tissue id: STT5751; patient number: 21; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5754; patient number: 22; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5756; patient number: 22; disease state: normal breast; tissue: breast; ', 'tissue id: STT5758; patient number: 22; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5761; patient number: 22; disease state: normal breast; tissue: breast; ', 'tissue id: STT5763; patient number: 22; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5825; patient number: 24; disease state: invasive ductal carcinoma; tissue: breast; ', 'tissue id: STT5828; patient number: 24; disease state: normal breast; tissue: breast; ', 'tissue id: STT5829; patient number: 24; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5830; patient number: 24; disease state: early neoplasia; tissue: breast; ', 'tissue id: STT5831; patient number: 24; disease state: normal breast; tissue: breast; ', 'tissue id: STT6088; patient number: 22; disease state: early neoplasia; tissue: breast; ' GSE161502 Homo sapiens 9 Expression profiling by high throughput sequencing GPL18573 The effect of mitochondrial uncoupling on triple-negative breast cancer 2020-11-15 Examination of two different mitochondrial uncouplers of human triple-negative breast cancer cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE161502 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA678529 https://www.ebi.ac.uk/ena/browser/view/PRJNA678529 https://www.ncbi.nlm.nih.gov/sra?term=SRP292615 [Overal design]MDA-MB-231 cells were treated with either 0.1% DMSO Vehicle or 20uM BAM15 for 16 hours and RNA was isolated for cellular transcriptome analysis.; [Treatment]'Cells at 80% confluence were treated with 0.1% DMSO Vehicle, 1uM BAM15 (in 0.1% DMSO), 10uM BAM15 (in 0.1% DMSO), 20uM BAM15 (in 0.1% DMSO) or 20uM DNP (in 0.1% DMSO) for 16 hours.'; [Growth]'MDA-MB-231 cells were cultured in high glucose DMEM supplemented with 10% fetal bovine serum (FBS), 1% penicillin-streptomycin (100 U/mL), and 0.2% amphotericin B. Cells (0.3x106) were seeded into 6-well plates, grown to 80% confluence.'; [Extraction]'RNA was harvested using the TRIzol Reagent, isopropanol precipitation, 3 washes with 75% ethanol, and solubulized in RNase-free water.\nLexogen Quant-Seq\nindexed and pooled samples, 50bp forward read'; [Cell type]'MDA-MB-231''cell type: MDA-MB-231; passages: 9; ' GSE150624 Homo sapiens 12 Expression profiling by array GPL17586 Molecular interplay between dormant bone marrow-resident cells (BMRCs) and CTCs in breast cancer. 2020-05-14 Despite widespread knowledge that bone marrow-resident breast cancer cells (BMRCs) affect tumor progression, signaling mechanisms of BMRCs implicated in maintaining long-term dormancy have not been characterized. To overcome these hurdles, we developed a novel experimental model of tumor dormancy employing circulating tumor cells (CTCs) derived from metastatic breast cancer patients (de novo CTCs), transplanted them in immunocompromised mice, and re-isolated these cells from xenografted mice bone marrow (ex vivo BMRCs) and blood (ex vivo CTCs) to perform downstream transcriptomic analyses. Here we report that the balance between mTORC1 vs mTORC2 signaling regulates BMRC mitotic and/or dormancy characteristics. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE150624 Molecular Interplay between Dormant Bone Marrow-Resident Cells (BMRCs) and CTCs in Breast Cancer. Cancers 6.162 https://doi.org/10.3390/cancers12061626 {Cancers (6.162): 10.3390/cancers12061626} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA632946 https://www.ebi.ac.uk/ena/browser/view/PRJNA632946 None [Overal design]Blood samples were collected from 6 (2 each of ER/PR+, HER2+ and triple negative) metastatic breast cancer patients in accordance to a protocol approved by Institutional Ethical Review Board at Houston Methodist Research Institute. After red blood cell lysis, the remaining buffy coat layer was subjected to FACS for enrichment of CTC populations by (i) doublet discrimination and dead cell elimination (DAPI-), followed by (ii) depletion of cells normally present in the peripheral blood using lineage-specific (CD45-/CD34-/CD105-/CD90-/CD73-) antibodies. Next, we implanted the residual CTC-enriched/lineage-negative cells into NOD scid-gamma (NSG) mice by intra-cardiac injection. Mice were euthanized after 4-8 months of in vivo selection, and bone marrow and blood were subjected to FACS to isolate ex vivo BMRCs and CTCs. The ex vivo BMRC/CTCs were defined as live (DAPI-), HLA-ABC+ (confirming human origin), PanCK+ (epithelial phenotype) or CD44+/CD24- (stem-like phenotype). Sorted cells were collected directly into a pre-chilled tube maintained at 4oC containing RNA lysis buffer and total RNA was collected, followed by RNA and cDNA amplifications, quality controls and gene expression arrays using the Affymetrix HTA 2.0 array. Only mice that were confirmed to be free of overt metastasis, were used for this study. Ex vivo BMRC/CTC gene expression was compared to whole gene expression data from CTCs isolated from 10 metastatic breast cancer patients (de novo CTCs) publicly available at GSE99394. Comparison between ex vivo BMRC/CTCs and de novo CTCs highlighted the transcriptomic landscape of dormant breast cancer BMRC/CTCs and identified mTORC2 signaling as a key regulator of metastatic dormancy.; [Treatment]'Ex vivo CTCs and BMRCs were isolated using a BD FACSAriaII (BD Biosciences) housed inside a BSL-2 facility allowing for collection of cells in sterile conditions. The flow cell was cleaned and sterilized before and after running each sample.'; [Growth]'NSG mice were injected with CTC-enriched cells obtained from metastatic breast cancer patients. After 4-8 months of in vivo selection, mice were euthanized and ex vivo BMRC/CTCs were isolated by FACS. Only samples from mice that did not develop overt metastasis (confirmed by gross and microscopic examination) were included in this study.'; [Extraction]'Sorted cells were collected directly into a pre-chilled tube maintained at 4oC containing RNA lysis buffer and total RNA was collected according to the manufacturer’s protocol (Macherey-Nagel, Inc.).'; [Cell type]'Source: ''subject status: metastatic breast cancer patient; subject/sample id: BrPt62; gender: female; primary tumor subtype: ER+/PR+; host strain: NGS; tissue/cell type: xenograft bone marrow-resident cells (BMRCs); ', 'subject status: metastatic breast cancer patient; subject/sample id: BrPt92; gender: female; primary tumor subtype: ER+/PR+; host strain: NGS; tissue/cell type: xenograft bone marrow-resident cells (BMRCs); ', 'subject status: metastatic breast cancer patient; subject/sample id: BrPt75; gender: female; primary tumor subtype: HER2+; host strain: NGS; tissue/cell type: xenograft bone marrow-resident cells (BMRCs); ', 'subject status: metastatic breast cancer patient; subject/sample id: BrPt91; gender: female; primary tumor subtype: HER2+; host strain: NGS; tissue/cell type: xenograft bone marrow-resident cells (BMRCs); ', 'subject status: metastatic breast cancer patient; subject/sample id: BrPt67; gender: female; primary tumor subtype: TNBC; host strain: NGS; tissue/cell type: xenograft bone marrow-resident cells (BMRCs); ', 'subject status: metastatic breast cancer patient; subject/sample id: BrPt73; gender: female; primary tumor subtype: TNBC; host strain: NGS; tissue/cell type: xenograft bone marrow-resident cells (BMRCs); ', 'subject status: metastatic breast cancer patient; subject/sample id: BrPt62; gender: female; primary tumor subtype: ER+/PR+; host strain: NGS; tissue/cell type: xenograft blood; ', 'subject status: metastatic breast cancer patient; subject/sample id: BrPt92; gender: female; primary tumor subtype: ER+/PR+; host strain: NGS; tissue/cell type: xenograft blood; ', 'subject status: metastatic breast cancer patient; subject/sample id: BrPt75; gender: female; primary tumor subtype: HER2+; host strain: NGS; tissue/cell type: xenograft blood; ', 'subject status: metastatic breast cancer patient; subject/sample id: BrPt91; gender: female; primary tumor subtype: HER2+; host strain: NGS; tissue/cell type: xenograft blood; ', 'subject status: metastatic breast cancer patient; subject/sample id: BrPt67; gender: female; primary tumor subtype: TNBC; host strain: NGS; tissue/cell type: xenograft blood; ', 'subject status: metastatic breast cancer patient; subject/sample id: BrPt73; gender: female; primary tumor subtype: TNBC; host strain: NGS; tissue/cell type: xenograft blood; ' GSE124432 Homo sapiens 1 Non-coding RNA profiling by array GPL7686 miRNA profiling in MMP-8 overexpressing MDA-MB-231 cells 2018-12-27 Matrix metalloproteinases (MMPs) have been traditionally implicated in cancer progression because of their ability to degrade the extracellular matrix. However, some members of the MMP family have recently been identified as proteases with antitumor properties. Thus, it has been described that collagenase-2 (MMP-8) has a protective role in tumor and metastasis progression, but the molecular mechanisms underlying these effects are unknown. We show herein that Mmp8 expression causes a decrease in miR-21 levels that in turn leads to a reduction in tumor growth and lung metastasis formation by MDA-MB-231 (4175) breast cancer cells. By using both in vitro and in vivo models, we demonstrate that the mechanism responsible for these MMP-8 beneficial effects involves cleavage of decorin by MMP-8 and a subsequent reduction of transforming growth factor ? (TGF-?) signaling that controls miR-21 levels. In addition, miR-21 downregulation induced by MMP-8 increases the levels of tumor suppressors such as programmed cell death 4, which may also contribute to the decrease in tumor formation and metastasis of breast cancer cells overexpressing this metalloproteinase. These findings reveal a new signaling pathway for cancer regulation controlled by MMP-8, and contribute to clarify the molecular mechanisms by which tumor-defying proteases may exert their protective function in cancer and metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124432 The anti-metastatic activity of collagenase-2 in breast cancer cells is mediated by a signaling pathway involving decorin and miR-21. Oncogene 6.634 https://doi.org/10.1038/onc.2013.267 {Oncogene (6.634): 10.1038/onc.2013.267} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA512001 https://www.ebi.ac.uk/ena/browser/view/PRJNA512001 None [Overal design]Dye swap-experiment comparing MMP8-overexpressing MDA-MB-231 cells versus control MDA-MB-231 cells .; [Treatment]'None'; [Growth]'Cells were grown in Dulbecco’s modified Eagle’s medium (Gibco) supplemented with 10% fetal bovine serum (Gibco) and 1% antibiotic antimycotic (Gibco)'; [Extraction]'Qiagen RNeasy'; [Cell type]'Source: ''cell line: MDA-MB-231 cell line; ' GSE33287 Homo sapiens 15 Expression profiling by array GPL10558 Unique signatures of estrogen independent growth of MCF-7 cells in low-estrogen versus complete estrogen depravation 2011-10-27 Despite the success of the aromatase inhibitors (AIs) in treating estrogen receptor positive breast cancer, 15-20% of patients receiving adjuvant AIs will relapse within 5-10 years of treatment initiation. Long term estrogen deprivation (LTED) of breast cancer cells in culture has been successfully used to mimic AI-induced estrogen depletion to dissect mechanisms of AI resistance. However, we hypothesized that a subset of patients receiving AI therapy may maintain low circulating concentrations of estrogens that influence the development of endocrine resistance. We sought to expand established LTED models to account for these observations. MCF-7 cells were grown in medium with charcoal stripped serum supplemented with defined concentrations of E2 or the estrogenic androgen metabolite 3βAdiol. Cells were selected in the EC10 and EC90 of E2 or 3βAdiol, or estrogen deprived. Estrogen-independence was evaluated during selection by assessing cell growth in the absence or presence of E2 or 3βAdiol. Following >7 months of selection, estrogen-independence developed in estrogen-deprived cells and cells maintained in low concentrations of steroid hormone. Functional analyses demonstrated that estrogen-deprived and low-steroid selected cells developed estrogen-independence via unique mechanisms, independent and dependent of ERα, respectively. Estrogen-independent growth in low-steroid selected cells could be blocked by kinase inhibitors. However, these cells were completely resistant to kinase inhibition in the presence of low steroid hormone concentrations. These data offer a novel perspective on the development of resistance to AI therapy, and may yield novel approaches to treat AI-resistant tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE33287 Mechanisms of estrogen-independent breast cancer growth driven by low estrogen concentrations are unique versus complete estrogen deprivation. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-012-2032-6 {Breast cancer research and treatment (3.471): 10.1007/s10549-012-2032-6} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA149285 https://www.ebi.ac.uk/ena/browser/view/PRJNA149285 None [Overal design]MCF-7 cells were selected for >7months in IMEM+10% Charcoal Stripped FBS, supplmented with defined steroid hormone conditions. Following outgrowth of estrogen-independent cells, cell lines were grown in estrogen-free conditions and gene expression analysis was performed to identify drivers of estrogen-independent growth. Cells were assessed in biological triplicates.; [Treatment]'Cells were treated with either 0.05% ethanol (vehicle) , 1pM or 50pM E2 concentrations, or 50pM or 1nM 3βAdiol concentrations. Prior to microarray, all cells were grown in 10% charcoal stripped serum only.'; [Growth]'MCF-7 cells were maintained in phenol red-free Improved Minimum Essential Medium supplemented with 10% charcoal-stripped calf serum and indicated hormones.'; [Extraction]'Total RNA was harvested using RNeasy mini columns (Qiagen, Valencia, CA) according to the manufacturer’s instructions.'; [Cell type]'Source: ''treatment dose: vehicle; ', 'treatment dose: 1 picomolar E2; ', 'treatment dose: 50 picomolar E2; ', 'treatment dose: 50 picomolar 3βAdiol; ', 'treatment dose: 1 nanomolar 3βAdiol; ' GSE91383 Homo sapiens 11 Expression profiling by high throughput sequencing GPL11154 The antineoplastic drug, trastuzumab, dysregulates metabolism in iPSC derived cardiomyocytes. 2016-12-09 Background: The targeted ERBB2 therapy, trastuzumab, has had a tremendous impact on management of patients with HER2+ breast cancer, leading to development and increased use of further HER2 targeted therapies. The major clinical side effect is cardiotoxicity but the mechanism is largely unknown. On the basis that gene expression is known to be altered in multiple models of heart failure, we examined differential gene expression of iPSC derived cardiomyocytes treated at day 11 with the ERBB2 targeted monoclonal antibody, trastuzumab for 48 hours and the small molecule tyrosine kinase inhibitor of EGFR and ERBB2. Methods: Transcriptome sequencing was performed on four replicates from each group (48 hours untreated, 48 hours trastuzumab and 48 hours lapatinib) and differential gene expression analyses were performed on each treatment group relative to untreated cardiomyocytes. Results: 517 and 1,358 genes were differentially expressed, p<0.05, respectively in cardiomyocytes treated with trastuzumab and lapatinib. Gene ontology analyses revealed in cardiomyocytes treated with trastuzumab, significant down-regulation of genes involved in small molecule metabolism (p=3.22x10-9) and cholesterol (p=0.01) and sterol (p=0.03) processing. Conclusions: Our study suggests dysregulation of cardiac gene expression and metabolism as key elements of ERBB2 signaling that could potentially be early biomarkers of cardiotoxicity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE91383 The antineoplastic drug, trastuzumab, dysregulates metabolism in iPSC-derived cardiomyocytes. Clinical and translational medicine 4.08 https://doi.org/10.1186/s40169-016-0133-2 {Clinical and translational medicine (4.08): 10.1186/s40169-016-0133-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA356882 https://www.ebi.ac.uk/ena/browser/view/PRJNA356882 https://www.ncbi.nlm.nih.gov/sra?term=SRP094851 [Overal design]Differential expression of iPSC-dervied cardiomyocytes treated with trastuzumab or lapatinib; [Treatment]'48 hours treatment with trastuzumab (100ug/ml) or lapatinib (2uM)'; [Growth]'manufacturers protocol (Cellular Dynamics)'; [Extraction]'Qiagen RNAeasy minikit\nIllumina TruSeq V2'; [Cell type]'iPSC-derived cardiomyocytes''cell type: iPSC-derived cardiomyocytes; treatment: untreated; dose: NA; ', 'cell type: iPSC-derived cardiomyocytes; treatment: trastuzumab; dose: 100ug/ml; ', 'cell type: iPSC-derived cardiomyocytes; treatment: lapatinib; dose: 2uM; ' GSE73857 Homo sapiens 5 Expression profiling by high throughput sequencing GPL11154 Newly constructed network models of different WNT signaling cascades applied to breast cancer expression data 2015-10-08 RNA-Seq profiling of MCF-7 and MDA-MB-231. We profiled RNA expression in the estrogen-receptor-positive (ER+) MCF-7 and the triple-negative MDA-MB-231 breast cancer cells. The objective was to find genes differentially expressed between these cell lines as potential drivers of invasiveness of the triple-negative MDA-MB-231. We further utilized the identified differential genes to validate expression-responsive module of non-canonical Wnt signaling pathway. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE73857 Newly Constructed Network Models of Different WNT Signaling Cascades Applied to Breast Cancer Expression Data. PloS one 2.776 https://doi.org/10.1371/journal.pone.0144014 {PloS one (2.776): 10.1371/journal.pone.0144014} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA298248 https://www.ebi.ac.uk/ena/browser/view/PRJNA298248 https://www.ncbi.nlm.nih.gov/sra?term=SRP064625 [Overal design]2 biological replicates of MCF-7 and 3 biological replicates of MDA-MB-231; [Treatment]'The ER+ and PR+ human breast cancer cell line MCF-7 was purchased from DSMZ and the triple-negtaive MDA-MB-231 breast cancer cell war pruchased from ATCC. Both cell lines were maintained in RPMI-1640 medium (PAA Laboratories Inc., Cölbe, Germany) supplemented with 10% heat-inactivated fetal calf serum (FCS, Invitrogen, Karlsruhe, Germany). For gene expression studies, cells were seeded on extracellular matrix (R&D Systems, Wiesbaden, Germany)-coated tissue culture wells.'; [Growth]'None'; [Extraction]"Total RNA for array experiments was isolated using TRIZOL reagent according to the manufacturer’s instructions (Invitrogen, Carlsbad, CA). RNA integrity for each sample was confirmed with the Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA).\nLibrary preparation for RNA-Seq was performed using the TruSeq RNA Sample Preparation Kit (Illumina, Cat. N°RS-122-2002) starting from 1000 ng of total RNA according to Illumina's instructions. Accurate quantitation of cDNA libraries was performed by using the QuantiFluor™ dsDNA System (Promega). The size range of final cDNA libraries was determined applying the DNA 1000 chip on the Bioanalyzer 2100 from Agilent (280 bp). The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the HiSeq2000 following the manufacturer's protocols.\nNon stranded mRNA-Seq"; [Cell type]'ER+, PR+', 'Triple Negative''cell line: MCF7; cell type: ER+, PR+; ', 'cell line: MDA-MB231; cell type: Triple Negative; ' GSE17508 Homo sapiens 6 Expression profiling by array GPL570 Identification of human miR-22-responsive transcripts in MCF7 cells 2009-08-05 To examine the expression patterns of human miR-22-responsive transcripts in estrogen receptor alpha positive cell line MCF7, we transfected miR-22 duplex or negative control RNA duplex into MCF7 cells. Gene expression patterns were then evaluated using Affymetrix Human Genome U133 Plus 2.0 Array microarrays. Keywords: comparision of expression patterns in MCF7 cells with or without human miR-22 overexpression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17508 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA118775 https://www.ebi.ac.uk/ena/browser/view/PRJNA118775 None [Overal design]Total RNA was collected from two groups MCF7-NC (MCF7 cells transfected with negative control RNA duplex) and MCF7-miR (MCF7 cells transfected with miR-22 duplex) and hybridized to Affymetrix microarrays. Each group has three repeat samples.; [Treatment]'MCF7 cells were transfected with 50nm negative control RNA duplex or miR-22 duplex and total RNA was collected 24 hours after transfection.'; [Growth]'MCF7 cells were maintained in DMEM supplemented with 10% fetal bovine serum, 100U/mL penicillin, and 100mg/mL streptomycin 37℃ with 5% CO2.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''tissue: breast cancer; cell line: MCF7; ', 'tissue: breast cancer; cell line: MCF7; genome/variation: miR-22 duplex; ' GSE108565 Homo sapiens 14 Expression profiling by array GPL16025 Identification of the molecular signature of distinctive breast cancer associated fibroblasts (CAFs) 2017-12-27 Cancer associated fibroblasts (CAFs) are highly heterogeneous and different subsets of CAFs may exhibit distinct functions, To identify the molecular signature of distinctive CAFs , we compared mRNA expression profiles of CAFs isolated from tumors in sensitive patients and resistant ones before neo-adjuvant chemotherapy. Compared the CAFs from sensitive samples, those from refractory samples exhibited a distinctive signature. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE108565 CD10+GPR77+ Cancer-Associated Fibroblasts Promote Cancer Formation and Chemoresistance by Sustaining Cancer Stemness. Cell 36.216 https://doi.org/10.1016/j.cell.2018.01.009 {Cell (36.216): 10.1016/j.cell.2018.01.009} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA427700 https://www.ebi.ac.uk/ena/browser/view/PRJNA427700 None [Overal design]A fourteen chip study using total RNA recovered from CAFs of 7 sensitive breast cancer patients and 7 resistant ones before neo-adjuvant chemotherapy. Each chip measures the expression 45033 genes were collected from the authoritative data source including NCBI.; [Treatment]'None'; [Growth]'Primary cancer associated fibroblasts (CAFs) and breast cancer cells were isolated from breast invasive ductal carcinoma samples obtained from vacuum-assisted biopsies or mastectomies'; [Extraction]'Total RNA was extracted using TRIzol Reagent (Invitrogen, Carlsbad, CA) according to manufacturer’s instructions, RNA quantity and quality were measured by NanoDrop ND-1000. RNA integrity was assessed by standard denaturing agarose gel electrophoresis.'; [Cell type]'Source: ''tissue: Cancer associated fibroblasts (CAFs) from neo-adjuvant chemotherapy resistant breast cancer; neo-adjuvant chemotherapy: resistant; ', 'tissue: Cancer associated fibroblasts (CAFs) from neo-adjuvant chemotherapy sensitive breast cancer; neo-adjuvant chemotherapy: sensitive; ' GSE93193 Homo sapiens 4 Expression profiling by array GPL14550 Inhibition of CDK8 Mediator Kinase Suppresses Estrogen Receptor Signaling and Growth of Estrogen Receptor Positive Breast Cancer 2017-01-05 Hormone therapy targeting estrogen receptor (ER) is the principal treatment for ER-positive breast cancers but many cancers develop resistance to anti-estrogens. Cyclin-dependent kinase 8 (CDK8) is a transcriptional regulator of several oncogenic pathways. Expression levels of CDK8 and ERα are inversely correlated in breast cancers suggesting a functional association between CDK8 and ER. CDK8 inhibition by selective small-molecule inhibitors, by shRNA knockdown or by CRISPR-Cas9 knockout suppressed estrogen-induced transcription, with no significant effects on ERα protein expression or phosphorylation. CDK8 inhibition also abrogated the mitogenic effect of estrogen on ER-positive breast cancer cells and potentiated growth inhibition by the ER antagonist fulvestrant. In vivo, administration of a CDK8 inhibitor suppressed ER-positive breast cancer xenograft growth and augmented the effects of fulvestrant with no apparent toxicity. CDK8 inhibitors also suppressed the development of estrogen independence in ER-positive breast cancer cells. These results identify CDK8 as a novel drug target for breast cancer therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93193 Inhibition of CDK8 mediator kinase suppresses estrogen dependent transcription and the growth of estrogen receptor positive breast cancer. Oncotarget None https://doi.org/10.18632/oncotarget.14894 {Oncotarget (None): 10.18632/oncotarget.14894} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA360278 https://www.ebi.ac.uk/ena/browser/view/PRJNA360278 None [Overal design]Examining the effects of 2.5 µM Senexin A for 24 hr followed by 10 nM E2 for 12 hours compared to single agent treatments in estrogen-deprived MCF7 cells; [Treatment]'Cells were seeded in biological duplicates under ED conditions, treated with 2.5 µM Senexin A for 24 hours and then treated with 10 nM E2 for 12 hours.'; [Growth]'MCF7 cells weregrown in phenol-red free DMEM/Hams F12 with 10% FBS, 1% penicillin-streptomycin and 2 mM L-glutamine, 1 mM sodium pyruvate (Sigma) and 5 mg insulin (Sigma). After three days, cells were plated in either phenol-red free RPMI-1640 or phenol-red free DMEM/Hams F12 with 10% charcoal-dextran-stripped FBS (Fisher Scientific), (with all additives indicated above) and allowed to grow for 24-72 hours prior to treatment.'; [Extraction]'Total RNA was extracted using RNAeasy Mini Kit (Qiagen) and RNA quality was tested using Bioanalyser.'; [Cell type]'Source: ''cell line: MCF7; tissue: breast cancer; ' GSE80778 Mus musculus 15 Expression profiling by array GPL10787 Targeting tumor mitochondrial metabolism overcomes resistance to antiangiogenics 2016-04-28 Epithelial malignancies are effectively treated by antiangiogenics; however, acquired resistance is a major problem in cancer therapeutics. Epithelial tumors commonly have mutations in the MAPK/Pi3K-AKT pathways, which leads to high-rate aerobic glycolysis. Here, we show how novel multikinase inhibitor antiangiogenics (TKIs) induce hypoxia correction in spontaneous breast and lung tumor models. When this happens, the tumors down-regulate glycolysis and switch to long-term reliance on mitochondrial respiration. A transcriptomic, metabolomic and phosphoproteomic study revealed that this metabolic switch is mediated by down-regulation of HIF1α and AKT and up-regulation of AMPK, allowing uptake and degradation of fatty acids and ketone bodies. The switch renders mitochondrial respiration necessary for tumor survival. Agents like phenformin or ME344 induce synergistic tumor control when combined with TKIs, especially in a sequential schedule, leading to metabolic synthetic lethality. Our study uncovers new mechanistic insights in the process of tumor resistance to TKIs, and may have clinical applicability. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80778 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA319971 https://www.ebi.ac.uk/ena/browser/view/PRJNA319971 None [Overal design]Treatment induced gene expression in mouse mammary tumors was measured after treatment to B20, nintedanib or vehicle compounds.; [Treatment]'Treatment with the different drugs was started at 7 weeks of age. B20-4.1.1 (Genentech, San Francisco, CA, USA) was prepared in 1× PBS and administered at 5 mg/kg intraperitoneally twice per week. Nintedanib (Boehringer-Ingelheim, Ingelheim, Germany) was administered at 85 mg/kg/d by oral gavage.'; [Growth]'None'; [Extraction]'Tumors were dissected. Total RNA was extracted and purified using RNeasy Mini-Kit (Qiagen, Valencia, CA, USA) following the manufacturer’s instructions.'; [Cell type]'Source: ''tissue: mammary tumor; treatment: B20; gender: female; ', 'tissue: mammary tumor; treatment: nintedanib; gender: female; ', 'tissue: mammary tumor; gender: female; treatment: before any treatment; ', 'tissue: mammary tumor; treatment: vehicle; gender: female; treatment: before any treatment; ', 'tissue: mammary tumor; treatment: vehicle; gender: female; ' GSE64827 Homo sapiens 6 Expression profiling by array GPL6104 Human umbilical cord matrix mesenchymal stem cells suppress the growth of breast cancer by expression of tumor suppressor genes [human] 2015-01-09 Human and rat umbilical cord matrix mesenchymal stem cells (UCMSC) possess the ability to control the growth of breast carcinoma cells. Comparative analyses of two types of UCMSC suggest that rat UCMSC-dependent growth regulation is significantly stronger than that of human UCMSC. Their different tumoricidal abilities were clarified by analyzing gene expression profiles in the two types of UCMSC. Microarray analysis revealed differential gene expression between untreated naïve UCMSC and those co-cultured with species-matched breast carcinoma cells. The analyses screened 17 differentially expressed genes that are commonly detected in both human and rat UCMSC. The comparison between the two sets of gene expression profiles identified two tumor suppressor genes, adipose-differentiation related protein (ADRP) and follistatin (FST), that were specifically up-regulated in rat UCMSC, but down-regulated in human UCMSC when they were co-cultured with the corresponding species' breast carcinoma cells. Over-expression of FST, but not ADRP, in human UCMSC enhanced their ability to suppress the growth of MDA-231 cells. The growth of MDA-231 cells was also significantly lower when they were cultured in medium conditioned with FST, but not ADRP over-expressing human UCMSC. In the breast carcinoma lung metastasis model generated with MDA-231 cells, systemic treatment with FST-overexpressing human UCMSC significantly attenuated the tumor burden. These results suggest that FST may play an important role in exhibiting stronger tumoricidal ability in rat UCMSC than human UCMSC and also implies that human UCMSC can be transformed into stronger tumoricidal cells by enhancing tumor suppressor gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64827 Human umbilical cord matrix mesenchymal stem cells suppress the growth of breast cancer by expression of tumor suppressor genes. PloS one 2.776 https://doi.org/10.1371/journal.pone.0123756 {PloS one (2.776): 10.1371/journal.pone.0123756} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA272144 https://www.ebi.ac.uk/ena/browser/view/PRJNA272144 None [Overal design]Human UCMSC and MDA-231 breast carcinoma cells were cultured indirectly for 48 hours using Transwell culture dish. Naïve human UCMSC were cultured under same condition without the addition of carcinoma cells.; [Treatment]'MDA-231 cells (5x10^5 cells) were added in Transwell inserts for 48 hours.'; [Growth]'Human UCMSC (5x10^4 cells) were seeded in defined medium in the bottom of a 6-well Transwell culture dish and allowed to settle for 24 hours. The human biological samples were sourced ethically with no donor-identifying information and their research use was approved by the Kansas State University Institutional Review Board (Protocol # 3515).'; [Extraction]"RNA was extracted from naïve and MDA-231 co-cultured UCMSC cells using TRIzol® reagent (Invitrogen) using the standard manufacturer's protocol. Samples were assessed for quality and quantity using an Agilent 2100 Bioanalyzer with RNA 6000 Nano Chips (Agilent Technologies)."; [Cell type]'umbilical cord matrix mesenchymal stem cells (UCMSC)''cell type: umbilical cord matrix mesenchymal stem cells (UCMSC); co-culture: none; ', 'cell type: umbilical cord matrix mesenchymal stem cells (UCMSC); co-culture: MDA-231 breast carcinoma cells; ' GSE52567 Homo sapiens 11 Expression profiling by array GPL6480 The RON receptor tyrosine kinase promotes metastasis by triggering epigenetic reprogramming through the thymine glycosylase MBD4 (gene expression array) 2013-11-20 Metastasis is the major cause of death in cancer patients, yet the genetic/epigenetic programs that drive metastasis are poorly understood. Here, we report a novel epigenetic reprogramming pathway that is required for breast cancer metastasis. Concerted differential DNA methylation is initiated by activation of the RON receptor tyrosine kinase by its ligand, macrophage stimulating protein (MSP). Through PI3K signaling, RON/MSP promotes expression of the G:T mismatch-specific thymine glycosylase MBD4. RON/MSP and MBD4-dependent aberrant DNA methylation results in misregulation of a specific set of genes. Knockdown of MBD4 reverses methylation at these specific loci, and blocks metastasis. We also show that the MBD4 glycosylase catalytic residue is required for RON/MSP-driven metastasis. Analysis of human breast cancers revealed that this epigenetic program is significantly associated with poor clinical outcome. Furthermore, inhibition of Ron kinase activity with a new pharmacological agent blocks metastasis of patient-derived breast tumor grafts in vivo. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE52567 The RON receptor tyrosine kinase promotes metastasis by triggering MBD4-dependent DNA methylation reprogramming. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2013.12.010 {Cell reports (7.815): 10.1016/j.celrep.2013.12.010} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA229394 https://www.ebi.ac.uk/ena/browser/view/PRJNA229394 None [Overal design]To determine the molecular mechanisms by which RON/MSP drives breast cancer metastasis, we performed microarray gene expression profiling of MCF7, MCF7-RON/MSP and MCF7-RON/MSP-shMBD4 cells.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA for gene expression analysis by microarray was isolated with the RNeasy Kit (Qiagen) and tested for integrity on RNA 6000 NanoChips using an Agilent 2100 Bioanalyzer.'; [Cell type]'Source: ''cell line: MCF-7; treatment: none; ', 'cell line: MCF-7; treatment: RON and MSP; ', 'cell line: MCF-7; treatment: RON and MSP and shMBD4; ' GSE38867 Homo sapiens 28 Non-coding RNA profiling by array GPL15019 MicroRNAs expression profiling during breast cancer progression 2012-06-21 MicroRNAs (miRNAs) are known to be deregulated in human breast cancer (BC). The purpose of the current study was to investigate the expression of miRNAs in different stages of BC to assess their biological value in BC progression. MiRNA expression was assessed in a series of BC patients (n=7) with distinct stages of tumour progression (Normal, in-situ (DCIS), primary invasive BC and nodal metastases) to evaluate miRNA differential expression. We used an Agilent miRNA microarray based platform which uses miRBase 16 to screen for 1205 Homo sapiens (hsa) and 144 human viral miRNA candidates. To validate the microarray data, the expression of two deregulated miRNAs was measured by TaqMan quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE38867 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA169159 https://www.ebi.ac.uk/ena/browser/view/PRJNA169159 None [Overal design]This study was conducted Formalin Fixed and Paraffin Embedded (FFPE) specimens from 7 female patients. Twenty μm thick FFPE sections were cut and mounted on PALM Membrane Slides. Under direct microscopic visualization, tissues of interest were micro-dissected using PALM non-contact Laser catapulsion instrument (P.A.L.M. Microlaser Technologies, Carl Zeiss Ltd). Total RNA, including miRNAs, was extracted with the TRIzol reagent (Invitrogen, supplied by Fisher Scientific UK Ltd) according to the manufacturer’s instructions. Total RNA was quantified with Quant-iT RiboGreen RNA Quantitation Kit (Fisher Scientific UK Ltd), which is an accurate method of measuring total RNA with a detection limit of 0.001-1ng/µl. RNA purity and RNA integrity number (RIN) were determined on an Agilent 2100 Bioanalyzer and RNA 6000 NanoLabChip Kits (both Agilent Technologies, Santa Clara, USA), and the RIN of all the samples was >2 but <3. This is expected for FFPE breast samples and is acceptable by Agilent Technologies, Santa Clara, USA, for FFPE samples to undergo miRNA microarray analysis. MiRNAs extracted from laser microdissected tissue components were profiled using Agilent microRNA microarray profiling system (Agilent Technologies, Santa Clara, USA). Total RNA samples were spiked using the MicroRNA Spike-In Kit (Agilent Technologies, Santa Clara, USA) to evaluate efficiencies of labelling and hybridisation. Total RNA was treated with Calf Intestinal Alkaline Phosphatase (CIP), and then 100 ng of total RNA was used per sample to initiate a labelling reaction. Ligation master mix for T4 RNA ligase, which includes Cyanine 3-Cytidine biphosphate (Cyanine 3-pCp) (Complete miRNA Labelling and Hyb Kit, Agilent Technologies, Santa Clara, USA) was used to label the dephosphorylated RNA. Cyanine-3-labelled miRNA samples were hybridised to human miRNA microarrays (Release 16.0, 8x60K) (Agilent Technologies, Santa Clara, USA) at 55°C for 20 hrs. Microarray slides were washed with increasing stringency (Gene Expression Wash Buffers, Agilent Technologies, Santa Clara), and subsequently dried with acetonitrile (Sigma-Aldrich, St. Louis, USA). Fluorescent signal intensities were detected on an Agilent Microarray Scanner (Agilent Technologies, Santa Clara, USA) using the Scan Control A.8.4.1 Software (Agilent Technologies, Santa Clara, USA) and extracted from the images with the Feature Extraction 10.7.3.1 Software (Agilent Technologies, Santa Clara, USA).; [Treatment]'Mastectomised breast and the axillary lymph nodes kept in formalin'; [Growth]'None'; [Extraction]'Twenty μm thick FFPE sections were cut and mounted on PALM Membrane Slides. Under direct microscopic visualization, tissues of interest were micro-dissected using PALM non-contact Laser catapulsion instrument (P.A.L.M. Microlaser Technologies, Carl Zeiss Ltd). Total RNA, including miRNAs, was extracted with the TRIzol reagent (Invitrogen, supplied by Fisher Scientific UK Ltd) according to the manufacturer’s instructions. Total RNA was quantified with Quant-iT RiboGreen RNA Quantitation Kit (Fisher Scientific UK Ltd), which is an accurate method of measuring total RNA with a detection limit of 0.001-1ng/µl. RNA purity and RNA integrity number (RIN) were determined on an Agilent 2100 Bioanalyzer and RNA 6000 NanoLabChip Kits (both Agilent Technologies, Santa Clara, USA).'; [Cell type]'Source: ''gender: female; age: 62 years; tissue origin: breast; tissue: normal breast tissue; ', 'gender: female; age: 62 years; tissue origin: breast; tissue: ductal carcinoma in situ; ', 'gender: female; age: 62 years; tissue origin: breast; tissue: invasive breast cancer tissue; ', 'gender: female; age: 62 years; tissue origin: breast; tissue: metastatic breast cancer tissue; ', 'gender: female; age: 36 years; tissue origin: breast; tissue: normal breast tissue; ', 'gender: female; age: 36 years; tissue origin: breast; tissue: ductal carcinoma in situ; ', 'gender: female; age: 36 years; tissue origin: breast; tissue: invasive breast cancer tissue; ', 'gender: female; age: 36 years; tissue origin: breast; tissue: metastatic breast cancer tissue; ', 'gender: female; age: 38 years; tissue origin: breast; tissue: normal breast tissue; ', 'gender: female; age: 38 years; tissue origin: breast; tissue: ductal carcinoma in situ; ', 'gender: female; age: 38 years; tissue origin: breast; tissue: invasive breast cancer tissue; ', 'gender: female; age: 38 years; tissue origin: breast; tissue: metastatic breast cancer tissue; ', 'gender: female; age: 28 years; tissue origin: breast; tissue: normal breast tissue; ', 'gender: female; age: 28 years; tissue origin: breast; tissue: ductal carcinoma in situ; ', 'gender: female; age: 28 years; tissue origin: breast; tissue: invasive breast cancer tissue; ', 'gender: female; age: 28 years; tissue origin: breast; tissue: metastatic breast cancer tissue; ', 'gender: female; age: 52 years; tissue origin: breast; tissue: normal breast tissue; ', 'gender: female; age: 52 years; tissue origin: breast; tissue: ductal carcinoma in situ; ', 'gender: female; age: 52 years; tissue origin: breast; tissue: invasive breast cancer tissue; ', 'gender: female; age: 52 years; tissue origin: breast; tissue: metastatic breast cancer tissue; ', 'gender: female; age: 56 years; tissue origin: breast; tissue: normal breast tissue; ', 'gender: female; age: 56 years; tissue origin: breast; tissue: ductal carcinoma in situ; ', 'gender: female; age: 56 years; tissue origin: breast; tissue: invasive breast cancer tissue; ', 'gender: female; age: 56 years; tissue origin: breast; tissue: metastatic breast cancer tissue; ' GSE134656 Homo sapiens 54 Expression profiling by high throughput sequencing GPL20301 Characterization of FOXA1 mutations in breast cancer (RNA-seq) 2019-07-22 Invasive Lobular Carcinoma (ILC) is the second most frequent breast cancer (BCa) type and encompasses 10-15% of BCa cases. FOXA1 specific mutations are enriched in this subtype of BCa, however their role in breast cancer pathogenesis is still ill-defined. FOXA1, together with estrogen receptor (ER), is a key transcription factor for the correct activation of estrogen-dependent gene expression and, consequently, for mammary gland development and BCa identity. FOXA1 has the capability to bind to and de-compact heterochromatin to render it accessible for other nuclear proteins, such as ER, and allow activation of their transcriptional programs upon estrogen stimulation. In this project, we aim to elucidate the role of FOXA1 missense mutations in altering its binding to DNA, chromatin accessibility, ER-dependent transcription and their implication in limiting the sensitivity to standard-of-care anti-hormonal therapy, commonly used in ER-positive BCa patients. To this end, we have generated BCa cell lines expressing these FOXA1 mutations and we will employ ATAC-Seq, RIME assays, ChIP-Seq and RNA-Seq to ascertain their effect on DNA accessibility, DNA binding capability, as well as binding of transcriptional coregulators, such as ER, to chromatin. We will extend our analyses to our internal BCa patient datasets with detailed clinical annotation to study the correlation between presence of FOXA1 mutations and response to anti-hormonal therapy of ER-positive BCa patients. The results of this project will allow to understand how the different mutations in the Forkhead domain can alter FOXA1 and ER function, transcriptional regulation and response to anti-hormonal therapy in ER-positive BCa patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE134656 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA556015 https://www.ebi.ac.uk/ena/browser/view/PRJNA556015 https://www.ncbi.nlm.nih.gov/sra?term=SRP215936 [Overal design]RNA-Seq analysis of MCF7 cells overexpressing either empty vector (EV), FOXA1 wild-type (WTNS) or FOXA1 mutant (SY242CS, H247Y, S250F, F266L) constructs, in triplicates.; [Treatment]'DMSO and E2 conditions were subjected to DMSO or E2 treatment for 6h'; [Growth]'Cells were seeded in full media; the following day media was changed to either estrogen depleted media (for DMSO and E2 groups) or same DMEM/F12 50/50 full media (for FM); cells were incubated for 72h; the day of cell harvesting media was refreshed'; [Extraction]'Cells were snap frozen and RNA was extracted with RNeasy Kit from Qiagen (#74106), DNase treatment was performed during the extraction\nLibraries were performed by Genewiz'; [Cell type]'breast cancer', 'V5', 'V6', 'V7', 'V8', 'V9', 'V10', 'V11', 'V12', 'V13', 'V14', 'V15', 'V16', 'V17', 'V18', 'V19', 'V20', 'V21', 'V22', 'V23', 'V24', 'V25', 'V26', 'V27', 'V28', 'V29', 'V30', 'V31', 'V32', 'V33', 'V34', 'V35', 'V36', 'V37', 'V38', 'V39', 'V40', 'V41', 'V42', 'V43', 'V44', 'V45', 'V46', 'V47', 'V48', 'V49', 'V50', 'V51', 'V52', 'V53', 'V54', 'V55', 'V56', 'V57''cell line: MCF7; cell type: breast cancer; ', 'cell line: MCF7; cell type: V5; ', 'cell line: MCF7; cell type: V6; ', 'cell line: MCF7; cell type: V7; ', 'cell line: MCF7; cell type: V8; ', 'cell line: MCF7; cell type: V9; ', 'cell line: MCF7; cell type: V10; ', 'cell line: MCF7; cell type: V11; ', 'cell line: MCF7; cell type: V12; ', 'cell line: MCF7; cell type: V13; ', 'cell line: MCF7; cell type: V14; ', 'cell line: MCF7; cell type: V15; ', 'cell line: MCF7; cell type: V16; ', 'cell line: MCF7; cell type: V17; ', 'cell line: MCF7; cell type: V18; ', 'cell line: MCF7; cell type: V19; ', 'cell line: MCF7; cell type: V20; ', 'cell line: MCF7; cell type: V21; ', 'cell line: MCF7; cell type: V22; ', 'cell line: MCF7; cell type: V23; ', 'cell line: MCF7; cell type: V24; ', 'cell line: MCF7; cell type: V25; ', 'cell line: MCF7; cell type: V26; ', 'cell line: MCF7; cell type: V27; ', 'cell line: MCF7; cell type: V28; ', 'cell line: MCF7; cell type: V29; ', 'cell line: MCF7; cell type: V30; ', 'cell line: MCF7; cell type: V31; ', 'cell line: MCF7; cell type: V32; ', 'cell line: MCF7; cell type: V33; ', 'cell line: MCF7; cell type: V34; ', 'cell line: MCF7; cell type: V35; ', 'cell line: MCF7; cell type: V36; ', 'cell line: MCF7; cell type: V37; ', 'cell line: MCF7; cell type: V38; ', 'cell line: MCF7; cell type: V39; ', 'cell line: MCF7; cell type: V40; ', 'cell line: MCF7; cell type: V41; ', 'cell line: MCF7; cell type: V42; ', 'cell line: MCF7; cell type: V43; ', 'cell line: MCF7; cell type: V44; ', 'cell line: MCF7; cell type: V45; ', 'cell line: MCF7; cell type: V46; ', 'cell line: MCF7; cell type: V47; ', 'cell line: MCF7; cell type: V48; ', 'cell line: MCF7; cell type: V49; ', 'cell line: MCF7; cell type: V50; ', 'cell line: MCF7; cell type: V51; ', 'cell line: MCF7; cell type: V52; ', 'cell line: MCF7; cell type: V53; ', 'cell line: MCF7; cell type: V54; ', 'cell line: MCF7; cell type: V55; ', 'cell line: MCF7; cell type: V56; ', 'cell line: MCF7; cell type: V57; ' GSE24717 Homo sapiens 22 Expression profiling by array GPL571 Using a Stem Cell-Based Signature to Guide Therapeutic Selection in Cancer 2010-10-15 Given the very substantial heterogeneity of most human cancers, it is likely that most cancer therapeutics will be active in only a small fraction of any population of patients. As such, the development of new therapeutics, coupled with methods to match a therapy with the individual patient, will be critical to achieving significant gains in disease outcome. One such opportunity is the use of expression signatures to identify key oncogenic phenotypes that can serve not only as biomarkers but also as a means of identifying therapeutic compounds that might specifically target these phenotypes. Given the potential importance of targeting tumors exhibiting a stem-like phenotype, we have developed an expression signature that reflects common biological aspects of various stem-like characteristics. The Consensus Stemness Ranking (CSR) signature is upregulated in cancer stem cell enriched samples, at advanced tumor stages and is associated with poor prognosis in multiple cancer types. Using two independent computational approaches we utilized the CSR signature to identify clinically useful compounds that could target the CSR phenotype. In vitro assays confirmed selectivity of several predicted compounds including topoisomerase inhibitors and resveratrol towards breast cancer cell lines that exhibit a high-CSR phenotype. Importantly, the CSR signature could predict clinical response of breast cancer patients to a neoadjuvant regimen that included a CSR-specific agent. Collectively, these results suggest therapeutic opportunities to target the CSR phenotype in a relevant cohort of cancer patients. This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24717 Using a stem cell-based signature to guide therapeutic selection in cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-10-1735 {Cancer research (8.378): 10.1158/0008-5472.CAN-10-1735} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA132341 https://www.ebi.ac.uk/ena/browser/view/PRJNA132341 None [Overal design]Refer to individual Series.; [Treatment]'No treatment'; [Growth]'Subconfuent breast cancer cell lines', 'CD133+ and CD133-\xa0glioma cells were separated from tumor xenografts (4105 and 4302), cultured in serum-free media for 48 hours in the presence of absence of laminin, which led to adherent growth of\xa0glioma stem cells while\xa0preserving\xa0stemness.'; [Extraction]'RNeasy mini kit (Qiagen)'; [Cell type]'breast cancer cell', 'Source: ''cell type: breast cancer cell; cell line: BT483; ', 'cell type: breast cancer cell; cell line: BT20; ', 'cell type: breast cancer cell; cell line: MDA-MB-361; ', 'cell type: breast cancer cell; cell line: Hs578t; ', 'cell type: breast cancer cell; cell line: MDA-MB-231; ', 'cell type: breast cancer cell; cell line: MDA-MB-157; ', 'cell type: breast cancer cell; cell line: SKBR3; ', 'cell type: breast cancer cell; cell line: BT474; ', 'cell type: breast cancer cell; cell line: MCF7; ', 'cell type: breast cancer cell; cell line: HCC1806; ', 'cell type: breast cancer cell; cell line: T47D; ', 'cell type: breast cancer cell; cell line: ZR75; ', 'cell type: breast cancer cell; cell line: HCC1428; ', 'cell type: breast cancer cell; cell line: BT549; ', 'tissue: glioblastoma xenografts; ' GSE54439 synthetic construct 6 Non-coding RNA profiling by array GPL8786 miRNA expression data from MCF-7 cells, overexpressing ANXA1 2014-01-27 Annexin 1 (ANXA1), an endogenous anti-inflammatory protein which modulates cellular processes such as proliferation, differentiation and apoptosis has been implicated in cancer initiation and progression. ANXA1 was previously shown to be regulated by hsa-miR-196a and promoted cell proliferation and anchorarge-dependent growth and suppressed apoptosis. However, whether ANXA1 itself regulates miRNA expression is unknown. Therefore, in this study, we investigated the regulation of miRNA by ANXA1 in breast cancer cells. Using microarray technology, 12 miRNAs were found to be significantly and consistently downregulated in MCF-7 cells (MCF-V5) overexpressing ANXA1 overexpressing MCF-7 cells (MCF-V5). Hsa-miR-26b* and hsa-miR-562 were chosen for further investigation.The data suggest that miR-26b* and miR-562 may play a role in ANXA1-induced migration and possibly angiogenesis by targeting NFKB and point towards a potential therapeutic target for breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54439 Annexin-A1 regulates microRNA-26b* and microRNA-562 to directly target NF-κB and angiogenesis in breast cancer cells. PloS one 2.776 https://doi.org/10.1371/journal.pone.0114507 {PloS one (2.776): 10.1371/journal.pone.0114507} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA236526 https://www.ebi.ac.uk/ena/browser/view/PRJNA236526 None [Overal design]Breast cancer MCF-7 cells (MCF-V5) overexpressing ANXA1 were cultured for RNA extraction and hybridization on Affymetrix miRNA microarrays. These were compared against the control, which were MCF-7 cells (MCF-EV) carrying an empty expression vector. Expression analyses were carried out in triplicates; [Treatment]'MCF-7_EV and MCF-7_V5 cells were cultured as described in Bist et. al (2013) and harvested after 24hrs of growth.'; [Growth]'Human breast cancer cell line MCF7 were obtained from the American Type Culture Collection. The cells were grown as monolayers in Dulbecco’s Modified Eagle’s Medium (DMEM) supplemented with 10% heat-inactivated fetal bovine serum (FBS, Biowest), 1% L-glutamine (GIBCO) and 1% penicillin-streptomycin (Hyclone) at 37oC in a humid atmosphere containing 5% CO2. MCF-7_EV and MCF-7_V5 cells were derived as described in Bist et. al, 2013. (1). Bist P, Shu S, Lee H, Arora S, Nair S, Lim JY, Dayalan J, Gasser S, Biswas SK, Fairhurst AM, Lim LH. Annexin-A1 regulates TLR-mediated IFN-β production through an interaction with TANK-binding kinase 1. J Immunol. 2013 Oct 15;191(8):4375-82. doi: 10.4049/jimmunol.1301504. Epub 2013 Sep 18. PubMed PMID: 24048896.'; [Extraction]'Total cellular RNA was isolated with TRIzol (Invitrogen) according to manufacturer’s instructions. Enriched miRNA was isolated from cell pellets using mirPremier miRNA isolation kit (Sigma) according to the manufacturer’s protocol. The enriched miRNA was quantified using a NanoDrop spectrophotometer (NanoDrop Technology) where 1 A260 unit is 33ug/ml of small RNA. The integrity of the miRNA was determined using an Agilent Bioanaylzer (Agilent Technology).'; [Cell type]'Source: ''tissue: MCF-7 cells; vector: empty expression vector; age: 24hrs; ', 'tissue: MCF-7 cells; vector: overexpressing ANXA1; age: 24hrs; ' GSE98831 Mus musculus 8 Expression profiling by high throughput sequencing GPL17021 BRCA1 Regulates Carbohydrate Metabolism Through its RING Domain and Transcription Factor Oct1 2017-05-11 The tumor suppressor BRCA1 regulates DNA damage responses and multiple other processes. Among these, BRCA1 heterodimerizes with BARD1 to ubiquitylate targets via its N-terminal RING domain. Here we show that BRCA1 promotes oxidative metabolism via degradation of Oct1, a transcription factor with pro-glycolytic/tumorigenic effects. BRCA1 E3 ubiquitin ligase mutation skews cells towards a glycolytic metabolic profile while elevating Oct1 protein. CRISPR-mediated Oct1 deletion reverts the glycolytic phenotype. RNAseq confirms the deregulation of metabolic genes. BRCA1 mediates direct Oct1 ubiquitylation and degradation, and mutation of two ubiquitylated Oct1 lysines insulates the protein against BRCA1-mediated destabilization. Oct1 deletion in MCF-7 breast cancer cells does not perturb growth in standard culture, but inhibits growth in soft agar and xenografts. Oct1 protein levels correlate positively with tumor aggressiveness, and inversely with BRCA1, in primary breast cancer samples. These results identify BRCA1 as an Oct1 ubiquitin ligase that catalyzes Oct1 degradation to promote oxidative metabolism. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98831 BRCA1 through Its E3 Ligase Activity Regulates the Transcription Factor Oct1 and Carbohydrate Metabolism. Molecular cancer research : MCR 4.484 https://doi.org/10.1158/1541-7786.MCR-17-0364 {Molecular cancer research : MCR (4.484): 10.1158/1541-7786.MCR-17-0364} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA386332 https://www.ebi.ac.uk/ena/browser/view/PRJNA386332 https://www.ncbi.nlm.nih.gov/sra?term=SRP106907 [Overal design]mRNA profiles of BRCA1-I26A mutant MEFs treated with control CRISPR lentiviral vector, or an Oct1-specific CRISPR construct; [Treatment]'Following infection, cells were allowed to grow for 2 d before sorting GFP+ cells to perform RNAseq.'; [Growth]'DMEM with 10% calf serum, supplemental glutamine. Cells were subconfluent when infected, sorted, replated and collected for RNAseq'; [Extraction]'Total RNA was prepared using Trizol reagent. Illumina TruSeq mRNA library preparation kit was used with 1 ug of total RNA for the construction of sequencing libraries.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'immortalized MEFs (BRCA1-I26A mutant)''experiment: Oct1 Mutant; cell type: immortalized MEFs (BRCA1-I26A mutant); strain: C57BL/6; ', 'experiment: Control; cell type: immortalized MEFs (BRCA1-I26A mutant); strain: C57BL/6; ' GSE105777 Homo sapiens 426 Expression profiling by array GPL10558 Major impact of sampling methodology on gene expression in estrogen receptor positive breast cancer 2017-10-23 To investigate the impact of sampling methodology on gene expression data from primary estrogen receptor positive (ER+) breast cancer biopsies. Analysis of global gene-expression measured in core-cut biopsies at baseline and surgery from patients randomised to receive either 2-week’s presurgical aromatase inhibitor (AI, n=157) or no presurgical treatment (n=56) revealed genes most markedly altered in the AI group (e.g. FOS, DUSP1, RGS1, FOSB) were equally altered in the no-treatment group; some widely investigated genes that were apparently unaffected in the AI group (e.g. MYC) were counter-altered in the Control group masking actual AI-dependent changes. In the absence of a Control group these artefactual changes would likely lead to the most affected genes being the erroneous focus of research. The findings are likely relevant to all archival collections of ER+ breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE105777 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA415551 https://www.ebi.ac.uk/ena/browser/view/PRJNA415551 None [Overal design]Global gene-expression measured in core-cut biopsies at baseline and surgery from patients randomised to receive either 2-week’s presurgical aromatase inhibitor (AI, n=157) or no presurgical treatment (n=112).; [Treatment]'None'; [Growth]'None'; [Extraction]"mRNA from baseline (B) and surgery (S) tumour biopsies were extracted with RNeasy Mini Kit (Qiagen), as per the manufacturer's instructions, and quantification performed using the Agilent 2100 Bioanalyzer (Santa Clara, CA, USA).", "mRNA from untreated paired biopsies were extracted with RNeasy Mini Kit (Qiagen), as per the manufacturer's instructions, and quantification performed using the Agilent 2100 Bioanalyzer (Santa Clara, CA, USA)."; [Cell type]'Source: ''group: treated; Sex: female; timepoint: baseline (B); her2: Positive; ', 'group: treated; Sex: female; timepoint: baseline (B); her2: Negative; ', 'group: treated; Sex: female; timepoint: surgery (S); her2: Positive; ', 'group: treated; Sex: female; timepoint: surgery (S); her2: Negative; ', 'Sex: female; disease: primary ER+ breast carcinoma; group: untreated; sampling time: surgery; subtype: LumA; tissue: breast tumour; ', 'Sex: female; disease: primary ER+ breast carcinoma; group: untreated; sampling time: diagnosis; subtype: LumA; tissue: breast tumour; ', 'Sex: female; disease: primary ER+ breast carcinoma; group: untreated; sampling time: surgery; subtype: LumB; tissue: breast tumour; ', 'Sex: female; disease: primary ER+ breast carcinoma; group: untreated; sampling time: diagnosis; subtype: LumB; tissue: breast tumour; ', 'Sex: female; disease: primary ER+ breast carcinoma; group: untreated; sampling time: surgery; subtype: Normal; tissue: breast tumour; ', 'Sex: female; disease: primary ER+ breast carcinoma; group: untreated; sampling time: diagnosis; subtype: Her2; tissue: breast tumour; ', 'Sex: female; disease: primary ER+ breast carcinoma; group: untreated; sampling time: diagnosis; subtype: Normal; tissue: breast tumour; ' GSE35118 Homo sapiens 14 Expression profiling by array GPL6244 Primary TNBC tumor in the presence or absence of SHP2 2012-01-15 The first bona fide PTP proto-oncogene was the Src-homology 2 domain-containing phosphatase SHP2 (encoded by PTPN11), an ubiquitously expressed PTP that transduces mitogenic, pro-survival, cell fate and/or pro-migratory signals from numerous growth factor-, cytokine- and extracellular matrix receptors. In malignancies, SHP2 is hyperactivated either downstream of oncoproteins or by mutations.We provide analysis of a primary triple-negative breast tumor grown as xenografts in the presence or absence of SHP2 for 30 days. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE35118 Tyrosine phosphatase SHP2 promotes breast cancer progression and maintains tumor-initiating cells via activation of key transcription factors and a positive feedback signaling loop. Nature medicine 30.641 https://doi.org/10.1038/nm.2645 {Nature medicine (30.641): 10.1038/nm.2645} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA156015 https://www.ebi.ac.uk/ena/browser/view/PRJNA156015 None [Overal design]A primary triple-negative breast tumor (BT8) was transduced with a doxycycline-inducible lentiviral vector expressing a CTRL miR or SHP2 miR1 or SHP2 miR2. Cells from each group were injected in imuunodeficient mice and after tumor development, the knockdown of SHP2 was induced for 30 days in vivo. At day 30, tumors were dissected and RNA isolated for gene expression analysis.; [Treatment]'Doxycycline in drinking water (2 g per liter). The treatment started after tumor development and continued until the end of the experiment (day 30). The drinking water containing doxycycline was refreshed every two days.'; [Growth]'Primary TNBC cells were injected orthotopically into the fat pad of mammary gland 2/3 of imuunodeficient mice. After tumor development, we depleted SHP2 for 30 days in vivo.'; [Extraction]'Tumors were dissected and total RNA was isolated with a standard TRIZOL extraction method.'; [Cell type]'Source: ''xenografted cells: Primary triple-negative breast cancer (BT8); tissue isolated: tumor developed in recipient mice; ', 'xenografted cells: Primary triple-negative breast cancer (BT8); transduced with: doxycycline-inducible lentiviral vector expressing a CTRL miR; tissue isolated: tumor developed in recipient mice; ', 'xenografted cells: Primary triple-negative breast cancer (BT8); transduced with: doxycycline-inducible lentiviral vector expressing a SHP2 miR1; tissue isolated: tumor developed in recipient mice; ', 'xenografted cells: Primary triple-negative breast cancer (BT8); transduced with: doxycycline-inducible lentiviral vector expressing a SHP2 miR2; tissue isolated: tumor developed in recipient mice; ' GSE48906 Homo sapiens 96 Expression profiling by array GPL570 Neoadjuvant anastrozole alone or with gefitinib in early breast cancer 2013-07-16 Trial 223 was a placebo-controlled trial of neoadjuvant anastrozole alone or with gefitinib in early breast cancer. We used patients from arm B and C: anastrozole 1mg/d for the duration of the 16 week period plus placebo 1 tablet/d orally for 2 weeks. Patients in arm B were followed by gefitinib 250mg/d orally for 14 weeks whereas patients in arm C continued with placebo for 14 weeks. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48906 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA212259 https://www.ebi.ac.uk/ena/browser/view/PRJNA212259 None [Overal design]96 samples; [Treatment]'None'; [Growth]'None'; [Extraction]'Rneasy'; [Cell type]'Source: ''Sex: female; core: IRSS 001A; arm: c; ki67-1: nd; ', 'Sex: female; core: IRSS 019A; arm: b; ki67-1: 13; ki67-2: 3.9; ki67-6.1: 6.1; ', 'Sex: female; ', 'Sex: female; core: IRSS 020A; arm: c; ki67-1: 33.5; ki67-2: 23; ki67-6.1: 34.7; ', 'Sex: female; core: IRSS 021A; arm: b; ki67-1: 37.8; ki67-2: 4.4; ki67-6.1: 4.8; ', 'Sex: female; core: IRSS 024A; arm: c; ki67-1: 32.9; ki67-2: nd; ki67-6.1: 6.2; ', 'Sex: female; core: IRSS 025A; arm: b; ki67-1: nd; ', 'Sex: female; core: IRSS 027A; arm: c; ki67-1: 23.84; ki67-2: 2.02; ki67-6.1: 12.02; ', 'Sex: female; core: IRSS 029A; arm: c; ki67-1: 8.3; ki67-2: 3.1; ki67-6.1: 1.6; ', 'Sex: female; core: IRSS 031A; arm: c; ki67-1: 13.9; ki67-2: 9.6; ki67-6.1: 5.7; ', 'Sex: female; core: IRSS 032A; arm: b; ki67-1: nd; ', 'Sex: female; core: IRSS 033A; arm: c; ki67-1: 19.4; ki67-2: 7.7; ki67-6.1: 12.9; ', 'Sex: female; core: IRSS 002A; arm: b; ki67-1: 11.2; ki67-2: 3.7; ki67-6.1: 6.7; ', 'Sex: female; core: IRSS 034A; arm: c; ki67-1: nd; ', 'Sex: female; core: IRSS 036A; arm: b; ki67-1: 18.3; ki67-6.1: 1.95; ', 'Sex: female; core: IRSS 037A; arm: b; ki67-1: 21.9; ki67-2: 25.9; ki67-6.1: 29; ', 'Sex: female; core: IRSS 038A; arm: c; ki67-1: 32.37; ki67-2: 17.51; ki67-6.1: 9.62; ', 'Sex: female; core: IRSS 039A; arm: b; ki67-1: nd; ', 'Sex: female; core: IRSS 044A; arm: c; ki67-1: nd; ', 'Sex: female; core: IRSS 048A; arm: b; ki67-1: nd; ', 'Sex: female; core: IRSS 050A; arm: b; ki67-1: 8.41; ki67-2: 0.16; ki67-6.1: 0.09; ', 'Sex: female; core: IRSS 051A; arm: b; ki67-1: 58.8; ki67-2: 30.05; ki67-6.1: 50.31; ', 'Sex: female; core: IRSS 004A; arm: b; ki67-1: 16.4; ki67-2: 1.3; ki67-6.1: 1.8; ', 'Sex: female; core: IRSS 053A; arm: b; ki67-1: 8.4; ki67-2: 9.8; ki67-6.1: 21.1; ', 'Sex: female; core: IRSS 057A; arm: b; ki67-1: 13.76; ki67-2: nd; ki67-6.1: 0.86; ', 'Sex: female; core: IRSS 062A; arm: c; ki67-1: 20.36; ki67-2: nd; ki67-6.1: nd; ', 'Sex: female; core: IRSS 074A; arm: c; ki67-1: nd; ', 'Sex: female; core: IRSS 076A; arm: b; ki67-1: 20.06; ki67-2: nd; ki67-6.1: 2.98; ', 'Sex: female; core: IRSS 079A; arm: b; ki67-1: 17.48; ki67-2: 4.45; ki67-6.1: 0.81; ', 'Sex: female; core: IRSS 080A; arm: b; ki67-1: 23.39; ki67-2: 3.54; ki67-6.1: 4.62; ', 'Sex: female; core: IRSS 082A; arm: b; ki67-1: 49.56; ki67-2: 59.67; ki67-6.1: 31.72; ', 'Sex: female; core: IRSS 083A; arm: c; ki67-1: nd; ', 'Sex: female; core: IRSS 084A; arm: b; ki67-1: nd; ', 'Sex: female; core: IRSS 085A; arm: b; ki67-1: nd; ', 'Sex: female; core: IRSS 087A; arm: b; ki67-1: nd; ', 'Sex: female; core: IRSS 010A; arm: c; ki67-1: 5.2; ki67-2: 1.5; ki67-6.1: 0.2; ', 'Sex: female; core: IRSS 012A; arm: b; ki67-1: 13.6; ki67-6.1: 0.7; ', 'Sex: female; core: IRSS 014A; arm: c; ki67-1: 22.5; ki67-2: 0.9; ki67-6.1: 0.8; ', 'Sex: female; core: IRSS 015A; arm: b; ki67-1: 14.3; ki67-2: 5.7; ki67-6.1: 5.9; ', 'Sex: female; core: IRSS 018A; arm: c; ki67-1: 20.11; ki67-2: 5.6; ki67-6.1: 13.4; ' GSE130503 Homo sapiens 4 Expression profiling by high throughput sequencing GPL16791 RNA-seq to profile the transcriptome changes induced by the EZH2 degrader MS1943 2019-04-30 To gain mechanistic insights into how MS1943 induces cell death, MDA-MB-468 cells were treated with 5 µM of MS1943 or DMSO control and changes of gene expression were assessed after 3 days of treatment. Interestingly, MS1943-treated cells were characterized by a unique set of deregulated genes that could readily separate them from control cells. We identified 8,730 significant differentially expressed genes with a false discovery rate (FDR) at 5%, in which 2,120 genes have an absolute log fold change above 1. We next performed gene set enrichment analyses (GSEA) that capture pathways perturbed towards both directions simultaneously using the 24,448 ranked genes identified in our dataset and annotated in ENSEMBL (version 94) against the KEGG pathways and the hallmarks gene set collection (MSigDB V6.2). Induction of the unfolded protein response (UPR) / endoplasmic reticulum (ER)-stress pathway was commonly identified using both types of analyses and we therefore decided to pursue this further. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130503 Discovery of a first-in-class EZH2 selective degrader. Nature chemical biology 12.154 https://doi.org/10.1038/s41589-019-0421-4 {Nature chemical biology (12.154): 10.1038/s41589-019-0421-4} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA540486 https://www.ebi.ac.uk/ena/browser/view/PRJNA540486 https://www.ncbi.nlm.nih.gov/sra?term=SRP194267 [Overal design]Examination of difference in gene expression in one breast cancer cell line, MDA-MB-468, between treated with 5 µM of MS1943 (n=2) and treated with DMSO as control (n=2).; [Treatment]'We sequenced duplicated RNA samples (DMSO treated versus MS1943 treated [5 µM for 3 days])'; [Growth]'2E6 MDA-MB-468 cells were seeded in 10 cm dishes in duplicates and drugged at the indicated concentrations.'; [Extraction]'Cell samples were purified using Qiagen RNeasy Plus Mini Kit according to the protocols in RNeasy® Plus Mini Handbook published by Qiagen.\nRNA-Seq libraries were constructed from the PolyA selected mRNA according to the protocol for the TruSeq RNA Library Prep Kit v2 (Illumina).'; [Cell type]'Triple negative breast cancer cell line''cell type: Triple negative breast cancer cell line; cell line: MDA-MD-468; passage: 12; treated with: DMSO; ', 'cell type: Triple negative breast cancer cell line; cell line: MDA-MD-468; passage: 12; treated with: MS1943 degrader; ' GSE77491 Homo sapiens 12 Expression profiling by array GPL10558 Genome-wide transcriptome profile of CYTOR (LINC00152)-silenced MDA-MB-231 breast cancer cell line 2016-02-02 The transcriptional profile of MDA-MB-231 cells silenced for CYTOR (LINC00152, long intergenic non-protein coding RNA 152) was compared to LNA-control-treated MDA-MB-231 cells to identify potential CYTOR targets. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE77491 Portraying breast cancers with long noncoding RNAs. Science advances 12.804 https://doi.org/10.1126/sciadv.1600220 {Science advances (12.804): 10.1126/sciadv.1600220} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA310629 https://www.ebi.ac.uk/ena/browser/view/PRJNA310629 None [Overal design]MDA-MB-231 cells were treated with LNA targeting CYTOR or with LNA control (from Exiqon), and total RNA was obtained.; [Treatment]"Cells were treated with LNA gapmeRs (Exiqon) according to the manufacturer's instructions. Briefly, 300,000 cells were transfected in 6-well plates with 30 nM LNA gapmeRs and 5 μl Lipofectamine 2000 in 2 ml total volume and incubated for 24 h."; [Growth]'MDA-MB-231 cells were grown in DMEM (Gibco) supplemented with 10% FBS (Gibco). They were maintained at 37°C in 5% CO2.'; [Extraction]"RNA purification was performed with the RNeasy kit (Qiagen) according to the manufacturer's instructions. DNase treatment was performed with a DNA-free DNase kit (Ambion) according to the manufacturer's protocol."; [Cell type]'breast cancer cell line''cell line: MDA-MB-231; cell type: breast cancer cell line; lna type: CYTOR (LINC00152); batch: 2; ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; lna type: CYTOR (LINC00152); batch: 1; ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; lna type: Control; batch: 2; ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; lna type: Control; batch: 1; ' GSE74214 Homo sapiens 18 Methylation profiling by array GPL13534 Genome-wide single base resolution profiling of 5-methylcytosine in human breast tissue 2015-10-20 The underlying biological mechanisms through which epidemiologically defined breast cancer risk factors contribute to disease risk remain poorly understood. Here we investigated the impact cancer risk factors have on the normal breast epigenome by analyzing DNA methylation genome-wide (Infinium 450K array) in cancer-free women. We tested the relation of established breast cancer risk factors with DNA methylation adjusting for potential variation in cell-type proportions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74214 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA299572 https://www.ebi.ac.uk/ena/browser/view/PRJNA299572 None [Overal design]Non-diseased breast tissue (n=18) DNA was subjected to bisulfite conversion with an input of 4ug per sample using the TrueMethyl® kit v.1.1 (Cambridge Epigenetix) protocol optimized for Illumina HumanMethylation450 arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'Tumor DNA was extracted with the QIAmp DNeasy tissue kit (Qiagen) according to the manufacturer’s instructions.'; [Cell type]'Source: ''tissue: Breast tissue; Sex: Female; subject bmi: 23.79; subject age: 48; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 24.96; subject age: 23; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 19.53; subject age: 15; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 14.59; subject age: 59; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 24.86; subject age: 44; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 28.61; subject age: 17; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 24.80; subject age: 80; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 22.71; subject age: 13; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 15.94; subject age: 58; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 38.22; subject age: 58; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 37.63; subject age: 59; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 62.73; subject age: 68; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 32.65; subject age: 36; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 22.75; subject age: 70; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 24.80; subject age: 70; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 40.17; subject age: 51; ', 'tissue: Breast tissue; Sex: Female; subject bmi: 25.75; subject age: 69; ' GSE80594 Homo sapiens 12 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL11154; GPL18573 PI3K/AKT signaling regulates H3K4 methylation in breast cancer 2016-04-22 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80594 PI3K/AKT Signaling Regulates H3K4 Methylation in Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2016.05.046 {Cell reports (7.815): 10.1016/j.celrep.2016.05.046} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA319402 https://www.ebi.ac.uk/ena/browser/view/PRJNA319402 None [Overal design]Refer to individual Series; [Treatment]'The medium was changed to medium containing either MK2206 or DMSO for 24 hours.'; [Growth]'Cells were maintained at 37oC and 5% CO2 in RPMI or DMEM + 10% FBS and Pen-Strep.'; [Extraction]'RNA was extracted using RNeasy\nLibraries were made from total RNA using the Illumina TruSeq Stranded mRNA Library Prep Kit', 'Cells were crosslinked, lysed in SDS lysis buffer, and sonicated.\nThruPLEX-FD Prep kit, Rubicon Genomics'; [Cell type]'T47D''cell type: T47D; treatment: AKT inhibitor MK2206; ', 'cell type: T47D; treatment: DMSO; ', 'cell type: T47D; chip antibody: H3K4me3 Abcam (Ab8580); treatment: DMSO; ', 'cell type: T47D; chip antibody: H3K4me3 Abcam (Ab8580); treatment: MK2206; ', 'cell type: T47D; chip antibody: KDM5A #1416 (gift Kaelin Lab DFCI); treatment: DMSO; ', 'cell type: T47D; chip antibody: KDM5A #1416 (gift Kaelin Lab DFCI); treatment: MK2206; ' GSE28503 Homo sapiens 4 Expression profiling by array GPL570 Expression data for knockdown of POLRMT or RNA PolII in MCF-7 cell line 2011-04-08 Transcription of mRNA in mammalian is mainly performed by RNA polymerase II (PolII). POLRMT is responsible for the production of cytoplasmic and nuclear form of mitochondrial RNA polymerase. The former (mtRNAP) participates in transcription of RNA in the mitochondria while the latter (spRNAP-IV) is responsible for some mRNA transcription in the nucleus. The nature and amount of genes transcribed by spRNAP-IV still remains unclear. Thus, we scanned for possible candidate genes by using Affymetrix. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28503 Transcription of muscle actin genes by a nuclear form of mitochondrial RNA polymerase. PloS one 2.776 https://doi.org/10.1371/journal.pone.0022583 {PloS one (2.776): 10.1371/journal.pone.0022583} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA153941 https://www.ebi.ac.uk/ena/browser/view/PRJNA153941 None [Overal design]MCF-7 cell line was subjected to siRNA knockdown of either non-targeting, POLRMT, or PolII for 72 hours; [Treatment]'MCF-7 cell line was subjected to siRNA knockdown of either non-targeting, POLRMT, or PolII for 72 hours'; [Growth]'Cells were grown to 85 % confluence in 10 cm tissue culture dish.'; [Extraction]'Each 10 cm dish was washed with 1x PBS for three times. Total RNA was extracted according to the RNeasy® Mini Kit Spin Protocol (QIAGEN). The integrity of the RNA extract was checked by 1.2 % (w/v) agarose gel electrophoresis and the concentration of RNA was estimated by ultraviolet spectrophotometry.'; [Cell type]'Source: ''cell line: MCF-7 breast cancer cell line; cell line source: 69 year old female; genotype/variation: control; ', 'cell line: MCF-7 breast cancer cell line; cell line source: 69 year old female; genotype/variation: POLRMT knockdown; ', 'cell line: MCF-7 breast cancer cell line; cell line source: 69 year old female; genotype/variation: PolII knockdown; ' GSE85247 Homo sapiens 4 Expression profiling by array GPL10558 Epigenetically regulated Fibronectin leucine rich transmembrane protein 2 (FLRT2) shows tumor suppressor activity in breast cancer cells 2016-08-05 To investigate the role of FLRT2 in breast cancer, its expression was knocked down and upregulated in mammary cell lines. Our results show that FLRT2 has tumor suppressor activity in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE85247 Epigenetically regulated Fibronectin leucine rich transmembrane protein 2 (FLRT2) shows tumor suppressor activity in breast cancer cells. Scientific reports 4.011 https://doi.org/10.1038/s41598-017-00424-0 {Scientific reports (4.011): 10.1038/s41598-017-00424-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA337938 https://www.ebi.ac.uk/ena/browser/view/PRJNA337938 None [Overal design]Total RNA is obtained from MCF-10A and 7 where FLRT2 is knocked down and upregulated using lipofectamine 2000; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with QIAzol Lysis reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''cell line: MCF-10A; ', 'cell line: MCF-7; ' GSE160878 Homo sapiens 21 Methylation profiling by genome tiling array GPL23976 A novel DNA methylation signature in Merkel Cell Carcinoma 2020-11-05 Merkel cell carcinoma (MCC) is a rare but aggressive skin cancer with neuroendocrine features. Although the role of epigenetic in tumorigenesis has been documented in most type of cancer, it is overlooked in MCC. The treatment options for MCC is limited and the five-year survival rate remains as low as 33%. In addition, recent studies have suggested multiple mechanisms of epigenetic dysregulation that may contribute to loss H3K27me3 and the tumorigenesis in MCC but not well studied. In this study, we conducted DNA methylation analysis of an existing retrospective cohort of clinically annotated MCC samples, which included samples from 8 primary tumors, three metastatic skin tumors, four metastatic lymph node tumors, and five paired normal tissue samples. Global DNA methylation profile was performed using Illumina Infinium MethylationEPIC array. Two MCC cell lines were also analyzed for DNA methylation and gene expression (RNA-seq) to confirm the correlation between DNA methylation and gene expression for MCC. Our analysis revealed 24,497 loci (14,456 genes) that showed significantly different DNA methylation pattern in the four groups (ANOVA p-value < 0.05 and standard deviation of mean of groups > 0.25) namely adjacent normal, primary tumor, metastatic skin, and metastatic lymph node in MCC patients. By GO terms analysis, the genes correlated with DNA methylation alteration associated with nervous system, cell adhesion, signal transduction, and development pathways. We also observed 870 probes differentially methylated in MCPyV positive and MCPyV negative tumor (FDR adjusted p-value < 0.05 and delta change greater than 0.4 or less than -0.4). Furthermore, using expression and DNA methylation data from two MCC cell lines (MS1 and MCC13) as validation, we identified 964 MCC specific genes directly regulated by DNA methylation either at promoter or gene body, which are highly enriched in nervous system related pathways. By this approach, we not only identify DNA methylation markers for MCC and MCPyV status but also genes regulated by DNA methylation in MCC, MCPyV status, and neuroendocrine features. Most importantly, our results may also suggest overexpression of KDM6B and EZHIP by loss of DNA methylation in their promoter may contribute to loss of H3K27me3 in MCC. In addition, we observed the DNA methylation profile of MS1 resembled MCC patient sample, while DNA methylation profile of MCC13 cell line was similar to small cell lung carcinoma (SCLC), which suggested that MCC13 cell line may originally come from SCLC. Taken together, we have demonstrated dramatic DNA methylation alteration along with four unique patterns in normal, primary and metastatic MCC. Our finding provides DNA methylation markers not only for diagnosis or prognosis of MCC and MCPyV status but also correlate gene expression status of MCC specific genes with important functional roles in MCC tumorigenesis, MCPyV expression, neuroendocrine feature and H3K27me3 status. The identification of DNA methylation alteration in MCC also provides foundation for potential implication of epigenetic therapy for MCC patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE160878 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA674759 https://www.ebi.ac.uk/ena/browser/view/PRJNA674759 None [Overal design]20 samples: 5 normal; 8 primary; 4 Metastatic lymph node; 3 Metastatic skin; [Treatment]'NA'; [Growth]'NA'; [Extraction]'Following bisulfite treatment (ZYMO research EZ DNA Methylation kit), DNA methylation data were generated using the Illumina Infinium MethylationEPIC BeadChip array at the USC Norris Molecular Genomics Core Facility).'; [Cell type]'Source: ''gender: M; tissue: skin; tumor stage: III; race: HISP; age: 58; mcpyv_ihc: 0; recurrence: 0; immunosuppressed?: NO; tumor location: chest; surgery: WLE + LND; radiation: NO; systemic: NO; date of dx: 2014-10-31; date of relapse: NA; date of last follow-up: 2017-09-07; status: LOST; patient: 1; ', 'gender: M; tissue: lymph node; tumor stage: III; race: HISP; age: 58; mcpyv_ihc: 0; recurrence: 0; immunosuppressed?: NO; tumor location: chest; surgery: WLE + LND; radiation: NO; systemic: NO; date of dx: 2014-10-31; date of relapse: NA; date of last follow-up: 2017-09-07; status: LOST; patient: 1; ', 'gender: F; tissue: skin; tumor stage: I; race: WHITE; age: 82; mcpyv_ihc: 1; recurrence: 0; immunosuppressed?: NO; tumor location: H/N; surgery: WLE; radiation: NO; systemic: NO; date of dx: 2015-04-24; date of relapse: NA; date of last follow-up: 2015-10-14; status: LOST; additional info: Metastatic Breast CA; patient: 2; ', 'gender: M; tissue: skin; tumor stage: III; race: WHITE; age: 53; mcpyv_ihc: 1; recurrence: 1; immunosuppressed?: NO; tumor location: LE; surgery: WLE + LND; radiation: YES; systemic: chemo, PD-1, CTLA-4, TVEC; date of dx: 2010-01-27; date of relapse: 8/19/2011, 7/18/2014, 8/15/2015, 7/7/2016; date of last follow-up: 2019-05-21; status: ALIVE; patient: 3; ', 'gender: M; tissue: skin; race: WHITE; age: 53; mcpyv_ihc: 1; recurrence: 1; patient: 3; ', 'gender: M; tissue: skin; tumor stage: III; race: WHITE; age: 72; mcpyv_ihc: 1; recurrence: 1; immunosuppressed?: NO; tumor location: LE; surgery: WLE + LND; radiation: YES; systemic: chemo; date of dx: 2012-04-01; date of relapse: 2014-04-28; date of last follow-up: 2016-06-25; status: LOST; patient: 4; ', 'gender: M; tissue: skin; race: WHITE; age: 72; mcpyv_ihc: 1; recurrence: 1; patient: 4; ', 'gender: M; tissue: skin; tumor stage: III; race: HISP; age: 49; mcpyv_ihc: 1; recurrence: 1; immunosuppressed?: NO; tumor location: H/N; surgery: WLE + LND; radiation: YES; systemic: NO; date of dx: 2016-01-14; date of relapse: NA; date of last follow-up: 2019-07-22; status: ALIVE; patient: 5; ', 'gender: M; tissue: skin; tumor stage: I; race: HISP; age: 66; mcpyv_ihc: 0; recurrence: 0; immunosuppressed?: YES (TRANSPLANT); tumor location: H/N; surgery: WLE; radiation: NO; systemic: NO; date of dx: 2016-08-29; date of relapse: NA; date of last follow-up: 2017-01-27; status: HOSPICE; additional info: mCSCC, CHF; patient: 6; ', 'gender: M; tissue: lymph node; tumor stage: IIII; race: HISP; age: 53; mcpyv_ihc: 0; recurrence: 0; immunosuppressed?: NO; tumor location: H/N; surgery: WLE + LND; radiation: YES; systemic: chemo; date of dx: 2016-08-31; date of relapse: NA; date of last follow-up: 2019-08-27; status: ALIVE; patient: 7; ', 'gender: M; tissue: skin; tumor stage: III; race: WHITE; age: 82; mcpyv_ihc: 0; recurrence: 1; immunosuppressed?: NO; tumor location: H/N; surgery: WLE + LND; radiation: NO; systemic: NO; date of dx: 2016-12-16; date of relapse: 2018-02-02; date of last follow-up: 2018-05-25; status: LOST; patient: 8; ', 'gender: M; tissue: skin; tumor stage: II; race: HISP; age: 51; mcpyv_ihc: 1; recurrence: 0; immunosuppressed?: NO; tumor location: LE; surgery: WLE + LND; radiation: NO; systemic: NO; date of dx: 2017-02-14; date of relapse: NA; date of last follow-up: 2017-11-09; status: DEAD; additional info: UNKNOWN COD; patient: 9; ', 'gender: F; tissue: skin; tumor stage: II; race: WHITE; age: 88; mcpyv_ihc: 1; recurrence: 1; immunosuppressed?: NO; tumor location: H/N; surgery: WLE; radiation: YES; systemic: NO; date of dx: 2018-03-23; date of relapse: 2019-06-01; date of last follow-up: 2019-08-27; status: ALIVE; patient: 10; ', 'gender: M; tissue: skin; tumor stage: III; race: WHITE; age: 86; mcpyv_ihc: 0; recurrence: 0; immunosuppressed?: NO; tumor location: UNK; surgery: LND; radiation: YES; systemic: NO; date of dx: 2019-01-11; date of relapse: NA; date of last follow-up: 2019-07-26; status: ALIVE; patient: 11; ', 'gender: M; tissue: lymph node; tumor stage: III; race: WHITE; age: 86; mcpyv_ihc: 0; recurrence: 0; immunosuppressed?: NO; tumor location: UNK; surgery: LND; radiation: YES; systemic: NO; date of dx: 2019-01-11; date of relapse: NA; date of last follow-up: 2019-07-26; status: ALIVE; patient: 11; ', 'gender: F; age: 59; mcpyv_ihc: 1; ', 'gender: F; age: 80; mcpyv_ihc: 0; ' GSE147471 Homo sapiens 45 Expression profiling by array GPL23159 GEP signatures in tumors from women with high grade early breast cancer [PrimitiveTumor]. 2020-03-24 Several molecular signatures are able to predict the activity of adjuvant chemotherapy in breast cancer patients. However, no molecular data are already available to detect microenvironment molecular signature that can identify patients who are good candidates for treatment with immune checkpoint inhibitors (ICIs). For this reason, in a series of women with operable high grade breast cancer (HGBC), we tried to combine the ECM3 and IFN molecular signatures reflecting different aspects of tumor microenvironment that can better draw the picture of the tumor microenvironment in which the immune cells are in close contact with extracellular matrix. Grade 3 primary tumors https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE147471 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA614942 https://www.ebi.ac.uk/ena/browser/view/PRJNA614942 None [Overal design]All gene expression data considered were from previously untreated patients. Cox regression and Kaplan-Meier analysis were used to assess associations with Overall Survival (OS). Characterization of the tumor immune microenvironment was achieved evaluating gene expression patterns scores of tumor infiltrating lymphocytes and their phenotypes as assessed by immunohistochemistry.; [Treatment]'NA'; [Growth]'NA'; [Extraction]"RNA was extracted with miRNeasy FFPE kit (Qiagen) in accordance with the manufacture's protocol."; [Cell type]'Source: ''type: Primitive; origin_material: FFPE; grade: G3; ' GSE149677 Mus musculus 2 Other GPL17021 Large domains of heterochromatin direct the formation of short mitotic chromosome loops 2020-04-30 During mitosis chromosomes reorganise into highly compact, rod-shaped forms, thought to consist of consecutive chromatin loops around a central protein scaffold. Condensin complexes are involved in chromatin compaction, but the contribution of other chromatin proteins, DNA sequence and histone modifications is less understood. A large region of fission yeast DNA inserted into a mouse chromosome was previously observed to adopt a mitotic organisation distinct from that of surrounding mouse DNA. Here we show that a similar distinct structure is common to a large subset of insertion events in both mouse and human cells and is coincident with the presence of high levels of heterochromatic H3 lysine 9 trimethylation (H3K9me3). Hi-C and microscopy indicate that the heterochromatinised fission yeast DNA is organised into smaller chromatin loops than flanking euchromatic mouse chromatin. We conclude that heterochromatin alters chromatin loop size, thus contributing to the distinct appearance of heterochromatin on mitotic chromosomes, such as at centromeres. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE149677 Large domains of heterochromatin direct the formation of short mitotic chromosome loops. eLife 7.551 https://doi.org/10.7554/eLife.57212 {eLife (7.551): 10.7554/eLife.57212} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA629586 https://www.ebi.ac.uk/ena/browser/view/PRJNA629586 https://www.ncbi.nlm.nih.gov/sra?term=SRP259379 [Overal design]HI-C experiment on Interphase and Mitotic phase F1.1 cell line respectively; [Treatment]'None'; [Growth]'F1.1 cells were synchronised for mitotic Hi-C by a thymidine block. Cells were arrested for 18 hours by the addition of 2mM thymidine and collected by mitotic shake off 5 and then 8 hours after release. Cells were fixed in 1% PFA and collected as for ChIP'; [Extraction]'Hi-C experiment were conducted using HindIII (Naumova et al. 2013).\nHi-C libraries prepared as previously described (Naumova et al. 2013).'; [Cell type]'mouse mammary tumour''cell type: mouse mammary tumour; cell line: F1.1; ' GSE132528 Mus musculus 21 Expression profiling by high throughput sequencing GPL13112 Expression of deregulated MYC with activated NeuNT in mammary gland developed mammary tumors with molecular heterogeneity 2019-06-11 The goal of this study is to investigate the role of deregulated c-MYC in cooperation with activated NeuNT (mutated rat HER2) in mammary tumor molecular heterogeneity. We monitored female mice through two cycles of pregnancy/lactation in order to activate Blg-Cre expression in mammary gland after the second cycle. MYC-NeuNT mice develop tumors between 4 and 12 weeks post Blg-Cre activation, H&E images from these tumors showed histologic heterogeneity. NeuNT mice developed tumors between 28 to 44 weeks post Blg-Cre activation that also showed histologic heterogeneity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132528 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA548309 https://www.ebi.ac.uk/ena/browser/view/PRJNA548309 https://www.ncbi.nlm.nih.gov/sra?term=SRP201078 [Overal design]ROSA-LSL-MYC mice were crossed with LSL-NeuNT and Blg-Cre mice to get mice that express both MYC and NeuNT in response to Cre-mediated recombination in the mammary gland. We monitored the female mice through two cycles of pregnancy/lactation then activated and waited for tumors to reach 20mm in diameter (end point). We collected 14 tumors from MYC-NeuNT mice, 4 tumors from NeuNT mice , and 3 normal mammary gland samples from control Myc mice without Blg-Cre. One piece of tissue from each sample was used to extact total RNA with Trizol according to manufactuer's protocol.; [Treatment]'At 8 weeks of age, start breeding MYC-NeuNT and NeuNT females with male mice through two cycles of pregnancy. Monitor tumor growth twice every week.'; [Growth]'Generate MYC-NeuNT and NeuNT mice, passing two cycles of pregnancy/lactation. MYC-NeuNT mice developed tumors between 4 and 12 weeks post Blg-Cre activation and NeuNT mice developed tumors between 28 - 44 weeks post Blg-Cre activation.'; [Extraction]"Total RNA was extracted with Trizol according to manufacturer's protocol.\nSequencing libraries were constructed using an Illumina TruSeq RNAseq kit. Briefly, poly(A)+ RNA was isolated from 1ug of total RNA (per sample) using oligo-dT coated magnetic beads. The recovered RNA was then chemically fragmented. First strand cDNA was generated using random hexamers as primers for reverse transcriptase. Following second strand synthesis, the ends of the double stranded fragments were repaired and then a single “A” nucleotide was added to each end. Illumina adaptors were ligated to the cDNAs. Limited round (11-cycle) PCR was used to amplify the material to yield the final libraries. Library concentration was determined using real time PCR with primers complementary to the Illumina adaptors. Sample libraries were diluted and applied to an Illumina single read flow cell at a concentration appropriate to generate about 180 million reads per lane. All libraries were prepared with indexing barcodes to permit multiplexing in a single lane. 100 cycle single read sequencing was used to generate base call files. Illumina’s CASAVA package was used to assemble the reads into standard fastq formatted data."; [Cell type]'Source: ''tissue: mammary gland tumor; tumor size (diameter): 20mm; genotype: MYC-NeuNT; ', 'tissue: normal mammary gland; genotype: MYC without Blg-Cre; ', 'tissue: mammary gland tumor; tumor size (diameter): 20mm; genotype: NeuNT; ' GSE18996 Mus musculus 12 Expression profiling by array GPL4134 ShcA is a Paracrine Integrator of the Adaptive Immune Response during Breast Cancer Progression 2009-11-12 Using transgenic mouse models of breast cancer, we demonstrate that loss of ShcA signaling within mammary tumors results in extensive CD4+ T cell infiltration, activation and induction of a humoral immune response. Our studies reveal that ShcA signaling during early breast cancer progression is required to establish and maintain an immunosuppressive state that favors tumor growth. Consistent with these transgenic studies, high ShcA levels correlate with poor outcome and reduced CTL infiltration in primary human breast cancers. Conversely, elevated expression of a ShcA-regulated immune signature, generated from ShcA-null mammary tumors, is a predictor of good prognosis in HER2-positive and basal breast cancer patients. These observations define a novel role for ShcA in polarizing the immune response to facilitate tumorigenesis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE18996 Receptor tyrosine kinase signaling favors a protumorigenic state in breast cancer cells by inhibiting the adaptive immune response. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-10-2229 {Cancer research (8.378): 10.1158/0008-5472.CAN-10-2229} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA120665 https://www.ebi.ac.uk/ena/browser/view/PRJNA120665 None [Overal design]NIC SHC null Tumors vs. pooled MMPV-NIC reference, some replicate dye swaps; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was isolated from samples using the RNeasy Midi Kit (Qiagen)'; [Cell type]'Source: ''tissue: ShcA-null mammary tumor; ', 'reference: Pooled NIC tumor; ', 'tissue: Pooled NIC tumor; ' GSE76453 Homo sapiens 12 Expression profiling by high throughput sequencing GPL11154 The Chromatin-Looping Factor ZNF143 Engages at Looping Promoters to Favor the Estrogen Response in Breast Cancer (RNA-seq) 2015-12-31 Estrogen signaling in breast cancer cells relies on long-range chromatin interactions connecting distal regulatory elements bound by the estrogen receptor 1 (ESR1) to target gene promoters. This ensures stimulus and subtype-specific transcriptional responses. Expanding on the function of CTCF and the cohesin complex in breast cancer, we demonstrate that the chromatin-looping factor ZNF143 binds the promoter of most early-response estrogen target genes connected to distal regulatory elements in ESR1-positive breast cancer cells. Its chromatin occupancy is unaffected by estrogen stimulation, supporting a stable three-dimensional genomic architecture within the early response to estrogen. Its loss abrogates the estrogen-induced transcriptional response and growth of breast cancer cells. When taking into account CTCF, ZNF143 and cohesin complex subunits, we show that chromatin-looping factors are genetically altered in over 20% of ESR1-positive primary breast tumors. Furthermore, the overexpression of ZNF143, CTCF and RAD21, a cohesin complex subunit, in ESR1-positive breast tumors associates with a worse clinical outcome. Overall, our results suggest that ZNF143 is a new critical effector of the estrogen response and highlights the contribution of the chromatin looping machinery to ESR1-positive breast cancer development. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76453 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA307350 https://www.ebi.ac.uk/ena/browser/view/PRJNA307350 https://www.ncbi.nlm.nih.gov/sra?term=SRP067977 [Overal design]mRNA profiles of MCF-7 cells (siCtl or siZNF143) under vehicle (EtOH) or E2 (10 uM 17-beta oestradiol) stimulation; [Treatment]'MCF-7 cells were transfected with siZNF143 (Ambion siRNA ID: s15194) or a scrambled control siRNA and starved of oestrogen for 48hrs. They were stimulated with 10 nM 17-beta oestradiol for 3 hours prior to RNA extraction.'; [Growth]'MCF-7 cells were grown in DMEM supplemented with 10% FBS and 1% P/S'; [Extraction]"RNA was harvested using Qiagen's Rneasy Plus Mini Kit\nRNA libraries were prepared for sequencing using standard Illumina protocols."; [Cell type]'Source: ''cell line: MCF-7; transfection: scrambled control siRNA; treatment: vehicle; ', 'cell line: MCF-7; transfection: scrambled control siRNA; treatment: 10 uM 17-beta oestradiol for 3 hours; ', 'cell line: MCF-7; transfection: siZNF143; treatment: vehicle; ', 'cell line: MCF-7; transfection: siZNF143; treatment: 10 uM 17-beta oestradiol for 3 hours; ' GSE134817 Homo sapiens 180 Expression profiling by high throughput sequencing GPL11154 Promoter activity profiling reveals on- and off-target transcriptional responses to drug treatment 2019-07-24 Owing to safety concerns or insufficient potential for efficacy, only 0.01% to 0.02% of new drug candidates are approved for marketing. Drugs already on the market may be withdrawn or restricted to certain uses due to adverse effects (AEs) discovered after market introduction. Comprehensively investigating the on-/off-target effects of drugs can help expose AEs during the drug development process. In this study, we developed an integrative framework for systematic identification of on-/off-target pathways and elucidation of the underlying mechanisms, by combining expression profiling after drug treatment with gene perturbation of the primary drug target. Expression profiles from statin-treated cells and HMG-CoA reductase knockdowns were analyzed using the framework, allowing for identification of not only reported adverse effects but also novel candidates of off-target effects from statin treatment. Our findings may provide new insights for finding new usages or potential side effects of drug treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE134817 A framework for identification of on- and off-target transcriptional responses to drug treatment. Scientific reports 4.011 https://doi.org/10.1038/s41598-019-54180-4 {Scientific reports (4.011): 10.1038/s41598-019-54180-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA556524 https://www.ebi.ac.uk/ena/browser/view/PRJNA556524 https://www.ncbi.nlm.nih.gov/sra?term=SRP216293 [Overal design]CAGE profiling in three different cell types after treatment with four different statins and two siRNAs targeting HMG-CoA reductase (HMGCR), including replicates and control samples.; [Treatment]'In the statin treatment, Atorvastatin, Fluvastatin, Rosuvastatin and Simvastatin were added to the culture medium at the final concentration of 30 uM for MCF-7 and THP-1 and 10 uM for HepG2 for 6 and 48 h. In the siRNA treatment, 2 siRNAs against HMGCR gene (HSS104864and HSS179267, Thermo Fisher SCIENTIFIC) and negative control siRNA (Stealth RNAi siRNA Negative Control, Med GC, Thermo Fisher SCIENTIFIC) were transfected using Lipofectamine RNAiMAX\u3000Transfection Reagent (Thermo Fisher Scientific) and incubated for 48 h. The HMGCR knockdown efficiency for HSS104864 and HSS179267 was 80% and 81% (HepG2), 42% and 52% (MCF-7) and 77% and 70% (THP-1), respectively.'; [Growth]'HepG2 and MCF-7 cells were cultured in DMEM high glucose (Gibco) supplemented with 10% inactivated fetal bovine serum (Gibco), 100 U/mL penicillin, 100 μg/mL streptomycin (Gibco) and 1 mM sodium pyruvate (Gibco). THP-1cells were cultured in RPMI-1640 (Gibco) supplemented with 10% inactivated fetal bovine serum (Gibco), 100 U/mL penicillin and 100 μg/mL streptomycin (Gibco).'; [Extraction]'After the treatments, total RNA was extracted from the cells using RNeasy kit (Qiagen).\n8-plex nAnT-iCAGE protocol (Murata M, et al. Detecting expressed genes using CAGE. Methods Mol. Biol. 2014;1164:67–85. doi: 10.1007/978-1-4939-0805-9_7.)'; [Cell type]'Source: ''cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ato; treatment time: 6; library id: CNhi10321; barcode: ACG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ato; treatment time: 6; library id: CNhi10321; barcode: GCT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10321; barcode: ACC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10321; barcode: CAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10321; barcode: AGT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10321; barcode: GCG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10321; barcode: ATG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10321; barcode: TAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ato; treatment time: 6; library id: CNhi10322; barcode: ACC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Flu; treatment time: 6; library id: CNhi10322; barcode: ATG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Flu; treatment time: 6; library id: CNhi10322; barcode: TAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Flu; treatment time: 6; library id: CNhi10322; barcode: ACG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ros; treatment time: 6; library id: CNhi10322; barcode: GCT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Sim; treatment time: 6; library id: CNhi10322; barcode: CAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Sim; treatment time: 6; library id: CNhi10322; barcode: AGT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Sim; treatment time: 6; library id: CNhi10322; barcode: GCG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10323; barcode: AGT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10323; barcode: GCG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10323; barcode: ATG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10323; barcode: TAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10323; barcode: ACG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10323; barcode: GCT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ros; treatment time: 6; library id: CNhi10323; barcode: ACC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ros; treatment time: 6; library id: CNhi10323; barcode: CAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ato; treatment time: 48; library id: CNhi10324; barcode: ACC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ato; treatment time: 48; library id: CNhi10324; barcode: CAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ato; treatment time: 48; library id: CNhi10324; barcode: AGT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Flu; treatment time: 48; library id: CNhi10324; barcode: ACG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Flu; treatment time: 48; library id: CNhi10324; barcode: GCT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Sim; treatment time: 48; library id: CNhi10324; barcode: GCG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Sim; treatment time: 48; library id: CNhi10324; barcode: TAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Flu; treatment time: 48; library id: CNhi10325; barcode: ACC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ros; treatment time: 48; library id: CNhi10325; barcode: CAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ros; treatment time: 48; library id: CNhi10325; barcode: AGT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ros; treatment time: 48; library id: CNhi10325; barcode: GCG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10332; barcode: ACC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10332; barcode: CAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: siRNA; treatment: si104864; treatment time: 48; library id: CNhi10332; barcode: AGT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10332; barcode: GCG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10333; barcode: ACG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10333; barcode: GCT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: siRNA; treatment: si104864; treatment time: 48; library id: CNhi10333; barcode: ACC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10333; barcode: CAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10334; barcode: ATG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10334; barcode: TAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: siRNA; treatment: si104864; treatment time: 48; library id: CNhi10334; barcode: ACG; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10334; barcode: GCT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Sim; treatment time: 48; library id: CNhi10357; barcode: TAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Flu; treatment time: 48; library id: CNhi10371; barcode: ACC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ros; treatment time: 48; library id: CNhi10371; barcode: CAC; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ros; treatment time: 48; library id: CNhi10371; barcode: AGT; ', 'cell line: HepG2; tissue/cell type source: hepatocellular carcinoma; treatment group: Statins; treatment: Ros; treatment time: 48; library id: CNhi10371; barcode: GCG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Ato; treatment time: 6; library id: CNhi10315; barcode: GCT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10315; barcode: CAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10315; barcode: AGT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10315; barcode: GCG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10315; barcode: ATG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10315; barcode: TAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10315; barcode: ACG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Ato; treatment time: 6; library id: CNhi10316; barcode: ACC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Ato; treatment time: 6; library id: CNhi10316; barcode: CAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Flu; treatment time: 6; library id: CNhi10316; barcode: TAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Flu; treatment time: 6; library id: CNhi10316; barcode: ACG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Flu; treatment time: 6; library id: CNhi10316; barcode: GCT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Sim; treatment time: 6; library id: CNhi10316; barcode: AGT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Sim; treatment time: 6; library id: CNhi10316; barcode: GCG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Sim; treatment time: 6; library id: CNhi10316; barcode: ATG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10317; barcode: GCG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10317; barcode: ATG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10317; barcode: TAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10317; barcode: ACG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10317; barcode: GCT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Ros; treatment time: 6; library id: CNhi10317; barcode: ACC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Ros; treatment time: 6; library id: CNhi10317; barcode: CAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Ros; treatment time: 6; library id: CNhi10317; barcode: AGT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Ato; treatment time: 48; library id: CNhi10318; barcode: AGT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Ato; treatment time: 48; library id: CNhi10318; barcode: GCG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Ato; treatment time: 48; library id: CNhi10318; barcode: ATG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10318; barcode: CAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Sim; treatment time: 48; library id: CNhi10318; barcode: TAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Sim; treatment time: 48; library id: CNhi10318; barcode: ACG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Sim; treatment time: 48; library id: CNhi10318; barcode: GCT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Flu; treatment time: 48; library id: CNhi10319; barcode: ACC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Flu; treatment time: 48; library id: CNhi10319; barcode: CAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Flu; treatment time: 48; library id: CNhi10319; barcode: AGT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Ros; treatment time: 48; library id: CNhi10319; barcode: GCG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Ros; treatment time: 48; library id: CNhi10319; barcode: ATG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: Statins; treatment: Ros; treatment time: 48; library id: CNhi10319; barcode: TAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: si104864; treatment time: 48; library id: CNhi10330; barcode: GCT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10330; barcode: CAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10330; barcode: AGT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10330; barcode: GCG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10330; barcode: ATG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10330; barcode: TAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10330; barcode: ACG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: si104864; treatment time: 48; library id: CNhi10331; barcode: ACC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: si104864; treatment time: 48; library id: CNhi10331; barcode: CAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10331; barcode: AGT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10331; barcode: GCG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10331; barcode: ATG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10369; barcode: GCT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10369; barcode: AGT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10369; barcode: CAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10369; barcode: GCG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10369; barcode: ATG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10369; barcode: TAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10369; barcode: ACG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: si104864; treatment time: 48; library id: CNhi10370; barcode: ACC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: si104864; treatment time: 48; library id: CNhi10370; barcode: CAC; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10370; barcode: AGT; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10370; barcode: GCG; ', 'cell line: MCF-7; tissue/cell type source: breast cancer; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10370; barcode: ATG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10325; barcode: ATG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10325; barcode: TAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10325; barcode: ACG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10325; barcode: GCT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ato; treatment time: 6; library id: CNhi10326; barcode: AGT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ato; treatment time: 6; library id: CNhi10326; barcode: GCG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ato; treatment time: 6; library id: CNhi10326; barcode: ATG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10326; barcode: ACC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10326; barcode: CAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Sim; treatment time: 6; library id: CNhi10326; barcode: TAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Sim; treatment time: 6; library id: CNhi10326; barcode: ACG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Sim; treatment time: 6; library id: CNhi10326; barcode: GCT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Flu; treatment time: 6; library id: CNhi10327; barcode: ACC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Flu; treatment time: 6; library id: CNhi10327; barcode: CAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Flu; treatment time: 6; library id: CNhi10327; barcode: AGT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10327; barcode: ACG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10327; barcode: GCT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ros; treatment time: 6; library id: CNhi10327; barcode: GCG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ros; treatment time: 6; library id: CNhi10327; barcode: ATG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ros; treatment time: 6; library id: CNhi10327; barcode: TAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ato; treatment time: 48; library id: CNhi10328; barcode: ATG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ato; treatment time: 48; library id: CNhi10328; barcode: TAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ato; treatment time: 48; library id: CNhi10328; barcode: ACG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10328; barcode: ACC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10328; barcode: CAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10328; barcode: AGT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10328; barcode: GCG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Sim; treatment time: 48; library id: CNhi10328; barcode: GCT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Flu; treatment time: 48; library id: CNhi10329; barcode: AGT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Flu; treatment time: 48; library id: CNhi10329; barcode: GCG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Flu; treatment time: 48; library id: CNhi10329; barcode: ATG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ros; treatment time: 48; library id: CNhi10329; barcode: TAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ros; treatment time: 48; library id: CNhi10329; barcode: ACG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ros; treatment time: 48; library id: CNhi10329; barcode: GCT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Sim; treatment time: 48; library id: CNhi10329; barcode: ACC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Sim; treatment time: 48; library id: CNhi10329; barcode: CAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: siRNA; treatment: si104864; treatment time: 48; library id: CNhi10332; barcode: ACG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10332; barcode: GCT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10332; barcode: ATG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10332; barcode: TAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10333; barcode: AGT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10333; barcode: GCG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: siRNA; treatment: si104864; treatment time: 48; library id: CNhi10333; barcode: ATG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10333; barcode: TAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10334; barcode: ACC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: siRNA; treatment: NC; treatment time: 48; library id: CNhi10334; barcode: CAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: siRNA; treatment: si104864; treatment time: 48; library id: CNhi10334; barcode: AGT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: siRNA; treatment: si179267; treatment time: 48; library id: CNhi10334; barcode: GCG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10371; barcode: ATG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10371; barcode: TAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10371; barcode: ACG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10371; barcode: GCT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ato; treatment time: 6; library id: CNhi10372; barcode: AGT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ato; treatment time: 6; library id: CNhi10372; barcode: GCG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ato; treatment time: 6; library id: CNhi10372; barcode: ATG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10372; barcode: ACC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 6; library id: CNhi10372; barcode: CAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Sim; treatment time: 6; library id: CNhi10372; barcode: TAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Sim; treatment time: 6; library id: CNhi10372; barcode: ACG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Sim; treatment time: 6; library id: CNhi10372; barcode: GCT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Flu; treatment time: 6; library id: CNhi10373; barcode: ACC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Flu; treatment time: 6; library id: CNhi10373; barcode: CAC; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Flu; treatment time: 6; library id: CNhi10373; barcode: AGT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10373; barcode: ACG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Non; treatment time: 48; library id: CNhi10373; barcode: GCT; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ros; treatment time: 6; library id: CNhi10373; barcode: GCG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ros; treatment time: 6; library id: CNhi10373; barcode: ATG; ', 'cell line: THP-1; tissue/cell type source: monocyte; treatment group: Statins; treatment: Ros; treatment time: 6; library id: CNhi10373; barcode: TAC; ' GSE84080 Homo sapiens 6 Expression profiling by high throughput sequencing GPL16791 Regulators of cellular heterogeneity in basal-like breast cancer influence symmetric versus asymmetric division rates (Expression profiles) 2016-07-06 Differentiation events contribute to cellular heterogeneity within tumors and influence disease progression and response to therapy. Here we dissect the mechanisms controlling intratumoral heterogeneity within basal-like breast cancers. We show that cancer cells can transition between a differentiation state related to that of normal luminal progenitors and a state closer to that of mature luminal cells, and that this occurs through asymmetric cell divisions. The Polycomb factor EZH2 and the Notch pathway act to increase the rates of symmetric divisions that produce progenitor-like cells, while the FOXA1 transcription factor promotes asymmetric divisions that reduce the numbers of such cells. Through functional screening, we identified a group of regulators that control cancer cell differentiation state and the relative proportions of tumor cell subpopulations. Our findings highlight the regulation of asymmetric cell divisions as a mechanism controlling intratumoral heterogeneity, and identify molecular pathways that control breast cancer cellular composition. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE84080 Regulation of Cellular Heterogeneity and Rates of Symmetric and Asymmetric Divisions in Triple-Negative Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2018.08.053 {Cell reports (7.815): 10.1016/j.celrep.2018.08.053} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA327998 https://www.ebi.ac.uk/ena/browser/view/PRJNA327998 https://www.ncbi.nlm.nih.gov/sra?term=SRP077979 [Overal design]Expression profiles of three cell subpopulations – K18+, K18+K14+ and K18+Vim+ – sorted from the breast cancer cell lines HCC70 and MDA-MB-468; [Treatment]'For staining of cells for differentiation markers by FACS, the cells were detached by trypsin-EDTA, fixed and permeabilized for 10 min in 100% methanol on ice, and stained with antibodies against K18 (sc-31700, Santa Cruz), K14, and vimentin (NCL-L-VIM- V9, Novocastra), followed by conjugated secondary antibodies.'; [Growth]'Cell lines were obtained from ATCC. HCC70 cells were grown in RPMI medium containing 10% FBS, and MDA-MB-468 cells in Leibovitz L15 medium containing 10% FBS and supplemented with penicillin and streptomycin.'; [Extraction]'To extract RNA from fixed and stained cell subpopulations isolated by FACS from cell lines and mRNA was extracted using the Recover All Total Nucleic Acid Isolation Kit (Ambion).\nLibraries were prepared and libraries were prepared and sequenced using Illumina’s RNA sequencing protocol'; [Cell type]'Source: ''cell line: HCC70 breast cancer cell line; cell population: Keratin 18+; ', 'cell line: HCC70 breast cancer cell line; cell population: Keratin 18+ Keratin14+; ', 'cell line: HCC70 breast cancer cell line; cell population: Keratin 18+ Vimentin+; ', 'cell line: MDA-MB-468 breast cancer cell line; cell population: Keratin 18+; ', 'cell line: MDA-MB-468 breast cancer cell line; cell population: Keratin 18+ Keratin14+; ', 'cell line: MDA-MB-468 breast cancer cell line; cell population: Keratin 18+ Vimentin+; ' GSE43610 Mus musculus 6 Expression profiling by array GPL7202 Dual Roles of the Transcription Factor Grainyhead-like 2 (GRHL2) in Breast Cancer 2013-01-18 Using a retrovirus-mediated cDNA expression cloning approach we identified the grainyhead-like 2 (GRHL2) transcription factor as novel protooncogene. Overexpression of GRHL2 in NIH3T3 cells induced striking morphological changes, an increase in cell proliferation, anchorage-independent growth, and tumor growth in vivo. By combining a microarray analysis and a phylogenetic footprinting analysis with various biochemical assays we identified the epidermal growth factor receptor family member Erbb3 as a novel GRHL2 target gene. In breast cancer cell lines, shRNA-mediated knockdown of GRHL2 expression or functional inactivation of GRHL2 using dominant-negative GRHL2 proteins induce downregulation of ERBB3 gene expression, a striking reduction in cell proliferation and morphological and phenotypical alterations characteristic of an epithelial-to-mesenchymal transition (EMT), thus implying dual roles of GRHL2 in breast carcinogenesis. Interestingly, we could further demonstrate that expression of GRHL2 is directly suppressed by the transcription factor zinc-finger-enhancer binding protein 1 (ZEB1) which in turn is a direct target for repression by GRHL2, suggesting that the EMT transcription factors GRHL2 and ZEB1 form a double negative regulatory feedback loop in breast cancer cells. Finally, a comprehensive immunohistochemical analysis of GRHL2 expression in primary breast cancers showed loss of GRHL2 expression at the invasive front of primary tumors. A pathophysiological relevance of GRHL2 in breast cancer metastasis is further demonstrated by our finding of a statistically significant association between loss of GRHL2 expression in primary breast cancers and lymph-node metastasis. We thus demonstrate a crucial role of GRHL2 in breast carcinogenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43610 Dual roles of the transcription factor grainyhead-like 2 (GRHL2) in breast cancer. The Journal of biological chemistry 4.106 https://doi.org/10.1074/jbc.M113.456293 {The Journal of biological chemistry (4.106): 10.1074/jbc.M113.456293} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA186816 https://www.ebi.ac.uk/ena/browser/view/PRJNA186816 None [Overal design]To evaluate the role of the GRHL2 transcription factor in carcinogenessis we overexpressed the human GRHL2 protein in NIH3T3 cells. Parental NIH3T3 cells do not express the orthologic protein. Alterations in genome-wide transcriptional profiles were determined by microarray analysis.; [Treatment]'FLAG-tagged human GRHL2 cDNA was subcloned into the pIRES-N1 expression vector under the control of cytomegalovirus promoter (pIRES-N1-GRHL2). NIH3T3 cells were transfected with pIRES-N1-GRHL2 using Lipofectamine 2000 (Invitrogen). Stably transfected cells were selected with 500 µg/ml G418.'; [Growth]'NIN3T3 cells were cultured in DMEM conaining 10% FCS in 10% CO2 atmosphere'; [Extraction]'Total RNA was extracted from parental and GRHL2-expressing NIH3T3 cells using the RNeasy Kit (Qiagen). For each cell culture three samples taken from different passages were utilized for expression profiling.'; [Cell type]'Source: ''cell line: NIH3T3; ' GSE152580 Homo sapiens 12 Expression profiling by high throughput sequencing GPL16791 Deciphering the gene expression network regulated by ETV7 2020-06-16 Cancer stem cells (CSCs) represent a population of cells within the tumor able to drive tumorigenesis and known to be highly resistant to conventional chemotherapy and radiotherapy. In this work, we show a new role for ETV7, a transcriptional repressor member of the ETS family, in promoting breast cancer stem-like cells plasticity and resistance to chemo- and radiotherapy in breast cancer (BC) cells. We observed that MCF7 and T47D BC-derived cells stably over-expressing ETV7 showed reduced sensitivity to the chemotherapeutic drug 5-Flouororuacil and to radiotherapy, accompanied by an adaptive proliferative behavior observed in different culture conditions. We further noticed that alteration of ETV7 expression could significantly affect the population of breast CSCs, measured by CD44+/CD24low cell population and mammosphere formation efficiency. By transcriptome profiling, we identified a signature of Interferon-responsive genes significantly repressed in cells over-expressing ETV7, which could be responsible for the increase in the breast CSCs population, as this could be partially reverted by the treatment with IFN-b. Lastly, we show that the expression of the IFN-responsive genes repressed by ETV7 could have prognostic value in breast cancer, as low expression of these genes was associated with a worse prognosis. Therefore, we propose a novel role for ETV7 in breast cancer stem cells’ plasticity and associated resistance to conventional chemotherapy and radiotherapy, which involves the repression of a group of IFN-responsive genes, potentially reversible upon IFN-b treatment. We, therefore, suggest that an in-depth investigation of this mechanism could lead to novel breast CSCs targeted therapies and to the improvement of combinatorial regimens, possibly involving the therapeutic use of IFN-b, with the aim of avoiding resistance development and relapse in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE152580 ETV7 regulates breast cancer stem-like cell features by repressing IFN-response genes. Cell death & disease 5.959 https://doi.org/10.1038/s41419-021-04005-y {Cell death & disease (5.959): 10.1038/s41419-021-04005-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA639783 https://www.ebi.ac.uk/ena/browser/view/PRJNA639783 https://www.ncbi.nlm.nih.gov/sra?term=SRP267516 [Overal design]We analyzed gene expression from 2 breast cancer-derived cell lines (MCF7 and T47D) stably transfected with ETV7 or an empty vector (pAIP backbone) as a control. Three biological replicates for each condition (4 Samples) have been prepared and processed.; [Treatment]'Cells were plated cultured as above and no treatment was applied.'; [Growth]'Cells were grown in DMEM medium (Gibco, ThermoFisher Scientific, Milan, Italy) supplemented with 10% FBS (Gibco), 2mM L-Glutamine (Gibco) and a mixture of 100U/ml Penicillin / 100μg/ml Streptomycin (Gibco). Cells were cultured at 37°C with 5% CO2 in a humidified atmosphere. Selction was maintained growing MCF7 and T47D cells in growth medium additioned with Puromycin (Life Technologies) 0.75 and 1.5 μg/ml, respectively.'; [Extraction]'Total RNA was extracted using the Illustra RNA spin Mini Kit (GE Healthcare, Milan, Italy), checkd for quality and purity the Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA, USA) selecting RNA extracts with a RIN (RNA integrity number) value > 8.\nRNA (1 mg) was then converted into cDNA libraries according to the Illumina TruSeq Stranded mRNA Sample Preparation Guide (Illumina, San Diego, CA, USA) following manufacturer’s instructions.'; [Cell type]'Source: ''cell line: MCF7; treatment: Empty; tissue: Luminal Breast Cancer; ', 'cell line: MCF7; treatment: ETV7; tissue: Luminal Breast Cancer; ', 'cell line: T47D; treatment: Empty; tissue: Luminal Breast Cancer; ', 'cell line: T47D; treatment: ETV7; tissue: Luminal Breast Cancer; ' GSE93109 Homo sapiens 48 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL11532; GPL16791 Patient-derived luminal breast cancer xenografts with progestins 2017-01-04 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93109 None None None None None 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA360064 https://www.ebi.ac.uk/ena/browser/view/PRJNA360064 None [Overal design]Refer to individual Series; [Treatment]'Chronic E2/E2+MPA treatment upon transplant', 'Chronic E2/E2+P4 treatment upon transplant', 'Mice were treated using silastic pellets as described in Sartorius et al, Breast Cancer Res Treat 2003 (PMID 12846413)'; [Growth]'Xenografts were grown in NOD/SCID/Il2rgnull mice', 'Tumors were partitioned into 10 mm^3 pieces and placed into recipient NSG mice under various hormone conditons as in Kabos et al Breast Cancer Res Treat 2012 (PMID 22821401)'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions.\nRNA libraries were prepared for sequencing using the Illumina TruSeq Stranded mRNA LT Sample Prep Kit at the University of Colorado Denver Genomics and Microarray Core facility.", 'Tissue was pulverized and crosslinked. Lysates were produced from sonicated nuclei and ER or PR were isolated with antibody.\nLibraries were prepared at the University of Colorado Denver Genomics and Microarray Core facility using the NuGEN Ovation Ultralow Library System v2 .', "Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''xenograft: UCD4; treatment: estrogen; ', 'xenograft: UCD4; treatment: estrogen+MPA; ', 'xenograft: UCD65; treatment: estrogen; ', 'xenograft: UCD65; treatment: estrogen+MPA; ', 'xenograft: UCD4; treatment: estrogen; chip antibody: input; ', 'xenograft: UCD4; treatment: estrogen; chip antibody: ER (sc-543X, Santa Cruz Biotechnology), lot# F1215; ', 'xenograft: UCD4; treatment: estrogen; chip antibody: PR (sc-7208X, Santa Cruz Biotechnology), lot# H1415; ', 'xenograft: UCD4; treatment: estrogen; chip antibody: IgG (sc-2027, Santa Cruz Biotechnology), lot # H2615; ', 'xenograft: UCD4; treatment: estrogen plus progesterone; chip antibody: input; ', 'xenograft: UCD4; treatment: estrogen plus progesterone; chip antibody: ER (sc-543X, Santa Cruz Biotechnology), lot# F1215; ', 'xenograft: UCD4; treatment: estrogen plus progesterone; chip antibody: PR (sc-7208X, Santa Cruz Biotechnology), lot# H1415; ', 'xenograft: UCD4; treatment: estrogen plus progesterone; chip antibody: IgG (sc-2027, Santa Cruz Biotechnology), lot # H2615; ', 'tissue: breast tumor xenograft; treatment: placebo; ', 'tissue: breast tumor xenograft; treatment: estradiol; ', 'tissue: breast tumor xenograft; treatment: estradiol and medroxyprogesterone acetate; ', 'tissue: breast tumor xenograft; treatment: estradiol and progesterone; ' GSE98273 Homo sapiens 5 Expression profiling by high throughput sequencing GPL17303 RNA-sequencing in MDA-231-D cells transfected with ZEB1 or ZEB2 siRNAs 2017-04-27 We searched for roles of ZEB1and/or ZEB2 during EMT by RNA-seq in breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98273 ZEB1-regulated inflammatory phenotype in breast cancer cells. Molecular oncology 5.962 https://doi.org/10.1002/1878-0261.12098 {Molecular oncology (5.962): 10.1002/1878-0261.12098} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA384523 https://www.ebi.ac.uk/ena/browser/view/PRJNA384523 https://www.ncbi.nlm.nih.gov/sra?term=SRP105333 [Overal design]Expression of mRNA in a basal type breast cancer cell line MDA-231-D transfected with ZEB1 or ZEB2 siRNAs.; [Treatment]'MDA-231-D cells were transfected with siRNAs.'; [Growth]'MDA-231-D human mammary gland triple-negative cancer cell line, a highly bone metastatic clone of MDA-MB-231, was established as described (Ehata et al., Cancer Sci 98: 127-133, 2007) and cultured in Dulbecco’s modified Eagle’s medium (DMEM: #11965, Thermo Fisher Scientific, Waltham, MA, USA).'; [Extraction]'Total RNAs were extracted as described previously (Mizutani et al., 2011, J Biol Chem).\nLibraries were prepared using Dynabeads mRNA DIRECT Purification Kit (Life Technologies) and Ion Total RNA-seq kit v2 (Thermo Scientific). Sequencing was performed as described (Sakurai et al., 2016, Oncogene).'; [Cell type]'Source: ''sirna: Negative control siRNA (12935-112, Thermo Fisher Scientific); tgf-beta treatment: no; histology: basal type breast cancer; ', 'sirna: ZEB1 siRNA (HSS110548, Thermo Fisher Scientific); tgf-beta treatment: no; histology: basal type breast cancer; ', 'sirna: ZEB1 siRNA (HSS186235, Thermo Fisher Scientific); tgf-beta treatment: no; histology: basal type breast cancer; ', 'sirna: ZEB1 siRNA (HSS114854, Thermo Fisher Scientific); tgf-beta treatment: no; histology: basal type breast cancer; ', 'sirna: ZEB1 siRNA (HSS190654, Thermo Fisher Scientific); tgf-beta treatment: no; histology: basal type breast cancer; ' GSE180508 Mus musculus; Homo sapiens 12 Expression profiling by high throughput sequencing GPL21626; GPL21697 Sensory nerves enhance triple negative breast cancer migration and metastasis through PlexinB3 signaling 2021-07-20 We identified sensory nerves as more abundant in triple-negative human breast tumors. Human triple negative breast cancer (TNBC) cells (MDA-MB-231, SUM159) were co-cultured with mice primary sensory neurons from dorsal root ganglia (DRG). Breast can-cer cells were found to attach to neurons and have higher migration speed and prolifera-tion rate. Species-specific RNA sequencing highlighted cell migration and adhesion among the most upregulated pathways for cancer cells in coculture. We identified a novel mechanism where cancer’s PlexinB3 interacted with neuron’s Sema5A to regulate attachment and migration along nerve fibers. These findings demonstrate that sensory nerves induced a drastic shift in TNBC cells gene expression, and that dirupting the nerve-cancer is a viable strategy to impede metastasis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE180508 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA748434 https://www.ebi.ac.uk/ena/browser/view/PRJNA748434 https://www.ncbi.nlm.nih.gov/sra?term=SRP329161 [Overal design]Bulk RNA-seq of human TNBC cells and mouse DRG neurons in coculture; [Treatment]'MDA-MB-231-GFP cells were added on D3 of DRG seeding. Control 231 cells were seeded on PDL/laminin coated glass bottom wells. Same neuronal media was used'; [Growth]'DRGs were dissected, isolated into single cell and seeded on PDL/laminin coated glass bottom wells. Media used: Neurobasal, 2% B27, 1% Glutamax, 1% Antibiotic-Antimycotic, 25ng/ml NGF, 10ng/ml GDNF'; [Extraction]'Lysates were prepared using Quick-RNA miniprep kit (R1057, Zymo Research)\nRNA libraries were prepared for sequencing using standard Illumina protocols (TruSeq stranded mRNA)'; [Cell type]'Source: ''cell line: MDA-MB-231-GFP; strain: N/A; age: N/A; tissue: N/A; treatment: untreated; ', 'cell line: N/A; strain: SW-F; age: 7 weeks; tissue: Dorsal root ganglia; treatment: untreated; ', 'cell line: MDA-MB-231-GFP; strain: N/A; age: N/A; tissue: N/A; treatment: cultured in DRG conditioned media; ', 'cell line: MDA-MB-231-GFP; strain: SW-F; age: 7 weeks; tissue: Dorsal root ganglia; treatment: co-cultured with DRG; ' GSE32394 Homo sapiens 19 Expression profiling by array GPL11097 Two types of estrogen receptor-positive (ER+) and -negative (ER-) breast cancer will be compared with glycan structure analyses 2011-09-26 ER+ve and ER-ve breast cancers tend to show different patterns of metastasis, with ER+ve tumours having a propensity to metastasize to the bone while ER-ve tumours tend to induce visceral metastasis. Glycans can play an important role in metastasis through their interactions with glycan binding proteins. Moreover we, and others have also shown that expression of particular tumor-associated glycoforms of the mucin MUC1, allows it to interact with lectins of the immune system. We now have data showing differences in the level of expression of some glycosyltransferases in ER+ve and ER-ve of breast cancer suggesting the expression of different O-linked glycoforms. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32394 Selectin ligand sialyl-Lewis x antigen drives metastasis of hormone-dependent breast cancers. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-11-1139 {Cancer research (8.378): 10.1158/0008-5472.CAN-11-1139} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA147945 https://www.ebi.ac.uk/ena/browser/view/PRJNA147945 None [Overal design]RNA will be isolated from ER+ve and ER-ve primary breast cancers supplied by the Guy’s and St Thomas’ Research Breast Tissue Bank. Tumor tissue will be macro-dissected from thick cryostat sections by visual comparison with a representative H&E section. We will verify the level of expression of ER and document the expression of ST3Gal-I and ST6GalNAc-II by RT-qPCR. We have already isolated RNA from a number of tumours and shown we can obtain RNA of good quality with a RNA integrity number, as measured with an Agilent Bioanalyser, of >4.5 Since there is likely to be variability among primary tumors, ideally we analyzed of 10 ER negative and 9 ER positive tumours.; [Treatment]'None'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''Sex: female; estrogen receptor status: ER+; disease state: Breast Cancer; ', 'Sex: female; estrogen receptor status: ER-; disease state: Breast Cancer; ', 'Sex: unknown; estrogen receptor status: ER-; disease state: Breast Cancer; ' GSE95304 Homo sapiens 20 Expression profiling by high throughput sequencing GPL11154 Systematic Functional Perturbations Uncover a Prognostic Genetic Network Driving Human Breast Cancer [RNA-Seq] 2017-02-23 Gene-expression patterns of primary breast cancers aid clinicians in predicting the risk of metastatic disease. Some prognostic signatures have recently been prospectively validated, highlighting their clinical value. Such classifiers conceivably comprise biomarker genes that, in fact, functionally contribute to the oncogenic and metastatic properties of the tumors, but this has not been investigated systematically. We previously reported that the transcription factor Fra-1 not only has an essential role in breast cancer, but also drives the expression of a highly prognostic gene set. Here, we systematically perturbed the function of 31 individual Fra-1-dependent poor-prognosis genes and examined their impact on breast cancer growth in vivo. Because of the considerable number of genes in this gene set, we anticipated that the contribution of single genes to breast cancer progression would be limited. In contrast, we find that stable shRNA depletion of each of nine individual signature genes strongly inhibits breast cancer growth and aggressiveness. Several factors within this nine-gene set regulate each other's expression, suggesting that together they form a network. The nine-gene set is regulated by estrogen, ERBB2 and EGF signaling, all established breast cancer factors. We also uncover three transcription factors, MYC, E2F1 and TP53, which act alongside Fra-1 at the core of this network. ChIP-Seq analysis reveals that a substantial number of genes are bound, and regulated, by all four transcription factors. The nine-gene set retains significant prognostic power and includes several potential therapeutic targets, including the bifunctional enzyme PAICS, which catalyzes purine biosynthesis. Depletion of PAICS largely cancelled breast cancer expansion, exemplifying a prognostic gene with breast cancer activity. Our data uncover a core genetic and prognostic network driving human breast cancer. We propose that pharmacological inhibition of components within this network, such as PAICS, may be used in conjunction with the Fra-1 prognostic classifier towards personalized management of poor prognosis breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95304 Systematic functional perturbations uncover a prognostic genetic network driving human breast cancer. Oncotarget None https://doi.org/10.18632/oncotarget.16244 {Oncotarget (None): 10.18632/oncotarget.16244} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA376601 https://www.ebi.ac.uk/ena/browser/view/PRJNA376601 https://www.ncbi.nlm.nih.gov/sra?term=SRP100645 [Overal design]RNA-Seq experiment to examine mRNA levels in metastatic breast cancer cell line (MDA-MB-231 LM2) after treatment with shRNA for scrambled control or shRNA for transcription factors for FOSL1 (Fra-1), E2F1, TP53, MYC, or EZH2 (two biological replicates for each gene and control); [Treatment]'Vectors containing a scrambled sequence or a shRNA targeting luficerase gene (Sigma) were used. References of pLKO.1 vectors used in experiments are listed in Supplementary Table 1. Lentiviral particles were produced by transfection of the HEK293T cell line and supernatants were collected 48 h after transfection. Supernatants were used to infect sub-confluent cultures in the presence of 5 ug/ml polybrene overnight. Puromycin (2 ug/ml) was then used to select for stable cell lines.'; [Growth]"MDA-MB-231 LM2 cells (an MDA-MB-231 derivative that specifically metastasizes to the lung, known as LM2, obtained by Minn et al. Nature, 2005) were cultured in Dulbecco's Modified Eagle Medium, supplied with l-glutamine (1%), PenStrep(1%), and FBS (10%) (all Gibco, Life technologies)."; [Extraction]'~5 x 106 cells were harvested and RNA was extracted from exponentially growing cells using TRIzol reagent (Life Technologies).\nLibraries were prepared for sequencing using standard Illumina TrueSeq protocols. Libraries were pooled and sequenced 51 bp on a HiSeq2000.'; [Cell type]'metastatic breast cancer''cell line: MDA-MB-231 LM2; cell type: metastatic breast cancer; treatment: shScramble; ', 'cell line: MDA-MB-231 LM2; cell type: metastatic breast cancer; treatment: shFra1; ', 'cell line: MDA-MB-231 LM2; cell type: metastatic breast cancer; treatment: shMYC; ', 'cell line: MDA-MB-231 LM2; cell type: metastatic breast cancer; treatment: shE2F1; ', 'cell line: MDA-MB-231 LM2; cell type: metastatic breast cancer; treatment: shTP53; ', 'cell line: MDA-MB-231 LM2; cell type: metastatic breast cancer; treatment: shEZH2; ' GSE51999 Homo sapiens 41 Expression profiling by array GPL4133 Phosphatome profiling of estrogen receptor negative breast cancer 2013-11-01 Purpose: To characterize the expression of phosphatases in estrogen receptor negative breast cancer Little is known about the role of phosphatases in the major estrogen receptor negative breast cancer phenotypes (i.e. those overexpressing ERBB2 and the triple negative). We carried out microarray phosphatome profiling in 41 estrogen receptor negative (ER-) breast cancer patients (as determined by immunohistochemistry (IHC)) containing both ERBB2+ and ERBB2- in order to characterize the differences between these groups by Statistical Analysis of Microarrays (SAM). Our findings point to the importance of the MAPK and PI3K pathways in ER- BCs as some of the most differentially expressed phosphatases (like DUSP4 and DUSP6) share ERK as substrate, or regulate the PI3K pathway (INPP4B, PTEN). These observations are also confirmed by pathway and GSEA analysis. It is shown that both ER- ERBB2+ and triple negative breast cancers have a distinctive pattern of phosphatase RNA expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE51999 Microarray phosphatome profiling of breast cancer patients unveils a complex phosphatase regulatory role of the MAPK and PI3K pathways in estrogen receptor-negative breast cancers. International journal of oncology 3.571 https://doi.org/10.3892/ijo.2014.2648 {International journal of oncology (3.571): 10.3892/ijo.2014.2648} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA226662 https://www.ebi.ac.uk/ena/browser/view/PRJNA226662 None [Overal design]Surgical specimens from primary breast cancers that were estrogen receptor negative according to immunohistochemistry; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted with Rneasy columns (QIAGEN)'; [Cell type]'Source: ''gender: Female; erbb2 status (by ihc): Negative; age: 53; tumor grade: G3; tumor diameter: 65; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 54; tumor grade: G3; tumor diameter: 27; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 65; tumor grade: G3; tumor diameter: 20; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 80; tumor grade: G2; tumor diameter: 21; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 73; tumor grade: G2; tumor diameter: 25; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 44; tumor grade: G2; tumor diameter: 25; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 69; tumor grade: G3; tumor diameter: 30; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 78; tumor grade: G3; tumor diameter: 22; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 66; tumor grade: G3; tumor diameter: 22; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 72; tumor grade: G2; tumor diameter: 25; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 58; tumor grade: NA; tumor diameter: 42; ', 'reference composition: 10 human tumor cell lines; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 80; tumor grade: G3; tumor diameter: 18; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 62; tumor grade: G3; tumor diameter: 24; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 34; tumor grade: NA; tumor diameter: 14; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 36; tumor grade: G2; tumor diameter: 75; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 53; tumor grade: G3; tumor diameter: 40; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 68; tumor grade: G3; tumor diameter: 40; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 73; tumor grade: G3; tumor diameter: 17; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 38; tumor grade: G3; tumor diameter: 25; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 51; tumor grade: G2; tumor diameter: 30; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 59; tumor grade: G3; tumor diameter: 25; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 61; tumor grade: G3; tumor diameter: 55; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 51; tumor grade: G3; tumor diameter: 30; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 55; tumor grade: G3; tumor diameter: 40; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 67; tumor grade: G3; tumor diameter: 25; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 66; tumor grade: NA; tumor diameter: 60; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 61; tumor grade: G2; tumor diameter: 20; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 46; tumor grade: G3; tumor diameter: 30; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 58; tumor grade: G3; tumor diameter: 33; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 78; tumor grade: G2; tumor diameter: 17; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 77; tumor grade: G2; tumor diameter: 30; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 78; tumor grade: G3; tumor diameter: 25; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 69; tumor grade: G2; tumor diameter: 24; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 62; tumor grade: G2; tumor diameter: 30; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 65; tumor grade: G3; tumor diameter: 30; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 58; tumor grade: G3; tumor diameter: 28; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 65; tumor grade: G2; tumor diameter: 19; ', 'gender: Female; erbb2 status (by ihc): Negative; age: 47; tumor grade: G3; tumor diameter: 20; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 50; tumor grade: G1; tumor diameter: 23; ', 'gender: Female; erbb2 status (by ihc): Positive; age: 66; tumor grade: G2; tumor diameter: 20; ', 'gender: Female; erbb2 status (by ihc): NA; age: 54; tumor grade: NA; tumor diameter: 30; ' GSE40056 synthetic construct 12 Non-coding RNA profiling by array GPL8786 A systematic evaluation of miRNA: mRNA interactions involved in the migration and invasion of breast cancer cells [miRNA Array] 2012-08-11 In this study we performed a systematic evaluation of functional miRNA-mRNA interactions associated with the aggressiveness of breast cancer cells using a combination of integrated miRNA and mRNA expression profiling, bioinformatics prediction, and functional assays. Analysis of the miRNA expression identified 11 miRNAs that were differentially expressed, including 7 down-regulated (miR-200c, miR-205, miR-203, miR-141, miR-34a, miR-183, and miR-375) and 4 up-regulated miRNAs (miR-146a, miR-138, miR-125b1 and miR-100), in aggressive cell lines when compared to normal and less aggressive cell lines. Transient overexpression of miR-200c, miR-205, and miR-375 in MDA-MB-231 cells led to the inhibition of cell migration and invasion. The integrated analysis of miRNA and mRNA expression identified 35 known and novel target genes of miR-200c, miR-205, and mir-375, including CFL2, LAMC1, TIMP2, ZEB1, CDH11, PRKCA, PTPRJ, PTPRM, LDHB, and SEC23A. Surprisingly, the majority of these genes (27 genes) were target genes of miR-200c, suggesting that it plays a more important role in regulating the aggressiveness of breast cancer cells. We characterized one of the target genes of miR-200c, CFL2, and demonstrated that CFL2 is overexpressed in aggressive breast cancer cell lines and can be significantly down-regulated by exogenous miR-200c. Tissue microarray analysis further revealed that CFL2 expression in primary breast cancer tissue correlated with tumor grade. To our knowledge, this study is the first systematic screening of functional miRNA target genes in aggressive breast cancer cells. The results obtained from this study may improve our understanding of the role of these candidate miRNAs and their target genes in relation to breast cancer aggressiveness and ultimately lead to the identification of novel biomarkers associated with prognosis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE40056 A systematic evaluation of miRNA:mRNA interactions involved in the migration and invasion of breast cancer cells. Journal of translational medicine 4.098 https://doi.org/10.1186/1479-5876-11-57 {Journal of translational medicine (4.098): 10.1186/1479-5876-11-57} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA172635 https://www.ebi.ac.uk/ena/browser/view/PRJNA172635 None [Overal design]Affymetrix miRNA 1.0 arrays were performed according to the manufacturer's directions on small RNA extracted from 12 breast cancer cell lines including 4 aggressive cell lines, 6 less aggressive cell lines and 2 imortalized breast epithelium cell lines; [Treatment]'none'; [Growth]'Breast cancer cell lines BT474, MDA-MB-468, T47D, ZR-75-1, MCF7, SK-BR3, MDA-MB-231, HS578T, BT549, SUM159 cell line were cultured in DMEM media with 10% fetal bovine serum (FBS). Immortalized breast epithelium cell lines MCF10A and MCF12A were cultured in DMEM/F12 supplemented with 5% horse serum, 20 ng/mL EGF, 10 μg/mL insulin, 100 ng/ml cholera toxin, and 500 ng/ml hydrocortisone.'; [Extraction]'Total RNA was extracted using the QiazolTM Lysis reagent (Qiagen, Valencia, CA, USA). Small molecular weight RNA was extracted using the mirVanaTM miRNA Isolation Kit (Invitrogen, Carlsbad, CA, USA) according to the manufacturer’s protocol.'; [Cell type]'Breast cancer cells', 'Immortalized breast epithelium cells''cell line: BT474; tissue: breast; cell line type: Less-aggressive cell line; cell type: Breast cancer cells; molecule subtype: small RNA; ', 'cell line: MDA-MB-468; tissue: breast; cell line type: Less-aggressive cell line; cell type: Breast cancer cells; molecule subtype: small RNA; ', 'cell line: T47D; tissue: breast; cell line type: Less-aggressive cell line; cell type: Breast cancer cells; molecule subtype: small RNA; ', 'cell line: ZR-75-1; tissue: breast; cell line type: Less-aggressive cell line; cell type: Breast cancer cells; molecule subtype: small RNA; ', 'cell line: MCF7; tissue: breast; cell line type: Less-aggressive cell line; cell type: Breast cancer cells; molecule subtype: small RNA; ', 'cell line: SK-BR3; tissue: breast; cell line type: Less-aggressive cell line; cell type: Breast cancer cells; molecule subtype: small RNA; ', 'cell line: MDA-MB-231; tissue: breast; cell line type: Aggressive cell line; cell type: Breast cancer cells; molecule subtype: small RNA; ', 'cell line: HS578T; tissue: breast; cell line type: Aggressive cell line; cell type: Breast cancer cells; molecule subtype: small RNA; ', 'cell line: BT549; tissue: breast; cell line type: Aggressive cell line; cell type: Breast cancer cells; molecule subtype: small RNA; ', 'cell line: SUM159; tissue: breast; cell line type: Aggressive cell line; cell type: Breast cancer cells; molecule subtype: small RNA; ', 'cell line: MCF10A; tissue: breast; cell line type: Immortalized breast epithelium cell line; cell type: Immortalized breast epithelium cells; molecule subtype: small RNA; ', 'cell line: MCF12A; tissue: breast; cell line type: Immortalized breast epithelium cell line; cell type: Immortalized breast epithelium cells; molecule subtype: small RNA; ' GSE42568 Homo sapiens 121 Expression profiling by array GPL570 Breast Cancer Gene Expression Analysis 2012-11-27 Analysis of 104 breast cancer biopsies (removed prior to any treatment with tamoxifen or chemotherapeutic agents) from patients aged between 31 years and 89 years at the time of diagnosis (mean age = 58 years). Twenty were less than 50 years and seventy-seven women were 50 years, or older, at diagnosis. The size of the tumours ranged between 0.6 cm and 8.0 cm (mean = 2.79 cm). Eighteen tumours were T1 (<2 cm) in maximal dimension; 83 were T2 (2–5 cm) and 3 tumours were T3 (>5 cm). Eighty-two were invasive ductal carcinoma, 17 were invasive lobular and five were tumours of special type (two tubular and three mucinous). Eleven tumours were grade 1; 40 were grade 2; and 53 were grade 3. Sixty-seven tumours were oestrogen receptor (ER) positive and 34 were ER negative (ER status was determined by Enzyme Immuno-Assay (EIA); a positive result was defined as more than 200 fmol/g protein). ER status was not available for 3 patients. Forty-five tumours had no axillary metastases and 59 tumours had metastasised to axillary lymph nodes. Sixty-nine women were treated with post-operative tamoxifen; 26 did not receive tamoxifen. Fifty patients were treated with adjuvant systemic chemotherapy (CMF +/− adriamycin); 45 patients did not receive chemotherapy. Details regarding tamoxifen and systemic chemotherapy were not available for 9 patients. Maximal follow-up was 3,026 days with a mean follow-up of 1,887 days. 17 normal breast tissues were also assayed. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE42568 Correlating transcriptional networks to breast cancer survival: a large-scale coexpression analysis. Carcinogenesis 4.004 https://doi.org/10.1093/carcin/bgt208 {Carcinogenesis (4.004): 10.1093/carcin/bgt208} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA182286 https://www.ebi.ac.uk/ena/browser/view/PRJNA182286 None [Overal design]Gene expression profiling of 104 breast cancer and 17 normal breast biopsies.; [Treatment]'Tissues were stored at -70°C/-80°C prior to RNA isolation.'; [Growth]'None'; [Extraction]"Samples were homogenised, on ice, in 1 ml TriReagent (Sigma; Poole, UK) and total RNA was subsequently isolated according to the manufacturer's instructions. RNA quantity and purity were assessed at 260 nm and 280 nm using a Nanodrop (ND-1000; Labtech. International); an Agilent Bioanalyser (Agilent 2100; Agilent Technologies) was used to assess RNA qualitatively after isolation and, subsequently, following biotin-labelling and after fragmentation."; [Cell type]'Source: ''tissue: normal breast; age: NA; er_status: NA; size: NA; grade: NA; lymph node status: NA; relapse free survival time_days: NA; relapse free survival event: NA; overall survival time_days: NA; overall survival event: NA; ', 'tissue: breast cancer; age: 74.03; er_status: 1; size: 0.6; grade: 2; lymph node status: 1; relapse free survival time_days: 3026; relapse free survival event: 0; overall survival time_days: 3026; overall survival event: 0; ', 'tissue: breast cancer; age: 67.26; er_status: 1; size: 5; grade: 2; lymph node status: 1; relapse free survival time_days: 755; relapse free survival event: 1; overall survival time_days: 755; overall survival event: 1; ', 'tissue: breast cancer; age: 53.35; er_status: 1; size: 3.5; grade: 1; lymph node status: 0; relapse free survival time_days: 3014; relapse free survival event: 0; overall survival time_days: 3014; overall survival event: 0; ', 'tissue: breast cancer; age: 43.72; er_status: 1; size: 1.5; grade: 3; lymph node status: 1; relapse free survival time_days: 406; relapse free survival event: 1; overall survival time_days: 1726; overall survival event: 1; ', 'tissue: breast cancer; age: 51.47; er_status: 0; size: 2.7; grade: 3; lymph node status: 0; relapse free survival time_days: 2225; relapse free survival event: 0; overall survival time_days: 2225; overall survival event: 0; ', 'tissue: breast cancer; age: 42.49; er_status: 0; size: 5; grade: 3; lymph node status: 1; relapse free survival time_days: 252; relapse free survival event: 1; overall survival time_days: 285; overall survival event: 1; ', 'tissue: breast cancer; age: 52.01; er_status: 0; size: 2.5; grade: 3; lymph node status: 0; relapse free survival time_days: 2138; relapse free survival event: 0; overall survival time_days: 2138; overall survival event: 0; ', 'tissue: breast cancer; age: 43.4; er_status: 1; size: 1; grade: 2; lymph node status: 0; relapse free survival time_days: 2449; relapse free survival event: 0; overall survival time_days: 2449; overall survival event: 0; ', 'tissue: breast cancer; age: 45.86; er_status: 0; size: 1.8; grade: 3; lymph node status: 0; relapse free survival time_days: 2080; relapse free survival event: 1; overall survival time_days: 2456; overall survival event: 1; ', 'tissue: breast cancer; age: 78.6; er_status: 1; size: 2.3; grade: 2; lymph node status: 1; relapse free survival time_days: 346; relapse free survival event: 1; overall survival time_days: 420; overall survival event: 1; ', 'tissue: breast cancer; age: 56.89; er_status: 0; size: 3.5; grade: 3; lymph node status: 0; relapse free survival time_days: 1110; relapse free survival event: 1; overall survival time_days: 1110; overall survival event: 1; ', 'tissue: breast cancer; age: 54.36; er_status: 0; size: 4; grade: 3; lymph node status: 1; relapse free survival time_days: 332; relapse free survival event: 1; overall survival time_days: 488; overall survival event: 1; ', 'tissue: breast cancer; age: 49.03; er_status: 0; size: 8; grade: 3; lymph node status: 1; relapse free survival time_days: 368; relapse free survival event: 1; overall survival time_days: 2718; overall survival event: 0; ', 'tissue: breast cancer; age: 51.46; er_status: 0; size: 2.5; grade: 3; lymph node status: 1; relapse free survival time_days: 362; relapse free survival event: 1; overall survival time_days: 767; overall survival event: 1; ', 'tissue: breast cancer; age: 63.88; er_status: 0; size: 3; grade: 2; lymph node status: 1; relapse free survival time_days: 1216; relapse free survival event: 1; overall survival time_days: 1216; overall survival event: 1; ', 'tissue: breast cancer; age: 43.89; er_status: 0; size: 1; grade: 3; lymph node status: 1; relapse free survival time_days: 2462; relapse free survival event: 0; overall survival time_days: 2462; overall survival event: 0; ', 'tissue: breast cancer; age: 76.49; er_status: 1; size: 3; grade: 3; lymph node status: 1; relapse free survival time_days: 888; relapse free survival event: 1; overall survival time_days: 1862; overall survival event: 1; ', 'tissue: breast cancer; age: 68.57; er_status: 1; size: 2.3; grade: 3; lymph node status: 1; relapse free survival time_days: 212; relapse free survival event: 1; overall survival time_days: 1223; overall survival event: 1; ', 'tissue: breast cancer; age: 82.14; er_status: 1; size: 1.5; grade: 1; lymph node status: 0; relapse free survival time_days: 3019; relapse free survival event: 0; overall survival time_days: 3019; overall survival event: 0; ', 'tissue: breast cancer; age: 73.05; er_status: 1; size: 3; grade: 3; lymph node status: 1; relapse free survival time_days: 155; relapse free survival event: 1; overall survival time_days: 155; overall survival event: 1; ', 'tissue: breast cancer; age: 77.3; er_status: 1; size: 1.5; grade: 1; lymph node status: 0; relapse free survival time_days: 947; relapse free survival event: 0; overall survival time_days: 947; overall survival event: 0; ', 'tissue: breast cancer; age: 65.07; er_status: 0; size: 4.5; grade: 3; lymph node status: 1; relapse free survival time_days: 552; relapse free survival event: 1; overall survival time_days: 552; overall survival event: 1; ', 'tissue: breast cancer; age: 47.59; er_status: 0; size: 5; grade: 2; lymph node status: 1; relapse free survival time_days: 1641; relapse free survival event: 1; overall survival time_days: 2903; overall survival event: 0; ', 'tissue: breast cancer; age: 57.59; er_status: 0; size: 2.5; grade: 3; lymph node status: 1; relapse free survival time_days: 2438; relapse free survival event: 0; overall survival time_days: 2438; overall survival event: 0; ', 'tissue: breast cancer; age: 38.6; er_status: 1; size: 3; grade: 3; lymph node status: 0; relapse free survival time_days: 1627; relapse free survival event: 0; overall survival time_days: 1627; overall survival event: 0; ', 'tissue: breast cancer; age: 49.59; er_status: 1; size: 3; grade: 3; lymph node status: 1; relapse free survival time_days: 1224; relapse free survival event: 1; overall survival time_days: 1708; overall survival event: 1; ', 'tissue: breast cancer; age: 80.3; er_status: 0; size: 2; grade: 3; lymph node status: 0; relapse free survival time_days: 2237; relapse free survival event: 0; overall survival time_days: 2237; overall survival event: 0; ', 'tissue: breast cancer; age: 58.52; er_status: 1; size: 2.5; grade: 3; lymph node status: 1; relapse free survival time_days: 845; relapse free survival event: 1; overall survival time_days: 845; overall survival event: 1; ', 'tissue: breast cancer; age: 46.08; er_status: 0; size: 3.5; grade: 2; lymph node status: 1; relapse free survival time_days: 602; relapse free survival event: 1; overall survival time_days: 2957; overall survival event: 0; ', 'tissue: breast cancer; age: 50.62; er_status: 0; size: 5; grade: 3; lymph node status: 1; relapse free survival time_days: 577; relapse free survival event: 1; overall survival time_days: 913; overall survival event: 1; ', 'tissue: breast cancer; age: 50.62; er_status: 1; size: 3.5; grade: 3; lymph node status: 1; relapse free survival time_days: 138; relapse free survival event: 1; overall survival time_days: 138; overall survival event: 1; ', 'tissue: breast cancer; age: 42.95; er_status: 0; size: 5.5; grade: 3; lymph node status: 1; relapse free survival time_days: 459; relapse free survival event: 1; overall survival time_days: 1058; overall survival event: 1; ', 'tissue: breast cancer; age: 73.38; er_status: 0; size: 1.5; grade: 2; lymph node status: 0; relapse free survival time_days: 2759; relapse free survival event: 0; overall survival time_days: 2759; overall survival event: 0; ', 'tissue: breast cancer; age: 53.75; er_status: 1; size: 3.5; grade: 3; lymph node status: 1; relapse free survival time_days: 2405; relapse free survival event: 1; overall survival time_days: 2764; overall survival event: 0; ', 'tissue: breast cancer; age: 72.74; er_status: 1; size: 3.5; grade: 3; lymph node status: 1; relapse free survival time_days: 1157; relapse free survival event: 1; overall survival time_days: 1157; overall survival event: 1; ', 'tissue: breast cancer; age: 54.6; er_status: 1; size: 3; grade: 3; lymph node status: 0; relapse free survival time_days: 546; relapse free survival event: 0; overall survival time_days: 546; overall survival event: 0; ', 'tissue: breast cancer; age: 53.28; er_status: 1; size: 3; grade: 2; lymph node status: 0; relapse free survival time_days: 2582; relapse free survival event: 0; overall survival time_days: 2582; overall survival event: 0; ', 'tissue: breast cancer; age: 54.69; er_status: 1; size: 2.3; grade: 3; lymph node status: 1; relapse free survival time_days: 2460; relapse free survival event: 0; overall survival time_days: 2460; overall survival event: 0; ', 'tissue: breast cancer; age: 48.01; er_status: 1; size: 4; grade: 3; lymph node status: 1; relapse free survival time_days: 978; relapse free survival event: 1; overall survival time_days: 1338; overall survival event: 1; ', 'tissue: breast cancer; age: 60.12; er_status: 1; size: 1.5; grade: 1; lymph node status: 0; relapse free survival time_days: 2626; relapse free survival event: 0; overall survival time_days: 2626; overall survival event: 0; ', 'tissue: breast cancer; age: 52.82; er_status: 1; size: 2; grade: 3; lymph node status: 1; relapse free survival time_days: 2948; relapse free survival event: 0; overall survival time_days: 2948; overall survival event: 0; ', 'tissue: breast cancer; age: 62.81; er_status: 0; size: 2.5; grade: 2; lymph node status: 0; relapse free survival time_days: 2416; relapse free survival event: 0; overall survival time_days: 2416; overall survival event: 0; ', 'tissue: breast cancer; age: 43.48; er_status: NA; size: 2; grade: 3; lymph node status: 1; relapse free survival time_days: 124; relapse free survival event: 1; overall survival time_days: 194; overall survival event: 1; ', 'tissue: breast cancer; age: 72.49; er_status: 1; size: 2; grade: 2; lymph node status: 0; relapse free survival time_days: 2897; relapse free survival event: 0; overall survival time_days: 2897; overall survival event: 0; ', 'tissue: breast cancer; age: 54.34; er_status: 0; size: 2; grade: 2; lymph node status: 0; relapse free survival time_days: 2899; relapse free survival event: 0; overall survival time_days: 2899; overall survival event: 0; ', 'tissue: breast cancer; age: 73.68; er_status: 1; size: 2.2; grade: 3; lymph node status: 1; relapse free survival time_days: 2829; relapse free survival event: 0; overall survival time_days: 2829; overall survival event: 0; ', 'tissue: breast cancer; age: 78.8; er_status: 1; size: 3; grade: 2; lymph node status: 0; relapse free survival time_days: 2561; relapse free survival event: 1; overall survival time_days: 2785; overall survival event: 0; ', 'tissue: breast cancer; age: 74.34; er_status: 1; size: 2.5; grade: 2; lymph node status: 0; relapse free survival time_days: 2740; relapse free survival event: 0; overall survival time_days: 2740; overall survival event: 0; ', 'tissue: breast cancer; age: 74.02; er_status: 1; size: 3; grade: 1; lymph node status: 0; relapse free survival time_days: 1235; relapse free survival event: 0; overall survival time_days: 1235; overall survival event: 0; ', 'tissue: breast cancer; age: 75.15; er_status: 1; size: 2; grade: 2; lymph node status: 0; relapse free survival time_days: 2092; relapse free survival event: 1; overall survival time_days: 2092; overall survival event: 1; ', 'tissue: breast cancer; age: 67.83; er_status: 1; size: 2.5; grade: 2; lymph node status: 1; relapse free survival time_days: 2535; relapse free survival event: 0; overall survival time_days: 2535; overall survival event: 0; ', 'tissue: breast cancer; age: 50.21; er_status: 1; size: 2; grade: 2; lymph node status: 1; relapse free survival time_days: 2211; relapse free survival event: 0; overall survival time_days: 2211; overall survival event: 0; ', 'tissue: breast cancer; age: 69.58; er_status: 1; size: 1.5; grade: 2; lymph node status: 0; relapse free survival time_days: 2275; relapse free survival event: 1; overall survival time_days: 2275; overall survival event: 1; ', 'tissue: breast cancer; age: 31.06; er_status: 0; size: 2; grade: 3; lymph node status: 1; relapse free survival time_days: 390; relapse free survival event: 1; overall survival time_days: 390; overall survival event: 1; ', 'tissue: breast cancer; age: 71.06; er_status: 1; size: 2; grade: 3; lymph node status: 0; relapse free survival time_days: 2184; relapse free survival event: 0; overall survival time_days: 2184; overall survival event: 0; ', 'tissue: breast cancer; age: 60.72; er_status: 1; size: 3; grade: 3; lymph node status: 1; relapse free survival time_days: 436; relapse free survival event: 1; overall survival time_days: 919; overall survival event: 1; ', 'tissue: breast cancer; age: 65.08; er_status: 0; size: 2.8; grade: 3; lymph node status: 1; relapse free survival time_days: 634; relapse free survival event: 1; overall survival time_days: 917; overall survival event: 0; ', 'tissue: breast cancer; age: 67.24; er_status: 1; size: 2; grade: 2; lymph node status: 1; relapse free survival time_days: 2758; relapse free survival event: 0; overall survival time_days: 2758; overall survival event: 0; ', 'tissue: breast cancer; age: 56.88; er_status: 1; size: 2; grade: 3; lymph node status: 1; relapse free survival time_days: 977; relapse free survival event: 0; overall survival time_days: 977; overall survival event: 0; ', 'tissue: breast cancer; age: 69.42; er_status: 1; size: 1.5; grade: 2; lymph node status: 0; relapse free survival time_days: 365; relapse free survival event: 1; overall survival time_days: 1997; overall survival event: 0; ', 'tissue: breast cancer; age: 65.68; er_status: 1; size: 2.5; grade: 2; lymph node status: 1; relapse free survival time_days: 1854; relapse free survival event: 0; overall survival time_days: 1854; overall survival event: 0; ', 'tissue: breast cancer; age: 61.42; er_status: 0; size: 2; grade: 3; lymph node status: 0; relapse free survival time_days: 1793; relapse free survival event: 0; overall survival time_days: 1793; overall survival event: 0; ', 'tissue: breast cancer; age: 46.97; er_status: 0; size: 3; grade: 3; lymph node status: 1; relapse free survival time_days: 545; relapse free survival event: 1; overall survival time_days: 545; overall survival event: 1; ', 'tissue: breast cancer; age: 52.26; er_status: 0; size: 1.5; grade: 3; lymph node status: 1; relapse free survival time_days: 725; relapse free survival event: 1; overall survival time_days: 1409; overall survival event: 1; ', 'tissue: breast cancer; age: 56.1; er_status: 1; size: 3; grade: 1; lymph node status: 1; relapse free survival time_days: 2943; relapse free survival event: 0; overall survival time_days: 2943; overall survival event: 0; ', 'tissue: breast cancer; age: 59.56; er_status: 1; size: 3.5; grade: 3; lymph node status: 1; relapse free survival time_days: 421; relapse free survival event: 1; overall survival time_days: 1044; overall survival event: 1; ', 'tissue: breast cancer; age: 50.94; er_status: 1; size: 3; grade: 3; lymph node status: 0; relapse free survival time_days: 2489; relapse free survival event: 0; overall survival time_days: 2489; overall survival event: 0; ', 'tissue: breast cancer; age: 75.81; er_status: NA; size: 2.2; grade: 3; lymph node status: 0; relapse free survival time_days: 1332; relapse free survival event: 1; overall survival time_days: 1332; overall survival event: 1; ', 'tissue: breast cancer; age: 59; er_status: 1; size: 3.5; grade: 3; lymph node status: 1; relapse free survival time_days: 755; relapse free survival event: 1; overall survival time_days: 1915; overall survival event: 1; ', 'tissue: breast cancer; age: 48.27; er_status: 1; size: 3.5; grade: 3; lymph node status: 1; relapse free survival time_days: 1950; relapse free survival event: 0; overall survival time_days: 1950; overall survival event: 0; ', 'tissue: breast cancer; age: 38.9; er_status: 1; size: 3; grade: 2; lymph node status: 1; relapse free survival time_days: 276; relapse free survival event: 1; overall survival time_days: 1080; overall survival event: 1; ', 'tissue: breast cancer; age: 46.59; er_status: 1; size: 1; grade: 2; lymph node status: 0; relapse free survival time_days: 2266; relapse free survival event: 0; overall survival time_days: 2266; overall survival event: 0; ', 'tissue: breast cancer; age: 48.84; er_status: 0; size: 2; grade: 3; lymph node status: 0; relapse free survival time_days: 1692; relapse free survival event: 0; overall survival time_days: 1692; overall survival event: 0; ', 'tissue: breast cancer; age: 47.39; er_status: 0; size: 4; grade: 2; lymph node status: 0; relapse free survival time_days: 2302; relapse free survival event: 0; overall survival time_days: 2302; overall survival event: 0; ', 'tissue: breast cancer; age: 67.7; er_status: 0; size: 2.5; grade: 3; lymph node status: 1; relapse free survival time_days: 365; relapse free survival event: 1; overall survival time_days: 365; overall survival event: 1; ', 'tissue: breast cancer; age: 46.31; er_status: 0; size: 2.5; grade: 2; lymph node status: 0; relapse free survival time_days: 2211; relapse free survival event: 0; overall survival time_days: 2211; overall survival event: 0; ', 'tissue: breast cancer; age: 71.64; er_status: 1; size: 4; grade: 3; lymph node status: 1; relapse free survival time_days: 1980; relapse free survival event: 1; overall survival time_days: 2344; overall survival event: 0; ', 'tissue: breast cancer; age: 66.66; er_status: 1; size: 2.5; grade: 2; lymph node status: 0; relapse free survival time_days: 1864; relapse free survival event: 1; overall survival time_days: 1864; overall survival event: 0; ', 'tissue: breast cancer; age: 68.29; er_status: 1; size: 2; grade: 2; lymph node status: 0; relapse free survival time_days: 2484; relapse free survival event: 0; overall survival time_days: 2484; overall survival event: 0; ', 'tissue: breast cancer; age: 67.75; er_status: 0; size: 5; grade: 1; lymph node status: 0; relapse free survival time_days: 424; relapse free survival event: 1; overall survival time_days: 526; overall survival event: 1; ', 'tissue: breast cancer; age: 47.13; er_status: 1; size: 2; grade: 2; lymph node status: 0; relapse free survival time_days: 2955; relapse free survival event: 0; overall survival time_days: 2955; overall survival event: 0; ', 'tissue: breast cancer; age: 44.52; er_status: 0; size: 1.5; grade: 1; lymph node status: 1; relapse free survival time_days: 84; relapse free survival event: 1; overall survival time_days: 2650; overall survival event: 0; ', 'tissue: breast cancer; age: 55.89; er_status: 0; size: 4; grade: 2; lymph node status: 0; relapse free survival time_days: 2384; relapse free survival event: 0; overall survival time_days: 2384; overall survival event: 0; ', 'tissue: breast cancer; age: 55.57; er_status: 1; size: 2.4; grade: 2; lymph node status: 0; relapse free survival time_days: 2689; relapse free survival event: 0; overall survival time_days: 2689; overall survival event: 0; ', 'tissue: breast cancer; age: 51.23; er_status: 1; size: 1.9; grade: 1; lymph node status: 0; relapse free survival time_days: 2641; relapse free survival event: 0; overall survival time_days: 2641; overall survival event: 0; ', 'tissue: breast cancer; age: 54.31; er_status: 1; size: 3.8; grade: 3; lymph node status: 0; relapse free survival time_days: 423; relapse free survival event: 0; overall survival time_days: 423; overall survival event: 0; ', 'tissue: breast cancer; age: 68.76; er_status: 1; size: 4.2; grade: 2; lymph node status: 1; relapse free survival time_days: 1682; relapse free survival event: 0; overall survival time_days: 1682; overall survival event: 0; ', 'tissue: breast cancer; age: 56.04; er_status: 1; size: 4; grade: 1; lymph node status: 1; relapse free survival time_days: 2052; relapse free survival event: 0; overall survival time_days: 2052; overall survival event: 0; ', 'tissue: breast cancer; age: 60.55; er_status: 1; size: 0.7; grade: 3; lymph node status: 1; relapse free survival time_days: 288; relapse free survival event: 1; overall survival time_days: 475; overall survival event: 0; ', 'tissue: breast cancer; age: 89.93; er_status: 1; size: 3; grade: 3; lymph node status: 0; relapse free survival time_days: 2243; relapse free survival event: 0; overall survival time_days: 2243; overall survival event: 0; ', 'tissue: breast cancer; age: 73.79; er_status: 1; size: 3.2; grade: 2; lymph node status: 0; relapse free survival time_days: 2197; relapse free survival event: 0; overall survival time_days: 2197; overall survival event: 0; ', 'tissue: breast cancer; age: 61.41; er_status: 1; size: 1.5; grade: 2; lymph node status: 1; relapse free survival time_days: 2576; relapse free survival event: 0; overall survival time_days: 2576; overall survival event: 0; ', 'tissue: breast cancer; age: 57.23; er_status: 1; size: 3; grade: 3; lymph node status: 1; relapse free survival time_days: 2556; relapse free survival event: 0; overall survival time_days: 2556; overall survival event: 0; ', 'tissue: breast cancer; age: 56.1; er_status: 1; size: 3; grade: 2; lymph node status: 0; relapse free survival time_days: 2225; relapse free survival event: 0; overall survival time_days: 2225; overall survival event: 0; ', 'tissue: breast cancer; age: 75.75; er_status: 0; size: 3; grade: 2; lymph node status: 0; relapse free survival time_days: 441; relapse free survival event: 1; overall survival time_days: 2022; overall survival event: 1; ', 'tissue: breast cancer; age: 41.17; er_status: 1; size: 2.5; grade: 3; lymph node status: 0; relapse free survival time_days: 2713; relapse free survival event: 0; overall survival time_days: 2713; overall survival event: 0; ', 'tissue: breast cancer; age: 53.07; er_status: 1; size: 2.5; grade: 3; lymph node status: 1; relapse free survival time_days: 2790; relapse free survival event: 0; overall survival time_days: 2790; overall survival event: 0; ', 'tissue: breast cancer; age: 55.95; er_status: 1; size: 3.5; grade: 2; lymph node status: 0; relapse free survival time_days: 2622; relapse free survival event: 0; overall survival time_days: 2622; overall survival event: 0; ', 'tissue: breast cancer; age: 60.39; er_status: 0; size: 6; grade: 3; lymph node status: 1; relapse free survival time_days: 634; relapse free survival event: 1; overall survival time_days: 2909; overall survival event: 0; ', 'tissue: breast cancer; age: 46.09; er_status: 1; size: 2; grade: 2; lymph node status: 1; relapse free survival time_days: 2952; relapse free survival event: 0; overall survival time_days: 2952; overall survival event: 0; ', 'tissue: breast cancer; age: 47.82; er_status: NA; size: 3; grade: 1; lymph node status: 1; relapse free survival time_days: 1209; relapse free survival event: 1; overall survival time_days: 2989; overall survival event: 0; ', 'tissue: breast cancer; age: 48.43; er_status: 1; size: 3.5; grade: 2; lymph node status: 1; relapse free survival time_days: 2105; relapse free survival event: 0; overall survival time_days: 2105; overall survival event: 0; ', 'tissue: breast cancer; age: 70.44; er_status: 1; size: 2; grade: 2; lymph node status: 1; relapse free survival time_days: 639; relapse free survival event: 1; overall survival time_days: 927; overall survival event: 1; ', 'tissue: breast cancer; age: 62.51; er_status: 1; size: 1.5; grade: 2; lymph node status: 1; relapse free survival time_days: 2962; relapse free survival event: 0; overall survival time_days: 2962; overall survival event: 0; ' GSE45133 Homo sapiens 7 Expression profiling by high throughput sequencing GPL9115; GPL11154 Breakpoint analysis of transcriptional and genomic profiles uncovers novel gene fusions spanning multiple human cancer types (RNA-seq) 2013-03-13 We report the design and implementation of a "breakpoint analysis" pipeline to discover novel gene fusions by tell-tale transcript level or genomic DNA copy number transitions occurring within genes. We use this method to prioritize candidate rearrangements from high density array CGH datasets as well as exon-resolution expression microarrays. We mine both publicly available data as well as datasets generated in our laboratory. Several gene fusion candidates were chosen for further characterization, and corresponding samples were profiled using paired end RNA sequencing to discover the identity of the gene fusion. Using this approach, we report the discovery and characterization of novel gene fusions spanning multiple cancer subtypes including angiosarcoma, pancreatic cancer, anaplastic astrocytoma, melanoma, breast cancer, and T-cell acute lymphoblastic leukemia. Taken together, this study provides a robust approach for gene fusion discovery, and our results highlight a more widespread role of fusion genes in cancer pathogenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE45133 Breakpoint analysis of transcriptional and genomic profiles uncovers novel gene fusions spanning multiple human cancer types. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1003464 {PLoS genetics (5.224): 10.1371/journal.pgen.1003464} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA192951 https://www.ebi.ac.uk/ena/browser/view/PRJNA192951 https://www.ncbi.nlm.nih.gov/sra?term=SRP019207 [Overal design]Breakpoint analysis for the discovery of novel gene fusions across human cancers; [Treatment]'No treatment performed'; [Growth]'Cell lines were cultured in RPMI + 10% FBS until 60-70% confluent. Total RNA was then harvested using the Rneasy Mini Kit (Qiagen)'; [Extraction]'mRNA Seq-8 Sample Prep Kit (Illumina)'; [Cell type]'Source: ''cell line: A172, A431, D538MG; cancer subtype: A172-GBM, A431-epidermoid carcinoma, D538MG-anaplastic astrocytoma; ', 'cell line: SUPT7, ONS76, SH-4; cancer subtype: SUPT7-TALL, ONS76-GBM, SH-4-melanoma; ', 'cell line: CHL-1, DKMG, JURKAT; cancer subtype: CHL-1-melanoma, DKMG-GBM, JURKAT-TALL; ', 'cell line: PL5; cancer subtype: pancreatic cancer; ', 'cell line: HCC1954; cancer subtype: breast cancer; ', 'cell line: BT-549; cancer subtype: breast cancer; ', 'cell line: SUPT13; cancer subtype: T-ALL; ' GSE48064 Homo sapiens 214 Genome variation profiling by SNP array GPL6801 Respective Prognostic Value of Genomic Grade and Histological Proliferation Markers in Early Stage (pN0) Breast Carcinoma 2013-06-18 Phenotypic and genomic characterization of Early Stage Breast Carcinoma using Training set (n=109) Validation set (n=105) of SNP6 arrays https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48064 Genomic instability: a stronger prognostic marker than proliferation for early stage luminal breast carcinomas. PloS one 2.776 https://doi.org/10.1371/journal.pone.0076496 {PloS one (2.776): 10.1371/journal.pone.0076496} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA209040 https://www.ebi.ac.uk/ena/browser/view/PRJNA209040 None [Overal design]Affymetrix SNP6.0 arrays were performed according to the manufacturer's directions on DNA extracted from cryopreserved breast tumoral samples.; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was extracted from tumor fragments using a standard phenol/chloroform procedure. DNA quality and quantity was assessed using a Nanodrop Spectrophotometer and agarose gel electrophoresis.'; [Cell type]'Source: ''group: validation set; tissue: breast cancer tissue; ', 'group: training set; tissue: breast cancer tissue; ' GSE102402 Homo sapiens 2 Expression profiling by array GPL6480 Posttranscriptional upregulation of HER3 by HER2 mRNA induces Trastuzumab Resistance in breast cancer 2017-08-09 To explore HER2 3’-UTR-dependent transcriptional programs, we analyzed gene-expression profiles of T47D cells transfected with HER2 3’-UTR. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE102402 Posttranscriptional upregulation of HER3 by HER2 mRNA induces trastuzumab resistance in breast cancer. Molecular cancer 10.679 https://doi.org/10.1186/s12943-018-0862-5 {Molecular cancer (10.679): 10.1186/s12943-018-0862-5} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA397673 https://www.ebi.ac.uk/ena/browser/view/PRJNA397673 None [Overal design]Comparative microarray analysis of mRNA for T47D cells transfected with pCDNA3.1-HER2 3’-UTR and pCDNA3.1 as a control was performed on Agilent Whole Human Genome Microarray.; [Treatment]'T47D cells transfected with pcDNA3.1 plasmid containing HER2 3’-UTR or the empty pcDNA3.1 vector (3.1) as a mock.'; [Growth]'T47D cell line was cultured with RPMI1640 supplemented with 10% fetal bovine serum.'; [Extraction]'Total RNA was extracted using TRIZOL Reagent (Cat#15596-018 , Life technologies, Carlsbad, CA, US) following the manufacturer’s instructions and checked for a RIN number to inspect RNA integrity by an Agilent Bioanalyzer 2100 (Agilent technologies, Santa Clara, CA, US). Qualified total RNA was further purified by RNeasy micro kit (Cat#74004, QIAGEN, GmBH, Germany) and RNase-Free DNase Set (Cat#79254, QIAGEN, GmBH, Germany).'; [Cell type]'Source: ''cell line: T47D; transfected with: pCDNA3.1-HER2 3’-UTR; ', 'cell line: T47D; transfected with: pCDNA3.1; ' GSE173839 Homo sapiens 105 Expression profiling by array GPL20078 Durvalumab with olaparib and paclitaxel for high-risk HER2-negative stage II/III breast cancer: Results from the adaptively randomized I-SPY2 platform trial 2021-05-04 Durvalumab with olaparib was one of the experimental regimens evaluated in I-SPY 2, a neoadjuvant platform trial for high risk, early stage breast cancer, and graduated in the HER2- and HR+HER2- signatures. We hypothesized that (pre-treatment) expression-based immune signatures may predict response to the immune checkpoint inhibitor durvalumab and signatures related to DNA repair deficiency (DRD) may associate with response to olaparib. In this analysis, we assessed 13 expression based signatures related to immune, DRD, proliferation and estrogen signaling as specific predictor of pathologic complete response (pCR) to durvalumab/olaparib. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE173839 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA727320 https://www.ebi.ac.uk/ena/browser/view/PRJNA727320 None [Overal design]RNA extracted from pretreatment biopsies were profiled using Agilent 44 K expression arrays (GPL20078). I-SPY2 changed biopsy requirements from fresh frozen (FF) tissue to formalin fixed paraffin embedded (FFPE) tissues in May 2018; therefore, patients on the durvalumab/olaparib arm had RNA extracted from FFPE biopsies (N=71). As microarray-based gene expression levels may differ between FF and FFPE tissues, we restricted the control set in the biomarker analysis to patients who received treatment in the control arm and had FFPE-derived gene expression data (N=34). The sample characteristics and their values represent: HER2: the status of the HER2 gene. 1 = positive; 0 = negative. HR: the status of hormone (estrogen and progesterone) receptors 1 = positive; 0 = negative. pCR: the status of a pathological complete response (pCR) 1 = complete response; 0 = failed complete response MP: MP status MammaPrint High 1: 0 ; MammaPrint (ultra)-High2: 1 . Arm: arm of the trial per patient ‘durvalumab/olaparib’; control; [Treatment]'None'; [Growth]'None'; [Extraction]'Performed by Agendia Inc (Irvine, CA)'; [Cell type]'Source: ''tissue: breast cancer; her2: 0; hr: 0; pcr: 0; mp: 0; arm: durvalumab/olaparib; ', 'tissue: breast cancer; her2: 0; hr: 1; pcr: 1; mp: 1; arm: durvalumab/olaparib; ', 'tissue: breast cancer; her2: 0; hr: 0; pcr: 1; mp: 1; arm: control; ', 'tissue: breast cancer; her2: 0; hr: 0; pcr: 0; mp: 1; arm: durvalumab/olaparib; ', 'tissue: breast cancer; her2: 0; hr: 1; pcr: 0; mp: 0; arm: durvalumab/olaparib; ', 'tissue: breast cancer; her2: 0; hr: 1; pcr: 0; mp: 1; arm: durvalumab/olaparib; ', 'tissue: breast cancer; her2: 0; hr: 1; pcr: 0; mp: 0; arm: control; ', 'tissue: breast cancer; her2: 0; hr: 1; pcr: 0; mp: 1; arm: control; ', 'tissue: breast cancer; her2: 0; hr: 0; pcr: 0; mp: 1; arm: control; ', 'tissue: breast cancer; her2: 0; hr: 0; pcr: 0; mp: 0; arm: control; ', 'tissue: breast cancer; her2: 0; hr: 0; pcr: 1; mp: 1; arm: durvalumab/olaparib; ', 'tissue: breast cancer; her2: 0; hr: 0; pcr: -1; mp: 1; arm: control; ', 'tissue: breast cancer; her2: 0; hr: 1; pcr: -1; mp: 0; arm: control; ', 'tissue: breast cancer; her2: 0; hr: 1; pcr: 1; mp: 1; arm: control; ', 'tissue: breast cancer; her2: 0; hr: 0; pcr: 1; mp: 0; arm: control; ', 'tissue: breast cancer; her2: 0; hr: 1; pcr: -1; mp: 1; arm: control; ', 'tissue: breast cancer; her2: 0; hr: 1; pcr: 1; mp: 0; arm: durvalumab/olaparib; ' GSE14744 Homo sapiens 56 Genome variation profiling by SNP array GPL8036 FFPE study using MIP copy number platform - breast cancer II 2009-02-06 A major challenge to the study of tumor DNA copy number (CN) in clinical specimens is the lack of appropriate fresh frozen samples and thus a dependence on Formalin-Fixed Paraffin Embedded (FFPE) banked samples, which typically have more extensive clinical follow up information. However, on most high density CN platforms, DNA from FFPE tissues generally underperforms or suffers high failure rates compared to fresh frozen samples because of DNA degradation and cross-linking. Molecular Inversion Probe (MIP) technology has been applied successfully to obtain high quality CN and genotype data from DNA isolated from cell lines and frozen tumor samples. Since the MIP probes require only a small (~40 bp) target binding site, we reasoned they may be well suited to assess FFPE samples. In this study, we successfully applied MIP technology with a panel of 50,000 markers to CN determination in FFPE samples. Using an input of 37 ng genomic DNA, we demonstrated high quali ty CN data with MIP technology from 93 FFPE samples from seven diverse collections. We found that the performance of FFPE DNA for CN determination was comparable to that of DNA obtained from matched frozen tumor, with only a modest loss in performance of DNA. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE14744 High quality copy number and genotype data from FFPE samples using Molecular Inversion Probe (MIP) microarrays. BMC medical genomics 2.568 https://doi.org/10.1186/1755-8794-2-8 {BMC medical genomics (2.568): 10.1186/1755-8794-2-8} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA114335 https://www.ebi.ac.uk/ena/browser/view/PRJNA114335 None [Overal design]Various collections of FFPE samples have been assayed by MIP; [Treatment]'None'; [Growth]'None'; [Extraction]"genomic DNA extracted from a FFPE block. It's a customer sample"; [Cell type]'Source: ''disease state: primary tumor; sample: FFPE form; tissue: Breast; ', 'disease state: normal tissue; sample: FFPE form; tissue: Breast; ' GSE72935 Homo sapiens 15 Expression profiling by array GPL16699 Targeting metastasis stem cells through the fatty acid receptor CD36 (I) 2015-09-11 Metastasis is the leading cause of cancer-related deaths. For most human cancers, the identity of the cells that initiate and promote metastasis is still unknown, hampering our ability to develop therapies to prevent or inhibit the spread of tumour cells to distant sites. Using an orthotopic model of human oral squamous cell carcinoma (OSCC), we have now identified a subpopulation of CD44bright cells within the primary lesion with the highest potential to develop lymph node and lung metastasis. This population is slow-cycling, expresses high levels of the receptor CD36 at the cell membrane and relies on fatty acid metabolism to thrive in lymph nodes and bronchoalveolar environments. Importantly, inhibition of CD36 by either shRNA or neutralizing monoclonal antibodies severely impairs metastatic spread of primary OSCC patient samples and established cell lines. Further underscoring its importance, CD36 overexpression in poorly disseminating tumours confers an aggressive metastatic behavior. Analyses of public gene expression data indicate that the presence of the signature-defining CD36+ cells also strongly correlates with a poor prognosis in patients with lung SCC, ovarian cancer, bladder cancer, or luminal breast cancer. By identifying metastasis-promoting cells and then targeting them with CD36 inhibition, novel anti-metastatic therapies could be developed for patients with these types of tumours. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72935 Targeting metastasis-initiating cells through the fatty acid receptor CD36. Nature 43.070 https://doi.org/10.1038/nature20791 {Nature (43.070): 10.1038/nature20791} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA296106 https://www.ebi.ac.uk/ena/browser/view/PRJNA296106 None [Overal design]4 biological replicates from SCC-25 cell line were included (set 8A, set 8B, set 9B and set 10A). From each biological replicate, 3 independent cell populations were sorted DID+,DID- and CD44. From set 8B, an additional technical replicate was done.; [Treatment]'None'; [Growth]'Cells were grown in an orthotopic xenograft model in NOD-SCIDγ mice (NSG)'; [Extraction]'Total RNA was extracted from FACS sorted cells with RNAClean XP kit– Agentcourt A63987 following the manufacturer’s instructions and immediately amplified using the TransPlex Complete Whole Transcriptome Amplification Kit (Sigma WTA2) to generate the cDNA'; [Cell type]'Source: ''disease state: orthotopic xenograft model of human OSCC; cell line: SCC-25; sorted cell population: DID+; ', 'disease state: orthotopic xenograft model of human OSCC; cell line: SCC-25; sorted cell population: DID-; ', 'disease state: orthotopic xenograft model of human OSCC; cell line: SCC-25; sorted cell population: CD44; ' GSE41527 Homo sapiens 8 Expression profiling by array GPL6255 Outer ECM-attached vs. inner cells of MCF10A acini at day 6 of morphogenesis 2012-10-11 Basal-like carcinoma is a subtype of breast cancer that is characterized by poor prognosis and high intratumor heterogeneity. Using a basal-like breast epithelial line, we have identified two anti-correlated gene-expression programs that arise among single extracellular matrix (ECM)-attached cells during organotypic 3D culture. The first program contains TGFBR3, a high-affinity receptor for transforming growth factor β (TGFβ) and other related ligands. The second program contains the JUND transcription factor together with the basal-like marker, KRT5. By disrupting the TGFBR3 and JUND programs individually, we reveal an important circuit for 3D morphogenesis that is wired together by four negative-feedback loops. Computational modeling of this circuit showed that it could exhibit damped, antiphase oscillations when excited with small impulses of TGFβ-like ligand. We directly visualize the circuit's spontaneous dynamics in organotypic cultures by using live-cell imaging with engineered pathway reporters. Importantly, we show that the essence of the JUND-TGFBR3 expression circuit holds true in early basal-like tumors that heterogeneously express KRT5. Correlated JUND-KRT5 expression depends critically on contact with stromal ECM and local expression of tenascin C. This work illustrates how complex tumor heterogeneities can be deconstructed into intrinsic single-cell expression circuits that are modulated by the microenvironment. Gene expression analysis of outer ECM-attached vs. inner cells of MCF10A-5E clones grown in organotypic 3D culture at day 6. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41527 A time- and matrix-dependent TGFBR3-JUND-KRT5 regulatory circuit in single breast epithelial cells and basal-like premalignancies. Nature cell biology 17.728 https://doi.org/10.1038/ncb2930 {Nature cell biology (17.728): 10.1038/ncb2930} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA177354 https://www.ebi.ac.uk/ena/browser/view/PRJNA177354 None [Overal design]Total RNA was isolated from ~50 outer ECM-attached cells and ~50 inner cells, each separately microdissected from 8 micron sections of MCF10A structures at day 6 of morphogenesis. Total RNA was amplified in quadruplicate, and hybridized to HumanRef-8 v2.0 Expression BeadChips (Illumina).; [Treatment]'Acini were allowed to grow to day 6.'; [Growth]'MCF10A-5E cells diluted to 12,500 cells/ml in assay medium (DMEM/F12, 2% Horse serum, Hydrocortisone 0.5 μg/ml, Cholera toxin 100 ng/ml, Insulin 10 μg/ml, & 1% Pen/Strep) with 5 ng/ml EGF and 2% Matrigel were seeded into a well of a chamber slide coated with 100% Matrigel. Cells were refed every 4 days with assay medium containing 5 ng/ml EGF and 2% Matrigel.'; [Extraction]'Day 6 acini were cut into 8 μm sections and fixed onto slides. Microdissection of 50 cells per sample was performed on a Pixcell II instrument (Arcturus) using Capsure HS LCM caps (Arcturus). Samples were eluted from the microdissection caps using digestion buffer (1.25× MMLV reverse transcriptase buffer (Invitrogen), 100 μM dNTPs (Roche), 0.08 OD ml−1 oligo(dT)24 and 250 μg ml−1 proteinase K (Sigma)) and incubated at 42 °C for 1 h. Sample processing was done by using poly(A) PCR.'; [Cell type]'breast epithelial cells''cell line: MCF10A-5E; cell type: breast epithelial cells; growth stage: day 6 of morphogenesis; acini cell type: inner non-ECM-attached cells; ', 'cell line: MCF10A-5E; cell type: breast epithelial cells; growth stage: day 6 of morphogenesis; acini cell type: outer ECM-attached cells; ' GSE25314 Homo sapiens 16 Expression profiling by array GPL6947 FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response (part I) 2010-11-12 Estrogen Receptor-a (ER) is the key feature in the majority of breast cancers and ER binding to the genome correlates with the Forkhead protein FOXA1 (HNF3a), but mechanistic insight is lacking. We now show that FOXA1 is the defining factor that governs differential ER-chromatin interactions. We show that almost all ER-chromatin interactions and gene expression changes are dependent on the presence of FOXA1 and that FOXA1 dictates genome-wide chromatin accessibility. Furthermore, we show that CTCF is an upstream negative regulator of FOXA1-chromatin interactions. In ER responsive breast cancer cells, the dependency on FOXA1 for tamoxifen-ER activity is absolute and in tamoxifen resistant cells, ER binding occurs independently of ligand, but in a FOXA1 dependent manner. Importantly, expression of FOXA1 in non-breast cancer cells is sufficient to alter ER binding and response to endocrine treatment. As such, FOXA1 is the primary determinant that regulates estrogen-ER activity and endocrine response in breast cancer cells and is sufficient to program ER functionality in non-breast cancer contexts. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE25314 FOXA1 is a key determinant of estrogen receptor function and endocrine response. Nature genetics 25.455 https://doi.org/10.1038/ng.730 {Nature genetics (25.455): 10.1038/ng.730} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA142545 https://www.ebi.ac.uk/ena/browser/view/PRJNA142545 None [Overal design]breast cancer MCF-7 cell lines were treaated in the presence of Estrogen, Estrogen plus Tamoxifen, Tamoxifen or a vehicle. MCF-7 cells were hormone-depleted for 3 d and treated with 100 nM estrogen or 1 microM Tamoxifen for 6 h. There were four biological replicates for each of the four different groups.; [Treatment]'Estrogen was added at a final concentration of 100 nM and tamoxifen at 1 microM'; [Growth]'MCF-7 human cell lines were grown as described previously (Neve et al. 2006, Cancer Cell 10:515–527).'; [Extraction]'Total RNA was extracted using the QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. A DNase I digestion was included. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''treatment: vehicle (control); cell line: MCF-7; ', 'treatment: estrogen; cell line: MCF-7; ', 'treatment: estrogen and tamoxifen; cell line: MCF-7; ', 'treatment: tamoxifen; cell line: MCF-7; ' GSE145955 Homo sapiens 8 Expression profiling by high throughput sequencing GPL21290 RNA sequencing from T47D and MCF-7 breast cancer cells 2020-02-26 We report the RNA sequencingn onT47D and MCF-7 cells infected by either vehicle or shMEN1 virus https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE145955 Menin and Menin-Associated Proteins Coregulate Cancer Energy Metabolism. Cancers 6.162 https://doi.org/10.3390/cancers12092715 {Cancers (6.162): 10.3390/cancers12092715} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA608867 https://www.ebi.ac.uk/ena/browser/view/PRJNA608867 https://www.ncbi.nlm.nih.gov/sra?term=SRP250795 [Overal design]Investigate downstream genes of MEN1 in breast cancer cells.; [Treatment]'T47D and MCF-7 cells were infected of either vehicle virus or shMEN1 virus to knockdown MEN1 gene expression.'; [Growth]'T47D and MCF-7 breast cancer cell line were cultured in DMEM medium with 10%FBS and 1% penicillin/streptomycin aired with 5%CO2 at 37℃.'; [Extraction]"Total RNA was extracted by using the PureLink RNA Mini Kit, and each treatment had 2 biological replicates.\nLibraries were prepared according to Illumina's instructions accompanying the Nextera XT DNA Library Prep Kit with Nextera XT Index Kit v2 Set A and B index primers."; [Cell type]'Source: ''tissue: T47D breast cancer cell line; ', 'tissue: MCF-7 breast cancer cell line; ' GSE159275 Homo sapiens 9 Expression profiling by high throughput sequencing GPL11154 PELP1/SRC-3-dependent regulation of metabolic kinases drives therapy resistant ER+ breast cancer [3D] 2020-10-08 Trascriptome analysis of mcf7 cell lines were performed https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE159275 PELP1/SRC-3-dependent regulation of metabolic PFKFB kinases drives therapy resistant ER+ breast cancer. Oncogene 6.634 https://doi.org/10.1038/s41388-021-01871-w {Oncogene (6.634): 10.1038/s41388-021-01871-w} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA668175 https://www.ebi.ac.uk/ena/browser/view/PRJNA668175 https://www.ncbi.nlm.nih.gov/sra?term=SRP286808 [Overal design]MCF-7 PELP1 cells expressing LXSN, WT PELP1, or cytoplasmic (cyto) PELP1 were used to create tumorsphere 3D culture: Single cells were plated serum-free mammary epithelial basal medium containing 1% methylcellulose, 1% B27 supplement, 1% penicillin–streptomycin, 5 mg/mL insulin, 20 ng/mL EGF, 1 ng/mL hydrocortisone, and 100 mmol/L beta-mercaptoethanol in ultra-low attachment plates and cultured for 6 days prior to RNA isolation. RNA was extracted with RNAeasy Mini Kit and sequenced with Illumina HiSeq 2000; [Treatment]'None'; [Growth]'None'; [Extraction]'RNeasy Mini Kit (Qiagen)\nTruSeq RNA v2; average insert size of 200 selected'; [Cell type]'breast cancer''cell line: mcf7; cell type: breast cancer; expression: LXSN; ', 'cell line: mcf7; cell type: breast cancer; expression: cytoplasmic PELP1; ', 'cell line: mcf7; cell type: breast cancer; expression: wildtype PELP1; ' GSE106729 Homo sapiens 6 Non-coding RNA profiling by array GPL16956 Identification of glucose-regulated lncRNAs in triple-negative breast cancer cells 2017-11-09 To comprehensively identify the glucose-regulated lncRNAs, we have employed ArraryStar LncRNA Microarry discovery platform to detect lncRNA expression in glucose-starved and glucose-stimulated triple-negative breast cancer cells. Differentially expressed LncRNAs with statistical significance were identified through Volcano Plot filtering between two groups. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE106729 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA417802 https://www.ebi.ac.uk/ena/browser/view/PRJNA417802 None [Overal design]Glucose-induced lncRNA expression in MDA-MB-231 cells was measured at 4 hours after exposure to 25 mM glucose. Three independent experiments were performed at each condition (- or + glucose) using different batch of cells for each experiment.; [Treatment]'MDA-MB-231 cells were subjected to glucose starvation overnight in glucose-free DMEM supplemented with 10% fetal bovine serum (FBS). The next morning, glucose-starved cells were either continuously maintained in glucose-free DMEM or stimulated with DMEM containg 25 mM glucose for 4 hr.'; [Growth]'MDA-MB-231 cells were maintained in Dulbecco modified essential medium (DMEM) supplemented with 10% fetal bovine serum (FBS) at 37 °C in 5% CO2 (v/v).'; [Extraction]"Total RNAs were isolated from glucose-starved and - stimulated cells using RNeasy Plus RNA Purification Kit (Qiagen, Valencia CA) following the manufacturer's recommendations. RNA quantity and quality were measured by NanoDrop ND-2000 and RNA integrity was assessed by Bioanalyzer."; [Cell type]'Source: ''tissue: breast; derived from metastatic site: pleural effusion; gender: Female; age: 51; ' GSE13577 Homo sapiens 24 Expression profiling by array GPL570; GPL571 SIRT1-Dependent Gene Regulation Through Promoter-Directed Recruitment of a Nuclear NAD+ Synthase 2008-11-12 In mammals, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) constitute a nuclear NAD+ salvage pathway, regulating cellular functions of the NAD+-dependent deacetylase SIRT1. However, little is known about the molecular mechanisms by which NAD+ biosynthesis controls gene transcription in the nucleus. In this study, we show that stable knockdown of NAMPT or NMNAT-1 in MCF-7 breast cancer cells significantly reduced total cellular NAD+ levels. Expression microarray analyses demonstrate that both enzymes have broad and overlapping functions in gene regulation. SIRT1 is a key mediator of NAMPT- and NMNAT-1-dependent gene regulation, and is found at promoters of many of the target genes. Furthermore, SIRT1 deacetylase activity at these promoters is regulated by NAMPT and NMNAT-1. Most significantly, NMNAT-1 interacts with SIRT1 and is recruited to target gene promoters by SIRT1. Our results reveal an unexpected mechanism for the direct control of SIRT1 deacetylase activity at target gene promoters by NMNAT-1. Interactions between NMNAT-1 and SIRT1 at gene promoters may provide a platform for integration of multiple signaling pathways that regulate transcription. This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE13577 Enzymes in the NAD+ salvage pathway regulate SIRT1 activity at target gene promoters. The Journal of biological chemistry 4.106 https://doi.org/10.1074/jbc.M109.016469 {The Journal of biological chemistry (4.106): 10.1074/jbc.M109.016469} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA110679 https://www.ebi.ac.uk/ena/browser/view/PRJNA110679 None [Overal design]Refer to individual Series. Each of the 3 Series has its own matching luciferase knockdown controls and the three data sets were generated independently of each other.; [Treatment]'None', 'MCF-7 cells were cultured in estrogen-free media for 72 hours prior to hormone treatment. Control cells were treated with vehicle (ethanol) for 3 hours.', 'MCF-7 cells were cultured in estrogen-free media for 72 hours prior to hormone treatment. E2 samples were treated with 10-7M estradiol for 3 hours.'; [Growth]'None', "MCF-7 cells were maintained in Eagle's minimum essential medium supplemented with 5% calf serum and antibiotics."; [Extraction]'Total RNA was prepared using Trizol Reagent according to the manufacturer’s instructions (Invitrogen) and was further purified using RNeasy columns (Qiagen).', "Total RNA was prepared using Trizol reagent according to the manufacturer's instructions (Invitrogen) and was further purified using RNeasy columns (Qiagen)"; [Cell type]'Source: ''' GSE153646 Homo sapiens 8 Expression profiling by high throughput sequencing GPL23227 Fibroblasts direct differentiation of human breast epithelial progenitors 2020-07-01 Background: Breast cancer arises within specific regions in the human breast referred to as the terminal duct lobular units (TDLUs). These are relatively dynamic structures characterized by sex hormone driven cyclic epithelial turnover. TDLUs consist of unique parenchymal entities embedded within a fibroblast-rich lobular stroma. Here, we established and characterized a new human breast lobular fibroblast cell line against its interlobular counterpart with a view to assessing the role of region-specific stromal cues in the control of TDLU dynamics. Methods: Primary lobular and interlobular fibroblasts were transduced to express human telomerase reverse transcriptase (hTERT). Differentiation of the established cell lines along lobular and interlobular pathways was determined by immunocytochemical staining and genome-wide RNA sequencing. Their functional properties were further characterized by analysis of mesenchymal stem cell (MSC) differentiation repertoire in culture and in vivo. The cells’ physiological relevance for parenchymal differentiation was examined in heterotypic co-culture with fluorescence-activated cell sorting (FACS)-purified normal breast primary luminal or myoepithelial progenitors. The co-cultures were immunostained for quantitative assessment of epithelial branching morphogenesis, polarization, growth, and luminal epithelial maturation. In extension, myoepithelial progenitors were tested for luminal differentiation capacity in culture and in mouse xenografts. To unravel the significance of transforming growth factor-beta (TGF-β)-mediated crosstalk in TDLU-like morphogenesis and differentiation, fibroblasts were incubated with the TGF-β signaling inhibitor, SB431542, prior to heterotypic co-culture with luminal cells. Results: hTERT immortalized fibroblast cell lines retained critical phenotypic traits in culture and linked to primary fibroblasts. Cell culture assays and transplantation to mice showed that the origin of fibroblasts determines TDLU-like and ductal-like differentiation of epithelial progenitors. Whereas lobular fibroblasts supported a high level of branching morphogenesis by luminal cells, interlobular fibroblasts supported ductal-like myoepithelial characteristics. TDLU-like morphogenesis, at least in part, relied on intact TGF-β signaling. Conclusions: The significance of the most prominent cell type in normal breast stroma, the fibroblast, in directing epithelial differentiation is largely unknown. Through establishment of lobular and interlobular fibroblast cell lines, we here demonstrate that epithelial progenitors are submitted to stromal cues for site-specific differentiation. Our findings lend credence to considering stromal subtleties of crucial importance in the development of normal breast and, in turn, breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE153646 Fibroblasts direct differentiation of human breast epithelial progenitors. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-020-01344-0 {Breast cancer research : BCR (5.676): 10.1186/s13058-020-01344-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA643540 https://www.ebi.ac.uk/ena/browser/view/PRJNA643540 https://www.ncbi.nlm.nih.gov/sra?term=SRP269579 [Overal design]Duplicate primary lobular and interlobular breast fibroblastic cells. Duplicate immortalized lobular and interlobular breast fibroblastic cells.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted using Trizol (Thermo Fischer) and a spin column method according to the manufacturer’s instructions (Zymo Research)\nDNAse treated total RNA samples were enriched for mRNAs using oligo dT magnetic beads. mRNAs were fragmented into 200 bp-size fragments and the first strands of cDNAs were synthesized by using random-hexamers. In order to generate the library products, after the second strand synthesis, double strands cDNAs were purified by magnetic beads followed by addition of adenine to the 3’ends and ligation of sequencing adaptors to the fragments. These fragments were amplified by PCR using ABI StepOnePlus Real-Time PCR System, and the quantity and quality was checked by Agilent 2100 Bioanalyzer. Sequencing was performed using BGISeq 500'; [Cell type]'Lobular fibroblastic cells', 'Interlobular fibroblastic cells''cell type: Lobular fibroblastic cells; htert immortalized: No; passage #: 9; ', 'cell type: Interlobular fibroblastic cells; htert immortalized: No; passage #: 9; ', 'cell type: Lobular fibroblastic cells; htert immortalized: Yes; passage #: 24; ', 'cell type: Interlobular fibroblastic cells; htert immortalized: Yes; passage #: 25; ' GSE98515 Homo sapiens 12 Expression profiling by high throughput sequencing GPL18460 Expression profiling of MCF-7 cells with treatment of TCDD 2017-05-03 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98515 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA385317 https://www.ebi.ac.uk/ena/browser/view/PRJNA385317 None [Overal design]Refer to individual Series; [Treatment]'6hrs treatment with either vehicle (DMSO) or TCDD', '6hrs treatment withTCDD'; [Growth]'250,000 MCF-7 cells were seeded in 35 mm plates in DMEM supplemented with 10 % FBS for 24 hr, followed by overnight serum-starvation in phenol red-free DMEM'; [Extraction]'Total RNA purification kits from Qiagen (Valencia, CA) were used according to manufacturers instructions\nLibraries were prepared from 1 µg of total RNA using a TruSeq RNA Prep Kit (Illumina Inc., San Diego, CA)'; [Cell type]'Source: ''treatment: DMSO; concentration: N/A; ', 'treatment: TCDD; concentration: 10nM; ', 'treatment: TCDD; concentration: 100nM; cell line: MCF-7; ' GSE29036 Homo sapiens 30 Expression profiling by array GPL13482 Global gene expression analysis of heterotypic interactions between cancer cells and osteoblasts in vitro 2011-05-03 Bone is the most common site of breast cancer metastasis, and this type of metastasis is a main cause of morbidity. Because breast cancer is a heterogeneous disease, the interactions between the cancer cells and the skeletal host cells, such as osteoblasts, might be diverse. Thus far, these tumor-osteoblast interactions have not yet been well characterized using a genomic approach. We hypothesized that gene expression signatures induced by tumor-osteoblast interactions might be of clinical relevance. To examine these gene expression signatures, we established an ex vivo co-culture model with benign human cells and a panel of 5 malignant breast epithelial cells in combination with primary human osteoblasts and determined associated gene expression changes using cDNA microarrays. This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE29036 Global gene expression analysis of the interaction between cancer cells and osteoblasts to predict bone metastasis in breast cancer. PloS one 2.776 https://doi.org/10.1371/journal.pone.0029743 {PloS one (2.776): 10.1371/journal.pone.0029743} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA140251 https://www.ebi.ac.uk/ena/browser/view/PRJNA140251 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None', 'osteoblast co-culture; Human mammary epithelial cells (HMEC) (Cambrex Bio Science Walkersville, Walkersville, MD) were expanded in mammary epithelial basal medium that was supplemented with bovine pituitary extract, human EGF, insulin and antibiotics (Clonetics, Cambrex Bio Science Walkersville, Walkersville, MD). MCF-7, T47D, MDA-MB231, SKBR-3, Hs578T, (ATCC, Atlanta, GA) were propagated in DMEM with 4.5% glucose (Gibco, Grand Island, NY) that was supplemented with 10% FBS (HyClone, Logan, UT), glutamine, 100 U/ml penicillin and 100 ??g/ml streptomycin (Gibco, Grand Island, NY). Normal human Osteoblasts (NHOST) (Lonza Walkersville, Walkersville, MD) were expanded in Clonetics Osteoblast Basal Medium (OBM???) (Lonza Walkersville, Walkersville, MD) supplemented with osteoblast growth medium (OGM TM) SingleQuots?? (Lonza Walkersville, Walkersville, MD) with 10 % FBS. For the co-culture experiments, the cells were cultivated for 48 hours at equal density of 30???000 cells/cm2 (15???000 tumor cells /cm2 and 15???000 normal human Osteoblast cells /cm2) in Clonetics Osteoblast Basal Medium (OBM???) supplemented with 0.2% FBS without any further additives. This medium served as a good universal media for all the cells in the study'; [Extraction]"MessageAmpII; Total RNA was amplified using the Message AmpTM II aRNA Kit (Ambion, Austin, TX), according to the manufacturer's instructions", "RNeasy; Total RNA was isolated using the RNeasy mini kit (QIAGEN), according to the manufacturer's instructions.; Protocol Type = Extract preparation; Performer: Michal,,Rajski\nMessageAmp II; RNA was amplified using the Message AmpTM II aRNA Kit (Ambion, Austin, TX) according to the manufacturer's instructions"; [Cell type]'Source: ''reference: stratagene human reference plus doping controls.; ', 'cells: HMEC sample B plus doping controls.; ', 'cells: normal human osteoblasts sample B3 plus doping controls.; ', 'cells: normal human osteoblasts and HMEC coculture B plus doping controls.; ', 'cells: HMEC sample A plus doping controls.; ', 'cells: normal human osteoblasts and HMEC coculture A plus doping controls.; ', 'cells: normal human osteoblasts sample A3 plus doping controls.; ', 'cells: normal human osteoblasts sample B plus doping controls.; ', 'cells: Hs578t sample B plus doping controls.; ', 'cells: Hs578t sample A plus doping controls.; ', 'cells: normal human osteoblasts and Hs578t coculture B plus doping controls.; ', 'cells: normal human osteoblasts sample A; ', 'cells: normal human osteoblasts and Hs578t coculture A plus doping controls.; ', 'cells: normal human osteoblasts and MCF-7 coculture A plus doping controls.; ', 'cells: normal human osteoblasts sample A2 plus doping controls.; ', 'cells: MCF-7 sample A plus doping controls.; ', 'cells: normal human osteoblasts and MCF-7 coculture B plus doping controls.; ', 'cells: normal human osteoblasts sample B2 plus doping controls.; ', 'cells: MCF-7 sample B plus doping controls.; ', 'cells: normal human osteoblasts and MDA-MB-231 coculture B plus doping controls.; ', 'cells: MDA-MB-231 sample A plus doping controls.; ', 'cells: MDA-MB-231 sample B plus doping controls.; ', 'cells: normal human osteoblasts and MDA-MB-231 coculture A plus doping controls.; ', 'cells: normal human osteoblasts and SKBR3 coculture A plus doping controls.; ', 'cells: SKBR3 sample B plus doping controls.; ', 'cells: normal human osteoblasts and SKBR3 coculture B plus doping controls.; ', 'cells: SKBR3 sample A plus doping controls.; ', 'cells: T47D sample A; ', 'cells: normal human osteoblasts and T47D coculture B plus doping controls.; ', 'cells: normal human osteoblasts and T47D coculture A plus doping controls.; ', 'cells: T47D sample B; ' GSE148483 Homo sapiens 24 Expression profiling by high throughput sequencing GPL18573 Patient-derived scaffolds uncover breast cancer promoting properties of the microenvironment 2020-04-10 Tumor cells interact with the microenvironment that specifically supports and promotes tumor development. Key components in the tumor environment have been linked to various aggressive cancer features and can further influence the presence of subpopulations of cancer cells with specific functions, including cancer stem cells and migratory cells. To model and further understand the influence of specific microenvironments we have developed an experimental platform using cell-free patient-derived scaffolds (PDSs) from primary breast cancers infiltrated with standardized breast cancer cell lines. This PDS culture system induced a series of orchestrated changes in differentiation, epithelial-mesenchymal transition, stemness and proliferation of the cancer cell population, where an increased cancer stem cell pool was confirmed using functional assays. Furthermore, global gene expression profiling showed that PDS cultures were similar to xenograft cultures. Mass spectrometry analyses of cell-free PDSs identified subgroups based on their protein composition that were linked to clinical properties, including tumor grade. Finally, we observed that an induction of epithelial-mesenchymal transitionrelated genes in cancer cells growing on the PDSs were significantly associated with clinical disease recurrences in breast cancer patients. Patient-derived scaffolds thus mimics in vivo-like growth conditions and uncovers unique information about the malignancy-inducing properties of tumor microenvironment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148483 Patient-derived scaffolds uncover breast cancer promoting properties of the microenvironment. Biomaterials 10.273 https://doi.org/10.1016/j.biomaterials.2019.119705 {Biomaterials (10.273) doi:10.1016/j.biomaterials.2019.119705}; {Data in brief (None) doi:10.1016/j.dib.2020.105860}; 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA624359 https://www.ebi.ac.uk/ena/browser/view/PRJNA624359 https://www.ncbi.nlm.nih.gov/sra?term=SRP256212 [Overal design]RNA samples from two breast cancer cell lines, MCF7 and MDA-MB-231, extracted from three different culture conditions: adherent 2D culture (6 replicates for each cell line), patient-derived scaffolds (3 replicates for each cell line), mice xenografts (3 replicates for each cell line).; [Treatment]'None'; [Growth]"Cell lines were cultured under normal cell culture conditions, MCF7 cells in Dulbecco's modified Eagle's medium (DMEM) complete media and MDA-MB-231 in RPMI 1640 complete media.\nFor patient-derived scaffold (PDS) culture, tumor pieces were decellularized using detergent wash. The PDSs were cut into 3x3 mm pieces, maximum 2 mm thick, and added to 48-well culture plates. Cells were added onto the PDSs in complete media and cultured for 21 days before analysis. PDS pieces were regulalry transferred to new wells with fresh media.\nFor xenograft culture, cells were dissociated using Accutase and resuspended in DMEM media mixed 1:1 with matrigel. Cells were injected subcutaneously into flanks of NOG mice. Tumors were extraced after 32 days."; [Extraction]'Samples were lyzed in either lysis buffer containing 1 µg/µl BSA and 2.5% glycerol or in QIAzol lysis reagent. PDS and xenograft samples were homogenized using a stainless steel bead in TissueLyzer II. RNA was extracted using Qiagen miRNeasy Mini Kit including DNase treatment. RNA concentration was measured with nanodrop and RNA quality was randomly assessed with Agilent RNA 6000 Nano Kit using Bioanalyser 2100.\nThe library was generated using the Smart-seq2 protocol (Picelli, Faridani et al. 2014) with some modifications.'; [Cell type]'Source: ''cell line: MCF7; cell culture method: Adherent 2D culture; ', 'cell line: MCF7; cell culture method: Patient-derived scaffold (PDS) culture; ', 'cell line: MCF7; cell culture method: Xenograft culture; ', 'cell line: MDA-MB-231; cell culture method: Adherent 2D culture; ', 'cell line: MDA-MB-231; cell culture method: Patient-derived scaffold (PDS) culture; ', 'cell line: MDA-MB-231; cell culture method: Xenograft culture; ' GSE55503 Homo sapiens 12 Expression profiling by array GPL10558 Effects of siRNA targeting PRKCD in breast cancer cells 2014-03-03 The aim was to identify genes that were commonly influenced by a siRNA targeting PRKCD in breast cancer cell lines. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55503 Down Regulation of CLDND1 Induces Apoptosis in Breast Cancer Cells. PloS one 2.776 https://doi.org/10.1371/journal.pone.0130300 {PloS one (2.776): 10.1371/journal.pone.0130300} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA239804 https://www.ebi.ac.uk/ena/browser/view/PRJNA239804 None [Overal design]MDA-MB-468 and BT-549 breast cancer cell lines were treated with control siRNA or siRNA targeting PRKCD. Three samples in each group were analyzed.; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen Rneasy'; [Cell type]'Source: ''cell line: MDA-MB-468 breast cancer cell line; treatment: siControl; ', 'cell line: MDA-mB-468 breast cancer cell line; treatment: siPRKCD; ', 'cell line: BT-549 breast cancer cell line; treatment: siControl; ', 'cell line: BT-549 breast cancer cell line; treatment: siPRKCD; ' GSE143944 Homo sapiens 12 Expression profiling by high throughput sequencing GPL24676 Transcriptional profiling of ribociclib-treated sensitive and ribociclib resistant CAMA-1 cells 2020-01-20 We report transcriptional response to ribociclib treatment in resistant and sensitive CAMA-1 cells using RNA sequencing. Acquired ribociclib resistant cells were generated by treating CAMA-1 cells over a period of 5 month. Cells were then treated with ribociclib or DMSO control and processed for RNA sequencing. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE143944 Exploiting collateral sensitivity controls growth of mixed culture of sensitive and resistant cells and decreases selection for resistant cells in a cell line model. Cancer cell international 3.439 https://doi.org/10.1186/s12935-020-01337-1 {Cancer cell international (3.439): 10.1186/s12935-020-01337-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA602306 https://www.ebi.ac.uk/ena/browser/view/PRJNA602306 https://www.ncbi.nlm.nih.gov/sra?term=SRP243450 [Overal design]Examination of transcriptional response to ribociclib in sensitive and resistant CAMA-1 cells. In total, 12 samples (2 cell lines with 2 treatments, 3 replicates) were analyzed.; [Treatment]'24 hours after plating ribociclib treatment of 1 uM (final concentration) or same volume of vehicle control (DMSO) were initiated. After 12 hours of treatment, cells were trypsinized, washed and pellets were stored in -80C until RNA isolation.'; [Growth]'CAMA-1 cells were continuously treated with 1 uM ribociclib for 1 month followed by 250 nM for 4 months to develop resistance. Dose response experiments confirmed the ribociclib-resistant nature of treated cells. Parental, sensitive and adapted, resistant cells were independently plated at 500,000 cells/well in 6-well cell culture plates in triplicate.'; [Extraction]"RNA was isolated using the commercially available kit (RNEasy Plus Mini Kit, Qiagen, Cat. No.: 74136) following the manufacturer's instruction.\nRNA-seq libraries were prepared using Illumina TruSeq Stranded Total RNA library Prep Ribo-zero Gold following manufacturer’s protocol.\nRNA-Seq, paired-end reads, stranded"; [Cell type]'Source: ''cell line: CAMA-1; treatment: DMSO; ribociclib sensitivity: sensitive; ', 'cell line: CAMA-1; treatment: 1 uM ribociclib; ribociclib sensitivity: sensitive; ', 'cell line: CAMA-1; treatment: DMSO; ribociclib sensitivity: resistant; ', 'cell line: CAMA-1; treatment: 1 uM ribociclib; ribociclib sensitivity: resistant; ' GSE112432 Homo sapiens 2 Expression profiling by array GPL16686 Nuclear localization of intracellular domain of LDL receptor-related protein 1B induced expresion data 2018-03-28 We have generated a MCF-7 Tet-On model system for inducible nuclear expression of intracellular domain of LRP1b using the pTRE-Tight vector system (Clontech Takara, Ohtsu, Japan). Expression data of MCF-7 without and with induction of Doxycycline, sample 1 and sample 2, respectively. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112432 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA445987 https://www.ebi.ac.uk/ena/browser/view/PRJNA445987 None [Overal design]We have generated a MCF-7 Tet-On model system for inducible expression of intracellular domain of LRP1b using the pTRE-Tight vector system (Clontech Takara, Ohtsu, Japan). Human cDNA, which encoded a intracellular lesion of LRP1B, was amplified by PCR using sense primer 5’-ACCATGGGTAAAAGAAAAAGAAGGACAAAAAC-3’ (underline indicates the introduced start codon) and antisense primer 5’-AGGGATCCTCACTGATTATGCCACTGTCTCTCTTATAC-3’(double underline and underline indicates the introduced BamH1 site and internal stop codon, respectively), cloned to pTarget-T vector (Promega), and subsequently verified by sequencing. Next, Mlu1 and BamH1 fragment, which contained the coding region of intracellular domain of LRP1B was subcloned to Mlu1-BamH1 site of pTRE3G-ZsGreen1 vector (Clontech Takara). After verified by sequencing of the inserted lesion, the vector was designated pTRE3G-ZsGreen1-cLRP1B vector. A stable Tet-On 3G MCF-7 cell line, which was a host for Tet-inducible gene expression systems, was established using a pCMV-Tet3G vector and Xfect transfection reagent (Clontech Takara), subsequently transfected with pTRE3G-ZsGreen1-cLRP1B vector according to the manufacture’s protocol. Finally, a doxycycline (Dox) controlled expression of intracellular domain of LRP1B was established in MCF-7 cells. We established six MCF cell clones, in which intracellular domain of LRP1B was tightly regulated by doxycycline (Dox) at 100ng/ml.; [Treatment]'MCF-7 cell clones, in which intracellular domain of LRP1B was tightly regulated by doxycycline (Dox) at 100ng/ml.'; [Growth]'Cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM; Gibco Life Technologies, Grand Island, NY, USA) containing 10% heat-inactivated fetal bovine serum (FBS).'; [Extraction]'RNA was extracted by using Qiagen RNA Easy kits.'; [Cell type]'Source: ''tissue: Human breast cancer cells; cell line: MCF-7; ' GSE50564 Homo sapiens 12 Expression profiling by array; Third-party reanalysis GPL570 IMPACT: Unraveling intracellular signal transduction and pathway crosstalk by exploring pathway landscape 2013-09-04 Understanding complicated modularization and crosstalk of intracellular signal transduction pathways holds the key to battle against drug resistance in human cancer research. We propose an integrative approach, namely Inferring Modularization of PAthway CrossTalk (IMPACT), to identify aberrant pathway modules and their between-module crosstalk by exploring pathway landscape that is reconstructed from a sampling strategy. The pathway identification method (i.e., IMPACT) was applied to breast cancer data to uncover aberrant pathway modules, which were further investigated with cell line studies to understand drug resistance in breast cancer. The patient datasets we mentioned are published and are available in the GEO database as GSE6532 and GSE17705. The re-processed GSE6532 and GSE17705 patient datasets are linked below as supplementary files. The GSE6532_matrix.txt and GSE17705_matrix.txt are processed by Affy Gene console with plier as normailization. But importantly, we also used 'Combat' method (http://www.bu.edu/jlab/wp-assets/ComBat/Abstract.html) to remove potential institutional batch effect. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50564 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA218218 https://www.ebi.ac.uk/ena/browser/view/PRJNA218218 None [Overal design]Four MCF7 derived cell models were included in the study: MCF7-STR, MCF7RR-STR, LCC1 and LCC2 cell lines. MCF7-STR and MCF7RR-STR were grown in phenol red-free IMEM supplemented with 5% charcoal-stripped calf serum and 1nM estradiol for 72 h prior to RNA extraction. LCC1 and LCC2 cells were grown in phenol red-free IMEM supplemented with 5% charcoal-stripped calf serum. The cell line data were used to validate computational results derived from patient datasets.; [Treatment]'Stripped cells were grown over 96 hours (4 successive days) in phenol-red free IMEM media supplemented with 5% Charcoal-Stripped Calf Serum. Every 24 hours the media was removed and replaced with fresh phenol-red free IMEM media supplemented with 5% Charcoal-Stripped Calf Serum (3 times total).'; [Growth]'Cells were grown in phenol-red free IMEM media supplemented with 5% Charcoal-Stripped Calf Serum. Both Control and Treated cells were kept in a 37C incubator with 5% C02 and regulated humidity.'; [Extraction]'Total RNA was extracted from cell lines using TRIzol, cleaned using the QIAGEN Rneasy Mini Kit, and its quality confirmed using an Agilent 2100 Bioanalyzer and RNA 6000 LabChips'; [Cell type]'Source: ''cell line: MCF7-STR; gender: Female; age: 69 years; race: Caucasian; ', 'cell line: MCF7RR-STR; gender: Female; age: 69 years; race: Caucasian; ', 'cell line: LCC1; gender: Female; age: 69 years; race: Caucasian; ', 'cell line: LCC2; gender: Female; age: 69 years; race: Caucasian; ' GSE41894 Homo sapiens 12 Expression profiling by array GPL10558 Prolactin-induced protein (PIP) regulates proliferation of luminal A type breast cancer cells in a hormone-independent manner 2012-10-28 RNA was extracted from cells using Aurum Total RNA kit from Bio-Rad Laboratories, Inc., Hercules, CA following the manufacturer’s recommendations. Gene expression profiling was performed using the BeadChip HumanHT-12 v4 Expression kit from Illumina®, which contains 47,231 gene-probes (Illumina® Inc., San Diego, CA). The raw signal intensities were imported and analyzed using the GenomeStudio® data software. After background subtraction and normalization, the signal intensity values were exported to the Partek® genomics expression analysis suite using “Partek's Report Plug-in” option in the GenomeStudio® software. Differentially expressed genes in the dox- versus vehicle-treated samples were identified using the “gene expression” workflow in the Partek® software. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41894 Prolactin-induced protein (PIP) regulates proliferation of luminal A type breast cancer cells in an estrogen-independent manner. PloS one 2.776 https://doi.org/10.1371/journal.pone.0062361 {PloS one (2.776): 10.1371/journal.pone.0062361} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA178414 https://www.ebi.ac.uk/ena/browser/view/PRJNA178414 None [Overal design]T47D cells hoaboring a doxycycline inducible shPIP construct were treated for 24 or 48 hours with 250 ng/mL of doxycycline and their mRNAs analyzed in biological triplicates (a total of 12 samples) using Illumina‘s HumanHT-12 v4 BeadChips. The samples for each time point comprised of three samples each for doxycycline or equal volume of water as vehicle control.; [Treatment]'Doxycycline was added to the culture mdium for either for 24 or 48 hours to induce the knockdown of PIP mRNA. Control samples were prepared by treating the cells with equal volume of water (usually 2.5 uL per mL).'; [Growth]'T47D cells were maintained in RPMI-1640 medium supplemented with 10% fetal bovine serum from Clontech, CA.'; [Extraction]'RNA was extracted from cells using Aurum Total RNA kit from Bio-Rad Laboratories, Inc., Hercules, CA following the manufacturer’s recommendations.'; [Cell type]'Source: ''agent: Doxycycline; time point: 48 Hour; shRNA: Dox-inducible shRNA for PIP; ', 'agent: vehicle; time point: 48 Hour; shRNA: Dox-inducible shRNA for PIP; ', 'agent: vehicle; time point: 24 Hour; shRNA: Dox-inducible shRNA for PIP; ', 'agent: Doxycycline; time point: 24 Hour; shRNA: Dox-inducible shRNA for PIP; ' GSE92598 Homo sapiens 35 Expression profiling by array GPL17586 mTORC1 and -2 Coordinate Transcriptional and Translational Reprogramming in Resistance to DNA Damage and Replicative Stress in Breast Cancer Cells 2016-12-19 mTOR coordinates growth signals with metabolic pathways and protein synthesis and is hyperactivated in many human cancers. We have characterized the coordinated mTORC1 and -2 transcription and translation response using genome-wide translatome and transcriptome profiling on cells inhibited in mTORC1/2 with PP242 or only mTORC1 with RAD001, with or without concurrent IR. In this dataset, we include the expression data obtained from SUM149 cells treated with RAD001 + IR, RAD001, PP242+IR, PP242, IR, DMSO. We include both total (transcriptional) data as well as polysome arrays. These data are used to obtain differentially expressed genes in all treatments compared to DMSO in both polysome and transcriptional data. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE92598 mTORC1 and -2 Coordinate Transcriptional and Translational Reprogramming in Resistance to DNA Damage and Replicative Stress in Breast Cancer Cells. Molecular and cellular biology 3.735 https://doi.org/10.1128/MCB.00577-16 {Molecular and cellular biology (3.735): 10.1128/MCB.00577-16} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA358095 https://www.ebi.ac.uk/ena/browser/view/PRJNA358095 None [Overal design]35 samples were analyzed. We examined the following comparisons using Limma with a p-value < 0.05, log fold-change > 1.5: PP242 vs. DMSO, PP242+IR vs. DMSO, RAD001 vs DMSO, RAD001 + IR vs DMSO, IR vs DMSO in polysome samples, total sampes, and using translational efficiency.; [Treatment]'not applicable'; [Growth]'Mouse forelimbs dissected from day 11.5 mouse embryos'; [Extraction]'Shh mutant phenotypes were manually identified as wild-type or mutants. All other samples were snap frozen in liquid N2 and genotyped. Either single or dual samples of equivalent genotyped samples (2-4 forelimbs) were used for all other samples. All samples contained 5μg of carrier glycogen and were prepared using Trizol. Samples were then treated with the RiobMinusâ„¢ rRNA reduction kit (Invitrogen), cDNA synthesis and amplification was performed using the WT cDNA synthesis and amplification kit (Affymetrix).'; [Cell type]'Source: ''cell line: SUM149; ' GSE16873 Homo sapiens 40 Expression profiling by array GPL96 Early Dysregulation of Cell Adhesion and Extracellular Matrix Pathways in Breast Cancer Progression 2009-06-29 Proliferative breast lesions, such as simple ductal hyperplasia (SH) and atypical ductal hyperplasia (ADH), are candidate precursors to ductal carcinoma in situ (DCIS) and invasive cancer. To better understand their relationship to more advanced disease, we used microdissection and DNA microarrays to profile the gene expression of patient-matched histologically normal (HN), ADH, and DCIS from 12 patients with ER+ sporadic breast cancer. SH were profiled from a subset of cases. We found 837 differentially expressed genes between DCIS-HN and 447 between ADH-HN, with >90% of the ADH-HN genes also present among the DCIS-HN genes. Only 61 genes were identified between ADH-DCIS. Expression differences were reproduced in an independent cohort of patient-matched lesions by qRT-PCR. Many breast cancer-related genes and pathways were dysregulated in ADH and maintained in DCIS. Particularly, cell adhesion and extracellular matrix (ECM) interactions were overrepresented. Focal adhesion was the top pathway in each gene set. We conclude that ADH and DCIS share highly similar gene expression and are distinct from HN. In contrast, SH appear more similar to HN. These data provide genetic evidence that ADH (but not SH) are often precursors to cancer and suggest cancer-related genetic changes, particularly adhesion and ECM pathways, are dysregulated prior to invasion and even before malignancy is apparent. These findings could lead to novel risk stratification, prevention, and treatment approaches. Patient-matched (HN, SH, ADH, DCIS) samples were isolated from within patients with ER+ sporadic breast cancers via laser capture microdissection. Use of patient-matched samples decreases between patient variations. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE16873 Early dysregulation of cell adhesion and extracellular matrix pathways in breast cancer progression. The American journal of pathology 3.762 https://doi.org/10.2353/ajpath.2009.090115 {The American journal of pathology (3.762): 10.2353/ajpath.2009.090115} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA117579 https://www.ebi.ac.uk/ena/browser/view/PRJNA117579 None [Overal design]Forty total samples were analyzed via Affymetrix U133A. Patient age ranged from 48-92. Case numbers correspond to individual patients. Each sample is identified by case number, histologic lesion and corresponding microarray ID.; [Treatment]'Samples were microdissected from lightly H&E stained serial frozen tissue sections.'; [Growth]'None'; [Extraction]'Following the manufacturer’s protocol, total RNA was extracted and purified using the Picopure RNA Isolation Kit (Arcturus Engineering).'; [Cell type]'epithelial''tissue: laser capture microdissected human breast; cell type: epithelial; disease state: histologically normal; age range: 48-92 years old; ', 'tissue: laser capture microdissected human breast; cell type: epithelial; disease state: simple ductal hyperplasia; age range: 48-92 years old; ', 'tissue: laser capture microdissected human breast; cell type: epithelial; disease state: atypical ductal hyperplasia; age range: 48-92 years old; ', 'tissue: laser capture microdissected human breast; cell type: epithelial; disease state: ductal carcinoma in situ; age range: 48-92 years old; ' GSE102616 Homo sapiens 47 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing GPL11154; GPL20301; GPL21290 ZFX acts as a transcriptional activator in multiple types of human tumors by binding downstream of transcription start sites at the majority of CpG island promoters 2017-08-14 We performed ChIP-seq in four cancer cell lines to identify ZFX binding sites throughout the human genome. We also performed RNA-seq analysis after knockdown of ZFX by siRNA in prostate and breast cancer cells. Using Nucleosome Occupancy and Methylome Sequencing (NOMe-seq), we show that ZFX binds between the open chromatin region at the TSS and the first downstream nucelosome, suggesting that ZFX may play a critical role in promoter architecture. We also showed that ZNF711 may function redundantly with ZFX in MCF7 by performing ZNF711 ChIP-seq and RNA-seq analysis after knockdown of ZFX, ZNF711, and both ZFX and ZNF711. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE102616 A high-resolution 3D epigenomic map reveals insights into the creation of the prostate cancer transcriptome. Nature communications 11.878 https://doi.org/10.1038/s41467-019-12079-8 {Genome research (9.944) doi:10.1101/gr.228809.117}; {Nature communications (11.878) doi:10.1038/s41467-019-12079-8}; 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA398222 https://www.ebi.ac.uk/ena/browser/view/PRJNA398222 https://www.ncbi.nlm.nih.gov/sra?term=SRP115395 [Overal design]ChIP-seq, NOMe-seq and RNA-seq; [Treatment]'For transient knockdown, cells were transfected in triplicate with 100nM of siRNA oligonucleotides targeting human ZFX (Cat# L006572000005), ZNF711 (Cat# L008444020005) or control oligonucleotides (Cat# D0018101005) using SMART pool Dharmafect transfection reagent 3 (Cat# T200301) for C42B and reagent 1 (Cat# T200101) for MCF7 (Dharmacon, Lafayette, CO, USA). Cells were incubated for 24 hours and transfected again with the same concentration of siRNAs and the incubation was continued for an additional 24 hours.'; [Growth]'The human kidney HEK293T (ATCC# CRL-3216), colon HCT116 (ATCC# CCL-247), and breast cancer MCF7 (ATCC# HTB-22) cells were obtained from ATCC (https://www.atcc.org/). The human prostate cancer C42B cells were obtained from ViroMed Laboratories (Minneapolis, MN, USA). The corresponding medium of each cell lines (DMEM for HEK293T, McCoy’s 5A for HCT116, RPMI 1640 for C42B, DMEM for MCF7) was supplemented 10% fetal bovine serum (Gibco by Thermo Fisher Scientific, Waltham, MA, USA) and 1% penicillin and streptomycin at 37ºC with 5% CO2. All cell stocks were authenticated at the USC Norris Cancer Center cell culture facility by comparison to the ATCC and/or published genomic criteria for that specific cell line; all cells are documented to be free of mycoplasma.', 'The human kidney HEK293T (ATCC# CRL-3216), colon HCT116 (ATCC# CCL-247), and breast cancer MCF7 (ATCC# HTB-22) cells were obtained from ATCC (https://www.atcc.org/). The human prostate cancer C42B cells were obtained from ViroMed Laboratories (Minneapolis, MN, USA). The human normal prostate epithelial cells (PrEC) were obtained from Lonza (Cat# CC-2555, Lonza, Walkersville, MD, USA) The corresponding medium of each cell lines (DMEM for HEK293T, McCoy’s 5A for HCT116, RPMI 1640 for C42B, DMEM for MCF7) was supplemented 10% fetal bovine serum (Gibco by Thermo Fisher Scientific, Waltham, MA, USA) and 1% penicillin and streptomycin at 37ºC with 5% CO2. PrEC cells were grown with PrEGM Bullet Kit (Prostate Epithelial Cell Growth Medium with supplements), which were obtained from Lonza (Cat# CC-3166, Walkersville, MD, USA).'; [Extraction]'For RNA-seq, RNA was extracted using Trizol reagent (15596-026) (Life technologies, Carlsbad, CA) following its protocol.\nFor ChIP-seq, cells were crosslinked using 1% formaldehyde andl lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody.\nFor NOMe-seq, after isolating nuclei from the cells, M.CviPI was treated to methylate accessible GpCs. After purifying M.CvPI-treated DNA, sonication was performed. Bisulfite treatment of M.CviPI-methylated DNA resulted to convert all unmethylated Cs to Ts.\nRNA-seq libraries were made using KAPA Stranded mRNA-Seq Kit with KAPA mRNA Capture Beads (KK8420) (Kapa Biosystems, Woburn, MA).\nChIP-seq: Libraries were barcoded (NEXTflex™ DNA Barcodes) (Bio Scientific, Austin, TX).\nNOMe-seq: Libraries were generated using the Accel-NGS Methyl-Seq DNA Library Kit for Illumina Platforms.', 'For ChIP-seq, cells were crosslinked using 1% formaldehyde andl lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody.\nChIP-seq: Libraries were barcoded (NEXTflex™ DNA Barcodes) (Bio Scientific, Austin, TX).'; [Cell type]'Source: ''tissue: Human breast cancer cell line MCF7; cell line: MCF7; chip antibody: ZFX; sirna: none; ', 'tissue: Human breast cancer cell line MCF7; cell line: MCF7; chip antibody: ZNF711; sirna: none; ', 'tissue: Human breast cancer cell line MCF7; cell line: MCF7; chip antibody: none; sirna: none; ', 'tissue: Human prostate cancer cell line C42B; cell line: C42B; chip antibody: ZFX; sirna: none; ', 'tissue: Human prostate cancer cell line C42B; cell line: C42B; chip antibody: none; sirna: none; ', 'tissue: Human colon cancer cell line HCT116; cell line: HCT116; chip antibody: ZFX; sirna: none; ', 'tissue: Human colon cancer cell line HCT116; cell line: HCT116; chip antibody: none; sirna: none; ', 'tissue: Human kidney cancer cell line HEK293T; cell line: HEK293T; chip antibody: ZFX; sirna: none; ', 'tissue: Human kidney cancer cell line HEK293T; cell line: HEK293T; chip antibody: none; sirna: none; ', 'tissue: Human prostate cancer cell line C42B; cell line: C42B; chip antibody: none; sirna: siZFX; ', 'tissue: Human prostate cancer cell line C42B; cell line: C42B; chip antibody: none; sirna: siCtrl; ', 'tissue: Human breast cancer cell line MCF7; cell line: MCF7; chip antibody: none; sirna: siZFX; ', 'tissue: Human breast cancer cell line MCF7; cell line: MCF7; chip antibody: none; sirna: siCtrl; ', 'tissue: Human breast cancer cell line MCF7; cell line: MCF7; chip antibody: none; sirna: siZNF711; ', 'tissue: Human breast cancer cell line MCF7; cell line: MCF7; chip antibody: none; sirna: Both siZFX and siZNF711; ', 'tissue: Human normal prostate epithelial cell PrEC; cell line: PrEC; chip antibody: ZFX; sirna: none; ', 'tissue: Human prostate cancer cell line C42B; cell line: C42B; chip antibody: POLR2A; sirna: none; ', 'tissue: Human prostate cancer cell line C42B; cell line: C42B; chip antibody: H3K4me3; sirna: none; ' GSE41561 Homo sapiens 16 Genome binding/occupancy profiling by high throughput sequencing GPL10999; GPL11154 A novel proteomic approach reveals GREB1 as an Estrogen Receptor co-factor 2012-10-12 Methods for identifying protein-protein interactions have mostly been limited to tagged exogenous expression approaches. We now establish a rapid, robust and comprehensive method for finding interacting proteins using endogenous proteins from limited cell numbers. We apply this approach called ‘Rapid IP-Mass Spectrometry of Endogenous proteins (RIME)’ to identify ER, FoxA1 and E2F4 interacting proteins in breast cancer cells. From small numbers of starting cells, we find a comprehensive collection of known ER, FoxA1 and E2F4 targets, plus a number of novel unexpected interactors. One of the most ER (and FoxA1) associated interactors is GREB1, an estrogen induced gene with almost no known function. We apply RIME, in parallel with ER ChIP-seq, to identify ER protein interactors and ER binding events from solid tumor xenografts, resulting in the validation of the ER-GREB1 interactions. Furthermore, we establish a method for identifying endogenous interacting proteins from solid primary breast cancer samples, whih we apply to validate ER interactions with GREB1 and additional co-factors. Mechanistically, we show that GREB1 is recruited with ER to the chromatin where it functions as an essential estrogen-mediated regulatory factor required for effective ER transcriptional activity. Our novel approach enables, for the first time, the ability for discovery and validation of protein-protein interactions in whole tissue and solid tumors, revealing significant insight into ER regulatory factors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41561 Endogenous purification reveals GREB1 as a key estrogen receptor regulatory factor. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2013.01.010 {Cell reports (7.815): 10.1016/j.celrep.2013.01.010} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA177430 https://www.ebi.ac.uk/ena/browser/view/PRJNA177430 https://www.ncbi.nlm.nih.gov/sra?term=SRP016108 [Overal design]Examination of ERGREB1 and E2F4 genomic binding patterns in cell line and xenograft tumour models; [Treatment]'Tamoxifen or ICI 182 drug treatments done at 100nM concentration for the indicated time'; [Growth]'MCF7 cells were grown in DMEM with 10% FBS.'; [Extraction]'DNA extracted according to Schmidt D.(Methods,2009)\nLibrary constructed according to Schmidt D.(Methods,2009)'; [Cell type]'Source: ''cell line: MCF7; library id: JC347; antibody: E2F4; sc-866 (santa cruz) Lot-(A2804); treatment: MCF7 cells in complete DMEM media treated with 100nm Tamoxifen for 48hrs; ', 'cell line: MCF7; library id: JC348; antibody: E2F4; sc-866 (santa cruz) Lot-(A2804); treatment: MCF7 cells in complete DMEM media treated with 100nm ICI 182780 for 48hrs; ', 'cell line: MCF7; library id: JC379; antibody: none; treatment: Input; ', 'cell line: MCF7; library id: JC398; antibody: ER; sc-534 (santa cruz) Lot-(HC-20); treatment: MCF7 cells in Complete DMEM media; ', 'cell line: MCF7; library id: JC424; antibody: GREB1; ab72999 (abcam) Lot-(ab12563); treatment: MCF7 cells in Complete DMEM media (rep1); ', 'cell line: MCF7; library id: JC425; antibody: GREB1; ab72999 (abcam) Lot-(ab12563); treatment: MCF7 cells in Complete DMEM media and 4 hours of 100nM ICI 182780(rep1); ', 'cell line: MCF7; library id: JC430; antibody: ER; sc-534 (santa cruz) Lot-(HC-20); treatment: MCF7 cells in Complete DMEM media; ', 'cell line: MCF7; library id: JC465; antibody: GREB1; ab72999 (abcam) Lot-(ab12563); treatment: MCF7 cells in Complete DMEM media (rep2); ', 'cell line: MCF7; library id: JC466; antibody: GREB1; ab72999 (abcam) Lot-(ab12563); treatment: MCF7 cells in Complete DMEM media and 4 hours of 100nM ICI 182780(rep2); ', 'cell line: MCF7; library id: JC546; antibody: ER; sc-534 (santa cruz) Lot-(HC-20); treatment: MCF7 xenograft tumour in mouse; ', 'cell line: MCF7; library id: JC629; antibody: GREB1; HPA024616 (sigma)Lot-(A57971); treatment: MCF7 xenograft tumour in mouse; ', 'cell line: MCF7; library id: JC830; antibody: COT2; R&D systems PP-H7147-00-Lot(A2); treatment: MCF7 cells in Complete DMEM media; ', 'cell line: MCF7; library id: JC832; antibody: KLF4; R&D systems AF3640-Lot(xvh0310101); treatment: MCF7 cells in Complete DMEM media; ', 'cell line: MCF7; library id: JC888; antibody: IgG; sc-2027 (santa cruz)-Lot(c2712); treatment: MCF7 cells in Complete DMEM media; ', 'cell line: MCF7; library id: JC907; antibody: RXRA; sc-553 (santa cruz)-Lot(E0411); treatment: MCF7 cells in Complete DMEM media; ', 'cell line: MCF7; library id: JC945; antibody: TLE3; ab94972(abcam)-Lot(GR54354-1); treatment: MCF7 cells in Complete DMEM media; ' GSE65194 Homo sapiens 178 Expression profiling by array GPL570 Expression profiling of breast cancer samples from Institut Curie (Maire cohort) --Affy CDF 2015-01-22 Transcriptome analysis of 130 breast cancer samples (41 TNBC ; 30 Her2 ; 30 Luminal B and 29 Luminal A), 11 normal breast tissue samples and 14 TNBC cell lines. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE65194 Polo-like kinase 1: a potential therapeutic option in combination with conventional chemotherapy for the management of patients with triple-negative breast cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-12-2633 {PloS one (2.776) doi:10.1371/journal.pone.0122333}; {PloS one (2.776) doi:10.1371/journal.pone.0063712}; {Cancer research (8.378) doi:10.1158/0008-5472.CAN-12-2633}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA273413 https://www.ebi.ac.uk/ena/browser/view/PRJNA273413 None [Overal design]This dataset contains 178 arrays. 153 arrays were used to analyze 130 unique breast cancer samples from as many patients and 23 technical duplicates. In addition 11 “Normal” samples from healthy breast tissue obtained from mammoplasty are included, as well as a collection of 14 breast cancer cell lines. Data production involved different array batches and hybridation series which were accounted for in the pre-processing of the data.; [Treatment]'None'; [Growth]'Tumor samples were obtained from patients treated at the hospital of Institut Curie (Biological Resource Center, Paris, France). Healthy samples were obtained from mammary plastic surgery. Cell lines were grown from the American Type Culture Collection (ATCC),'; [Extraction]'Total RNA was extracted and purified from frozen tumor samples using the RNeasy Mini Kit (Qiagen) followed by the RNA clean up kit (Macherey Nagel), according to manufacturers’ instructions.'; [Cell type]'Source: ''sample_group: TNBC; array_batch: B3; hybridation batch: H1; ', 'sample_group: TNBC; array_batch: B7; hybridation batch: H4; ', 'sample_group: Her2; array_batch: B1; hybridation batch: H2; ', 'sample_group: Her2; array_batch: B7; hybridation batch: H4; ', 'sample_group: TNBC; array_batch: B6; hybridation batch: H4; ', 'sample_group: TNBC; array_batch: B2; hybridation batch: H2; ', 'sample_group: Her2; array_batch: B6; hybridation batch: H4; ', 'sample_group: TNBC; array_batch: B1; hybridation batch: H1; ', 'sample_group: TNBC; array_batch: B8; hybridation batch: H4; ', 'sample_group: TNBC; array_batch: B4; hybridation batch: H3; ', 'sample_group: Her2; array_batch: B4; hybridation batch: H2; ', 'sample_group: Her2; array_batch: B2; hybridation batch: H2; ', 'sample_group: TNBC; array_batch: B4; hybridation batch: H2; ', 'sample_group: TNBC; array_batch: B4; hybridation batch: H1; ', 'sample_group: Her2; array_batch: B1; hybridation batch: H3; ', 'sample_group: Her2; array_batch: B4; hybridation batch: H1; ', 'sample_group: Her2; array_batch: B5; hybridation batch: H3; ', 'sample_group: TNBC; array_batch: B1; hybridation batch: H3; ', 'sample_group: Her2; array_batch: B8; hybridation batch: H4; ', 'sample_group: TNBC; array_batch: B3; hybridation batch: H2; ', 'sample_group: Her2; array_batch: B5; hybridation batch: H1; ', 'sample_group: Her2; array_batch: B3; hybridation batch: H1; ', 'sample_group: TNBC; array_batch: B5; hybridation batch: H2; ', 'sample_group: TNBC; array_batch: B1; hybridation batch: H2; ', 'sample_group: TNBC; array_batch: B2; hybridation batch: H1; ', 'sample_group: TNBC; array_batch: B2; hybridation batch: H3; ', 'sample_group: Her2; array_batch: B2; hybridation batch: H3; ', 'sample_group: TNBC; array_batch: B5; hybridation batch: H3; ', 'sample_group: TNBC; array_batch: B5; hybridation batch: H1; ', 'sample_group: Luminal A; array_batch: B2; hybridation batch: H2; ', 'sample_group: Luminal A; array_batch: B4; hybridation batch: H2; ', 'sample_group: Luminal A; array_batch: B5; hybridation batch: H2; ', 'sample_group: Luminal A; array_batch: B3; hybridation batch: H1; ', 'sample_group: Luminal A; array_batch: B1; hybridation batch: H1; ', 'sample_group: Luminal A; array_batch: B3; hybridation batch: H3; ', 'sample_group: Luminal A; array_batch: B4; hybridation batch: H3; ', 'sample_group: Luminal A; array_batch: B5; hybridation batch: H3; ', 'sample_group: Luminal A; array_batch: B2; hybridation batch: H1; ', 'sample_group: Luminal A; array_batch: B5; hybridation batch: H1; ', 'sample_group: Luminal A; array_batch: B3; hybridation batch: H2; ', 'sample_group: Luminal A; array_batch: B2; hybridation batch: H3; ', 'sample_group: Luminal A; array_batch: B1; hybridation batch: H3; ', 'sample_group: Luminal A; array_batch: B4; hybridation batch: H1; ', 'sample_group: Luminal A; array_batch: B1; hybridation batch: H2; ', 'sample_group: Luminal B; array_batch: B5; hybridation batch: H2; ', 'sample_group: Luminal B; array_batch: B1; hybridation batch: H2; ', 'sample_group: Luminal B; array_batch: B4; hybridation batch: H3; ', 'sample_group: Luminal B; array_batch: B1; hybridation batch: H3; ', 'sample_group: Luminal B; array_batch: B2; hybridation batch: H3; ', 'sample_group: Luminal B; array_batch: B2; hybridation batch: H2; ', 'sample_group: Luminal B; array_batch: B5; hybridation batch: H1; ', 'sample_group: Luminal B; array_batch: B3; hybridation batch: H2; ', 'sample_group: Luminal B; array_batch: B1; hybridation batch: H1; ', 'sample_group: Luminal B; array_batch: B5; hybridation batch: H3; ', 'sample_group: Luminal B; array_batch: B3; hybridation batch: H3; ', 'sample_group: Luminal B; array_batch: B2; hybridation batch: H1; ', 'sample_group: Luminal B; array_batch: B3; hybridation batch: H1; ', 'sample_group: Luminal B; array_batch: B4; hybridation batch: H1; ', 'sample_group: CellLine; array_batch: B1; hybridation batch: H1; cell line: 184B5; ', 'sample_group: Healthy; array_batch: B1; hybridation batch: H2; ', 'sample_group: CellLine; array_batch: B1; hybridation batch: H2; cell line: MDA-MB-436; ', 'sample_group: Healthy; array_batch: B1; hybridation batch: H3; ', 'sample_group: CellLine; array_batch: B1; hybridation batch: H3; cell line: HCC1143; ', 'sample_group: CellLine; array_batch: B2; hybridation batch: H1; cell line: HCC1187; ', 'sample_group: Healthy; array_batch: B2; hybridation batch: H1; ', 'sample_group: Healthy; array_batch: B2; hybridation batch: H2; ', 'sample_group: CellLine; array_batch: B2; hybridation batch: H2; cell line: BT20; ', 'sample_group: CellLine; array_batch: B2; hybridation batch: H3; cell line: HCC1937; ', 'sample_group: Healthy; array_batch: B2; hybridation batch: H3; ', 'sample_group: CellLine; array_batch: B3; hybridation batch: H1; cell line: MCF-12A; ', 'sample_group: CellLine; array_batch: B3; hybridation batch: H2; cell line: HCC38; ', 'sample_group: Healthy; array_batch: B3; hybridation batch: H3; ', 'sample_group: CellLine; array_batch: B3; hybridation batch: H3; cell line: Hs 578T; ', 'sample_group: Healthy; array_batch: B4; hybridation batch: H1; ', 'sample_group: CellLine; array_batch: B4; hybridation batch: H2; cell line: MDA-MB-468; ', 'sample_group: CellLine; array_batch: B4; hybridation batch: H3; cell line: BT-549; ', 'sample_group: Healthy; array_batch: B5; hybridation batch: H1; ', 'sample_group: CellLine; array_batch: B5; hybridation batch: H1; cell line: HCC70; ', 'sample_group: Healthy; array_batch: B5; hybridation batch: H2; ', 'sample_group: CellLine; array_batch: B5; hybridation batch: H2; cell line: MDA-MB-157; ', 'sample_group: CellLine; array_batch: B5; hybridation batch: H3; cell line: MDA-MB-231; ' GSE47493 Mus musculus 20 Expression profiling by array GPL7202 ΔNp63 promotes stem cell activity in mammary gland development and basal-like breast cancer by enhancing Fzd7 expression and Wnt signaling 2013-05-29 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47493 ΔNp63 promotes stem cell activity in mammary gland development and basal-like breast cancer by enhancing Fzd7 expression and Wnt signalling. Nature cell biology 17.728 https://doi.org/10.1038/ncb3040 {Nature cell biology (17.728): 10.1038/ncb3040} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA205866 https://www.ebi.ac.uk/ena/browser/view/PRJNA205866 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'cell preparation: Single cell suspensions were prepared from the mammary glands of virgin mice using mechanical and enzymatic dissociation as detail described in Tiede BJ et al., 2009, PLoS ONE 4(11): e8035. doi:10.1371/journal.pone.0008035\nFACS sorting protocol: Various subpopulations of mammary epithelial cells were sorted using flow cytometry based on combination of a set of surface markers. The marker profiles and FACS gating parameters are detailed in Tiede BJ et al., 2009, PLoS ONE 4(11): e8035. doi:10.1371/journal.pone.0008035\nTotal RNA were extracted using RNAeasy mini-prep kit from Qiagen', 'Cell preparation protocol: Single cell suspensions were prepared from the mammary glands of virgin and pregnant wild type and transgenic mice using mechanical and enzymatic dissociation as detail described in Tiede BJ et al., 2009, PLoS ONE 4(11): e8035. doi:10.1371/journal.pone.0008035\nFACS sorting protocol: Various subpopulations of mammary epithelial cells were sorted using flow cytometry based on combination of a set of surface markers and/or GFP expression. The marker profiles and FACS gating parameters are detailed in Tiede BJ et al., 2009, PLoS ONE 4(11): e8035. doi:10.1371/journal.pone.0008035\nTotal RNA were extracted using RNAeasy mini-prep kit from Qiagen'; [Cell type]'Source: ''strain: C57/B6; genotype/variation: wild type; mg condition: Virgin; enrichment: MaSC; ', 'cell lines: Mix of 11 mouse cell lines; ', 'strain: C57/B6; genotype/variation: wild type; mg condition: Virgin; enrichment: luminal progenitor; ', 'strain: C57/B6; genotype/variation: DNP63 KO heterozygous; mg condition: Virgin; enrichment: MaSC; ', 'strain: C57/B6; genotype/variation: DNP63 KO heterozygous; mg condition: Virgin; enrichment: luminal progenitor; ', 'strain: C57/B6; genotype/variation: wild type; mg condition: Virgin; enrichment: none; ', 'strain: C57/B6; genotype/variation: DNP63 KO heterozygous; mg condition: Virgin; enrichment: none; ', 'strain: FVB/N-J; genotype/variation: wild type; mg condition: Virgin; enrichment: MaSC; ', 'strain: FVB/N-J; genotype/variation: wild type; mg condition: Virgin; enrichment: luminal progenitor; ', 'strain: FVB/N-J; genotype/variation: wild type; mg condition: Virgin; enrichment: none; ', 'strain: FVB/N-J; genotype/variation: wild type; mg condition: pregnant; enrichment: MaSC; ', 'strain: FVB/N-J; genotype/variation: wild type; mg condition: pregnant; enrichment: luminal progenitor; ', 'strain: FVB/N-J; genotype/variation: wild type; mg condition: pregnant; enrichment: none; ', 'strain: FVB/N-Luciferase transgenic mouse L2G85; genotype/variation: transgenic mouse L2G85; mg condition: Virgin; enrichment: MaSC; ', 'strain: FVB/N-Luciferase transgenic mouse L2G85; genotype/variation: transgenic mouse L2G85; mg condition: Virgin; enrichment: none; ' GSE142221 Homo sapiens 51 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL20301 FOXA1 suppresses cancer immunity independent of DNA binding 2019-12-17 Exclusion of lymphocytes from tumors is a major barrier for effective immuno- and chemo-therapy of cancer. We found that FOXA1 overexpression inversely correlates with expression of antigen processing and presentation and interferon signaling genes in different cancer types. FOXA1 binds to STAT proteins and inhibits expression of antigen presentation and interferon response genes and tumor immunity independent of the forkhead domain - DNA binding function. Increased FOXA1 also correlates with immunotherapy resistance in murine triple negative breast tumor and bladder cancer in patients and chemo-resistance in breast cancer patients. Our results reveal that FOXA1 is a key immune suppressor, suggesting that FOXA1 overexpression may predict tumor resistance to immuno- and chemo-therapies and that depletion of FOXA1 may therapeutically convert cancers from ‘immune-cold’ to ‘immune-hot’ diseases. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE142221 None None None None None 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA596242 https://www.ebi.ac.uk/ena/browser/view/PRJNA596242 https://www.ncbi.nlm.nih.gov/sra?term=SRP237953 [Overal design]To determine the inhibitory effect of FOXA1 variants on the DNA binding ability of STAT2, cells were expressed of Vetor as control, FOXA1-WT, FOXA1-R261G and FOXA1△αH3, and then the endogenous FOXA1 in LNCaP cells was knocked down by specific siRNA for next STAT2 chromatin immunoprecipitation sequencing (ChIP-seq).; [Treatment]'LNCaP cells was treated with vehicle (PBS) or 100ng/L IFNα for 24 hours.', 'LNCaP cells was treated with vehicle (PBS) or 100ng/L IFNα for 6 hours.'; [Growth]'Cells were maintained at 37°C and 5% CO2 in RPMI 1640 containing 10% fetal bovine serum (FBS) and 1% antibiotic/antimycotic (Thermo Fisher Scientific).FGF-2 (NS expansion medium).'; [Extraction]"Lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody.\nLibraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit (Part# 0801-0303). Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation DNA was PCR amplified with Illumina primers for 15 cycles and library fragments of ~250 bp (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the Genome Analyzer following the manufacturer's protocols.", "RNeasy Mini Kit (Cat No.74104, QIAGEN)\nLibraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit (Part# 0801-0303). Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation DNA was PCR amplified with Illumina primers for 15 cycles and library fragments of ~250 bp (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the Genome Analyzer following the manufacturer's protocols."; [Cell type]'prostate cancer''cell line: LNCaP; cell type: prostate cancer; passages: 20-30; knockdown: vector control; rescue: N/A; chip antibody: anti-STAT2 #72604S, Cell Signaling Technology; ', 'cell line: LNCaP; cell type: prostate cancer; passages: 20-30; knockdown: shFOXA1; rescue: N/A; chip antibody: anti-STAT2 #72604S, Cell Signaling Technology; ', 'cell line: LNCaP; cell type: prostate cancer; passages: 20-30; knockdown: shFOXA1; rescue: FOXA1-WT; chip antibody: anti-STAT2 #72604S, Cell Signaling Technology; ', 'cell line: LNCaP; cell type: prostate cancer; passages: 20-30; knockdown: shFOXA1; rescue: FOXA1-R261G; chip antibody: anti-STAT2 #72604S, Cell Signaling Technology; ', 'cell line: LNCaP; cell type: prostate cancer; passages: 20-30; knockdown: shFOXA1; rescue: FOXA1-delta_alphaH3; chip antibody: anti-STAT2 #72604S, Cell Signaling Technology; ', 'cell line: LNCaP; cell type: prostate cancer; passages: 20-30; knockdown: N/A; rescue: N/A; chip antibody: anti-FOXA1 #ab23738, Abcam; ', 'cell type: prostate cancer; passages: 20-30; chip antibody: IgG #3900, Cell Signaling Technology; ', 'cell type: prostate cancer; passages: 20-30; chip antibody: anti-STAT2 #72604S, Cell Signaling Technology; ', 'cell type: prostate cancer; passages: 20-30; ' GSE94523 Homo sapiens 111 Expression profiling by array GPL3676 Tamoxifen-associated endometrial tumors expose differential enhancer activity for Estrogen Receptor alpha [Microarray Expression] 2017-02-06 Tamoxifen, a small molecule inhibitor that binds the Estrogen Receptor alpha (ERα), blocks breast cancer progression while increasing the risk for endometrial cancer. In this study, we assessed genome-wide ERα-chromatin interactions in surgical specimens of endometrial tumors from patients who were previously treated for breast cancer with tamoxifen, and endometrial tumors from patients who were treated without tamoxifen. We compared ERα and signal at differential ERα sites in endometrial tumors of nine patients who received tamoxifen with endometrial tumors with six patients who never used tamoxifen. In addition, we performed H3K27ac (a marker for activity) ChIPs on the above mentioned endometrial tumors, and assed this signal at differential ERα sites. Compared to endometrial tumors of non-users, tamoxifen-associated endometrial tumors exposed higher H3K27ac intensities at ERα sites that are enriched in tamoxifen-associated endometrial tumors. Four tamoxifen-associated endometrial tumors that we used in our analysis have been previously published as Tumor A, B, D, and E in GSE81213. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE94523 Estrogen receptor α wields treatment-specific enhancers between morphologically similar endometrial tumors. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1615233114 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1615233114} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA371413 https://www.ebi.ac.uk/ena/browser/view/PRJNA371413 None [Overal design]Gene expression profiling in 111 endometrial tumors; [Treatment]'No treatment'; [Growth]'Tissued from patients'; [Extraction]'Thirty 30-µm cryosections of fresh-frozen endometrial tumors that contained at least 50% tumor were used for RNA isolation using Trizol (#15596-026, Invitrogen) according to manufacturer’s instructions. RNA was purified using RNeasy Mini Kit (#74104, Qiagen), and treated with DNAse using RNase-Free DNase Set (#79254, Qiagen).'; [Cell type]'Source: ''tissue: endometrioid adenocarcinoma; ', 'tissue: Endometrial tumor; ' GSE90104 Homo sapiens 6 Expression profiling by array GPL16951 Improvement of antiproliferative activity of betulinic acid by fluorine substitution 2016-11-21 Gene expression profiling of betulinic acid and fluorinated betulinic acid-treated MCF-7 human breast cancer cells. We used Phalanx Biotech Human Whole Genome OneArray HOA6.2 Array to determine differential gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE90104 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA354421 https://www.ebi.ac.uk/ena/browser/view/PRJNA354421 None [Overal design]Samples were collected from betulinic acid and fluorinated betulinic acid-treated MCF-7 cells.; [Treatment]'Cells were treated with 40 uM betulinic acid or 40 uM fluorinated betulinic acid for 24 h.'; [Growth]'MCF-7 cells were cultured in DMEM/F12 medium supplemented with 10% (v/v) FBS, 100 units/ml penicillin, and 100 ug/ml streptomycin.'; [Extraction]'RNA extraction by Trizol. RNA purity was checked by optical density of NanoDrop ND-1000 and agarose electrophoresis with the result of A260/A280≧1.8, no gDNA contamination. RNA integrity was measured by Agilent RNA 6000 Nano Assay (RIN≧7).'; [Cell type]'human breast cancer cells''cell line: MCF-7; cell type: human breast cancer cells; treated with: none (control); ', 'cell line: MCF-7; cell type: human breast cancer cells; treated with: 40 uM betulinic acid for 24 hr; ', 'cell line: MCF-7; cell type: human breast cancer cells; treated with: 40 uM fluorinated betulinic acid for 24hr; ' GSE143626 Homo sapiens 344 Other; Expression profiling by high throughput sequencing; Expression profiling by array GPL11154; GPL16288; GPL16686; GPL18573 Deregulation of ribosomal protein expression and translation promotes breast cancer metastasis 2020-01-14 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE143626 Deregulation of ribosomal protein expression and translation promotes breast cancer metastasis. Science (New York, N.Y.) 41.037 https://doi.org/10.1126/science.aay0939 {Science (New York, N.Y.) (41.037): 10.1126/science.aay0939} 'total RNA', 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA601126 https://www.ebi.ac.uk/ena/browser/view/PRJNA601126 None [Overal design]Refer to individual Series; [Treatment]'Control or a CMV promoter-driven, lentiviral encoded vector to ectopically express RPL15. Lentiviral expression constructs for RPL15 (Accession: BC071672) were obtained from the CCSB-Broad Lentiviral Expression Library.', 'MCF10A cells were split the day before initiating treatment with TGF-beta (5ng/mL) for 3 days and then harvested or split and re-treated with TGF-beta for a total of 6 days.Untreated control cells and TGF-beta treated cells were harvested for RNA.', 'Patients with a diagnosis of ER and/or PR positive metastatic breast cancer provided informed consent for de-identified blood collection, as per institutional review board approved protocol (DF/HCC 05-300) at Massachusetts General Hospital. Approximately 6-12 mL of fresh whole blood was processed through the microfluidic CTC-iChip as previously described [PMID: 24577360] within 4 hours from the blood draw. Before processing, whole blood samples were incubated with biotinylated antibodies against CD45 (R&D Systems, clone 2D1), CD66b (AbD Serotec, clone 80H3) and followed by incubation with Dynabeads MyOne Streptavidin T1 (Invitrogen) to achieve magnetic labelling of white blood cells. This mixture was processed through the CTC-iChip. To identify CTCs, the CTC-enriched product was stained with Alexa Fluor 488-conjugated antibodies against EpCAM (Cell Signaling Technology, #5198), Cadherin 11 (R&D Systems, FAB17901G), and HER2 (BioLegend, #324410). To identify contaminating white blood cells the product was stained with TexasRed-conjugated antibodies against CD45 (BD Biosciences, BDB562279), CD14 (BD Biosciences, BDB562334), and CD16 (BD Biosciences, BDB562320). The stained product was viewed under a fluorescent microscope where single CTCs were identified based on intact cellular morphology, Alexa Fluor 488-positive staining and lack of TexasRed staining. Cells of interest were individually micromanipulated with a 10 mm transfer tip on an Eppendorf Transfer-Man NK 2 micromanipulator and lysed.'; [Growth]'CTCs were grown in suspension in ultra-low attachment plates (Corning) in tumor sphere media, consisting of RPMI-1640 with GlutaMAX supplemented with EGF (20ng/mL), FGF (20ng/mL), 1X B27, and 1X antibiotic/antimycotic (Life Technologies), in 4% O2, as previously described (PUBMED IDs 27556950 and 25013076). CTC lines were routinely checked for mycoplasma (MycoAlert, Lonza), and were authenticated by RNA-seq and DNA-seq.', 'MCF10A were grown as previously described [PUBMED ID 12798140].'; [Extraction]'Ribosome profiling was performed as previously described (PUBMED ID 22836135). Briefly, 10 million RPL15- or control-expressing Brx-142 cells were treated with 0.1 mg/ml cyclohexamide for 1 minute, washed with cold PBS containing cycloheximide and lysed. A range of RNase I (Thermofisher) concentrations was tested, and an optimal concentration was chosen that did not lead to degradation of the ribosome protected fragments. RNase I (Thermofisher) treatment was performed and the monosomes were isolated by gel filtration MicroSpin S-400 HR Columns (GE Healthcare). After RNA extraction using RNA Clean & Concentrator-25 kit (Zymo Research), rRNA was depleted (Ribo-Zero Gold rRNA Removal Kit, Illumina), and ribosome-protected fragments were purified by PAGE. The fragments were end- repaired with PNK (NEB).\nLibraries were prepared using a TruSeq small RNA Library Prep Kit (Illumina) and sequenced on a NextSeq 500 Illumina (76 bp single-end reads).', 'RNA was extracted using the RNeasy Mini Kit (Qiagen).\nThe SMART-Seq HT Kit (Takara Bio USA) was used according to the manufacturer’s instructions.', 'Polysome fractions were combined and RNA isolated with TRIzol reagent.', "RNA was extracted as previously described (Tang, F., Barbacioru, C., Nordman, E., Li, B., Xu, N., Bashkirov, V.I., Lao, K., and Surani, M.A. (2010). RNA-Seq analysis to capture the transcriptome landscape of a single cell. Nat Protoc 5, 516-535).\nLibraries were constructed as previously described (Tang, F., Barbacioru, C., Nordman, E., Li, B., Xu, N., Bashkirov, V.I., Lao, K., and Surani, M.A. (2010). RNA-Seq analysis to capture the transcriptome landscape of a single cell. Nat Protoc 5, 516-535). Briefly, to generate cDNA, samples were treated with reverse transcription master mix (0.05 uL RNase inhibitor, 0.07uL T4 gene 32 protein, and 0.33uL SuperScript III Reverse Transcriptase per 1X volume) and incubated on thermocycler at 50C for 30 minutes and 70C for 15 minutes. To remove free primer, 1.0uL of EXOSAP mix was added to each sample, which was incubated at 37C for 30 minutes and inactivated at 80C for 25 minutes. Next, a 3'-poly-A tail was added to the cDNA in each sample by incubating in master mix (0.6uL 10X PCR Buffer II, 0.36uL 25mM MgCl2, 0.18uL 100mM dATP, 0.3uL Terminal Transferase, 0.3uL RNase H, and 4.26uL H2O per 1X volume) at 37C for 15 minutes and inactivated at 70C for 10 minutes. A second strand cDNA was synthesis by dividing each sample into 4 and incubating in master mix (2.2uL 10X High Fidelity PCR Buffer, 1.76uL 2.5mM each dNTP, 0.066uL UP2 Primer at 100uM, 0.88uL 50mM MgSO4, 0.44uL Platinum Taq DNA Polymerase, and 13.654uL H2O per 1X volume) at 95C for 3 minutes, 50C for 2 minutes, and 72C for 10 minutes. DNA was sheared using a Covaris S2 system and then prepared for ABI 5500XL library construction with end polishing, size selection of 200-500 bp using AMPure XP, ABI barcode adaptor ligation, amplification and purification with AMPure XP, and then pooling of barcoded samples for emulsion PCR wiht template beads preparation. Samples were then loaded per protocol on the ABI 5500XL.\nRNA-Seq using oligo-dT cDNA synthesis and amplification of cDNA libraries using custom universal PCR primers", 'Single CTCs were isolated from fresh whole blood following leukocyte depletion using the microfluidic CTC-iChip as described in PMID 23552373. Single cells were individually micromanipulated using a 10 μm transfer tip on an Eppendorf TransferMan NK 2 micromanipulator, transferred into PCR tubes containing RNA protective lysis buffer, and flash frozen in liquid nitrogen.\nClontech SMARTer Ultra Low Input Kit for RNA v3 for cDNA synthesis and the Nextera XT kit for library construction'; [Cell type]'Source: ''tissue: circulating tumor cell - derived cell line; rpl15 overexpressing: control; batch: batch1; molecule subtype: ribosome-bound mRNA; ', 'tissue: circulating tumor cell - derived cell line; rpl15 overexpressing: RPL15 overexpressing; batch: batch1; molecule subtype: ribosome-bound mRNA; ', 'tissue: circulating tumor cell - derived cell line; rpl15 overexpressing: control; batch: batch2; molecule subtype: ribosome-bound mRNA; ', 'tissue: circulating tumor cell - derived cell line; rpl15 overexpressing: RPL15 overexpressing; batch: batch2; molecule subtype: ribosome-bound mRNA; ', 'tissue: circulating tumor cell - derived cell line; rpl15 overexpressing: control; ', 'tissue: circulating tumor cell - derived cell line; rpl15 overexpressing: RPL15 overexpressing; ', 'cell line: MCF10A; tissue: breast cancer; treatment: none; molecule subtype: mRNA; ', 'cell line: MCF10A; tissue: breast cancer; treatment: 3 days TGF-b; molecule subtype: mRNA; ', 'cell line: MCF10A; tissue: breast cancer; treatment: 6 days TGF-b; molecule subtype: mRNA; ', 'cell line: MCF10A; tissue: breast cancer; treatment: none; molecule subtype: Polysome; ', 'cell line: MCF10A; tissue: breast cancer; treatment: 3 days TGF-b; molecule subtype: Polysome; ', 'cell line: MCF10A; tissue: breast cancer; treatment: 6 days TGF-b; molecule subtype: Polysome; ', 'patient: Brx71; overall survival days: 454; overall survival event: 1; ', 'patient: Brx50; overall survival days: 31; overall survival event: 1; ', 'patient: Brx61; ', 'patient: Brx74; overall survival days: 914; overall survival event: 0; ', 'patient: Brx10; overall survival days: 621; overall survival event: 1; ', 'patient: Brx72; ', 'patient: Brx73; overall survival days: 651; overall survival event: 0; ', 'patient: BR21; overall survival days: 220; overall survival event: 1; ', 'patient: Brx83; overall survival days: 568; overall survival event: 1; ', 'patient: Brx86; overall survival days: 99; overall survival event: 1; ', 'patient: Brx86; overall survival days: 98; overall survival event: 1; ', 'patient: Brx78; overall survival days: 580; overall survival event: 1; ', 'patient: Brx82; ', 'patient: Brx95; overall survival days: 835; overall survival event: 0; ', 'patient: Brx95; overall survival days: 834; overall survival event: 0; ', 'patient: Brx87; overall survival days: 485; overall survival event: 1; ', 'patient: Brx90; overall survival days: 596; overall survival event: 0; ', 'patient: Brx100; overall survival days: 98; overall survival event: 0; ', 'patient: Brx98; overall survival days: 755; overall survival event: 0; ', 'patient: Brx97; overall survival days: 786; overall survival event: 1; ', 'patient: Brx100; overall survival days: 97; overall survival event: 0; ', 'patient: Brx107; overall survival days: 754; overall survival event: 0; ', 'patient: Brx35; overall survival days: 567; overall survival event: 1; ', 'patient: Brx70; ', 'patient: Brx116; overall survival days: 637; overall survival event: 0; ', 'patient: Brx121; overall survival days: 651; overall survival event: 0; ', 'patient: Brx122; overall survival days: 636; overall survival event: 0; ', 'patient: Brx120; ', 'patient: Brx109; overall survival days: 92; overall survival event: 1; ', 'patient: Brx117; overall survival days: 501; overall survival event: 0; ', 'patient: Brx35; overall survival days: 510; overall survival event: 1; ', 'patient: Brx93; ', 'patient: Brx126; overall survival days: 615; overall survival event: 0; ', 'patient: Brx130; overall survival days: 83; overall survival event: 0; ', 'patient: Brx134; overall survival days: 593; overall survival event: 0; ', 'patient: Brx163; ', 'patient: Brx90; overall survival days: 126; overall survival event: 0; ', 'patient: Brx146; ', 'patient: Brx164; overall survival days: 395; overall survival event: 1; ', 'patient: Brx116; overall survival days: 342; overall survival event: 0; ', 'patient: Brx117; overall survival days: 216; overall survival event: 0; ', 'patient: Brx03; ', 'patient: BR29; overall survival days: 999; overall survival event: 0; ', 'patient: BR29; overall survival days: 998; overall survival event: 0; ', 'patient: Brx66; overall survival days: 1007; overall survival event: 0; ', 'patient: Brx53; overall survival days: 219; overall survival event: 1; ', 'patient: Brx53; overall survival days: 246; overall survival event: 1; ', 'patient: Brx12; ', 'patient: Brx52; ', 'patient: Brx17; ', 'patient: BrTr08; overall survival days: 28; overall survival event: 0; ', 'patient: Brx11; ', 'patient: BrTr11; overall survival days: 125; overall survival event: 1; ', 'patient: BrTr12; ', 'patient: BRx-102; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-10; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-110; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-110; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-129; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-129; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-129; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-139; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-139; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-152; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-170; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-171; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-172; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-172; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-18; clinical her2: HER2+; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-18; clinical her2: HER2+; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-42; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-42; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-82; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-82; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-82; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-97; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-97; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-122; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-122; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-129; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-131; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-132; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-136; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-146; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-16; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-16; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-172; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-18; clinical her2: HER2+; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-183; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-189; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-189; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-189; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-193; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-194; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-42; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-47; clinical hormone receptor: HR+; clinical her2: HER2+; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-47; clinical hormone receptor: HR+; clinical her2: HER2+; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-55; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-55; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-65; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-96; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-110; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-110; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-111; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-131; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-132; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-156; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-156; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-16; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-164; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-180; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-180; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-188; number uniquely mapped reads: fail; ptprc expression: fail; ', 'patient: BRx-193; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-194; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-206; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-212; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-212; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-213; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-213; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-221; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-233; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-233; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-233; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-239; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-239; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-245; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-245; clinical hormone receptor: HR-; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-267; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-267; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: fail; ptprc expression: pass; ', 'patient: BRx-267; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-278; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: pass; ', 'patient: BRx-278; clinical hormone receptor: HR+; clinical her2: HER2-; number uniquely mapped reads: pass; ptprc expression: fail; ', 'patient: BRx-47; clinical hormone receptor: HR+; clinical her2: HER2+; number uniquely mapped reads: pass; ptprc expression: fail; ' GSE85350 Homo sapiens 33 Expression profiling by array GPL17586 Bisphenol A alternatives can effectively substitute for estradiol in promoting cell growth through estrogen receptor alpha in human breast cancer cells 2016-08-09 Plasticizers with estrogenic activity, such as bisphenol A (BPA), have been reported to have potential adverse health effects in humans, especially in fetal and infant stages. Due to mounting evidence and public pressure BPA is being phased out by the plastics manufacturing industry and is being replaced by other bisphenol variants in “BPA-free” products. We have compared estrogenic activity of 7 bisphenol analogues (BPA; bisphenol S, BPS; bisphenol F, BPF; bisphenol AP, BPAP; bisphenol AF, BPAF; bisphenol Z, BPZ; bisphenol B, BPB) in human breast cancer cell lines. We used microarrays to detail the alterations in gene expression profiles associated with MCF-7 cell line exposure to bisphenol A analogues https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE85350 Editor's Highlight: Transcriptome Profiling Reveals Bisphenol A Alternatives Activate Estrogen Receptor Alpha in Human Breast Cancer Cells. Toxicological sciences : an official journal of the Society of Toxicology 3.564 https://doi.org/10.1093/toxsci/kfx101 {Toxicological sciences : an official journal of the Society of Toxicology (3.564): 10.1093/toxsci/kfx101} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA338240 https://www.ebi.ac.uk/ena/browser/view/PRJNA338240 None [Overal design]MCF-7 cells treated during a period of 48h with the BPA alternatives and the natural hormone 17β-estradiol were subjected to a full transcriptome profiling using the Affymetrix microarray platform.; [Treatment]'MCF-7 cells were seeded into 96-well plates with DMEM medium containing 10% FBS at a density of 20,000 cells per well. After 24 h of steroid deprivation in hormone free medium (charcoal stripped FBS), the cells were stimulated with test substances for 48 h in triplicate in three independent experiments.'; [Growth]'None'; [Extraction]"RNA extraction was performed using the Agencourt RNAdvance Cell V2 kit according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MCF-7; exposure time: 48h; experimental group: Bisphenol AF; treatment: Bisphenol AF; concentration (nm): 80; ', 'cell line: MCF-7; exposure time: 48h; experimental group: Bisphenol AP; treatment: Bisphenol AP; concentration (nm): 1000; ', 'cell line: MCF-7; exposure time: 48h; experimental group: Bisphenol A; treatment: Bisphenol A; concentration (nm): 400; ', 'cell line: MCF-7; exposure time: 48h; experimental group: Bisphenol B; treatment: Bisphenol B; concentration (nm): 300; ', 'cell line: MCF-7; exposure time: 48h; experimental group: Bisphenol F; treatment: Bisphenol F; concentration (nm): 1000; ', 'cell line: MCF-7; exposure time: 48h; experimental group: Bisphenol Z; treatment: Bisphenol Z; concentration (nm): 400; ', 'cell line: MCF-7; exposure time: 48h; experimental group: Bisphenol S; treatment: Bisphenol S; concentration (nm): 1500; ', 'cell line: MCF-7; exposure time: 48h; experimental group: E2_1nM; treatment: Estradiol; concentration (nm): 1; ', 'cell line: MCF-7; exposure time: 48h; experimental group: E2_100pM; treatment: Estradiol; concentration (nm): 0.1; ', 'cell line: MCF-7; exposure time: 48h; experimental group: E2_10pM; treatment: Estradiol; concentration (nm): 0.01; ', 'cell line: MCF-7; exposure time: 48h; experimental group: Control; treatment: Control; concentration (nm): 0; ' GSE51233 Homo sapiens 6 Non-coding RNA profiling by array GPL8227 Development of micoRNA expression signatures for invasive ductal breast carcinoma 2013-09-27 To further develop gene expression approach to miRNA biomarker discovery, we have employed miRNA microarray expression profiling as a discovery platform to identify miRNA with the potential to regulated the gene expression signatures in the process of tumor development. Human FFPE tissues from grade 1, 2 and 3 were used to profile miRNA. The miRNA targeted genes were also studied for expression along with the selected miRNA, from this signature in the same RNA samples by real-time PCR, confirming the selected miRNA has regulatory action on the target gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE51233 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA221780 https://www.ebi.ac.uk/ena/browser/view/PRJNA221780 None [Overal design]miRNA were profiled with less number of samples from each grade using miRNa microarray hybridization. Confirmation of the expression was carried out with more (20 from each grade)number of samples and targetted gene expression regulation was confirmed using RT PCR.; [Treatment]'None'; [Growth]'None'; [Extraction]"RNA extraction using Ambion's Tri-reagent method as per manufacturer protocol (part no.AM9738). RNA concentration was estimated using Agilent Nanodrop Bioanalyser Spectrophotometer."; [Cell type]'Source: ''tissue: Female breast formalin fixed biopsy blocks; gender: female; age: 32y; ', 'tissue: Female breast formalin fixed biopsy blocks; gender: female; age: 37y; ', 'tissue: Female breast formalin fixed biopsy blocks; gender: female; age: 35y; ', 'tissue: Female breast formalin fixed biopsy blocks; gender: female; age: 55y; ', 'tissue: Female breast formalin fixed biopsy blocks; gender: female; age: 50y; ' GSE59829 Homo sapiens 123 Expression profiling by array GPL8179 Mir-30e* is an independent subtype-specific prognostic marker in breast cancer 2014-07-28 Both gene and miRNA expression patterns separately correlate with survival in breast cancer suggesting that the development of models using both miRNAs and gene markers might improve their prediction performance. In this study miRNAs significantly associated with development of distant metastasis were identified and further investigated and validated in the publicly available dataset from the METABRIC. A combined outcome prediction model using gene expression, miRNA expression and clinico-pathological features was implemented. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59829 miR-30e* is an independent subtype-specific prognostic marker in breast cancer. British journal of cancer 5.416 https://doi.org/10.1038/bjc.2015.206 {British journal of cancer (5.416): 10.1038/bjc.2015.206} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA256342 https://www.ebi.ac.uk/ena/browser/view/PRJNA256342 None [Overal design]Fresh-frozen primary tumors were obtained from 123 patients with operable breast cancer previously untreated, pathologically defined as axillary node-negative and undergoing radical or conservative surgery at the Istituto Nazionale Tumori of Milano (INTM) between1990 and 1998. Patients were selected in order to have a comparable pattern of classical risk factors (age, tumor size).; [Treatment]'None'; [Growth]'Tissue samples collected at time of surgery were stored at -80°C until RNA extraction.'; [Extraction]'Tissue was pulverized using a Mikrodismembrator (Braun Biotech International , Germany). Total RNA was extracted with the Trizol reagent (Invitrogen, Carlsbad, CA) according to manufacture instructions.'; [Cell type]'Source: ''distant_metastasis: 0; dfs (months): 83; age: 61; tumor_size: 2.5; histotype: other; esr1_status: 1; erbb2_status: 1; ', 'distant_metastasis: 0; dfs (months): 83; age: 59; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 173; age: 61; tumor_size: 3.5; histotype: CDI; esr1_status: 0; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 95; age: 67; tumor_size: 2.8; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 82; age: 57; tumor_size: 1.7; histotype: CDI; esr1_status: 0; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 185; age: 43; tumor_size: 2.5; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 93; age: 68; tumor_size: 4; histotype: other; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 120; age: 49; tumor_size: 1; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 91; age: 45; tumor_size: 2.5; histotype: CDI; esr1_status: 0; erbb2_status: 1; ', 'distant_metastasis: 0; dfs (months): 91; age: 57; tumor_size: 2.2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 172; age: 45; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 87; age: 47; tumor_size: 4; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 170; age: 65; tumor_size: 2.5; histotype: CDI+CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 72; age: 60; tumor_size: 3.5; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 180; age: 44; tumor_size: 3; histotype: other; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 79; age: 65; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 122; age: 68; tumor_size: 4.5; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 89; age: 65; tumor_size: 2.3; histotype: other; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 132; age: 52; tumor_size: 1.8; histotype: CDI; esr1_status: 0; erbb2_status: 1; ', 'distant_metastasis: 0; dfs (months): 117; age: 47; tumor_size: 2; histotype: CDI; esr1_status: 0; erbb2_status: 1; ', 'distant_metastasis: 0; dfs (months): 117; age: 53; tumor_size: 1.7; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 124; age: 41; tumor_size: 1.4; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 148; age: 44; tumor_size: 1.5; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 168; age: 50; tumor_size: 2.3; histotype: CDI; esr1_status: 0; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 159; age: 50; tumor_size: 2.3; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 159; age: 62; tumor_size: 2.8; histotype: CDI; esr1_status: 0; erbb2_status: 1; ', 'distant_metastasis: 0; dfs (months): 93; age: 62; tumor_size: 1.6; histotype: CDI+CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 160; age: 51; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 71; age: 58; tumor_size: 1.4; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 127; age: 37; tumor_size: 2.7; histotype: CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 111; age: 68; tumor_size: 1.1; histotype: CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 163; age: 43; tumor_size: 1.8; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 165; age: 59; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 152; age: 51; tumor_size: 3; histotype: CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 158; age: 57; tumor_size: 1.8; histotype: CDI; esr1_status: 1; erbb2_status: 1; ', 'distant_metastasis: 0; dfs (months): 152; age: 47; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 118; age: 63; tumor_size: 1.2; histotype: CDI+CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 77; age: 41; tumor_size: 1.6; histotype: CDI+CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 66; age: 37; tumor_size: 2.4; histotype: CDI; esr1_status: 0; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 135; age: 82; tumor_size: 4; histotype: other; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 145; age: 52; tumor_size: 1.8; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 112; age: 55; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 131; age: 48; tumor_size: 1.7; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 111; age: 40; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 136; age: 45; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 112; age: 52; tumor_size: 1.4; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 91; age: 50; tumor_size: 0.6; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 140; age: 49; tumor_size: 1.6; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 72; age: 76; tumor_size: 2.2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; 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esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 98; age: 75; tumor_size: 1.5; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 122; age: 48; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 124; age: 49; tumor_size: 2.6; histotype: CDI; esr1_status: 0; erbb2_status: 1; ', 'distant_metastasis: 0; dfs (months): 114; age: 42; tumor_size: 1.3; histotype: CDI+CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 114; age: 63; tumor_size: 1.7; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 0; dfs (months): 102; age: 69; tumor_size: 2; histotype: other; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 57; age: 62; tumor_size: 0.8; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 28; age: 67; tumor_size: 3; histotype: CDI; esr1_status: 0; erbb2_status: 0; ', 'distant_metastasis: 1; 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esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 33; age: 39; tumor_size: 2.4; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 21; age: 61; tumor_size: 2.7; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 16; age: 53; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 31; age: 67; tumor_size: 2.4; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 36; age: 59; tumor_size: 2.4; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 20; age: 58; tumor_size: 1.8; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 52; age: 51; tumor_size: 1.8; histotype: CDI; esr1_status: 0; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 41; age: 64; tumor_size: 2.2; histotype: CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 11; age: 67; tumor_size: 2.3; histotype: CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 9; age: 69; tumor_size: 3.9; histotype: CDI; esr1_status: 1; erbb2_status: 1; ', 'distant_metastasis: 1; dfs (months): 26; age: 70; tumor_size: 1.8; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 53; age: 51; tumor_size: 2; histotype: CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 12; age: 32; tumor_size: 2.5; histotype: CDI; esr1_status: 0; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 12; age: 37; tumor_size: 3.6; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 45; age: 56; tumor_size: 2.2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 19; age: 55; tumor_size: 3.8; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 50; age: 46; tumor_size: 2.8; histotype: CDI+CLI; esr1_status: 0; erbb2_status: 1; ', 'distant_metastasis: 1; dfs (months): 26; age: 40; tumor_size: 1.3; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 32; age: 78; tumor_size: 2.3; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 13; age: 50; tumor_size: 1.5; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 10; age: 66; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 19; age: 60; tumor_size: 1.7; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 52; age: 58; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 30; age: 70; tumor_size: 3; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 50; age: 85; tumor_size: 2.3; histotype: CDI; esr1_status: 1; erbb2_status: 1; ', 'distant_metastasis: 1; dfs (months): 55; age: 65; tumor_size: 1.5; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 41; age: 52; tumor_size: 1.6; histotype: CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 10; age: 62; tumor_size: 2.1; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 22; age: 39; tumor_size: 2.5; histotype: CDI; esr1_status: 1; erbb2_status: 1; ', 'distant_metastasis: 1; dfs (months): 11; age: 53; tumor_size: 0.7; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 15; age: 44; tumor_size: 2.2; histotype: CDI; esr1_status: 0; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 13; age: 45; tumor_size: 2.5; histotype: CDI+CLI; esr1_status: 1; erbb2_status: 1; ', 'distant_metastasis: 1; dfs (months): 57; age: 62; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 9; age: 69; tumor_size: 1.8; histotype: CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 16; age: 60; tumor_size: 1.3; histotype: CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 52; age: 71; tumor_size: 3.5; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 20; age: 56; tumor_size: 1.8; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 39; age: 43; tumor_size: 2; histotype: CDI; esr1_status: 0; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 58; age: 67; tumor_size: 2.5; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 25; age: 70; tumor_size: 2.3; histotype: CDI; esr1_status: 0; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 16; age: 61; tumor_size: 2.6; histotype: CLI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 30; age: 69; tumor_size: 1.5; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 24; age: 71; tumor_size: 3; histotype: CDI; esr1_status: 0; erbb2_status: 1; ', 'distant_metastasis: 1; dfs (months): 35; age: 78; tumor_size: 3.5; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 54; age: 52; tumor_size: 4; histotype: CDI; esr1_status: 0; erbb2_status: 1; ', 'distant_metastasis: 1; dfs (months): 52; age: 38; tumor_size: 2; histotype: CDI; esr1_status: 1; erbb2_status: 0; ', 'distant_metastasis: 1; dfs (months): 45; age: 38; tumor_size: 1.8; histotype: CDI; esr1_status: 0; erbb2_status: 1; ', 'distant_metastasis: 1; dfs (months): 49; age: 42; tumor_size: 1.5; histotype: CDI; esr1_status: 0; erbb2_status: 0; ' GSE47108 Homo sapiens 10 Expression profiling by array GPL6244 Gene expression profiling in true interval breast cancer reveals overactivation of mTOR signalling pathway 2013-05-20 Background: Interval breast cancers can occur through failure to detect an abnormality at the time of screening (missed interval cancer), or as a new event after a negative screen (true interval cancer). The development and progression of true interval tumors (TIBC) is known to be different than screen-detected tumors (SDBC). However, much work still needs to be done to understand the biological characteristics and clinical behaviour of these TIBC. Objectives: To characterize the gene expression profile in TIBC and SDBC aimed to identify biological markers that may be associated with the emergence of symptomatic breast cancer in the screening interval. Material and Methods: An unsupervised exploratory gene expression profile analysis was performed among 10 samples (discovery set, TIBC=5 and SDBC=5) using Affymetrix Human Gene 1.0 ST arrays and interpreted by Ingenuity Pathway Analysis. Differential expression of selected genes was confirmed in validation series of 91 patients (TIBC=12 and SDBC=79) by immunohistochemistry and 24 patients (TIBC=8 and SDBC=16) by RT-qPCR, expanding the analysis to other genes in same pathway (mTOR, 4E-BP1, eIF-4G and S6). Results: Exploratory gene expression analysis identified 1060 transcripts with a p value <0.05 and 132 transcripts with an adjusted p value <0.01 difference between TIBC and SDBC samples. Based on biological implications in breast cancer, four genes were selected for further validation: CP (ceruloplasmin) and RPS6KB2 (ribosomal protein S6 kinase, 70kDa, polypeptide 2) both up-regulated in TIBC vs SDBC and PTEN (phosphatase and tensin homolog) and TGFBR3 (transforming growth factor beta receptor III), down-regulated in TIBC vs SDBC. Their differential expression was confirmed by RT-qPCR and immunohistochemistry, suggesting mTOR pathway overexpression in TIBC at both mRNA and protein level. Further expanded analysis by immunohistochemistry for mTOR pathway activation, including expression of phosphorylated forms of mTOR, 4E-BP1, eIF-4G, RPS6KB2 and S6, confirmed the upregulation of this pathway in TIBC. Conclusions: TIBC and SDBC shows differential expression profile both at the gene and protein levels. The mTOR signaling is significantly upregulated in TIBC compared with SDBC, suggesting an enhanced aggressiveness of TIBC. Besides, CP may also represent novel immunohistochemical marker helpful in distinguishing between TIBC and SDBC. Further studies with larger sets of patients are guaranteed to verify these findings associated with TIBC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47108 Gene expression profiling in true interval breast cancer reveals overactivation of the mTOR signaling pathway. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 5.057 https://doi.org/10.1158/1055-9965.EPI-13-0761 {Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology (5.057): 10.1158/1055-9965.EPI-13-0761} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA203581 https://www.ebi.ac.uk/ena/browser/view/PRJNA203581 None [Overal design]5 TIBC samples where compared with 5 SDBC; [Treatment]'None'; [Growth]'None'; [Extraction]"RNA was extracted following Qiagen protocol according to the manufacturer's instructions."; [Cell type]'Source: ''tissue: breast cancer; condition: true interval tumors (TIBC); phenotype: TN; ', 'tissue: breast cancer; condition: screen-detected tumors (SDBC); phenotype: LumA; ', 'tissue: breast cancer; condition: true interval tumors (TIBC); phenotype: LumA; ', 'tissue: breast cancer; condition: screen-detected tumors (SDBC); phenotype: HER2+; ', 'tissue: breast cancer; condition: screen-detected tumors (SDBC); phenotype: LumB; ', 'tissue: breast cancer; condition: true interval tumors (TIBC); phenotype: LumB; ', 'tissue: breast cancer; condition: true interval tumors (TIBC); phenotype: HER2+; ' GSE131986 Mus musculus; Homo sapiens 223 Genome variation profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL18573; GPL21290; GPL21493 Acquired resistance to combined BET and CDK4/6 inhibition in triple-negative breast cancer 2019-05-30 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131986 Acquired resistance to combined BET and CDK4/6 inhibition in triple-negative breast cancer. Nature communications 11.878 https://doi.org/10.1038/s41467-020-16170-3 {Nature communications (11.878) doi:10.1038/s41467-020-16170-3}; {Oncogene (6.634) doi:10.1038/s41388-020-01479-6}; 'genomic DNA', 'polyA RNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA545501 https://www.ebi.ac.uk/ena/browser/view/PRJNA545501 None [Overal design]Refer to individual Series; [Treatment]'Cells were grown in vitro in the presence of DMSO, JQ1 (100 nM), paclitaxel (0.6 nM), palbociclib (160 nM), JQ1+paclitaxel, or JQ1+palbociclib, in triplicates, for up to 18 passages. Mice were treated for up to 2 weeks with vehicle, JQ1 (30-50 mg/kg daily), palbociclib (75 mg/kg daily), paclitaxel (10 mg/kg twice weekly), JQ1+palbociclib, or JQ1+paclitaxel, with 5 mice per group.', 'Cells were grown in vitro in the presence of DMSO, JQ1 (100 nM), paclitaxel (0.6 nM), palbociclib (160 nM), JQ1+paclitaxel, or JQ1+palbociclib, in triplicates, for up to 18 passages. Mice were treated for up to 2 weeks with vehicle, JQ1 (30-50 mg/kg daily), palbociclib (75 mg/kg daily), paclitaxel (10 mg/kg twice weekly), JQ1+palbociclib, or JQ1+paclitaxel, or for 1 week with JQ1 followed by 1 week with paclitaxel, 1 week with paclitaxel followed by 1 week with JQ1, or 1 week with JQ1+paclitaxel followed by 1 week with vehicle, with 5 mice per group.', 'Cells were grown in vitro in the presence of DMSO, JQ1 (100 nM), paclitaxel (0.6 nM), palbociclib (160 nM), JQ1+paclitaxel, or JQ1+palbociclib, in triplicates, for up to 18 passages.'; [Growth]'Cells were lentivirally infected with the ClonTracer barcode library (Bhang et al., 2015). Barcoded cells were passaged in vitro in the presence of drug or injected orthotopically into mammary fat pads of NOG mice to produce xenografts.', 'Cells were lentivirally infected with the ClonTracer barcode library (Bhang et al., 2015). Barcoded cells were passaged in vitro in the presence of drug.'; [Extraction]'DNA was extracted from frozen cultured cells and xenografts using the AllPrep DNA/RNA Mini Kit or the QIAamp DNA Mini Kit (Qiagen).\nPCR was used to amplify barcodes and introduce Illumina adaptors along with a 5 bp index sequence for multiplexing as described (Bhang et al., 2015). 2 µg of genomic DNA was used as template, and 15-16 samples were multiplexed. PCR products were run on 0.8% agarose NGS E-Gels (Invitrogen) to verify the correct library size, and bands were purified using the MinElute Gel Extraction Kit (Qiagen).', 'DNA was extracted from frozen cultured cells and xenografts using the AllPrep DNA/RNA Mini Kit or the QIAamp DNA Mini Kit (Qiagen). Equal amounts of DNA were pooled from replicates for library construction.\nDNA was fragmented to 250 bp (Covaris ultrasonication) and further purified using Agencourt AMPure XP beads. Size-selected DNA was ligated to sequencing adaptors with sample-specific barcodes using the KAPA Hyper Prep Kit. Libraries were pooled and sequenced on an Illumina MiSeq nano flow cell to estimate the library DNA concentration based on the number of barcode reads per sample. Libraries were pooled and captured using SureSelectXT Human All Exon v5 (Agilent) in 7 x 3-plex and 1 x 2-plex. Captures were performed using the SureSelectXT Reagent Kit (Agilent).', 'RNA was extracted from duplicate samples using the AllPrep DNA/RNA Mini Kit (Qiagen).\nLibraries were prepared using the Illumina TruSeq Stranded mRNA Library Prep Kit, and 16-18 samples were multiplexed per lane for NGS.', 'Equal numbers of cells from triplicates were combined, washed twice in PBS with 0.04% RNase-free BSA, diluted to 700 cells/µL, and filtered through a 35 µm nylon mesh prior to library preparation.\nLibraries were prepared using the Chromium Single Cell 3’ Library & Gel Bead Kit v2 and Single Cell A Chip (10X Genomics).'; [Cell type]'Source: ''cell line: SUM159; treatment: vehicle; time point: 2 wk; replicate: 1; ', 'cell line: SUM159; treatment: vehicle; time point: 2 wk; replicate: 2; ', 'cell line: SUM159; treatment: vehicle; time point: 2 wk; replicate: 3; ', 'cell line: SUM159; treatment: vehicle; time point: 2 wk; replicate: 4; ', 'cell line: SUM159; treatment: JQ1; time point: 2 wk; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: 2 wk; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: 2 wk; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: 2 wk; replicate: 4; ', 'cell line: SUM159; treatment: palbociclib; time point: 2 wk; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; time point: 2 wk; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; time point: 2 wk; replicate: 3; ', 'cell line: SUM159; treatment: palbociclib; time point: 2 wk; replicate: 4; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: 2 wk; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: 2 wk; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: 2 wk; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: 2 wk; replicate: 4; ', 'cell line: SUM159; treatment: pre-treatment; time point: 0 wk; replicate: 1; ', 'cell line: SUM159; treatment: pre-treatment; time point: 0 wk; replicate: 2; ', 'cell line: SUM159; treatment: pre-treatment; time point: 0 wk; replicate: 3; ', 'cell line: SUM159; treatment: pre-treatment; time point: 0 wk; replicate: 4; ', 'cell line: SUM159; treatment: vehicle; time point: 1 wk; replicate: 1; ', 'cell line: SUM159; treatment: vehicle; time point: 1 wk; replicate: 2; ', 'cell line: SUM159; treatment: vehicle; time point: 1 wk; replicate: 3; ', 'cell line: SUM159; treatment: vehicle; time point: 1 wk; replicate: 4; ', 'cell line: SUM159; treatment: JQ1; time point: 1 wk; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: 1 wk; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: 1 wk; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: 1 wk; replicate: 4; ', 'cell line: SUM159; treatment: paclitaxel; time point: 1 wk; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; time point: 1 wk; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; time point: 1 wk; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: 1 wk; replicate: 4; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 1 wk; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 1 wk; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 1 wk; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 1 wk; replicate: 4; ', 'cell line: SUM159; treatment: paclitaxel; time point: 2 wk; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; time point: 2 wk; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; time point: 2 wk; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: 2 wk; replicate: 4; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 2 wk; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 2 wk; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 2 wk; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 2 wk; replicate: 4; ', 'cell line: SUM159; treatment: pre-treatment; time point: passage 0; replicate: 1; ', 'cell line: SUM159; treatment: pre-treatment; time point: passage 0; replicate: 2; ', 'cell line: SUM159; treatment: pre-treatment; time point: passage 0; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 2; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 2; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 2; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 4; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 4; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 4; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 6; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 6; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 6; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 11; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 11; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 11; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 18; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 18; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 18; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: passage 2; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: passage 2; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: passage 2; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: passage 4; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: passage 4; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: passage 4; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: passage 6; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: passage 6; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: passage 6; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: passage 11; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: passage 11; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: passage 11; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: passage 18; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: passage 18; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: passage 18; replicate: 3; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 2; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 2; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 2; replicate: 3; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 4; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 4; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 4; replicate: 3; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 6; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 6; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 6; replicate: 3; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 11; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 11; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 11; replicate: 3; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 18; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 18; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 18; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 2; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 2; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 2; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 4; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 4; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 4; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 6; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 6; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 6; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 7; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 11; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 11; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 18; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 18; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 1; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 1; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 1; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 7; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 7; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 7; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 14; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 14; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 14; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: passage 7; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: passage 7; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: passage 7; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: passage 14; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: passage 14; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: passage 14; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 2; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 2; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 2; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 4; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 4; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 4; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 6; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 6; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 6; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 7; replicate: 1; ', 'cell line: SUM159; 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', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 7; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 7; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 9; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 9; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 9; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 14; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 14; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 14; replicate: 3; ', 'cell line: SUM159; treatment: pre-treatment; ', 'cell line: SUM159; treatment: DMSO; ', 'cell line: SUM159; treatment: paclitaxel; ', 'cell line: SUM159; treatment: JQ1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; ', 'cell line: SUM159; treatment: palbociclib; ', 'cell line: SUM159; treatment: JQ1+palbociclib; ', 'cell line: SUM159; treatment: vehicle; ', 'cell line: SUM159; treatment: JQ1->paclitaxel; ', 'cell line: SUM159; treatment: paclitaxel->JQ1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel->vehicle; ', 'cell line: NOD.Cg-Prkdcscid Il2rgtm1Sug/JicTac (NOG); treatment: N/A; ', 'cell line: CEPH1408 cells; treatment: N/A; ', 'cell line: SUM159; treatment: pre-treatment; replicate: 1; ', 'cell line: SUM159; treatment: pre-treatment; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+palbociclib; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; replicate: 2; ', 'cell line: SUM159; treatment: pre-treatment; index: SI-GA-E1; ', 'cell line: SUM159; treatment: DMSO; index: SI-GA-E2; ', 'cell line: SUM159; treatment: paclitaxel; index: SI-GA-E3; ', 'cell line: SUM159; treatment: JQ1; index: SI-GA-E4; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; index: SI-GA-E5; ', 'cell line: SUM159; treatment: palbociclib; index: SI-GA-E6; ', 'cell line: SUM159; treatment: JQ1; index: SI-GA-E7; ', 'cell line: SUM159; treatment: JQ1+palbociclib; index: SI-GA-E8; ' GSE131631 Homo sapiens 14 Expression profiling by high throughput sequencing GPL18573 Next Generation Sequencing and differential expression analysis in stem-like vs. non-stem breast cancer cells in response to HDAC1 and HDAC7 knockdown 2019-05-22 Purpose: We performed RNA-seq differential expression analysis after 72h HDAC1 and HDAC7 knockdown in order to evaluate the transcriptional regulation exerted by HDAC1 and HDAC7 in a stem-like (BPLER) vs. non-stem (HMLER) breast cancer (BrCa) cell model (please search for keywords "BPLER" or "HMLER" in GEO to access over 240 associated data sets). Results: HDAC7 knockdown by a pool of siRNAs resulted in altered expression of nearly three times the genes in BPLER vs. HMLER cells (2545 vs. 763), with the two cell types sharing altered expression of 328 genes. In stem-like BPLER cells, HDAC7 knockdown caused significant alterations in gene expression (1068 down and 1477 up). Fewer genes, less than half of BPLER, were altered in non-stem HMLER cells (448 down and 315 up), with 199 repressed and 129 activated genes shared between the two cell types. In contrast, 72h HDAC1 knockdown resulted in nearly equal numbers of altered genes in BPLER vs. HMLER cells (3187 vs. 2627), with the two cell types sharing altered expression of 637 genes. Moreover, the number of repressed (1570 vs. 1307) and activated (1617 vs. 1320) gene transcripts was similar in the two cell types In HMLER cells, HDAC7 knockdown resulted in alterations of significantly fewer gene transcripts compared to HDAC1 knockdown (508 vs. 2681), in both repressed (305 vs. 1362) and activated (203 vs. 1319) transcripts. Conclusions: Cumulatively, these results highlight that HDAC7 regulates nearly three times as many genes in stem-like compared to non-stem BrCa cells. In contrast, HDAC1 regulates equal number of genes in the same cell context, suggesting a predominant association of HDAC7 with the cancer stem cell phenotype. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131631 HDAC7 regulates histone 3 lysine 27 acetylation and transcriptional activity at super-enhancer-associated genes in breast cancer stem cells. Oncogene 6.634 https://doi.org/10.1038/s41388-019-0897-0 {Oncogene (6.634): 10.1038/s41388-019-0897-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA544243 https://www.ebi.ac.uk/ena/browser/view/PRJNA544243 https://www.ncbi.nlm.nih.gov/sra?term=SRP199194 [Overal design]RNA-seq differential expression analysis in stem-like BPLER (triplicate) vs. HMLER (duplicate) cells following HDAC1 and HDAC7 knockdown.; [Treatment]'BPLER and HMLER cells were plated in 10cm petri dish at 7.0x10e5 cell/plate respectively in BMI-T and MEGM (Lonza) medium 24h before transfection. Cells were transfected with pools, 50 nM each, of HDAC1 and HDAC7 specific double-stranded RNAs and non-specific (NS) siRNAs as control using Lipofectamine RNAiMAX (Invitrogen) in OptiMEM (GIBCO, Life Technologies) added directly to the medium. The cells were harvested 72h later for total RNA extraction.'; [Growth]'BPLER and HMLER cells were described before (Cancer Cell 12, 160-170, 2007). Both cell types and BPLER culture medium (BMI-T) are available from the Live Tissue Culture Service Center, University if Miami (contact LTCC@med.miami.edu).'; [Extraction]'Total RNA preparations were obtained with RNAzol® RT (Sigma) and cleaned with Turbo DNA-Free Kit (Ambion).\nDNase I-treated total RNA preparations were qualitatively validated by Eukaryote Total RNA 6000 Nano analysis on 2100 Bioanalyzer (Agilent) and libraries were prepared using the KAPA RNA HyperPrep kit according to manufacturer instructions (KAPA).'; [Cell type]'Breast primary epithelial cells''cell line: BPLER2; cell type: Breast primary epithelial cells; transforming gene: hTERT; SV40-LT/st; hRASV12; sirna: Non-targeting (NT); ', 'cell line: BPLER2; cell type: Breast primary epithelial cells; transforming gene: hTERT; SV40-LT/st; hRASV12; sirna: siHDAC7; ', 'cell line: BPLER2; cell type: Breast primary epithelial cells; transforming gene: hTERT; SV40-LT/st; hRASV12; sirna: siHDAC1; ', 'cell line: HMLER2; cell type: Breast primary epithelial cells; transforming gene: hTERT; SV40-LT/st; hRASV12; sirna: Non-targeting (NT); ', 'cell line: HMLER2; cell type: Breast primary epithelial cells; transforming gene: hTERT; SV40-LT/st; hRASV12; sirna: siHDAC7; ', 'cell line: HMLER2; cell type: Breast primary epithelial cells; transforming gene: hTERT; SV40-LT/st; hRASV12; sirna: siHDAC1; ' GSE59780 Homo sapiens 6 Expression profiling by array GPL570 Expression data from menadione, PERK inhibitor, or control-treated HMLE-shGFP and HMLE-Twist human mammary epithelial cells 2014-07-25 Malignant carcinomas that recur following therapy are typically de-differentiated and multi-drug resistant (MDR). De-differentiated cancer cells acquire MDR by upregulating reactive oxygen species (ROS)-scavenging enzymes and drug efflux pumps, but how these genes are upregulated in response to de-differentiation is not known. Here, we examine this question by using global transcriptional profiling to identify ROS-induced genes that are already upregulated in de-differentiated cells, even in the absence of oxidative damage. Using this approach, we found that the Nrf2 transcription factor, which is the master regulator of cellular response to oxidative stress, is pre-activated in de-differentiated cells. In de-differentiated cells, Nrf2 is not activated by oxidation but rather through a non-canonical mechanism involving its phosphorylation by the ER membrane kinase PERK. In contrast, differentiated cells require oxidative damage to activate Nrf2. Constitutive PERK-Nrf2 signaling protects de-differentiated cells from chemotherapy by reducing ROS levels and increasing drug efflux. These findings are validated in therapy-resistant basal breast cancer cell lines and animal models, where inhibition of the PERK-Nrf2 signaling axis reversed the MDR of de-differentiated cancer cells. Additionally, analysis of patient tumor datasets showed that a PERK pathway signature correlates strongly with chemotherapy resistance, tumor grade, and overall survival. Collectively, these results indicate that de-differentiated cells upregulate MDR genes via PERK-Nrf2 signaling, and suggest that targeting this pathway could sensitize drug-resistant cells to chemotherapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59780 De-differentiation confers multidrug resistance via noncanonical PERK-Nrf2 signaling. PLoS biology 8.386 https://doi.org/10.1371/journal.pbio.1001945 {PLoS biology (8.386): 10.1371/journal.pbio.1001945} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA256186 https://www.ebi.ac.uk/ena/browser/view/PRJNA256186 None [Overal design]Differentiated human breast epithelial cells (HMLE-shGFP) or de-differentiated cells (HMLE-Twist) were treated in culture with 40uM menadione for 2 hours or 1uM PERK inhibitor for 48 hours and compared to control DMSO-treated cells.; [Treatment]'Cells were treated for 40uM Menadione for 2 hours or 1uM PERK inhibitor for 48 hours.'; [Growth]'Cells were grown in a 1:1 mixture of DMEM+10%FBS, insulin, hydrocortisone and MEGM.'; [Extraction]'Total RNA was extracted from culture plates for each cell type using an RNeasy Mini kit coupled with an RNase-free DNase set (Qiagen).'; [Cell type]'HMLE''cell type: HMLE; genotype: SV40ER, hTERT; agent: DMSO; ', 'cell type: HMLE; genotype: SV40ER, hTERT; agent: Menadione; ', 'cell type: HMLE; genotype: SV40ER, hTERT; agent: PERKi; ' GSE126038 Homo sapiens 54 Expression profiling by array GPL20311 FGFR4 is a key regulator of tumor subtype differentiation in luminal breast cancer and metastatic disease 2019-02-04 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE126038 FGFR4 regulates tumor subtype differentiation in luminal breast cancer and metastatic disease. The Journal of clinical investigation 12.282 https://doi.org/10.1172/JCI130323 {The Journal of clinical investigation (12.282): 10.1172/JCI130323} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA520840 https://www.ebi.ac.uk/ena/browser/view/PRJNA520840 None [Overal design]Refer to individual Series; [Treatment]'Cell were infected with a FGFR4 expressing lentiviral vector or treated with BLU9931 at IC50 doses', 'Tumors treated with BLU9931 (0.6g/Kg/day) or Lapatinib (0.22g/kg/day) for 18 days'; [Growth]'MDA-MB-453, CAMA-1 and T47D are derived from metastatic carcinoma pericardial effusion and MCF7 derived from adenocarcinoma pleural effusion. Cell cultures were incubated at 37ºC in a humidified 5% CO2 atmosphere. All cell lines were maintained in complete growth media (corresponding media supplemented with a mix of penicillin/streptomycin plus fungizone (ratio 9:1) at 1% (GIBCO), 1% of L-GlutaMAX™ 200 mM and 10% of fetal bovine serum (FBS) (Sigma-Aldrich)).', 'PDX WHIM11 tumors were engrafted in the mammary fat pad of NSG mice by subcutaneous injection of 1.0 × 10^6 cells in RPMI:Matrigel (1:1) in a total volume of 200 μl'; [Extraction]'Cell line lysate was prepared using QIAshredder tubes (QIAGEN). RNA was isolated using the RNeasy Mini Kit (QUIAGEN) according to manufacturer protocol. Isolated RNA was quantified using a NanoDrop® Spectrophotometer.', 'Tumor tissue was disrupted using roto-stator homogenization. RNA was isolated using the RNeasy Mini Kit (QUIAGEN) according to manufacturer protocol. Isolated RNA was quantified using a NanoDrop® Spectrophotometer.'; [Cell type]'Source: ''reference: High-quality total RNA. Comprised of 10 different cell lines for broad gene coverage on human microarrays; ', 'cell line: MCF7 cell line; agent: Transduced with empty/control expressing lentiviral vector; ', 'cell line: MCF7 cell line; agent: Transduced with FGFR4 expressing lentiviral vector; ', 'cell line: T47D cell line; agent: Transduced with empty/control expressing lentiviral vector; ', 'cell line: T47D cell line; agent: Transduced with FGFR4 expressing lentiviral vector; ', 'cell line: CAMA-1 cell line; agent: Untreated (DMSO only at IC50 concentrations); ', 'cell line: CAMA-1 cell line; agent: Treated with BLU9931 for 48h at the IC50 doses; ', 'cell line: MDA-MB-453 cell line; agent: Untreated (DMSO only at IC50 concentrations); ', 'cell line: MDA-MB-453 cell line; agent: Treated with BLU9931 for 48h at the IC50 doses; ', 'tissue: WHIM11 tumor; agent: Untreated; ', 'tissue: WHIM11 tumor; agent: Lapatinib treated for 18 days; ', 'tissue: WHIM11 tumor; agent: BLU9931 treated for 18 days; ' GSE148452 Mus musculus 3 Expression profiling by high throughput sequencing GPL17021 RNA-sequencing expression of MMTV-Neu mouse mammary tumors 2020-04-10 We use RNA-seq to measure gene expression from mammary tumors from untreated MMTV-Neu mice. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148452 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA624305 https://www.ebi.ac.uk/ena/browser/view/PRJNA624305 https://www.ncbi.nlm.nih.gov/sra?term=SRP255960 [Overal design]mammary tumors from untreated MMTV-Neu mice.; [Treatment]'No Treatment'; [Growth]'Tumors were orthotopically injected in sygeneic hosts. Tumors were allowed to progress to a 5mm diameter, then grew for 7 days withouth any treatment'; [Extraction]'RNA was extracted using Qiagen Rneasy kits. mRNA quality was assessed using the Agilent Bioanalyzer.\nLibraries for mRNA-seq made using total RNA and the Illumina TruSeq mRNA sample preparation kit\nPaired end (2x50bp) sequencing was performed on the Illumina HiSeq 2000/2500 sequencer at the UNC High Throughput Sequencing Facility'; [Cell type]'Source: ''strain: FVB-MMTV-Neu; tissue: mammary tumor; ' GSE144221 Homo sapiens 25 Methylation profiling by high throughput sequencing GPL17301 DNA methylation markers panel can improve prediction of response to neoadjuvant chemotherapy in luminal B breast cancer 2020-01-24 Despite the advantages of neoadjuvant chemotherapy (NACT), associated toxicity is a serious complication that renders monitoring of the patients response to NACT highly important. Thus, prediction of tumor response to treatment is imperative to avoid exposure of potential non-responders to deleterious complications. We have performed genome-wide analysis of DNA methylation by XmaI-RRBS and selected CpG dinucleotides differential methylation of which discriminates luminal B breast cancer samples with different sensitivity to NACT. With this data, we have developed multiplex methylation sensitive restriction enzyme PCR (MSRE-PCR) protocol for determining the methylation status of 10 genes (SLC9A3, C1QL2, DPYS, IRF4, ADCY8, KCNQ2, TERT, SYNDIG1, SKOR2 and GRIK1) that distinguish BC samples with different NACT response. Analysis of these 10 markers by MSRE-PCR in biopsy samples allowed us to reveal three top informative combinations of markers, (1) IRF4 and C1QL2; (2) IRF4, C1QL2, and ADCY8; (3) IRF4, C1QL2, and DPYS, with the areas under ROC curves (AUCs) of 0.75, 0.78 and 0.74, respectively. A classifier based on IRF4 and C1QL2 better meets the diagnostic panel simplicity requirements, as it consists of only two markers. Diagnostic accuracy of the panel of these two markers is 0.75, with the sensitivity of 75% and specificity of 75%. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144221 DNA methylation markers panel can improve prediction of response to neoadjuvant chemotherapy in luminal B breast cancer. Scientific reports 4.011 https://doi.org/10.1038/s41598-020-66197-1 {Scientific reports (4.011): 10.1038/s41598-020-66197-1} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA603073 https://www.ebi.ac.uk/ena/browser/view/PRJNA603073 https://www.ncbi.nlm.nih.gov/sra?term=SRP244660 [Overal design]Reduced representation bisulfite sequencing by XmaI-RRBS (Tanas et al., 2017); [Treatment]'None'; [Growth]'None'; [Extraction]'Phenol:chloroform protocol after proteinase K treatment\nXmaI-RRBS protocol as in: Tanas AS, Borisova ME, Kuznetsova EB et al. Rapid and affordable genome-wide bisulfite DNA sequencing by XmaI-reduced representation bisulfite sequencing. Epigenomics. 9 (6), 833-847 (2017).'; [Cell type]'Tissue''cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 2; n: 1; age: 48; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Stabilization; t: 4; n: 3; age: 57; recist: SD; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Stabilization; t: 2; n: 0; age: 47; recist: SD; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Stabilization; t: 2; n: 0; age: 50; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Stabilization; t: 1; n: 1; age: 46; recist: SD; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 2; n: 0; age: 51; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 2; n: 1; age: 68; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 1; n: 1; age: 44; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 2; n: 0; age: 49; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 2; n: 1; age: 38; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Stabilization; t: 2; n: 0; age: 54; recist: SD; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 2; n: 1; age: 59; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 2; n: 1; age: 33; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 2; n: 0; age: 40; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Stabilization; t: 1; n: 1; age: 45; recist: SD; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 2; n: 1; age: 57; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Stabilization; t: 2; n: 1; age: 48; recist: SD; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Stabilization; t: 2; n: 0; age: 55; recist: SD; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 2; n: 1; age: 54; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 2; n: 3; age: 29; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Stabilization; t: 1; n: 1; age: 44; recist: SD; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Stabilization; t: 2; n: 1; age: 36; recist: SD; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Stabilization; t: 2; n: 0; age: 48; recist: SD; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 1; n: 1; age: 48; recist: PR; ', 'cell type: Tissue; tissue: LumB Breast Cancer; nact: Partial Regression; t: 1; n: 2; age: 54; recist: PR; ' GSE54465 Homo sapiens 24 Expression profiling by array GPL10558 Expression profiling of migrated and invaded breast cancer cells predicts early metastatic relapse and reveals Krüppel-like factor 9 as a potential suppressor of invasive growth in breast cancer 2014-01-28 Cell motility and invasion initiate metastasis. However, only a subpopulation of cancer cells within a tumor will ultimately become invasive. Due to this stochastic and transient nature, in an experimental setting, migrating and invading cells need to be isolated from the general population in order to study the gene expression profiles linked to these processes. This report describes microarray analysis on RNA derived from migrated or invaded subpopulations of triple negative breast cancer cells in a Transwell set-up, at two different time points during motility and invasion, pre-determined as “early” and “late” in real-time kinetic assessments. Invasion- and migration-related gene expression signatures were generated through comparison with non-invasive cells, remaining at the upper side of the Transwell membranes. Late-phase signatures of both invasion and migration indicated poor prognosis in a series of breast cancer data sets. Furthermore, evaluation of the genes constituting the prognostic invasion-related gene signature revealed Krüppel-like factor 9 (KLF9) as a putative suppressor of invasive growth in breast cancer. Next to loss in invasive vs non-invasive cell lines, KLF9 also showed significantly lower expression levels in the “early” invasive cell population, in several public expression data sets and in clinical breast cancer samples when compared to normal tissue. Overexpression of EGFP-KLF9 fusion protein significantly altered morphology and blocked invasion and growth of MDA-MB-231 cells in vitro. In addition, KLF9 expression correlated inversely with mitotic activity in clinical samples, indicating anti-proliferative effects. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54465 Expression profiling of migrated and invaded breast cancer cells predicts early metastatic relapse and reveals Krüppel-like factor 9 as a potential suppressor of invasive growth in breast cancer. Oncoscience 3.16 https://doi.org/10.18632/oncoscience.10 {Oncoscience (3.16): 10.18632/oncoscience.10} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA236585 https://www.ebi.ac.uk/ena/browser/view/PRJNA236585 None [Overal design]After selection of two time points (“early” and “late”), RNA from invasive and migratory MDA-MB-231 cells was isolated from Transwell membranes and hybridized onto an Illumina HumanHT-12 v4 Expression beadchip. Gene expressions of migrated/invaded subpopulations vs non-motile cells were compared.; [Treatment]'In vitro invasion experiments have been performed using a conventional 24-well Transwell system (Corning®), with 4x10^5 cells seeded on top of a 20% (v/v) Matrigel layer. Complete medium was added to the wells as chemoattractant and the Transwell plates were incubated at 37°C/5% CO2 during 20h (first timewindow) and 28h (second timewindow), as predetermined in real-time invasion assessments. An identical protocol as the above was followed for migration experiments, without application of an extracellular matrix substitute. Transwell migration plates were incubated during 6h30’ (first timewindow) and 24h (second timewindow). For both invasion and migration, the respective timeframes of incubation have immediately been followed by RNA-isolation.'; [Growth]'The MDA-MB-231 cells were cultured in RPMI1640 supplemented with 10% fetal bovine serum (FBS), 1% L-glutamine, 1% penicillin/streptomycin and 1% sodium pyruvate. All cell culture reagents were purchased from Invitrogen (Life Technologies, USA) unless mentioned otherwise. Cell lines were maintained at 37°C and 5% CO2/95% air in a humidified incubator. Although the MDA-MB-231 breast cancer cell line was purchased from the American Type Culture Collection (ATCC, USA) (http:// www.lgcstandards-atcc.org), cell line identity was validated in-house by short tandem repeat (STR) profiling using the Cell ID System (Promega, USA) according to the manufacturer’s instructions.'; [Extraction]'Total RNA was extracted using the RNAqueousTM Micro Kit (Life Technologies, USA) for nucleic acid extraction from small cell populations. All cell populations of interest were lysed directly on the membranes without prior enzymatic detachment.'; [Cell type]'Source: ''cell population: non-motile cells, reference for early migratory cell population; cell line: MDA-MB-231; ', 'cell population: early migratory cell population; cell line: MDA-MB-231; ', 'cell population: non-motile cells, reference for late migratory cell population; cell line: MDA-MB-231; ', 'cell population: late migratory cell population; cell line: MDA-MB-231; ', 'cell population: non-motile cells, reference for early invasive cell population; cell line: MDA-MB-231; ', 'cell population: early invasive cell population; cell line: MDA-MB-231; ', 'cell population: non-motile cells, reference for late invasive cell population; cell line: MDA-MB-231; ', 'cell population: late invasive cell population; cell line: MDA-MB-231; ' GSE5588 Homo sapiens 41 Expression profiling by array GPL4190; GPL4192; GPL4203 Comparison of RNA Amplification Techniques meeting the demands for the Expression Profiling of Clinical Cancer Samples 2006-08-24 For microarray experiments starting with nanogram amounts of RNA it is essential to implement reproducible and powerful RNA amplification techniques. Available methods were mainly tested for reproducibility, only a few studies concentrated on potential amplification bias. We evaluated three amplification protocols, which are less time-consuming than the commonly used T7-RNA polymerase based in vitro transcription protocols and therefore may be more suitable for clinical use: Template Switching (TS)-PCR (SMART-PCR Kit, BD), Ribo-SPIA (single primer isothermal amplification, Oviation, Nugen) and a random primer-based PCR. Additionally a more sensitive labeling method, Dendrimer-labeling (Genisphere), was evaluated. All methods were compared to unamplified RNA labelled at reverse transcription. Hybridizations were carried out on a targeted two-colour oligonucleotide microarray. From our results we conclude that RNA amplification with TS-PCR is highly reproducible and results in a reliable representation of the starting RNA population. We then assessed whether RNA amplification of clinical breast and thyroid cancer samples with TS-PCR showed robust performance when altered cycle numbers or partially degraded RNA were used. According to our experiments TS-PCR proved to be a very reliable method for global RNA amplification, even when starting from partially degraded RNA down to a RNA Integrity Number (RIN) of 4.3. Keywords: microarray expression profiling, RNA amplification techniques, RNA integrity https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE5588 Comparison of RNA amplification techniques meeting the demands for the expression profiling of clinical cancer samples. Virchows Archiv : an international journal of pathology 2.92 https://doi.org/10.1007/s00428-007-0522-4 {Virchows Archiv : an international journal of pathology (2.92): 10.1007/s00428-007-0522-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA95459 https://www.ebi.ac.uk/ena/browser/view/PRJNA95459 None [Overal design]To compare the methods under test we generated two pools of total RNA from breast cancer cell lines MCF7 and Hs578T, respectively, which were used for to test subsequent techniques. For each method a replication including a dye-swap hybridization was performed. Over all, non-amplifying methods were replicated two times and amplifying methods 4 times. Next, we investigated whether Ribo-SPIA and TS-PCR are suitable for amplification of rather heterogenous clinical breast cancer samples. Total RNA from (estrogen receptor) ER- (patient number 180/03) and ER+ (patient number 254/03) breast cancer samples were chosen as targets for hybridization. As tumor material was limited, only one hybridization of unamplified RNA could be performed. For Ribo-SPIA and TS-PCR (17, 19 and 26 cycles) a replicate including a dye-swap hybridization was carried out. To test test stability of TS-PCR with degraded samples, total RNA from both breast cancer samples was subjected to artificial degradation by heating to 50 degrees Celsius for 0, 25 and 50 minutes. Additionally, thyroid nodules from 3 different patients (604/05, 607/05 and 618/05) were disrupted into several pieces. TS-PCR was performed on total RNA from both breast cancer samples and different extracts from thyroid cancer subpieces, respectively. The amplification product was labeled with Cy3. Universal Reference RNA (Stratagene) was used as a common reference and labeled with Cy5.; [Treatment]'none', 'TumorSubpiece 2, Extract 3', 'Tumor Subpiece 2, Extract 1', 'Tumor Subpiece 7, Extract 3', 'Tumor Subpiece 7, Extract 1', 'Tumor Subpiece 7, Extract 2', 'Tumor Subpiece 1, Extract 1', 'Tumor Subpiece 1, Extract 2', 'Tumor Subpiece 1, Extract 3', 'Tumor Subpiece 4, Extract 1', 'Tumor Subpiece 4, Extract 3'; [Growth]'none', 'Inkubation for 0 min at 55 degrees Celsius after extraction', 'Inkubation for 25 min at 55 degrees Celsius after extraction', 'Inkubation for 50 min at 55 degrees Celsius after extraction'; [Extraction]'Total RNA from human breast cancer cell lines was extracted using Trizol (Invitrogen) followed by an RNeasy mini column clean up (Qiagen) according to the manufacturer’s protocol.', 'Hs578T\nbreast cancer cell line established from invasive human mammacarcinoma\nknown to be estrogen receptor negative', 'Total RNA from human breast cancer cell lines was extracted using Trizol (Invitrogen) followed by an RNeasy mini column clean up (Qiagen) according to the manufacturers protocol.', 'Total RNA from human breast cancer cell lines was extracted using Trizol (Invitrogen) followed by an RNeasy mini column clean up (Qiagen) according to the manufacturers protocol.ve', 'Total RNA from human breast cancer cell lines was extracted using Trizol (Invitrogen) followed by an RNeasy mini column clean up (Qiagen) according to the manufacturers protocol', 'Primary samples were dissected into smaller pieces if necessary and shock frozen in liquid nitrogen. RNA later ice (Ambion) was applied to the samples at least one day before RNA isolation and then kept at -80 degrees Celsius. Samples were disrupted in liquid nitrogen with a mortar and pestle-like device developed in our laboratory. Samples were homogenized using Qiashredder Columns (Qiagen) and total RNA was isolated by an RNeasy mini column (Qiagen). Total RNA was concentrated by ethanol precipitation and dissolved in appropriate amount of DEPC-treated distilled water (dH2O).', 'none, is commercially available as total RNA'; [Cell type]'Source: ''' GSE108883 Homo sapiens 40 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL18573 Role of SUMOylation in differential ERα transcriptional repression by SERMs and pure antiestrogens in breast cancer cells 2018-01-08 RNA-seq: Gene expression profiling in MCF-7 cells treated with vehicle (0), estradiol (E2), the Selective ER Modulator 4-hydroxytamoxifen (OHT), or the pure antiestrogen fulvestrant (ICI). ChIP-seq: Genome-wide DNA binding profile of ERα and SUMO2/3 in MCF-7 cells treated with vehicle, E2 or ICI. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE108883 None None None None None 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA429003 https://www.ebi.ac.uk/ena/browser/view/PRJNA429003 https://www.ncbi.nlm.nih.gov/sra?term=SRP128564 [Overal design]RNA-seq: MCF-7 cells cultured in estrogen-depleted media were treated with vehicle, 5 nM E2, 100 nM OHT or 100 nM ICI for 16 h. Fold-Change of mRNA levels compared to vehicle was determined for each treatment condition (3 biological replicates for each). ChIP-seq: MCF-7 cells cultured in estrogen-depleted media were treated with vehicle, 5 nM E2 or 100 nM ICI for 30 min or 3 h. ChIP-seq with an antibody for ERα (Santa Cruz Biotechnology sc-543) was performed, and ERα peaks were called for each condition (3 biological replicates) relative to the corresponding input samples. MCF-7 cells cultured in estrogen-depleted media were treated with vehicle or 100 nM ICI for 30 min or 3 h. ChIP-seq with an antibody for SUMO2/3 (Cedarlane M114-3) was performed, and SUMO2/3 peaks were called for each condition (2 biological replicates) relative to the corresponding input samples.; [Treatment]'MCF-7 cells were treated with vehicle for 30 min', 'MCF-7 cells were treated with 100 nM ICI for 30 min', 'MCF-7 cells were treated with 5 nM E2 for 30 min', 'MCF-7 cells were treated with vehicle for 3h', 'MCF-7 cells were treated with ICI for 3h', 'MCF-7 cells were treated with E2 for 3h', 'pool of cells with different treatments', 'MCF-7 cells were treated with 5 nM E2 for 16 h.', 'MCF-7 cells were treated with 100 nM ICI for 16 h.', 'MCF-7 cells were treated with 100 nM OHT for 16 h.', 'MCF-7 cells were treated with vehicule for 16 h.'; [Growth]'MCF-7 cells were maintained at 37°C, 5% CO2 in AMEM supplemented with 10% FBS, 1% L-glutamine and 1% penicillin-streptomycin. Three days before experiments, cells were switched to phenol red-free DMEM containing charcoal-stripped FBS, 2% L-glutamine and 1% penicillin-streptomycin.'; [Extraction]"Nuclei were lysed. ERα-DNA complexes complexes were isolated with the appropriate antibody.\nLibraries were prepared according to Roche's instructions. KAPA DNA HyperPrep Library Kit.", "Nuclei were lysed. SUMO2/3-DNA complexes were isolated with the appropriate antibody.\nLibraries were prepared according to Roche's instructions. KAPA DNA HyperPrep Library Kit.", "Nuclei were lysed and samples were sonicated to fragment chromatin.\nLibraries were prepared according to Roche's instructions. KAPA DNA HyperPrep Library Kit.", "Cell pellets were lysed with QIAzol and RNA was extracted per manufacturer's instructions.\nLibraries were prepared according to Roche's instructions. KAPA Stranded RNA-seq Library Preparation Kit."; [Cell type]'MCF-7 cells''cell type: MCF-7 cells; chip antibody: ERα HC-20 (Santa Cruz Biotechnology sc-543); ', 'cell type: MCF-7 cells; chip antibody: SUMO2/3 (Cedarlane M114-3); ', 'cell type: MCF-7 cells; chip antibody: none; ', 'cell type: MCF-7 cells; chip antibody: N/A; ' GSE155273 Mus musculus 6 Expression profiling by high throughput sequencing GPL17021 Xenografted breast epithelia reveal differences in growth stimulation among contraceptive progestins related to androgenic properties [mouse] 2020-07-28 Hormonal contraception exposes women to different synthetic progesterone receptor (PR) agonists, progestins, and transiently increases breast cancer risk. How progestins affect the breast epithelium is poorly understood because we lack adequate models to study this. We hypothesized that individual progestins differentially affect cell proliferation in the normal breast epithelium and hence breast cancer risk. Using mouse mammary tissue ex vivo, we show that testosterone-related progestins strongly induce the PR target and mediator of PR signaling induced cell proliferation Receptor Activator of NF-κB Ligand (Rankl), previously implicated in breast carcinogenesis, whereas other progestins fail to do so. We developed xenografts of normal human breast epithelial cells (HBECSs) to the milk ducts of immunocompromised female mice and show that they remain hormone-responsive. Using HBECSs from 36 women, we show that testosterone-related progestins, desogestrel, gestodene, and levonorgestrel, induce PSA (KLK3) and promote their proliferation, whereas the anti-androgenic progestins, which have shown anti-androgenic properties in reporter assays, chlormadinone acetate and cyproterone acetate, do not. Pharmacological inhibition of the androgen receptor (AR) inhibits PR agonist and levonorgestrel-induced RANKL expression and both pharmacological and genetic AR inhibition reduce levonorgestrel-driven breast epithelial cell proliferation in vivo. Prolonged exposure to androgenic progestins elicits hyperproliferation with cytologic changes. Thus, different progestins have distinct biological activities in the breast epithelium that should be taken into account for more informed choices in hormonal contraception. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE155273 Contraceptive progestins with androgenic properties stimulate breast epithelial cell proliferation. EMBO molecular medicine 10.624 https://doi.org/10.15252/emmm.202114314 {EMBO molecular medicine (10.624): 10.15252/emmm.202114314} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA649234 https://www.ebi.ac.uk/ena/browser/view/PRJNA649234 https://www.ncbi.nlm.nih.gov/sra?term=SRP273956 [Overal design]3 paired biological replicates of mouse organoids stimulated with either ETOH or promegestone (R5020).; [Treatment]'None'; [Growth]'We transcriptionally profiled 3 biological replicates of mouse organoids treated with either ETOH or R5020 using RNA-seq'; [Extraction]'RNA was extracted from epithelial-enriched material using miRNeasy Mini Kit (Qiagen).\nLibraries were preparred using Truseq Stranded RNA producing single-end reads of 100 bp and sequenced on Illumina Hiseq 2500 instrument.'; [Cell type]'Source: ''tissue/cell type: Mouse Mammary Organoids Enriched in Epithelial Cells; treatment: ETOH; ', 'tissue/cell type: Mouse Mammary Organoids Enriched in Epithelial Cells; treatment: promegestone (R5020); ' GSE52789 Homo sapiens 7 Genome binding/occupancy profiling by high throughput sequencing GPL11154 UVB induces a major genome-wide rearrangement of RNA polymerase II at transcribed human genes 2013-11-27 Abstract Background: Faithful transcription of DNA is constantly threatened by different endogenous and environmental genotoxic effects. Transcription coupled repair has been described to quickly remove DNA lesions from the transcribed strand of active genes, permitting rapid resumption of blocked transcription. This repair mechanism has been well characterized in the past using individual target genes. However, the precise mechanism by which RNA polymerase II (Pol II) transcription is affected following UV irradiation during the repair processes genome-wide is not well understood. Results: We investigated the effect of a non-lethal dose of UVB on global DNA-bound Pol II distribution in human cells. We find that about 90% of the promoters of expressed genes show reduced Pol II occupancy 2-4 hours following UVB irradiation, and that the presence of Pol II is restored to “normal”, or higher, levels 5-6 hours after irradiation. We also identified a smaller set of genes, where the presence of Pol II at the promoter regions does not decrease after UVB irradiation, but often increases throughout the entire transcription units. Interestingly, at promoters, where Pol II promoter clearance occurs, TFIIH but not TBP follows the behavior of Pol II suggesting that at these genes TFIIH may be sequestered for DNA repair upon UVB treatment. Conclusions: Thus, our study reveals a global negative regulatory mechanism that targets Pol II transcription initiation on the large majority of transcribed genes following sublethal UVB irradiation, and a small subset of genes (including regulators of repair, cell growth and survival), where Pol II escapes this negative regulation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE52789 UVB induces a genome-wide acting negative regulatory mechanism that operates at the level of transcription initiation in human cells. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1004483 {PLoS genetics (5.224): 10.1371/journal.pgen.1004483} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA230028 https://www.ebi.ac.uk/ena/browser/view/PRJNA230028 https://www.ncbi.nlm.nih.gov/sra?term=SRP033363 [Overal design]Following genome-wide RNA Polymerase II redistribution over time upon UVB irradiation; [Treatment]'MCF-7 cells were irradiated with 55J/m2 UVB then Pol II ChIP was carried out at different time points'; [Growth]'MCF-7 cells were cultured in DMEM +10% FCS + insulin + antibiotics'; [Extraction]"Standard ChIP protocol\nIllumina HiSeq 2000 platform, according to manufacturer's protocol"; [Cell type]'Source: ''cell line: MCF-7; passages: 10 – 20; treatment: Non-treated; antibody: RNA Polymerase II ChIP (sc-224x); ', 'cell line: MCF-7; passages: 10 – 20; treatment: UVB irradiated; antibody: RNA Polymerase II ChIP (sc-224x); ' GSE20868 Homo sapiens 6 Methylation profiling by array GPL8490 Epigenetic portraits of human breast cancers (HCT116 cell line data) 2010-03-12 Breast cancer is a molecularly, biologically and clinically heterogeneous group of disorders. Understanding this diversity is essential to improving diagnosis and optimising treatment. Both genetic and acquired epigenetic abnormalities participate in cancer, but information is scant on the involvement of the epigenome in breast cancer and its contribution to the complexity of the disease. Here we used the Infinium Methylation Platform to profile at single-CpG resolution (over 14,000 genes interrogated) the methylomes of 119 breast tumours. It emerges that many genes whose expression is linked to the ER status are epigenetically controlled (or/ we show that the two major phenotypes of breast cancers determined by ER status are widely involving epigenetic regulatory mechanisms), offering the prospect of a novel approach to treating ER-positive tumours. We have distinguished methylation-profile-based tumour clusters, some coinciding with known “expression subtypes” but also new entities that may provide a meaningful basis for refining breast tumour typology. We show that methylation patterns may reflect the cellular origins of tumours. Having highlighted an unexpectedly strong epigenetic component in the regulation of key immune pathways, we show that a set of immune genes have high prognostic value in specific tumour categories. By laying the ground for better understanding of breast cancer heterogeneity and improved tumour taxonomy, the precise epigenetic portraits drawn here should contribute to better management of breast cancer patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE20868 DNA methylation profiling reveals a predominant immune component in breast cancers. EMBO molecular medicine 10.624 https://doi.org/10.1002/emmm.201100801 {EMBO molecular medicine (10.624): 10.1002/emmm.201100801} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA129631 https://www.ebi.ac.uk/ena/browser/view/PRJNA129631 None [Overal design]6 methylation profiling of HCT116 cell lines. Study of epigenetic variation (methylation) linked to gene expression. No replicate, no reference sample.; [Treatment]'Cells were harvested after 5 or 6 passages. They were detached from the culture flask using a cell scraper.'; [Growth]'HCT116 cells were maintained in McCoy’s 5A medium (Gibco) supplemented with 10% fetal calf serum (Gibco).'; [Extraction]'Genomic DNA from HCT116 cells was extracted using the QIAamp DNA Mini Kit according to the supplier’s instructions (Qiagen, Hilden, Germany). This included the recommended proteinase K and RNase A digestions. DNA was quantitated with the NanoDrop® ND-1000 UV-Vis Spectrophotometer (NanoDrop Technologies, Wilmington, DE, USA).'; [Cell type]'HCT116 cell line''methylation barcode: 4564612127_A; cell type: HCT116 cell line; genome/variation: wild type; ', 'methylation barcode: 4564612127_D; cell type: HCT116 cell line; genome/variation: wild type; ', 'methylation barcode: 4564612127_E; cell type: HCT116 cell line; genome/variation: wild type; ', 'methylation barcode: 4564612127_B; cell type: HCT116 cell line; genome/variation: DNMT1 and DNMT3B double knock out; ', 'methylation barcode: 4564612127_C; cell type: HCT116 cell line; genome/variation: DNMT1 and DNMT3B double knock out; ', 'methylation barcode: 4564612127_F; cell type: HCT116 cell line; genome/variation: DNMT1 and DNMT3B double knock out; ' GSE6532 Homo sapiens 741 Expression profiling by array GPL96; GPL97; GPL570 Definition of clinically distinct molecular subtypes in estrogen receptor positive breast carcinomas using genomic grade 2006-12-14 Purpose: A number of microarray studies have reported distinct molecular profiles of breast cancers (BC): basal-like, ErbB2-like and two to three luminal-like subtypes. These were associated with different clinical outcomes. However, although the basal and the ErbB2 subtypes are repeatedly recognized, identification of estrogen receptor (ER)-positive subtypes has been inconsistent. Refinement of their molecular definition is therefore needed. Materials and methods: We have previously reported a gene-expression grade index (GGI) which defines histological grade based on gene expression profiles. Using this algorithm, we assigned ER-positive BC to either high or low genomic grade subgroups and compared these to previously reported ER-positive molecular classifications. As further validation, we classified 666 ER-positive samples into subtypes and assessed their clinical outcome. Results: Two ER-positive molecular subgroups (high and low genomic grade) could be defined using the GGI. Despite tracking a single biological pathway, these were highly comparable to the previously described luminal A and B classification and significantly correlated to the risk groups produced using the 21-gene recurrence score. The two subtypes were associated with statistically distinct clinical outcome in both systemically untreated and tamoxifen-treated populations. Conclusions: The use of genomic grade can identify two clinically distinct ER-positive molecular subtypes in a simple and highly reproducible manner across multiple datasets. This study emphasizes the important role of proliferation-related genes in predicting prognosis in ER-positive BC. Keywords: disease state analysis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE6532 PIK3CA mutations associated with gene signature of low mTORC1 signaling and better outcomes in estrogen receptor-positive breast cancer. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.0907011107 {Journal of clinical oncology : official journal of the American Society of Clinical Oncology (None) doi:10.1200/JCO.2006.07.1522}; {BMC genomics (3.501) doi:10.1186/1471-2164-9-239}; {Proceedings of the National Academy of Sciences of the United States of America (9.580) doi:10.1073/pnas.0907011107}; {BMC medical genomics (2.568) doi:10.1186/1755-8794-2-37}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA98807 https://www.ebi.ac.uk/ena/browser/view/PRJNA98807 None [Overal design]dataset of microarray experiments from primary breast tumors used to assess the reationship between GGI, molecular subtypes, and tamoxifen resistance. No replicate, no reference sample.; [Treatment]'None'; [Growth]'None'; [Extraction]"Isolation of RNA was performed using the Trizol method (Invitrogen) according to the manufacturer's instructions and was purified using RNeasy mini-columns (Qiagen, Valencia, CA). The quality of the RNA obtained from each tumour sample was assessed based on the RNA profile generated by the bioanalyzer (Agilent Inc)olation of RNA was performed using the Trizol method (Invitrogen) according to the manufacturer's instructions and was purified using RNeasy mini-columns (Qiagen, Valencia, CA). The quality of the RNA obtained from each tumour sample was assessed based on the RNA profile generated by the bioanalyzer (Agilent Inc)", 'Isolation of RNA was performed using the Trizol method (Invitrogen) according to the manufacturers instructions and was purified using RNeasy mini-columns (Qiagen, Valencia, CA). The quality of the RNA obtained from each tumour sample was assessed based on the RNA profile generated by the bioanalyzer (Agilent Inc)olation of RNA was performed using the Trizol method (Invitrogen) according to the manufacturers instructions and was purified using RNeasy mini-columns (Qiagen, Valencia, CA). The quality of the RNA obtained from each tumour sample was assessed based on the RNA profile generated by the bioanalyzer (Agilent Inc)'; [Cell type]'Source: ''sample name: KIT_82A83; grade: 3; ggi: 0.621223; ', 'sample name: KIT_6B85; grade: 1; ggi: 0.510982; ', 'sample name: KIT_8B87; grade: 1; ggi: -2.23099; ', 'sample name: KIT_289C75; grade: 1; ggi: -1.6602; ', 'sample name: KIT_39C24; grade: 1; ggi: -1.22899; ', 'sample name: KIT_104B91; grade: 3; ggi: 0.712751; ', 'sample name: KIT_313A87; grade: 3; ggi: 1.61792; ', 'sample name: KIT_48A46; grade: 1; ggi: -1.96308; ', 'sample name: KIT_55A79; grade: 3; ggi: 1.09356; ', 'sample name: KIT_311A27; grade: 3; ggi: 1.09473; ', 'sample name: KIT_69A93; grade: 3; ggi: 0.442752; ', 'sample name: KIT_46A25; grade: 3; ggi: 1.94314; ', 'sample name: KIT_76A44; grade: 3; ggi: 0.641204; ', 'sample name: KIT_72A92; grade: 1; ggi: -1.12932; ', 'sample name: KIT_114B68; grade: 1; ggi: -0.226757; ', 'sample name: KIT_138B34; grade: 1; ggi: -1.77498; ', 'sample name: KIT_173B43; grade: 1; ggi: -1.60262; ', 'sample name: KIT_194B60; grade: 3; ggi: 1.39321; ', 'sample name: KIT_207C08; grade: 1; ggi: -1.04536; ', 'sample name: KIT_131B79; grade: 3; ggi: 0.631926; ', 'sample name: KIT_135B40; grade: 1; ggi: -1.05798; ', 'sample name: KIT_139B03; grade: 3; ggi: 1.29211; ', 'sample name: KIT_162B98; grade: 3; ggi: -0.0805463; ', 'sample name: KIT_252C64; grade: 3; ggi: 1.122; ', 'sample name: OXFT_2220; grade: 1; ggi: -1.1865; ', 'sample name: OXFT_2190; grade: 1; ggi: -0.0646606; ', 'sample name: OXFT_2152; grade: 3; ggi: -1.48307; ', 'sample name: OXFT_2221; grade: 3; ggi: 0.00432486; ', 'sample name: OXFT_209; grade: 3; ggi: 2.51046; ', 'sample name: OXFT_1769; grade: 1; ggi: -0.0938409; ', 'sample name: OXFT_928; grade: 1; ggi: -2.46578; ', 'sample name: OXFT_2093; grade: 1; ggi: -0.821333; ', 'sample name: OXFT_1770; grade: 1; ggi: -0.233113; ', 'sample name: OXFT_630; grade: 1; ggi: -2.25362; ', 'sample name: OXFT_1342; grade: 3; ggi: 2.46201; ', 'sample name: OXFT_2340; grade: 1; ggi: -0.423715; ', 'sample name: OXFT_2338; grade: 3; ggi: 1.83407; ', 'sample name: OXFT_2341; grade: 1; ggi: -0.128292; ', 'sample name: OXFT_1902; grade: 3; ggi: 1.54786; ', 'sample name: OXFT_1982; grade: 1; ggi: -2.15729; ', 'sample name: OXFT_5210; grade: 3; ggi: 1.43675; ', 'sample name: OXFT_2027; grade: 3; ggi: -0.495184; ', 'sample name: OXFT_1133; grade: 1; ggi: -1.03916; ', 'sample name: OXFT_1441; grade: 3; ggi: 0.992788; ', 'sample name: OXFT_1432; grade: 1; ggi: -0.931815; ', 'sample name: OXFT_1125; grade: 1; ggi: -1.4746; ', 'sample name: OXFT_1070; grade: 1; ggi: -1.17797; ', 'sample name: OXFT_700; grade: 1; ggi: -2.22663; ', 'sample name: OXFT_742; grade: 3; ggi: 0.342894; ', 'sample name: OXFT_738; grade: 1; ggi: -1.55124; ', 'sample name: OXFT_669; grade: 3; ggi: -0.368934; ', 'sample name: OXFT_3597; grade: 3; ggi: 0.496276; ', 'sample name: OXFT_638; grade: 1; ggi: -1.12038; ', 'sample name: OXFT_2188; grade: 3; ggi: 0.411223; ', 'sample name: OXFT_2069; grade: 3; ggi: 2.04336; ', 'sample name: OXFT_596; grade: 3; ggi: 2.71614; ', 'sample name: OXFT_619; grade: 3; ggi: 1.50798; ', 'sample name: OXFT_680; grade: 1; ggi: -0.495882; ', 'sample name: OXFT_443; grade: 3; ggi: 2.57167; ', 'sample name: OXFT_2092; grade: 1; ggi: 0.538565; ', 'sample name: OXFT_1579; grade: 1; ggi: 0.546113; ', 'sample name: OXFT_4904; grade: 1; ggi: 0.424396; ', 'sample name: OXFT_511; grade: 3; ggi: 0.405457; ', 'sample name: OXFT_736; grade: 1; ggi: -1.63122; ', 'sample name: KIU_101B88; node: 0; size: 1.2; grade: 3; ggi: 2.48005; age: 40; er: 0; time rfs: 2280; distant rfs: 0; ', 'sample name: KIU_105B13; node: 0; size: 1.3; grade: 1; ggi: -0.633592; age: 46; er: 1; time rfs: 2675; distant rfs: 0; ', 'sample name: KIU_106B55; node: 0; size: 6; grade: 1; ggi: -1.02972; age: KJ67; er: 1; time rfs: 426; distant rfs: 1; ', 'sample name: KIU_111B51; node: 0; size: 3.3; grade: 3; ggi: 1.04395; age: 41; er: 1; time rfs: 182; distant rfs: 1; ', 'sample name: KIU_113B11; node: 0; size: 3.2; grade: 3; ggi: 0.683559; age: 38; er: 1; time rfs: KJX46; distant rfs: 1; ', 'sample name: KIU_120B73; node: 0; size: 1.6; grade: 2; ggi: 1.05919; age: 34; er: 1; time rfs: 3952; distant rfs: 0; ', 'sample name: KIU_124B25; node: 0; size: 2.1; grade: 2; ggi: -1.23306; age: 46; er: 1; time rfs: 1824; distant rfs: 1; ', 'sample name: KIU_127B00; node: 0; size: 2.2; grade: 3; ggi: 0.679034; age: 57; er: 1; time rfs: 699; distant rfs: 1; ', 'sample name: KIU_134B33; node: 0; size: 2.8; grade: 2; ggi: 0.31585; age: 63; er: 1; time rfs: 730; distant rfs: 1; ', 'sample name: KIU_136B04; node: 0; size: 1.7; grade: 2; ggi: -1.17846; age: 54; er: 1; time rfs: 882; distant rfs: 1; ', 'sample name: KIU_140B91; node: 0; size: 1.2; grade: 2; ggi: -1.42336; age: 61; er: 1; time rfs: 2827; distant rfs: 0; ', 'sample name: KIU_144B49; node: 0; size: 2.1; grade: 2; ggi: -1.11827; age: 40; er: 1; time rfs: 2006; distant rfs: 0; ', 'sample name: KIU_151B84; node: 0; size: 1.5; grade: 2; ggi: -0.749794; age: KJ69; er: 1; time rfs: 2523; distant rfs: 0; ', 'sample name: KIU_155B52; node: 0; size: 1.3; grade: 1; ggi: -1.41523; age: KJ69; er: 0; time rfs: 3648; distant rfs: 0; ', 'sample name: KIU_163B27; node: 0; size: 0.8; grade: 1; ggi: -1.27328; age: 49; er: 1; time rfs: 2250; distant rfs: 0; ', 'sample name: KIU_164B81; node: 0; size: 2.3; grade: 2; ggi: 0.999075; age: 62; er: 0; time rfs: 3587; distant rfs: 0; ', 'sample name: KIU_172B19; node: 0; size: 2.3; grade: 3; ggi: 0.36665; age: 42; er: 1; time rfs: 3131; distant rfs: 1; ', 'sample name: KIU_177B67; node: 0; size: 1.8; grade: 1; ggi: -1.91747; age: 41; er: 1; time rfs: 2493; distant rfs: 1; ', 'sample name: KIU_184B38; node: 0; size: 1; grade: 1; ggi: -0.995142; age: 63; er: 1; time rfs: 3162; distant rfs: 0; ', 'sample name: KIU_188B13; node: 0; size: 1.4; grade: 2; ggi: -0.174684; age: 60; er: 0; time rfs: 3496; distant rfs: 0; ', 'sample name: KIU_196B81; node: 0; size: 1.4; 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', 'samplename: GUYT_50143; ID: 50143; series: GUYT; age: 59; grade: 3; size: 2.00; er: 1; pgr: 0; node: 1; t.rfs: 5518; e.rfs: 0; t.dmfs: 5518; e.dmfs: 0; ', 'samplename: GUYT_50146; ID: 50146; series: GUYT; age: 61; grade: 2; size: 2.50; er: 1; pgr: 1; node: 1; t.rfs: 2585; e.rfs: 0; t.dmfs: 2585; e.dmfs: 0; ', 'samplename: GUYT_50148; ID: 50148; series: GUYT; age: 62; grade: 2; size: 3.00; er: 1; pgr: 1; node: 1; t.rfs: 5189; e.rfs: 0; t.dmfs: 5189; e.dmfs: 0; ', 'samplename: GUYT_50149; ID: 50149; series: GUYT; age: 43; grade: 2; size: 2.50; er: 1; pgr: 1; node: 1; t.rfs: 4462; e.rfs: 0; t.dmfs: 4462; e.dmfs: 0; ', 'samplename: GUYT_50150; ID: 50150; series: GUYT; age: 56; grade: 2; size: 2.00; er: 1; pgr: 0; node: 0; t.rfs: 4774; e.rfs: 1; t.dmfs: 4774; e.dmfs: 1; ', 'samplename: GUYT_50151; ID: 50151; series: GUYT; age: 53; grade: NA; size: 4.00; er: 1; pgr: 1; node: 0; t.rfs: 5132; e.rfs: 0; t.dmfs: 5132; e.dmfs: 0; ', 'samplename: GUYT_50153; ID: 50153; series: GUYT; age: 59; grade: NA; size: 1.10; er: 1; pgr: 1; node: 1; t.rfs: 5274; e.rfs: 0; t.dmfs: 5274; e.dmfs: 0; ', 'samplename: GUYT_50154; ID: 50154; series: GUYT; age: 58; grade: 1; size: 3.00; er: 1; pgr: 1; node: 1; t.rfs: 5311; e.rfs: 0; t.dmfs: 5311; e.dmfs: 0; ', 'samplename: GUYT_50155; ID: 50155; series: GUYT; age: 53; grade: NA; size: 5.00; er: 1; pgr: 0; node: 1; t.rfs: 188; e.rfs: 1; t.dmfs: 188; e.dmfs: 1; ', 'samplename: GUYT_50156; ID: 50156; series: GUYT; age: 66; grade: 1; size: 2.50; er: 1; pgr: 1; node: 1; t.rfs: 4756; e.rfs: 0; t.dmfs: 4756; e.dmfs: 0; ', 'samplename: GUYT_50158; ID: 50158; series: GUYT; age: 67; grade: 3; size: 1.50; er: 1; pgr: 0; node: 1; t.rfs: 1242; e.rfs: 0; t.dmfs: 1242; e.dmfs: 0; ', 'samplename: GUYT_50159; ID: 50159; series: GUYT; age: 63; grade: 3; size: 3.00; er: 1; pgr: 0; node: 1; t.rfs: 1923; e.rfs: 1; t.dmfs: 1923; e.dmfs: 1; ', 'samplename: GUYT_50160; ID: 50160; series: GUYT; age: 61; grade: NA; size: 1.50; er: 1; pgr: 1; node: 1; t.rfs: 4465; e.rfs: 1; t.dmfs: 4465; e.dmfs: 1; ', 'samplename: GUYT_50162; ID: 50162; series: GUYT; age: 66; grade: 2; size: 2.00; er: 1; pgr: 1; node: 0; t.rfs: 5214; e.rfs: 0; t.dmfs: 5214; e.dmfs: 0; ', 'samplename: GUYT_50163; ID: 50163; series: GUYT; age: 61; grade: 2; size: 1.40; er: 1; pgr: 0; node: 1; t.rfs: 428; e.rfs: 1; t.dmfs: 428; e.dmfs: 1; ', 'samplename: GUYT_50166; ID: 50166; series: GUYT; age: 57; grade: NA; size: 3.00; er: 1; pgr: 1; node: 0; t.rfs: 4797; e.rfs: 0; t.dmfs: 4797; e.dmfs: 0; ', 'samplename: GUYT_50168; ID: 50168; series: GUYT; age: 59; grade: 2; size: 3.80; er: 1; pgr: 1; node: 0; t.rfs: 1237; e.rfs: 1; t.dmfs: 1237; e.dmfs: 1; ', 'samplename: GUYT_50169; ID: 50169; series: GUYT; age: 56; grade: 2; size: 3.00; er: 1; pgr: 1; node: 1; t.rfs: 4852; e.rfs: 0; t.dmfs: 4852; e.dmfs: 0; ', 'samplename: GUYT_50172; ID: 50172; series: GUYT; age: 61; grade: 1; size: 2.00; er: 1; pgr: 1; node: 1; t.rfs: 5189; e.rfs: 0; t.dmfs: 5189; e.dmfs: 0; ', 'samplename: GUYT_50173; ID: 50173; series: GUYT; age: 67; grade: 1; size: 1.90; er: 1; pgr: 1; node: 0; t.rfs: 5054; e.rfs: 0; t.dmfs: 5054; e.dmfs: 0; ', 'samplename: GUYT_50174; ID: 50174; series: GUYT; age: 68; grade: NA; size: 3.00; er: 1; pgr: 1; node: 1; t.rfs: 378; e.rfs: 0; t.dmfs: 378; e.dmfs: 0; ', 'samplename: GUYT_50176; ID: 50176; series: GUYT; age: 59; grade: 2; size: 4.00; er: 1; pgr: 1; node: 1; t.rfs: 927; e.rfs: 1; t.dmfs: 927; e.dmfs: 1; ', 'samplename: GUYT_50177; ID: 50177; series: GUYT; age: 50; grade: 3; size: 3.00; er: 1; pgr: 1; node: 1; t.rfs: 4973; e.rfs: 0; t.dmfs: 4973; e.dmfs: 0; ', 'samplename: GUYT_50178; ID: 50178; series: GUYT; age: 63; grade: 3; size: 3.00; er: 1; pgr: 1; node: 1; t.rfs: 3795; e.rfs: 1; t.dmfs: 3795; e.dmfs: 1; ', 'samplename: GUYT_50179; ID: 50179; series: GUYT; age: 50; grade: 1; size: 1.80; er: 1; pgr: 1; node: 1; t.rfs: 4628; e.rfs: 0; t.dmfs: 4628; e.dmfs: 0; ', 'samplename: GUYT_50181; ID: 50181; series: GUYT; age: 53; grade: 1; size: 1.20; er: 1; pgr: 1; node: 0; t.rfs: 4816; e.rfs: 0; t.dmfs: 4816; e.dmfs: 0; ', 'samplename: GUYT_50182; ID: 50182; series: GUYT; age: 70; grade: 2; size: 2.50; er: 1; pgr: 1; node: 1; t.rfs: 4988; e.rfs: 0; t.dmfs: 4988; e.dmfs: 0; ', 'samplename: GUYT_50183; ID: 50183; series: GUYT; age: 77; grade: 1; size: 1.60; er: 1; pgr: 1; node: 1; t.rfs: 4517; e.rfs: 0; t.dmfs: 4517; e.dmfs: 0; ', 'samplename: GUYT_50184; ID: 50184; series: GUYT; age: 68; grade: 2; size: 1.90; er: 1; pgr: 1; node: 1; t.rfs: 3592; e.rfs: 0; t.dmfs: 3592; e.dmfs: 0; ', 'samplename: GUYT_50188; ID: 50188; series: GUYT; age: 71; grade: 1; size: 1.50; er: 1; pgr: 0; node: 0; t.rfs: 4435; e.rfs: 0; t.dmfs: 4435; e.dmfs: 0; ', 'samplename: GUYT_50190; ID: 50190; series: GUYT; age: 72; grade: 3; size: 1.20; er: 1; pgr: 1; node: 0; t.rfs: 2853; e.rfs: 0; t.dmfs: 2853; e.dmfs: 0; ', 'samplename: GUYT_50192; ID: 50192; series: GUYT; age: 86; grade: 2; size: 1.85; er: 1; pgr: 1; node: 0; t.rfs: 1699; e.rfs: 0; t.dmfs: 1699; e.dmfs: 0; ', 'samplename: GUYT_50193; ID: 50193; series: GUYT; age: 82; grade: 1; size: 1.80; er: 1; pgr: 1; node: 1; t.rfs: 3579; e.rfs: 0; t.dmfs: 3579; e.dmfs: 0; ', 'samplename: GUYT_50200; ID: 50200; series: GUYT; age: 82; grade: 3; size: 2.50; er: 1; pgr: 0; node: 0; t.rfs: 4155; e.rfs: 0; t.dmfs: 4155; e.dmfs: 0; ', 'samplename: GUYT_50204; ID: 50204; series: GUYT; age: 78; grade: 2; size: 1.70; er: 1; pgr: 1; node: 0; t.rfs: 4461; e.rfs: 0; t.dmfs: 4461; e.dmfs: 0; ', 'samplename: GUYT_50210; ID: 50210; series: GUYT; age: 65; grade: NA; size: 3.00; er: 1; pgr: 1; node: 1; t.rfs: 3304; e.rfs: 1; t.dmfs: 3304; e.dmfs: 1; ', 'samplename: GUYT_50211; ID: 50211; series: GUYT; age: 63; grade: 2; size: 1.50; er: 1; pgr: 1; node: 0; t.rfs: 3004; e.rfs: 1; t.dmfs: 3004; e.dmfs: 1; ', 'samplename: GUYT_50213; ID: 50213; series: GUYT; age: 65; grade: 2; size: 2.00; er: 1; pgr: 1; node: 1; t.rfs: 4428; e.rfs: 0; t.dmfs: 4428; e.dmfs: 0; ', 'samplename: GUYT_50218; ID: 50218; series: GUYT; age: 51; grade: 1; size: 1.50; er: 1; pgr: 1; node: 0; t.rfs: 4144; e.rfs: 0; t.dmfs: 4144; e.dmfs: 0; ', 'samplename: GUYT_50219; ID: 50219; series: GUYT; age: 65; grade: 3; size: 1.70; er: 1; pgr: 1; node: 0; t.rfs: 4324; e.rfs: 0; t.dmfs: 4324; e.dmfs: 0; ', 'samplename: GUYT_50221; ID: 50221; series: GUYT; age: 73; grade: 3; size: 2.90; er: 1; pgr: 1; node: 1; t.rfs: 3349; e.rfs: 0; t.dmfs: 3349; e.dmfs: 0; ', 'samplename: GUYT_50223; ID: 50223; series: GUYT; age: 67; grade: 3; size: 2.60; er: 1; pgr: 0; node: 1; t.rfs: 1270; e.rfs: 1; t.dmfs: 1270; e.dmfs: 1; ', 'samplename: GUYT_50225; ID: 50225; series: GUYT; age: 58; grade: 1; size: 3.50; er: 1; pgr: 1; node: 1; t.rfs: 4481; e.rfs: 0; t.dmfs: 4481; e.dmfs: 0; ', 'samplename: GUYT_50228; ID: 50228; series: GUYT; age: 74; grade: 3; size: 1.50; er: 1; pgr: 1; node: 1; t.rfs: 3429; e.rfs: 0; t.dmfs: 3429; e.dmfs: 0; ', 'samplename: GUYT_50230; ID: 50230; series: GUYT; age: 64; grade: 2; size: 1.30; er: 1; pgr: 1; node: 0; t.rfs: 4514; e.rfs: 0; t.dmfs: 4514; e.dmfs: 0; ', 'samplename: GUYT_50233; ID: 50233; series: GUYT; age: 57; grade: 1; size: 1.30; er: 1; pgr: 0; node: 1; t.rfs: 4596; e.rfs: 0; t.dmfs: 4596; e.dmfs: 0; ', 'samplename: GUYT_50235; ID: 50235; series: GUYT; age: 60; grade: 1; size: 1.30; er: 1; pgr: 1; node: 1; t.rfs: 4554; e.rfs: 0; t.dmfs: 4554; e.dmfs: 0; ', 'samplename: GUYT_50236; ID: 50236; series: GUYT; age: 72; grade: 2; size: 2.50; er: 1; pgr: 1; node: 0; t.rfs: 2263; e.rfs: 0; t.dmfs: 2263; e.dmfs: 0; ', 'samplename: GUYT_50237; ID: 50237; series: GUYT; age: 79; grade: 1; size: 2.70; er: 1; pgr: 1; node: 0; t.rfs: 4454; e.rfs: 0; t.dmfs: 4454; e.dmfs: 0; ', 'samplename: GUYT_50238; ID: 50238; series: GUYT; age: 58; grade: 2; size: 3.40; er: 1; pgr: 0; node: 0; t.rfs: 767; e.rfs: 1; t.dmfs: 767; e.dmfs: 1; ', 'samplename: GUYT_50239; ID: 50239; series: GUYT; age: 62; grade: NA; size: 1.40; er: 1; pgr: 1; node: 0; t.rfs: 1574; e.rfs: 0; t.dmfs: 1574; e.dmfs: 0; ', 'samplename: GUYT_50243; ID: 50243; series: GUYT; age: 81; grade: 2; size: 2.00; er: 1; pgr: 0; node: 0; t.rfs: 2278; e.rfs: 0; t.dmfs: 2278; e.dmfs: 0; ', 'samplename: GUYT_50246; ID: 50246; series: GUYT; age: 77; grade: 1; size: 1.50; er: 1; pgr: 1; node: 1; t.rfs: 2750; e.rfs: 0; t.dmfs: 2750; e.dmfs: 0; ', 'samplename: GUYT_50247; ID: 50247; series: GUYT; age: 67; grade: 2; size: 4.00; er: 1; pgr: 0; node: 0; t.rfs: 443; e.rfs: 1; t.dmfs: 443; e.dmfs: 1; ', 'samplename: GUYT_50248; ID: 50248; series: GUYT; age: 67; grade: 3; size: 7.50; er: 1; pgr: 0; node: 1; t.rfs: 3211; e.rfs: 0; t.dmfs: 3211; e.dmfs: 0; ', 'samplename: GUYT_50251; ID: 50251; series: GUYT; age: 70; grade: 2; size: 1.60; er: 1; pgr: 1; node: 1; t.rfs: 3751; e.rfs: 1; t.dmfs: 3751; e.dmfs: 1; ', 'samplename: GUYT_50252; ID: 50252; series: GUYT; age: 48; grade: 3; size: 2.10; er: 1; pgr: 0; node: 0; t.rfs: 3973; e.rfs: 0; t.dmfs: 3973; e.dmfs: 0; ', 'samplename: GUYT_50254; ID: 50254; series: GUYT; age: 76; grade: 3; size: 1.50; er: 1; pgr: 1; node: 0; t.rfs: 2622; e.rfs: 0; t.dmfs: 2622; e.dmfs: 0; ', 'samplename: GUYT_50257; ID: 50257; series: GUYT; age: 67; grade: 2; size: 2.20; er: 1; pgr: 0; node: 1; t.rfs: 4222; e.rfs: 0; t.dmfs: 4222; e.dmfs: 0; ' GSE28556 Mus musculus 24 Expression profiling by array GPL6885 Fasting Cycles Retard Growth of Tumors and Sensitize a Range of Cancer Cell Types to Chemotherapy 2011-04-12 Short-term starvation (STS or fasting) provides protection to normal cells, mice, and possibly patients from a variety of chemotherapy drugs, but the possibility that it may also protect tumor cells renders its translational potential uncertain. Here we show that fasting cycles can be as effective as toxic chemotherapy drugs, and increase chemotherapy efficacy in the treatment of melanoma, glioma, breast cancer, and neuroblastoma. In vitro, STS sensitizes to chemotherapy 15 of the 17 cancer cell lines tested. In combination with chemotherapy STS results in a synergistic 20-fold increase in DNA damage, increased phosphorylation of pro-aging genes AKT and S6 kinase, reduced expression of stress resistance transcription factors FOXO3a and NFkB, elevated superoxide, and activated caspase-3; all changes not observed in normal tissues. Several of these effects are linked to the activity of heme oxygenase 1 (HO-1), whose modulation was sufficient to regulate chemotherapy-dependent cell death in breast cancer cells. These studies suggest that multiple fasting cycles have the potential to replace certain toxic chemotherapy drugs and to sensitize a wide range of tumors to chemotherapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28556 Fasting cycles retard growth of tumors and sensitize a range of cancer cell types to chemotherapy. Science translational medicine 17.161 https://doi.org/10.1126/scitranslmed.3003293 {Science translational medicine (17.161): 10.1126/scitranslmed.3003293} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA139071 https://www.ebi.ac.uk/ena/browser/view/PRJNA139071 None [Overal design]To obtain an unbiased view of the gene expression changes occurring in cancer cells in response to fasting, we performed genome-wide microarray analyses, using Illumina's Sentrix MouseRef-8 v2 Expression BeadChips (Illumina, San Diego, CA), on the subcutaneous 4T1 breast cancer tumor mass, heart, muscle and liver tissues from balb-c mice that were either fasted for 48 hours or fed an ad lib diet. Three mice from each of the starvation and the ad lib fed groups were used for the array studies.; [Treatment]'Heart tissue from mice that fasted for 48 hours.', 'Heart tissue from mice that were fed an ad lib diet.', 'Liver tissue from mice that fasted for 48 hours.', 'Liver tissue from mice that were fed an ad lib diet.', 'Subcutaneous 4T1 breast cancer tumor mass from mice that were fasted for 48 hours.', 'Subcutaneous 4T1 breast cancer tumor mass from mice that were fed an ad lib diet.', 'Muscle tissue from mice that fasted for 48 hours.', 'Muscle tissue from mice that were fed an ad lib diet.'; [Growth]'None'; [Extraction]"RNA was extracted from heart tissue using 1.0mm glass beads (BioSpec Products, Inc.) in a Precellys 24 Tissue Homogenizer (Bertin Technologies) and Qiagen RNeasy Mini Kits according to manufacturer's specifications. Quality and quantity of the total RNA was checked with the Agilent 2100 bioanalyzer using RNA 6000 Nano chips.", "RNA was extracted from liver tissue using 1.0mm glass beads (BioSpec Products, Inc.) in a Precellys 24 Tissue Homogenizer (Bertin Technologies) and Qiagen RNeasy Mini Kits according to manufacturer's specifications. Quality and quantity of the total RNA was checked with the Agilent 2100 bioanalyzer using RNA 6000 Nano chips.", "RNA was extracted from a subcutaneous 4T1 breast cancer tumor mass using 1.0mm glass beads (BioSpec Products, Inc.) in a Precellys 24 Tissue Homogenizer (Bertin Technologies) and Qiagen RNeasy Mini Kits according to manufacturer's specifications. Quality and quantity of the total RNA was checked with the Agilent 2100 bioanalyzer using RNA 6000 Nano chips.", "RNA was extracted from a subcutaneous 4T1 breast cancer tumor mass using 1.0mm glass beads (BioSpec Products, Inc.) and a Precellys 24 Tissue Homogenizer (Bertin Technologies) and Qiagen RNeasy Mini Kits according to manufacturer's specifications. Quality and quantity of the total RNA was checked with the Agilent 2100 bioanalyzer using RNA 6000 Nano chips.", "RNA was extracted from muscle tissue using 1.0mm glass beads (BioSpec Products, Inc.) in a Precellys 24 Tissue Homogenizer (Bertin Technologies) and Qiagen RNeasy Mini Kits according to manufacturer's specifications. Quality and quantity of the total RNA was checked with the Agilent 2100 bioanalyzer using RNA 6000 Nano chips."; [Cell type]'Source: ''tissue: Heart tissue; strain: Balb-c mice; treatment: fasted for 48 hours; ', 'tissue: Heart tissue; strain: Balb-c mice; treatment: fed an ad lib diet; ', 'tissue: Liver tissue; strain: Balb-c mice; treatment: fasted for 48 hours; ', 'tissue: Liver tissue; strain: Balb-c mice; treatment: fed an ad lib diet; ', 'tissue: Subcutaneous 4T1 breast cancer tumor mass tissue; strain: Balb-c mice; treatment: fasted for 48 hours; ', 'tissue: Subcutaneous 4T1 breast cancer tumor mass tissue; strain: Balb-c mice; treatment: fed an ad lib diet; ', 'tissue: Muscle tissue; strain: Balb-c mice; treatment: fasted for 48 hours; ', 'tissue: Muscle tissue; strain: Balb-c mice; treatment: fed an ad lib diet; ' GSE21834 Homo sapiens 21 Expression profiling by array; Non-coding RNA profiling by array GPL570; GPL5106 Identification of the receptor tyrosine kinase AXL in triple negative breast cancer as a novel target for the human miR-34a microRNA 2010-05-14 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE21834 Identification of the receptor tyrosine kinase AXL in breast cancer as a target for the human miR-34a microRNA. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-011-1690-0 {Breast cancer research and treatment (3.471): 10.1007/s10549-011-1690-0} 'other', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA126915 https://www.ebi.ac.uk/ena/browser/view/PRJNA126915 None [Overal design]Refer to individual Series; [Treatment]'Cells were untreated.', 'MDA-MB-231 cells (600,000 cells/well) were reverse transfected in 6 well dishes with either AllStar negative control, Qmimic, or Dmimic at 10 nM final concentration using Lipofectamine 2000 (10.5 ul/well),'; [Growth]'Cells were grown in RPMI 1640 basal medium + 10% FBS in a T75 flask at 37C with 5% carbon dioxide. Cells were harvested at 80-90% confluency for total RNA extraction.', 'Cells were grown in DMEM/F12 basal medium supplemented with 5% horse serum, 20 ng/ml final epidermal growth factor, 0.5 ug/ml final hydrocortisone, 100 ng/ml final cholera toxin, and 10 ug/ml final insulin in a T75 flask at 37C with 5% carbon dioxide. Cells were harvested at 80-90% confluency for total RNA extraction.', 'MDA-MB-231 cells were grown in T75 flasks containing RPMI 1640 basal medium + 10% Fetal Bovine Serum at 37C with 5% CO2. Cells at 80-90% confluency were used in transfections.'; [Extraction]"The small RNA fraction was extracted from these cells using Qiagen's miRNeasy kit by following the manufacturer's protocol.", "At 48 hrs post-transfection, total RNA was extracted from each well using Qiagen's miRNeasy extraction kit according to the manufacturer's instructions."; [Cell type]'Source: ''estrogen receptor: negative; progesterone receptor: negative; her-2: negative; cell line: MB231; ', 'cell line: MCF10A; ', 'estrogen receptor: positive; progesterone receptor: positive; her-2: negative; cell line: MCF7; ', 'estrogen receptor: positive; progesterone receptor: negative; her-2: negative; cell line: MCF7; ', 'estrogen receptor: negative; progesterone receptor: negative; her-2: positive; cell line: SKBR3; ', 'cell line: MDA-MB-231; ' GSE60650 Mus musculus 12 Expression profiling by high throughput sequencing GPL13112 From mouse to humans: detecting preventing vaccination targets associated to melanoma cancer stem cells 2014-08-22 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60650 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA259189 https://www.ebi.ac.uk/ena/browser/view/PRJNA259189 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'The adherent B16 epithelial cells were cultured in DMEM supplemented with 20% FCS (GIBCO, Grand Island, NY). Single B16 cells were plated in ultra low attachment flasks (Corning Life Sciences, Chorges, France) at 6 x 10^4 viable cells/ml in serum-free DMEM-F12 medium (Cambrex BioScience, Venviers, Belgium) supplemented with 20 ng/ml basic fibroblast growth factor (bFGF), 20 ng/ml epidermal growth factor (EGF), 5 µg/ml insulin, and 0.4% bovine serum albumin (BSA), all from Sigma-Aldrich (St. Louis, MO). Nonadherent spherical clusters of cells, named mammospheres, were collected by gentle centrifugation after 7 days.', 'The adherent CT26 epithelial cells were cultured in DMEM supplemented with 20% FCS (GIBCO, Grand Island, NY). Single CT26 cells were plated in ultra low attachment flasks (Corning Life Sciences, Chorges, France) at 6 x 104 viable cells/ml in serum-free DMEM-F12 medium (Cambrex BioScience, Venviers, Belgium) supplemented with 20 ng/ml basic fibroblast growth factor (bFGF), 20 ng/ml epidermal growth factor (EGF), 5 μg/ml insulin, and 0.4% bovine serum albumin (BSA), all from Sigma-Aldrich (St. Louis, MO). Nonadherent spherical clusters of cells, named mammospheres, were collected by gentle centrifugation after 7 days.', 'The adherent TUBO epithelial cells were cultured in DMEM supplemented with 20% FCS (GIBCO, Grand Island, NY). Single TUBO cells were plated in ultra low attachment flasks (Corning Life Sciences, Chorges, France) at 6 x 104 viable cells/ml in serum-free DMEM-F12 medium (Cambrex BioScience, Venviers, Belgium) supplemented with 20 ng/ml basic fibroblast growth factor (bFGF), 20 ng/ml epidermal growth factor (EGF), 5 μg/ml insulin, and 0.4% bovine serum albumin (BSA), all from Sigma-Aldrich (St. Louis, MO). Nonadherent spherical clusters of cells, named mammospheres, were collected by gentle centrifugation after 7 days.'; [Extraction]'Total RNA extraction was done with Rneasy QIAGEN kit following manufacturer instruction. Quality of RNA was evaluated by Bioanalyser and quantified with Nanodrop.\nLibraries construction and indexing was done using Illumina TrueSeq unstranded Illumina kit following manufacturer instructions using 1 microgram of total RNA.'; [Cell type]'epithelial bulk', 'mammospheres p1', 'spheroids p1''cell type: epithelial bulk; cell line: B16; disease status: melanoma; ', 'cell type: mammospheres p1; cell line: B16; disease status: melanoma; ', 'cell type: epithelial bulk; cell line: CT26; disease status: colon carcinoma; ', 'cell type: spheroids p1; cell line: CT26; disease status: colon carcinoma; ', 'cell type: epithelial bulk; cell line: TUBO; disease status: breast cancer; ', 'cell type: mammospheres p1; cell line: TUBO; disease status: breast cancer; ' GSE157109 Homo sapiens 6 Expression profiling by high throughput sequencing GPL24676 Gene expression profiling data following TRIM8 knockdown in MCF-7 cells 2020-08-29 Breast cancer (BC) is the most common female malignancies worldwide, and 70% of cases are estrogen receptor α (ERα) positive. In this study, we report that the E3 ubiquitin ligase TRIM8 acts as a novel regulator of ER signaling. TRIM8 is downregulated in BC and is associated with poor prognosis. In addition, the protein level of TRIM8 is negatively correlated with ERα expression. To investigate whether TRIM8 mediated estrogen signaling pathway, we generated a knockdown model of TRIM8 in human MCF7 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE157109 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA660124 https://www.ebi.ac.uk/ena/browser/view/PRJNA660124 https://www.ncbi.nlm.nih.gov/sra?term=SRP279307 [Overal design]Gene expression profiling of MCF-7 cells were transfected with TRIM8 siRNA or control siRNA. Three biological replicates were used for each group.; [Treatment]'MCF7 cells were transfected with the control or TRIM8 siRNAs. Transfection was perfomed with Lipofectamine RNAiMAX reagent (13778100, Invitrogen).'; [Growth]'The cells were cultured in a humidified environment consisting of 95% air and 5% CO2 at 37°C, and cultured in DMEM (Gibco, China) supplemented with 10% FBS (Gibco, Australia).'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions\nRNA libraries were prepared for sequencing using standard Illumina protocols"; [Cell type]'breast cancer''cell line: MCF-7; cell type: breast cancer; ' GSE18592 Homo sapiens 18 Expression profiling by array GPL6244 Estrogen Coordinates Translation and Transcription Revealing a Role for NRSF in Human Breast Cancer Cells 2009-10-15 Analysis of estrogen receptor (ER)-positive MCF7 cell total RNA expression and polysome-assiciated RNA expression following treatment with estradiol (E2) and vehicle (etoh). We used expression microarrays to measure polysome association and total RNA abundance in E2 treated MCF7. These data, along with previously published data, show that genes that are upregulated by estrogen treatment are biased towards association with polysomes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE18592 Estrogen coordinates translation and transcription, revealing a role for NRSF in human breast cancer cells. Molecular endocrinology (Baltimore, Md.) 3.628 https://doi.org/10.1210/me.2009-0436 {Molecular endocrinology (Baltimore, Md.) (3.628): 10.1210/me.2009-0436} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA121331 https://www.ebi.ac.uk/ena/browser/view/PRJNA121331 None [Overal design]MCF7 cells were grown in hormone depleted media for three days before a 1 hour treatment with E2 or 0.1 % ethanol (vehicle). Total RNA was collected using standard methods and polysome-association RNA from the same cells were collected using sucrose gradient fractionation. Both RNA populations were purified, labeled, and hybridized to Affymetrix Human Genest arrays.; [Treatment]'Cells were split on day 0, then switched to phenol red free DMEM with 5% charcol-dextran-treated serum on day 1. The media was changed daily. On day 4, the cells were treated with 10nM estradiol (E2) or vehicle control (etoh) for one hour.'; [Growth]'Cells maintained in DMEM with 10% FBS, split 1:4 every 3 days.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions. Polysome-associated RNA was collected from fractionation of a sucrose gradient and then purified by precipitating in guanadine-HCL and ethanol. Both sets were cleaned up using RNeasy with on-the-column DNase I treatment."; [Cell type]'Source: ''agent: estrogen; fraction: total RNA; cell line: MCF7; ', 'agent: estrogen; fraction: polysome-associated RNA; cell line: MCF7; ', 'agent: ethanol; fraction: total RNA; cell line: MCF7; ', 'agent: ethanol; fraction: polysome-associated RNA; cell line: MCF7; ', 'agent: estrogen; fraction: monosome-associated RNA; cell line: MCF7; ', 'agent: ethanol; fraction: monosome-associated RNA; cell line: MCF7; ' GSE117949 Homo sapiens 12 Expression profiling by array GPL17586 The thyroid hormone receptor β inhibits self-renewal capacity of breast cancer stem cells (Adherent MCF7 cells) 2018-07-31 Since the thyroid hormone receptor β (TRβ) appears to suppress breast tumor growth and metastasis, we have analyzed the possibility that this receptor could affect cancer stem cell biology using TRβ-expressing MCF-7 cells (MCF7-TRβ cells) treated with the thyroid hormone T3. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE117949 Thyroid Hormone Receptor β Inhibits Self-Renewal Capacity of Breast Cancer Stem Cells. Thyroid : official journal of the American Thyroid Association 7.786 https://doi.org/10.1089/thy.2019.0175 {Thyroid : official journal of the American Thyroid Association (7.786): 10.1089/thy.2019.0175} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA483784 https://www.ebi.ac.uk/ena/browser/view/PRJNA483784 None [Overal design]Gene expression was compared among MCF7 control cells (transduced with a selector Neo gene), MCF7-TRβ cells and both of them treated with T3. Three replicates were analyzed per each group.; [Treatment]'When indicated, T3 was added to a final concentration of 25 nM.'; [Growth]"Cells were maintained in Dulbecco's Modified Eagle Medium GlutaMAX™ supplemented with 1% L-glutamine (Gibco-BRL Life Technologies), 10% fetal bovine serum (Sigma) and 1% penicillin/streptomycin (Gibco-BRL Life Technologies) at 37°C in a humidified atmosphere of 5% CO2."; [Extraction]"Total RNA was extracted from cells using RNeasy Mini Kit (Qiagen) according to the manufacturer's instructions."; [Cell type]'Luminal breast cancer cell line''cell type: Luminal breast cancer cell line; cell line: MCF7; ' GSE77604 Homo sapiens 3 Genome variation profiling by genome tiling array GPL4560 Genomic profiling of Estrogen receptor positive BRCA1-mutated breast cancer [human 3.5k BAC array] 2016-02-05 Purpose: As estrogen receptor (ER)-positive breast cancer in BRCA1 mutation carriers arises at an older age with less aggressive tumor characteristics than ER negative BRCA1 mutated breast cancer, it has been suggested that these tumors are ?sporadic? and not BRCA1-driven. With the introduction of targeted treatments specific for tumors with a non-functioning BRCA1 or BRCA2 gene, the question whether the BRCA genes are impaired in the tumor, is highly relevant. Therefore, we performed genomic profiling of BRCA1-mutated ER+ tumors. Experimental design: Genomic profiling, BRCA1 promoter methylation assessment, and loss of heterozygosity analysis were done on 16 BRCA1-mutated ER+ tumors. Results were compared with 57 BRCA1-mutated ER- tumors, 36 BRCA2-mutated ER+ associated tumors, and 182 sporadic ER+ tumors [GSE9021, GSE9114, GSE16511, GSE50407]. Results: The genomic profile of BRCA1-mutated ER+ tumors was different from BRCA1-mutated ER- breast tumors, but highly similar to BRCA2-mutated ER+ tumors. In 83% of the BRCA1-mutated ER+ tumors, loss of the wildtype BRCA1 allele was observed. In addition, clinico-pathological variables in BRCA1-mutated ER+ cancer were also more similar to BRCA2-mutated ER+ and sporadic ER+ breast cancer than to BRCA1 mutated ER- cancers. Conclusions: As BRCA1-mutated ER+ tumors show a BRCAness copy number profile and LOH, it is likely that the loss of a functional BRCA1 protein plays a role in tumorigenesis in BRCA1-mutated ER+ tumors. Therefore, we hypothesize that these tumors are sensitive to drugs targeting the BRCA1 gene defect, providing new targeted treatment modalities for advanced BRCA-deficient, ER-positive breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE77604 BRCA1-Mutated Estrogen Receptor-Positive Breast Cancer Shows BRCAness, Suggesting Sensitivity to Drugs Targeting Homologous Recombination Deficiency. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-16-0198 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-16-0198} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA310999 https://www.ebi.ac.uk/ena/browser/view/PRJNA310999 None [Overal design]This submission includes the data of 3 Estrogen receptor positive BRCA1-mutated breast cancers; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA is extracted as described in: Joosse et al. (Br Can Res Tr, 2009)'; [Cell type]'Source: ''tumor type: invasive breast cancer; age (yrs): 38; histology: IDC (invasive ductal carcinoma); grade: ND; er_perc: 100; her2: neg; ', 'sample type: Promega normal female reference DNA; catalog number: G1521; ', 'tumor type: invasive breast cancer; age (yrs): 41; histology: ILC (invasive lobular carcinoma); grade: ND; er_perc: 75; her2: neg; ', 'tumor type: invasive breast cancer; age (yrs): 42; histology: IDC (invasive ductal carcinoma); grade: ND; er_perc: 5; her2: neg; ' GSE6246 Mus musculus 12 Expression profiling by array GPL339 Gene expression profiling: breast cancer formation in WAP-SVT/t transgenic animals 2006-11-08 Microarray studies revealed that as a first hit, SV40 T/t-antigen causes deregulation of 462 genes in mammary gland cells (ME-cells) of WAP-SVT/t transgenic animals. The majority of deregulated genes are cell-proliferation specific and Rb-E2F dependent, causing ME-cell proliferation and gland hyperplasia but not breast cancer formation. In the breast tumor cells, a further 207 genes are differentially expressed, most of them belonging to the cell communication category. In tissue culture, breast tumor cells frequently switch off WAP-SVT/t transgene expression and regain the morphology and growth characteristics of normal-ME-cells, although the tumor-revertant cells are aneuploid and only 114 genes regain the expression level of normal-ME-cells. The profile of retransformants shows that only 38 deregulated genes appear to be tumor-relevant and that none of them is considered to be a typical breast cancer gene. Keywords: Tumorigenesis, Breast cancer, SV40 T/t antigen https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE6246 Gene expression profiling: cell cycle deregulation and aneuploidy do not cause breast cancer formation in WAP-SVT/t transgenic animals. Journal of molecular medicine (Berlin, Germany) 4.746 https://doi.org/10.1007/s00109-004-0625-1 {Journal of molecular medicine (Berlin, Germany) (4.746): 10.1007/s00109-004-0625-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA97521 https://www.ebi.ac.uk/ena/browser/view/PRJNA97521 None [Overal design]We have analyzed nine mammary gland tissue segments from three normal NMRI, three WAP-SVT/t mice on the first day of lactation and from three WAP-SVT/t breast cancers (583-tumor 1, 585-tumor 2, 597-tumor 3) as well as three distinct breast cancer derived cell lines (ME-A cells, revertant-ME-B cells and ME-B-T/t cells).; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was isolated from mammary gland tissue segments stored in liquid nitrogen. The frozen tissue segments were ground to a fine powder using a liquid nitrogen chilled mortar and pestle. Total RNA was extracted with RNAzol reagent in accordance with the manufacturer’s protocol (PeQLab, Biotechnology), and the isolated RNA was treated with RNasefree DNase (DNA-free Ambion, Austin, Tex., USA). The integrity of RNA was verified with the Agilent Bioanalyzer (Agilent Technologies) by the presence of prominent 28S and 18S bands on agarose gels and an A260/280 ratio in the range of 1.9–2.1.'; [Cell type]'Source: ''Strain: NMRI, female, mammary gland on the first day of lactation; ', 'This animal synthesizes the SV40 T/t- antigens selectively in the mammary gland epithelial cells. Strain: NMRI, female, mammary gland on the first day of lactation.; ', 'This animal synthesizes the SV40 T/t- antigens selectively in the mammary gland epithelial cells. Strain: NMRI, female, breast cancer.; ', '' GSE161418 Homo sapiens 12 Expression profiling by high throughput sequencing GPL20301 Innate immune response to G-quadruplex binders in cancer cells 2020-11-13 G-quadruplex (G4) is non-canonical nucleic acid structure involved in a plethora of fundamental biological processes. In past decades, it has been studied as a promising pharmaceutical target for anticancer therapy. However, no G4-targeting agent has shown significant clinical effects up to date. Pyridostatin (PDS), a well-known G4 binder, can induce double-stranded DNA breaks and genome instability. We have recently shown that Pyridostatin (Pyridostatin) and other G4 binders can trigger micronuclei formation in cancer cells at non-cytotoxic concentrations. As micronuclei can play a crucial role in linking genome instability to innate immunity, we have here wondered whether G4 binders can induce immune gene activation in human MCF-7 breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE161418 G-quadruplex binders as cytostatic modulators of innate immune genes in cancer cells. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkab500 {Nucleic acids research (11.147): 10.1093/nar/gkab500} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA678279 https://www.ebi.ac.uk/ena/browser/view/PRJNA678279 https://www.ncbi.nlm.nih.gov/sra?term=SRP292489 [Overal design]By using RNA seq technology, we show that non-cytotoxic doses of Pyridostatin (PDS) can activate Interferon beta- and IRF3-dependent genes leading to an innate immune gene response in human cancer cells. In addition, immune gene activation follows the induction of micronuclei formation supporting cytoplasmic DNA as a trigger of immune gene activation.; [Treatment]'PDS samples were treated with pyridostatin 10 microM for 24 hours. All samples were cultured 72h in drug free medium before collection'; [Growth]'None'; [Extraction]'rep1 and rep2 of each group were extracted using NucleoSpin RNA kit, rep3 and rep4 using TRI Reagent\nNEBNext Ultra Directional RNA library prep'; [Cell type]'Source: ''cell line: MCF-7; tissue: mammary gland, breast; disease: adenocarcinoma; treatment: control at time 0; ', 'cell line: MCF-7; tissue: mammary gland, breast; disease: adenocarcinoma; treatment: control at time 4 (days); ', 'cell line: MCF-7; tissue: mammary gland, breast; disease: adenocarcinoma; treatment: pyridostatin 10 microM at time 4 (days); ' GSE171958 Homo sapiens 27 Methylation profiling by array; Expression profiling by high throughput sequencing GPL18573; GPL21145 Multi-omics data integration reveals correlated regulatory features of triple negative breast cancer 2021-04-12 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE171958 None None None None None 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA721449 https://www.ebi.ac.uk/ena/browser/view/PRJNA721449 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'MCF10A cells were cultured in DMEM/F12 supplemented with 20ng/mL hEGF, 100ng/mL cholera toxin, 10ug/mL bovine insulin, 500ng/mL hydrocortisone, 5% horse serum, and 1% Penicillin/Streptomycin. MDA-MB-231 cells were cultured in DMEM and supplemented with 10% FBS and 1% Penicillin/Streptomycin. HCC1937 cells were cultured in RPMI supplemented with 10% FBS and 1% Penicillin/Streptomycin.'; [Extraction]'Genomic DNA (500 ng) was bisulfite treated and purified using the EZ DNA Methylation-Gold kit (Zymo Research, Irvine, CA) according to the manufacturer’s protocol (Bibikova et al).', 'RNAseq #74101 (RNAseq)\nIllumina TruSeq Stranded mRNA Sample Preparation Kit v2'; [Cell type]'Source: ', 'BRCA1-wild-type ductal primary breast tumor', 'Triple-Negative Breast Cancer', 'normal breast epithelial''cell line: MCF10A; tissue: benign proliferative breast tissue; ', 'cell line: HCC1937; tissue: breast cancer; ', 'cell line: MDA-MB-231; tissue: breast cancer; ', 'cell type: BRCA1-wild-type ductal primary breast tumor; cell line: HCC1937; ', 'cell type: Triple-Negative Breast Cancer; cell line: MDA-231; ', 'cell type: normal breast epithelial; cell line: MCF10A; ' GSE94001 Homo sapiens 2 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Genome-wide changes in FOXA1 binding after MEN1 silencing in MCF-7 cells 2017-01-24 We performed ChIP-seq using FOXA1 antibodies in MCF-7 cells after induction of small hairpin RNA's directed at the MEN1 mRNA or a control sequence. We demonstrate that at menin-bound loci FOXA1 binding is disrupted by MEN1 silencing. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE94001 Enhancer-Mediated Oncogenic Function of the Menin Tumor Suppressor in Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2017.02.025 {Cell reports (7.815): 10.1016/j.celrep.2017.02.025} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA363044 https://www.ebi.ac.uk/ena/browser/view/PRJNA363044 https://www.ncbi.nlm.nih.gov/sra?term=SRP097678 [Overal design]Comparison of genome-wide FOXA1 binding after ShMEN1 induction vs ShCtrl; [Treatment]"MCF-7 cells that had been lentivirally infected with constructs for inducible expression of small hairpin RNA's directed against the MEN1 mRNA (ShMEN1#1) or a control sequence were synchronized for 72 hrs in phenol red-free medium (DMEM) containing 10% charcoal dextran-treated fetal bovine serum (CDT medium). Expression of small hairpin RNA's was induced by adding 100 ng/ml for 72 hrs."; [Growth]'Cells were maintained at 37oC and 5% CO2 in DMEM + 10% FBS and Pen-Strep.'; [Extraction]'Cells were crosslinked, lysed in a buffer containing SDS and sonicated.\nThruPLEX-FD Prep kit, Rubicon Genomics'; [Cell type]'Source: ''cell line: MCF7; chip antibody: FOXA1 antibodies mixed ab5089, ab23738; induction: ShCtrl; ', 'cell line: MCF7; chip antibody: FOXA1 antibodies mixed ab5089, ab23738; induction: ShMEN1; ' GSE13449 Homo sapiens 6 Expression profiling by array GPL571 Expression analysis upon NAMPT knockdown in MCF-7 cells 2008-11-03 NAMPT is an enzyme in the mammalian NAD+ salvage pathway. Expression microarray analysis was used to study the effect of NAMPT knockdown on gene expression in MCF-7 breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE13449 Enzymes in the NAD+ salvage pathway regulate SIRT1 activity at target gene promoters. The Journal of biological chemistry 4.106 https://doi.org/10.1074/jbc.M109.016469 {The Journal of biological chemistry (4.106): 10.1074/jbc.M109.016469} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA113977 https://www.ebi.ac.uk/ena/browser/view/PRJNA113977 None [Overal design]Stable knockdown of NAMPT was achieved using a retroviral shRNA construct. An shRNA directed against Luciferase was used to generate the Luc control cells. Three independent biological replicates with matching Luc controls were analyzed using Affymetrix U133 A2.0 microarrays.; [Treatment]'None'; [Growth]"MCF-7 cells were maintained in Eagle's minimum essential medium supplemented with 5% calf serum and antibiotics."; [Extraction]"Total RNA was prepared using Trizol reagent according to the manufacturer's instructions (Invitrogen) and was further purified using RNeasy columns (Qiagen)"; [Cell type]'Source: ''' GSE8598 Homo sapiens 22 Genome variation profiling by genome tiling array GPL5672 Lobular Carcinoma in situ CGH 2007-07-26 We examined a set of human breast cancers that were laser-microdissected from archived formalin fixed paraffin embedded (FFPE) tissue. These samples represent an important resource; however, they also represent a challenging aCGH application, as they tend to have significant amounts of noise. Our goal was to use known aberrations within these samples as a benchmark for determining the ability to differentiate between sample noise and real signal. Keywords: CGH https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE8598 Assessing the significance of conserved genomic aberrations using high resolution genomic microarrays. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.0030143 {PLoS genetics (5.224): 10.1371/journal.pgen.0030143} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA105277 https://www.ebi.ac.uk/ena/browser/view/PRJNA105277 None [Overal design]Human genomic DNA from a pool of individuals were hybridized to the Cy5 channel and labeled using indeirect amino alyl dUTP. The genomic DNA was extracted from LCM cells from LCIS and labelled with Cy3 using DOP amplification amino-alyl dUTP.; [Treatment]'None'; [Growth]'None'; [Extraction]'Commercial human DNA obtained from female genomic DNA. A pool was used to reduce variation between arrays.', 'Extracted cells were digested with proteinase K and DOP amplified and labeled.'; [Cell type]'Source: ''We hybridized our samples to the array, where the reference channel consisted of a pool of degenerate oligonucleotide–primed PCR amplification products from a commercial DNA source. Aliquots of labeled target and reference DNA were cohybridized to each BAC microarray with 100 μg of human Cot-1 DNA (Invitrogen, http: //www.invitrogen.com) to block repetitive sequences.; ', 'A skilled histotechnologist cut and mounted single 10-μm thick paraffin sections of each target tissue onto PET-membrane slides used with the SL μCUT System (Molecular Machines & Industries, http: //www.molecular-machines.com). We deparaffinized, rehydrated and stained the sections with hematoxylin. Within 1–2 h, we placed each section into a microdissection unit that sandwiches the tissue section between a clean glass slide and the membrane and microdissected it with the SL μCUT System (Molecular Machines & Industries).; ' GSE55470 Homo sapiens 67 Expression profiling by array GPL14951 Gene expression profiling of circulating tumor cells in breast cancer 2014-02-28 CTCs are the purpoted intermediates of metastatic dissemination and are likely to contain cellular clones responsible for disease progression representing a preferred source for identification of druggable targets. Unfortunately a molecular characterization of CTCs is seriously hampered by their low numbers even in metastatic patients and by the elevated contamination of isolated CTCs with leukocytes. With the final goal of providing a reliable assay allowing to obtain valuable information on CTC features in the clinical setting, we have developed a method based on capture with beads linked to EpCAM and to MUC1 exploiting a commercially available kit and performing an extensive gene expression profiling with the DASL platform. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55470 Gene expression profiling of circulating tumor cells in breast cancer. Clinical chemistry 6.891 https://doi.org/10.1373/clinchem.2014.229476 {Clinical chemistry (6.891): 10.1373/clinchem.2014.229476} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA239696 https://www.ebi.ac.uk/ena/browser/view/PRJNA239696 None [Overal design]For spike-in experiments, low pre-defined numbers of cells derived from established breast cancer cell lines (MCF7 and MDA-MB-468) were spiked into 5 mL of whole blood of healthy donor and captured using AdnaTest EMT-1/StemCell Select kit. Total RNA isolated from the captured cells together with total RNA isolated from the same in vitro cultered cells was processed in duplicate or triplicate onto Illumina Whole-Genome DASL HT platform. Finally, gene expression profiling was carried out on CTCs isolated from blood of 7 patients with advanced breast cancer. According with the characteristics of the study, data normalization was not applicable; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA extraction was performed according to the manufacturer’s instructions and RNA was eluted in 5 or 10 ul of RNase-free water (Ambion), depending on the experimental setting.'; [Cell type]'Source: ''experiment: 1; sample type: blood with AdnaWash; cell number 5ml: 0; donor: d1; replicate: a; tissue: blood; ', 'experiment: 1; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 200; donor: d1; replicate: a; tissue: blood; ', 'experiment: 1; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 100; donor: d1; replicate: a; tissue: blood; ', 'experiment: 1; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 50; donor: d1; replicate: a; tissue: blood; ', 'experiment: 1; sample type: blood without AdnaWash; cell number 5ml: 0; donor: d1; replicate: a; tissue: blood; ', 'experiment: 1; sample type: spiked cells; cell line: MCF7; cell number 5ml: 200; donor: d1; replicate: a; tissue: blood; ', 'experiment: 1; sample type: spiked cells; cell line: MCF7; cell number 5ml: 100; donor: d1; replicate: a; tissue: blood; ', 'experiment: 1; sample type: spiked cells; cell line: MCF7; cell number 5ml: 50; donor: d1; replicate: a; tissue: blood; ', 'experiment: 1; sample type: RNA; cell line: MDA-MB-468; rna quantity (ng): 100; donor: d1; replicate: a; ', 'experiment: 1; sample type: RNA; cell line: MDA-MB-468; rna quantity (ng): 10; donor: d1; replicate: a; ', 'experiment: 1; sample type: RNA; cell line: MDA-MB-468; rna quantity (ng): 1; donor: d1; replicate: a; ', 'experiment: 1; sample type: RNA; cell line: MDA-MB-468; rna quantity (ng): 0.5; donor: d1; replicate: a; ', 'experiment: 1; sample type: blood with AdnaWash; cell number 5ml: 0; donor: d1; replicate: b; tissue: blood; ', 'experiment: 1; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 200; donor: d1; replicate: b; tissue: blood; ', 'experiment: 1; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 100; donor: d1; replicate: b; tissue: blood; ', 'experiment: 1; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 50; donor: d1; replicate: b; tissue: blood; ', 'experiment: 1; sample type: blood without AdnaWash; cell number 5ml: 0; donor: d1; replicate: b; tissue: blood; ', 'experiment: 1; sample type: spiked cells; cell line: MCF7; cell number 5ml: 200; donor: d1; replicate: b; tissue: blood; ', 'experiment: 1; sample type: spiked cells; cell line: MCF7; cell number 5ml: 100; donor: d1; replicate: b; tissue: blood; ', 'experiment: 1; sample type: spiked cells; cell line: MCF7; cell number 5ml: 50; donor: d1; replicate: b; tissue: blood; ', 'experiment: 1; sample type: RNA; cell line: MDA-MB-468; rna quantity (ng): 100; donor: d1; replicate: b; ', 'experiment: 1; sample type: RNA; cell line: MDA-MB-468; rna quantity (ng): 10; donor: d1; replicate: b; ', 'experiment: 1; sample type: RNA; cell line: MDA-MB-468; rna quantity (ng): 1; donor: d1; replicate: b; ', 'experiment: 1; sample type: RNA; cell line: MDA-MB-468; rna quantity (ng): 0.5; donor: d1; replicate: b; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 50; donor: d1; replicate: a; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 25; donor: d1; replicate: a; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 10; donor: d1; replicate: a; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 5; donor: d1; replicate: a; tissue: blood; ', 'experiment: 2; sample type: RNA; cell line: MCF7; rna quantity (ng): 100; donor: d1; replicate: a; ', 'experiment: 2; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 50; donor: d1; replicate: a; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 25; donor: d1; replicate: a; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 10; donor: d1; replicate: a; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 5; donor: d1; replicate: a; tissue: blood; ', 'experiment: 2; sample type: RNA; cell line: MDA-MB-468; rna quantity (ng): 100; donor: d1; replicate: a; ', 'experiment: 2; sample type: blood with AdnaWash; cell number 5ml: 0; donor: d1; replicate: a; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 50; donor: d2; replicate: a; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 50; donor: d1; replicate: b; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 25; donor: d1; replicate: b; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 10; donor: d1; replicate: b; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 5; donor: d1; replicate: b; tissue: blood; ', 'experiment: 2; sample type: RNA; cell line: MCF7; rna quantity (ng): 100; donor: d1; replicate: b; ', 'experiment: 2; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 50; donor: d1; replicate: b; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 25; donor: d1; replicate: b; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 10; donor: d1; replicate: b; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 5; donor: d1; replicate: b; tissue: blood; ', 'experiment: 2; sample type: RNA; cell line: MDA-MB-468; rna quantity (ng): 100; donor: d1; replicate: b; ', 'experiment: 2; sample type: blood with AdnaWash; cell number 5ml: 0; donor: d1; replicate: b; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 50; donor: d2; replicate: b; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 50; donor: d1; replicate: c; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 25; donor: d1; replicate: c; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 10; donor: d1; replicate: c; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 5; donor: d1; replicate: c; tissue: blood; ', 'experiment: 2; sample type: RNA; cell line: MCF7; rna quantity (ng): 100; donor: d1; replicate: c; ', 'experiment: 2; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 50; donor: d1; replicate: c; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 25; donor: d1; replicate: c; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 10; donor: d1; replicate: c; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MDA-MB-468; cell number 5ml: 5; donor: d1; replicate: c; tissue: blood; ', 'experiment: 2; sample type: RNA; cell line: MDA-MB-468; rna quantity (ng): 100; donor: d1; replicate: c; ', 'experiment: 2; sample type: spiked cells; cell number 5ml: 0; donor: d1; replicate: c; tissue: blood; ', 'experiment: 2; sample type: spiked cells; cell line: MCF7; cell number 5ml: 50; donor: d2; replicate: c; tissue: blood; ', 'experiment: 3; sample type: clinical sample; cell number 5ml: 203; er status: pos; pr status: neg; her2 status: neg; tissue: circulating tumor cells; ', 'experiment: 3; sample type: clinical sample; cell number 5ml: 7; er status: pos; pr status: pos; her2 status: neg; tissue: circulating tumor cells; ', 'experiment: 3; sample type: clinical sample; er status: pos; pr status: pos; her2 status: neg; tissue: circulating tumor cells; ', 'experiment: 3; sample type: clinical sample; cell number 5ml: 13; er status: pos; pr status: neg; her2 status: neg; tissue: circulating tumor cells; ', 'experiment: 3; sample type: clinical sample; cell number 5ml: 0; er status: pos; pr status: neg; her2 status: neg; tissue: circulating tumor cells; ', 'experiment: 3; sample type: clinical sample; cell number 5ml: 13; er status: pos; pr status: pos; her2 status: neg; tissue: circulating tumor cells; ', 'experiment: 3; sample type: clinical sample; cell number 5ml: 19; er status: pos; pr status: pos; her2 status: neg; tissue: circulating tumor cells; ' GSE15944 Rattus norvegicus 10 Expression profiling by array GPL1355 Differentially expressed genes after treatment with hydroxytyrosol in DMBA-induced rat breast tumors 2009-05-04 The aim of this study was to compare the gene expression profile changes of DMBA-induced rat breast tumors after treatment with hydroxytyrosol (a natural compound from virgin olive oil). To this end, a cDNA microarray experiment was performed (Affymetrix’s Rat Genome 230 2.0 array). This gene expression study was carried out on the tumor biopsy samples prior to hydroxytyrosol treatment, and compared with matched tumor biopsy samples after completion of the hydroxytyrosol treatment schedule. The result of this study was the identification of several genes related to apoptosis, cell cycle arrest, proliferation, differentiation, survival and transformation-related genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15944 Hydroxytyrosol inhibits growth and cell proliferation and promotes high expression of sfrp4 in rat mammary tumours. Molecular nutrition & food research 4.653 https://doi.org/10.1002/mnfr.201000220 {Molecular nutrition & food research (4.653): 10.1002/mnfr.201000220} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA116997 https://www.ebi.ac.uk/ena/browser/view/PRJNA116997 None [Overal design]Breast tumors were induced with a single oral dose of 7,12-dimethylbenz(alpha)anthracene (100 mg/kg body weight) in female Sprague-Dawley rats to test the antitumor power of orally administrated hydroxytyrosol (0.5 mg/kg body weight 5 days/week for 6 weeks). Gene expression analysis was performed in paired samples as follows: HT final trucut tumor vs initial trucut tumor (HT final vs basal). For this assay, 5 samples were chosen according to histopathologic criteria (Bloom-Richardson grade II). Gene expression profiling was carried out using Affymetrix’s GeneChip technology, using the Rat Genome 230 v2.0 array from this provider. All the protocols and apparatus were recommended by Affymetrix. Total RNA from frozen mammary tumors was extracted by RNeasy Mini kit and homogenized by QIAshredder columns according to manufacturer’s instructions. The quality and quantity of the obtained RNA was checked out through agarose electrophoresis and later spectrophotometry at 260/280 nm. Biotinylated cRNA was synthesized following the IVT labeling kit from Affymetrix and purified by the GeneChip Sample Cleanup Module from Affymetrix. The quality and quantity of the obtained cRNA was again checked out through agarose electrophoresis and posterior spectrophotometry at 260/280 nm. After hybridization, slides were washed and scanned following the manufacturer’s standard protocol. Intensity values were normalized by Robust Multichip Average method and subsequently these were filtered to remove the control sequences and those with a hybridization signal close to background. The spike controls were: BioB, BioC, BioD and Cre; because BioB was the least abundant in the samples, it was used to estimate the sensitivity of the experiment. The housekeeping control was GAPDH. After non-supervised clustering using Pearson correlation coefficient, statistical significance of gene expression was estimated by Student’s T test for paired samples using GeneSpring GX 7.3 software (Agilent).; [Treatment]'RNA was preserved using RNAlater (Quiagen) for 24h and frozen at -80ºC until RNA extraction protocol'; [Growth]'None'; [Extraction]'Total RNA was extracted using a RNeasy Mini Kit from Qiagen, and later homogenized with QIAshredder (Quiagen) columns. Quality and quantity was assessed by agarose electrophoresis and spectrophotometric analysis (Absorbance 260/280 nm)'; [Cell type]'Source: ''strain: Sprague-Dawley; gender: female; age: 12 weeks; tissue: Breast tumor. Trucut Biopsy of breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene before treatment with hydroxytyrosol. Such biopsy was taken when tumor had 2cm3 volume; biopsy dimensions: 0.7 cm x 2.5 mm; treatment: none; sample: 66D2 (basal); ', 'strain: Sprague-Dawley; gender: female; age: 19 weeks; tissue: Breast tumor. Breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene at the moment of sacrifice.; treatment: hydroxytyrosol (0,5 mg/kg weight/day, 5 days/week, for 6 weeks) by gavage after trucut biopsy.; sacrifice: 7th week post-biopsy; sample: 66D2 (final); ', 'strain: Sprague-Dawley; gender: female; age: 12 weeks; tissue: Breast tumor. Trucut Biopsy of breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene before treatment with hydroxytyrosol. Such biopsy was taken when tumor had 2cm3 volume; biopsy dimensions: 0.7 cm x 2.5 mm; treatment: none; sample: 67D3(basal); ', 'strain: Sprague-Dawley; gender: female; age: 19 weeks; tissue: Breast tumor. Breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene at the moment of sacrifice.; treatment: hydroxytyrosol (0,5 mg/kg weight/day, 5 days/week, for 6 weeks) by gavage after trucut biopsy.; sacrifice: 7th week post-biopsy; sample: 67D3 (final); ', 'strain: Sprague-Dawley; gender: female; age: 12 weeks; tissue: Breast tumor. Trucut Biopsy of breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene before treatment with hydroxytyrosol. Such biopsy was taken when tumor had 2cm3 volume; biopsy dimensions: 0.7 cm x 2.5 mm; treatment: none; sample: 45D3 (basal); ', 'strain: Sprague-Dawley; gender: female; age: 19 weeks; tissue: Breast tumor. Breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene at the moment of sacrifice.; treatment: hydroxytyrosol (0,5 mg/kg weight/day, 5 days/week, for 6 weeks) by gavage after trucut biopsy.; sacrifice: 7th week post-biopsy; sample: 45D3 (final); ', 'strain: Sprague-Dawley; gender: female; age: 12 weeks; tissue: Breast tumor. Trucut Biopsy of breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene before treatment with hydroxytyrosol. Such biopsy was taken when tumor had 2cm3 volume; biopsy dimensions: 0.7 cm x 2.5 mm; treatment: none; sample: 49I1 (basal); ', 'strain: Sprague-Dawley; gender: female; age: 19 weeks; tissue: Breast tumor. Breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene at the moment of sacrifice.; treatment: hydroxytyrosol (0,5 mg/kg weight/day, 5 days/week, for 6 weeks) by gavage after trucut biopsy.; sacrifice: 7th week post-biopsy; sample: 49I1 (final); ', 'strain: Sprague-Dawley; gender: female; age: 12 weeks; tissue: Breast tumor. Trucut Biopsy of breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene before treatment with hydroxytyrosol. Such biopsy was taken when tumor had 2cm3 volume; biopsy dimensions: 0.7 cm x 2.5 mm; treatment: none; sample: 51I1 (basal); ', 'strain: Sprague-Dawley; gender: female; age: 19 weeks; tissue: Breast tumor. Breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene at the moment of sacrifice.; treatment: hydroxytyrosol (0,5 mg/kg weight/day, 5 days/week, for 6 weeks) by gavage after trucut biopsy.; sacrifice: 7th week post-biopsy; sample: 51I1 (final); ' GSE56704 Mus musculus 45 Expression profiling by array GPL11533 Densely Ionizing Radiation Effects on the Microenvironment Promote Aggressive Trp53 Null Mammary Carcinomas 2014-04-10 Densely ionizing radiation is a major component of the space radiation environment and has potentially greater carcinogenic effect compared to sparsely ionizing radiation that is prevalent in the terrestrial environment. It is unknown to what extent the irradiated microenvironment contributes to the differential carcinogenic potential of densely ionizing radiation. To address this gap, 10-week old BALB/c mice were irradiated with 100 cGy sparsely ionizing g-radiation or 10, 30, or 80 cGy of densely ionizing, 350 MeV/amu Si particles and transplanted 3 days later with syngeneic Trp53 null mammary fragments. Tumor appearance was monitored for 600 days. Tumors arising in Si-particle irradiated mice had a shorter median time to appearance, grew faster and were more likely to metastasize. Most tumors arising in sham-irradiated mice were ER-positive, pseudo-glandular and contained both basal keratin 14 and luminal keratin 8/18 cells (designated K14/18), while most tumors arising in irradiated hosts were K8/18 positive (designated K18) and ER negative. Comparison of K18 vs K14/18 tumor expression profiles showed that genes increased in K18 tumors were associated with ERBB2 and KRAS while decreased genes overlapped with those down regulated in metastasis and by loss of E-cadherin. Consistent with this, K18 tumors grew faster than K14/18 tumors and more mice with K18 tumors developed lung metastases compared to mice with K14/18 tumors. However, K18 tumors arising in Si-particle irradiated mice grew even faster and were more metastatic compared to control mice. A K18 Si-irradiated host profile was enriched in genes involved in mammary stem cells, stroma, and Notch signaling. Thus systemic responses to densely ionizing radiation enriches for a ER-negative, K18-positive tumor, whose biology is more aggressive compared to similar tumors arising in non-irradiated hosts. Key Words: ionizing radiation; breast cancer; heavy ion radiation;initiation; promotion https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE56704 Densely ionizing radiation acts via the microenvironment to promote aggressive Trp53-null mammary carcinomas. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-14-1212 {Cancer research (8.378): 10.1158/0008-5472.CAN-14-1212} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA244345 https://www.ebi.ac.uk/ena/browser/view/PRJNA244345 None [Overal design]3 different dose of Si were used. Total RNA was extracted from mammary tumors derived from transplantations of non-irradiated p53null mammary fragments into irradiated hosts. We analyzed a total of 45 Trp53-null tumors: 18 from sham-irradiated hosts, 9 from 10 cGy Si-irradiated hosts, 10 from 30 cGy Si-irradiated hosts, and 8 from irradiated hosts.; [Treatment]'Host mice were either irradiated or not, three days before transplantation.'; [Growth]'Trp53-null mammary fragments were orthotoically transplanted into the inguinal mammary fat pads of 10 week-old wild-type BALB/c female host mice that had their endogenous epithelium removed at 3wks of age. The development of Trp-null mammary tumors were monitored for 600 days. Survival surgery were performed to remove the tumors once they reach the size of 1cm3. Tumor then were frozen in liquid nitrogen for RNA extraction.'; [Extraction]"Total RNA was extracted using Trizol Reaget (Invitrogen), according to manufacturer's instructions."; [Cell type]'Source: ''strain (donor): BALB/c; tissue (donor): Trp53-null mammary fragments; strain (host): BALB/c; protocol (host): Irradiated with 80 cGy Si; disease state (host): Trp53-null mammary tumors; ', 'strain (donor): BALB/c; tissue (donor): Trp53-null mammary fragments; strain (host): BALB/c; protocol (host): Irradiated with 30 cGy Si; disease state (host): Trp53-null mammary tumors; ', 'strain (donor): BALB/c; tissue (donor): Trp53-null mammary fragments; strain (host): BALB/c; protocol (host): Irradiated with 10 cGy Si; disease state (host): Trp53-null mammary tumors; ', 'strain (donor): BALB/c; tissue (donor): Trp53-null mammary fragments; strain (host): BALB/c; protocol (host): Sham-irradiated; disease state (host): Trp53-null mammary tumors; ' GSE155506 Homo sapiens 40 Expression profiling by high throughput sequencing GPL15520 Benchmarking full-length transcript single cell mRNA sequencing protocols 2020-07-31 Here we present a performance evaluation of three different plate-based scRNA-seq protocols. Two commercially available kits; NEBNext Single Cell/ Low Input RNA Library Prep Kit (NEB), SMART-seq HT kit (Takara), and non-commercially available protocol Genome & transcriptome sequencing (G&T). We evaluated each kit based upon sensitivity, reproducibility, ease of use and price point per cell. This evaluation is specifically relevant for implementation of scRNA-seq in e.g. diagnostics, requiring high sensitivity in regards of gene detection, high reproducibility between samples, minimum hands on time and smooth sample preparation for technicians, as well as keeping a reasonable price point per patient. G&T protocol delivered the highest detection of genes per single cell, at the absolute lowest price point. Takara's kit delivered likewise high gene detection per single cell, and high reproducibility between sample, however at the absolute highest price points. Here we present pros and cons of each protocol, sequencing breast cancer cell line T47D. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE155506 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA649961 https://www.ebi.ac.uk/ena/browser/view/PRJNA649961 https://www.ncbi.nlm.nih.gov/sra?term=SRP274620 [Overal design]Assessment of three plate-based full-length scRNA-seq protocols on T47D breast cancer cells.; [Treatment]'T47D single cell suspension was prepared by removal of growth medium and subsequent washing of cell layer using 10 ml PBS. Cells were disaggregated with 2 ml TrypLETM Express Enzyme (1X) (cat nr. 12604013, GibcoTM, USA) for approximately 2 min in an incubator at 37 C. Reaction was stopped adding full growth media (RPMI-1640+GlutaMAXTM (cat nr. 61870-010, GibcoTM, UK) + 10% Fetal Bovine Serum (FBS) + 5% Penicillin/ Streptamycin) in double the amount of TrypLETM. Suspension was spun down 3 min 1200 rpm. Cells were washed once in PBS, resuspended in FACS buffer (PBS + 0.04 % bovine serum albumin (BSA)), and filtered using a 100 μm strainer.'; [Growth]'Cells were cultured in 15 ml Complete growth medium in Nunclon Delta coated flasks with 75 cm2 culture area. Cells were grown in an incubator at 37 Cand 5% CO2. Cells had a doubling time of 32 h, and were passaged twice a week at dilution 1 : 4 using TrypLETM Express Enzyme (1 X)(Cat. nr. 12604013, GIBCOTM, NY, USA). Cell line was maintained in cell culture\xa0flasks with 75 cm2 culture area.'; [Extraction]'NEBNext Single Cell/ Low Input RNA Library Prep Kit (NEB), SMART-seq HT kit (Takara), and non-commercially available protocol Genome & transcriptome sequencing (G&T).'; [Cell type]'Breast cancer cell line''cell line: T47D; cell type: Breast cancer cell line; passages: P10; ' GSE45202 Homo sapiens 3 Expression profiling by high throughput sequencing GPL11154 Amplitude modulation of androgen signaling by c-MYC [RNA-Seq] 2013-03-15 Androgen-stimulated growth of the molecular apocrine breast cancer is mediated by an androgen receptor (AR)-regulated transcriptional program. Through profiling the genomic licalizations of AR and its co-regulators FOXA1 and TCF7L2 in MDA-MB-453 breast cancer cells, we revealed the molecular details of the AR-centered regulatory network. We further identified that c-MYC is a key downstream target co-regulated by AR, FOXA1 and TCF7L2, and reinforces the transctiopnal activation of androgen-responsive genes in this subtype of breast cancers. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE45202 Amplitude modulation of androgen signaling by c-MYC. Genes & development 8.990 https://doi.org/10.1101/gad.209569.112 {Genes & development (8.990): 10.1101/gad.209569.112} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA193203 https://www.ebi.ac.uk/ena/browser/view/PRJNA193203 https://www.ncbi.nlm.nih.gov/sra?term=SRP019498 [Overal design]MDA-MB-453 breast cancer cells were transfected with control of MYC siRNA for 48 h, followed by treatment with 10nM DHT or vehicle for 6 h. The cells were subjected to mRNA purification and library praparation for RNA-seq on Illumina HiSeq2000 platform.; [Treatment]'The MDA-MB-453 cells were transfected with siRNA and then grown in the phenol red-free medium supplemented with 5% charcoal/dextran-treated fetal bovine serum for 48 h, followed by treatment of vehicle or 10 nM DHT for 6 h.'; [Growth]'The MDA-MB-453 cells were maintained in DMEM supplemented with 10% fetal bovinw serum at 37oC incubator'; [Extraction]"Total RNA was prepared using RNeasy Mini Kit (Qiagen) according to the manufacturer's instruction. The polyadenylated mRNA was purified using oligo d(T)25 beads (NEB).\n1 ng of mRNA was used for library preparation using Encore Complete RNA-seq kit (NuGEN) according to the manufacturer's instruction."; [Cell type]'breast cancer''cell line: MDA-MB-453; cell type: breast cancer; ' GSE74142 Homo sapiens 15 Other; Expression profiling by high throughput sequencing GPL9052; GPL18573 NAD+ Analog-sensitive PARPs Reveal a Role for PARP-1 in Transcription Elongation 2015-10-19 The PARP family of proteins comprises 17 members, about two thirds of which are active mono- or poly(ADP-ribosyl)transferase enzymes that transfer the ADP-ribose moiety of NAD+ onto target proteins. In many cases, ADP-ribosylation, which plays critical roles in human diseases (e.g., cancer, heart disease, and neuropathies) is associated with abrogation of the molecular functions of the target. Discerning ADP-ribosylation events mediated by a specific PARP is challenging, since all PARPs use the same substrate (i.e., NAD+) and the available inhibitors lack the specificity needed to make such conclusions. In order to identify the direct and specific targets of individual PARP family members, we have developed a chemical and genetic approach known as analog sensitivity, in which alteration of a single conserved amino acid in the active site of the PARP protein creates a pocket that allows use of an unnatural NAD+ analog containing a steric moiety. We have functionalized the steric moiety with alkyne for use in click chemistry reactions. This approach, which is transferable to other PARP family members, creates substrate specificity where none previously existed, allowing PARP-specific post-translational modification followed by target visualization, or isolation of ADP-ribosylated targets using click chemistry techniques. We have used this technology in conjunction with mass spectrometry to identify hundreds of targets both unique to, as well as shared among, the nuclear PARP proteins, PARP-1, PARP-2, and PARP-3. We have also determined the genome-wide distribution of PARP-1-specific ADP-ribosylation by coupling this analog-sensitive PARP approach with chromatin cross-linking in method that we call “Click-ChIP-seq”. We observed that PARP-1-specific ADP-ribosylation is enriched at transcriptionally active promoters in proximity to sites of PARP-1 enrichment. In addition, we observed that NELF, an important regulator of RNA Polymerase II (Pol II) pausing, is not only a target of ADP-ribosylation by PARP-1 but also spatially correlated with chromatin-associated ADP-ribose and PARP-1 in Click-ChIP-seq and ChIP-seq assays, respectively. Given these observations, we hypothesized that ADP-ribosylation might modulate NELF function and result altered Pol II pausing. We have explored this possibility using global run-on coupled with deep sequencing (GRO-seq) in MCF-7 cells in which PARP-1 was depleted by RNAi-mediated knockdown. PARP-1 depletion caused an increase in Pol II pausing genome-wide. Taken together, these results suggest the intriguing possibility that ADP-ribosylation of NELF by PARP-1 may be an important and heretofore unknown step in the release of Pol II into productive elongation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74142 Chemical genetic discovery of PARP targets reveals a role for PARP-1 in transcription elongation. Science (New York, N.Y.) 41.037 https://doi.org/10.1126/science.aaf7865 {Science (New York, N.Y.) (41.037): 10.1126/science.aaf7865} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA299156 https://www.ebi.ac.uk/ena/browser/view/PRJNA299156 https://www.ncbi.nlm.nih.gov/sra?term=SRP064970 [Overal design]Using GRO-seq (knockdown of Luciferase [control] with or without PARP inhibitor [PJ34] treatment and knockdown of PARP-1) and RNA-seq (knockdown of Luciferase [control] with or without CDK inhibitor [DRB] treatment and knockdown of PARP-1) in MCF-7 human breast cancer cells. Using GRO-seq upon 17b-estradiol (E2) treatment in MCF-7 cells.; [Treatment]'Prior to all experiments, MCF-7 cells were grown for 3 days in phenol red-free MEM Eagle medium supplemented with 5% charcoal-dextran-treated calf serum and then treated with either vehicle (ethanol) or 100 nM estradiol for 40 minutes.', 'GRO-seq: Prior to all experiments, MCF-7 cells were grown for 3 days in phenol red-free MEM Eagle medium supplemented with 5% charcoal-dextran-treated calf serum. RNA-seq: Prior to all experiments, MCF-7 cells were grown for 3 days in phenol red-free MEM Eagle medium supplemented with 5% charcoal-dextran-treated calf serum and 1 µg/mL Doxycycline for 4 days prior to treatment with DRB or vehicle (DMSO) treatment for 3 hours prior to RNA harvest.', 'Prior to all experiments, MCF-7 cells were grown for 3 days in phenol red-free MEM Eagle medium supplemented with 5% charcoal-dextran-treated calf serum (CDCS). For experiments, cells were treated with 100 nM E2 or vehicle (ethanol) for 40 minutes.'; [Growth]'MCF-7 cells were maintained in Minimum Essential Medium Eagle supplemented with 5% calf serum containing 0.5 μg/mL puromycin and 800 μg/mL G418.', 'MCF-7 cell lines were obtained from the ATCC used for GRO-seq and proliferation assays described herein. MCF-7 cells were maintained in Minimum Essential Medium Eagle supplemented with 5% calf serum.'; [Extraction]'MCF-7 cells were washed three times with ice-cold PBS and then resuspended for swelling in ice-cold Hypotonic Lysis Buffer [10 mM Tris•HCl, pH 7.4, 0.5% NP-40, 10% Glycerol, 3 mM CaCl2, 2 mM MgCl2, and 1 mM DTT containing 1x protease inhibitor cocktail (Sigma-Aldrich) and 4 units/mL SUPERase-In (Ambion)]. The swollen cells were collected by centrifugation at 1000 RCF for 10 min at 4°C and then resuspended in 1.5 ml of lysis buffer and pipetted up and down through a narrow opening tip 30 to 50 times to lyse the cells and release the nuclei. The nuclei were collected by centrifugation and washed once with 1 mL of Hypotonic Lysis Buffer. After a final collection by centrifugation, the resulting pellets of nuclei were resuspended in 500 μL of Freezing Buffer (50 mM Tris•HCl, pH 8.3, 40% glycerol, 5 mM MgCl2, 0.1 mM EDTA, and 4 units/mL of SUPERase-In per mL), counted, frozen in liquid nitrogen in 100 μL aliquots containing 5 x 106 nuclei, and stored at -80°C until use.\nNuclear run-on and GRO-seq library preparation were performed as previously described {Core, 2008;Hah, 2011}. Briefly, nuclear run-on reactions were performed for ~100 bases in the presence of sarksoyl (to prevent reengagement of RNA polymerases), rNTPs, α32P-CTP, and 5-bromo-UTP. The nascent RNAs were isolated, hydrolyzed to ~100 bases, and enriched using α-BrdUTP antibody-conjugated agarose beads (Santa Cruz). The bound RNAs were washed several times and eluted. The 5’ RNA cap was removed and the ends were repaired in preparation for adapter ligation. Small RNA adapters were ligated to the 5’ end, followed by another bead binding enrichment using α-BrdUTP antibody-conjugated agarose beads. These steps were repeated using a 3’ adapter. The resulting RNAs were reverse transcribed, amplified using PCR, and analyzed by high throughput sequencing using an Illumina 1G Genome Analyzer.', 'GRO-seq: MCF-7 cells were washed three times with ice-cold PBS and then resuspended for swelling in ice-cold Hypotonic Lysis Buffer [10 mM Tris•HCl, pH 7.4, 0.5% NP-40, 10% Glycerol, 3 mM CaCl2, 2 mM MgCl2, and 1 mM DTT containing 1x protease inhibitor cocktail (Sigma-Aldrich) and 4 units/mL SUPERase-In (Ambion)]. The swollen cells were collected by centrifugation at 1000 RCF for 10 min at 4°C and then resuspended in 1.5 ml of lysis buffer and pipetted up and down through a narrow opening tip 30 to 50 times to lyse the cells and release the nuclei. The nuclei were collected by centrifugation and washed once with 1 mL of Hypotonic Lysis Buffer. After a final collection by centrifugation, the resulting pellets of nuclei were resuspended in 500 μL of Freezing Buffer (50 mM Tris•HCl, pH 8.3, 40% glycerol, 5 mM MgCl2, 0.1 mM EDTA, and 4 units/mL of SUPERase-In per mL), counted, frozen in liquid nitrogen in 100 μL aliquots containing 5 x 106 nuclei, and stored at -80°C until use. RNA-seq: Following 3 hours of treatment, RNA was harvested using QIAGEN RNeasy Kit.\nGRO-seq: Nuclear run-on and GRO-seq library preparation were performed as previously described {Core, 2008;Hah, 2011}. Briefly, nuclear run-on reactions were performed for ~100 bases in the presence of sarksoyl (to prevent reengagement of RNA polymerases), rNTPs, α32P-CTP, and 5-bromo-UTP. The nascent RNAs were isolated, hydrolyzed to ~100 bases, and enriched using α-BrdUTP antibody-conjugated agarose beads (Santa Cruz). The bound RNAs were washed several times and eluted. The 5’ RNA cap was removed and the ends were repaired in preparation for adapter ligation. Small RNA adapters were ligated to the 5’ end, followed by another bead binding enrichment using α-BrdUTP antibody-conjugated agarose beads. These steps were repeated using a 3’ adapter. The resulting RNAs were reverse transcribed, amplified using PCR, and analyzed by high throughput sequencing using an Illumina 1G Genome Analyzer. RNA-seq: RNA was prepared for sequencing as previously described (Sun, M. et al. Mol. Cell 2015).', 'MCF-7 cells were washed three times with ice-cold PBS and then resuspended for swelling in ice-cold Hypotonic Lysis Buffer [10 mM Tris•HCl, pH 7.4, 0.5% NP-40, 10% Glycerol, 3 mM CaCl2, 2 mM MgCl2, and 1 mM DTT containing 1x protease inhibitor cocktail (Sigma-Aldrich) and 4 units/mL SUPERase-In (Ambion)]. The swollen cells were collected by centrifugation at 1000 RCF for 10 min at 4°C and then resuspended in 1.5 ml of lysis buffer and pipetted up and down through a narrow opening tip 30 to 50 times to lyse the cells and release the nuclei. The nuclei were collected by centrifugation and washed once with 1 mL of Hypotonic Lysis Buffer. After a final collection by centrifugation, the resulting pellets of nuclei were resuspended in 500 µL of Freezing Buffer (50 mM Tris•HCl, pH 8.3, 40% glycerol, 5 mM MgCl2, 0.1 mM EDTA, and 4 units/mL of SUPERase-In per mL), counted, frozen in liquid nitrogen in 100 µL aliquots containing 5 x 106 nuclei, and stored at -80°C until use. (PMID: 7256882)\nGRO-seq libraries were prepared as described previously with some minor modifications (PMID: 24564208).'; [Cell type]'human breast cancer cells', 'human Estrogen receptor alpha+ breast cancer cells''cell line: MCF7; cell type: human breast cancer cells; gender: female; ', 'cell line: MCF-7; cell type: human breast cancer cells; gender: female; ', 'cell line: MCF-7; cell type: human Estrogen receptor alpha+ breast cancer cells; genotype: LucKD; treatment: 100 nM E2; biological replicate: Replicate1; ', 'cell line: MCF-7; cell type: human Estrogen receptor alpha+ breast cancer cells; genotype: LucKD; treatment: 100 nM E2; biological replicate: Replicate2; ', 'cell line: MCF-7; cell type: human Estrogen receptor alpha+ breast cancer cells; genotype: PARP-1KD; treatment: 100 nM E2; biological replicate: Replicate1; ', 'cell line: MCF-7; cell type: human Estrogen receptor alpha+ breast cancer cells; genotype: PARP-1KD; treatment: 100 nM E2; biological replicate: Replicate2; ' GSE42742 Mus musculus 56 Expression profiling by array GPL1261 Murine microenvironment metaprofiles associate with human cancer etiology and intrinsic subtypes 2012-12-05 We developed a mouse model that captures radiation effects on host biology by transplanting unirradiated Trp53 null mammary tissue to sham or irradiated hosts. Gene expression profiles of tumors that arose in irradiated mice are distinct from those that arose in naïve hosts. Host irradiation induces a metaprofile consisting of gene modules representing stem cells, cell motility, macrophages and autophagy. Human orthologs of the host irradiation metaprofile discriminated between radiation-preceded and sporadic human thyroid cancers. An irradiated host centroid was strongly associated with estrogen receptor negative breast cancer. When applied to sporadic human breast cancers, the irradiated host metaprofile strongly associated with basal-like and claudin-low breast cancer intrinsic subtypes. Comparing host irradiation in the context of TGFβ levels showed that inflammation was robustly associated with claudin-low tumors. The association of the irradiated host metaprofiles with estrogen receptor negative status and claudin-low subtype suggests that host processes similar to those induced by radiation underlie sporadic cancers. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE42742 Murine microenvironment metaprofiles associate with human cancer etiology and intrinsic subtypes. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-12-3554 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-12-3554} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA182988 https://www.ebi.ac.uk/ena/browser/view/PRJNA182988 None [Overal design]Total RNA was extracted from mammary tumors derived from transplantations of non-irradiated p53null mammary fragments into irradiated hosts. We analyized a total of 32 p53null tumors from irradiated wild type mice: 9 from sham-irradiated hosts, and 23 from irradiated hosts. We also analyzed 24 tumors from irradiated TGFb1 heterozygote hosts: 6 from sham-irradiated hosts, and 18 from irradiated hosts.; [Treatment]'Host mice were either irradiated or not, three days before transplantation.'; [Growth]'p53null tumors developed from p53null mammary fragments that were orthotoically transplanted into the inguinal mammary fat pads of female host mice that had their endogenous epithelium removed at 3wks of age.'; [Extraction]"Total RNA was extracted using Trizol Reaget (Invitrogen), according to manufacturer's instructions."; [Cell type]'Source: ''strain: BALB/c; tissue: transplanted p53null mammary tumor; host genotype/variation: sham-irradiated wild-type; ', 'strain: BALB/c; tissue: transplanted p53null mammary tumor; host genotype/variation: irradiated wild-type; ', 'strain: BALB/c; tissue: transplanted p53null mammary tumor; host genotype/variation: sham-irradiated TGFb1 heterozygote; ', 'strain: BALB/c; tissue: transplanted p53null mammary tumor; host genotype/variation: irradiated TGFb1 heterozygote; ' GSE115602 Homo sapiens 8 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Enhancer Release and Retargeting” Activates Disease Susceptibility Genes (ChIP-Seq) 2018-06-11 We used genome wide ChIP-seq to examine the chromatin histone changes after the knockdown of one of cohesin subunit, RAD21, in MCF7 breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115602 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA475557 https://www.ebi.ac.uk/ena/browser/view/PRJNA475557 https://www.ncbi.nlm.nih.gov/sra?term=SRP150231 [Overal design]Examination of h3k4me1,h3k4me3 histone modifications by ChIP-seq.; [Treatment]'To induce the estrogen gene transcriptional responses, MCF-7 cells at 60-80% confluency were first hormone-stripped for 3 days in phenol-free DMEM media plus 5% charcoal dextran treated FBS (Omega Scientific, CA), and they were then treated with 100nM 17β-estradiol (E2) (Sigma) for indicated time points (usually for 1 hour).'; [Growth]'We originally purchased MCF-7 from ATCC, which were maintained in DMEM (Gibco® #10566) media supplemented with 10% FBS (Omega Scientific, CA) in a 5% CO2 humidified incubator at 37°C (MCF-7 without stripping).'; [Extraction]'Cells were cross-linked with 1% formaldehyde at room temperature for 10 min. Or for some cases, cells were double cross-linked with 1mM DSG (ProteoChem) for 1 hr first and then for 10minutes by 1% formaldehyde. In both situations, the crosslinking was quenched by addition of 0.125M glycine for 10 minutes. ChIP chromatin was fragmented using (Diagenode) Bioruptor®300 (20-40 cycles, 30sec on, 30sec off, 4°C). Subsequently, the soluble chromatin was harvested by 16,100g centrifugation, pre-cleared with 10-20ul Dynabeads G (Life Technologies), and was then incubated with 1-5 μg of antibodies at 4°C overnight. The next morning, immuno-precipitated complexes were collected using 30ul Dynabeads protein G (Invitrogen) per reaction. The immune-complexes were subjected to washes with wash buffer I for once, with wash buffer II for twice, and with Tris-EDTA (TE) + 0.1% triton x-100 for once, with TE for once, the beads were incubated at 55°C for 2hrs with proteinase K and de-crosslinked at 65°C for overnight. The final ChIP DNA was extracted and purified using QIAquick spin columns (Qiagen).\nThe library was processed that the extracted DNA was ligated to specific adaptors for Illumina’s HiSeq system using KAPA Hyper Prep Kit (Kapa Biosystems)'; [Cell type]'MCF7 breast cancer cell''cell type: MCF7 breast cancer cell; passages: ~200; chip antibody: SMC1a (bethyl, A300-055A); ', 'cell type: MCF7 breast cancer cell; passages: ~200; chip antibody: H3K4me3 (abcam, ab8580); ', 'cell type: MCF7 breast cancer cell; passages: ~200; chip antibody: H3K4me1 (abcam, ab8895); ' GSE165289 Homo sapiens 6 Expression profiling by high throughput sequencing GPL20301 Genome wide expression change by RNF31 knocking down in MCF-7 cells 2021-01-21 We aim to the investigate the role of RNF31 in breast cancer progression. MCF-7 cells were used as the model and RNF31 was silenced by siRNA. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE165289 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA693877 https://www.ebi.ac.uk/ena/browser/view/PRJNA693877 https://www.ncbi.nlm.nih.gov/sra?term=SRP302775 [Overal design]The MCF-7 cells were treated with 50nM stramble siRNA and siRCF31. After 48 hours, cells were harvested and the total RNA was extacted by Qiagen kit. The RNA sample was sent to BGI for RNA expression anaylsis.; [Treatment]'cells were treated with 50nM siRNF31 or siControl'; [Growth]'cells were cultured in DMEM with 10% FBS.'; [Extraction]"The total RNA was extracted from cells by the qiagen RNA exaction kit\nLibraries were prepared according to Illumina's instructions accompanying the RNA Sample Kit (Part# 0801-0303)."; [Cell type]'Source: ''passage: 15-18 passage; cell line: MCF-7; treatment: scramble siRNA; ', 'passage: 15-18 passage; cell line: MCF-7; treatment: siRCF31; ' GSE76540 Homo sapiens 6 Expression profiling by array GPL570 Expression data from MCF-7 and MCF-7/ADR cells 2016-01-05 Chemoresistance in breast cancer has been a great interest in past studies, however, the development of rational therapeutic strategies targeting chemoresistant cells is still a challenge for clinical oncology.The resistant property of MCF7/ADR cells was confirmed by long term culture with Dox, cell viability, and PARP cleavage assays. Microarray analysis was performed to compare the global differences of gene expression between MCF-7 and MCF-7/ADR cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76540 Gas6/Axl Axis Contributes to Chemoresistance and Metastasis in Breast Cancer through Akt/GSK-3β/β-catenin Signaling. Theranostics 8.063 https://doi.org/10.7150/thno.15083 {Theranostics (8.063): 10.7150/thno.15083} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA307671 https://www.ebi.ac.uk/ena/browser/view/PRJNA307671 None [Overal design]MCF-7 and MCF-7/ADR gene expression profiles were analyzed. Total RNA were prepared for analysis with Affymetrix Human U133 Plus 2.0 arrays according to the manufacturer’s instructions.; [Treatment]'MCF-7 and MCF-7/ADR cells were cultured in RPMI-1640 medium with 10% fetal calf serum. MCF-7/ADR cells were cultured in the presence of a low concentration of Dox (1 µg/ml) and passaged for 1 week in drug-free medium before the experiments.'; [Growth]'RPMI-1640 medium with 10% fetal calf serum.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''disease state: Breast cancer; cell line: MCF-7; ', 'disease state: Breast cancer; cell line: MCF-7/ADR; ' GSE89107 Rattus norvegicus 20 Methylation profiling by high throughput sequencing GPL10287 DNA Methylation Targets Influenced by Bisphenol A and/or Genistein Are Associated with Survival Outcomes in Breast Cancer Patients 2016-10-24 Early postnatal exposures to Bisphenol A (BPA) and genistein (GEN) have been reported to predispose for and against mammary cancer, respectively, in adult rats. Since the changes in cancer susceptibility occurs in the absence of the original chemical exposure, we have investigated the potential of epigenetics to account for these changes. DNA methylation studies reveal that prepubertal BPA exposure alters signaling pathways that contribute to carcinogenesis. Prepubertal exposure to GEN and to BPA + GEN suggests pathways involved in maintenance of cellular function, indicating that the presence of GEN either reduces or counters some of the alterations caused by the carcinogenic properties of BPA. We subsequently evaluated the potential of epigenetic changes in the rat mammary tissues to predict survival in breast cancer patients via The Cancer Genomic Atlas (TCGA). We identified 12 genes that showed strong predictive values for long-term survival in estrogen receptor positive patients. Importantly, two genes associated with improved long term survival, HPSE and RPS9, were identified to be hypomethylated in mammary glands of rats exposed prepuberally to GEN or to GEN + BPA respectively, reinforcing the suggested cancer suppressive properties of GEN. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE89107 DNA Methylation Targets Influenced by Bisphenol A and/or Genistein Are Associated with Survival Outcomes in Breast Cancer Patients. Genes 3.331 https://doi.org/10.3390/genes8050144 {Genes (3.331): 10.3390/genes8050144} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA350299 https://www.ebi.ac.uk/ena/browser/view/PRJNA350299 https://www.ncbi.nlm.nih.gov/sra?term=SRP091986 [Overal design]We conducted MBDCap-seq on mammary glands procured from 100 day-old rats exposed prepubertally to vehicle control, BPA, GEN, or BPA + GEN (n = 5/ group); [Treatment]'From PND2 through PND20 only, the offspring nursed via the lactating dams. Animals were weaned at PND20 and provided AIN-76A diet and water without further treatment/exposure. GEN was provided by DSM Nutritional Products (Basel, Switzerland). BPA, sesame oil, and all other chemicals were from Sigma Chemical Co. (St. Louis, MO). Offspring were weaned at PND21 and fed AIN-76A diet. At PND100, female offspring were killed in the estrous phase.'; [Growth]'Seven week old female Sprague-Dawley rats were purchased from Charles River Laboratories (Wilmington, MA). Animals were housed in a temperature controlled facility with a 12-h light : dark cycle. These animals were bred with proven Sprague-Dawley studs, fed phytoestrogen-free AIN-76A diet (Harlan Teklad, Madison WS), housed in polypropylene cages and water provided via glass bottles (all polycarbonate/BPA free). On the day of birth (designated as PND zero), offspring were sexed and litters were culled to 10 offspring per lactating dam.'; [Extraction]"The fourth abdominal mammary glands were rapidly dissected from live ketamine/xylazine anesthetized animals (to minimize proteolysis), snap-frozen in liquid nitrogen, and stored at -80 ºC for later analysis. Methylated DNA was obtained by the MethylMiner Methylated DNA Enrichment Kit (Invitrogen).\nEluted DNA was used to generate libraries following the standard protocols from Illumina. Next, MBDCap-seq libraries were sequenced using the Illumina Genome Analyzer II as per manufacturer's instructions. Image analysis and base calling were performed with the standard Illumina pipeline."; [Cell type]'Source: ''strain: Sprague-Dawley; Sex: Female; days after birth: 100; ' GSE113650 Homo sapiens 6 Expression profiling by high throughput sequencing GPL18573 RNA-seq analysis of breast cancer 2018-04-25 Background: We searched triple negative breast cancer (TNBC) specifically expressing candidates for target therapy. Methods: High expressing genes in three TNBC cell lines compared to three non-TNBC cell lines were evaluated by using RNA sequencing (log2 ratio>5, q<0.05). By integrating the shRNA library screening and public gene expression databases, we identifyied candidates for therapeutic targets. The expression significance of the candidates was examined by using immunohistochemistry of 248 clinical breast cancer patients. Results: One hundred seventy one genes were detected as highly expressed genes in TNBC cell lines than non-TNBC cell lines, and 13 genes were picked up as candidates not expressing in non-cancerous tissues. Integrated analysis with shRNA screening identified three candidates as TBNC specific molecular targets. Protein staining were stronger in breast cancer tissues, especially TNBC, than in the normal tissues. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113650 Carboxypeptidase A4 accumulation is associated with an aggressive phenotype and poor prognosis in triple-negative breast cancer. International journal of oncology 3.571 https://doi.org/10.3892/ijo.2019.4675 {International journal of oncology (3.571): 10.3892/ijo.2019.4675} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA453538 https://www.ebi.ac.uk/ena/browser/view/PRJNA453538 https://www.ncbi.nlm.nih.gov/sra?term=SRP142602 [Overal design]Gene expression profiles of 6 breast cancer cell lines were generated by RNA-seq using Illumina NextSeq 500 system.; [Treatment]'None'; [Growth]'Cells were cultured in PRMI 1640 medium supplemented with 100 U/mL of penicillin, 100 U/mL of streptomycin, and 10% fetal bovine serum in a humidified atmosphere of 5% CO2 at 37°C.'; [Extraction]'Total RNA was extracted using NucleoSpin RNA (TaKaRa Bio, Shiga, Japan/MACHEREY-NAGEL, Düren, Germany). The quality of RNA was assessed with RNA integrity number (RIN) using Agilent RNA6000 Pico Kit and Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA, USA). Samples used for transcrptome analysis had on average a RIN value of 9.4 and a minimum RIN value of 8.9.\nLibrary preparation was performed using TruSeq RNA Sample Prep Kit v2 (Illumina, San Diego, CA, USA) from 1 µg of total RNA according to the manufacturer’s protocol.'; [Cell type]'Source: ''cell line: MCF7; subtype: Luminal (non-TNBC); ', 'cell line: BT474; subtype: Luminal (non-TNBC); ', 'cell line: T47D; subtype: Luminal (non-TNBC); ', 'cell line: MDA-MB-468; subtype: Basal-like TNBC; ', 'cell line: HCC70; subtype: Basal-like TNBC; ', 'cell line: HCC1143; subtype: Basal-like TNBC; ' GSE83611 Homo sapiens 9 Expression profiling by high throughput sequencing GPL17303 Field cancerized fibroblasts in primary culture, P2 2016-06-22 Fibroblasts cultured from human breast cancer and adjacent normal tissues at 1cm and 5cm from the margin. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE83611 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA326500 https://www.ebi.ac.uk/ena/browser/view/PRJNA326500 https://www.ncbi.nlm.nih.gov/sra?term=SRP076912 [Overal design]3 patient sets of fibroblasts from tumor, and patient matched adjacent normal at 1cm and 5cm from tumor.; [Treatment]'None'; [Growth]'Primary culture according to Stampfer, 1985 PMID: 3857588. Grown in DMEM 10%FBS. Passage 2 cells'; [Extraction]'Qiagen RNAEasy kit\nDNaseI treatment, Thermo Fisher Ribo Minus, Ion Total RNASeq Library Kit v2'; [Cell type]'fibroblasts''cell type: fibroblasts; tissue: breast; culture protocol: primary culture Passage 2; tumor status: adjacent normal tissue; patient id: 53; ', 'cell type: fibroblasts; tissue: breast; culture protocol: primary culture Passage 2; tumor status: tumor tissue; patient id: 53; ', 'cell type: fibroblasts; tissue: breast; culture protocol: primary culture Passage 2; tumor status: adjacent normal tissue; patient id: 55; ', 'cell type: fibroblasts; tissue: breast; culture protocol: primary culture Passage 2; tumor status: tumor tissue; patient id: 55; ', 'cell type: fibroblasts; tissue: breast; culture protocol: primary culture Passage 2; tumor status: adjacent normal tissue; patient id: 60; ', 'cell type: fibroblasts; tissue: breast; culture protocol: primary culture Passage 2; tumor status: tumor tissue; patient id: 60; ' GSE26457 Homo sapiens 113 Expression profiling by array GPL570 Defining the Genomic Signature of the Parous Breast 2011-01-05 It is widely accepted that a woman’s lifetime risk of developing breast cancer at menopause is reduced by early full term pregnancy and multiparity. This phenomenon is associated with the development and differentiation of the breast, which ultimately imprints a specific genomic profile in the mammary epithelium. In the present work we demonstrate that this profile represents a permanent signature that could be associated with the breast cancer risk reduction conferred by pregnancy. We have compared the gene expression profile of normal breast biopsies performed in 71 parous (P) and 42 nulliparous (NP) postmenopausal women. All samples were hybridized to Affymetrix HG_U133 Plus 2.0 oligonucleotide arrays. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26457 Pregnancy-induced chromatin remodeling in the breast of postmenopausal women. International journal of cancer 4.982 https://doi.org/10.1002/ijc.27323 {BMC medical genomics (2.568) doi:10.1186/1755-8794-5-46}; {International journal of cancer (4.982) doi:10.1002/ijc.27323}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA136563 https://www.ebi.ac.uk/ena/browser/view/PRJNA136563 None [Overal design]We compared the gene expression profile of normal breast core biopsies from 71 parous (women that had a full term pregnancy) and 42 nulliparous (women that never completed a pregnancy) postmenopausal women from Sweden. All samples were hybridized to Affymetrix HG_U133 Plus 2.0 oligonucleotide arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA from core needle biopsies specimens was isolated using the Qiagen Allprep RNA/DNA Mini Kit according to manufacturer's instructions (Qiagen, Alameda, CA, USA)"; [Cell type]'Source: ''parity: nulliparous; phase: Discovery; batch: D.1; gravida: 0; ', 'parity: nulliparous; phase: Discovery; batch: D.7; gravida: 0; ', 'parity: nulliparous; phase: Discovery; batch: D.4; gravida: 1; ', 'parity: nulliparous; phase: Discovery; batch: D.5; gravida: 0; ', 'parity: nulliparous; phase: Discovery; batch: D.3; gravida: 0; ', 'parity: nulliparous; phase: Discovery; batch: D.6; gravida: 0; ', 'parity: nulliparous; phase: Discovery; batch: D.6; gravida: 1; ', 'parity: nulliparous; phase: Discovery; batch: D.7; gravida: 1; ', 'parity: nulliparous; phase: Discovery; batch: D.4; gravida: 0; ', 'parity: nulliparous; phase: Discovery; batch: D.2; gravida: 1; ', 'parity: nulliparous; phase: Discovery; batch: D.8; gravida: 0; ', 'parity: parous; phase: Discovery; batch: D.8; gravida: 1; ', 'parity: parous; phase: Discovery; batch: D.4; gravida: 1; ', 'parity: parous; phase: Discovery; batch: D.5; gravida: 1; ', 'parity: parous; phase: Discovery; batch: D.7; gravida: 1; ', 'parity: parous; phase: Discovery; batch: D.3; gravida: 1; ', 'parity: parous; phase: Discovery; batch: D.6; gravida: 1; ', 'parity: parous; phase: Discovery; batch: D.2; gravida: 1; ', 'parity: nulliparous; phase: Validation; batch: V.1; gravida: 1; ', 'parity: nulliparous; phase: Validation; batch: V.5; gravida: 0; ', 'parity: nulliparous; phase: Validation; batch: V.6; gravida: 0; ', 'parity: nulliparous; phase: Validation; batch: V.2; gravida: 0; ', 'parity: nulliparous; phase: Validation; batch: V.4; gravida: 0; ', 'parity: nulliparous; phase: Validation; batch: V.7; gravida: 0; ', 'parity: nulliparous; phase: Validation; batch: V.3; gravida: 1; ', 'parity: nulliparous; phase: Validation; batch: V.1; gravida: 0; ', 'parity: nulliparous; phase: Validation; batch: V.4; gravida: 1; ', 'parity: nulliparous; phase: Validation; batch: V.5; gravida: 1; ', 'parity: parous; phase: Validation; batch: V.2; gravida: 1; ', 'parity: parous; phase: Validation; batch: V.5; gravida: 1; ', 'parity: parous; phase: Validation; batch: V.6; gravida: 1; ', 'parity: parous; phase: Validation; batch: V.7; gravida: 1; ', 'parity: parous; phase: Validation; batch: V.8; gravida: 1; ', 'parity: parous; phase: Validation; batch: V.1; gravida: 1; ', 'parity: parous; phase: Validation; batch: V.3; gravida: 1; ', 'parity: parous; phase: Validation; batch: V.4; gravida: 1; ' GSE74943 Homo sapiens 6 Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing GPL9442; GPL10999 Epigenetic activation of the prostaglandin receptor EP4 promotes resistance to endocrine therapy for breast cancer 2015-11-12 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74943 Epigenetic activation of the prostaglandin receptor EP4 promotes resistance to endocrine therapy for breast cancer. Oncogene 6.634 https://doi.org/10.1038/onc.2016.397 {Oncogene (6.634): 10.1038/onc.2016.397} 'polyA RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA301974 https://www.ebi.ac.uk/ena/browser/view/PRJNA301974 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'MCF7 LTED cells were maintained in RPMI 1640 without phenol red supplemented with 5% charcoal stripped fetal bovine serum, 10 mM HEPES, 4.5 g/L glucose, 2 mM L-glutamine, 1 mM sodium pyruvate, and 50 µg/ml gentamicin.'; [Extraction]'Total RNA (10 ug) was isolated , DNase treated, and twice oligo(dT) selected using the Dynabeads mRNA purification kit (Invitrogen).\nRNA-seq libraries were constructed using the NEBNext Kit from New England Biolabs. MCF7-LTED_1 libraries were constructed with custom 4 bp barcodes and sequenced with an Illumina GAIIx (32 bp single-end reads). MCF7_LTED_2 libraries were constructed with standard Illumina indexed primers and sequenced using Illumina HiSeq 2000 (42 bp single-end reads).', 'Genomic DNA was isolated from 3 x 10^6 cells using the Quick-gDNA MiniPrep kit from Zymo Research (Irvine, CA) according to the manufacturers instructions. The quality of the isolated high molecular weight DNA was confirmed by agarose gel electrophoresis.\nMethyl-MAPS libraries were prepared according to the protocol in Edwards et al Genome Research 2010. In brief, genomic DNA was split and unmethylated and methylated compartments were independently obtained by limit digestions of 10–15 ug of DNA with McrBC or five tetranucleotide methylation-sensitive restriction endonucleases (RE; HpaII, HhaI, AciI, BstUI, HpyCH4IV). Digested fragments were size selected by gel-electrophoresis for fragments >800 bp. Mate-pair SOLiD sequencing libraries were then prepared using custom 6 bp barcodes. As part of the Methyl-MAPS protocol, EcoP15I CAP linkers are ligated onto the ends of the fragments. The fragments are then circularized with biotinylated internal adapters, and digested with EcoP15I, which cleaves the DNA 25-27 bp away from its recognition site. Consequently, although we sequence 35 bp for both the F3 and R3 tags, only 25 bp comprise the genomic sequence tag. Each library was loaded on two sequencing slides.'; [Cell type]'long-term estradiol deprived (LTED) MCF-7 cells''cell type: long-term estradiol deprived (LTED) MCF-7 cells; ', 'cell type: long-term estradiol deprived (LTED) MCF-7 cells; genomic dna digested with: methylation-sensitive restriction endonucleases (RE); genomic dna fraction: methylated; ', 'cell type: long-term estradiol deprived (LTED) MCF-7 cells; genomic dna digested with: Methylation-dependent restriction enzyme McrBC; genomic dna fraction: unmethylated; ' GSE74910 Homo sapiens 3 Methylation profiling by high throughput sequencing GPL16791 Digital Restriction Enzyme Analysis of Methylation (DREAM) of normal breast epithelial cells and MCF7 genomic DNA 2015-11-11 We analyzed levels of 5-methyl cytosine nnnn CCCGGG target sites by sequential restriction digest by SmaI and XmaI enzymes, ligating Illumina adaptors to the restriction fragments and reading methylation-specific signatures at the ends of restriction fragments by paired ends Illumina high throughput sequencing. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74910 Transcriptional Selectivity of Epigenetic Therapy in Cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-16-0834 {Cancer research (8.378): 10.1158/0008-5472.CAN-16-0834} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA301889 https://www.ebi.ac.uk/ena/browser/view/PRJNA301889 https://www.ncbi.nlm.nih.gov/sra?term=SRP066051 [Overal design]Digital restriction enzyme analysis of methylation (DREAM) was performed to determine the methylation profile of normal breast epithelial cells and MCF7 genomic DNA. Genomic DNA spiked in with unmethylated, partially methylated and fully methylated standards was sequentially cut at CCCGGG sites with the methylation-sensitive enzyme SmaI (blunt ends) and its methylation-tolerant neoschizomer XmaI (5'CCGG overhangs), creating different end sequences that represented methylation status of the CCCGGG sites. These end sequences were analyzed by Illumina high throughput sequencing. Methylation status at individual CCCGGG sites across the genome was determined by counting the methylated reads with the CCGGG signature and unmethylated reads with the GGG signature at the beginnings of the sequencing reads after alignment to the human genome.; [Treatment]'none'; [Growth]'MCF7 cell line was cultured in DMEM medium with 10% fetal bovine serum, normal breast epithelial cells were grown in 1:1 DMEM/F12 medium with 2.4 g/L sodium bicarbonate, 5% chelated horse serum, 20 ng/ml EGF (BD Biosciences), 100 ng/ml cholera toxin (Sigma-Aldrich), 10 mg/L insulin (Sigma-Aldrich), 0.5 mg/L hydrocortisone (Sigma-Aldrich), and 0.04 mM calcium chloride (Sigma-Aldrich)'; [Extraction]"phenol-chloroform\nFive micrograms of genomic DNA spiked with 500 ng of methylation standards with defined methylation levels of 0, 25, 50, and 100% were digested with 100 units of SmaI endonuclease (NEB) for 3 hours at 25°C. Subsequently, 100 units of XmaI endonuclease (NEB) were added and the digestion was continued for an additional 16 hours at 37°C. Digested DNA was purified using the QIAquick PCR purification kit (Qiagen, Valencia, CA) and eluted in TRIS-HCl 10 mM pH 8.5 (EB). Eluted DNA was supplemented with NEB buffer #2, dCTP, dGTP and dATP (0.4 mM final concentration of each), 15 units of Klenow Fragment (3'→5' exonuclease deficient) DNA polymerase (NEB) and incubated for 30 minutes at 37°C. This step filled in the recesses at 3' DNA ends created by XmaI digestion and added 3' dA tails to all fragments. Illumina paired end (Quail et al. 2008) or barcoded Truseq (Illumina, San Diego, CA) sequencing adapters were then ligated at 10:1 adapter:fragment ratio using Rapid T4 DNA ligase (Enzymatics, Beverly, MA). The ligation mix was size selected by electrophoresis in 2% agarose. Two slices corresponding to 250-350 bp and 350-500 bp sizes based on a 100 bp DNA ladder (NEB) were cut out and DNA was extracted from agarose. DNA eluted from the slices was separately amplified with Illumina paired end PCR primers (Quail et al. 2008) using iProof high-fidelity DNA polymerase (Bio-Rad Laboratories, Hercules, CA) and 18 cycles of amplification. Resulting sequencing libraries were purified with AMPure magnetic beads (Agencourt, Beverly, MA)."; [Cell type]'Source: ''tissue of origin: breast; disease: adjacent normal tissue from 69 year old patient with lobular carcinoma in situ; gender: female; ', 'tissue of origin: breast; disease: adjacent normal tissue from 49 year old patient with infiltrating ductal carcinoma; gender: female; ', 'tissue of origin: breast cancer cell line; disease: mammary gland, breast; derived from metastatic site: pleural effusion; ER positive; gender: female; ' GSE37719 Homo sapiens 16 Non-coding RNA profiling by array GPL15462 miR-155 regulates the ability of circulating cancer cells to colonize and establish metastasis 2012-05-02 Abstract: Metastases are established through a complex multistep process by which tumor cells disseminate from the primary tumor and expand at distant sites. Traditionally, studies on metastasis have focused on proteins and protein-coding genes, but recently microRNAs (miRNAs) have achieved increasing interest. miRNAs involved in the metastatic process are poorly defined, and while the use of clinical tissue samples or in vitro assessment for study of the first phases of the metastatic process is not feasible; such processes may be studies using in vivo models created by inoculation of human cell lines into mice. We have used such a model system consisting of three isogenic human cancer cell lines that are equally tumorigenic in mice, but while two of these cell lines give rise to metastasis at different rates, the last one disseminates single cells that remain dormant in distant organs. Using a global LNA- based miRNA microarray platform, 28 miRNAs were found to be significantly altered between the metastatic and non-metastatic cell lines, with mir-155 being the miRNA exhibiting the largest difference in expression level and central in a network analysis. Examining the potential targets of miR-155 identified calumenin, solute carrier family 26 (sulfate transporter) member 2 (SLC26A2), Integrin αV, and CD73, which showed an inverse expression pattern to miR-155 in the metastatic and non-metastatic cell lines as determined by immunocytochemical staining. The miRNAs identified in this study could be markers of the ability of cancer cells to colonize at distant organs. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37719 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA163093 https://www.ebi.ac.uk/ena/browser/view/PRJNA163093 None [Overal design]global microRNA profiling of three breast cancer cell lines with different metastatic potential derived from MDA-435; [Treatment]'None'; [Growth]"The human cancer cell lines NM-2C5-GFP (NM-2C5), M-4A4-GFP (M-4A4) and M-4A4-LM3-GFP (LM3) (American Type Culture Collection (ATCC), derived from the cell line MDA-MB-435 Manassas, VA, USA) were cultured in Dulbecco's Modified Eagle's Medium (DMEM) with GlutamaxTM-I, glucose and sodium pyrovate (Gibco, Invitrogen, Carlsbad, California, USA) supplemented with 10% fetal bovine serum (FBS) (Gibco, Invitrogen), 1% Non-essential amino acids (Gibco, Invitrogen) and 1% Penicillin/Streptomycin (100 Units/ml Penicillin, 100 μg/ml Streptomycin) (Gibco, Invitrogen)."; [Extraction]'Total RNA was isolated using TRIzol (Invitrogen) from cell lines NM-2C5-GFP, M-4A4-GFP and M- 4A4-LM3-GFP according to the manufacturer’s instructions.'; [Cell type]'Source: ''cell line: LM3-GFP; metastatic status: metastatic; ', 'cell line: M4A4-GFP; metastatic status: metastatic; ', 'cell line: MDA-MB-435; metastatic status: parental; ', 'cell line: NM-2C5-GFP; metastatic status: non-metastatic; ' GSE63354 Mus musculus; Homo sapiens 20 Expression profiling by array GPL570; GPL1261 Regulation of Epithelial-Mesenchymal Transition in Breast Cancer Cells by Cell Contact and Adhesion 2014-11-17 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE63354 Regulation of epithelial-mesenchymal transition in breast cancer cells by cell contact and adhesion. Cancer informatics 1.210 https://doi.org/10.4137/CIN.S18965 {Cancer informatics (1.210): 10.4137/CIN.S18965} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA267555 https://www.ebi.ac.uk/ena/browser/view/PRJNA267555 None [Overal design]Refer to individual Series; [Treatment]'Treatment with MMP3', 'Culture at differing densities'; [Growth]'Cells were grown in DMEM+2% FCS', 'MCF10A cells were grown in DMEM/F12 (Gibco), supplemented with 5% horse serum (Gibco), 20 ng/ml EGF (Peprotech), 0.5 μg/ml hydrocortisone (Sigma), 100 ng/ml cholera toxin (Sigma), 10 μg/ml insulin (Sigma) and 100 μg/ml gentamicin (Gibco)'; [Extraction]'Phenol/Chloroform'; [Cell type]'Source: ''tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 50K; agent: control; experiment: A; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 100K; agent: control; experiment: A; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 250K; agent: control; experiment: A; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 50K; agent: MMP-3; experiment: A; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 100K; agent: MMP-3; experiment: A; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 250K; agent: MMP-3; experiment: A; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 25K; agent: control; experiment: B; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 50K; agent: control; experiment: B; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 100K; agent: control; experiment: B; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 250K; agent: control; experiment: B; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 25K; agent: MMP-3; experiment: B; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 50K; agent: MMP-3; experiment: B; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 100K; agent: MMP-3; experiment: B; ', 'tissue: mammary gland; cell line: SCp2 mouse mammary epithelial cells; cell density: 250K; agent: MMP-3; experiment: B; ', 'tissue: mammary gland; cell line: MCF10A human breast epithelial cells; cell density: 50K; ', 'tissue: mammary gland; cell line: MCF10A human breast epithelial cells; cell density: 100K; ', 'tissue: mammary gland; cell line: MCF10A human breast epithelial cells; cell density: 200K; ', 'tissue: mammary gland; cell line: MCF10A human breast epithelial cells; cell density: 400K; ', 'tissue: mammary gland; cell line: MCF10A human breast epithelial cells; cell density: 600K; ', 'tissue: mammary gland; cell line: MCF10A human breast epithelial cells; cell density: 800K; ' GSE98714 Homo sapiens 10 Genome binding/occupancy profiling by high throughput sequencing; Third-party reanalysis GPL16791 Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer [ChIP-seq] 2017-05-09 DNA replication timing is known to facilitate the establishment of the epigenome, however, the intimate connection between replication timing and changes to the genome and epigenome in cancer remain largely uncharacterised. Here, we perform Repli-Seq and integrated epigenome analyses and demonstrate that genomic regions that undergo long-range epigenetic deregulation in prostate cancer also show concordant differences in replication timing. A subset of altered replication timing domains are conserved across cancers from different tissue origins. Notably, late-replicating regions in cancer cells display a loss of DNA methylation, and a switch in heterochromatin features from H3K9me3-marked constitutive to H3K27me3-marked facultative heterochromatin. Finally, analysis of 214 prostate and 35 breast cancer genomes reveal that late-replicating regions are prone to cis and early-replication to trans chromosomal rearrangements. Together, our data suggests that the nature of chromosomal rearrangement in cancer is related to the spatial and temporal positioning and altered epigenetic states of early-replicating compared to late-replicating loci. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98714 Replication timing and epigenome remodelling are associated with the nature of chromosomal rearrangements in cancer. Nature communications 11.878 https://doi.org/10.1038/s41467-019-08302-1 {Nature communications (11.878): 10.1038/s41467-019-08302-1} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA386038 https://www.ebi.ac.uk/ena/browser/view/PRJNA386038 https://www.ncbi.nlm.nih.gov/sra?term=SRP106747 [Overal design]ChIP-seq was conducted in 2 human prostate cell lines: normal prostate epithelial cells (PrEC) and prostate cancer cells (LNCaP); [Treatment]'None'; [Growth]"Cell lines were cultured according to manufacturer's instructions."; [Extraction]'Cells (7x10^6 per sample) were scraped, centrifuged and washed with PBS. Cell pellets were resuspended in nuclear extraction buffer (10mM Tris-HCl pH7.4, 12.5mM NaCl, 3mM MgCl, 0.1mM EDTA, 0.5% IGEPAL) and dounced until nuclei were visible under light microscope with 0.4% Trypan Blue staining. DNase1 (Roche, #04716728001) was added to nuclei pellets of LNCaP (24U) and PrEC (12U) and incubated at 37°C for 15 minutes. DNaseI reactions were terminated by the addition of 36mM EDTA and Proteinase K was added before incubating at 55°C overnight. DNA was purified by phenol-chloroform extraction and ethanol precipitation. Samples were separated using electrophoresis on a 1% agarose gel. 100-300bp sections were excised and purified using the QIAquick Gel Extraction kit. Library preparation and sequencing were performed by the USC Epigenome Center.\nLibraries were prepared using the Illumina TruSeq Chip Library Prep Kit. The resulting libraries were sequenced on the Illumina HiSeq 2000 or 2500 platform configured for 50bp single-end reads.', 'Cells (10^6 per ChIP) were cross-linked in suspension for 10 min in media containing 1% formaldehyde before quenching with 1.25mM glycine. The cells were washed twice with ice cold PBS containing protease inhibitors (1mM phenylmethylsulfonyl fluoride (PMSF), 1µg/ml aprotinin and 1µg/ml pepstatin A), harvested and treated with SDS lysis buffer for 10 min on ice. Chromatin lysate was sonicated to generate a majority of fragments between 200 and 500bp. 10µg of each antibody was used per ChIP. No antibody controls were also included, and no precipitation was observed by quantitative Real-Time PCR analysis. Input samples were processed in parallel. The antibody/protein complexes were collected by Protein A/G PLUS agarose beads (Santa Cruz, sc-2003) and washed several times. The immune complexes were eluted with 1% SDS and 0.1M NaHCO3, treated with proteinase K for 1 hour, followed by DNA purification using phenol/chloroform extraction and ethanol precipitation, and finally resuspended in 30µl H2O. The ChIP DNA was quantitated using Qubit and 10ng was used for Illumina library preparation using Illumina ChIP-seq DNA Sample Prep Kit.\nLibraries were prepared using the Illumina TruSeq Chip Library Prep Kit. The resulting libraries were sequenced on the Illumina HiSeq 2000 or 2500 platform configured for 50bp single-end reads.', 'Cells were cross-linked for 10 min in media containing 1% formaldehyde before quenching with 1.25mM glycine. Cell pellets were collected and resuspended in cell lysis buffer (1% Igepal, 85mM KCL, 5mM PIPES pH 8) to a concentration of 1mL per 10^7 cells, incubated on ice for 15 mins, and dounced 20x. Nuclear pellets were collected at 430xg for 5min at 4C and resuspended in nuclear lysis buffer (50mM Tris pH8, 10mM EDTA, 1% SDS, protease inhibitors), 20uL per 10^6 cells, and incubated on ice for 30 min. Lysates were sonicated to fragment lengths of 200 to 500bp. The sonicated lysate was spun at 16,100g for 10 mins at 4°C and aliquoted. The chromatin was diluted 5x in IP dilution buffer (50mM Tris pH 7.4, 1mM EDTA, 150mM NaCl, 1% Igepal, 0.25% Na Deoxychlorate and protease inhibitors). 5ug of chromatin in 250uL total volume is used per ChIP. Preloaded magnetic beads (Dynabeads M280 Streptavidin, Invitrogen #11205D) with anti-H3K9me3 (Diagenode, C15500003) or control-antibody were made by washing 68uL of beads with TBS/0.5% BSA 2x, followed by incubating with antibodies (1.8ug diluted in 105uL TBS/0.5% BSA) for 1 hr at 4C on a rotator. Excess streptavidin biotin-binding sites were blocked with 2x washes of 200uL of 5uM biotin (Sigma Aldrich, B4501) in TBS/0.5% BSA, rotating for 10 min at 4C. Beads were washed 2x with IP dilution buffer, then the chromatin added and incubated O/N at 4C on a rotator. The antibody/protein complexes were collected, washed several times and eluted in 1% SDS and 50mM NaHCO3. Crosslinks were reversed for 6hr at 65C in elution buffer with 200mM NaCl, treated with 1uL of 10ug/uL RNase A and 1uL of 20mg/mL Proteinase K. DNA was purified, the library was prepared (Illumina TruSeq Chip Library Prep Kit).\nLibraries were prepared using the Illumina TruSeq Chip Library Prep Kit. The resulting libraries were sequenced on the Illumina HiSeq 2500 platform configured for 50bp single-end reads.', 'Cells (10^7 per ChIP) were cross-linked in suspension for 10 min in PBS containing 1% formaldehyde before quenching with 1.25mM glycine. Pellets were collected and resuspended in hypertonic buffer (10mM Tris pH 7.5, 5mM NaCl, 1.5mM MgCl2, 0.5mM DTT, 0.5mM PMSF protease inhibitor), incubated on ice for 30 mins, and dounced 50x. MgCl2 was then adjusted to 5mM, NP-40 (IGEPAL) was added to final concentration of 0.1%, incubated on ice for 10 mins, before centrifugation at 2400g for 10 mins. The pellet was resuspended in MNase buffer (20mM Tris pH 7.5, 15mM NaCl, 1mM CaCl2) at 25 million cells/ml, incubated for 5 mins at 37°C, 0.5U MNase was added per 1 million cells and then incubated at 37°C for 5 mins. Digestion was stopped with 10mM final EDTA in ice for 10 mins. Samples were diluted to 8 million cells/ml with lysis buffer (50mM Tris pH8, 10mM EDTA, 0.5% SDS, 0.5mM PMSF and prostease inhibitors) before sonication. The sonicated lysate was spun at 16,100g for 10 mins at 4°C and aliquoted. The chromatin was diluted 5x in NP-40 buffer (20mM Tris pH 8, 5mM EDTA, 150mM NaCl, 1% NP-40 and protease inhibitors, SDS 0.1%), pre-cleared with Santa Cruz A/G beads for 1 hr at 4°C, spun at 1000rpm for 1 min at 4°C, before adding antibody 5ug lamin B1 (Abcam, #ab16048) and 10ug lamin A/C (Santa Cruz. #sc7292) for overnight incubation with rotation. ChIP material was collected and washed 3x in 1 ml ice-cold RIPA buffer. Crosslink was reversed and DNA eluted for 6 h on a shaker at 37°C in elution buffer (50mM NaCl, 20mM Tris-HCl, pH 7.5, 5mM EDTA, 1% SDS) containing 0.5μg/ml RNase A and 2μg/ml Proteinase K. DNA was purified, the library was prepared (Illumina TruSeq Chip Library Prep Kit).\nLibraries were prepared using the Illumina TruSeq Chip Library Prep Kit. The resulting libraries were sequenced on the Illumina HiSeq 2500 platform configured for 50bp single-end reads.'; [Cell type]'Source: ''tissue: Prostate; cell line: PrEC; chip-antibody: DNase1 (Roche, #04716728001); ', 'tissue: Prostate; cell line: PrEC; chip-antibody: H3K36me3 (Abcam, #ab9050); ', 'tissue: Prostate; cell line: PrEC; chip-antibody: H3K9me3 (Diagenode, #C15500003); ', 'tissue: Prostate; cell line: PrEC; chip-antibody: Lamin A/C (Santa Cruz, #sc7292); ', 'tissue: Prostate; cell line: PrEC; chip-antibody: Lamin B1 (Abcam, #ab16048); ', 'tissue: Prostate; cell line: LNCaP; chip-antibody: DNase1 (Roche, #04716728001); ', 'tissue: Prostate; cell line: LNCaP; chip-antibody: H3K36me3 (Abcam, #ab9050); ', 'tissue: Prostate; cell line: LNCaP; chip-antibody: H3K9me3 (Diagenode, #C15500003); ', 'tissue: Prostate; cell line: LNCaP; chip-antibody: Lamin A/C (Santa Cruz, #sc7292); ', 'tissue: Prostate; cell line: LNCaP; chip-antibody: Lamin B1 (Abcam, #ab16048); ' GSE60725 synthetic construct 16 Non-coding RNA profiling by array GPL17107 MicroRNA profiling of Human Breast Cancer 2014-08-25 Total RNA was isolated from epithelial tissues of different grades and stages of human breast cancer samples using mirVana kit and RNA integrity number (RIN) was determined in Agilent Bioanalyzer (2100) to assess the suitability for microarray assays. Sixteen samples were individually analyzed using miRCURY™ LNA arrays version 11.0 (Exiqon, Denmark). The LNA array slides were scanned using Agilent G2565BA Microarray Scanner System (Agilent Technologies, Inc., USA) and image analysis was carried out using ImaGene 8.0 software (BioDiscovery, Inc., USA). The quantified signals were background corrected (Normexp with offset value 10 14 and normalized using global Lowess (Locally Weighted Scatterplot Smoothing) regression algorithm. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60725 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA259365 https://www.ebi.ac.uk/ena/browser/view/PRJNA259365 None [Overal design]Three condition experiment Grade 2, stage II vs its adjacent normals (AN) and Grade 3, stage III vs it AN, Grade 2 vs Grade 3, Grade 2, stage II 5 biological replicates, Grade 3 stage III 5 biological replicates, AN 3 biological replicates each; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was extracted using mirVana™ miRNA isolation kit following manufacturer's instructions."; [Cell type]'stage III Grade 3', 'Source: ', 'stage II Grade 2', 'adjacent normal''cell type: stage III Grade 3; tissue: Epithelial Tissue; ', 'sample type: Reference RNA; ', 'cell type: stage II Grade 2; tissue: Epithelial Tissue; ', 'cell type: adjacent normal; tissue: Epithelial Tissue; ' GSE118728 Mus musculus 27 Expression profiling by array GPL11383 Identification of Jun loss that promotes resistance to HDAC inhibitor Entinostat through Myc signaling in Luminal breast cancer (expression) 2018-08-17 The histone deacetylase inhibitor Entinostat is in phase III trials for patients with metastatic estrogen receptor-positive breast cancer. Predictors of sensitivity and resistance, however, remain unknown. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE118728 Identification of Jun loss promotes resistance to histone deacetylase inhibitor entinostat through Myc signaling in luminal breast cancer. Genome medicine 10.886 https://doi.org/10.1186/s13073-018-0597-3 {Genome medicine (10.886): 10.1186/s13073-018-0597-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA486661 https://www.ebi.ac.uk/ena/browser/view/PRJNA486661 None [Overal design]A total of 8 cell lines and 9 mouse models of breast cancer were treated with Entinostat. Luminal cell lines were treated with or without Entinostat at their IC50 doses, and MMTV/Neu luminal mouse tumors were treated with Entinostat until progression. We investigated these models using gene expression profiling by microarray and copy number by arrayCGH. We also utilized the network-based Dawnrank algorithm, that integrates DNA and RNA data, to identify driver genes of resistance. The impact of a number of candidate drivers was investigated in The Cancer Genome Atlas and the METABRIC; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen Rneasy Kit'; [Cell type]'Source: ''', 'sample type: MMTV/Neu; treatment: Untreated; ', 'sample type: MMTV/Neu; treatment: Entinostat_3wks; ', 'sample type: MMTV/Neu; treatment: Entinostat_6wks; ', 'sample type: MMTV/Neu; treatment: Entinostat_Progression; ' GSE83591 Homo sapiens 109 Expression profiling by array GPL14550 Gene expression profiles of tumor epithelium and tumor-associated stroma of HER2+ breast tumors, plus normal epithelium and stroma from HER2+ and HER2- breast tumors 2016-06-21 Breast cancer is a heterogeneous disease. This heterogeneity can be observed at multiple levels, including gene expression, chromosomal aberrations, and disease pathology. A clear understanding of these differences is important since they impact upon treatment efficacy and clinical outcome. Many studies have shown that the tumor microenvironment also plays a critical role in cancer initiation and progression. Although genomic technologies have been used to gain a better understanding of the impact of gene expression heterogeneity on breast cancer outcome by identifying gene expression signatures associated with clinical outcome, histopathological breast cancer subtypes, and a variety of cancer-related pathways and processes, relatively little is known about the spectrum of heterogeneity in the tumor microenvironment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE83591 Discovery of Stromal Regulatory Networks that Suppress Ras-Sensitized Epithelial Cell Proliferation. Developmental cell 9.190 https://doi.org/10.1016/j.devcel.2017.04.024 {Developmental cell (9.190): 10.1016/j.devcel.2017.04.024} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA326438 https://www.ebi.ac.uk/ena/browser/view/PRJNA326438 None [Overal design]107 samples isolated by laser capture microdissection; in total, 40 samples of tumor epithelium, 39 samples of tumor stroma, 14 samples of normal epithelium and 14 samples of normal stroma; 2 samples possess biological replicates; each subjected to gene expression profiling in a common reference design using Agilent whole human genome oligonucleotide arrays.; [Treatment]"Tissue compartments isolated from OCT-embedded frozen human tissue samples by laser capture microscopy following HistoGene staining and pathologist's evaluation.", 'N/A'; [Growth]'N/A'; [Extraction]'Normal and tumor epithelium and stroma were separately microdissected from tissue samples using a PixCell IIe LCM system (Arcturus). All microdissections were performed within three hours of tissue staining. Total RNA was extracted from each population of microdissected cells using an Arcturus PicoPure RNA Isolation Kit (Cat# 12204-01).', 'Universal Human Reference RNA (Stratagene, ID #740000, La Jolla, California, USA).'; [Cell type]'Source: ''disease state: HER2+ breast cancer; breast tissue compartment: Tumor epithelium; ', 'sample type: Reference; ', 'disease state: HER2+ breast cancer; breast tissue compartment: Tumor stroma; ', 'disease state: Breast cancer; breast tissue compartment: Normal epithelium; ', 'disease state: Breast cancer; breast tissue compartment: Normal stroma; ' GSE142562 Homo sapiens 2 Expression profiling by high throughput sequencing GPL15520 Transcriptomic profiling by RNA-Seq of MCF-7 cells edited by CRISPR/Cas9 in the FASN locus 2019-12-24 We report a preliminary RNA-Seq data of MCF-7 cells edited in the FASN locus using CRISPR/Cas9. MCF-7 cells were edited by CRISPR/Cas9, screened by Surveyor assay, purified by limiting dilutions, validated by sanger sequencing, and characterized by diverse cellular analyses. Then, RNA from edited cells and non-edited controls were processed by TruSeq-RNA-Library-Prep-Kit and sequenced in a illumina equipment. Reads were aligned to hg38 in Galaxy using RNA-Star and transcripts were counted by FeatureCounts. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE142562 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA597467 https://www.ebi.ac.uk/ena/browser/view/PRJNA597467 https://www.ncbi.nlm.nih.gov/sra?term=SRP238680 [Overal design]A CRIPSR/Cas9 edited clone and a edited-negative cells as control.; [Treatment]'CRISPR/Cas9, PX459 plasmid'; [Growth]'DMEM-F12 + 10%FBS'; [Extraction]'GenElute Mammalian Total RNA Miniprep Kit\nTruSeq-RNA-Library-Prep-Kit'; [Cell type]'Source: ''genotype: Mutant; ', 'genotype: Control; ' GSE66083 Homo sapiens 25 Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing; Third-party reanalysis GPL16791; GPL17811 Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth 2015-02-19 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE66083 Genome-wide association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth. Nature cell biology 17.728 https://doi.org/10.1038/ncb3216 {Nature cell biology (17.728): 10.1038/ncb3216} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA275842 https://www.ebi.ac.uk/ena/browser/view/PRJNA275842 None [Overal design]Refer to individual Series; [Treatment]'None', "Cells were transfected on day 2 with siRNA oligonucleotides (final concentration 33nM) by using RNAi MAX (Life Technologies), following a direct transfection protocol as indicated by manifacturer's instructions. On day 3, medium was renewed. On day 4, cells were washed with 1XHBSS and harvested for RNA extraction."; [Growth]'MDA MB 231 cells were cultured in DMEM:F12 + 10% FBS.', 'Cells were seeded at low confluence on day 1 in standard growth medium (DMEM/F12 with 2mM Glutamine, 17.5mM D-glucose, without antibiotics, 10% Fetal Bovine Serum).'; [Extraction]'Cross-linked chromatin was sheared by sonication and immunoprecipitated with YAP, TAZ, TEAD4 and JUN antibodies. DNA was purified by phenol/chloroform extraction and ethanol precipitation.\nNuGEN Ovation Ultralow Library Prep System kit', "Trizol extraction of total RNA, followed by DNAseI digestion to reduce genomic DNA contaminations, was performed according to the manufacturer's instructions."; [Cell type]'Source: ', 'breast cancer''cell line: MDA-MB-231; chip antibody: YAP EP1674Y (Abcam, ab-52771, lot GR75026-5); ', 'cell line: MDA-MB-231; chip antibody: WWTR1 (Sigma, HPA007415,lot C78623); ', 'cell line: MDA-MB-231; chip antibody: Rabbit IgG (Sigma, I5006); ', 'cell line: MDA-MB-231; chip antibody: TEF-3 (N-G2) (SCBT, sc-101184, lot C2812); ', 'cell line: MDA-MB-231; chip antibody: JUN (BD Bioscience, 610326, lot 3263734); ', 'cell line: MDA-MB-231; chip antibody: Mouse IgG (SCBT, sc-2025, lot A1813); ', 'cell line: MDA-MB-231; cell type: breast cancer; transfection construct: Control siRNA; ', 'cell line: MDA-MB-231; cell type: breast cancer; transfection construct: YAP/TAZ siRNA #1; ', 'cell line: MDA-MB-231; cell type: breast cancer; transfection construct: YAP/TAZ siRNA #2; ' GSE22035 Homo sapiens 43 Expression profiling by array GPL570 Gene expression data in estrogen receptor alpha positive breast tumors with and without PIK3CA mutations. 2010-05-27 PI3K/AKT pathway plays one of pivotal roles in breast cancer development and maintenance. PIK3CA, coding PIK3 catalytic subunit, is the oncogene which shows the high frequency of gain-of-function mutations leading to the PI3K/AKT pathway activation in breast cancer. In particular in the ERα-positive breast tumors PIK3CA mutations have been observed in 30% to 40%. However, genes expressed in connection to the pathway activation in breast tumorigenesis remain largely unknown. To identify downstream relevant target genes (and signaling pathways) turned on by the aberrant PI3K/AKT signal in breast tumors, we analyzed gene expression by pangenomic oligonucleotide microarray in a series of 43 ERα-positive tumors with and without PIK3CA mutations. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22035 Gene expression profiling reveals new aspects of PIK3CA mutation in ERalpha-positive breast cancer: major implication of the Wnt signaling pathway. PloS one 2.776 https://doi.org/10.1371/journal.pone.0015647 {PloS one (2.776): 10.1371/journal.pone.0015647} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA128895 https://www.ebi.ac.uk/ena/browser/view/PRJNA128895 None [Overal design]43 ERα-positive breast tumors including 14 tumors with PIK3CA mutations and 29 tumors without PIK3CA mutattions were used as screening set for microarray.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted from breast tissue samples by using acid-phenol guanidium method.'; [Cell type]'Source: ''tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 65 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 60 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 76 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 67 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 72 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 73 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 74 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 57 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 69 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 55 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 52 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 68 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 70 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 62 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 78 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 64 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 53 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 75 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 79 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 61 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 71 years; ', 'tissue: primary unilateral non-metastatic postmenopausal ERα-positive breast tumor; gender: woman; age: 46 years; ' GSE159806 Mus musculus 5 Expression profiling by high throughput sequencing GPL17021 Regulatory T cells support breast cancer progression by opposing IFN-γ -dependent functional reprogramming of myeloid cells 2020-10-21 Regulatory T (Treg) cell infiltration of solid tumors often correlates with poor prognosis, but their tumor suppressive function lacks mechanistic understanding. Through a combination of transgenic mice, cell fate mapping, adoptive transfer and co-injection strategies, we demonstrate that Treg cell ablation-dependent anti-tumor effects in murine breast cancer require intratumoral recruitment of CCR2+ inflammatory monocytes, which primarily differentiate into tumor-associated macrophages (TAMs), and lead to reprogramming of their function in an IFN--dependent manner. Furthermore, transcriptomic signatures from murine TAMs in Treg cell-ablated conditions correlate with increased overall survival in human breast cancer. Our studies highlight the strong myeloid dependency of breast cancer, and provide the basis for the development of therapeutic strategies based on manipulation of the IFN- signaling pathway in monocytes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE159806 Regulatory T Cells Support Breast Cancer Progression by Opposing IFN-γ-Dependent Functional Reprogramming of Myeloid Cells. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2020.108482 {Cell reports (7.815): 10.1016/j.celrep.2020.108482} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA670498 https://www.ebi.ac.uk/ena/browser/view/PRJNA670498 https://www.ncbi.nlm.nih.gov/sra?term=SRP288045 [Overal design]We mechanistically dissect the tumor-promoting function of Treg cells in poorly immunogenic breast cancer, describing the critical role of TAMs in the anti-tumor phenotype observed upon Treg cell ablation, and the dependency on CD4+ T cell-produced IFN-γ for their functional reprogramming; [Treatment]'EO771 orthotopic mammary tumors were treated with two doses of 50ug/kg of diphteria toxin to ablate Treg cells, and TAMs were sorted 4 days after treatment. Control tumors were left untreated.'; [Growth]'N/A'; [Extraction]'TAMs (defined as CD45+ CD11B+ Ly6G- F4/80+ cells) were sorted from EO771 orthotopic breast tumors as described, and collected into TrizolLS (Thermo Fisher) for subsequent RNA isolation. RNA isolation was performed following manufacturer’s protocols. Initial quality control was performed using an Agilent Bioanalizer System through the Pathology Tissue and Data Acquisition and Analysis Core (TDAAC). All samples were sent to the Brigham Young University DNA sequencing core for further library construction and sequencing.\nKAPA Stranded mRNA-Seq Kit was used for library preparation. Samples were sequenced on the Illumina Hi-Seq 2500 according to Illumina’s sequencing-by-synthesis protocol. 125bp paired-end reads were generated, yielding on average 87M reads per sample.'; [Cell type]'freshly sorted TAMs''cell type: freshly sorted TAMs; treatment: Treg cell ablated; strain: C57/BL6; ', 'cell type: freshly sorted TAMs; treatment: Control; strain: C57/BL6; ' GSE136105 Homo sapiens 18 Expression profiling by high throughput sequencing GPL16791 Gene expression profiling in lung and breast cancer cells treated by Bloom-specific siRNAs 2019-08-21 A549 and MDA-MB-231 cells were transfected with the Bloom-specific siRNA. Total RNA was extracted using Trizol at 48 hours after transfection. RNA-SEQ was carried out to profile the gene expression in both culture conditions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE136105 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA561309 https://www.ebi.ac.uk/ena/browser/view/PRJNA561309 https://www.ncbi.nlm.nih.gov/sra?term=SRP218977 [Overal design]The goal of this experiment was to profie the genes that are regulated by Bloom (BLM RecQ like helicase) in cancer cells. Gene expression was probed globally using RNA-SEQ.; [Treatment]'The cell were transfected either a control siRNA or three distinct Bloom-specific siRNAs in A549 cells or one Bloom-specific siRNA in MDA-MB-231 cells.'; [Growth]'A549 and MDA-MB-231 cells were cultured in DMEM+10% FBS.'; [Extraction]'Total cell RNA was extracted when cells were ~80% confluent in 2D culture and on day 4 in 3D culture using TRIZOL.\nLibraries were constructed using the Illumina TruSeq Stranded Total RNA Library Prep Kit/Ribo-Zero Gold kit.'; [Cell type]'Lung Cancer', 'Breast Cancer''cell line: A549; cell type: Lung Cancer; tissue type: Lung; genotype: BLM.siRNA1; ', 'cell line: A549; cell type: Lung Cancer; tissue type: Lung; genotype: BLM.siRNA2; ', 'cell line: A549; cell type: Lung Cancer; tissue type: Lung; genotype: BLM.siRNA3; ', 'cell line: A549; cell type: Lung Cancer; tissue type: Lung; genotype: control; ', 'cell line: MDA-MB-231; cell type: Breast Cancer; tissue type: Breast; genotype: BLM.siRNA1; ', 'cell line: MDA-MB-231; cell type: Breast Cancer; tissue type: Breast; genotype: control; ' GSE39623 Homo sapiens 22 Expression profiling by array GPL6947 GATA3 acts upstream of FOXA1 in mediating ER binding by shaping enhancer accessibility 2012-07-24 Estrogen Receptor (ESR1) drives growth in the majority of human breast cancers by binding to regulatory elements and inducing transcription events that promote tumor growth. Differences in enhancer occupancy by ESR1, contribute to the diverse expression profiles and clinical outcome observed in breast cancer patients. GATA3 is an ESR1 co-operating transcription factor mutated in breast tumors, however its genomic properties are not fully defined. In order to investigate the composition of enhancers involved in estrogen-induced transcription and the potential role of GATA3, we performed extensive ChIP-sequencing in unstimulated breast cancer cells and following estrogen treatment. We find that GATA3 is pivotal in mediating enhancer accessibility at regulatory regions involved in ESR1-mediated transcription. GATA3 silencing resulted in a global redistribution of co-factors and active histone marks prior to estrogen stimulation. These global genomic changes altered the ESR1 binding profile that subsequently occurred following estrogen, with events exhibiting both loss and gain in binding affinity, implying a GATA3 mediated re-distribution of ESR1 binding. The GATA3-mediated re-distributed ESR1 profile correlated with changes in gene expression, suggestive of its functionality. Chromatin loops at the TFF locus involving ESR1 bound enhancers occurred independently of ESR1 when GATA3 was silenced, indicating that GATA3, when present on the chromatin, may serve as a licensing factor for estrogen- ESR1 mediated interactions between cis-regulatory elements. Together these experiments suggest that GATA3 directly impacts ESR1 enhancer accessibility and may potentially explain the contribution of mutant-GATA3 in the heterogeneity of ESR1+ breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39623 GATA3 acts upstream of FOXA1 in mediating ESR1 binding by shaping enhancer accessibility. Genome research 9.944 https://doi.org/10.1101/gr.139469.112 {Genome research (9.944): 10.1101/gr.139469.112} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA171279 https://www.ebi.ac.uk/ena/browser/view/PRJNA171279 None [Overal design]MCF7 cells were transfected with siRNA and cultured in hormone deprived conditions for a further 3 days. Cells were subsequently treated with 100nM estrogen (E2) or control (Veh) for 6 hrs. We performed two independent biological experiments each using three different siRNAs against GATA3 individually (six siGATA3 replicates in total). For siControl we used RNA from five biological replicates.; [Treatment]"We used three different siRNAs against GATA3: ON-TARGET plus siRNA J-0033781-09 and two additional custom made targeting the 3'UTR of the RefSeq NM_002051. The sense sequences of the custom made ones are siGATA3-Custom-1: AAACUAGGUCUGAUAUUCAUU and siGATA3-Custom-2: CUUUAUUGCAUCUGGGUAGUU. AllStars Negative Control siRNA (Cat nr: 1027281, Qiagen) was used as a negative control. All siRNA experiments were at a final concentration of 50nM. Transfections were conducted using Lipofectamine 2000 (Invitrogen)."; [Growth]'MCF7 cells were cultured in DMEM and ZR-75-1 cells in RPMI media (Invitrogen) at 10% FCS. For hormonal deprivation, cells were cultured for 3 days in phenol-red free DMEM or RPMI respectively, supplemented with 5% charcoal-treated serum. E2 (Sigma) was added at a final concentration of 100nM for 6 hours.'; [Extraction]'RNA was extracted using TRIzol RNA Isolation reagents from Life Technologies as per manufacturer guidelines'; [Cell type]'Source: ''treatment: E2; knockdown: siGATA-v1; sigata variant: v1; cell line: MCF7; ', 'treatment: vehicle; knockdown: siGATA-v2; sigata variant: v2; cell line: MCF7; ', 'treatment: E2; knockdown: sINT; cell line: MCF7; ', 'treatment: vehicle; knockdown: sINT; cell line: MCF7; ', 'treatment: vehicle; knockdown: siGATA-v0; sigata variant: v0; cell line: MCF7; ', 'treatment: vehicle; knockdown: siGATA-v1; sigata variant: v1; cell line: MCF7; ', 'treatment: E2; knockdown: siGATA-v0; sigata variant: v0; cell line: MCF7; ', 'treatment: E2; knockdown: siGATA-v2; sigata variant: v2; cell line: MCF7; ' GSE18931 Homo sapiens 6 Expression profiling by array GPL570 The biological and molecular heterogeneity of breast cancers correlate with their cancer stem cell content 2009-11-06 Pathways that govern normal stem cell (SC) function are often subverted in cancer. Here, we report the isolation to near purity of human normal mammary SC (hNMSCs), from cultured mammospheres, based on their ability to retain the lipophilic dye PKH26 as a consequence of their quiescent nature. We demonstrated that PKH26-positive cells possess all the characteristics of hNMSCs. The transcriptional profile of PKH26-positive cells (hNMSC signature) was able to predict biological and molecular features of breast cancers. By using markers of the hNMSC signature, we could prospectively isolate SCs from the normal gland and from breast tumors. Poorly-differentiated aggressive (G3) cancers displayed higher content of prospectively isolated cancer SCs, than well-differentiated less aggressive (G1) cancers. By comparing G3 and G1 tumors in xenotransplantation experiments, we directly demonstrated that G3s are enriched in cancer SCs. Our data support the notion that the heterogeneous phenotypical and molecular traits of human breast cancers are a function of their SC content. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE18931 Biological and molecular heterogeneity of breast cancers correlates with their cancer stem cell content. Cell 36.216 https://doi.org/10.1016/j.cell.2009.12.007 {Cell (36.216): 10.1016/j.cell.2009.12.007} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA121041 https://www.ebi.ac.uk/ena/browser/view/PRJNA121041 None [Overal design]Epithelial cells, from reductive mammoplasties, labeled with PKH26 (Sigma, 10-7 M, 5 min) and subjected to FACS analysis using a FACS Vantage SE flow cytometer (Becton&Dickinson) to yield PKH-POS and PKH-NEG cells, were prepared for RNA extraction and hybridization on Affymetrix microarrays. Three independent pools of cells were used, and six Gene Expression Arrays were obtained. No replicates are available.; [Treatment]'None'; [Growth]'Epithelial cells, from reductive mammoplasties , were allowed to adhere for 24 h in complete SC medium. Cells were trypsinized, filtered through a 100um and a 40um cell strainer, resuspendend in PBS (500,000/ml), and labeled with PKH26 (Sigma, 10-7 M, 5 min). Labeled cells were plated (30,000 cells/ml) in suspension. After 7-10 days, mammospheres were harvested, dissociated enzymatically (0.05% trypsin/0.5 mM EDTA for 10 min, plus filtering though a 40um cell strainer), and subjected to FACS analysis using a FACS Vantage SE flow cytometer (Becton&Dickinson) to yield PKH-POS and PKH-NEG cells.'; [Extraction]'Total RNA was extracted using the Arcturus PicoPure RNA Isolation Kit (Arcturus Engineering, CA, USA) according to the manufacturer’s instructions, and analyzed with the Agilent 2100 Bioanalyzer (Agilent Technologies).'; [Cell type]'Mammary Epithelial Cells''cell type: Mammary Epithelial Cells; ' GSE31118 Homo sapiens 21 Expression profiling by array GPL14010 Estrogen-dependent gene expression in human breast cancer cells relies upon proteosome-dependent monoubiquitination of histone H2B 2011-08-02 The estrogen receptor-alpha (ERα) determines breast cancer cell phenotype and is a prognostic indicator. A better understanding of the mechanisms controlling ERα function may uncover improved strategies for the treatment of breast cancer. Proteasome inhibition was previously reported to regulate estrogen-induced transcription but the mechanisms by which it influences ERα function remain controversial. In this study we investigated the transcriptome-wide effects of the proteasome inhibitor Velcade on estrogen-regulated transcription in MCF7 human breast cancer cells and demonstrate a specific global decrease in estrogen-induced transcription. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE31118 Estrogen-dependent gene transcription in human breast cancer cells relies upon proteasome-dependent monoubiquitination of histone H2B. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-11-1896 {Cancer research (8.378): 10.1158/0008-5472.CAN-11-1896} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA144663 https://www.ebi.ac.uk/ena/browser/view/PRJNA144663 None [Overal design]This set contains 21 microarray samples. 3 controls, 3 estrogen stimulated, 3 Bortezomib + estrogen stimulated, 2* 3 siRNA controls, 3 siRNA PSMB3 knockdowns, 3 siRNA PSMB5 knockdowns; [Treatment]'Where indicated, cells were pretreated with 50 nM Bortezomib for 15 minutes followed by 10 nM 17-β-estradiol for 24 hours.'; [Growth]'Cells were grown in phenol-red free DMEM containing 5% charcoal-dextran treated FBS for 48 hours prior to treatment with Bortezomib or estrogen.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions"; [Cell type]'Source: ''group: Control; cell line: MCF7; ', 'group: E2; cell line: MCF7; ', 'group: Bort+E2; cell line: MCF7; ', 'group: siRNA_Ctrl1; cell line: MCF7; ', 'group: siRNA_Ctrl2; cell line: MCF7; ', 'group: siRNA_PSMB3; cell line: MCF7; ', 'group: siRNA_PSMB5; cell line: MCF7; ' GSE35525 Homo sapiens 8 Expression profiling by array GPL570 Pivotal role of HMGA1 gene signature in highly metastatic breast cancer 2012-02-03 Analysis of MDA-MB-231 breast cancer cells depleted for High Mobility Group A1 (HMGA1) using siRNA. HMGA1 is involved in invasion and metastasis in breast cancer cells. Results identify the specific transcriptional program induced by HMGA1 in highly metastatic breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE35525 HMGA1 promotes metastatic processes in basal-like breast cancer regulating EMT and stemness. Oncotarget None https://doi.org/10.18632/oncotarget.1136 {Oncotarget (None): 10.18632/oncotarget.1136} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA152247 https://www.ebi.ac.uk/ena/browser/view/PRJNA152247 None [Overal design]MDA-MB-231 cells were transfected with HMGA1-specific siRNA or a control siRNA. Transfections were performed by using Lipofectamin RNAiMAX (Invitrogen) according to the manufacturer's procedure. Seventy-two hours after transfection, samples were processed for total RNA extraction and hybridization on Affymetrix microarrays. Four biological replicas (A, B, C, D) were used for each of the two conditions, for a total of 8 samples.; [Treatment]'None'; [Growth]'None'; [Extraction]"TRIzol (Invitrogen) followed by RNeasy column cleanup (Qiagen) using the manufacturers' protocols."; [Cell type]'breast cancer cells''cell line: MDA-MB-231; cell type: breast cancer cells; sirna: control; ', 'cell line: MDA-MB-231; cell type: breast cancer cells; sirna: HMGA1; ' GSE150038 Homo sapiens 6 Expression profiling by high throughput sequencing GPL23525 HDAC inhibitor PCI-24781 inhibits metastasis in breast cancer 2020-05-07 RNA-seq analysis was performed to identify key signaling responding to PCI-24781 in MDA-MB-231 https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE150038 The histone deacetylase inhibitor PCI-24781 impairs calcium influx and inhibits proliferation and metastasis in breast cancer. Theranostics 8.063 https://doi.org/10.7150/thno.48314 {Theranostics (8.063): 10.7150/thno.48314} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA630975 https://www.ebi.ac.uk/ena/browser/view/PRJNA630975 https://www.ncbi.nlm.nih.gov/sra?term=SRP260440 [Overal design]Four independent sample groups were exposed to PCI-24781 and controls were treated with DMSO for 24 h and 48 h (DMSO-treated groups: DMSO 24 h, DMSO 48 h; PCI-24781-treated groups: 100 nM 24 h; 100 nM 48 h; 200 nM 24 h; 200 nM 48 h) in MDA-MB-231 and were analyzed through RNA-seq.; [Treatment]'Cells were treated for 24h or 48h in adherent conditions with 100 nM and 200 nM PCI-24781 or DMSO.'; [Growth]'MDA-MB-231 cells were cultured in a humidified incubator equilibrated with 5% CO2 at 37 °C. The media (Dulbecco Modified Eagle Medium (DMEM)) was supplemented with 10% fetal bovine serum (FBS), 100 units/mL penicillin, and 100 mg/mL streptomycin'; [Extraction]'RNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''cell line: MDA-MB-231; treatment: DMSO; treatment duration: 24h; dose: n/a; ', 'cell line: MDA-MB-231; treatment: DMSO; treatment duration: 48h; dose: n/a; ', 'cell line: MDA-MB-231; treatment: PCI-24781; treatment duration: 24h; dose: 100 nM; ', 'cell line: MDA-MB-231; treatment: PCI-24781; treatment duration: 48h; dose: 100 nM; ', 'cell line: MDA-MB-231; treatment: PCI-24781; treatment duration: 24h; dose: 200 nM; ', 'cell line: MDA-MB-231; treatment: PCI-24781; treatment duration: 48h; dose: 200 nM; ' GSE165884 Homo sapiens 8 Non-coding RNA profiling by array GPL21825 Hsa_circ_0001583 a novel biomarker for breast cancer related to immune response 2021-02-01 The differently expressed circRNAs were analysis by microarray. There were 256 differentially upregulated circRNAs and 277 differentially downregulated circRNAs based on fold change ≥2.0 and p<0.05. We found hsa_circ_0001583 expression was up-regulated in BC groups (p<0.05) by RT-qPCR. Therefore, we though hsa_circ_0001583 may serve as a novel kind of biomarker for BC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE165884 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA698539 https://www.ebi.ac.uk/ena/browser/view/PRJNA698539 None [Overal design]A total of 4 pairs of breast cancer tissue samples and adjacent nontumor tissue samples were obtained from five BC patients. The circRNA expression profiles were detected with microarray, and validated by RT-qPCR.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA isolation was performed using TRIzol reagent according to the manufacturer’s protocol.The purity and concentration of total RNA samples were determined with NanoDrop ND-1000.'; [Cell type]'Source: ''tissue: breast; gender: female; age: 42y; ', 'tissue: breast; gender: female; age: 47y; ', 'tissue: breast; gender: female; age: 54y; ', 'tissue: breast; gender: female; age: 64y; ' GSE124965 Homo sapiens 12 Expression profiling by array GPL6480 Gene expression analysis of miR-214 over-expressing melanoma cells (MA-2) 2019-01-11 Growing evidence shows a strong interplay between post-transcriptional regulation, mediated by miRs and epigenetic regulation. Nevertheless, the number of experimentally validated miRs (called epimiRs) involved in these regulatory circuitries is still very small. Material & methods:We propose a pipeline to prioritize candidate epi-miRs and to identify potential epigenetic interactors of any given miR starting from miR transfection experiment datasets. Results & conclusion: We identified 34 candidate epi-miRs: 19 of them are known epi-miRs, while 15 are new. Moreover, using an in-house generated gene expression dataset, we experimentally proved that a component of the polycomb-repressive complex 2, the histone methyltransferase enhancer of zeste homolog 2 (EZH2), interacts with miR-214, a well-known prometastatic miR in melanoma and breast cancer, highlighting a miR-214-EZH2 regulatory axis potentially relevant in tumor progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124965 Investigating the epi-miRNome: identification of epi-miRNAs using transfection experiments. Epigenomics 4.404 https://doi.org/10.2217/epi-2019-0050 {Epigenomics (4.404): 10.2217/epi-2019-0050} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA514711 https://www.ebi.ac.uk/ena/browser/view/PRJNA514711 None [Overal design]Gene expression profiling was carried out on controls and miR-214 overexpressing cells by using the Whole Human Genome Microarray platform (G4112F, Agilent Technologies). Total RNA was obtained from approximately 106 cells for each biological replicate. Three biological replicates were analyzed for controls and miR-214 overexpressing cells respectively for a total of 12 microarray experiments.; [Treatment]'To obtain transient pre-miR expression, cells were plated in 6-well plates at 30–50% confluency and transfected 24 h later using RNAiFect (Qiagen, Stanford, CA) reagent, according to the manufacturer’s instructions, with 75nM pre-miR. For transient cDNA overexpression, cells were plated in 6-well plates at 90% confluency and transfected 24 h later using LipofectamineTM2000 (Invitrogen Life Technologies) reagent, according to the manufacturer’s instruction. Cells were tested for gene expression 48 or 72 h later.'; [Growth]'MA-2 cells were provided by R.O. Hynes (Massachusetts Institute of Technology, Cambridge, MA) and maintained in Dulbecco’s Modified Eagle’s Medium containing 10mM Glutamax and 4.5 g/ml glucose (DMEM GlutamaxTM, GIBCO Invitrogen Life Technologies, Carlsbad, CA), supplemented with 10% heat-inactivated FCS (Seromed, GmbH), 1mM sodium pyruvate, 25mM HEPES pH 7.4, 1 MEM vitamin solution, 1X MEM non-essential amino acids and 100 mg/ml gentamicin (all from GIBCO Invitrogen Life Technologies).'; [Extraction]'Total RNA was isolated from 106 cells by using Trizol® Reagent (Thermo Fisher) according to the manufacturer’s protocol. Total RNA was quantified using the ND-1000 spectrophotometer (Nanodrop), while RNA integrity and content of microRNAs (%) in each samples were assessed by capillary electrophoresis using the RNA 6000 Nano LabChip using the Agilent Bioanalyzer 2100 (Agilent Technologies). Only total RNA samples with R.I.N. (RNA Integrity Number) values of 6, or higher, were used for microarray analysis.'; [Cell type]'MA2 melanoma cells''cell type: MA2 melanoma cells; transfection: precursor of miR-214; time point: 48h post-transfection; biological replicate: 1; ', 'cell type: MA2 melanoma cells; transfection: precursor of miR-214; time point: 48h post-transfection; biological replicate: 2; ', 'cell type: MA2 melanoma cells; transfection: precursor of miR-214; time point: 48h post-transfection; biological replicate: 3; ', 'cell type: MA2 melanoma cells; transfection: precursor of miR-214; time point: 72h post-transfection; biological replicate: 1; ', 'cell type: MA2 melanoma cells; transfection: precursor of miR-214; time point: 72h post-transfection; biological replicate: 2; ', 'cell type: MA2 melanoma cells; transfection: precursor of miR-214; time point: 72h post-transfection; biological replicate: 3; ', 'cell type: MA2 melanoma cells; transfection: negative control; time point: 48h post-transfection; biological replicate: 1; ', 'cell type: MA2 melanoma cells; transfection: negative control; time point: 48h post-transfection; biological replicate: 2; ', 'cell type: MA2 melanoma cells; transfection: negative control; time point: 48h post-transfection; biological replicate: 3; ', 'cell type: MA2 melanoma cells; transfection: negative control; time point: 72h post-transfection; biological replicate: 1; ', 'cell type: MA2 melanoma cells; transfection: negative control; time point: 72h post-transfection; biological replicate: 2; ', 'cell type: MA2 melanoma cells; transfection: negative control; time point: 72h post-transfection; biological replicate: 3; ' GSE62817 Mus musculus 14 Expression profiling by array GPL1261 SPR509: Lung metastasis 2014-10-29 Determine gene expression differences between normal, metastatic and non-metastatic mouse lung tissue. Priming of the organ-specific premetastatic sites is thought to be an important yet incompletely understood step during metastasis. In this study, we show that the metastatic tumors we examined overexpress granulocyte-colony stimulating factor (G-CSF), which expands and mobilizes Ly6G+Ly6C+ granulocytes and facilitates their subsequent homing at distant organs even before the arrival of tumor cells. Moreover, G-CSF-mobilized Ly6G+Ly6C+ cells produce the Bv8 protein, which has been implicated in angiogenesis and mobilization of myeloid cells. Anti-G-CSF or anti-Bv8 antibodies significantly reduced lung metastasis. Transplantation of Bv8 null fetal liver cells into lethally irradiated hosts also reduced metastasis. We identified an unexpected role for Bv8: the ability to stimulate tumor cell migration through activation of one of the Bv8 receptors, prokineticin receptor (PKR)-1. Finally, we show that administration of recombinant G-CSF is sufficient to increase the numbers of Ly6G+Ly6C+ cells in organ-specific metastatic sites and results in enhanced metastatic ability of several tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE62817 Granulocyte-colony stimulating factor promotes lung metastasis through mobilization of Ly6G+Ly6C+ granulocytes. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1015855107 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1015855107} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA266417 https://www.ebi.ac.uk/ena/browser/view/PRJNA266417 None [Overal design]67NR and 4T1mouse breast carcinoma cell lines were injected into fourth mammary fat pad; lung tissue was collected when tumor reached volume of 50mm3. RNA was extracted using Qiagen kit.; [Treatment]'Six days after tumor cell inoculation (or when tumors reached about 50 mm3), mice were euthanized, and lungs were perfused with PBS to completely remove blood from the lung vasculature. Cleaned lung lobes were immersed in RNAlater (Qiagen) to stabilize RNA.'; [Growth]'BALB/c mice were injected with nonmetastatic 67NR or metastatic 4T1 cells. Control (naïve) mice received PBS only.'; [Extraction]'Total DNA-free RNA was prepared from PBS-perfused lungs with the RNeasy kit (Qiagen) according to the manufacturer’s protocol'; [Cell type]'Source: ''strain: BALB/c; treatment: 4T1 mouse breast carcinoma cell line injected into fourth mammary fat pad of BALB/c mouse; tissue: Lung, Metastatic; ', 'strain: BALB/c; treatment: 67NR mouse breast carcinoma cell line injected into fourth mammary fat pad of BALB/c mouse; tissue: Lung, Non-metastatic; ', 'strain: BALB/c; treatment: PBS control; tissue: Lung, Normal; ' GSE15311 Mus musculus 280 Expression profiling by SAGE GPL11 Cancer Genome Anatomy Project (CGAP) Mouse SAGE 2009-03-19 This series represents the Cancer Genome Anatomy Project SAGE library collection. Libraries contained herein were either produced through CGAP funding, or donated to CGAP. The Cancer Genome Anatomy Project (CGAP: http://cgap.nci.nih.gov) is an interdisciplinary program established and administered by the National Cancer Institute (NCI: http://www.nci.nih.gov) to generate the information and technological tools needed to decipher the molecular anatomy of the cancer cell. SAGE libraries are named according to the following convention: * SAGE_Organ_histology_code_unique identifier, e.g., SAGE_Colon_adenocarcinoma_CL_Caco2 * Codes: B = bulk; CL = cell line; CS = short-term cell culture; MD = micro-dissected; AP = antibody purified. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15311 An anatomy of normal and malignant gene expression. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.152324199 {Human molecular genetics (4.544) doi:10.1093/hmg/10.7.663}; {Proceedings of the National Academy of Sciences of the United States of America (9.580) doi:10.1073/pnas.152324199}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA115841 https://www.ebi.ac.uk/ena/browser/view/PRJNA115841 None [Overal design]280 libraries; [Treatment]'None'; [Growth]'None'; [Extraction]'N/A'; [Cell type]'Adrenal glands', 'Source: ', 'normal', 'medulloblastoma tumor from a patch +/- heterozygous KO mouse.', 'Visual Cortex', 'Brain - Visual Cortex', 'Future forebrain', 'Whole telencephalon', 'Dorsal Telencephalon', 'ventral telencephalon', 'Brain - Optic Cup', 'Diencephalon', 'Brain - SVZ/VZ. Ventral Telencephalon', 'Brain - SVZ/VZ. Dorsal Telencephalon', 'prestriatum', 'hypothalamus', 'epithalamus', 'Branchial Arch', 'Cerebellar granule cell precursor', 'normal cerebellar granule cell precursors', 'normal granular cell precursors', 'Fertilized eggs', 'Whole embryo - extra-embryonic tissue', 'Morula', 'Blastocysts, dividing egg', 'Ventricles', 'Large intestine - mesoderm', 'large intestine', 'Mammary Adenocarcinoma', 'Mammary adenocarcinoma', 'Normal mammary gland', 'Normal mouse mammary epithelium', 'Normal mouse mammary epithelium pseudopregnant', 'Normal mouse mammary epithelium, pseudopregnant', 'Inguinal without lymph node (L+R)', 'Mammary gland at 5 days lactation, Inguinal without lymph node (L+R)', '6 days post weaning, Inguinal without lymph node (L+R)', 'pregnancy stage TS15 (9.5dpc), Inguinal without lymph node (L+R)', 'Embryo - ectoplacental cone', 'Normal epidermis', 'Skin Squamous Cell Carcinomas, pool', 'small intestine - mesenchyme', 'small intestine', 'urogenital sinus epithelium', 'Mesenchyme', 'Urogenital sinus female', '18.5 days, whole mouse embryo''organ/tissue: adrenal gland; tissue preparation: microscope dissected; age: P84; sex: unknown; cell type: Adrenal glands; ', 'organ/tissue: adrenal gland; tissue preparation: microscope dissected; age: TS22; sex: unknown; ', 'organ/tissue: bladder; tissue preparation: microscope dissected; age: P84; sex: unknown; ', 'organ/tissue: bladder; tissue preparation: microscope dissected; age: TS22; sex: unknown; ', 'organ/tissue: bladder; tissue preparation: microscope dissected; age: 16.5 days post coitum. reposition of umbilical hernia. theiler stage 24; sex: unknown; ', 'organ/tissue: bone marrow; tissue preparation: flow-sorted; sex: unknown; other information: CBA/Ca mouse bone marrow was cultured for 7 days in GM-CSF to generate dendritic cells (>90% CD11c+). [SAGEMap name: bmDC (mouse)]; ', 'organ/tissue: bone marrow; tissue preparation: flow-sorted; sex: unknown; other information: CBA/Ca mouse bone marrow was cultured with GM-CSF for 9 days to generate dendritic cells. Recombinant mouse IL-10(20ng/ml) was added from day 6 and bacterial derived LPS also added for the last 20 hrs of culture. [SAGEMap name: bmDC (IL-10+LPS)]; ', 'organ/tissue: bone marrow; tissue preparation: flow-sorted; sex: unknown; other information: CBA/Ca mouse bone marrow cells were culture with GM-CSF for 7 days in the presence of 1 alpha 25 dihydroxyvitamin D3 (10^-7M) from day 3. [SAGEMap name: bmDC (Vitamin D3 treated)]; ', 'organ/tissue: bone marrow; tissue preparation: flow-sorted; sex: unknown; other information: CBA/Ca mouse bone marrow was cultured in GM-CSF for 6 days to generate dendritic cells. These were treated for a further 36 hrs with recombinant mouse IL-10. [SAGEMap name: bmDC (IL-10 treated)]; ', 'organ/tissue: bone; tissue preparation: microscope dissected; age: P84; sex: unknown; cell type: normal; ', 'organ/tissue: cerebellum; tissue preparation: bulk; sex: unknown; cell type: medulloblastoma tumor from a patch +/- heterozygous KO mouse.; mutations: germline patch KO mouse; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: P07; sex: unknown; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: P07; sex: unknown; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: post natal day 20; sex: male; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: post natal day 27; sex: male; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: 27d; sex: male; cell type: Visual Cortex; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: 27d; sex: male; cell type: Brain - Visual Cortex; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: P27; sex: male; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: P35; sex: unknown; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: P35; sex: unknown; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: 42d; sex: unknown; cell type: Visual Cortex; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: p84; sex: unknown; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: P84; sex: unknown; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: P84-P90; sex: male; cell type: normal; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: 104d; sex: male; cell type: Brain - Visual Cortex; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: p84; sex: male; ', 'organ/tissue: brain; tissue preparation: other; age: P84-P90; sex: male; cell type: normal; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: TS13; sex: unknown; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: TS13; sex: unknown; cell type: Future forebrain; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: TS15; sex: unknown; cell type: Whole telencephalon; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: E9.5/TS15; sex: unknown; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: TS17; sex: unknown; cell type: Dorsal Telencephalon; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: TS17; sex: unknown; cell type: ventral telencephalon; ', 'organ/tissue: eye; tissue preparation: microscope dissected; age: TS17; sex: male; cell type: Brain - Optic Cup; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: TS17; sex: unknown; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: TS19; sex: unknown; cell type: Diencephalon; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: E11.5/TS19; sex: unknown; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: TS20; sex: male; cell type: Brain - SVZ/VZ. Ventral Telencephalon; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: TS20; sex: unknown; cell type: Brain - SVZ/VZ. Dorsal Telencephalon; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: TS20; sex: unknown; cell type: prestriatum; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: TS20; sex: unknown; cell type: hypothalamus; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: TS20; sex: unknown; cell type: epithalamus; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: E12.5/TS20; sex: unknown; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: E12.5T/S20; sex: unknown; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: E13.5/TS21; sex: unknown; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: E13.5; sex: male; cell type: normal; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: E13.5; sex: male; cell type: normal; mutations: fierce; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: E13.5; sex: male; cell type: normal; mutations: Tg(Hum); ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: E13.5/TS21; sex: unknown; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: E15.5; sex: male; cell type: normal; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: E15.5; sex: male; cell type: normal; mutations: Tg(Hum); ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: E15.5; sex: male; cell type: normal; mutations: fierce; ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: E15.5/TS23; sex: unknown; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: E17.5/TS25; sex: unknown; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: E17.5; sex: male; cell type: normal; mutations: fierce; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: E17.5; sex: male; cell type: normal; ', 'organ/tissue: brain; tissue preparation: laser capture microdissected; age: E17.5; sex: male; cell type: normal; mutations: Tg(Hum); ', 'organ/tissue: brain; tissue preparation: microscope dissected; age: TS25; sex: male; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: TS15; sex: unknown; cell type: Branchial Arch; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: TS17; sex: unknown; cell type: Branchial Arch; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: TS17; sex: unknown; ', 'organ/tissue: cerebellum; tissue preparation: cell line; age: postnatal day 8; sex: unknown; cell type: Cerebellar granule cell precursor; mutations: none; other information: Granule cell precursor isolated on postnatal day 8 and cultured for 18 hr in serum-free medium containing 3 ug/ml sonic hedgehog. Matched untreated Granular Cell control is mSAGE_Cerebellum_CS_GCPcontrol; ', 'organ/tissue: cerebellum; tissue preparation: short term culture; age: postnatal day 8; sex: unknown; cell type: normal cerebellar granule cell precursors; mutations: none; other information: Mouse primary granule cell precursors, isolated on postnatal day 8 and cultured for 18 hours in serum-free medium. Matched control for mSAGE_Cerebellum_CP_GCP+SHH (sonic hedgehog treated precursor cells).; ', 'organ/tissue: cerebellum; tissue preparation: other; age: postnatal day 8; sex: unknown; cell type: normal granular cell precursors; mutations: none; other information: Granular cell precursor cells from normal, 8-day old mice were purified by enzymatic digestion and percoll gradient centrifugation, pelleted and snap-frozen.; ', 'organ/tissue: whole body; tissue preparation: microscope dissected; sex: male and female; cell type: Fertilized eggs; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: TS10; sex: male and female; ', 'organ/tissue: other; tissue preparation: microscope dissected; age: TS10; sex: unknown; cell type: Whole embryo - extra-embryonic tissue; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: 7.5 dpc/TS11; sex: unknown; ', 'organ/tissue: whole body; tissue preparation: microscope dissected; age: TS3; sex: unknown; cell type: Morula; ', 'organ/tissue: other; tissue preparation: microscope dissected; age: 6.5 dpc/TS8; sex: unknown; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: E6.5; sex: unknown; cell type: normal; mutations: Foxa2 -/-; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: E6.5; sex: unknown; cell type: normal; mutations: Foxh1 -/-; ', 'organ/tissue: whole body; tissue preparation: microscope dissected; age: TS5; sex: male and female; cell type: Blastocysts, dividing egg; ', 'organ/tissue: whole body; tissue preparation: microscope dissected; age: 5.5 dpc/TS7; sex: unknown; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: E7.5; sex: unknown; cell type: normal; mutations: Foxh1 -/-; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: E7.5; sex: unknown; cell type: normal; mutations: Foxa2 -/-; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: 6.5 dpc/TS9; sex: unknown; ', 'organ/tissue: stem cell; tissue preparation: microscope dissected; age: cells; sex: unknown; ', 'organ/tissue: stem cell; tissue preparation: microscope dissected; age: Unspecified; sex: unknown; cell type: normal; ', 'organ/tissue: stem cell; tissue preparation: cell line; sex: unknown; other information: Dendritic cells were produced by directed differentiation of the CBA/Ca mouse derived embryonic stem cell line ESF 116 (Fairchild et al, Curr. Biol. 10:1515-8 (2000)).; ', 'organ/tissue: stem cell; tissue preparation: cell line; sex: unknown; other information: Dendritic cells were generated from the CBA/Ca mouse derived embryonic stem cell line ESF 116 (Fairchild P., et al., Curr. Biol. 10:1515-8 (2000)). These were mature by treatment with bacterial derived LPS overnight (Fairchild et al, Methods in Enzymology, in press (2003)). cDNA was preamplified (SMART) before SAGE analysis. [SAGEMap name: ES derived DCs (LPS treated)]; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: 8.0 dpc/TS12; sex: unknown; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: TS13; sex: unknown; ', 'organ/tissue: esophagus; tissue preparation: microscope dissected; age: 12.5 dpc/TS20; sex: unknown; ', 'organ/tissue: esophagus; tissue preparation: microscope dissected; age: 16.5 dpc/TS24; sex: unknown; ', 'organ/tissue: uncharacterized tissue; tissue preparation: cell line; sex: unknown; ', 'organ/tissue: limb; tissue preparation: bulk; sex: unknown; other information: SAGE expression profile of developing forelimb. Used to define unique patterns of transcription between developing forelimbs and hindlimbs. (NCBI name: mouse_forelimb); ', 'organ/tissue: heart; tissue preparation: microscope dissected; age: 8.5 dpc/TS13; sex: unknown; ', 'organ/tissue: heart; tissue preparation: microscope dissected; age: TS14; sex: unknown; ', 'organ/tissue: heart; tissue preparation: microscope dissected; age: TS15; sex: unknown; ', 'organ/tissue: heart; tissue preparation: microscope dissected; age: 9.5 dpc/TS15; sex: unknown; ', 'organ/tissue: heart; tissue preparation: microscope dissected; age: 11.5 days post coitum. lens vesicle completely separated from surface. theiler stage 19; sex: unknown; ', 'organ/tissue: heart; tissue preparation: microscope dissected; age: TS19; sex: unknown; cell type: Ventricles; ', 'organ/tissue: heart; tissue preparation: microscope dissected; age: 12.5 days post coitum. earliest signs of fingers. theiler stage 20; sex: unknown; ', 'organ/tissue: heart; tissue preparation: microscope dissected; age: E8.5; sex: unknown; cell type: normal; mutations: Foxh1 -/-; ', 'organ/tissue: limb; tissue preparation: bulk; sex: unknown; other information: SAGE expression profile of developing hindlimbs. Used to define unique patterns of transcription between developing forelimbs and hindlimbs. (NCBI name: mouse_hindlimb); ', 'organ/tissue: brain; tissue preparation: bulk; sex: unknown; other information: Two wild house mice lines were genetically selected for short and long attack latency. Mice with an attack latency >600s were considered long attack latency mice (LAL). RNA from the hippocampus of 14 LAL mice was pooled and used as input material for a SAGE library. (NCBI name: mouse hippocampus: long attack latency (LAL) mice); ', 'organ/tissue: brain; tissue preparation: bulk; sex: unknown; other information: Two wild house mice lines were genetically selected for short and long attack latency. Mice with an attack latency <50s were considered short attack latency mice (SAL). RNA from the hippocampus of 14 SAL mice was pooled and used as input material for the SAGE library. (NCBI nmae: mouse hippocampus: short attack latency (SAL) mice); ', 'organ/tissue: brain; tissue preparation: bulk; age: 7 weeks; sex: male; mutations: Wildtype; ', 'organ/tissue: kidney; tissue preparation: microscope dissected; age: TS27; sex: unknown; ', 'organ/tissue: kidney; tissue preparation: microscope dissected; age: 12 weeks; sex: unknown; ', 'organ/tissue: kidney; tissue preparation: microscope dissected; age: E12/ TS20; sex: unknown; ', 'organ/tissue: kidney; tissue preparation: microscope dissected; age: TS19; sex: unknown; ', 'organ/tissue: kidney; tissue preparation: microscope dissected; age: E12/TS20; sex: unknown; ', 'organ/tissue: kidney; tissue preparation: microscope dissected; age: TS24; sex: unknown; ', 'organ/tissue: gastrointestinal tract; tissue preparation: microscope dissected; age: TS20; sex: unknown; cell type: Large intestine - mesoderm; ', 'organ/tissue: tissues; tissue preparation: microscope dissected; age: E12; sex: unknown; cell type: normal; ', 'organ/tissue: gastrointestinal tract; tissue preparation: microscope dissected; age: 12.5 dpc/TS20; sex: unknown; ', 'organ/tissue: gastrointestinal tract; tissue preparation: microscope dissected; age: TS25; sex: unknown; cell type: large intestine; ', 'organ/tissue: limb; tissue preparation: microscope dissected; age: 10.5 dpc/TS17; sex: unknown; ', 'organ/tissue: limb; tissue preparation: microscope dissected; age: TS22; sex: male and female; ', 'organ/tissue: limb; tissue preparation: microscope dissected; age: 13.5 dpc/TS22; sex: unknown; mutations: Pax3 -/-; ', 'organ/tissue: limb; tissue preparation: microscope dissected; age: 15.5 dpc/TS23; sex: unknown; ', 'organ/tissue: liver; tissue preparation: microscope dissected; age: adult; sex: male; ', 'organ/tissue: liver; tissue preparation: microscope dissected; age: 12.5 days post coitum. earliest signs of fingers. theiler stage 20; sex: unknown; ', 'organ/tissue: liver; tissue preparation: microscope dissected; age: 9.5 dpc/TS15; sex: unknown; ', 'organ/tissue: liver; tissue preparation: microscope dissected; age: 18.5 dpc/TS26; sex: unknown; ', 'organ/tissue: lung; tissue preparation: microscope dissected; age: TS27; sex: unknown; ', 'organ/tissue: lung; tissue preparation: other; age: P109; sex: male; cell type: normal; ', 'organ/tissue: lung; tissue preparation: microscope dissected; age: 11.5 dpc/TS19; sex: unknown; ', 'organ/tissue: lung; tissue preparation: microscope dissected; age: TS19; sex: unknown; ', 'organ/tissue: lung; tissue preparation: microscope dissected; age: TS25; sex: unknown; ', 'organ/tissue: lung; tissue preparation: microscope dissected; age: TS26; sex: unknown; ', 'organ/tissue: lymph node; tissue preparation: microscope dissected; age: P63; sex: male; cell type: normal; mutations: PBCrePten(flox/flox); ', 'organ/tissue: lymph node; tissue preparation: microscope dissected; age: P63; sex: male; cell type: normal; mutations: PBCrePten(flox/-); ', 'organ/tissue: lymph node; tissue preparation: microscope dissected; age: P84; sex: unknown; other information: lymph nodes, mesenteric; ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 10 months; sex: female; cell type: Mammary Adenocarcinoma; mutations: p53; other information: P53 mammary tumor (TG7) derived from the PNIa transplantable mammary duct outgrowth line, Balb/C mice Medina et al. FASEB J., 2002; 16(8):881-3); ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 10 months; sex: female; cell type: Mammary adenocarcinoma; mutations: p53; other information: P53 mammary tumor (T2532 ) derived from mammary isograft in untreated Balb/C mice.; ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 10 months; sex: female; cell type: Mammary adenocarcinoma; mutations: p53; other information: P53 mammary tumor (T2539) derived from mammary isograft in untreated Balb/C mice.; ', 'organ/tissue: mammary gland; tissue preparation: bulk; sex: female; cell type: Normal mammary gland; mutations: C3(1)SV40 Tag; other information: Bulk mammary gland from C3(1)SV40 Tag untreated mice. Pool; ', 'organ/tissue: mammary gland; tissue preparation: bulk; sex: female; cell type: Normal mammary gland; mutations: C3(1)SV40 Tag; other information: Bulk mammary gland from C3(1)SV40 Tag mice treated with LGD1069 (RXR ligand). Pool; ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 15 weeks; sex: female; cell type: Normal mouse mammary epithelium; mutations: p53; other information: Balb/c mammary epithelium from transplants grown into cleared fat pads of syngeneic hosts. Genotype = P53 mammary gland transplants, that received no treatment, harvested 7 wks post-transplatation. Ref. Oncogene (2002) 21, 6366-6376; ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 15 wk; sex: female; cell type: Normal mouse mammary epithelium pseudopregnant; mutations: p53; other information: Balb/c mammary epithelium from transplants grown into cleared fat pads of syngeneic hosts. Genotype = P53 mammary gland transplants, that received hormonal treatment by means of pituitary isografts, harvested 7 wk post-transplatation and 5 wk of hormonal treatment. Ref. Oncogene (2002) 21, 6366-6376; ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 15 weeks; sex: female; cell type: Normal mouse mammary epithelium; mutations: p53 wild type; other information: Balb/c mammary epithelium from transplants grown into cleared fat pads of syngeneic hosts. Genotype = P53wild type mammary gland, transplants that received no treatment, harvested 7 wks post-transplatation. Ref. Oncogene (2002) 21, 6366-6376; ', 'organ/tissue: mammary gland; tissue preparation: bulk; age: 15 wk; sex: female; cell type: Normal mouse mammary epithelium, pseudopregnant; mutations: p53 wild type; other information: Balb/c mammary epithelium from transplants grown into cleared fat pads of syngeneic hosts. Genotype = P53 wild type mammary gland transplants, that received hormonal treatment by means of pituitary isografts, harvested 7 wk post-transplatation and 5 wk of hormonal treatment. Ref. Oncogene (2002) 21, 6366-6376; ', 'organ/tissue: mammary gland; tissue preparation: microscope dissected; age: 35d; sex: female; cell type: Inguinal without lymph node (L+R); ', 'organ/tissue: mammary gland; tissue preparation: microscope dissected; age: p84; sex: female; cell type: Mammary gland at 5 days lactation, Inguinal without lymph node (L+R); ', 'organ/tissue: mammary gland; tissue preparation: microscope dissected; age: 12w; sex: female; cell type: 6 days post weaning, Inguinal without lymph node (L+R); ', 'organ/tissue: mammary gland; tissue preparation: microscope dissected; age: 12w; sex: female; cell type: pregnancy stage TS15 (9.5dpc), Inguinal without lymph node (L+R); ', 'organ/tissue: mammary gland; tissue preparation: microscope dissected; sex: female; ', 'organ/tissue: embryonic tissue; tissue preparation: cell line; sex: unknown; ', 'organ/tissue: muscle; tissue preparation: microscope dissected; age: TS25; sex: unknown; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: 8.5 dpc/TS13; sex: unknown; ', 'organ/tissue: ovary; tissue preparation: microscope dissected; age: P0 /TS27; sex: female; ', 'organ/tissue: ovary; tissue preparation: microscope dissected; age: 21d; sex: female; ', 'organ/tissue: ovary; tissue preparation: microscope dissected; age: TS22; sex: female; ', 'organ/tissue: pancreas; tissue preparation: microscope dissected; age: 6 weeks; sex: unknown; ', 'organ/tissue: pancreas; tissue preparation: microscope dissected; age: 10 weeks; sex: unknown; ', 'organ/tissue: pancreas; tissue preparation: microscope dissected; age: 10.5 dpc/TS17; sex: unknown; other information: PDX1 Pancreas GFP+, SAGELite; ', 'organ/tissue: pancreas; tissue preparation: microscope dissected; age: 12.5 dpc/TS20; sex: unknown; other information: NGN3 Pancreas GFP+, SAGELite; ', 'organ/tissue: pancreas; tissue preparation: microscope dissected; age: 12.5 dpc/TS20; sex: unknown; other information: NGN3 Pancreas GFP-, SAGELite; ', 'organ/tissue: pancreas; tissue preparation: other; age: E13.5; sex: unknown; cell type: normal; mutations: NGN3 GFP+; ', 'organ/tissue: pancreas; tissue preparation: microscope dissected; age: 14.5 days post coitum. fingers separate distally. theiler stage 22; sex: unknown; ', 'organ/tissue: pancreas; tissue preparation: microscope dissected; age: E14.5; sex: unknown; cell type: normal; mutations: WT Tle6; ', 'organ/tissue: pancreas; tissue preparation: microscope dissected; age: E14.5; sex: unknown; cell type: normal; mutations: Tle 6; ', 'organ/tissue: pancreas; tissue preparation: microscope dissected; age: 16.5 days post coitum. reposition of umbilical hernia. theiler stage 24; sex: unknown; ', 'organ/tissue: pancreas; tissue preparation: microscope dissected; age: 18.5 days post coitum. long whiskers. theiler stage 26; sex: unknown; ', 'organ/tissue: pituitary gland; tissue preparation: microscope dissected; age: P0/TS27; sex: unknown; ', 'organ/tissue: tissues; tissue preparation: microscope dissected; age: P0; sex: male; cell type: normal; ', 'organ/tissue: pituitary gland; tissue preparation: microscope dissected; age: P84; sex: male; ', 'organ/tissue: pituitary; tissue preparation: microscope dissected; age: 14.5 dpc/TS23; sex: unknown; ', 'organ/tissue: other; tissue preparation: microscope dissected; age: TS10; sex: unknown; cell type: Embryo - ectoplacental cone; ', 'organ/tissue: placenta; tissue preparation: microscope dissected; age: TS15; sex: unknown; ', 'organ/tissue: placenta; tissue preparation: microscope dissected; age: TS22; sex: unknown; ', 'organ/tissue: prostate; tissue preparation: microscope dissected; age: TS27; sex: male; ', 'organ/tissue: prostate; tissue preparation: microscope dissected; age: P63; sex: unknown; cell type: normal; mutations: Pten -/-; ', 'organ/tissue: prostate; tissue preparation: microscope dissected; age: P63; sex: male; cell type: normal; mutations: Pten +/-; ', 'organ/tissue: prostate; tissue preparation: microscope dissected; age: P84; sex: male; ', 'organ/tissue: retina; tissue preparation: bulk; age: Postnatal day 0.5; sex: male and female; mutations: Wildtype; other information: Postnatal 0.5 whole retina (consists of a number of individuals of different sexes). Strain=C57BL/6.; ', 'organ/tissue: retina; tissue preparation: bulk; age: Postnatal day 10.5; sex: male and female; mutations: Wildtype; other information: Postnatal 10.5 whole retina (consists of a number of individuals of different sexes). Strain= C57BL/6 x Sv129.; ', 'organ/tissue: retina; tissue preparation: bulk; age: Postnatal day 10.5; sex: male and female; mutations: Crx; other information: Postnatal 10.5 whole retina of mice homozygous for a mutation in the Crx gene (consists of a number of individuals of different sexes). Strain=C57BL/6 x Sv129.; ', 'organ/tissue: retina; tissue preparation: bulk; age: Postnatal day 2.5; sex: male and female; mutations: Wildtype; other information: Postnatal 2.5 whole retina (consists of a number of individuals of different sexes). Strain=C57BL/6.; ', 'organ/tissue: retina; tissue preparation: bulk; age: Postnatal day 4.5; sex: male and female; mutations: Wildtype; other information: Postnatal 4.5 whole retina (consists of a number of individuals of different sexes). Strain=C57BL/6.; ', 'organ/tissue: retina; tissue preparation: bulk; age: Postnatal day 6.5; sex: male and female; mutations: Wildtype; other information: Postnatal 6.5 whole retina (consists of a number of individuals of different sexes). Strain=C57BL/6.; ', 'organ/tissue: retina; tissue preparation: bulk; age: 7 weeks; sex: male; mutations: Wildtype; other information: Postnatal day ~50 adult male whole retina. Strain=C57BL/6.; ', 'organ/tissue: retina; tissue preparation: microscope dissected; age: 7 weeks; sex: male; mutations: Wildtype; other information: Postnatal day ~50 adult male microdissected photoreceptor layer of retina. Strain=C57BL/6.; ', 'organ/tissue: retina; tissue preparation: bulk; age: Embryonic day 12.5; sex: male and female; mutations: Wildtype; other information: Embryonic 12.5 whole retina (consists of a number of individuals of different sexes). Strain=C57BL/6.; ', 'organ/tissue: retina; tissue preparation: bulk; age: Embryonic day 14.5; sex: male and female; mutations: Wildtype; other information: Embryonic 14.5 whole retina (consists of a number of individuals of different sexes). Strain=C57BL/6.; ', 'organ/tissue: retina; tissue preparation: bulk; age: Embryonic day 16.5; sex: male and female; mutations: Wildtype; other information: Embryonic 16.5 whole retina (consists of a number of individuals of different sexes). Strain=C57BL/6.; ', 'organ/tissue: retina; tissue preparation: bulk; age: Embryonic day 18.5; sex: male and female; other information: Embryonic 18.5 whole retina (consists of a number of individuals of different sexes). Strain=C57BL/6.; ', 'organ/tissue: skin; tissue preparation: bulk; age: 6-8 wk; sex: female; cell type: Normal epidermis; mutations: none; other information: Epidermal scrapes from the dorsal skin of female SKH-1 mice, untreated. Pool of various female mice.; ', 'organ/tissue: skin; tissue preparation: bulk; age: 6-8 wk; sex: female; cell type: Normal epidermis; mutations: E2F1; other information: Epidermal scrapes from the dorsal skin of female SKH-1, Genotype= E2F1 mice, untreated. Pool of various female mice.; ', 'organ/tissue: skin; tissue preparation: bulk; age: 6-8 wk; sex: female; cell type: Normal epidermis; mutations: E2F1; other information: Epidermal scrapes from the dorsal skin of female SKH-1, Genotype = E2F1 mice, treated with UV light irradiation (8h post-treatment). Pool of various female mice.; ', 'organ/tissue: skin; tissue preparation: bulk; age: 6-8 wk; sex: female; cell type: Normal epidermis; mutations: E2F1 wild type; other information: Epidermal scrapes from the dorsal skin of female SKH-1, Genotype = E2F1 Wild type mice, untreated. Pool of various female mice.; ', 'organ/tissue: skin; tissue preparation: bulk; age: 6-8 wk; sex: female; cell type: Normal epidermis; mutations: E2F1 wild type; other information: Epidermal scrapes from the dorsal skin of female SKH-1, Genotype = E2F1 Wild type mice, treated with UV light irradiation (8h post-treatment). Pool of various female mice.; ', 'organ/tissue: skin; tissue preparation: microscope dissected; age: P84; sex: male; cell type: normal; ', 'organ/tissue: skin; tissue preparation: microscope dissected; age: 13.5 dpc/TS21; sex: unknown; ', 'organ/tissue: skin; tissue preparation: microscope dissected; age: E13.5; sex: unknown; cell type: normal; ', 'organ/tissue: skin; tissue preparation: microscope dissected; age: 16.5 dpc/TS24; sex: unknown; ', 'organ/tissue: skin; tissue preparation: bulk; age: 30 wk; sex: female; cell type: Skin Squamous Cell Carcinomas, pool; other information: Skin Squamous Cell Carcinomas induced in SKH-1 female mice by UV irradiation. Pool of various tumors.; ', 'organ/tissue: gastrointestinal tract; tissue preparation: microscope dissected; age: TS20; sex: unknown; cell type: small intestine - mesenchyme; ', 'organ/tissue: gastrointestinal tract; tissue preparation: microscope dissected; age: 12.5 dpc TS20; sex: unknown; ', 'organ/tissue: gastrointestinal tract; tissue preparation: microscope dissected; age: TS25; sex: unknown; cell type: small intestine; ', 'organ/tissue: spleen; tissue preparation: microscope dissected; age: P84; sex: unknown; ', 'organ/tissue: spleen; tissue preparation: microscope dissected; age: 16.5 days post coitum. reposition of umbilical hernia. theiler stage 22; sex: unknown; ', 'organ/tissue: spleen; tissue preparation: microscope dissected; age: TS23; sex: unknown; ', 'organ/tissue: spleen; tissue preparation: microscope dissected; age: 18.5 days post coitum. long whiskers. theiler stage 26; sex: unknown; ', 'organ/tissue: stomach; tissue preparation: microscope dissected; age: TS20; sex: unknown; ', 'organ/tissue: stomach; tissue preparation: microscope dissected; age: TS25; sex: male and female; ', 'organ/tissue: white blood cells; tissue preparation: flow-sorted; age: 6-10 wks; sex: unknown; other information: LCMV specific CD8 T cells tranferred to LCMV infected syngeneic animals, then isolated from spleen.; ', 'organ/tissue: white blood cells; tissue preparation: flow-sorted; age: 6-10 wks; sex: unknown; other information: LCMV specific CD8 T cells tranferred to uninfected syngeneic animals, then isolated from spleen.; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; sex: unknown; other information: CD4+CD25negative spleen cells were purified from naive CBA/Ca mice by MACS sorting. T cells were activated overnight by solid phase anti-CD3. cDNA was preamplified (SMART) before SAGE analysis. [SAGEMap name: CD4+CD25neg activated]; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; sex: unknown; other information: CD4+CD25negative spleen cells were purified from naive CBA/Ca mice by MACS sorting. cDNA was preamplified (SMART) before SAGE analysis.[SAGEMap name: CD4+CD25neg spleen]; ', 'organ/tissue: white blood cells; tissue preparation: antibody purified; sex: unknown; other information: CD4+CD25+ T cells were purified from naive CBA/Ca mouse spleen cells by MACS sorting. cDNA was preamplified (SMART) before SAGE analysis. [SAGEMap name: CD4+CD25+ spleen]; ', 'organ/tissue: white blood cells; tissue preparation: cell line; sex: unknown; ', 'organ/tissue: white blood cells; tissue preparation: flow-sorted; age: 6-10 wks; sex: unknown; other information: Intra-epithelial lymphocytes from mouse small intestine expressing T cell receptor alpha/beta.; ', 'organ/tissue: white blood cells; tissue preparation: flow-sorted; age: 6-10 wks; sex: unknown; other information: Intra-epithelial lymphocytes from mouse small intestine expressing T cell receptor gamma/delta.; ', 'organ/tissue: white blood cells; tissue preparation: cell line; sex: unknown; other information: A CD4+ Treg/Tr1-like H-Y + H2Ek specific line grown from the accepted male skin grafts of female A1(M) TCR transgenic mice. mRNA was derived from CD4+ T cells (>99%) 7 days from last stimulation, and contains <0.1% mast cells. cDNA was preamplified (SMART) before SAGE analysis.[SAGEMap name: Treg line SKA from skin graft]; ', 'organ/tissue: testis; tissue preparation: microscope dissected; age: P1; sex: male; ', 'organ/tissue: testis; tissue preparation: microscope dissected; age: P21; sex: male; ', 'organ/tissue: testis; tissue preparation: microscope dissected; age: p84; sex: male; ', 'organ/tissue: testis; tissue preparation: bulk; sex: unknown; other information: Adult mice were treated with busulphan (30mg/Kg). RNA was extracted from testes 60 days later. At this stage the testes were largely devoid of germ-cells. (NCBI name: Adult testis -somatic cells); ', 'organ/tissue: testis; tissue preparation: bulk; sex: unknown; other information: RNA was extracted from testes of Wv/Wv fetuses at day 18 post coitum. These testes are largely devoid of germ cells and SAGE library will represent somatic cells of the fetal testis. (NCBI name: fetal testis somatic cells); ', 'organ/tissue: testis; tissue preparation: microscope dissected; age: TS22; sex: male; ', 'organ/tissue: testis; tissue preparation: microscope dissected; age: TS24; sex: male; ', 'organ/tissue: thymus; tissue preparation: microscope dissected; age: P84; sex: male; ', 'organ/tissue: thymus; tissue preparation: microscope dissected; age: TS23; sex: unknown; ', 'organ/tissue: thymus; tissue preparation: microscope dissected; age: 18.5 days post coitum. long whiskers. theiler stage 26; sex: unknown; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: TS24; sex: male; cell type: urogenital sinus epithelium; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: 16.5 days post coitum. reposition of umbilical hernia. theiler stage 24; sex: male; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: TS24; sex: male; cell type: Mesenchyme; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: TS24; sex: female; cell type: Urogenital sinus female; ', 'organ/tissue: embryonic tissue; tissue preparation: microscope dissected; age: 16.5 dpc/TS24; sex: female; ', 'organ/tissue: uterus; tissue preparation: microscope dissected; age: P0/TS27; sex: female; ', 'organ/tissue: uterus; tissue preparation: microscope dissected; age: p21; sex: female; ', 'organ/tissue: vascular; tissue preparation: antibody purified; sex: unknown; ', 'organ/tissue: whole body; tissue preparation: cell line; sex: unknown; ', 'organ/tissue: whole body; tissue preparation: cell line; sex: unknown; other information: SAGE identification of differentiation responsive genes in P19 embryonic cells induced to form cardiomyocytes in vitro. P19 embryonic carcinoma (EC) cells, induced to form cardiomyocytes in vitro, day 3+0.5 of differentiation protocol. Total number of 51,822 SAGE tags sequenced. 50,983 SAGE tags analyzed after clean-up (extraction of poly(A) tags, linker-generated tags, and tags originated from clones producing 4 tags or less). (NCBI name: P19 embryonic carcinoma (EC) cells, day 3+0.5); ', 'organ/tissue: whole body; tissue preparation: cell line; sex: unknown; other information: SAGE identification of differentiation responsive genes in P19 embryonic cells induced to form cardiomyocytes in vitro. P19 embryonic carcinoma (EC) cells, induced to form cardiomyocytes in vitro, day 3+3.0 of differentiation protocol. Total number of 54,236 SAGE tags sequenced. 53,022 SAGE tags analyzed after clean-up (extraction of poly(A) tags, linker-generated tags, and tags originated from clones producing 4 tags or less). (NCBI name: P19 embryonic carcinoma (EC) cells, day 3+3.0); ', 'organ/tissue: whole body; tissue preparation: cell line; sex: unknown; other information: SAGE identification of differentiation responsive genes in P19 embryonic cells induced to form cardiomyocytes in vitro. Undifferentiated P19 embryonic carcinoma (EC) cells. Total number of 65,677 SAGE tags sequenced. 64,952 SAGE tags analyzed after clean-up (extraction of poly(A) tags, linker-generated tags, and tags originated from clones producing 4 tags or less). (NCBI name: Undifferentiated P19 embryonic carcinoma (EC) cells; ', 'organ/tissue: whole body; tissue preparation: bulk; age: 18.5 days; sex: female; cell type: 18.5 days, whole mouse embryo; mutations: CARM; other information: Pool of 2 female Embryos 18.5 days (129/B6), treated with DES 15mg 4h prior to euthanized. Genotype = CARM; ', 'organ/tissue: whole body; tissue preparation: bulk; age: 18.5 days; sex: female; cell type: 18.5 days, whole mouse embryo; mutations: CARM wild type; other information: Pool of 2 female embryos 18.5 days (129/B6), treated with DES (diethylbestrol) 15mg, 4h prior to euthanisia. Genotype = CARM wild type; ' GSE31863 Homo sapiens 143 Expression profiling by array GPL14374 Gene expression profiling in primary breast cancer distinguishes patients developing local recurrence after breast-conservation surgery, with or without postoperative radiotherapy. 2011-09-02 Gene expression profiling of breast tumors for prognosis of local reccurence. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE31863 Gene expression profiling in primary breast cancer distinguishes patients developing local recurrence after breast-conservation surgery, with or without postoperative radiotherapy. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr1997 {Breast cancer research : BCR (5.676): 10.1186/bcr1997} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA145079 https://www.ebi.ac.uk/ena/browser/view/PRJNA145079 None [Overal design]Dual channel arrays with a tumor sample in one channel and a common reference in the other channel.; [Treatment]"Frozen tumor samples were collected from patients representing the following four groups: (a) LR+RT+ (local recurrence developed after radiotherapy), (b) LR-RT+ (no local recurrence after radiotherapy), (c) LR+RT- (local recurrence developed, no radiotherapy given), and (d) LR-RT- (no local recurrence, no radiotherapy given). All patients were operated on with breast-conservation surgery and axillary clearance with no lymph node involvement, tumor size of less than or equal to 30 mm (two patients had tumors measuring 32 and 40 mm, respectively, and one was T2 without any further information on size), tumor-free margins (>1 mm), no multicentricity, and with frozen tumor tissue with good RNA quality available. Local recurrence was defined as the appearance of a new breast tumor in the ipsilateral residual breast parenchyma in the overlying skin or in the scar. Patients with recurrence in the contralateral breast or with distant metastases prior or simultaneous to local recurrence were excluded. In the first inclusion, 102 patients from a randomized clinical trial in the South and West health care regions in Sweden and 19 patients from a population-based cohort study with a nested case-control study (Stockholm and South Sweden) were included (Tables 1 and 2). To perform gene expression profiling in a more homogenous material with regard to ER status and yet with a sufficient number of cases in all four subgroups, 22 additional ER+ tumors from the South-East and South health care regions were included in a second inclusion (Tables 1 and 2). The study was approved by the Ethics Committee at Lund University (Lund, Sweden). Patient and primary tumor characteristics and follow-up information were collected from the patients' medical records."; [Growth]'None'; [Extraction]'The samples were pulverized with a Micro-dismembrator II (B. Braun Biotech Int., Germany), and RNA was extracted using Trizol reagent (Invitrogen, Carlsbad, CA), and purified with Qiagen RNeasy Midi columns (Qiagen, Chatsworth, CA). The RNA concentration was determined using a Nanodrop Spectrophotometer (NanoDrop Technologies, Wilmington, DE). The RNA quality was assessed using an Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA) together with the reagents in the RNA 6000 Nano LabChip kit.'; [Cell type]'Source: ''series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 49; s_bioanalyzer_18s: 13.4; s_bioanalyzer_28s: 18.07; s_bioanalyzer_area: 143.98; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.35; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 23011-301; s_dnaind1: -1; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 180; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: n/a; s_meno: pre; s_original_study: SB91B; s_original_study_prog: SB91B; s_pgr_float: 440; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 5.4; s_spf_status_0low_1high: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 18; taxonomy_test_rin_float: 7.5; tissue_mg: 92.7; opdat: 19920706; extrdat: 20050101; time_in_freezer: 4562; ', 'sample type: reference; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: non_available; p_days_followup: 1918; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 57; s_bioanalyzer_18s: 9.77; s_bioanalyzer_28s: 5.11; s_bioanalyzer_area: 79.5; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.52; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: 1.13; s_dnaind2: 0.98; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 67; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 230; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 2.8; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 17; taxonomy_test_rin_float: 6.7; tissue_mg: 31; opdat: 19920708; extrdat: 20020101; time_in_freezer: 3464; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2310; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 63; s_bioanalyzer_18s: 5.41; s_bioanalyzer_28s: 4.66; s_bioanalyzer_area: 89.84; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.86; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: 1.08; s_dnaind2: 1.01; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 140; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: non_available; s_hgrade_lokrec: non_available; s_hgrade_lokrec_mitotic_count: non_available; s_hgrade_lokrec_pleomrph: non_available; s_hgrade_lokrec_tubules: non_available; s_histology_type: n/a; s_meno: Post; s_original_study: SB91A; s_pgr_float: 2; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 1.3; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; taxonomy_test_rin_float: 6.6; tissue_mg: 23; opdat: 19920928; extrdat: 20020101; time_in_freezer: 3382; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2296; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 54; s_bioanalyzer_18s: 7.6; s_bioanalyzer_28s: 8.48; s_bioanalyzer_area: 265.83; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.12; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: 1.87; s_dnaind2: 1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 300; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: non_available; s_hgrade_lokrec: non_available; s_hgrade_lokrec_mitotic_count: non_available; s_hgrade_lokrec_pleomrph: non_available; s_hgrade_lokrec_tubules: non_available; s_histology_type: n/a; s_meno: Post; s_original_study: SB91A; s_pgr_float: 0; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 17; s_spf_status_0low_1high: 1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 13; taxonomy_test_rin_float: 6.4; tissue_mg: 24; opdat: 19921102; extrdat: 20020101; time_in_freezer: 3347; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1946; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 70; s_age_above50year_0no_1yes: 1; s_age_year: 72; s_bioanalyzer_18s: 6.63; s_bioanalyzer_28s: 4.51; s_bioanalyzer_area: 237.07; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.68; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41001-301; s_dnaind1: 1.04; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 290; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Tubuloductal; s_meno: Post; s_original_study: SB91A; s_pgr_float: 260; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 2.2; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 11; taxonomy_test_rin_float: 6.1; tissue_mg: 26; opdat: 19930107; extrdat: 20020101; time_in_freezer: 3281; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1844; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 61; s_bioanalyzer_18s: 8.74; s_bioanalyzer_28s: 6.8; s_bioanalyzer_area: 367.6; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.78; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 1.9; s_dnaind2: 1.61; s_dnaind3: 0.98; s_dnaind4: -1; s_er_float: 220; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 800; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 3; s_spf_percent: 6.9; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 1; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; taxonomy_test_rin_float: 6.5; tissue_mg: 34; opdat: 19930111; extrdat: 20020101; time_in_freezer: 3277; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2292; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 64; s_bioanalyzer_18s: 9.82; s_bioanalyzer_28s: 8.4; s_bioanalyzer_area: 122.89; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.86; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 310; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 140; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 1.9; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 8; taxonomy_test_rin_float: 7; tissue_mg: 28; opdat: 19930111; extrdat: 20020101; time_in_freezer: 3277; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2416; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 65; s_bioanalyzer_18s: 10.16; s_bioanalyzer_28s: 10.11; s_bioanalyzer_area: 151.02; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.99; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 1.02; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 370; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 93; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 4.4; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 1; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; taxonomy_test_rin_float: 7.1; tissue_mg: 39; opdat: 19930125; extrdat: 20020101; time_in_freezer: 3263; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2232; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 67; s_bioanalyzer_18s: 16.26; s_bioanalyzer_28s: 18.84; s_bioanalyzer_area: 313.34; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.16; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 1.07; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 400; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_mucous; s_meno: Post; s_original_study: SB91A; s_pgr_float: 640; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 1.6; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 11; taxonomy_test_rin_float: 8.4; tissue_mg: 29; opdat: 19930316; extrdat: 20020101; time_in_freezer: 3213; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 50; s_bioanalyzer_18s: 9.44; s_bioanalyzer_28s: 11.81; s_bioanalyzer_area: 101.08; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.25; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 23010-301; s_dnaind1: -1; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 29; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: n/a; s_meno: pre; s_original_study: SB91B; s_original_study_prog: SB91B; s_pgr_float: 79; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 4.2; s_spf_status_0low_1high: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; taxonomy_test_rin_float: 6.2; tissue_mg: 60.6; opdat: 19930421; extrdat: 20050101; time_in_freezer: 4273; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 1938; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 63; s_bioanalyzer_18s: 14.7; s_bioanalyzer_28s: 16.17; s_bioanalyzer_area: 461.21; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.1; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 0.99; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 3.8; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 3; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 6.4; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 18; taxonomy_test_rin_float: 7.4; tissue_mg: 50; opdat: 19930506; extrdat: 20020101; time_in_freezer: 3162; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 1870; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 53; s_bioanalyzer_18s: 9.7; s_bioanalyzer_28s: 8.02; s_bioanalyzer_area: 202.44; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.83; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 1.39; s_dnaind2: 1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 6.8; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_medullary; s_meno: Post; s_original_study: SB91A; s_pgr_float: 2.3; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: -1; s_spf_status_0low_1high: non_available; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; taxonomy_test_rin_float: 6.9; tissue_mg: 33; opdat: 19930524; extrdat: 20020101; time_in_freezer: 3144; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 2173; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 1246; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 60; s_bioanalyzer_18s: 4.79; s_bioanalyzer_28s: 2.48; s_bioanalyzer_area: 44.27; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.52; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41013-301; s_dnaind1: 0.93; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 14; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 61; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 5; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 1; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; taxonomy_test_rin_float: 6.1; tissue_mg: 24; opdat: 19930621; extrdat: 20020101; time_in_freezer: 3116; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1919; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 57; s_bioanalyzer_18s: 7.66; s_bioanalyzer_28s: 7.1; s_bioanalyzer_area: 145.77; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.93; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 1.5; s_dnaind2: 0.98; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 100; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubular; s_meno: Post; s_original_study: SB91A; s_pgr_float: 97; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 24; s_spf_status_0low_1high: 1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; taxonomy_test_rin_float: 6.7; tissue_mg: 32; opdat: 19930811; extrdat: 20020101; time_in_freezer: 3065; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2262; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 70; s_age_above50year_0no_1yes: 1; s_age_year: 73; s_bioanalyzer_18s: 4.42; s_bioanalyzer_28s: 2.52; s_bioanalyzer_area: 244.27; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.57; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: 1.79; s_dnaind2: 2.02; s_dnaind3: 1; s_dnaind4: -1; s_er_float: 350; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 18; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 3; s_spf_percent: 9.2; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; taxonomy_test_rin_float: 5.7; tissue_mg: 26; opdat: 19931004; extrdat: 20020101; time_in_freezer: 3011; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2176; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 59; s_bioanalyzer_18s: 5.63; s_bioanalyzer_28s: -1; s_bioanalyzer_area: 164.29; s_bioanalyzer_manual: degraded; s_bioanalyzer_ratio: -1; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 94; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Lobular; s_meno: Post; s_original_study: SB91A; s_pgr_float: 300; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 4.6; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 18; taxonomy_test_rin_float: 5.6; tissue_mg: 31; opdat: 19931021; extrdat: 20020101; time_in_freezer: 2994; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_days_to_recurrence: 1127; p_local_recurrence_0no_1yes: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 60; s_bioanalyzer_18s: 11.1; s_bioanalyzer_28s: 13.6; s_bioanalyzer_area: 348.5; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.2; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: n/a; s_meno: post; s_original_study: non_available; s_pgr_float: 69; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 16; tissue_mg: 38; opdat: 19940209; extrdat: 20050101; time_in_freezer: 3979; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 49; s_bioanalyzer_18s: 4.62; s_bioanalyzer_28s: 3.56; s_bioanalyzer_area: 102.93; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.77; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: -1; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 55; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: n/a; s_meno: pre; s_original_study: SB91B; s_original_study_prog: SB91B; s_pgr_float: 180; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 3.9; s_spf_status_0low_1high: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; taxonomy_test_rin_float: 5.9; tissue_mg: 24; opdat: 19940218; extrdat: 20050101; time_in_freezer: 3970; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 1884; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 561; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 46; s_bioanalyzer_18s: 12.57; s_bioanalyzer_28s: 11.35; s_bioanalyzer_area: 108.64; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.9; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 2.63; s_dnaind2: 1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 12; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: SB91A; s_original_study_prog: SB91B; s_pgr_float: 75; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 17; s_spf_status_0low_1high: 1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 14; taxonomy_test_rin_float: 7; tissue_mg: 31; opdat: 19940221; extrdat: 20020101; time_in_freezer: 2871; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2114; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 1504; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 44; s_bioanalyzer_18s: 3.7; s_bioanalyzer_28s: 1.39; s_bioanalyzer_area: 85.14; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.37; s_bioanalyzer_rin: 5; s_bioanalyzer_rin6_0no_1yes: 0; s_clinic_code: 41013-301; s_dnaind1: 1.57; s_dnaind2: 1.71; s_dnaind3: 1; s_dnaind4: -1; s_er_float: 44; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubular; s_meno: Pre; s_original_study: SB91A; s_pgr_float: 440; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 3; s_spf_percent: 10; s_spf_status_0low_1high: 0; s_surgery_desc: 3; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; taxonomy_test_rin_float: 5.1; tissue_mg: 30; opdat: 19940309; extrdat: 20020101; time_in_freezer: 2855; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_days_to_recurrence: -1; p_local_recurrence_0no_1yes: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 47; s_bioanalyzer_18s: 13.2; s_bioanalyzer_28s: 14.8; s_bioanalyzer_area: 556.1; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.1; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 27011-301; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: n/a; s_meno: non_available; s_original_study: non_available; s_pgr_float: 270; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; tissue_mg: 53; opdat: 19941215; extrdat: 20050101; time_in_freezer: 3670; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 1519; p_days_to_death: -1; p_days_to_distant_recurrence: 1552; p_days_to_recurrence: 1413; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 61; s_bioanalyzer_18s: 7.6; s_bioanalyzer_28s: 6.73; s_bioanalyzer_area: 136.14; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.89; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 1.68; s_dnaind2: 1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 4.5; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubuloductal; s_meno: Post; s_original_study: SB91A; s_pgr_float: 8.5; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 16; s_spf_status_0low_1high: 1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 14; taxonomy_test_rin_float: 6.4; tissue_mg: 43; opdat: 19950518; extrdat: 20020101; time_in_freezer: 2420; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_days_to_recurrence: -1; p_local_recurrence_0no_1yes: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 56; s_bioanalyzer_18s: 11.5; s_bioanalyzer_28s: 20.6; s_bioanalyzer_area: 337.2; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.8; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: n/a; s_meno: non_available; s_original_study: SB91A; s_pgr_float: 79; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; tissue_mg: 60; opdat: 19950615; extrdat: 20050101; time_in_freezer: 3488; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_cause_of_death: brca; p_days_followup: 998; p_days_to_death: 998; p_days_to_distant_recurrence: 431; p_days_to_recurrence: 431; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 12; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 55; s_bioanalyzer_18s: 10.27; s_bioanalyzer_28s: 8.61; s_bioanalyzer_area: 82.3; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.84; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 1.78; s_dnaind2: 1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 82; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 0; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 10; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 13; taxonomy_test_rin_float: 6.7; tissue_mg: 34; opdat: 19951113; extrdat: 20020101; time_in_freezer: 2241; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1119; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 45; s_bioanalyzer_18s: 5.89; s_bioanalyzer_28s: 3.81; s_bioanalyzer_area: 60.2; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.65; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 130; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: SB91A; s_pgr_float: 32; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 5.2; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 1; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 25; taxonomy_test_rin_float: 6; tissue_mg: n/a; opdat: 19951228; extrdat: 20020101; time_in_freezer: 2196; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_days_to_recurrence: -1; p_local_recurrence_0no_1yes: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 62; s_bioanalyzer_18s: 19.3; s_bioanalyzer_28s: 21.1; s_bioanalyzer_area: 477.7; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.1; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: n/a; s_meno: post; s_original_study: SB91A; s_pgr_float: 36; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 16; tissue_mg: 65; opdat: 19960605; extrdat: 20050101; time_in_freezer: 3132; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_days_to_recurrence: -1; p_local_recurrence_0no_1yes: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 59; s_bioanalyzer_18s: 16.3; s_bioanalyzer_28s: 16.4; s_bioanalyzer_area: 175.6; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41001-301; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: n/a; s_meno: Post; s_original_study: SB91A; s_pgr_float: 250; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 11; tissue_mg: 27; opdat: 19960603; extrdat: 20050101; time_in_freezer: 3134; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_days_to_recurrence: -1; p_local_recurrence_0no_1yes: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 46; s_bioanalyzer_18s: 17; s_bioanalyzer_28s: 18.2; s_bioanalyzer_area: 231.7; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.1; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41011-301; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: n/a; s_meno: non_available; s_original_study: SB91A; s_pgr_float: 200; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 16; tissue_mg: 31; opdat: 19970124; extrdat: 20050101; time_in_freezer: 2899; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_days_to_recurrence: -1; p_local_recurrence_0no_1yes: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 51; s_bioanalyzer_18s: 15.5; s_bioanalyzer_28s: 18.3; s_bioanalyzer_area: 132.4; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.2; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 2; s_histology_type: n/a; s_meno: non_available; s_original_study: SB91A; s_original_study_prog: 7; s_pgr_float: 6; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; tissue_mg: 57; opdat: 19970217; extrdat: 20050101; time_in_freezer: 2875; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_days_to_recurrence: 1510; p_local_recurrence_0no_1yes: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 49; s_bioanalyzer_18s: 6.5; s_bioanalyzer_28s: 6.4; s_bioanalyzer_area: 282.7; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: n/a; s_meno: non_available; s_original_study: non_available; s_pgr_float: 410; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; tissue_mg: 31; opdat: 19970317; extrdat: 20050101; time_in_freezer: 2847; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_days_to_recurrence: -1; p_local_recurrence_0no_1yes: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 40; s_bioanalyzer_18s: 14.9; s_bioanalyzer_28s: 17.8; s_bioanalyzer_area: 273.5; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.2; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: n/a; s_meno: non_available; s_original_study: SB91A; s_pgr_float: 510; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; tissue_mg: 62; opdat: 19970526; extrdat: 20050101; time_in_freezer: 2777; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_neg; p_cause_of_death: brca; p_days_followup: 520; p_days_to_death: 520; p_days_to_distant_recurrence: 455; p_days_to_recurrence: 238; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 3; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 0; s_age_year: 50; s_bioanalyzer_18s: 8.28; s_bioanalyzer_28s: 12.07; s_bioanalyzer_area: 447.69; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.46; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 23010-301; s_dnaind1: 0.98; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 3.4; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Margareta; s_pgr_float: 7.3; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 7.3; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 16; taxonomy_test_rin_float: 6.9; tissue_mg: 61; opdat: 19880613; extrdat: 20020101; time_in_freezer: 4950; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_neg; p_cause_of_death: brca; p_days_followup: 259; p_days_to_death: 259; p_days_to_distant_recurrence: 230; p_days_to_recurrence: 230; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 57; s_bioanalyzer_18s: 11.92; s_bioanalyzer_28s: 17.72; s_bioanalyzer_area: 1378.66; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.49; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41011-301; s_dnaind1: 1.85; s_dnaind2: 1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 0; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Margareta; s_pgr_float: 5.7; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 23; s_spf_status_0low_1high: 1; s_surgery_desc: 3; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 18; taxonomy_test_rin_float: 7.8; tissue_mg: 130; opdat: 19880616; extrdat: 20020101; time_in_freezer: 4947; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2999; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 1030; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 30; s_age_above50year_0no_1yes: 0; s_age_year: 37; s_bioanalyzer_18s: 9.64; s_bioanalyzer_28s: 12.69; s_bioanalyzer_area: 1869.53; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.32; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 28011-301; s_dnaind1: 1.66; s_dnaind2: 0.75; s_dnaind3: 1; s_dnaind4: -1; s_er_float: 210; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Margareta; s_pgr_float: 1200; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 3; s_spf_percent: 6.3; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; taxonomy_test_rin_float: 7.7; tissue_mg: 95; opdat: 19881128; extrdat: 20020101; time_in_freezer: 4782; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1700; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 541; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 42; s_bioanalyzer_18s: 13.18; s_bioanalyzer_28s: 15.52; s_bioanalyzer_area: 700.75; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.18; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41001-301; s_dnaind1: 1.62; s_dnaind2: 1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 270; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubuloductal; s_meno: Pre; s_original_study: Margareta; s_pgr_float: 290; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: -1; s_spf_status_0low_1high: non_available; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; taxonomy_test_rin_float: 8.2; tissue_mg: 74; opdat: 19890913; extrdat: 20020101; time_in_freezer: 4493; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 2134; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 735; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 0; s_age_year: 50; s_bioanalyzer_18s: 16.34; s_bioanalyzer_28s: 19.65; s_bioanalyzer_area: 411.79; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.2; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 28010-301; s_dnaind1: 1.69; s_dnaind2: 1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 0; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: non_available; s_hgrade_lokrec: non_available; s_hgrade_lokrec_mitotic_count: non_available; s_hgrade_lokrec_pleomrph: non_available; s_hgrade_lokrec_tubules: non_available; s_histology_type: n/a; s_meno: Pre; s_original_study: Margareta; s_pgr_float: 0; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 23; s_spf_status_0low_1high: 1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; taxonomy_test_rin_float: 8.2; tissue_mg: 68; opdat: 19901115; extrdat: 20020101; time_in_freezer: 4065; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 3164; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 49; s_bioanalyzer_18s: 9.64; s_bioanalyzer_28s: 12.13; s_bioanalyzer_area: 144.98; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.26; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41013-301; s_dnaind1: 1.81; s_dnaind2: 0.98; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 2.7; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_medullary; s_meno: Pre; s_original_study: SB91A; s_pgr_float: 7.1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 18; s_spf_status_0low_1high: 1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 22; taxonomy_test_rin_float: 6.8; tissue_mg: 70; opdat: 19910122; extrdat: 20020101; time_in_freezer: 3997; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2610; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 68; s_bioanalyzer_18s: 8.37; s_bioanalyzer_28s: 7.98; s_bioanalyzer_area: 78.84; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.95; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 1.01; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Tubular; s_meno: Post; s_original_study: SB91A; s_pgr_float: 12; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 5.7; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 8; taxonomy_test_rin_float: 6.6; tissue_mg: 52; opdat: 19910131; extrdat: 20020101; time_in_freezer: 3988; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2487; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 59; s_bioanalyzer_18s: 4.83; s_bioanalyzer_28s: 3.06; s_bioanalyzer_area: 54.11; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.63; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 1.05; s_dnaind2: 0.98; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 190; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Tubuloductal; s_meno: Post; s_original_study: SB91A; s_pgr_float: 380; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 4.3; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; taxonomy_test_rin_float: 5.9; tissue_mg: 29; opdat: 19910128; extrdat: 20020101; time_in_freezer: 3991; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2947; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 65; s_bioanalyzer_18s: 9.05; s_bioanalyzer_28s: 6.16; s_bioanalyzer_area: 30.17; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.68; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 1.04; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 140; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 7.6; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 3.6; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 4; taxonomy_test_rin_float: 6.9; tissue_mg: 73; opdat: 19910208; extrdat: 20020101; time_in_freezer: 3980; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2941; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 61; s_bioanalyzer_18s: 11.38; s_bioanalyzer_28s: 13.55; s_bioanalyzer_area: 171.62; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.19; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 23010-301; s_dnaind1: 0.99; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 450; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubuloductal; s_meno: Post; s_original_study: SB91A; s_pgr_float: 230; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 2.4; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 13; taxonomy_test_rin_float: 6.9; tissue_mg: 57; opdat: 19910225; extrdat: 20020101; time_in_freezer: 3963; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2743; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 66; s_bioanalyzer_18s: 7.7; s_bioanalyzer_28s: 5.89; s_bioanalyzer_area: 52.95; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.77; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 23010-301; s_dnaind1: 1.02; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 110; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 23; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 5.4; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 18; taxonomy_test_rin_float: 6.5; tissue_mg: 55; opdat: 19910301; extrdat: 20020101; time_in_freezer: 3959; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 2563; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 60; s_bioanalyzer_18s: 8.83; s_bioanalyzer_28s: 7.89; s_bioanalyzer_area: 247.24; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.89; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: 1.72; s_dnaind2: 1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 2.9; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_medullary; s_meno: Post; s_original_study: SB91A; s_pgr_float: 8.9; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 14; s_spf_status_0low_1high: 1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 16; taxonomy_test_rin_float: 6.3; tissue_mg: 63; opdat: 19910311; extrdat: 20020101; time_in_freezer: 3949; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2945; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 55; s_bioanalyzer_18s: 10.08; s_bioanalyzer_28s: 9.37; s_bioanalyzer_area: 37.17; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.93; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41011-301; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 490; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubuloductal; s_meno: Post; s_original_study: SB91A; s_pgr_float: 620; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 3.4; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; taxonomy_test_rin_float: 7.2; tissue_mg: 45; opdat: 19910308; extrdat: 20020101; time_in_freezer: 3952; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 3076; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 61; s_bioanalyzer_18s: 5.37; s_bioanalyzer_28s: 3.02; s_bioanalyzer_area: 29.33; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.56; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 28010-301; s_dnaind1: 1.82; s_dnaind2: 1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 13; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 0; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 20; s_spf_status_0low_1high: 1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; taxonomy_test_rin_float: 6.4; tissue_mg: 48; opdat: 19910318; extrdat: 20020101; time_in_freezer: 3942; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 2972; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 52; s_bioanalyzer_18s: 7.52; s_bioanalyzer_28s: 6.07; s_bioanalyzer_area: 133.36; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.81; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 1.45; s_dnaind2: 0.98; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 3.1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 0.71; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: -1; s_spf_status_0low_1high: non_available; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; taxonomy_test_rin_float: 6.1; tissue_mg: 41; opdat: 19910322; extrdat: 20020101; time_in_freezer: 3938; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2593; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 42; s_bioanalyzer_18s: 3.74; s_bioanalyzer_28s: 1.99; s_bioanalyzer_area: 189.39; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.53; s_bioanalyzer_rin: 5; s_bioanalyzer_rin6_0no_1yes: 0; s_clinic_code: 41012-301; s_dnaind1: 0.99; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 56; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: SB91A; s_pgr_float: 140; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 3.4; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 1; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; taxonomy_test_rin_float: 5.4; tissue_mg: 35; opdat: 19910325; extrdat: 20020101; time_in_freezer: 3935; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: brca; p_days_followup: 2468; p_days_to_death: 2468; p_days_to_distant_recurrence: 1895; p_days_to_recurrence: 611; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 70; s_age_above50year_0no_1yes: 1; s_age_year: 73; s_bioanalyzer_18s: 8.94; s_bioanalyzer_28s: 8.87; s_bioanalyzer_area: 162.76; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.99; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 28010-301; s_dnaind1: 1.67; s_dnaind2: 0.98; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 340; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubuloductal; s_meno: Post; s_original_study: SB91A; s_pgr_float: 110; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 10; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 9; taxonomy_test_rin_float: 6.8; tissue_mg: 71; opdat: 19910403; extrdat: 20020101; time_in_freezer: 3926; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 3276; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 64; s_bioanalyzer_18s: 9.98; s_bioanalyzer_28s: 8.85; s_bioanalyzer_area: 348.07; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.89; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 1.07; s_dnaind2: 0.98; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 270; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 300; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 2.6; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 14; taxonomy_test_rin_float: 6.4; tissue_mg: 46; opdat: 19910422; extrdat: 20020101; time_in_freezer: 3907; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2948; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 70; s_age_above50year_0no_1yes: 1; s_age_year: 70; s_bioanalyzer_18s: 4.29; s_bioanalyzer_28s: 1.81; s_bioanalyzer_area: 83.04; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.42; s_bioanalyzer_rin: 3; s_bioanalyzer_rin6_0no_1yes: 0; s_clinic_code: 42010-301; s_dnaind1: 1.98; s_dnaind2: 1.82; s_dnaind3: 0.99; s_dnaind4: -1; s_er_float: 67; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Tubular; s_meno: Post; s_original_study: SB91A; s_pgr_float: 40; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 3; s_spf_percent: 5.1; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 7; taxonomy_test_rin_float: 3.4; tissue_mg: 25; opdat: 19910507; extrdat: 20020101; time_in_freezer: 3892; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 3054; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 55; s_bioanalyzer_18s: 9.08; s_bioanalyzer_28s: 9.35; s_bioanalyzer_area: 80.94; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.03; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41001-301; s_dnaind1: 1.55; s_dnaind2: 0.99; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 290; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Tubular; s_meno: Post; s_original_study: SB91A; s_pgr_float: 6; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 6.5; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 13; taxonomy_test_rin_float: 6.7; tissue_mg: 60; opdat: 19910507; extrdat: 20020101; time_in_freezer: 3892; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2379; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 67; s_bioanalyzer_18s: 8.87; s_bioanalyzer_28s: 7.78; s_bioanalyzer_area: 95.28; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.88; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 23011-301; s_dnaind1: 2.04; s_dnaind2: 1.01; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 610; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Tubular; s_meno: Post; s_original_study: SB91A; s_pgr_float: 250; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 4.2; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; taxonomy_test_rin_float: 6.9; tissue_mg: 70; opdat: 19910523; extrdat: 20020101; time_in_freezer: 3876; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 2288; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 43; s_bioanalyzer_18s: 17.8; s_bioanalyzer_28s: 19.23; s_bioanalyzer_area: 1159.11; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.08; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 1.85; s_dnaind2: 0.96; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 1.9; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: SB91A; s_pgr_float: 1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 21; s_spf_status_0low_1high: 1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; taxonomy_test_rin_float: 7.6; tissue_mg: 96; opdat: 19910604; extrdat: 20020101; time_in_freezer: 3864; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2621; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 67; s_bioanalyzer_18s: 11.93; s_bioanalyzer_28s: 16.13; s_bioanalyzer_area: 203.89; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.35; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 200; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 230; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 3.1; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; taxonomy_test_rin_float: 7.2; tissue_mg: 81; opdat: 19910624; extrdat: 20020101; time_in_freezer: 3844; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1854; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 66; s_bioanalyzer_18s: 10.41; s_bioanalyzer_28s: 14.41; s_bioanalyzer_area: 204.63; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.38; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41001-301; s_dnaind1: 0.98; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 180; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Tubular; s_meno: Post; s_original_study: SB91A; s_pgr_float: 760; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 2; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; taxonomy_test_rin_float: 7; tissue_mg: 74; opdat: 19910710; extrdat: 20020101; time_in_freezer: 3828; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2939; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 2889; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 45; s_bioanalyzer_18s: 9.38; s_bioanalyzer_28s: 10.53; s_bioanalyzer_area: 209.86; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.12; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: 0.98; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 58; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: non_available; s_hgrade_lokrec: non_available; s_hgrade_lokrec_mitotic_count: non_available; s_hgrade_lokrec_pleomrph: non_available; s_hgrade_lokrec_tubules: non_available; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: SB91A; s_pgr_float: 480; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 5.3; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; taxonomy_test_rin_float: 6.6; tissue_mg: 49; opdat: 19910717; extrdat: 20020101; time_in_freezer: 3821; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1939; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 63; s_bioanalyzer_18s: 5.5; s_bioanalyzer_28s: 2.3; s_bioanalyzer_area: 47.49; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.42; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41001-301; s_dnaind1: 1.98; s_dnaind2: 1.16; s_dnaind3: 1; s_dnaind4: -1; s_er_float: 82; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 1; s_histology_type: Tubular; s_meno: Post; s_original_study: SB91A; s_pgr_float: 36; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 3; s_spf_percent: 8.8; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 13; taxonomy_test_rin_float: 6.3; tissue_mg: 47; opdat: 19910805; extrdat: 20020101; time_in_freezer: 3802; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 3091; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 43; s_bioanalyzer_18s: 12.59; s_bioanalyzer_28s: 15.13; s_bioanalyzer_area: 204.53; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.2; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 28010-301; s_dnaind1: 0.99; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 190; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: SB91A; s_pgr_float: 100; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 4.3; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; taxonomy_test_rin_float: 7.2; tissue_mg: 74; opdat: 19910822; extrdat: 20020101; time_in_freezer: 3785; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2583; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 66; s_bioanalyzer_18s: 13.13; s_bioanalyzer_28s: 11.72; s_bioanalyzer_area: 584.71; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.89; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 1.1; s_dnaind2: 2.03; s_dnaind3: 1.01; s_dnaind4: -1; s_er_float: 550; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_mucous; s_meno: Post; s_original_study: SB91A; s_pgr_float: 11; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 3; s_spf_percent: 5.5; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; taxonomy_test_rin_float: 6.6; tissue_mg: 52; opdat: 19910826; extrdat: 20020101; time_in_freezer: 3781; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 3177; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 55; s_bioanalyzer_18s: 18.88; s_bioanalyzer_28s: 20.44; s_bioanalyzer_area: 568.12; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.08; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 27010-301; s_dnaind1: 1.04; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 270; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 150; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 2.6; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; taxonomy_test_rin_float: 7.8; tissue_mg: 71; opdat: 19910821; extrdat: 20020101; time_in_freezer: 3786; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2974; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 1283; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 1; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 52; s_bioanalyzer_18s: 12.24; s_bioanalyzer_28s: 11.43; s_bioanalyzer_area: 68.04; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.93; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41011-301; s_dnaind1: 1.01; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 520; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 260; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 9.5; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 29; taxonomy_test_rin_float: 7.8; tissue_mg: 69; opdat: 19911008; extrdat: 20020101; time_in_freezer: 3738; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2654; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 64; s_bioanalyzer_18s: 5.79; s_bioanalyzer_28s: 5.5; s_bioanalyzer_area: 251.54; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.95; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 0.92; s_dnaind2: 0.98; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 95; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 53; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 4.2; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; taxonomy_test_rin_float: 6.1; tissue_mg: 44; opdat: 19911014; extrdat: 20020101; time_in_freezer: 3732; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: brca; p_days_followup: 2877; p_days_to_death: 3277; p_days_to_distant_recurrence: 2244; p_days_to_recurrence: 1240; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 54; s_bioanalyzer_18s: 7.48; s_bioanalyzer_28s: 8.97; s_bioanalyzer_area: 230.4; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.2; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41013-301; s_dnaind1: 1.89; s_dnaind2: 0.98; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 110; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: non_available; s_hgrade_lokrec: non_available; s_hgrade_lokrec_mitotic_count: non_available; s_hgrade_lokrec_pleomrph: non_available; s_hgrade_lokrec_tubules: non_available; s_histology_type: n/a; s_meno: Post; s_original_study: SB91A; s_original_study_prog: SB91B; s_pgr_float: 90; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 14; s_spf_status_0low_1high: 1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; taxonomy_test_rin_float: 6.6; tissue_mg: 27.1; opdat: 19911021; extrdat: 20020101; time_in_freezer: 3725; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2541; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 55; s_bioanalyzer_18s: 14.15; s_bioanalyzer_28s: 15.58; s_bioanalyzer_area: 132.9; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.1; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 28012-301; s_dnaind1: 2.12; s_dnaind2: 1.98; s_dnaind3: 1.12; s_dnaind4: 0.99; s_er_float: 450; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 220; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 4; s_spf_percent: 3.9; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 18; taxonomy_test_rin_float: 7.4; tissue_mg: 47; opdat: 19911028; extrdat: 20020101; time_in_freezer: 3718; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2496; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 68; s_bioanalyzer_18s: 9.47; s_bioanalyzer_28s: 8.75; s_bioanalyzer_area: 69.7; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.92; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 1.89; s_dnaind2: 1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 830; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 840; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: -1; s_spf_status_0low_1high: non_available; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 17; taxonomy_test_rin_float: 7.3; tissue_mg: 40; opdat: 19911031; extrdat: 20020101; time_in_freezer: 3715; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 2624; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 69; s_bioanalyzer_18s: 5.17; s_bioanalyzer_28s: 4.68; s_bioanalyzer_area: 388.64; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.91; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41011-301; s_dnaind1: 1.63; s_dnaind2: 0.99; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 4.7; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 2.7; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 18; s_spf_status_0low_1high: 1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 9; taxonomy_test_rin_float: 5.8; tissue_mg: 30; opdat: 19911112; extrdat: 20020101; time_in_freezer: 3703; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2911; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 67; s_bioanalyzer_18s: 7.72; s_bioanalyzer_28s: 4.17; s_bioanalyzer_area: 363.53; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.54; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: 1.07; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 590; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_medullary; s_meno: Post; s_original_study: SB91A; s_pgr_float: 38; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 2.7; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; taxonomy_test_rin_float: 5.7; tissue_mg: 33; opdat: 19911118; extrdat: 20020101; time_in_freezer: 3697; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: other_disease; p_days_followup: 2549; p_days_to_death: 2549; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 521; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 62; s_bioanalyzer_18s: 10.74; s_bioanalyzer_28s: 11.7; s_bioanalyzer_area: 90.37; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.09; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 28011-301; s_dnaind1: 0.98; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 49; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Lobular; s_meno: Post; s_original_study: SB91A; s_pgr_float: 1.6; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 3.9; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; taxonomy_test_rin_float: 7.5; tissue_mg: 83; opdat: 19911230; extrdat: 20020101; time_in_freezer: 3655; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2342; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 66; s_bioanalyzer_18s: 9.85; s_bioanalyzer_28s: 9.89; s_bioanalyzer_area: 153.6; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: 0.98; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 450; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubular; s_meno: Post; s_original_study: SB91A; s_pgr_float: 670; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 4.7; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; taxonomy_test_rin_float: 7.3; tissue_mg: 35; opdat: 19920127; extrdat: 20020101; time_in_freezer: 3627; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_neg; p_cause_of_death: brca; p_days_followup: 1945; p_days_to_death: 1945; p_days_to_distant_recurrence: 1441; p_days_to_recurrence: 1764; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 12; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 49; s_bioanalyzer_18s: 7.8; s_bioanalyzer_28s: 5.4; s_bioanalyzer_area: 295.5; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.69; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: 0.99; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 4.6; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_medullary; s_meno: Pre; s_original_study: SB91A; s_original_study_prog: SB91B; s_pgr_float: 0; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 12; s_spf_status_0low_1high: 1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 17; taxonomy_test_rin_float: 6; tissue_mg: 26; opdat: 19920205; extrdat: 20020101; time_in_freezer: 3618; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2823; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 56; s_bioanalyzer_18s: 13.03; s_bioanalyzer_28s: 12.61; s_bioanalyzer_area: 239.78; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.97; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: 1.89; s_dnaind2: 0.99; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 350; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 330; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 3.4; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 17; taxonomy_test_rin_float: 7; tissue_mg: 40; opdat: 19920224; extrdat: 20020101; time_in_freezer: 3599; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2528; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 56; s_bioanalyzer_18s: 15.33; s_bioanalyzer_28s: 17.54; s_bioanalyzer_area: 522.55; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.14; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 1.12; s_dnaind2: 0.99; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 160; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 260; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 2.8; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; taxonomy_test_rin_float: 7.4; tissue_mg: 51; opdat: 19920304; extrdat: 20020101; time_in_freezer: 3590; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2602; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 68; s_bioanalyzer_18s: 6.25; s_bioanalyzer_28s: 4.78; s_bioanalyzer_area: 189.05; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.76; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: 1.57; s_dnaind2: 1.46; s_dnaind3: 1; s_dnaind4: -1; s_er_float: 340; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 3.1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 3; s_spf_percent: 11; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 17; taxonomy_test_rin_float: 6.2; tissue_mg: 32; opdat: 19920325; extrdat: 20020101; time_in_freezer: 3569; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2577; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 67; s_bioanalyzer_18s: 9.6; s_bioanalyzer_28s: 4.99; s_bioanalyzer_area: 196.7; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.52; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 1.47; s_dnaind2: 1.01; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 440; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: n/a; s_meno: Post; s_original_study: SB91A; s_pgr_float: 790; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: -1; s_spf_status_0low_1high: non_available; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; taxonomy_test_rin_float: 6.1; tissue_mg: 32; opdat: 19920506; extrdat: 20020101; time_in_freezer: 3527; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1857; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 0; s_age_year: 50; s_bioanalyzer_18s: 8; s_bioanalyzer_28s: 3.22; s_bioanalyzer_area: 42.51; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.4; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 1.85; s_dnaind2: 0.99; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 230; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 540; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 9.1; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 13; taxonomy_test_rin_float: 6.5; tissue_mg: 37; opdat: 19920506; extrdat: 20020101; time_in_freezer: 3527; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 46; s_bioanalyzer_18s: 18.69; s_bioanalyzer_28s: 22.87; s_bioanalyzer_area: 1092.13; s_bioanalyzer_manual: o k; s_bioanalyzer_ratio: 1.22; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 30001-301; s_dnaind1: -1; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 110; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: n/a; s_meno: pre; s_original_study: SB91B; s_original_study_prog: SB91B; s_pgr_float: 76; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 8; s_spf_status_0low_1high: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 26; taxonomy_test_rin_float: 7.9; tissue_mg: 105.3; opdat: 19920511; extrdat: 20050101; time_in_freezer: 4618; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2496; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 54; s_bioanalyzer_18s: 9.89; s_bioanalyzer_28s: 12.05; s_bioanalyzer_area: 228.63; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.22; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41011-301; s_dnaind1: 0.99; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 110; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubuloductal; s_meno: Post; s_original_study: SB91A; s_pgr_float: 75; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 3.1; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; taxonomy_test_rin_float: 6.9; tissue_mg: 45; opdat: 19920514; extrdat: 20020101; time_in_freezer: 3519; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2191; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 65; s_bioanalyzer_18s: 10.34; s_bioanalyzer_28s: 9.71; s_bioanalyzer_area: 190.43; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.94; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 1.03; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 370; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 940; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 2.2; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; taxonomy_test_rin_float: 6.6; tissue_mg: 38; opdat: 19920518; extrdat: 20020101; time_in_freezer: 3515; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 2338; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 349; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 30; s_age_above50year_0no_1yes: 0; s_age_year: 37; s_bioanalyzer_18s: 5.9; s_bioanalyzer_28s: 4.85; s_bioanalyzer_area: 57.57; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.82; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 42010-301; s_dnaind1: 1.82; s_dnaind2: 0.99; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 2.9; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: SB91A; s_pgr_float: 2; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: -1; s_spf_status_0low_1high: non_available; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 2; taxonomy_test_rin_float: 6.4; tissue_mg: 35; opdat: 19920526; extrdat: 20020101; time_in_freezer: 3507; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2426; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 57; s_bioanalyzer_18s: 6.58; s_bioanalyzer_28s: 5.54; s_bioanalyzer_area: 84.43; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.84; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 1.15; s_dnaind2: 1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 120; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubular; s_meno: Post; s_original_study: SB91A; s_pgr_float: 90; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 5.4; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; taxonomy_test_rin_float: 6.5; tissue_mg: 39; opdat: 19920525; extrdat: 20020101; time_in_freezer: 3508; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2448; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 61; s_bioanalyzer_18s: 6.07; s_bioanalyzer_28s: 3.63; s_bioanalyzer_area: 120.37; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.6; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: 41012-301; s_dnaind1: 0.99; s_dnaind2: -1; s_dnaind3: -1; s_dnaind4: -1; s_er_float: 160; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: SB91A; s_pgr_float: 210; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 5; s_spf_status_0low_1high: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 1; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 11; taxonomy_test_rin_float: 6.1; tissue_mg: 25; opdat: 19920624; extrdat: 20020101; time_in_freezer: 3478; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_neg; p_cause_of_death: non_available; p_days_followup: 2623; p_days_to_death: 4388; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 55; s_bioanalyzer_18s: 9.68; s_bioanalyzer_28s: 8.69; s_bioanalyzer_area: 150.63; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.9; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 3.7; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 13; tissue_mg: 66; opdat: 19920205; extrdat: 20020101; time_in_freezer: 3618; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2953; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 61; s_bioanalyzer_18s: -1; s_bioanalyzer_28s: -1; s_bioanalyzer_area: 11.82; s_bioanalyzer_manual: unreadable; s_bioanalyzer_ratio: -1; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: -1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Tubular; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: non_available; s_spf_percent: -1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 5; tissue_mg: 24; opdat: 19910102; extrdat: 20020101; time_in_freezer: 4017; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2591; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 52; s_bioanalyzer_18s: 7.47; s_bioanalyzer_28s: 7.18; s_bioanalyzer_area: 202.96; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.96; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.87; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubular; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: -1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 11; tissue_mg: 32; opdat: 19920203; extrdat: 20020101; time_in_freezer: 3620; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2267; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 47; s_bioanalyzer_18s: 2.77; s_bioanalyzer_28s: -1; s_bioanalyzer_area: 37.28; s_bioanalyzer_manual: unreadable; s_bioanalyzer_ratio: -1; s_bioanalyzer_rin: 4; s_bioanalyzer_rin6_0no_1yes: 0; s_clinic_code: non_available; s_dnaind1: -1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Tubular; s_meno: Pre; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: non_available; s_spf_percent: -1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; tissue_mg: 15; opdat: 19920318; extrdat: 20020101; time_in_freezer: 3576; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2488; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 997; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 48; s_bioanalyzer_18s: 14.41; s_bioanalyzer_28s: 14.43; s_bioanalyzer_area: 350.86; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Lobular; s_meno: Pre; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 5.2; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; tissue_mg: 76; opdat: 19920320; extrdat: 20020101; time_in_freezer: 3574; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1869; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 1112; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 58; s_bioanalyzer_18s: 13.27; s_bioanalyzer_28s: 17.04; s_bioanalyzer_area: 209.56; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.28; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 3.4; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; tissue_mg: 58; opdat: 19920407; extrdat: 20020101; time_in_freezer: 3556; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2564; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 1143; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 46; s_bioanalyzer_18s: 6.25; s_bioanalyzer_28s: 5.42; s_bioanalyzer_area: 140.88; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.87; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.96; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 1; s_spf_nbr_pop: 2; s_spf_percent: 14.3; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; tissue_mg: 41; opdat: 19920413; extrdat: 20020101; time_in_freezer: 3550; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_neg; p_cause_of_death: brca; p_days_followup: 1526; p_days_to_death: 1528; p_days_to_distant_recurrence: 1441; p_days_to_recurrence: 982; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 2; p_treat_chemo_0no_1yes: 1; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 63; s_bioanalyzer_18s: 16.39; s_bioanalyzer_28s: 17.81; s_bioanalyzer_area: 725.79; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.09; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.6; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: non_available; s_hgrade_lokrec: non_available; s_hgrade_lokrec_mitotic_count: non_available; s_hgrade_lokrec_pleomrph: non_available; s_hgrade_lokrec_tubules: non_available; s_histology_type: n/a; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 14.2; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; tissue_mg: 69; opdat: 19920826; extrdat: 20020101; time_in_freezer: 3415; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2511; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 1105; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 49; s_bioanalyzer_18s: 5.95; s_bioanalyzer_28s: 3.9; s_bioanalyzer_area: 60.36; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.66; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: -1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: non_available; s_spf_percent: -1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 17; tissue_mg: 27; opdat: 19921015; extrdat: 20020101; time_in_freezer: 3365; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2304; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 64; s_bioanalyzer_18s: 11; s_bioanalyzer_28s: 11.66; s_bioanalyzer_area: 113.92; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.06; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.75; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubular; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 10.3; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 14; tissue_mg: 52; opdat: 19921013; extrdat: 20020101; time_in_freezer: 3367; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: other_disease; p_days_followup: 1685; p_days_to_death: 1693; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 1133; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 2; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 67; s_bioanalyzer_18s: 7.68; s_bioanalyzer_28s: 6.1; s_bioanalyzer_area: 103.31; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.8; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.99; s_dnaind2: 2.56; s_dnaind3: 1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubular; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 3; s_spf_percent: 13.7; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 7; tissue_mg: 42; opdat: 19921015; extrdat: 20020101; time_in_freezer: 3365; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2257; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 339; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 45; s_bioanalyzer_18s: 14.49; s_bioanalyzer_28s: 14.19; s_bioanalyzer_area: 132.99; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.98; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 2.7; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 1; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 18; tissue_mg: 56; opdat: 19921002; extrdat: 20020101; time_in_freezer: 3378; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2323; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 44; s_bioanalyzer_18s: 14.63; s_bioanalyzer_28s: 16.37; s_bioanalyzer_area: 117.6; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.12; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Tubular; s_meno: Pre; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 5.4; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 13; tissue_mg: 54; opdat: 19921103; extrdat: 20020101; time_in_freezer: 3346; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2353; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 57; s_bioanalyzer_18s: 12.79; s_bioanalyzer_28s: 9.91; s_bioanalyzer_area: 59.77; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.77; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 6.9; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 22; tissue_mg: 72; opdat: 19921022; extrdat: 20020101; time_in_freezer: 3358; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_neg; p_cause_of_death: brca; p_days_followup: 1931; p_days_to_death: 2331; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 422; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 59; s_bioanalyzer_18s: 9.76; s_bioanalyzer_28s: 13.1; s_bioanalyzer_area: 147.6; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.34; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.11; s_dnaind2: 2.08; s_dnaind3: 1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 3; s_spf_percent: 17; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 30; tissue_mg: 78; opdat: 19921216; extrdat: 20020101; time_in_freezer: 3303; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2259; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 65; s_bioanalyzer_18s: 12.1; s_bioanalyzer_28s: 13.39; s_bioanalyzer_area: 328.43; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.11; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.77; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 19; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 40; tissue_mg: 69; opdat: 19930325; extrdat: 20020101; time_in_freezer: 3204; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: non_available; p_days_followup: 1957; p_days_to_death: 3342; p_days_to_distant_recurrence: 3206; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 67; s_bioanalyzer_18s: 13.15; s_bioanalyzer_28s: 13.58; s_bioanalyzer_area: 149.65; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.03; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.98; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 9.2; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 18; tissue_mg: 78; opdat: 19930513; extrdat: 20020101; time_in_freezer: 3155; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1922; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 62; s_bioanalyzer_18s: 11.65; s_bioanalyzer_28s: 16.26; s_bioanalyzer_area: 224.06; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.4; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: non_available; s_hgrade_lokrec: non_available; s_hgrade_lokrec_mitotic_count: non_available; s_hgrade_lokrec_pleomrph: non_available; s_hgrade_lokrec_tubules: non_available; s_histology_type: n/a; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 2.9; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 21; tissue_mg: 74; opdat: 19931014; extrdat: 20020101; time_in_freezer: 3001; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2021; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 67; s_bioanalyzer_18s: 6.14; s_bioanalyzer_28s: 4.1; s_bioanalyzer_area: 167.76; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.67; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.1; s_dnaind2: 1.25; s_dnaind3: 1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubulolobular; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 3; s_spf_percent: 2.6; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; tissue_mg: 47; opdat: 19931014; extrdat: 20020101; time_in_freezer: 3001; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1857; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 687; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 48; s_bioanalyzer_18s: 12.6; s_bioanalyzer_28s: 12.32; s_bioanalyzer_area: 249.69; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.98; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: n/a; s_meno: Pre; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 2.6; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 11; tissue_mg: 68; opdat: 19931012; extrdat: 20020101; time_in_freezer: 3003; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 1892; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 1; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 0; s_age_year: 50; s_bioanalyzer_18s: 16.61; s_bioanalyzer_28s: 23.31; s_bioanalyzer_area: 220.54; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.4; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 5.7; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 30; tissue_mg: 75; opdat: 19930928; extrdat: 20020101; time_in_freezer: 3017; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1848; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 58; s_bioanalyzer_18s: 9.67; s_bioanalyzer_28s: 7.82; s_bioanalyzer_area: 94.59; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.81; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.41; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 8.3; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 17; tissue_mg: 47; opdat: 19931214; extrdat: 20020101; time_in_freezer: 2940; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1888; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 64; s_bioanalyzer_18s: 12.39; s_bioanalyzer_28s: 11.51; s_bioanalyzer_area: 119.98; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.93; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Lobular; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 3.5; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; tissue_mg: 55; opdat: 19940120; extrdat: 20020101; time_in_freezer: 2903; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_neg; p_cause_of_death: brca; p_days_followup: 1290; p_days_to_death: 1314; p_days_to_distant_recurrence: 1091; p_days_to_recurrence: 323; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 2; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 47; s_bioanalyzer_18s: 4.64; s_bioanalyzer_28s: 3.61; s_bioanalyzer_area: 207.72; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.78; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.61; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: n/a; s_meno: Pre; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 1; s_spf_nbr_pop: 2; s_spf_percent: 14.9; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; tissue_mg: 31; opdat: 19941115; extrdat: 20020101; time_in_freezer: 2604; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 1562; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 710; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 66; s_bioanalyzer_18s: 5.71; s_bioanalyzer_28s: 3.58; s_bioanalyzer_area: 48.14; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.63; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: -1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 1; s_spf_nbr_pop: non_available; s_spf_percent: -1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 25; tissue_mg: 31; opdat: 19941129; extrdat: 20020101; time_in_freezer: 2590; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 3093; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 728; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 62; s_bioanalyzer_18s: 7.23; s_bioanalyzer_28s: 6.58; s_bioanalyzer_area: 76.37; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.91; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: -1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: non_available; s_spf_percent: -1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; tissue_mg: 42; opdat: 19910208; extrdat: 20020101; time_in_freezer: 3980; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2618; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 62; s_bioanalyzer_18s: 7.63; s_bioanalyzer_28s: 9.06; s_bioanalyzer_area: 127.42; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.19; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.15; s_dnaind2: 1.96; s_dnaind3: 1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 3; s_spf_percent: -1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 1; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 7; tissue_mg: 57; opdat: 19910115; extrdat: 20020101; time_in_freezer: 4004; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 1281; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 607; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 3; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 62; s_bioanalyzer_18s: 4.91; s_bioanalyzer_28s: 5.25; s_bioanalyzer_area: 131.18; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.07; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 7.3; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 18; tissue_mg: 52; opdat: 19950706; extrdat: 20020101; time_in_freezer: 2371; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2647; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 65; s_bioanalyzer_18s: 9.31; s_bioanalyzer_28s: 10.25; s_bioanalyzer_area: 69.95; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.1; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 5.4; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 20; tissue_mg: 48; opdat: 19910617; extrdat: 20020101; time_in_freezer: 3851; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2508; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 47; s_bioanalyzer_18s: 21.37; s_bioanalyzer_28s: 14.68; s_bioanalyzer_area: 16.1; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.69; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.28; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 4.2; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 16; tissue_mg: 26; opdat: 19910624; extrdat: 20020101; time_in_freezer: 3844; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2722; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 64; s_bioanalyzer_18s: 6.99; s_bioanalyzer_28s: 7.92; s_bioanalyzer_area: 138.66; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.13; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.78; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: non_available; s_hgrade_lokrec: non_available; s_hgrade_lokrec_mitotic_count: non_available; s_hgrade_lokrec_pleomrph: non_available; s_hgrade_lokrec_tubules: non_available; s_histology_type: n/a; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 10.5; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 9; tissue_mg: 51; opdat: 19910628; extrdat: 20020101; time_in_freezer: 3840; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 2700; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: -1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 54; s_bioanalyzer_18s: 8.29; s_bioanalyzer_28s: 7.23; s_bioanalyzer_area: 254.53; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.87; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.26; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: -1; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 13; tissue_mg: 48; opdat: 19910724; extrdat: 20020101; time_in_freezer: 3814; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 3; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 3171; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 1394; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 52; s_bioanalyzer_18s: 16.29; s_bioanalyzer_28s: 24.32; s_bioanalyzer_area: 329.52; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.49; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.78; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 21; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 9; tissue_mg: 76; opdat: 19910618; extrdat: 20020101; time_in_freezer: 3850; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 2696; p_days_to_death: -1; p_days_to_distant_recurrence: - 1; p_days_to_recurrence: 2326; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 1; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 63; s_bioanalyzer_18s: 14.42; s_bioanalyzer_28s: 20.13; s_bioanalyzer_area: 238.55; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.4; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.29; s_dnaind2: 1; s_dnaind3: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Goteborg; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 9.2; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 25; tissue_mg: 67; opdat: 19911014; extrdat: 20020101; time_in_freezer: 3732; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_days_to_recurrence: 360; p_local_recurrence_0no_1yes: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 40; s_bioanalyzer_18s: 10.6; s_bioanalyzer_28s: 9.7; s_bioanalyzer_area: 239.8; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.9; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: n/a; s_meno: pre; s_original_study: Linkoping; s_original_study_prog: 5; s_pgr_float: 5; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; tissue_mg: 31; opdat: 20030707; extrdat: 20050101; time_in_freezer: 544; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_days_to_recurrence: 4458; p_local_recurrence_0no_1yes: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 1; s_age_10year: 30; s_age_above50year_0no_1yes: 0; s_age_year: 34; s_bioanalyzer_18s: 9.4; s_bioanalyzer_28s: 9.9; s_bioanalyzer_area: 406.6; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.1; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: n/a; s_meno: non_available; s_original_study: Linkoping; s_original_study_prog: 0; s_pgr_float: 15; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; tissue_mg: 33; opdat: 19860206; extrdat: 20050101; time_in_freezer: 6904; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_days_to_recurrence: 750; p_local_recurrence_0no_1yes: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 46; s_bioanalyzer_18s: 11.9; s_bioanalyzer_28s: 11.4; s_bioanalyzer_area: 91; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: non_available; s_hgrade_lokrec: non_available; s_hgrade_lokrec_mitotic_count: non_available; s_hgrade_lokrec_pleomrph: non_available; s_hgrade_lokrec_tubules: non_available; s_histology_type: n/a; s_meno: pre; s_original_study: Linkoping; s_original_study_prog: 0; s_pgr_float: 12; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: -1; tissue_mg: 46; opdat: 19870604; extrdat: 20050101; time_in_freezer: 6421; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_days_to_recurrence: 3793; p_local_recurrence_0no_1yes: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 41; s_bioanalyzer_18s: 9.3; s_bioanalyzer_28s: 8.3; s_bioanalyzer_area: 68.6; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.9; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: n/a; s_meno: pre; s_original_study: Linkoping; s_original_study_prog: 1; s_pgr_float: 67; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; tissue_mg: 44; opdat: 19910124; extrdat: 20050101; time_in_freezer: 5091; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_days_to_recurrence: 1761; p_local_recurrence_0no_1yes: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 47; s_bioanalyzer_18s: 11.9; s_bioanalyzer_28s: 13.6; s_bioanalyzer_area: 233.5; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.1; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: n/a; s_meno: pre; s_original_study: Linkoping; s_original_study_prog: 5; s_pgr_float: 78; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: T2; tissue_mg: 59; opdat: 19920206; extrdat: 20050101; time_in_freezer: 4713; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_days_to_recurrence: 2351; p_local_recurrence_0no_1yes: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 48; s_bioanalyzer_18s: 10.1; s_bioanalyzer_28s: 11.8; s_bioanalyzer_area: 223.7; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.2; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: n/a; s_meno: non_available; s_original_study: Linkoping; s_original_study_prog: 5; s_pgr_float: 71; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 13; tissue_mg: 45; opdat: 19930105; extrdat: 20050101; time_in_freezer: 4379; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_days_to_recurrence: 2750; p_local_recurrence_0no_1yes: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 1; s_age_10year: 70; s_age_above50year_0no_1yes: 1; s_age_year: 73; s_bioanalyzer_18s: 11.2; s_bioanalyzer_28s: 9.9; s_bioanalyzer_area: 104.4; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.9; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: n/a; s_meno: pre; s_original_study: Linkoping; s_original_study_prog: 0; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 16; tissue_mg: 34; opdat: 19940519; extrdat: 20050101; time_in_freezer: 3880; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_days_to_recurrence: 2583; p_local_recurrence_0no_1yes: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 1; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 45; s_bioanalyzer_18s: 13.2; s_bioanalyzer_28s: 14.8; s_bioanalyzer_area: 237.6; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.1; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: n/a; s_meno: non_available; s_original_study: Linkoping; s_original_study_prog: 0; s_pgr_float: 26; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; tissue_mg: 33; opdat: 19970206; extrdat: 20050101; time_in_freezer: 2886; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_days_to_recurrence: 2024; p_local_recurrence_0no_1yes: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 56; s_bioanalyzer_18s: 4.3; s_bioanalyzer_28s: 4.7; s_bioanalyzer_area: 121; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.1; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: n/a; s_meno: non_available; s_original_study: Linkoping; s_original_study_prog: 9; s_pgr_float: 6; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; tissue_mg: 33; opdat: 19970825; extrdat: 20050101; time_in_freezer: 2686; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_cause_of_death: other_disease; p_days_followup: 6311; p_days_to_death: 6311; p_days_to_distant_recurrence: 3365; p_days_to_recurrence: 2665; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 2; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 30; s_age_above50year_0no_1yes: 0; s_age_year: 30; s_bioanalyzer_18s: 5.08; s_bioanalyzer_28s: 2.1; s_bioanalyzer_area: 145.35; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.41; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; tissue_mg: 26; opdat: 19830616; extrdat: 20020101; time_in_freezer: 6774; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 5117; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 3206; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 59; s_bioanalyzer_18s: 5.83; s_bioanalyzer_28s: 3.58; s_bioanalyzer_area: 77.61; s_bioanalyzer_manual: partly_degraded; s_bioanalyzer_ratio: 0.61; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; tissue_mg: 33; opdat: 19830502; extrdat: 20020101; time_in_freezer: 6819; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 5783; p_days_to_death: -1; p_days_to_distant_recurrence: 2079; p_days_to_recurrence: 2016; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 48; s_bioanalyzer_18s: 10.08; s_bioanalyzer_28s: 9.1; s_bioanalyzer_area: 404.2; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.9; s_bioanalyzer_rin: 6; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Ductal_tubular; s_meno: Pre; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 12; tissue_mg: 85; opdat: 19840528; extrdat: 20020101; time_in_freezer: 6427; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 3570; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 1890; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 56; s_bioanalyzer_18s: 14.58; s_bioanalyzer_28s: 12.27; s_bioanalyzer_area: 168.23; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.84; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 2.69; s_dnaind2: 1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 1; s_hgrade_lokrec: 3; s_hgrade_lokrec_mitotic_count: 3; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Ductal_UNS; s_meno: Post; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 20.6; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 10; tissue_mg: 55; opdat: 19860829; extrdat: 20020101; time_in_freezer: 5604; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_neg; p_cause_of_death: brca; p_days_followup: 1368; p_days_to_death: 1368; p_days_to_distant_recurrence: 886; p_days_to_recurrence: 482; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 20; s_age_above50year_0no_1yes: 0; s_age_year: 27; s_bioanalyzer_18s: 10.54; s_bioanalyzer_28s: 12.69; s_bioanalyzer_area: 301.08; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.2; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 5.5; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 1; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 14; tissue_mg: 72; opdat: 19861017; extrdat: 20020101; time_in_freezer: 5555; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_cause_of_death: brca; p_days_followup: 4639; p_days_to_death: 4639; p_days_to_distant_recurrence: 4460; p_days_to_recurrence: 947; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 46; s_bioanalyzer_18s: 12.01; s_bioanalyzer_28s: 13.6; s_bioanalyzer_area: 280.17; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.13; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 11; tissue_mg: 45; opdat: 19860217; extrdat: 20020101; time_in_freezer: 5797; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 6246; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: 2425; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 20; s_age_above50year_0no_1yes: 0; s_age_year: 28; s_bioanalyzer_18s: 10.01; s_bioanalyzer_28s: 8.2; s_bioanalyzer_area: 167.78; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.82; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 32; tissue_mg: 40; opdat: 19860317; extrdat: 20020101; time_in_freezer: 5769; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_pos; p_cause_of_death: brca; p_days_followup: 2611; p_days_to_death: 2611; p_days_to_distant_recurrence: 2353; p_days_to_recurrence: 1464; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 3; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 30; s_age_above50year_0no_1yes: 0; s_age_year: 39; s_bioanalyzer_18s: 5.77; s_bioanalyzer_28s: 6.53; s_bioanalyzer_area: 105.42; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.13; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 3; s_histology_type: Lobular; s_meno: Pre; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 14; tissue_mg: 21; opdat: 19870929; extrdat: 20020101; time_in_freezer: 5208; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 1; s_er_pos_neg: er_neg; p_cause_of_death: brca; p_days_followup: 1461; p_days_to_death: 1461; p_days_to_distant_recurrence: 849; p_days_to_recurrence: 531; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 1; p_local_recurrence_desc: 1; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 42; s_bioanalyzer_18s: 11.38; s_bioanalyzer_28s: 13.53; s_bioanalyzer_area: 486.65; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.19; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.24; s_dnaind2: 1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: non_available; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 8.6; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 17; tissue_mg: 47; opdat: 19890912; extrdat: 20020101; time_in_freezer: 4494; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 6933; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 30; s_age_above50year_0no_1yes: 0; s_age_year: 37; s_bioanalyzer_18s: 12.81; s_bioanalyzer_28s: 14.43; s_bioanalyzer_area: 388.57; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.13; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubular; s_meno: Pre; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: non_available; s_recurrence_0no_1yes: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; tissue_mg: 63; opdat: 19850430; extrdat: 20020101; time_in_freezer: 6090; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_neg; p_cause_of_death: alive; p_days_followup: 6243; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 49; s_bioanalyzer_18s: 18.76; s_bioanalyzer_28s: 24.82; s_bioanalyzer_area: 582.98; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.32; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.53; s_dnaind2: 1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: non_available; s_hgrade_lokrec: non_available; s_hgrade_lokrec_mitotic_count: non_available; s_hgrade_lokrec_pleomrph: non_available; s_hgrade_lokrec_tubules: non_available; s_histology_type: n/a; s_meno: Pre; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: non_available; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 20.7; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 1; s_tumor_size_mm: 22; tissue_mg: 96; opdat: 19870909; extrdat: 20020101; time_in_freezer: 5228; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 3381; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 40; s_age_above50year_0no_1yes: 0; s_age_year: 49; 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s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: pgr_pos; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 14.4; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 15; tissue_mg: 58; opdat: 19850802; extrdat: 20020101; time_in_freezer: 5996; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 6123; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 30; s_age_above50year_0no_1yes: 0; s_age_year: 33; s_bioanalyzer_18s: 10.23; s_bioanalyzer_28s: 10.68; s_bioanalyzer_area: 298.07; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.04; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1.54; s_dnaind2: 1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Ductal_UNS; s_meno: Pre; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: non_available; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 2; s_spf_percent: 5; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 8; tissue_mg: 49; opdat: 19860905; extrdat: 20020101; time_in_freezer: 5597; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 6591; p_days_to_death: -1; p_days_to_distant_recurrence: 5109; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 0; s_age_year: 50; s_bioanalyzer_18s: 9.27; s_bioanalyzer_28s: 7.89; s_bioanalyzer_area: 149.71; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.85; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 2; s_hgrade_lokrec_mitotic_count: 2; s_hgrade_lokrec_pleomrph: 3; s_hgrade_lokrec_tubules: 2; s_histology_type: Tubular; s_meno: Pre; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: pgr_neg; s_recurrence_0no_1yes: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 16; tissue_mg: 56; opdat: 19860725; extrdat: 20020101; time_in_freezer: 5639; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 2; s_er_pos_neg: er_pos; p_cause_of_death: alive; p_days_followup: 5625; p_days_to_death: -1; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 0; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 1; s_age_10year: 50; s_age_above50year_0no_1yes: 1; s_age_year: 52; s_bioanalyzer_18s: 16.7; s_bioanalyzer_28s: 19.49; s_bioanalyzer_area: 239.46; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 1.17; s_bioanalyzer_rin: 8; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_dnaind1: 1; s_dnaind2: -1; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 0; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 2; s_histology_type: Ductal_UNS; s_meno: non_available; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: non_available; s_recurrence_0no_1yes: 0; s_spf_nbr_pop: 1; s_spf_percent: 4.7; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 19; tissue_mg: 69; opdat: 19881222; extrdat: 20020101; time_in_freezer: 4758; ', 'series, 1 = lr+/rt+, 2 = lr-/rt+, 3 = lr+/rt-, 4 = lr-/rt-: 4; s_er_pos_neg: er_pos; p_cause_of_death: other; p_days_followup: 4977; p_days_to_death: 4977; p_days_to_distant_recurrence: -1; p_days_to_recurrence: -1; p_dead_followup_0no_1yes: 1; p_local_recurrence_0no_1yes: 0; p_local_recurrence_desc: 0; p_treat_chemo_0no_1yes: 0; p_treat_horm_0no_1yes: 0; p_treat_radio_0no_1yes: 0; s_age_10year: 60; s_age_above50year_0no_1yes: 1; s_age_year: 64; s_bioanalyzer_18s: 16.69; s_bioanalyzer_28s: 14.1; s_bioanalyzer_area: 138.22; s_bioanalyzer_manual: ok; s_bioanalyzer_ratio: 0.84; s_bioanalyzer_rin: 7; s_bioanalyzer_rin6_0no_1yes: 1; s_clinic_code: non_available; s_er_float: -1; characteristics: s_found_by_screening_0no_1yes:_ch1 1; s_hgrade3_lokrec_0no_1yes: 0; s_hgrade_lokrec: 1; s_hgrade_lokrec_mitotic_count: 1; s_hgrade_lokrec_pleomrph: 2; s_hgrade_lokrec_tubules: 1; s_histology_type: Ductal_tubular; s_meno: Post; s_original_study: Stockholm; s_pgr_float: -1; s_pgr_pos_neg: non_available; s_recurrence_0no_1yes: 0; s_surgery_desc: 1; s_surgery_extended_0no_1yes: 0; s_tumor_size20_0no_1yes: 0; s_tumor_size_mm: 6; tissue_mg: 51; opdat: 19880428; extrdat: 20020101; time_in_freezer: 4996; ' GSE35399 Homo sapiens 72 Expression profiling by array GPL10558 Elucidating the gene expression profiles of human mammary subpopulations 2012-01-29 The organisation of the mammary epithelial cell hierarchy and how these cells relate to the presentation of human breast tumours is poorly understood. Our results demonstrate that the luminal cell compartment of the mouse mammary gland can be resolved into terminally differentiated oestrogen receptor (ER)+ luminal cells, ER+ luminal progenitors and ER- luminal progenitors. The ER+ luminal progenitors are unique in regards to cell survival, as they are relatively insensitive to loss of oestrogen and progesterone when compared to the other types of mammary epithelial cells. Analysis of normal human breast tissue reveals a similar hierarchical organisation that is composed of terminally differentiated luminal cells and relatively differentiated (EpCAM+CD49f+ALDH-) and undifferentiated (EpCAM+CD49f+ALDH+) luminal progenitors. In addition, approximately one third of human breast samples examined contained an additional population that had a luminal progenitor phenotype, but is characterised by low expression of ERBB3 and low proliferative potential. Parent-progeny relationship experiments demonstrated that all luminal progenitor populations in both species are highly plastic and, at low frequencies, can generate progeny representing all mammary cell types. Gene expression profiling demonstrates that the ER- luminal progenitors in the mouse and the undifferentiated ALDH+ luminal progenitors in the human have gene signatures that resemble those obtained from basal-like breast tumours. Overall, our work reveals a more defined mammary cell hierarchy, which may in turn provide greater insight into the aetiology of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE35399 Phenotypic and functional characterisation of the luminal cell hierarchy of the mammary gland. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr3334 {Breast cancer research : BCR (5.676): 10.1186/bcr3334} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA152785 https://www.ebi.ac.uk/ena/browser/view/PRJNA152785 None [Overal design]Normal human breast tissues from reduction mammoplasties were dissociated into single cells and the epithelial cell populations were flow sorted. Total RNA was extracted for each group in 11 independent patient samples.; [Treatment]'None'; [Growth]'Discarded tissues from reduction mammoplasties received from Addenbrooke’s hospital. Freshly sorted cells were used for this study.'; [Extraction]'Human breast tissue were dissociated in collagenase and hyaluronidase for 14-16 h at 37°C, treated with ammonium chloride, trypsin, dispase, DNase and filtered to obtain a single cell suspension. Mammary cells were stained with fluorochrome-conjugated antibodies and the viability dye DAPI and were then passed through a cell sorter. Total RNA was extracted using a PicoPure RNA extraction kit. Total RNA was quality checked using a Bioanalyser.'; [Cell type]'luminal', 'basal', 'stromal''gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 1; ', 'gender: female; tissue: breast; cell type: basal; disease state: normal; patient: 1; ', 'gender: female; tissue: breast; cell type: stromal; disease state: normal; patient: 1; ', 'gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 2; ', 'gender: female; tissue: breast; cell type: stromal; disease state: normal; patient: 2; ', 'gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 3; ', 'gender: female; tissue: breast; cell type: basal; disease state: normal; patient: 3; ', 'gender: female; tissue: breast; cell type: stromal; disease state: normal; patient: 3; ', 'gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 4; ', 'gender: female; tissue: breast; cell type: basal; disease state: normal; patient: 4; ', 'gender: female; tissue: breast; cell type: stromal; disease state: normal; patient: 4; ', 'gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 5; ', 'gender: female; tissue: breast; cell type: basal; disease state: normal; patient: 5; ', 'gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 6; ', 'gender: female; tissue: breast; cell type: basal; disease state: normal; patient: 6; ', 'gender: female; tissue: breast; cell type: stromal; disease state: normal; patient: 6; ', 'gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 7; ', 'gender: female; tissue: breast; cell type: basal; disease state: normal; patient: 7; ', 'gender: female; tissue: breast; cell type: stromal; disease state: normal; patient: 7; ', 'gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 8; ', 'gender: female; tissue: breast; cell type: basal; disease state: normal; patient: 8; ', 'gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 9; ', 'gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 10; ', 'gender: female; tissue: breast; cell type: basal; disease state: normal; patient: 10; ', 'gender: female; tissue: breast; cell type: stromal; disease state: normal; patient: 10; ', 'gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 11; ', 'gender: female; tissue: breast; cell type: basal; disease state: normal; patient: 11; ', 'gender: female; tissue: breast; cell type: stromal; disease state: normal; patient: 11; ', 'gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 12; ', 'gender: female; tissue: breast; cell type: basal; disease state: normal; patient: 12; ', 'gender: female; tissue: breast; cell type: luminal; disease state: normal; patient: 13; ', 'gender: female; tissue: breast; cell type: basal; disease state: normal; patient: 13; ', 'gender: female; tissue: breast; cell type: stromal; disease state: normal; patient: 13; ' GSE39359 Homo sapiens 12 Expression profiling by array; Non-coding RNA profiling by array GPL6480; GPL11487 MiR-374a Promotes Epithelial-Mesenchymal Transition (EMT) and Metastasis of Breast Cancer 2012-07-13 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39359 MicroRNA-374a activates Wnt/β-catenin signaling to promote breast cancer metastasis. The Journal of clinical investigation 12.282 https://doi.org/10.1172/JCI65871 {The Journal of clinical investigation (12.282): 10.1172/JCI65871} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA170688 https://www.ebi.ac.uk/ena/browser/view/PRJNA170688 None [Overal design]Refer to individual Series; [Treatment]'pMSCV-miR-374a or empty vector was co-transfected with the pIK packaging plasmid in 293FT cells by using the standard calcium phosphate transfection method. Thirty-six hours after the co-transfection, supernatants were collected and incubated with cells to be infected for 24 hours in the presence of polybrene (2.5 μg/mL). Following infection, puromycin (1.5μg/mL) was used to select stably transduced cells for 10 days.', 'MDA-MB-435 cells were injected into the mammary fat pads of BALB/C nude mice. After 30 days, the animals were sacrificed, pulmonary metastatic nodules were isolated and minced, and cell culture was established using the obtained explants.'; [Growth]'The MCF-7 breast cancer cells were cultured in complete DMEM medium and supplied with 10% FBS.', 'The MDA-MB-435 breast cancer cells were cultured in complete DMEM medium and supplied with 10% FBS.'; [Extraction]"Total RNA was isolated using the RNeasy RNA isolation kit (Qiagen) following the supplier's protocol.", 'Total RNA was isolated using mirVanaTM miRNA isolation kit (Ambion, Austin, TX) following supplier’s protocol.'; [Cell type]'breast cancer cells', 'parental cells cultured from primary explant', 'metastatic cells cultured from pulmonary metastatic nodules''cell line: MCF-7; cell type: breast cancer cells; transduction: vector control; ', 'cell line: MCF-7; cell type: breast cancer cells; transduction: miR-374a precursor; ', 'cell line: MDA-MB-435; cell type: parental cells cultured from primary explant; ', 'cell line: MDA-MB-435; cell type: metastatic cells cultured from pulmonary metastatic nodules; ' GSE137408 Homo sapiens 18 Expression profiling by high throughput sequencing GPL11154 Splicing and gene expression changes in human MDAM-MB231 breast cancer cells with TRA2B knockdown 2019-09-13 RNA-seq data from human MDA-MB231 breast cancer cells expressing control or TRA2B-targeting shRNAs grown for 8 days in 3D culture in matrigel https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE137408 Differential Functions of Splicing Factors in Mammary Transformation and Breast Cancer Metastasis. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2019.10.110 {Cell reports (7.815): 10.1016/j.celrep.2019.10.110} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA565391 https://www.ebi.ac.uk/ena/browser/view/PRJNA565391 https://www.ncbi.nlm.nih.gov/sra?term=SRP221583 [Overal design]We examined the differential gene expression and splicing changes in MDA-MB231 cells expressing a DOX-inducible non targeting (shCTL) or TRA2B-targeting shRNA (TRA2Bsh1 and TRA2B sh2). For each shRNA, we compared -DOX vs +DOX.; [Treatment]'Cells were treated with DOX (2ug/ml) or DMSO. Media was replaced every 3 days.'; [Growth]'MDA-MB231 cells stably expressing a retroviral construct containing a control or TRA2B-targeting DOX inducible shRNAs were grown for 8 days in matrigel.'; [Extraction]'3D structures were removed from the matrigel and RNA was extracted using an RNAeasy extraction kit (Qiagen) which includes DNAseI treatment.\nLibraries were prepared using the RNA-seq stranded mRNA kit from Illumina and sequenced as 125 bp PE reads on a HiSeq2500'; [Cell type]'Source: ''construct: TRA2B shRNA 2; culture: 3D culture day 8; treatment: without DOX; barcode: CGATGT(A); ', 'construct: TRA2B shRNA 2; culture: 3D culture day 8; treatment: with DOX (2ug/ml); barcode: CAGATC(A); ', 'construct: TRA2B shRNA 1; culture: 3D culture day 8; treatment: without DOX; barcode: GTGAAA(C); ', 'construct: TRA2B shRNA 1; culture: 3D culture day 8; treatment: with DOX (2ug/ml); barcode: ACAGTG(A); ', 'construct: control shRNA; culture: 3D culture day 8; treatment: without DOX; barcode: ACAGTG(A); ', 'construct: control shRNA; culture: 3D culture day 8; treatment: without DOX; barcode: GCCAAT(A); ', 'construct: control shRNA; culture: 3D culture day 8; treatment: without DOX; barcode: GTGAAA(C); ', 'construct: control shRNA; culture: 3D culture day 8; treatment: with DOX (2ug/ml); barcode: CGATGT(A); ', 'construct: control shRNA; culture: 3D culture day 8; treatment: with DOX (2ug/ml); barcode: CCGTCC(C); ', 'construct: control shRNA; culture: 3D culture day 8; treatment: with DOX (2ug/ml); barcode: TGACCA; ' GSE77948 Mus musculus 6 Expression profiling by array GPL6096 Gene expression profiling of mammary epithelial cells from mice transiently exposed to tamoxifen 2016-02-16 The tumor suppressor gene p53 is frequently mutated in human breast cancer and is a marker for poor prognosis and resistance to chemotherapy. Transplantation of p53-null mouse mammary epithelium into syngeneic wild-type mice leads to normal mammary gland development followed by spontaneous mammary tumors that recapitulate many of the phenotypic, molecular, and genetic features of human breast cancer. Using this genetically engineered mouse model, we have examined the molecular mechanisms underlying tamoxifen-dependent tumor prevention. To determine whether the changes observed in the ERα cistrome after tamoxifen exposure are reflected in changes in estrogen responsive gene signatures in p53-null mammary epithelial cells (MECs), we performed global gene expression analysis by microarray profiling of MECs isolated from control and tamoxifen-exposed mice 4 weeks after tamoxifen withdrawal and treated with E2 for 8h. We identified 245 differentially regulated genes (P<0.01 and FC>1.4). Of these, 177 genes (72%) were persistently upregulated and 68 genes (28%) were persistently downregulated after transient exposure to tamoxifen. These results indicate that transient exposure to tamoxifen leads to lasting intrinsic changes in gene expression profiles of p53-null mammary epithelial cells that persist after tamoxifen withdrawal. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE77948 Reprogramming of the estrogen responsive transcriptome contributes to tamoxifen-dependent protection against tumorigenesis in the p53 null mammary epithelial cells. PloS one 2.776 https://doi.org/10.1371/journal.pone.0194913 {PloS one (2.776): 10.1371/journal.pone.0194913} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA312187 https://www.ebi.ac.uk/ena/browser/view/PRJNA312187 None [Overal design]Two experimental groups: Tamoxifen-treated group and control group. We used triplicate pools of mammary glands from control or tamoxifen-treated mice (5 mice per pool) for preparation of MEC’s total RNA isolation followed by Affymetrix array profiling using Affymetrix GeneChip Mouse Exon 1.0 ST array.; [Treatment]"The basic transplantation protocol was previously described. Briefly, the inguinal (#4) mammary fat pads of three-week-old Balb/c WT mice were cleared. Five weeks after fat pad clearance, 1-mm2 fragments of mammary duct from 8-week-old female p53-null mice were transplanted into both cleared inguinal mammary fat pads. The transplanted cells take 8 weeks to completely fill the fat pad, at which point the cells assume a steady-state level of proliferation. Thus, tamoxifen treatment was started at 8-week-old hosts' age to avoid any effects of the agents on the ability of the cells to grow and fill the fat pad. At 8 weeks of host age, mice received a 5 mg tamoxifen (TAM) pellet or sham (control) pellet subcutaneously (SC) on the back. The pellets remained in place for 13 weeks before removal. At 4 weeks or 8 weeks after cessation of tamoxifen, all mice were injected with 17β-Estradiol (100μg SC). After 8h of 17β-Estradiol (E2) treatment, all mice were sacrificed and #4 mammary gland transplants were collected. Mammary epithelial cells were isolated by collagenase digestion."; [Growth]'All donor and recipient mice were bred and maintained at Baylor College of Medicine. The donor mice were Balb/c p53-null mammary gland, and the recipient mice were Balb/c p53 WT. All mice were maintained in a conventional mouse facility with room temperature set at 22°C, with food and water provided ad libitum. The animal facility is accredited by the American Association of Laboratory Animal Care and all the animal experiments were approved by the Institutional Animal Care and Use Committee (IACUC) at Baylor College of Medicine. Mammary epithelial cells (MECs) were isolated following a protocol previously published. Briefly, #4 mammary gland transplants were collected and intramammary lymph nodes were removed. Each group of mammary glands were pooled, finely minced and transferred into a sterile 50 mL tube containing 10 mL of DMEM/F12 media with antibiotics supplemented with collagenase (2 mg/ml) and hyaluronidase 100U/ml mixture. The tubes were kept at a 45o angle in a 37oC shaker for 3h. The dispersion was further facilitated by mechanically shaking vigorously a few times. The mammary epithelial cells released by this digestion were centrifuged at 1000X g for 5 min and washed 4 times in PBS with 5% serum to eliminate fat cells and the remaining collagenase. Cells were re-suspended with serum-free PBS. Cell viability was assessed by trypan blue exclusion.'; [Extraction]"For microarray and quantitative Real-Time PCR (qPCR), total mammary epithelial cell RNA or total mammary gland RNA was isolated from #4 glands (lymph nodes removed) using the RNeasy Lipid Tissue Midi Kit according to the manufacturer's instructions (QIAGEN, Inc., Valencia, CA). Physical integrity of the RNA was assessed using the Agilent 2100 Bioanalyzer (Agilent Technologies, Inc., Santa Clara, CA); RNA quantitation was performed using the NanoDrop ND1000 spectrophotometer (NanoDrop Technologies, Wilmington, DE). For microarray and qPCR analysis, total RNA pooled from a set of three to five mice per treatment group was analyzed."; [Cell type]'mammary epithelial cells (MECs)''cell type: mammary epithelial cells (MECs); strain/background: Balb/c; genotype/variation: p53-null; treatment 1: control; treatment 2: 17-beta-estradiol (E2) for 8h; ', 'cell type: mammary epithelial cells (MECs); strain/background: Balb/c; genotype/variation: p53-null; treatment 1: tamoxifen; treatment 2: 17-beta-estradiol (E2) for 8h; ' GSE124843 Homo sapiens 24 Expression profiling by high throughput sequencing GPL16791 Integrative transcriptomic analysis reveals mechanisms controlling the reciprocity of epithelial and mesenchymal genes during epithelial-to-mesenchymal transition 2019-01-09 Epithelial-to-mesenchymal transition (EMT) is an important developmental process that is also activated during disease progressions. Many genes involved in EMT have been identified to date, but the key molecules governing the coupling between the dynamics of epithelial genes and that of the mesenchymal genes are unclear. In addition, it has been shown that there is a remarkable diversity of EMT phenotypes in different pathological conditions or microenvironments, but its mechanistic basis remains elusive. In this study, we used transcriptomic analysis to identify the roles of an EMT-inducing transcription factor ZEB1 in controlling epithelial and mesenchymal genes. We found that the mesenchymal genes exhibit a significant diversity in terms of their responsiveness to ZEB1. We applied machine learning approaches to the transcriptome data and identified three groups of M-genes that are controlled by EMT promoting factors via different types of regulatory circuits. We inferred the functional differences among the M-gene clusters in motility regulation of cultured cells and in survival of breast cancer patients. We characterized the roles of ZEB1 in controlling the reciprocity and reversibility of EMT using mathematical modeling. Our integrative analysis reveals the key roles of ZEB1 in coordinating the dynamics of a large number of genes during EMT, and it provides new insights into the mechanisms for the diversity of EMT phenotypes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124843 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA513977 https://www.ebi.ac.uk/ena/browser/view/PRJNA513977 https://www.ncbi.nlm.nih.gov/sra?term=SRP178052 [Overal design]MCF10A cells were treated by combinations of perturbations as follows: recombinant TGF-beta (200 nM) for 4 weeks, CRISPR/Cas9-mediated ZEB1 knockout, doxycycline-inducible expression of exogenous ZEB1, and TGF-beta type1 receptor inhibiotr (SB-431542, 10microM) treatment; [Treatment]'MCF10A cells were treated by combinations of perturbations as follows: recombinant TGF-beta (200 nM) for 4 weeks, CRISPR/Cas9-mediated ZEB1 knockout, doxycycline-inducible expression of exogenous ZEB1, and TGF-beta type1 receptor inhibiotr (SB-431542, 10microM) treatment'; [Growth]'MCF10A cells were grown in DMEM/F12(1:1) medium with 5% horse serum, epidermal growth factor (10 ng/mL), cholera toxin (100 ng/mL) and insulin (0.023 IU/mL)'; [Extraction]'Total RNA was extracted by Qiagen miRNeasy Mini Kit (QIAGEN Inc.) according to the manufacturer’s instructions.\nCAGE libraries were prepared as previously described (Murata et al., Methods Mol Biol 2014). Briefly, 3\u2009μg of total RNA from each sample was subjected to reverse transcription using SuperScript III Reverse Transcriptase (Life Technologies, Carlsbad, CA, USA) with random primers. The 5-end cap structure were biotinylated by sequential oxidation with NaIO4 and biotinylation with biotin hydrazide (Vector Laboratories, Burlingame, CA, USA). After RNase I treatment (Promega, Madison, WI, USA), the biotinylated cap structure was captured with streptavidin-coated magnetic beads (Life Technologies). After ligation of 5’ and 3’ adaptors, second-strand cDNAs were synthesized with DeepVent (exo−) DNA polymerase (New England BioLabs, Ipswich, MA, USA). The double-stranded cDNAs were treated with exonuclease I (New England BioLabs) and purified.'; [Cell type]'mammary epithelial cells''cell line: MCF10A; cell type: mammary epithelial cells; transgene: NA; passages: 10 to 15; treatment: control; ', 'cell line: MCF10A; cell type: mammary epithelial cells; transgene: NA; passages: 10 to 15; treatment: recombinant TGF-beta; ', 'cell line: MCF10A; cell type: mammary epithelial cells; transgene: ZEB1 knockout; passages: 10 to 15; treatment: control; ', 'cell line: MCF10A; cell type: mammary epithelial cells; transgene: ZEB1 knockout; passages: 10 to 15; treatment: recombinant TGF-beta; ', 'cell line: MCF10A; cell type: mammary epithelial cells; transgene: inducible ZEB1; passages: 10 to 15; treatment: DMSO; ', 'cell line: MCF10A; cell type: mammary epithelial cells; transgene: inducible ZEB1; passages: 10 to 15; treatment: DMSO + DOX; ', 'cell line: MCF10A; cell type: mammary epithelial cells; transgene: inducible ZEB1; passages: 10 to 15; treatment: TGF-beta type1 receptor inhibitor (SB-431542); ', 'cell line: MCF10A; cell type: mammary epithelial cells; transgene: inducible ZEB1; passages: 10 to 15; treatment: TGF-beta type1 receptor inhibitor (SB-431542) + DOX; ' GSE146822 Homo sapiens 13 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Mapping of epigenetic marks (H3K4me1, H3K4me3, H3K27ac), p300/CBP, PolII and CTCF on MDA-MB-231 genome 2020-03-11 In the article "Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers" by Bejjani et al., we mapped epigenetic marks (H3K4me1, H3K4me3, H3K27ac), p300/CBP, PolII and CTCF to characterize the binding sites of Fra-1 and Fra-2 on MDA-MB-231 genome. Data for Fra-1 and Fra-2 ChIP-seq are available on GEO database, accession number GSE132098 (Tolza et al., 2019, MCR 17, 1999-2014) https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE146822 Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkab053 {Nucleic acids research (11.147): 10.1093/nar/gkab053} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA612054 https://www.ebi.ac.uk/ena/browser/view/PRJNA612054 https://www.ncbi.nlm.nih.gov/sra?term=SRP252453 [Overal design]ChIP-seq were carried out on MDA-MB-231 cells using antibodies specific of epigenetic marks (H3K4me1, H3K4me3, H3K27ac), p300/CBP, PolII and CTCF; [Treatment]'experiments were carried out in 2 independent replicates except for p300/CBP'; [Growth]'MDA-MB-231 cells (ATCC, Rockville, MD, USA) were cultured cultured in Dulbecco’s modified Eagle’s medium containing 10% fetal calf serum and penicillin/streptomycin (100µg/ml each) in a humidified 5% CO2 atmosphere at 37°C. Cells freshly amplified and frozen after obtention from the ATCC were used every 3months and were routinely tested for the absence of mycoplasma contamination'; [Extraction]'Lysates were clarified from sonicated nuclei and protein-DNA complexes were isolated with the appropriate antibodies.\nChIP-seq libraries were prepared using the TruSeq ChIP sample reparation kit from Illumina by the MGX sequencing Platform (Montpellier, France)'; [Cell type]'breast cancer cell line''cell line: MDA-MB-231; cell type: breast cancer cell line; tumor type: triple negative - basal b; chip antibody: none (input); ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; tumor type: triple negative - basal b; chip antibody: H3K4me1 Ab8895 from Abcam; ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; tumor type: triple negative - basal b; chip antibody: H3K4me3 Ab8580 from Abcam; ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; tumor type: triple negative - basal b; chip antibody: H3K27ac Ab4729 from Abcam; ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; tumor type: triple negative - basal b; chip antibody: p300/CBP Ab14984 from Abcam; ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; tumor type: triple negative - basal b; chip antibody: pol II sc-55492 from Santa Cruz Biotechnology; ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; tumor type: triple negative - basal b; chip antibody: CTCF C15410210 from Diagenode; ' GSE118466 Mus musculus 8 Expression profiling by array GPL17400 Expression array of carcinoma cell Mmp14-targeted MMTV-PyMT mammary tumors 2018-08-13 Breast carcinoma cell invasion is thought to depend on the mobilization of the membrane-anchored matrix metalloproteinase, Mmp14/MT1-MMP, to drive the remodeling of extracellular matrix and trigger associated signaling cascades. However, the roles that this proteinase plays during breast tumor progression and invasion in vivo remain undefined. A highly penetrant syngeneic mouse model for luminal B breast cancer driven by the polyoma middle T (PyMT) antigen, in tandem with recently developed Mmp14-floxed mice and MMTV-Cre transgenics that express Cre recombinase throughout the mammary epithelial cell compartment, were used to characterize the impact of conditional Mmp14-targeting on breast carcinoma cell invasion programs in vivo. Transcriptome profiling of intact MMTV-PyMT carcinoma tumors was used to investigate the functional roles of carcinoma cell-derived MT1-MMP in MMTV-PyMT tumor progression and invasion in an unbiased fashion https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE118466 Divergent Matrix-Remodeling Strategies Distinguish Developmental from Neoplastic Mammary Epithelial Cell Invasion Programs. Developmental cell 9.190 https://doi.org/10.1016/j.devcel.2018.08.025 {Developmental cell (9.190): 10.1016/j.devcel.2018.08.025} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA485737 https://www.ebi.ac.uk/ena/browser/view/PRJNA485737 None [Overal design]Intact mammary tumor tissue was harvested from conditional knockout [MMTV-Cre+/Mmp14(f/f)] MMTV-PyMT mice and wild-type [Mmp14(f/f)] MMTV-PyMT littermates on a congenic FVB/NJ background at 3-4 months for RNA extraction and hybridization on Affymetrix microarrays.; [Treatment]'None'; [Growth]'Intact MMTV-PyMT mammary tumors were harvested from the inguinal and thoracic mammary glands of 3-4 month-old mice.'; [Extraction]'MMTV-PyMT mammary tumors were flash frozen in liquid nitrogen and homogenized in 1mL TRIzol (Ambion, Life Technologies). Total RNA was extracted with chloroform according to standard protocols and purified with QIAGEN Rneasy Mini-kit columns.'; [Cell type]'Source: ''strain background: congenic FVB/NJ; genotype/variation: wild-type [Mmp14(f/f)] MMTV-PyMT; age: 3-4 months; tissue: MMTV-PyMT mammary tumors; ', 'strain background: congenic FVB/NJ; genotype/variation: conditional knockout [MMTV-Cre+/Mmp14(f/f)] MMTV-PyMT; age: 3-4 months; tissue: MMTV-PyMT mammary tumors; ' GSE64725 Homo sapiens 100 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL18224 Post-zygotic structural variants in histologically normal breast tissue may predispose to sporadic breast cancer [SET 7] 2015-01-07 Sporadic breast cancer (SBC) is a common and heterogeneous disease. There is no reliable way of early prediction of risk for SBC in the general population. We studied 282 females with SBC concentrating on copy number aberrations in tumor-free breast tissue (uninvolved margin, UM) outside the area of primary tumor (PT). Totally 1162 UMs (1-14 per breast) were studied. PT and blood/skin as control was also analyzed. Comparative analysis between genetic profiles for UM(s), PT(s) and blood/skin from the same patient is the core of study design. We identified 108 patients with at least one aberrant UM specimen, representing 38.3% of all cases. Gains were the dominating mutations in microscopically normal breast cells and gain of ERBB2, with overexpression of HER2 protein, was the most common aberration in normal cells. Five additional receptor genes (EGFR, FGFR1, IGF1R, LIFR and NGFR) also showed gains, and these were occasionally present in combination with the gain of ERBB2. Up to 67.6% of patients showed gain of one or more of these genes in normal cells. The aberrations found in normal cells from UMs were previously described in cancer literature, which suggest their causative, driving role in this disease. We demonstrate that analysis of normal cells from cancer-bearing patients leads to identification of genetic signatures that may predispose to SBC. Early detection of signals suggesting a predisposition towards development of SBC, long before detectable tumors are formed, is a key to the anticipated shift into a preventive paradigm of personalized medicine of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64725 Signatures of post-zygotic structural genetic aberrations in the cells of histologically normal breast tissue that can predispose to sporadic breast cancer. Genome research 9.944 https://doi.org/10.1101/gr.187823.114 {Genome research (9.944): 10.1101/gr.187823.114} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA271755 https://www.ebi.ac.uk/ena/browser/view/PRJNA271755 None [Overal design]We studied 282 female breast cancer patients that were assessed as affected by sporadic disease at the time of diagnosis and all underwent mastectomy. In total, 1162 UMs (uninvolved margin tissues), ranging from 1 to 14 UMs per patient, taken outside the location of clinically characterized index primary tumor, were analyzed on Illumina arrays. For each subject, DNA from at least one control tissue was also analyzed, which was predominantly blood DNA, alternatively skin-derived DNA. We also studied primary tumor (PT), or up to 3 primary tumor foci from patients with diagnosis of multifocal disease. This GEO project contains the genotyping profiles (processed and normalized data including Log R Ratio and B allele frequency) for these 1162 UMs used in the study. Information on phenotypes (age at diagnosis, tumor focality, tumor grade, tumor molecular phenotype) is also provided, whenever available. The sixth 100 samples out of 811 experiments runned on platform GPL18224 (Infinium HumanOmniExpressExome); [Treatment]'None'; [Growth]'None'; [Extraction]'The tissues were stored at -70 degrees C prior to DNA extraction. The solid tissues were homogenized with a Tissuerupter (Qiagen). Proteinase K and Sarcosine was then added and the sample was incubated at 50oC over-night. The samples were transferred to PhaseLock Gel tubes and the DNA was purified with phenol/chloroform extraction. Due to very rich content of fat in UMs, phenol/chloroform extraction was repeated 6 times for all UMs, and 3 times for PTs and control samples from skin. The purified DNA was precipitated with sodium acetate, pH 5.4 and 95% ethanol. The DNA precipitate was dried before dissolving in water. Control samples of blood were extracted with QIAmp DNA Blood Maxi Kit (Qiagen).'; [Cell type]'Source: ''subject_code: GC146; gender: female; age at cancer diagnosis (yrs): 70; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: GC147; gender: female; age at cancer diagnosis (yrs): 70; tumor grade: 3; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: GGB040; gender: female; age at cancer diagnosis (yrs): 63; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; ', 'subject_code: GI004; gender: female; age at cancer diagnosis (yrs): 62; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; ', 'subject_code: GS166; gender: female; age at cancer diagnosis (yrs): 56; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: HB054; gender: female; age at cancer diagnosis (yrs): 47; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; ', 'subject_code: HL057; gender: female; age at cancer diagnosis (yrs): 71; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; ', 'subject_code: HZK162; gender: female; age at cancer diagnosis (yrs): 75; tumor grade: 1; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: ILN025; gender: female; age at cancer diagnosis (yrs): 70; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; ', 'subject_code: ILS024; gender: female; age at cancer diagnosis (yrs): 73; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; ', 'subject_code: JE009; gender: female; age at cancer diagnosis (yrs): 52; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ', 'subject_code: JM154; gender: female; age at cancer diagnosis (yrs): 74; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: JP149; gender: female; age at cancer diagnosis (yrs): 44; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: JW167; gender: female; age at cancer diagnosis (yrs): 53; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ', 'subject_code: KK151; gender: female; age at cancer diagnosis (yrs): 54; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ' GSE138078 Homo sapiens 6 Expression profiling by array GPL16686 PRRX1 overexpression in MDA-MB-231 breast cancer cells 2019-09-26 To investigate downstream targets of PRRX1, we used MDA-MB-231 (MDA231) breast cancer cells which express low level of PRRX1 to generate a stable cell line where human PRRX1 was ectopically overexpressed (MDA231-PRRX1), and performed comparative microarray analyses. Interestingly, we found many miRNAs that were upregulated in MDA231-PRRX1 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE138078 A gene regulatory network to control EMT programs in development and disease. Nature communications 11.878 https://doi.org/10.1038/s41467-019-13091-8 {Nature communications (11.878): 10.1038/s41467-019-13091-8} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA574460 https://www.ebi.ac.uk/ena/browser/view/PRJNA574460 None [Overal design]MDA231 cells were transduced with lentiviral vectors containing PRRX1, GFP and puromycine resistance cassette, and were selected with antibiotics. Pool of stably transduced cells were used for further analyses and microarray.; [Treatment]'Cells were transduced using a lentiviral system to stably express control GFP (MDA231-Control, MDA231-C) and PRRX1 (MDA231-PRRX1, MDA231-P)'; [Growth]'Cells were cultured in DMEM:F12 HAM media (1:1), and SUM149PT cells in F12 HAM media, supplemented with 10% heat inactivated fetal bovine serum (FBS) (Sigma), 10 μg/ml insulin (Roche), 1% Gentamicin (Sigma) and 1% amphotericin (Sigma).'; [Extraction]"RNA extractions were performed from cells in 70% confluency in 10cm plates, using miRvana kit following manufacturer's instructions."; [Cell type]'Triple-negative, mesenchymal''cell type: Triple-negative, mesenchymal; ' GSE46934 Homo sapiens 149 Non-coding RNA profiling by array GPL8227 Individual and combined effects of DNA methylation and copy number alterations on miRNA expression in breast tumors 2013-05-20 Background: The global effect of copy number and epigenetic alterations on miRNA expression in cancer is poorly understood. In the present study, we integrate genome-wide copy number, DNA methylation and miRNA expression and identify genetic mechanisms underlying miRNA dysregulation in breast cancer. Results: We identify 70 miRNAs whose expression was associated with aberrations in copy number or methylation, or both. Among these, five miRNA families are represented. Interestingly, the members of these families are encoded on different chromosomes and are complementarily altered by gain or hypomethylation across the patients. In an independent breast cancer cohort of 123 patients, 41 of the 70 miRNAs were confirmed with respect to aberration pattern and association to expression. In vitro functional experiments were performed in breast cancer cell lines with miRNA mimics to evaluate the phenotype of the replicated miRNAs. let-7e-3p, which in tumors is found associated with hypermethylation, is shown to induce apoptosis and reduce cell viability, and low let-7e-3p expression is associated with poorer prognosis. The overexpression of three other miRNAs associated with copy number gain, miR-21-3p, miR-148b-3p and miR-151a-5p, increases proliferation of breast cancer cell lines. In addition, miR-151a-5p enhances the levels of phosphorylated AKT protein. Conclusions: Our data provide novel evidence of the mechanisms behind miRNA dysregulation in breast cancer. The study contributes to the understanding of how methylation and copy number aberrations influence miRNA expression, emphasizing miRNA functionality through redundant encoding, and suggests novel miRNAs important in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE46934 Individual and combined effects of DNA methylation and copy number alterations on miRNA expression in breast tumors. Genome biology 14.028 https://doi.org/10.1186/gb-2013-14-11-r126 {Genome biology (14.028) doi:10.1186/gb-2013-14-11-r126}; {British journal of cancer (5.416) doi:10.1038/bjc.2014.113}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA203649 https://www.ebi.ac.uk/ena/browser/view/PRJNA203649 None [Overal design]The miRNA expression profiling of 149 breast cancer samples was performed using the 8x15k “Human miRNA Microarray Kit (V2)” with design id 019118 from Agilent (Agilent Technologies, Santa Clara, CA, USA). In brief, 100 ng total RNA was dephosphorylated, labeled and hybridized for 20 hours, following the manufacturer’s protocol. Scanning was performed on Agilent Scanner G2565A, signals were extracted using Feature Extraction v9.5 and the subsequent data processing was performed using the GeneSpring software v12.0 (Agilent Technologies). In brief, the miRNA signal intensities were log2-transformed and normalized to the 90th percentile, and miRNAs that were detected in less than 10% of the samples were excluded. This resulted in 448 unique mature miRNAs.; [Treatment]'Fresh frozen in liquid nitrogen'; [Growth]'Human primary tumors'; [Extraction]'TRIzol, following manufactors protocol'; [Cell type]'Source: ''tissue: breast tumor; sample no: 609; tumor size grade: 3; anaplasi grade: 3; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 4345; tumor size grade: 2; anaplasi grade: 3; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 31; tumor size grade: 1; anaplasi grade: 2; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 522; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4134; tumor size grade: 1; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3087; tumor size grade: 1; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3151; tumor size grade: 3; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4367; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3891; tumor size grade: 2; anaplasi grade: 99; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4049; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4275; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3184; tumor size grade: 1; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3134; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4103; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3388; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3027; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4370; tumor size grade: 1; anaplasi grade: 2; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 4005; tumor size grade: 3; anaplasi grade: 99; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 3718; tumor size grade: 2; anaplasi grade: 3; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 4305; tumor size grade: 3; anaplasi grade: 3; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 3071; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3279; tumor size grade: 2; anaplasi grade: 2; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 3348; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 3867; tumor size grade: 1; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3345; tumor size grade: 1; anaplasi grade: 3; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 4002; tumor size grade: 1; anaplasi grade: 99; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 4324; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 1251; tumor size grade: 3; anaplasi grade: 3; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 3095; tumor size grade: 3; anaplasi grade: 3; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 3814; tumor size grade: 2; anaplasi grade: 3; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 3111; tumor size grade: 3; anaplasi grade: 99; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3195; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3973; tumor size grade: 2; anaplasi grade: 99; er status: 1; her2 status: 99; ', 'tissue: breast tumor; sample no: 3969; tumor size grade: 3; anaplasi grade: 3; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 3720; tumor size grade: 1; anaplasi grade: 3; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4167; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3232; tumor size grade: 1; anaplasi grade: 2; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 4150; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4152; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3861; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3397; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3164; tumor size grade: 3; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3998; tumor size grade: 2; anaplasi grade: 3; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3516; tumor size grade: 1; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3328; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 1247; tumor size grade: 1; anaplasi grade: 2; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 3959; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 650; tumor size grade: 2; anaplasi grade: 2; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 3251; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 1408; tumor size grade: 2; anaplasi grade: 2; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 356; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 246; tumor size grade: 2; anaplasi grade: 3; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 1443; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 320; tumor size grade: 3; anaplasi grade: 2; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 115; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 258; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 544; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 457; tumor size grade: 3; anaplasi grade: 3; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 185; tumor size grade: 3; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 1352; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 3119; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4028; tumor size grade: 1; anaplasi grade: 2; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 235; tumor size grade: 2; anaplasi grade: 3; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 3599; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3801; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 4117; tumor size grade: 3; anaplasi grade: 2; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 3967; tumor size grade: 1; anaplasi grade: 2; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 3053; tumor size grade: 2; anaplasi grade: 3; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 1198; tumor size grade: 3; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 348; tumor size grade: 2; anaplasi grade: 99; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 4050; tumor size grade: 1; anaplasi grade: 2; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 4350; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 1517; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 753; tumor size grade: 3; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 147; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3046; tumor size grade: 1; anaplasi grade: 3; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 945; tumor size grade: 3; anaplasi grade: 3; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 1077; tumor size grade: 1; anaplasi grade: 3; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 1297; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 1374; tumor size grade: 1; anaplasi grade: 3; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 262; tumor size grade: 1; anaplasi grade: 2; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 1688; tumor size grade: 3; anaplasi grade: 3; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 1541; tumor size grade: 2; anaplasi grade: 2; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 3214; tumor size grade: 2; anaplasi grade: 2; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 1589; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 278; tumor size grade: 1; anaplasi grade: 3; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 478; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 702; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3168; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 699; tumor size grade: 3; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3223; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 579; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 127; tumor size grade: 2; anaplasi grade: 2; er status: 0; her2 status: 99; ', 'tissue: breast tumor; sample no: 1559; tumor size grade: 2; anaplasi grade: 2; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 533; tumor size grade: 2; anaplasi grade: 3; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 1292; tumor size grade: 1; anaplasi grade: 1; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 3797; tumor size grade: 2; anaplasi grade: 3; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 3398; tumor size grade: 1; anaplasi grade: 2; er status: 0; her2 status: 99; ', 'tissue: breast tumor; sample no: 4077; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 327; tumor size grade: 2; anaplasi grade: 2; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 1630; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4337; tumor size grade: 1; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 415; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 1437; tumor size grade: 2; anaplasi grade: 2; er status: 0; her2 status: 1; ', 'tissue: breast tumor; sample no: 1238; tumor size grade: 2; anaplasi grade: 1; er status: 0; her2 status: 99; ', 'tissue: breast tumor; sample no: 3497; tumor size grade: 3; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 206; tumor size grade: 2; anaplasi grade: 3; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 1075; tumor size grade: 1; anaplasi grade: 1; er status: 1; her2 status: 99; ', 'tissue: breast tumor; sample no: 3640; tumor size grade: 2; anaplasi grade: 3; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3448; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 243; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 1254; tumor size grade: 2; anaplasi grade: 3; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 3886; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3623; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 22; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 57; tumor size grade: 1; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3213; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3363; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 843; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 1419; tumor size grade: 1; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4342; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3055; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 3604; tumor size grade: 2; anaplasi grade: 1; er status: 0; her2 status: 99; ', 'tissue: breast tumor; sample no: 1277; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 1255; tumor size grade: 2; anaplasi grade: 3; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 1056; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 3166; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 1348; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 596; tumor size grade: 3; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4099; tumor size grade: 2; anaplasi grade: 3; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 949; tumor size grade: 2; anaplasi grade: 2; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 3696; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 265; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 162; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 905; tumor size grade: 2; anaplasi grade: 2; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 365; tumor size grade: 3; anaplasi grade: 99; er status: 1; her2 status: 99; ', 'tissue: breast tumor; sample no: 1034; tumor size grade: 2; anaplasi grade: 3; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 99; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3676; tumor size grade: 2; anaplasi grade: 3; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3888; tumor size grade: 1; anaplasi grade: 3; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 3317; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 3866; tumor size grade: 2; anaplasi grade: 3; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 3169; tumor size grade: 2; anaplasi grade: 1; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 1411; tumor size grade: 2; anaplasi grade: 3; er status: 0; her2 status: 0; ', 'tissue: breast tumor; sample no: 4059; tumor size grade: 3; anaplasi grade: 1; er status: 1; her2 status: 1; ', 'tissue: breast tumor; sample no: 960; tumor size grade: 2; anaplasi grade: 99; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 4192; tumor size grade: 1; anaplasi grade: 2; er status: 1; her2 status: 0; ', 'tissue: breast tumor; sample no: 1377; tumor size grade: 2; anaplasi grade: 2; er status: 1; her2 status: 0; ' GSE93337 Homo sapiens 8 Expression profiling by array GPL13667 FFPE samples profiled on HG-U219 array with Affymetrix's SensationPlusTM FFPE Amplification and 3'IVT Labeling kit 2017-01-09 The reliability of differential expression analysis on FFPE expression profiles from Affymetrix arrays is questionable, due to the wide range of percent-present values reported in studies which profiled FFPE samples on Affymetrix arrays. Moreover the validity of externally defined gene-modules in FFPE microarray expression profiles is unknown. Using eight breast cancer tumors with available frozen and FFPE samples, five sample-matched data sets were generated from different combination of Affymetrix arrays, amplification-and-labeling kit and sample preservation method. The reliability of differential expression analysis was investigated by developing de novo ER/HER2 pathway gene-modules from matched data sets and validating it on external data set using ROC analysis. Spearman's rank correlation coefficient of module scores between matched FFPE-frozen expression profiles was used to measure reliability of externally defined gene-modules in FFPE expression profiles. Independent of array/amplification-kit/sample preservation method used, de novo ER/HER2 gene-modules derived from all matching data sets showed similar prediction performance during independent validation (AUC range; ER: 0.92-0.95, HER2: 0.88-0.91), except for de novo HER2 gene-module derived from FFPE data set with 3'IVT kit (AUC: 0.67-0.72). Further not all gene-module based biological signals present in frozen expression profiles can be recovered from matching FFPE microarray expression profiles using the currently available FFPE specific sample preparation kits. The gene-module based biological signal extracted from FFPE RNA, using microarrays, may not be as reliable as that from their frozen counterpart, if the sample preparation protocol used with FFPE RNA failed to recover relevant genes involved in the biological signal. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93337 Feasibility of developing reliable gene expression modules from FFPE derived RNA profiled on Affymetrix arrays. PloS one 2.776 https://doi.org/10.1371/journal.pone.0203346 {PloS one (2.776): 10.1371/journal.pone.0203346} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA360631 https://www.ebi.ac.uk/ena/browser/view/PRJNA360631 None [Overal design]RNAs were extracted from eight FFPE preserved breast cancers. RNAs were amplified and labeled using Affymetrix's SensationPlusTM FFPE Amplification and 3'IVT Labeling kit, and profiled on Affymetrix® HG-U219 Array Plate according to Affymetrix's standard procedure.; [Treatment]'NA'; [Growth]'NA'; [Extraction]'Total RNA from FFPE sections was extracted using miRNeasy FFPE kit according to Qiagen recommendation.'; [Cell type]'Source: ''tissue: breast tumor; er status: negative; her2 status: negative; tissue preservation method: FFPE; ', 'tissue: breast tumor; er status: positive; her2 status: negative; tissue preservation method: FFPE; ', 'tissue: breast tumor; er status: negative; her2 status: positive; tissue preservation method: FFPE; ', 'tissue: breast tumor; er status: positive; her2 status: positive; tissue preservation method: FFPE; ' GSE117474 Mus musculus 14 Expression profiling by high throughput sequencing GPL17021 Mesenchymal Epithelial Transition (MET) Timecourse of NMuMG-E9 cells treated with TGFb 2018-07-22 Background: Epithelial-mesenchymal transition (EMT) has been implicated in metastasis, drug resistance, survival under stress and also conferring stem cell-like traits to cancer cells. However, several of the studies have been carried out using model systems that don’t appropriately recapitulate all stages of the dynamic process of EMT. Hence, there is a need to overcome this limitation by development of a model system that allows us to mimic each stage of EMT and accurately assess the plastic changes associated with it. Methods: We have derived a cancer cell line from the PyMT-MMTV model of breast cancer, named PyMT-1099 cells, and undertaken a detailed characterization of the morpho-genetic changes it undergoes during a TGFbeta-induced EMT. Further, we have also performed high throughput transcriptomics on PyMT-1099 cells undergoing EMT in a high resolution kinetic of TGFbeta treatment. Results: We show that PyMT-1099 cells undergo an EMT comparable to the classically used immortalized NMuMG cells as assessed by morphological, and marker expression changes on TGFbeta treatment. Further, PyMT-1099 cells can also migrate in vitro in response to TGFbeta treatment. These cells are also tumorigenic and lead to metastasis formation when transplanted into immunocompromised mice. Conclusion: In this study we report the development of PyMT-1099 cells as an excellent tool to model and study breast cancer-associated EMT both in vitro and in vivo and show that these cells overcome the limitations posed by other cellular systems currently being used to study EMT https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE117474 PyMT-1099, a versatile murine cell model for EMT in breast cancer. Scientific reports 4.011 https://doi.org/10.1038/s41598-018-30640-1 {Scientific reports (4.011): 10.1038/s41598-018-30640-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA482264 https://www.ebi.ac.uk/ena/browser/view/PRJNA482264 https://www.ncbi.nlm.nih.gov/sra?term=SRP154777 [Overal design]RNA-Seq of MET over a timecourse of 10 days on withdrawl of TGFbeta in NMuMG (E9) cells performed in biological duplicates; [Treatment]'For the MET timecourse, TGFbeta was withdrawn from NMuMG (E9) cells after 10d treatment. Cells were then seeded without TGFbeta for 1, 2, 3, 4, 7 or 10d. 10d TGFbeta treated cells (MET d0) served as the control for MET experiment.'; [Growth]'NMuMG (E9) cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) (Sigma-Aldrich, D5671) supplemented with 10% Fetal Bovine Serum (FBS, 10%; Sigma-Aldrich), 2 mM glutamine (Sigma-Aldrich, G7513), 100 U penicillin (Sigma-Aldrich) and 0.1 mg/ml streptomycin (Sigma-Aldrich). All cell lines were grown at 37°C, 5% CO2, 95% humidity.'; [Extraction]'Total RNA was isolated from the samples above using the miRNeasy Mini Kit (Qiagen, 217004) with on-column DNAse digestion according to the manufacturer’s instructions. 5\uf06dg of RNA was then subjected to rRNA depletion using the Ribozero magnetic gold kit (Epicentre, MRZG12324) followed by concentrating it using the RNeasy MinElute Cleanup Kit (Qiagen, 74204).\nRNA-Seq libraries were sequenced SR50 with Illumina HiSeq 2500 High Output v2 kit (Illumina) on an Illumina Illumina HiSeq 2500 using protocols defined by the manufacturer'; [Cell type]'Source: ''cell line: NMuMG; source tissue: Normal mammary gland; clone: Epithelial 9 (E9) clone; ', 'cell line: NMuMG; source tissue: Normal mammary gland; clone: Epithelial 9 (E9) clone; tgfbeta withdrawal for: d1; ', 'cell line: NMuMG; source tissue: Normal mammary gland; clone: Epithelial 9 (E9) clone; tgfbeta withdrawal for: d2; ', 'cell line: NMuMG; source tissue: Normal mammary gland; clone: Epithelial 9 (E9) clone; tgfbeta withdrawal for: d3; ', 'cell line: NMuMG; source tissue: Normal mammary gland; clone: Epithelial 9 (E9) clone; tgfbeta withdrawal for: d4; ', 'cell line: NMuMG; source tissue: Normal mammary gland; clone: Epithelial 9 (E9) clone; tgfbeta withdrawal for: d7; ', 'cell line: NMuMG; source tissue: Normal mammary gland; clone: Epithelial 9 (E9) clone; tgfbeta withdrawal for: d10; ' GSE41678 Homo sapiens 80 Expression profiling by array GPL6244 System-Wide Analysis Reveals a Complex Network of Tumor-Fibroblast Interactions Involved in Tumorigenicity 2012-10-18 We’ve undertaken a genome-wide approach to identify and test genes in fibroblasts that are both induced upon interaction with basal breast cancer cells in culture and upregulated in stromal cells from primary human breast cancers. Several of the upregulated genes encode secreted growth factors or cytokines. Using RNAi and a co-injection tumorigenicity assay, we determined that the majority of secreted factors selected for functional validation played significant, yet functionally diverse, roles in promoting tumorigenicity. Rather than a single major mediator, these results indicate multiple points of intervention to prevent fibroblasts from supporting basal breast cancer. Additionally, we show that breast cancer subtypes differ markedly in the expression of these and other stromally secreted proteins using data from microdissected stromal samples. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41678 System-wide analysis reveals a complex network of tumor-fibroblast interactions involved in tumorigenicity. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1003789 {PLoS genetics (5.224): 10.1371/journal.pgen.1003789} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA177918 https://www.ebi.ac.uk/ena/browser/view/PRJNA177918 None [Overal design]Induction of genes in four different fibroblast strains (HFFF2, HFF1, CCD1112Sk and Wi38) upon coculture with Cal51 and MDAMB231 human basal breast cancer cell lines. Monocultures of each group are used as the experimental control with each group having 3-4 independent biological replicates.; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was isolated using the miRNeasy Mini kit (Qiagen) according to the manufacturer's protocol. The optional on-column DNA digestion was performed, using the RNase-free DNase Set (Qiagen)."; [Cell type]'Source: ''cell: Fibroblast CCD1112Sk monocultured; ', 'cell: Fibroblast CCD1112Sk cocultured with epithelial Cal51 cells; ', 'cell: Epithelial cells Cal51 cocultured with fibroblast CCD1112Sk; ', 'cell: Fibroblast CCD1112Sk cocultured with epithelial MDAMB231 cells; ', 'cell: Epithelial cells MDAMB231 cocultured with fibroblast CCD1112Sk; ', 'cell: Fibroblast Wi38 monocultured; ', 'cell: Fibroblast Wi38 cocultured with epithelial Cal51 cells; ', 'cell: Epithelial cells Cal51 cocultured with fibroblast Wi38; ', 'cell: Fibroblast Wi38 cocultured with epithelial MDAMB231 cells; ', 'cell: Epithelial cells MDAMB231 cocultured with fibroblast Wi38; ', 'cell: Fibroblast HFF1 monocultured; ', 'cell: Fibroblast HFF1 cocultured with epithelial Cal51 cells; ', 'cell: Epithelial cells Cal51 cocultured with fibroblast HFF1; ', 'cell: Fibroblast HFF1 cocultured with epithelial MDAMB231 cells; ', 'cell: Epithelial cells MDAMB231 cocultured with fibroblast HFF1; ', 'cell: Fibroblast HFFF2 monocultured; ', 'cell: Fibroblast HFFF2 cocultured with epithelial Cal51 cells; ', 'cell: Epithelial cells Cal51 cocultured with fibroblast HFFF2; ', 'cell: Fibroblast HFFF2 cocultured with epithelial MDAMB231 cells; ', 'cell: Epithelial cells MDAMB231 cocultured with fibroblast HFFF2; ', 'cell: Epithelial cells Cal51 monocultured; ', 'cell: Epithelial cells MDAMB231 monocultured; ' GSE15937 Homo sapiens 3 Non-coding RNA profiling by array GPL8519 Small RNAs subcellular distribution in breast cancer and normal cell lines 2009-05-03 We detect the small RNAs subcellular distribution in breast cancer cell lines MCF-7 and MDA-MB-231, and normal cell line MCF-10A. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15937 None None None None None 'cytoplasmic RNA', 'nuclear RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA116983 https://www.ebi.ac.uk/ena/browser/view/PRJNA116983 None [Overal design]Each cell line, we detected the nuclear and cytoplasmic small RNAs expression intensity; and then we could get the nuclear-cytoplasmic-ratio.; [Treatment]'None'; [Growth]'None'; [Extraction]'Subcellular fractioning was executed according to the Subcellular fractionation protocol provided by Abcam (http://www.abcam.com/index.html?pageconfig=resource&rid=11473). Total RNA was extracted from the subcellular fractions with Trizol (Invitrogen).'; [Cell type]'Source: ''cell line: MCF_7; ', 'cell line: mda_mb_231; ', 'cell line: mcf10a; ' GSE23038 Homo sapiens 27 Expression profiling by array GPL571 Normal prostate cells were immortalized and cultured for 650 days till several transformation hallmarks were observed 2010-07-20 Duplication of chromosomal arm 20q occurs in prostate, cervical, colon, gastric, bladder, melanoma, pancreas and breast cancer, suggesting that 20q amplification may play a key causal role in tumorigenesis. According to an alternative view, chromosomal instabilities are mainly a common side effect of cancer progression. To test whether a specific genomic aberration might serve as a cancer initiating event, we established an in vitro system that models the evolutionary process of early stages of prostate tumor formation; normal prostate cells were immortalized and cultured for 650 days till several transformation hallmarks were observed. Gene expression patterns were measured and chromosomal aberrations were monitored by spectral karyotype analysis at different times. Several chromosomal aberrations, in particular duplication of chromosomal arm 20q, occurred early in the process and were fixed in the cell populations, while other aberrations became extinct shortly after their appearance. A wide range of bioinformatic tools, applied to our data and to data from several cancer databases, revealed that spontaneous 20q amplification can promote cancer initiation. Our computational model suggests that deregulation of some key pathways, such as MAPK, p53, cell cycle regulation and Polycomb group factors, in addition to activation of several genes like Myc, AML, B-Catenin and the ETS family transcription factors, are key steps in cancer development driven by 20q amplification. Finally we identified 13 cancer initiating genes, located on 20q13, which were significantly overexpressed in many tumors, with expression levels correlated with tumor grade and outcome; these probably play key roles in inducing malignancy via20q amplification. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23038 Mutant p53(R175H) upregulates Twist1 expression and promotes epithelial-mesenchymal transition in immortalized prostate cells. Cell death and differentiation 8.086 https://doi.org/10.1038/cdd.2010.94 {PloS one (2.776) doi:10.1371/journal.pone.0014632}; {Cell death and differentiation (8.086) doi:10.1038/cdd.2010.94}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA131175 https://www.ebi.ac.uk/ena/browser/view/PRJNA131175 None [Overal design]33 samples were analysised, 12 were in replicate; [Treatment]'EP156T immortalized prostate cell cultures were grown in MCDB-153+ media under standard tissue culture conditions'; [Growth]'None'; [Extraction]'cells were trypsinized and pelleted after 3 days at logarithmic growth stage'; [Cell type]'hTERT immortalized cells passage 0', 'hTERT immortalized cells passage 10', 'hTERT immortalized cells passage 20', 'hTERT immortalized cells, empty vector control, passage 30', 'hTERT immortalized cells, empty vector control, passage 40', 'hTERT immortalized cells, empty vector control, passage 50', 'hTERT immortalized cells, empty vector control, passage 60', 'hTERT immortalized cells, empty vector control, passage 70', 'hTERT immortalized cells, empty vector control, passage 80', 'hTERT immortalized cells, dominant negative peptide for p53 vector , passage 30', 'hTERT immortalized cells, dominant negative peptide for p53 vector , passage 40', 'hTERT immortalized cells, dominant negative peptide for p53 vector , passage 50', 'hTERT immortalized cells, dominant negative peptide for p53 vector , passage 60', 'hTERT immortalized cells, dominant negative peptide for p53 vector , passage 70', 'hTERT immortalized cells, dominant negative peptide for p53 vector , passage 80', 'hTERT immortalized cells, mutant p53 vector , passage 30', 'hTERT immortalized cells, mutant p53 vector , passage 40', 'hTERT immortalized cells, mutant p53 vector , passage 50', 'hTERT immortalized cells, mutant p53 vector , passage 60', 'hTERT immortalized cells, mutant p53 vector , passage 70', 'hTERT immortalized cells, mutant p53 vector , passage 80', 'hTERT immortalized cells, empty vector control + hRAS, passage 80', 'hTERT immortalized cells, dominant negative peptide for p53 vector + hRAS, passage 80', 'hTERT immortalized cells, mutant p53 vector + hRAS, passage 80', 'hTERT immortalized cells, passage 80', 'hTERT immortalized cells + dominant negative peptide for p53, passage 80', 'hTERT immortalized cells + mutant p53, passage 80''cell type: hTERT immortalized cells passage 0; ', 'cell type: hTERT immortalized cells passage 10; ', 'cell type: hTERT immortalized cells passage 20; ', 'cell type: hTERT immortalized cells, empty vector control, passage 30; ', 'cell type: hTERT immortalized cells, empty vector control, passage 40; ', 'cell type: hTERT immortalized cells, empty vector control, passage 50; ', 'cell type: hTERT immortalized cells, empty vector control, passage 60; ', 'cell type: hTERT immortalized cells, empty vector control, passage 70; ', 'cell type: hTERT immortalized cells, empty vector control, passage 80; ', 'cell type: hTERT immortalized cells, dominant negative peptide for p53 vector , passage 30; ', 'cell type: hTERT immortalized cells, dominant negative peptide for p53 vector , passage 40; ', 'cell type: hTERT immortalized cells, dominant negative peptide for p53 vector , passage 50; ', 'cell type: hTERT immortalized cells, dominant negative peptide for p53 vector , passage 60; ', 'cell type: hTERT immortalized cells, dominant negative peptide for p53 vector , passage 70; ', 'cell type: hTERT immortalized cells, dominant negative peptide for p53 vector , passage 80; ', 'cell type: hTERT immortalized cells, mutant p53 vector , passage 30; ', 'cell type: hTERT immortalized cells, mutant p53 vector , passage 40; ', 'cell type: hTERT immortalized cells, mutant p53 vector , passage 50; ', 'cell type: hTERT immortalized cells, mutant p53 vector , passage 60; ', 'cell type: hTERT immortalized cells, mutant p53 vector , passage 70; ', 'cell type: hTERT immortalized cells, mutant p53 vector , passage 80; ', 'cell type: hTERT immortalized cells, empty vector control + hRAS, passage 80; ', 'cell type: hTERT immortalized cells, dominant negative peptide for p53 vector + hRAS, passage 80; ', 'cell type: hTERT immortalized cells, mutant p53 vector + hRAS, passage 80; ', 'cell type: hTERT immortalized cells, passage 80; ', 'cell type: hTERT immortalized cells + dominant negative peptide for p53, passage 80; ', 'cell type: hTERT immortalized cells + mutant p53, passage 80; ' GSE131295 Homo sapiens 1 Methylation profiling by array GPL21145 Epigenetic analysis of DU-4475 human breast cell line 2019-05-15 Illumina Infinium MethylationEPIC Beadchip of DU-4475 human breast cancer cell line https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131295 Epigenetic inactivation of the splicing RNA-binding protein CELF2 in human breast cancer. Oncogene 6.634 https://doi.org/10.1038/s41388-019-0936-x {Oncogene (6.634): 10.1038/s41388-019-0936-x} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA543131 https://www.ebi.ac.uk/ena/browser/view/PRJNA543131 None [Overal design]Bisulphite converted DNA from DU-4475 breast cell line was hybridised to the Illumina Infinium MethylationEPIC Beadchip.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total DNA was isolated by standard procedures'; [Cell type]'DU-4475''cell type: DU-4475; tissue: breast; gender: Female; ' GSE146477 synthetic construct 6 Non-coding RNA profiling by array GPL14613 Microarray analysis of miRNA in breast cancer cell lines 2020-03-05 The project aimed to identify miRNA that varied with tumourigenicity in human breast cell lines. The second objective was to identify miRNA that had differential expression between cell lines that varied in accordance with the abundance of the tetraspanin CD9 in the cell lines and the degree to which endogenous factors within these cell lines interacted with the 3'UTR of CD9 as determined by dual luciferase assay. These miRNA were considered potential regulators of the abundance of CD9 in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE146477 Tetraspanin CD9 is Regulated by miR-518f-5p and Functions in Breast Cell Migration and In Vivo Tumor Growth. Cancers 6.162 https://doi.org/10.3390/cancers12040795 {Cancers (6.162): 10.3390/cancers12040795} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA610632 https://www.ebi.ac.uk/ena/browser/view/PRJNA610632 None [Overal design]Total RNA was isolated from commercial breast cancer cell lines and non-tumourigenic breast cell lines and the abundance of each miRNA was determined by hybridisation to affymetrix miRNA microarrays. RNA was combined from 3 independent cultures of each cell line prior to labelling for hybridisation to each array. Each cell line was therefore only assayed once by microarray.; [Treatment]'No treatment, cells were grown to 85% confluency prior to RNA extraction'; [Growth]'Cells were grown in culture using media as described in the repository from where each cell line was obtained. All cells were maintained at 37C in 5% CO2. All cells were either purchased within 4 years of use or validated to be the correct line using the Promega GenePrint 10 kit.'; [Extraction]'Cells were washed with PBS and then Trizol-LS added directly to the cells, the manufacturers protocol was followed with the addition of glycogen during precipitation which was carried out overnight at -20C'; [Cell type]'Source: ''cell line: HMEC; tumourigenic status: not tumourigenic; ', 'cell line: 184A1; tumourigenic status: not tumourigenic; ', 'cell line: MCF7; tumourigenic status: tumourigenic; ', 'cell line: T47D; tumourigenic status: tumourigenic; ', 'cell line: SKBR3; tumourigenic status: tumourigenic; ', 'cell line: MDA-MB-231; tumourigenic status: tumourigenic; ' GSE156332 Homo sapiens 3 Expression profiling by high throughput sequencing GPL16791 The UPR Transducer IRE1 Promotes Breast Cancer Malignancy by Degrading Tumor Suppressor microRNAs 2020-08-17 To understand the mechanistic basis by which inositol-requiring enzyme 1 (IRE1) is involved in luminal breast cancer malignancy, we analyzed the transcriptomic signature that IRE1 regulates in breast cancer. We suppressed the activity of IRE1 RNase in luminal breast cancer SUM52 line by adenoviral-based over-expression of the IRE1 dominant-negative K599A or K907A, and then performed RNA-sequencing (RNA-seq) analysis with IRE1 dominant-negative and control SUM52 cells. Through the RNA-seq analysis, we identified 98 genes that were commonly upregulated (65 genes) or downregulated (33 genes) in K599A-expressing SUM52 (SUM52-K599A) or K907A-expressing SUM52 (SUM52-K907A) cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE156332 The UPR Transducer IRE1 Promotes Breast Cancer Malignancy by Degrading Tumor Suppressor microRNAs. iScience None https://doi.org/10.1016/j.isci.2020.101503 {iScience (None): 10.1016/j.isci.2020.101503} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA657549 https://www.ebi.ac.uk/ena/browser/view/PRJNA657549 https://www.ncbi.nlm.nih.gov/sra?term=SRP277797 [Overal design]Total RNAs from SUM52 cells transducted with the IRE1 dominant-negative K599A, K907A, or control adenovirus were harvested, frozen, and sent to the LC Sciences (Houston, TX, USA) for next-generation sequencing.; [Treatment]'SUM52 cells were infected by adenoviruses of the IRE1 dominant-negative K599A, K907A, or control GFP.'; [Growth]"SUM52 cell line is cultured in Ham's F-12 medium supplemented with 5% fetal bovine serum, fungizone (0.5 µg/mL), gentamicin (5 µg/mL), hydrocortisone (1 µg/mL) and insulin (5 µg/mL)."; [Extraction]'Total RNA was extracted with an RNeasy Plus Mini Kit in accordance with the manufacturer’s protocol (Qiagen, Hilden, Germany).\nRNAs from SUM52 cells transducted with the IRE1 dominant-negative K599A, K907A, or control adenovirus were equally pooled (total 3 μg) and sequenced by LC Sciences. RNA was subjected to isolated poly(A) mRNA with poly-T oligo-attached magnetic beads (Invitrogen). Following purification, the poly(A)- or poly(A)+ RNA fractions were fragmented into small pieces using divalent cations under elevated temperature. Then the cleaved RNA fragments were reverse-transcribed to create the final cDNA library in accordance with the protocol for the mRNA-Seq sample preparation kit (Illumina, San Diego, USA). Approximately 1 µg of this RNA was prepared for Next Generation Sequencing using a version of the Illumina protocol, Directional_mRNA-Seq_SamplePrep_Guide_15018460_A.'; [Cell type]'Source: ''cell line: Luminal breast cancer cell line; ' GSE112963 Homo sapiens 13 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL11154; GPL16791 Endogenous interaction profiling identifies DDX5 as an oncogenic coactivator of transcription factor Fra-1 2018-04-11 Fra-1, a member of the activator protein 1 (AP-1) family, is overexpressed in triple-negative breast cancer (TNBC) and plays crucial roles in tumor growth. Here we report the identification of 118 proteins interacting with endogenous chromatin-bound Fra-1 in TNBC cells, highlighting DDX5 as the most enriched Fra-1-interacting protein. DDX5, a previously unrecognized protein in the Fra-1 transcriptional network, shows extensive overlap with Fra-1 cistrome and transcriptome that are highly associated with the TNBC cell growth. We provide evidence that DDX5 expression enhances Fra-1 transcriptional activity and potentiates Fra-1-driven cell proliferation. Furthermore, we show that the DDX5 target gene signature predicts poor clinical outcome in breast cancer patients. DDX5 protein level was higher in triple-negative basal-like tumors than in non-basal-like tumors, including luminal A, luminal B, and HER2-enriched subtypes. Collectively, by combining proteomic and genomic approaches we reveal a role for DDX5 as a regulatory protein of Fra-1 signaling and suggest DDX5 as a potential therapeutic target for TNBC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112963 Endogenous interaction profiling identifies DDX5 as an oncogenic coactivator of transcription factor Fra-1. Oncogene 6.634 https://doi.org/10.1038/s41388-019-0824-4 {Oncogene (6.634): 10.1038/s41388-019-0824-4} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA449621 https://www.ebi.ac.uk/ena/browser/view/PRJNA449621 None [Overal design]Refer to individual Series; [Treatment]'No treatment'; [Growth]'Cells were maintained in RPMI 1640 supplemented with 10% FBS.'; [Extraction]'Lysates were clarified from sonicated nuclei, IgG, Fra-1 and DDX5 complexes were isolated with antibody.\nChIP-seq libraries were prepared for sequencing using standard Illumina protocols', 'Total RNA was extracted using RNeasy Mini Kit (Qiagen, Valencia, CA).\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'ERalpha-negtive breast cancer cells''cell line: BT549; cell type: ERalpha-negtive breast cancer cells; chip antibody: normal rabbit IgG (sc-2027, Santa Cruz); ', 'cell line: BT549; cell type: ERalpha-negtive breast cancer cells; chip antibody: Fra-1 (R-20,sc-605, Santa Cruz); ', 'cell line: BT549; cell type: ERalpha-negtive breast cancer cells; chip antibody: DDX5 (ab21696, Abcam); ', 'cell line: BT549; cell type: ERalpha-negtive breast cancer cells; chip antibody: none; ', 'cell line: BT549; cell type: ERalpha-negtive breast cancer cells; genotype/variation: control; ', 'cell line: BT549; cell type: ERalpha-negtive breast cancer cells; genotype/variation: Fra-1 knockdown; ', 'cell line: BT549; cell type: ERalpha-negtive breast cancer cells; genotype/variation: DDX5 knockdown; ' GSE5816 Homo sapiens 42 Expression profiling by array GPL570 A Genome-wide Screen for Hypermethylated Genes in Lung Cancer 2006-09-12 Abstract Background: Promoter hypermethylation coupled with loss of heterozygosity at the same locus results in loss of gene function in many tumor cells. The “rules” governing which genes are methylated during the pathogenesis of individual cancers, how specific methylation profiles are initially established, or what determines tumor-type specific methylation are unknown. However, DNA methylation markers that are highly specific and sensitive for common tumors would be useful for the early detection of cancer, and those required for the malignant phenotype identify pathways important as therapeutic targets. Methods and Findings: In an effort to identify new cancer-specific methylation markers, we employed a high throughput global expression profiling approach in lung cancer cells. We identified 132 genes that have 5’ CpG islands, are induced from undetectable levels by 5-aza-2’-deoxycytidine (5-aza) in multiple non-small cell lung cancer cell lines, and are expressed in immortalized human bronchial epithelial cells. As expected, these genes were also expressed in normal lung, but often not in companion primary lung cancers. Methylation analysis of a subset (45/132) of these promoter regions in primary lung cancer (N=20) and adjacent non-malignant tissue showed that 31 genes had acquired methylation in the tumors, but did not show methylation in normal lung or lymphocytes. We studied the eight most frequently and specifically methylated genes from our lung cancer data set in breast cancer (N=37), colon cancer (N=24), and prostate cancer (N=24) along with counterpart non-malignant tissues. We found that seven loci were frequently methylated in both breast and lung cancers, with four showing extensive methylation in all four epithelial tumors. Conclusions: By using a systematic biological screen we identified multiple genes that are methylated with high penetrance in primary lung, breast, colon, and prostate cancers. The cross-tumor methylation pattern we observed for these novel markers suggests that we have identified a partial promoter hypermethylation signature for these common malignancies. These data suggest that while tumors in different tissues vary substantially with respect to gene expression, there may be commonalities in their promoter methylation profiles that represent potential targets for early detection screening or therapeutic intervention. Keywords: Cell line comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE5816 A genome-wide screen for promoter methylation in lung cancer identifies novel methylation markers for multiple malignancies. PLoS medicine 11.048 https://doi.org/10.1371/journal.pmed.0030486 {PLoS medicine (11.048): 10.1371/journal.pmed.0030486} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA97201 https://www.ebi.ac.uk/ena/browser/view/PRJNA97201 None [Overal design]Drug treatment: control, 100 nM, 1 uM Cancer vs. Normal Comparison: NSCLC vs. Normal; [Treatment]'Control treatment group. Dimethylsulfoxide qod for 6 days.', "Low dose treatment group. 5-aza-2'-deoxycytidine qod for 6 days.", "High dose (1000 nM) treatment group. 5-aza-2'-deoxycytidine qod for 6 days.", 'Control treatment group. DMSO qod for 6 days.', "Low dose treatment group (100 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "High dose treatment group (1000 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "H460 Low dose treatment group (100 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "A549 Low dose treatment group (100 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "HBEC2 Low dose treatment group (100 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "HBEC4 Low dose treatment group (100 nM). 5-aza-2'-deoxycytidine qod for 6 days.", 'HBEC4 Control treatment group. DMSO qod for 6 days.', 'HBEC3 Control treatment group. DMSO qod for 6 days.', 'H460 Control treatment group. DMSO qod for 6 days.', 'HBEC2-Rep2 Control treatment group. DMSO qod for 6 days.', 'HBEC3-Rep2 Control treatment group. DMSO qod for 6 days.', 'HBEC4-Rep2 Control treatment group. DMSO qod for 6 days.', 'A549 Control treatment group. DMSO qod for 6 days.', "HBEC4 High dose treatment group (1000 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "H1299 High dose treatment group (1000 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "H460 High dose treatment group (1000 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "HBEC2 High dose treatment group (1000 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "HBEC3 High dose treatment group (1000 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "HBEC4-Rep2 High dose treatment group (1000 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "HBEC2-Rep2 High dose treatment group (1000 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "HBEC3-Rep2 High dose treatment group (1000 nM). 5-aza-2'-deoxycytidine qod for 6 days.", 'Control treatment group. DMSO qod for 6 days.', "Low dose treatment group (100 nM). 5-aza-2'-deoxycytidine qod for 6 days.", "High dose treatment group (1000 nM). 5-aza-2'-deoxycytidine qod for 6 days.", 'Lose dose treatment group (100 nM). DMSO qod for 6 days.', 'High dose treatment group (1000 nM). DMSO qod for 6 days.', 'Control group treatment. DMSO qod for 6 days.', 'Control treatment group (DMSO). DMSO qod for 6 days.', "High dose treatment group. 1000 nM 5-aza-2'-deoxycytidine qod for 6 days.", 'High dose treatment group. 5-aza-2-deoxycytidine qod for 6 days.', 'High dose treatment. 5-aza-2-deoxycytidine qod for 6 days.'; [Growth]'See pulication for details.', 'See publication for details.'; [Extraction]'Trizol'; [Cell type]'Source: ''' GSE152312 Homo sapiens 18 Expression profiling by high throughput sequencing GPL18573 Effect of bone marrow microenvironment on the sensitivity of breast cancer cells to antiestrogens 2020-06-11 Hormonal therapy (HT) inhibits the growth of hormone receptor-positive (HR+) breast (BrCa) and prostate (PrCa) cancers. HT resistance frequently develops within the complex metastatic microenvironment of the host-organ (often the bone), a setting poorly recapitulated in two-dimensional (2D) culture systems. To address this limitation, we cultured HR+ BrCa/PrCa spheroids and patient-derived organoids in 3D extracellular matrices (ECM) alone or together with bone marrow stromal cells (BMSCs). In 3D monocultures, antiestrogens/antiandrogens induced anoikis by abrogating the anchorage-independent growth of HR+ cancer cells but had only modest effect against tumor cells residing in the ECM niche. In contrast, BMSCs induced hormone-independent growth of BrCa/PrCa spheroids and restored lumen filling in the presence of HR-targeting agents. Molecular and functional characterization of the BMSC-induced hormone-independence and HT resistance in anchorage-independent cells revealed distinct, context-dependent, mechanisms. Cocultures of ZR75-1 and LNCaP with BMSCs exhibited paracrine IL-6-induced HT resistance via attenuation of HR protein expression, which was reversed by inhibition of IL-6 or JAK signaling. This paracrine IL-6/JAK/STAT3-mediated HT resistance was also confirmed in patient-derived organoids cocultured with BMSCs. Distinctly, MCF7 and T47D spheroids retained ER protein expression in cocultures, but also acquired redundant compensatory signals enabling anchorage independence via ERK and PI3K bypass cascades activated in non-IL-6-dependent manner. In summary, the acquisition of anchorage-independent growth in HR+ tumors is abrogated by HR blockade, but can be restored in the metastatic microenvironment through pleiotropic hormone-independent mechanisms. Combined analysis of tumor and microenvironmental biomarkers in metastatic biopsies of HT-resistant patients can help the refinement of treatment approaches. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE152312 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA638946 https://www.ebi.ac.uk/ena/browser/view/PRJNA638946 https://www.ncbi.nlm.nih.gov/sra?term=SRP266970 [Overal design]RNA profiles of breast cancer cells in 3D cultures in the presence vs. absence of immortalized bone marrow stromal cells HS5; [Treatment]'No treatment'; [Growth]'The breast cancer cells were grown in matrigel alone or together with HS5 bone marrow stromal cells in DMEM/10% FBS for 8 days.'; [Extraction]'The gel was enzymatically disintegrated and the separation of tumor and stromal cell subpopulations was performed using mesenchymal cells depletion microbeads. Next, the RNA was extracted from the tumor cells using RNA extraction kit (Qiagen), The lysates were supplemented with ERCC RNA spike-in mix to adjust for the cell number and analyzed by RNA sequencing using Illumina NextSeq 500 Next Gen\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''culture setting: mono-culture; cell line: MCF7; ', 'culture setting: co-culture with HS5; cell line: MCF7; ', 'culture setting: mono-culture; cell line: ZR751; ', 'culture setting: co-culture with HS5; cell line: ZR751; ', 'culture setting: mono-culture; cell line: T47D; ', 'culture setting: co-culture with HS5; cell line: T47D; ' GSE87424 Mus musculus; Homo sapiens 167 Methylation profiling by genome tiling array; Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Genome variation profiling by high throughput sequencing GPL11154; GPL13112; GPL13534; GPL16791; GPL18573 Enhancer Remodeling During Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacological Targeting of the P-TEFb Complex 2016-09-28 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE87424 Enhancer Remodeling during Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacologic Targeting of the P-TEFb Complex. Cancer discovery 26.370 https://doi.org/10.1158/2159-8290.CD-16-0653 {Cancer discovery (26.370): 10.1158/2159-8290.CD-16-0653} 'genomic DNA', 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA344730 https://www.ebi.ac.uk/ena/browser/view/PRJNA344730 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'culture media: DMEM/F12 1:1 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone', 'culture media: F12 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone, 10 mM HEPES', 'culture media: HuMEC supplemented with 5% FBS and Gibco defined HuMEC supplements', 'culture media: RPMI 1640 supplemented with 10% FBS', 'F12 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone, 10 mM HEPES'; [Extraction]'Genomic DNA was isolated using Qiagen DNeasy Blood & Tissue kit and bisulfite conversion of genomic DNA was performed using Zymo Research EZ DNA Methylation kit', 'Whole cell lysates were sonicated resulting in an average chromatin fragment size of ~300 bp and immunoprecipiated with the indicated antibodies.\nAll libraries were constructed using KAPA Hyper Prep kits with Illumina TruSeq adapters, 18 cycles of amplification and dual SPRI size selection post-amplification, except where indicated, whereby the libraries were constructed using DNA SMART ChIP Seq kit (Clontech) with dual SPRI size selection following 18 cycles of amplification.\nlibrary preparation kit: KAPA Hyper Prep', 'Whole cell lysates were sonicated resulting in an average chromatin fragment size of ~300 bp and immunoprecipiated with the indicated antibodies.\nAll libraries were constructed using KAPA Hyper Prep kits with Illumina TruSeq adapters, 18 cycles of amplification and dual SPRI size selection post-amplification, except where indicated, whereby the libraries were constructed using DNA SMART ChIP Seq kit (Clontech) with dual SPRI size selection following 18 cycles of amplification.\nlibrary preparation kit: Clontech DNA SMART ChIP Seq kit', 'Whole cell lysates were sonicated resulting in an average chromatin fragment size of ~300 bp and immunoprecipiated with the indicated antibodies.\nAll libraries were constructed using KAPA Hyper Prep kits with Illumina TruSeq adapters, 18 cycles of amplification and dual SPRI size selection post-amplification, except where indicated, whereby the libraries were constructed using DNA SMART ChIP Seq kit (Clontech) with dual SPRI size selection following 18 cycles of amplification.\nlibrary preparation kit: Illumina TruSeq ChIP Library Prep kit', 'Total RNA was isolated using Qiagen RNeasy Plus kit.\n2 µg total RNA and 15 cycles of amplification were used for libraries constructed with Illumina TruSeq RNA Library Prep Kit v2. 4 µg total RNA and 10 cycles of amplification (using 0.5X recommended DNA template) were used for libraries constructed with KAPA Stranded mRNAseq kit or Illumina TruSeq RNA library kit v2.\nlibrary preparation kit: Illumina TruSeq RNA library kit v2', 'Total RNA was isolated using Qiagen RNeasy Plus kit.\n2 µg total RNA and 15 cycles of amplification were used for libraries constructed with Illumina TruSeq RNA Library Prep Kit v2. 4 µg total RNA and 10 cycles of amplification (using 0.5X recommended DNA template) were used for libraries constructed with KAPA Stranded mRNAseq kit or Illumina TruSeq RNA library kit v2.\nlibrary preparation kit: KAPA Stranded mRNAseq kit', 'Genomic DNA was isolated from EpCAM+/CD49f+ and EpCAM-/CD49f- FACS populations using Qiagen DNeasy Blood and Tissue Kit and subquently treated with Rnase A.\n300 ng genomic DNA was submitted to the UNC High Throughput Sequencing Facility for Illumina Nextera Rapid Capture exome enrichment.', 'Total RNA was isolated using Qiagen RNeasy Plus kit.\n2 µg total RNA and 15 cycles of amplification were used for libaries constructed with Illumina TruSeq RNA Library Prep Kit v2. 4 µg total RNA and 10 cycles of amplification (using 0.5X recommended DNA template) were used for libraries constructed with KAPA Stranded mRNAseq kit.', 'Total RNA was isolated with Qiagen RNeasy Mini kit.\nmRNA libraries were made with Illumina TruSeq RNA Sample Prep Kit starting with 0.5-1 micrograms of total RNA.'; [Cell type]'Source: ''cell line: SUM159 breast carcinoma cell line; treatment: DMSO; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f positive subpopulation; treatment: DMSO; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f positive subpopulation; treatment: 30nM trametinib; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f negative subpopulation; treatment: DMSO; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f negative subpopulation; treatment: 30nM trametinib; ', 'cell line: SUM149 breast carcinoma cell line, EpCAM/CD49f positive subpopulation; treatment: DMSO; ', 'cell line: SUM149 breast carcinoma cell line, EpCAM/CD49f positive subpopulation; treatment: 30nM trametinib; ', 'cell line: SUM149 breast carcinoma cell line, EpCAM/CD49f negative subpopulation; treatment: DMSO; ', 'cell line: SUM149 breast carcinoma cell line, EpCAM/CD49f negative subpopulation; treatment: 30nM trametinib; ', 'control vendor: Human WGA Methylated & Non-methylated DNA, Zymo Research; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 300nM JQ1; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 300nM JQ1; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 24h; chip antibody: MED1/CRSP1/TRAP220 Bethyl Laboratories A300-793A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 24h; chip antibody: MED1/CRSP1/TRAP220 Bethyl Laboratories A300-793A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 300nM JQ1; time: 24h; chip antibody: MED1/CRSP1/TRAP220 Bethyl Laboratories A300-793A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 300nM JQ1; time: 24h; chip antibody: MED1/CRSP1/TRAP220 Bethyl Laboratories A300-793A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 24h; chip antibody: p300 Santa Cruz Biotechnology sc-585X; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 24h; chip antibody: p300 Santa Cruz Biotechnology sc-585X; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 300nM JQ1; time: 24h; chip antibody: p300 Santa Cruz Biotechnology sc-585X; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 300nM JQ1; time: 24h; chip antibody: p300 Santa Cruz Biotechnology sc-585X; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 24h; chip antibody: histone H3K27ac Active Motif 39133; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 24h; chip antibody: histone H3K27ac Active Motif 39133; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 300nM JQ1; time: 24h; chip antibody: histone H3K27ac Active Motif 39133; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 300nM JQ1; time: 24h; chip antibody: histone H3K27ac Active Motif 39133; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 24h; chip antibody: CEBPβ Santa Cruz Biotechnology sc-150X; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 24h; chip antibody: CEBPβ Santa Cruz Biotechnology sc-150X; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 300nM JQ1; time: 24h; chip antibody: CEBPβ Santa Cruz Biotechnology sc-150X; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 300nM JQ1; time: 24h; chip antibody: CEBPβ Santa Cruz Biotechnology sc-150X; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 24h; chip antibody: histone H3K4me1 Active Motif 39297; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 24h; chip antibody: histone H3K4me1 Active Motif 39297; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 24h; chip antibody: histone H3K4me3 EMD Millipore 07-473; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 500nM trametinib; time: 24h; chip antibody: histone H3K4me3 EMD Millipore 07-473; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 24h; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: DMSO; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: 100nM trametinib; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: 300nM JQ1; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: 100nM trametinib 300nM JQ1; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: DMSO; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 1uM SGCCBP30; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 300nM JIB04; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 1uM SGCCBP30; time: 24h; chip antibody: p300 Santa Cruz Biotechnology sc-585X; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 300nM JIB04; time: 24h; chip antibody: p300 Santa Cruz Biotechnology sc-585X; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 8h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 8h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 30nM bortezomib; time: 8h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 30nM bortezomib; time: 8h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 48h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 48h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: dox; time: 48h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 48h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: shMYC, DMSO; time: 48h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: shMYC, 100nM trametinib; time: 48h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: shMYC, dox; time: 48h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: shMYC, DMSO; time: 48h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 72h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 1h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 4h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 72h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f positive subpopulation; treatment: DMSO; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f positive subpopulation; treatment: 30nM trametinib; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f positive subpopulation; treatment: DMSO; time: 24h; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f negative subpopulation; treatment: DMSO; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f negative subpopulation; treatment: 30nM trametinib; time: 24h; chip antibody: BRD4 Bethyl Laboratories A301-985A; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f negative subpopulation; treatment: DMSO; time: 24h; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f positive subpopulation; treatment: 30nM trametinib; time: 24h; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f negative subpopulation; treatment: 30nM trametinib; time: 24h; ', 'cell line: T11 orthotopic serial transplant cell line; treatment: DMSO; time: 24h; ', 'cell line: T11 orthotopic serial transplant cell line; treatment: 500nM trametinib; time: 24h; ', 'cell line: C3TAg GEMM cell line; treatment: DMSO; time: 24h; ', 'cell line: C3TAg GEMM cell line; treatment: 500nM trametinib; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 300nM JQ1; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 300nM JQ1; time: 24h; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: DMSO; time: 48h; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: 10nM trametinib; time: 48h; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: 300nM JQ1; time: 48h; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: 10nM trametinib 300nM JQ1; time: 48h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 3uMSGCCBP30; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 3uMSGCCBP30; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 500nM IBET151; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 500nM IBET151; time: 24h; ', 'xenograft: SUM159 breast carcinoma cell line xenograft; treatment: 2mpk trametinib; time: 48h; ', 'xenograft: SUM159 breast carcinoma cell line xenograft; treatment: 2mpk trametinib 30mpkIBET151; time: 48h; ', 'xenograft: SUM159 breast carcinoma cell line xenograft; treatment: 30mpkIBET151; time: 48h; ', 'xenograft: SUM159 breast carcinoma cell line xenograft; treatment: control; time: 48h; ', 'cell line: triple negative breast cancer cell line SUM-229PE; cell subpopulation: SUM229neg; ', 'cell line: triple negative breast cancer cell line SUM-229PE; cell subpopulation: SUM229pos; ', 'cell line: HCC1806 breast carcinoma cell line; culture media: RPMI 1640 supplemented with 10% FBS; library preparation kit: KAPA Stranded mRNAseq kit; ', 'cell line: EpCAM/CD49f positive SUM149 breast carcinoma subpopulation; culture media: HuMEC supplemented with 5% FBS and Gibco defined HuMEC supplements; library preparation kit: KAPA Stranded mRNAseq kit; ', 'cell line: MDAMB468 breast carcinoma cell line; culture media: RPMI 1640 supplemented with 10% FBS; library preparation kit: KAPA Stranded mRNAseq kit; ', 'cell line: SUM159 breast carcinoma cell line; culture media: DMEM/F12 1:1 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone; library preparation kit: KAPA Stranded mRNAseq kit; ', 'cell line: HS578T breast carcinoma cell line; culture media: RPMI 1640 supplemented with 10% FBS; library preparation kit: KAPA Stranded mRNAseq kit; ', 'cell line: PDX breast carcinoma cell line; culture media: RPMI 1640 supplemented with 10% FBS; library preparation kit: KAPA Stranded mRNAseq kit; ', 'disease state: TNBC; individual: Patient 6; protocol: pre-treatment needle core biospy; tumor sample subtype: claudin low; ', 'disease state: TNBC; individual: Patient 6; protocol: post-treatment surgical resection; tumor sample subtype: claudin low; ', 'disease state: TNBC; individual: Patient 5; protocol: pre-treatment needle core biospy; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 5; protocol: post-treatment surgical resection; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 7; protocol: pre-treatment needle core biospy; tumor sample subtype: normal breast; ', 'disease state: TNBC; individual: Patient 7; protocol: post-treatment surgical resection; tumor sample subtype: normal breast; ', 'disease state: TNBC; individual: Patient 8; protocol: pre-treatment needle core biospy; tumor sample subtype: claudin low; ', 'disease state: TNBC; individual: Patient 8; protocol: post-treatment surgical resection; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 1; protocol: pre-treatment needle core biospy; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 1; protocol: post-treatment surgical resection; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 2; protocol: pre-treatment needle core biospy; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 2; protocol: post-treatment surgical resection; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 9; protocol: pre-treatment needle core biospy; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 9; protocol: post-treatment surgical resection; tumor sample subtype: normal breast; ', 'disease state: TNBC; individual: Patient 10; protocol: pre-treatment needle core biospy; tumor sample subtype: claudin low; ', 'disease state: TNBC; individual: Patient 10; protocol: post-treatment surgical resection; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 4; protocol: pre-treatment needle core biospy; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 4; protocol: post-treatment surgical resection; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 3; protocol: pre-treatment needle core biospy; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 3; protocol: post-treatment surgical resection; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 11; protocol: pre-treatment needle core biospy; tumor sample subtype: basal; ', 'disease state: TNBC; individual: Patient 11; protocol: post-treatment surgical resection; tumor sample subtype: claudin low; ', 'disease state: TNBC; individual: Patient 12; protocol: pre-treatment needle core biospy; tumor sample subtype: normal breast; ', 'disease state: TNBC; individual: Patient 12; protocol: post-treatment surgical resection; tumor sample subtype: normal breast; ' GSE37087 Homo sapiens 8 Expression profiling by array GPL4133 Examination of the role of peptidylarginine deiminase 2 (PAD2) in gene expression in MCF-7 breast cancer cells 2012-04-06 To investigate the potential role of peptidylarginine deiminase 2 (PAD2) in gene expression, we created stable shRNA scrambled control and PAD2 knockdown MCF-7 breast cancer cell lines. After validating the specific knockdown of PAD2 at the mRNA and protein level, we utilized an Agilent microarray platform to compare the gene expression profile of the two cell lines to generate a candidate list of genes regulated by PAD2. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37087 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA158129 https://www.ebi.ac.uk/ena/browser/view/PRJNA158129 None [Overal design]Control and PAD2 knockdown cells were created by stably transfecting shRNA constructs into MCF-7 cells. Stable cells were selected using puromycin and knockdown validate at the mRNA and protein level. Microarray data represents 4 independent biological replicates contain control and PAD2 knockdown samples.; [Treatment]'None'; [Growth]'MCF7 control and PAD2 knockdown cells were grown with DMEM, 10% FBS, 1% antibiotic/antimycoctic in a humidified atmosphere of 5% CO2 at 37 degrees celcius. Stable clones were selected with 2ug/mL of puromycin'; [Extraction]'Total RNA was prepared using a Qiagen Rneasy mini kit including the on-column DNase digestion. Quality of RNA was assessed using an Agilent Bioanalyzer 2100.'; [Cell type]'Source: ''cell line: MCF7; treatment: control; ', 'cell line: MCF7; treatment: PAD2 KD; ' GSE47860 Homo sapiens 160 Expression profiling by array GPL17279 Expression profiling of peripheral blood gene expression of women with hereditary breast cancer and controls (set 1) 2013-06-11 We obtained peripheral blood samples for women from Utah (USA) and Ontario (Canada) who had a family history of breast cancer (or did not), who carried a BRCA1/2 mutation (or did not), and who had developed breast cancer (or had not). We classified the women into two groups: [1] those who had a family history of breast cancer (irrespective of BRCA1/2 mutation status) and had developed an early-onset breast tumor and [2] those who had a family history of breast cancer but had not developed a breast tumor or who did not have a family history of breast cancer (some of whom had developed sporadic breast cancer and and others who had not). We then used machine-learning methods to assess how well we could classify these women into either group. The Utah samples served as a training set, and the Ontario samples served as an independent validation set from a geographically distinct population. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47860 Integrative analyses reveal signaling pathways underlying familial breast cancer susceptibility. Molecular systems biology 9.800 https://doi.org/10.15252/msb.20156506 {Molecular systems biology (9.800): 10.15252/msb.20156506} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA208225 https://www.ebi.ac.uk/ena/browser/view/PRJNA208225 None [Overal design]For the Utah cohort, there are 124 samples total: 16 who had a family history of breast cancer and carried a BRCA mutation and had developed breast cancer, 23 with a family history of breast cancer but did not carry a BRCA1/2 mutation and had developed breast cancer, 22 with a family history of breast cancer and carried a BRCA1/2 mutation but had not developed breast cancer, 22 with a family history of breast cancer but did not carry a BRCA1/2 mutation and had not developed breast cancer, 22 with no family history of breast cancer and had developed breast cancer, and 19 with no family history of breast cancer and had not developed breast cancer. The Ontario cohort included 73 samples: 11 who had a family history of breast cancer and carried a BRCA mutation and had developed breast cancer, 17 with a family history of breast cancer but did not carry a BRCA1/2 mutation and had developed breast cancer, 14 with a family history of breast cancer and carried a BRCA1/2 mutation but had not developed breast cancer, 18 with a family history of breast cancer but did not carry a BRCA1/2 mutation and had not developed breast cancer, 8 with no family history of breast cancer and had developed breast cancer, and 5 with no family history of breast cancer and had not developed breast cancer. 36 of the Ontario samples were scanned and processed at Duke University; the remaining 37 samples were handled at Boston University. The batch-adjustment process was repeated twice independently: [1] all 124 Utah samples were adjusted jointly with the 36 Ontario samples that had been processed at Duke University (set 1) and [2] all 124 Utah samples were adjusted jointly with the 37 Ontario samples that had been processed at Boston University (set 2). This dataset represents set 1.; [Treatment]'Not applicable.'; [Growth]'Not applicable.'; [Extraction]'RNA was extracted using the RiboPure RNA Isolation Kit.'; [Cell type]'peripheral blood mononuclear cells''cell type: peripheral blood mononuclear cells; breast_cancer_family_history: no; developed_breast_cancer: no; cohort: Utah; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: no; developed_breast_cancer: yes; cohort: Utah; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: no; cohort: Utah; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: yes; cohort: Utah; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: yes; cohort: Utah; carries_brca_mutation: yes; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: no; cohort: Utah; carries_brca_mutation: yes; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: no; cohort: Ontario; carries_brca_mutation: yes; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: no; cohort: Ontario; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: no; developed_breast_cancer: yes; cohort: Ontario; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: yes; cohort: Ontario; carries_brca_mutation: yes; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: yes; cohort: Ontario; carries_brca_mutation: no; ' GSE106817 Homo sapiens 4046 Non-coding RNA profiling by array GPL21263 Integrated extracellular microRNA profiling for ovarian cancer screening 2017-11-13 A serum miRNA combination could be a powerful classifier for the detEsophageal Cancertion of patients with ovarian cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE106817 Integrated extracellular microRNA profiling for ovarian cancer screening. Nature communications 11.878 https://doi.org/10.1038/s41467-018-06434-4 {Nature communications (11.878): 10.1038/s41467-018-06434-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA418128 https://www.ebi.ac.uk/ena/browser/view/PRJNA418128 None [Overal design]Serum microRNA profiles of 4046 woman samples, which consist of 333 of ovarian cancers, 66 of borderline ovarian tumors, 29 of benign ovarian diseases, 2759 of non-cancer controls, and 859 of the other solid cancers.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted each from 300uL serum samples using 3D-Gene® RNA extraction reagent from liquid sample kit (Toray Industries, Inc.).'; [Cell type]'Source: ''tumor stage (figo): NA; age: uncertain; ', 'tumor stage (figo): NA; age: 52; ', 'tumor stage (figo): NA; age: 60; ', 'tumor stage (figo): NA; age: 57; ', 'tumor stage (figo): NA; age: 59; ', 'tumor stage (figo): NA; age: 45; ', 'tumor stage (figo): NA; age: 63; ', 'tumor stage (figo): NA; age: 54; ', 'tumor stage (figo): NA; age: 68; ', 'tumor stage (figo): NA; age: 48; ', 'tumor stage (figo): NA; age: 71; ', 'tumor stage (figo): NA; age: 64; ', 'tumor stage (figo): NA; age: 58; ', 'tumor stage (figo): NA; age: 55; ', 'tumor stage (figo): NA; age: 42; ', 'tumor stage (figo): NA; age: 46; ', 'tumor stage (figo): NA; age: 41; ', 'tumor stage (figo): NA; age: 85; ', 'tumor stage (figo): NA; age: 51; ', 'tumor stage (figo): NA; age: 65; ', 'tumor stage (figo): NA; age: 49; ', 'tumor stage (figo): NA; age: 39; ', 'tumor stage (figo): NA; age: 72; ', 'tumor stage (figo): 1C; age: 32; ', 'tumor stage (figo): 1C; age: 77; ', 'tumor stage (figo): 1A; age: 47; ', 'tumor stage (figo): 1C; age: 40; ', 'tumor stage (figo): 1C; age: 49; ', 'tumor stage (figo): 2C; age: 55; ', 'tumor stage (figo): 1A; age: 63; ', 'tumor stage (figo): 1A; age: 55; ', 'tumor stage (figo): 1A; age: 73; ', 'tumor stage (figo): 1A; age: 58; ', 'tumor stage (figo): 1A; age: 39; ', 'tumor stage (figo): 1A; age: 56; ', 'tumor stage (figo): 1C; age: 16; ', 'tumor stage (figo): 1A; age: 53; ', 'tumor stage (figo): 1A; age: 72; ', 'tumor stage (figo): 1A; age: 77; ', 'tumor stage (figo): 1A; age: 48; ', 'tumor stage (figo): 1A; age: 60; ', 'tumor stage (figo): 1A; age: 67; ', 'tumor stage (figo): 2C; age: 62; ', 'tumor stage (figo): 1C; age: 27; ', 'tumor stage (figo): 2C; age: 45; ', 'tumor stage (figo): 3A; age: 62; ', 'tumor stage (figo): 1C; age: 65; ', 'tumor stage (figo): 1A; age: 34; ', 'tumor stage (figo): 1A; age: 42; ', 'tumor stage (figo): 1B; age: 38; ', 'tumor stage (figo): 1A; age: 51; ', 'tumor stage (figo): 1A; age: 38; ', 'tumor stage (figo): 3B; age: 51; ', 'tumor stage (figo): 1C; age: 44; ', 'tumor stage (figo): 1C; age: 61; ', 'tumor stage (figo): 1A; age: 62; ', 'tumor stage (figo): 1A; age: 65; ', 'tumor stage (figo): 2C; age: 32; ', 'tumor stage (figo): 1A; age: 37; ', 'tumor stage (figo): 2B; age: 19; ', 'tumor stage (figo): 1C; age: 42; ', 'tumor stage (figo): 1A; age: 69; ', 'tumor stage (figo): 3C; age: 67; ', 'tumor stage (figo): 1A; age: 78; ', 'tumor stage (figo): 3C; age: 19; ', 'tumor stage (figo): 1C; age: 56; ', 'tumor stage (figo): 1A; age: 50; ', 'tumor stage (figo): 1C; age: 64; ', 'tumor stage (figo): 3A; age: 44; ', 'tumor stage (figo): 1C; age: 41; ', 'tumor stage (figo): XX; age: 56; ', 'tumor stage (figo): XX; age: 35; ', 'tumor stage (figo): 1A; age: 46; ', 'tumor stage (figo): 2C; age: 56; ', 'tumor stage (figo): 2C; age: 68; ', 'tumor stage (figo): 2C; age: 52; ', 'tumor stage (figo): 4; age: 40; ', 'tumor stage (figo): 4; age: 55; ', 'tumor stage (figo): 4; age: 52; ', 'tumor stage (figo): 2C; age: 59; ', 'tumor stage (figo): 4; age: 49; ', 'tumor stage (figo): 3C; age: 63; ', 'tumor stage (figo): 4; age: 54; ', 'tumor stage (figo): XX; age: 65; ', 'tumor stage (figo): 3C; age: 65; ', 'tumor stage (figo): 3C; age: 55; ', 'tumor stage (figo): 3C; age: 60; ', 'tumor stage (figo): 1A; age: 64; ', 'tumor stage (figo): XX; age: 66; ', 'tumor stage (figo): 1A; age: 31; ', 'tumor stage (figo): 3A; age: 42; ', 'tumor stage (figo): 3C; age: 54; ', 'tumor stage (figo): XX; age: 62; ', 'tumor stage (figo): 3A; age: 56; ', 'tumor stage (figo): 1C; age: 46; ', 'tumor stage (figo): 1C; age: 50; ', 'tumor stage (figo): 1C; age: 39; ', 'tumor stage (figo): XX; age: 59; ', 'tumor stage (figo): XX; age: 45; ', 'tumor stage (figo): 3C; age: 66; ', 'tumor stage (figo): 1C; age: 70; ', 'tumor stage (figo): 3C; age: 46; ', 'tumor stage (figo): 3C; age: 58; ', 'tumor stage (figo): 1C; age: 53; ', 'tumor stage (figo): 3C; age: 62; ', 'tumor stage (figo): 3C; age: 59; ', 'tumor stage (figo): 1C; age: 62; ', 'tumor stage (figo): 2B; age: 56; ', 'tumor stage (figo): 3C; age: 43; ', 'tumor stage (figo): 3C; age: 70; ', 'tumor stage (figo): 2C; age: 66; ', 'tumor stage (figo): 4; age: 56; ', 'tumor stage (figo): 1C; age: 54; ', 'tumor stage (figo): 1C; age: 38; ', 'tumor stage (figo): 2C; age: 73; ', 'tumor stage (figo): XX; age: 67; ', 'tumor stage (figo): 1C; age: 51; ', 'tumor stage (figo): 3C; age: 73; ', 'tumor stage (figo): 4; age: 42; ', 'tumor stage (figo): 2C; age: 47; ', 'tumor stage (figo): 4; age: 58; ', 'tumor stage (figo): 2C; age: 50; ', 'tumor stage (figo): 3C; age: 51; ', 'tumor stage (figo): XX; age: 53; ', 'tumor stage (figo): 2A; age: 47; ', 'tumor stage (figo): 1C; age: 28; ', 'tumor stage (figo): 4; age: 59; ', 'tumor stage (figo): 4; age: 60; ', 'tumor stage (figo): XX; age: 64; ', 'tumor stage (figo): 1C; age: 45; ', 'tumor stage (figo): 1C; age: 52; ', 'tumor stage (figo): 1A; age: 41; ', 'tumor stage (figo): XX; age: 78; ', 'tumor stage (figo): 1C; age: 43; ', 'tumor stage (figo): 3C; age: 53; ', 'tumor stage (figo): 3C; age: 36; ', 'tumor stage (figo): 1A; age: 25; ', 'tumor stage (figo): XX; age: 61; ', 'tumor stage (figo): 3C; age: 52; ', 'tumor stage (figo): 3A; age: 52; ', 'tumor stage (figo): XX; age: 50; ', 'tumor stage (figo): 1C; age: 76; ', 'tumor stage (figo): 3C; age: 72; ', 'tumor stage (figo): 1C; age: 29; ', 'tumor stage (figo): 1C; age: 47; ', 'tumor stage (figo): 3B; age: 65; ', 'tumor stage (figo): 1A; age: 52; ', 'tumor stage (figo): 3C; age: 34; ', 'tumor stage (figo): 4; age: 74; ', 'tumor stage (figo): 1C; age: 66; ', 'tumor stage (figo): 2C; age: 42; ', 'tumor stage (figo): 2C; age: 72; ', 'tumor stage (figo): 3C; age: 71; ', 'tumor stage (figo): 4; age: 66; ', 'tumor stage (figo): 4; age: 68; ', 'tumor stage (figo): 2C; age: 57; ', 'tumor stage (figo): 1C; age: 60; ', 'tumor stage (figo): 3C; age: 69; ', 'tumor stage (figo): 3A; age: 65; ', 'tumor stage (figo): 3C; age: 61; ', 'tumor stage (figo): XX; age: 74; ', 'tumor stage (figo): 2A; age: 58; ', 'tumor stage (figo): 1C; age: 48; ', 'tumor stage (figo): 3C; age: 74; ', 'tumor stage (figo): XX; age: 70; ', 'tumor stage (figo): 3C; age: 79; ', 'tumor stage (figo): 3C; age: 80; ', 'tumor stage (figo): XX; age: 63; ', 'tumor stage (figo): XX; age: 69; ', 'tumor stage (figo): 3A; age: 60; ', 'tumor stage (figo): 3C; age: 57; ', 'tumor stage (figo): 3C; age: 56; ', 'tumor stage (figo): 3B; age: 27; ', 'tumor stage (figo): 2C; age: 64; ', 'tumor stage (figo): 2C; age: 31; ', 'tumor stage (figo): 3C; age: 49; ', 'tumor stage (figo): 3C; age: 47; ', 'tumor stage (figo): 1A; age: 54; ', 'tumor stage (figo): XX; age: 52; ', 'tumor stage (figo): XX; age: 76; ', 'tumor stage (figo): XX; age: 57; ', 'tumor stage (figo): 4; age: 70; ', 'tumor stage (figo): XX; age: 41; ', 'tumor stage (figo): 3C; age: 68; ', 'tumor stage (figo): XX; age: 81; ', 'tumor stage (figo): 3C; age: 75; ', 'tumor stage (figo): 2C; age: 63; ', 'tumor stage (figo): 2C; age: 69; ', 'tumor stage (figo): 4; age: 63; ', 'tumor stage (figo): 1C; age: 57; ', 'tumor stage (figo): 3C; age: 50; ', 'tumor stage (figo): 3C; age: 48; ', 'tumor stage (figo): 3C; age: 30; ', 'tumor stage (figo): XX; age: 79; ', 'tumor stage (figo): 1A; age: 40; ', 'tumor stage (figo): XX; age: 47; ', 'tumor stage (figo): 3C; age: 39; ', 'tumor stage (figo): 3C; age: 64; ', 'tumor stage (figo): 1C; age: 37; ', 'tumor stage (figo): 3B; age: 45; ', 'tumor stage (figo): 2C; age: 82; ', 'tumor stage (figo): 3C; age: 82; ', 'tumor stage (figo): 2B; age: 67; ', 'tumor stage (figo): 3C; age: 76; ', 'tumor stage (figo): 4; age: 50; ', 'tumor stage (figo): 1C; age: 35; ', 'tumor stage (figo): XX; age: 72; ', 'tumor stage (figo): 3B; age: 72; ', 'tumor stage (figo): 2B; age: 70; ', 'tumor stage (figo): XX; age: 71; ', 'tumor stage (figo): 3B; age: 59; ', 'tumor stage (figo): 3C; age: 42; ', 'tumor stage (figo): 1C; age: 55; ', 'tumor stage (figo): 4; age: 65; ', 'tumor stage (figo): 4A; age: 52; ', 'tumor stage (figo): 3B; age: 40; ', 'tumor stage (figo): XX; age: 43; ', 'tumor stage (figo): 1C; age: 67; ', 'tumor stage (figo): XX; age: 68; ', 'tumor stage (figo): XX; age: 75; ', 'tumor stage (figo): 3A; age: 45; ', 'tumor stage (figo): 1B; age: 67; ', 'tumor stage (figo): 1C; age: 74; ', 'tumor stage (figo): 3B; age: 34; ', 'tumor stage (figo): 2B; age: 74; ', 'tumor stage (figo): 3C; age: 28; ', 'tumor stage (figo): 3A; age: 50; ', 'tumor stage (figo): XX; age: 51; ', 'tumor stage (figo): 3A; age: 67; ', 'tumor stage (figo): 4; age: 38; ', 'tumor stage (figo): 1C; age: 36; ', 'tumor stage (figo): 4; age: 47; ', 'tumor stage (figo): 1A; age: 59; ', 'tumor stage (figo): 4A; age: 49; ', 'tumor stage (figo): 3; age: 67; ', 'tumor stage (figo): 3C; age: 44; ', 'tumor stage (figo): 3C; age: 38; ', 'tumor stage (figo): 4B; age: 59; ', 'tumor stage (figo): 3A; age: 66; ', 'tumor stage (figo): 1C; age: 58; ', 'tumor stage (figo): 3B; age: 62; ', 'tumor stage (figo): 3B; age: 54; ', 'tumor stage (figo): 2C; age: 65; ', 'tumor stage (figo): 1A; age: 36; ', 'tumor stage (figo): 1C; age: 22; ', 'tumor stage (figo): 1A; age: 71; ' GSE43406 Homo sapiens 43 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL16483 Evaluating the restoration of DNA derived from archival formalin-fixed paraffin embedded tissues for genomic profiling by SNP-CGH analysis 2013-01-10 Pathology archives contain vast resources of clinical material in the form of formalin-fixed paraffin embedded (FFPE) tissue samples. Due to the methods of tissue fixation and storage, the integrity of DNA and RNA available from FFPE tissue is compromised, meaning obtaining informative data regarding epigenetic, genomic and expression alterations can be challenging. Here we have investigated the utility of repairing damaged DNA derived from FFPE tumours prior to single nucleotide polymorphism (SNP) arrays for whole genome DNA copy number analysis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43406 Evaluating the repair of DNA derived from formalin-fixed paraffin-embedded tissues prior to genomic profiling by SNP-CGH analysis. Laboratory investigation; a journal of technical methods and pathology 3.684 https://doi.org/10.1038/labinvest.2013.54 {Laboratory investigation; a journal of technical methods and pathology (3.684): 10.1038/labinvest.2013.54} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA185989 https://www.ebi.ac.uk/ena/browser/view/PRJNA185989 None [Overal design]To investigate whether repairing the DNA might improve performance in SNP array assay, we used the DNA Restore protocol from Illumina as a pre-treatment step prior to applying the DNA to the Infinium assay using the Human CytoSNP FFPE-12v2.1 arrays. DNA was extracted from FFPE samples spanning five decades involving tumor material obtained from surgical specimens and post-mortems. Various aspects of the protocol were assessed, including the method of DNA extraction, the role of Quality Control quantitative PCR in predicting sample success and the effect of DNA restoration on assay performance, data quality and the prediction of copy number aberrations (CNAs). In total 8 cases were analysed in this experiment, involving 43 SNP arrays of tumour and matched normal DNA samples, replicates and other control arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'Tumour cores were punched from the FFPE blocks to enrich for tumour epithelial cells. Extraction of genomic DNA from these FFPE cores was performed using two different methods: the DNeasy Blood and Tissue Kit (QIAGEN) and the High Pure DNA Template Preparation Kit (Roche). Both methods were performed according to the manufacturer’s instructions with the following exceptions for both techniques: (i) some tissue samples were pre-treated in 1M sodium thiocyanate overnight at 37oC to remove cross-links and (ii) for all cases an extended tissue digestion step was performed over three nights with supplementary Proteinase K added every 24 hours. Eluted DNA was assessed for purity using the Nanodrop-2000 and double stranded DNA was quantified using the Qubit® fluorometer (Invitrogen) as per manufacturer’s instructions.'; [Cell type]'Source: ''year of diagnosis: 1974; sample type: Autopsy; tissue type: FFPE; tissue histology: NA; tumor immunophenotype: NA; dna extraction method: Qiagen; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1974; sample type: Autopsy; tissue type: FFPE; tissue histology: NA; tumor immunophenotype: NA; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1980; sample type: Autopsy; tissue type: FFPE; tissue histology: NA; tumor immunophenotype: NA; dna extraction method: Qiagen; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1987; sample type: Surgical; tissue type: FFPE; tissue histology: NA; tumor immunophenotype: NA; dna extraction method: Qiagen; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1987; sample type: Surgical; tissue type: FFPE; tissue histology: NA; tumor immunophenotype: NA; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1987; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER -ve; PgR -ve; HER2 -ve; dna extraction method: Qiagen; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1987; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER -ve; PgR -ve; HER2 -ve; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1987; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER -ve; PgR -ve; HER2 -ve; dna extraction method: Qiagen; sodium thiocyanate treatment performed: YES; ffpe restore performed: NO; ', 'year of diagnosis: 1987; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER -ve; PgR -ve; HER2 -ve; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: NO; ', 'year of diagnosis: 1988; sample type: Surgical; tissue type: FFPE; tissue histology: NA; tumor immunophenotype: NA; dna extraction method: Qiagen; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1988; sample type: Surgical; tissue type: FFPE; tissue histology: NA; tumor immunophenotype: NA; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1988; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER -ve; PgR -ve; HER2 3+; dna extraction method: Qiagen; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1988; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER -ve; PgR -ve; HER2 3+; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1989; sample type: Surgical; tissue type: FFPE; tissue histology: NA; tumor immunophenotype: NA; dna extraction method: Qiagen; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1989; sample type: Surgical; tissue type: FFPE; tissue histology: NA; tumor immunophenotype: NA; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1989; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER +ve; PgR +ve; HER2 -ve; dna extraction method: Qiagen; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1989; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER +ve; PgR +ve; HER2 -ve; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1990; sample type: Surgical; tissue type: FFPE; tissue histology: NA; tumor immunophenotype: NA; dna extraction method: Qiagen; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1990; sample type: Surgical; tissue type: FFPE; tissue histology: NA; tumor immunophenotype: NA; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1990; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER +ve; PgR +ve; HER2 3+; dna extraction method: Qiagen; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 1990; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER +ve; PgR +ve; HER2 3+; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 2010; sample type: Blood; tissue type: whole blood; tissue histology: NA; tumor immunophenotype: NA; dna extraction method: Qiagen blood maxi kit; sodium thiocyanate treatment performed: NO; ffpe restore performed: NO; ', 'year of diagnosis: 2010; sample type: Surgical; tissue type: fresh frozen; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER +ve; PgR +ve; HER2 3+; dna extraction method: Qiagen; sodium thiocyanate treatment performed: NO; ffpe restore performed: NO; ', 'year of diagnosis: 2010; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER +ve; PgR +ve; HER2 3+; dna extraction method: Roche; sodium thiocyanate treatment performed: NO; ffpe restore performed: YES; ', 'year of diagnosis: 2010; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER +ve; PgR +ve; HER2 3+; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: NO; ', 'year of diagnosis: 2010; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER +ve; PgR +ve; HER2 3+; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 2010; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER +ve; PgR -ve; HER2 -ve; dna extraction method: Roche; sodium thiocyanate treatment performed: YES; ffpe restore performed: YES; ', 'year of diagnosis: 2010; sample type: Surgical; tissue type: FFPE; tissue histology: IDC-NST, grade 3; tumor immunophenotype: ER +ve; PgR -ve; HER2 -ve; dna extraction method: Roche; sodium thiocyanate treatment performed: NO; ffpe restore performed: YES; ' GSE165678 Homo sapiens 30 Expression profiling by high throughput sequencing GPL24676 RNA sequencing data from MCF7 luminal breast cancer cells expressing STAT5a phospho-point mutants 2021-01-28 Purpose: The goal of this study was to generate mRNA profiles for MCF7 breast cancer cells expressing phospho-deficient STAT5a point mutants with treatment of prolactin (PRL) to determine differential global genomic effects in breast cancer. This data was compared to in vitro studies using the same cells to determine phenotypic outcomes of the STAT5a point mutations. Methods: mRNA profiles of prolactin (PRL) treated or untreated MCF7 cells expressing wild type (WT)-STAT5a, or phospho-deficient point mutants Y694F-, S726A-, or S780A-STAT5a were generated in triplicate by sequencing on the S4 flow cell platform of the Illumina NovaSEQ 6000 System (Illumina, Inc), generating ≥50 million 150 bp paired-end (PE) reads per sample. All libraries were prepared and sequenced in a single batch/flow cell lane. Results: RNA-sequencing and subsequent Ingenuity Pathway Analysis predicted that loss of each phospho-site differentially affected both prolactin-induced gene expression as well as functional pathways of breast cancer (e.g. cell survival, proliferation, and colony formation). Gene set analysis for transcription factor activity (using ENCODE project ChIP-sequencing and the web platform Enrichr), illustrated multiple transcription factors at work in MCF7 cells expressing each phospho-deficient STAT5a point mutant, indicating that these point mutants have roles regulating STAT5a activity at various enhancer/promoters in a enhancer/promoter specific context. Conclusion: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE165678 Serine residues 726 and 780 have nonredundant roles regulating STAT5a activity in luminal breast cancer. Scientific reports 4.011 https://doi.org/10.1038/s41598-021-92830-8 {Scientific reports (4.011): 10.1038/s41598-021-92830-8} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA695443 https://www.ebi.ac.uk/ena/browser/view/PRJNA695443 https://www.ncbi.nlm.nih.gov/sra?term=SRP303606 [Overal design]mRNA profiling of MCF7 cells containing either WT-STAT5a, or point mutants Y694F-, S726A-, or S780A-STAT5a treated or untreated for 2 hours with prolactin (PRL).; [Treatment]'Following 24 hour serum starvation, (DMEM supplemented with 0.1% BSA), three biological replicates were treated with PRL (250 ng/ml) for two hours.'; [Growth]'MCF7 breast cancer cells were grown in DMEM supplemented with 10% fetal bovine serum (FBS) and 1% penicillin/streptomycin (P/S). Endogenous STAT5a was targeted by shRNA, and stable knockdown was achieved by viral transduction and antibiotic selection. These MCF7 cells with STAT5a knockdown were then rescued: stable rescue with indicated STAT5a species was done by viral transduction and antibiotic selection. Confirmation of rescues was performed by Western Blot. Cells were grown in an incubator at 37C with 5% CO2, and routinely passaged.'; [Extraction]'Cells were washed with 1x PBS, placed on ice, and RNA was harvested using Trizol reagent and the PureLink™ RNA Mini Kit (Thermo Fisher Scientific, 12183018A) with Dnase treatment.\nmRNA library was prepared by polyA selection with ≥500 ng RNA using the Universal Plus mRNA-Seq Library Preparation Kit (NuGEN) following manufacturer’s protocol.'; [Cell type]'Source: ''cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: wild type (WT)-STAT5a; treatment: untreated; biological replicate: biological rep 1; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: wild type (WT)-STAT5a; treatment: untreated; biological replicate: biological rep 2; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: wild type (WT)-STAT5a; treatment: untreated; biological replicate: biological rep 3; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: wild type (WT)-STAT5a; treatment: treated with PRL for 2 hours; biological replicate: biological rep 1; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: wild type (WT)-STAT5a; treatment: treated with PRL for 2 hours; biological replicate: biological rep 2; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: wild type (WT)-STAT5a; treatment: treated with PRL for 2 hours; biological replicate: biological rep 3; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant Y694F-STAT5a; treatment: untreated; biological replicate: biological rep 1; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant Y694F-STAT5a; treatment: untreated; biological replicate: biological rep 2; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant Y694F-STAT5a; treatment: untreated; biological replicate: biological rep 3; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant Y694F-STAT5a; treatment: treated with PRL for 2 hours; biological replicate: biological rep 1; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant Y694F-STAT5a; treatment: treated with PRL for 2 hours; biological replicate: biological rep 2; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant Y694F-STAT5a; treatment: treated with PRL for 2 hours; biological replicate: biological rep 3; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant S726A-STAT5a; treatment: untreated; biological replicate: biological rep 1; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant S726A-STAT5a; treatment: untreated; biological replicate: biological rep 2; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant S726A-STAT5a; treatment: untreated; biological replicate: biological rep 3; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant S726A-STAT5a; treatment: treated with PRL for 2 hours; biological replicate: biological rep 1; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant S726A-STAT5a; treatment: treated with PRL for 2 hours; biological replicate: biological rep 2; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant S726A-STAT5a; treatment: treated with PRL for 2 hours; biological replicate: biological rep 3; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant S780A-STAT5a; treatment: untreated; biological replicate: biological rep 1; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant S780A-STAT5a; treatment: untreated; biological replicate: biological rep 2; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant S780A-STAT5a; treatment: untreated; biological replicate: biological rep 3; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant S780A-STAT5a; treatment: treated with PRL for 2 hours; biological replicate: biological rep 1; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant S780A-STAT5a; treatment: treated with PRL for 2 hours; biological replicate: biological rep 2; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: point mutant S780A-STAT5a; treatment: treated with PRL for 2 hours; biological replicate: biological rep 3; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: empty vector (EV) control; treatment: untreated; biological replicate: biological rep 1; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: empty vector (EV) control; treatment: untreated; biological replicate: biological rep 2; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: empty vector (EV) control; treatment: untreated; biological replicate: biological rep 3; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: empty vector (EV) control; treatment: treated with PRL for 2 hours; biological replicate: biological rep 1; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: empty vector (EV) control; treatment: treated with PRL for 2 hours; biological replicate: biological rep 2; ', 'cell line: MCF7; stat5a knockdown: Endogenous STAT5a knockdown; stat5a rescue: empty vector (EV) control; treatment: treated with PRL for 2 hours; biological replicate: biological rep 3; ' GSE99060 Homo sapiens 18 Expression profiling by high throughput sequencing GPL17303 Transcriptomic analysis in breast cancer cell lines after CDK4/6 inhibition 2017-05-18 We measured changes in expression of 20,812 genes in human breast cancer cell lines after treatment with abemaciclib https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99060 CDK4/6 inhibition triggers anti-tumour immunity. Nature 43.070 https://doi.org/10.1038/nature23465 {Nature (43.070): 10.1038/nature23465} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA387164 https://www.ebi.ac.uk/ena/browser/view/PRJNA387164 https://www.ncbi.nlm.nih.gov/sra?term=SRP107319 [Overal design]Examination of changes in gene expression in 3 cell lines, in triplicate; [Treatment]'Abemaciclib concentration 500nM for MDA-MB_361 and MDA-MB453; 250nM for MCF7'; [Growth]'Cells were cultured in sterile dishes in media as described. Cells were plated at densities such that final density at time of RNA collection was between 60-70%.'; [Extraction]'RNA was extracted using Macherey Nagel kit.\ncDNA libraries were constructed using\xa0the Ion AmpliSeq Transcriptome Human Gene Expression Kit (Thermo Fisher)\nThe Ion AmpliSeq Transcriptome Human Gene Expression Kit is designed for targeted amplification of over 20,000 human RefSeq genes. A short amplicon (~110 bp) is amplified for each targeted gene (Thermo Fisher).'; [Cell type]'Source: ''cell line: MDA-MB-361 breast carcinoma cell line; agent: control; ', 'cell line: MDA-MB-361 breast carcinoma cell line; agent: abemaciclib; ', 'cell line: MDA-MB-453 breast carcinoma cell line; agent: control; ', 'cell line: MDA-MB-453 breast carcinoma cell line; agent: abemaciclib; ', 'cell line: MCF7 breast carcinoma cell line; agent: control; ', 'cell line: MCF7 breast carcinoma cell line; agent: abemaciclib; ' GSE38499 Homo sapiens 4 Expression profiling by RT-PCR GPL15666 Real-time quantitative PCR analysis of MDA MB 231 cells 2012-06-05 MDA-MB-231 breast cancer cells were infected with either Ad-GFP, Ad-FLI1, or Ad-PDEF https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE38499 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA168022 https://www.ebi.ac.uk/ena/browser/view/PRJNA168022 None [Overal design]qPCR gene expression profiling of MDA-MB-231 breast cancer cells were infected with either Ad-GFP, Ad-FLI1, or Ad-PDEF.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted with RNeasy Mini Kit.'; [Cell type]'adenocarcinoma''cell line: MDA-MB-231; cell type: adenocarcinoma; activation agent: Control; time: 72 hours; ', 'cell line: MDA-MB-231; cell type: adenocarcinoma; activation agent: Ad-GFP; time: 72 hours; ', 'cell line: MDA-MB-231; cell type: adenocarcinoma; activation agent: Ad-GFP-FLI1; time: 72 hours; ', 'cell line: MDA-MB-231; cell type: adenocarcinoma; activation agent: Ad-GFP-PDEF; time: 72 hours; ' GSE31223 Mus musculus 30 Expression profiling by high throughput sequencing GPL11002; GPL13112 Gene expression of polyoma middle T antigen induced mammary tumors [RNA_Seq : MOLF x PyMT] 2011-08-04 Mouse genetic crosses were established between the PyMT model of metastatic breast cancer and MOLF strain. Tumors were harvested from the animals for gene expression analysis to identify genes and network modules associated with progression to distant metastatic disease. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE31223 An integrated systems genetics screen reveals the transcriptional structure of inherited predisposition to metastatic disease. Genome research 9.944 https://doi.org/10.1101/gr.166223.113 {Proceedings of the National Academy of Sciences of the United States of America (9.580) doi:10.1073/pnas.1117872109}; {Genome research (9.944) doi:10.1101/gr.166223.113}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA154115 https://www.ebi.ac.uk/ena/browser/view/PRJNA154115 https://www.ncbi.nlm.nih.gov/sra?term=SRP007956 [Overal design]30 samples from the MOLF cross were assayed using Illumina next generation sequencers; [Treatment]'None'; [Growth]'None'; [Extraction]"Illumina mRNA Library Preparation Protocol (Total RNA extracted from mammary tissue, Purify mRNA by poly-A selection, Fragment mRNA, Synthesize the First Strand cDNA, Synthesize the Second Strand cDNA, Perform End Repair, Adenylate 3' ends, Ligate the Adapters, Purify the cDNA Templates on a gel to select a size range)"; [Cell type]'Source: ''strain background: ((MOLF x PyMT) x FVB) backcross animal; tissue: MOLF x PyMT backcross mammary tumor; ' GSE168485 Hominidae 8 Expression profiling by high throughput sequencing GPL29824 Addition-elimination mechanism activated nucleotide transition sequencing for RNA dynamics profiling 2021-03-08 The temporal information of intracellular transcripts is essential to understand their functional roles, yet routine RNA-seq methods only measure RNA species at a steady state. Here we develop addition-elimination mechanism activated nucleotide transition sequencing (AENT-seq) for transcriptome-wide profiling of RNA dynamics. In AENT-seq, intracellular transcripts are metabolically labeled with 4-thiouridine (4sU), and then isolated total RNA are subjected to 4sU-to-cytosine (C) transition reactions based on a mild addition-elimination chemistry. N2H4•H2O is demonstrated to convert 4sU to 4-hydrazino cytosine (C*) in RNA-friendly aqueous conditions. The C* is recorded as natural C during extension reactions with a high efficiency of ~95%. This 4sU-to-C transition marks 4sU-containing nascent transcripts, and it enables subsequent sequencing analysis of RNA dynamics with single-nucleotide resolution. We applies our AENT-seq to simply investigate transcript dynamic information of several genes involved in cancer progression and metastasis. This method avoids harsh chemical conditions and harmful reagents involved in previous approaches, allowing rapid dissemination and extensive applications of the technique. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE168485 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA707546 https://www.ebi.ac.uk/ena/browser/view/PRJNA707546 https://www.ncbi.nlm.nih.gov/sra?term=SRP309806 [Overal design]Next generation sequencing (NGS) provided the numbers and locations of 4sU-to-C (T-to-C) transition in the mapping reads of mRNA transcripts; [Treatment]'None'; [Growth]'None'; [Extraction]'cells were cultured with 4sU for different time (0h, 1h, 4h, and 8h), and RNA was harvested using Trizol reagent. Novogene RNA library Prep Kit was used with 1 ug of total RNA for the construction of sequencing libraries.\nA total amount of 1 µg RNA per sample was used as input material for the RNA sample preparations. Briefly, mRNA was purified from total RNA using poly-T oligo-attached magnetic beads. Fragmentation was carried out using divalent cations under elevated temperature in First Strand Synthesis Reaction Buffer. First strand cDNA was synthesized using random hexamer primer and RNase H. In order to select cDNA fragments of preferentially 100~200 bp in length, the library fragments were purified with AMPure XP system (Beckman Coulter, Beverly, USA). Adapter ligation at 25°C for 10min before PCR . Then PCR was performed with Phusion HighFidelity DNA polymerase, Universal PCR primers and Index (X) Primer. At last, PCR products were purified (AMPure XP system) and library quality was assessed on the Agilent Bioanalyzer 2100 system.'; [Cell type]'Human breast cancer cells''cell line: MDA-MB-231; cell type: Human breast cancer cells; treatment: untreated; ', 'cell line: MDA-MB-231; cell type: Human breast cancer cells; treatment: treated with 4sU for 1 hours; ', 'cell line: MDA-MB-231; cell type: Human breast cancer cells; treatment: treated with 4sU for 4 hours; ', 'cell line: MDA-MB-231; cell type: Human breast cancer cells; treatment: treated with 4sU for 8 hours; ', 'cell line: MCF-7; cell type: Human breast cancer cells; treatment: untreated; ', 'cell line: MCF-7; cell type: Human breast cancer cells; treatment: treated with 4sU for 1 hours; ', 'cell line: MCF-7; cell type: Human breast cancer cells; treatment: treated with 4sU for 4 hours; ', 'cell line: MCF-7; cell type: Human breast cancer cells; treatment: treated with 4sU for 8 hours; ' GSE110686 Homo sapiens 2 Expression profiling by high throughput sequencing GPL16791 Single-cell RNA-seq of six thousand purified CD3+ T cells from human primary TNBCs 2018-02-15 CD3+ T cells were isolated by FACS from primary tumour tissues of two triple-negative breast cancer patients. Sorted cells were submitted to a 10X Genomics Chromium System for single cell capture. cDNA synthesis and library preparation were done according to the protocol supplied by the manufacturer. Libraries were sequenced on an Illumina HiSeq 2500 High Output Mode using V4 clustering and sequencing chemistry to achieve 100 bp paired-end reads. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE110686 Single-cell profiling of breast cancer T cells reveals a tissue-resident memory subset associated with improved prognosis. Nature medicine 30.641 https://doi.org/10.1038/s41591-018-0078-7 {Nature medicine (30.641): 10.1038/s41591-018-0078-7} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA434278 https://www.ebi.ac.uk/ena/browser/view/PRJNA434278 https://www.ncbi.nlm.nih.gov/sra?term=SRP132943 [Overal design]Transcriptional profiling was completed for 5,174 CD3+ T cells from the first patient and 1,137 CD3+ T cells from the second patient.; [Treatment]'None'; [Growth]'None'; [Extraction]'Primary tumour tissues were resected from two patients with triple-negative breast cancer. Tissues were treated with collagenase and mechanically dissociated. Single cell suspensions were generated and the viable cells were FACS sorted for CD3+ T cells on a BD FACSAria II Cell Sorter (BD Biosciences). Sorted cells were then counted, assessed for viability and resuspended. Cell suspensions were loaded onto a Chromium Single Cell Chip along with the reverse transcription (RT) mastermix and single cell 3’ gel beads, aiming for 2000 – 6000 cells per channel.\nFollowing generation of single cell gel bead-in-emulsions (GEMs), reverse transcription was performed using a C1000 Touch Thermal Cycler with a Deep Well Reaction Module (Bio-Rad Laboratories, Hercules, CA, USA). Amplified cDNA was purified using SPRIselect beads (Beckman Coulter, Lane Cove, NSW, Australia) and sheared to approximately 200bp with a Covaris S2 instrument (Covaris, Woburn, MA, USA) using the manufacturer’s recommended parameters. Sequencing libraries were generated with unique sample indices (SI) for each sample. Libraries were sequenced on an Illumina HiSeq 2500 High Output Mode using V4 clustering and sequencing chemistry to achieve paired-end 100 bp reads..'; [Cell type]'Source: ''breast cancer subtypes: triple negative; number of cells: 5174; number of channels: 2; ', 'breast cancer subtypes: triple negative; number of cells: 1137; number of channels: 1; ' GSE19777 Homo sapiens 9 Expression profiling by array GPL570 Antisense miRNA-221/222 (si221/222) and control inhibitor (GFP) treated fulvestrant-resistant breast cancer cells 2010-01-07 Full title: Expression data from antisense miRNA-221/222 (si221/222) and control inhibitor (GFP) treated fulvestrant-resistant breast cancer cells The expression of miR-221/222 were found to be upregulated in fulvestrant resistant breast cancer cells MCF7-FR compared to its drug-sensitive counterpart MCF7. To investigate the role of miR-221/222 in acquired resistance to fulvestrant, we lowered the level of miR-221/222 in MCF7-FR cells using miRNA inhibitors (antagomirs), and compared gene expression profiles before and after treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE19777 MicroRNA-221/222 confers breast cancer fulvestrant resistance by regulating multiple signaling pathways. Oncogene 6.634 https://doi.org/10.1038/onc.2010.487 {Oncogene (6.634): 10.1038/onc.2010.487} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA121861 https://www.ebi.ac.uk/ena/browser/view/PRJNA121861 None [Overal design]Fulvestrant-resistant breast cancer cells MCF7-FR (originated from drug-sentitive breast cancer model cell line MCF7) were transient-transfected by antigomirs targeting miR221 or miR222 (i.e. si221, si222). All three cell lines, MCF7-FR, siR221, siRNA222 were subjected to gene expression profiling.; [Treatment]'None', "For transfection assays, cells were plated in antibiotic-free media and transfected with Lipofectamine 2000 (Invitrogen, Carlasbad, CA) according to the manufacturer's instructions. Antagomirs were transfected at 100nM concentrations."; [Growth]'MCF7-FR cells were growing in phenol red-free medium with 10% charcoal-stripped fetal bovine serum (FBS) and 10E-7 mol/L fulvestrant'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''treatment: control; cell line: MCF7-FR; ', 'treatment: si221; cell line: MCF7-FR; ', 'treatment: si222; cell line: MCF7-FR; ' GSE134992 Homo sapiens 3 Non-coding RNA profiling by high throughput sequencing GPL18573 Serum tRNA-derived fragments (tRFs) as potential candidates for diagnosis of non-triple-negative breast cancer 2019-07-28 Breast cancer is one of the most common cancers in the world and non-triple-negative breast cancer (non-TNBC) accounts for 80-90% of all invasive breast cancers. Early detection of breast cancer is considered as key to successful treatment. Conventionally,breast imaging and needle core biopsy are used for detection and monitoring of disease progression. However, small volume changes may be ignored on imaging and traditional biopsy is spatially and temporally limited, leading to a significant lag time in detecting cancer progression. This thus prompted renewed focus on early and accurate diagnosis. In this article, we committed to investigate whether there exists accurate molecule in peripheral blood which can help diagnose breast cancer. tRNA-derived fragments (tRFs) have been reported to be involved in many pathological processes, but whether it can serve as biomarkers for the diagnosis of breast cancer remains unclear. Using high-throughput sequencing technology, we identified 4021 differentially expressed tRFs in normal breast epithelial cell lines and non-triple-negative breast cancer cell lines and 8 tRFs were selected to construct a signature to predict the non-TNBC. Further, qRT-PCR was conducted to verify its expression and to analyze the correlation between dysregulated tRFs and breast cancer. The results indicated that tDR-7816, tDR-5334, tDR-4733 might be promising biomarkers. Through further bioinformatics analysis, we predicted that tDR-7816 influences xenobiotic metabolic process that support the oncogenesis of breast cancer. Taken together, our results provide a rationale for using circulating tDR-7816 expression as a novel potential biomarker to diagnose early non-TNBC patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE134992 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA557046 https://www.ebi.ac.uk/ena/browser/view/PRJNA557046 https://www.ncbi.nlm.nih.gov/sra?term=SRP216608 [Overal design]Examination of differentially expressed tRFs in non-triple-negative breast cancer cell lines and normal cell lines.; [Treatment]'None'; [Growth]'Human breast cancer cell lines MCF-7 and SKBR-3 were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA). Human normal breast epithelial cell line HBL-100 was obtained from Cell bank of Chinese Academy of Sciences (Shanghai, China). SKBR-3 cells were cultured in RPMI-1640 (Multicell, USA), MCF-7 and HBL-100 cells were cultured in DMEM (Gibco, UK) supplemented with 10% Fetal Bovine Serum (FBS, Gibco), 100 U/ml penicillin and 100 μg/ml streptomycin (Multicell, USA). Cells were cultured at 37°C in a humidified atmosphere containing 5% CO2 and the cell medium was replaced every 48 h.'; [Extraction]'Total RNA was extracted from cells using Trizol reagent (Life Technologies, USA). We do the following treatments before library preparation for total RNA samples: 3’-aminoacyl (charged) deacylation to 3’-OH for 3’ adaptor ligation, 3’-cP (2’,3’-cyclic phosphate) removal to 3’-OH for 3’ adaptor ligation, 5’-OH (hydroxyl group) phosphorylation to 5’-P for 5’-adaptor ligation, m1A and m3C demethylation for efficient reverse transcription. Sequencing libraries are size-selected for the RNA biotypes to be sequenced using an automated gel cutter. The libraries are qualified and absolutely quantified using Agilent BioAnalyzer 2100.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'estrogen-sensitive cells', 'HER2/ERBB2 amplified cells', 'normal breast epithelial cells''cell type: estrogen-sensitive cells; tissue: breast adenocarcinoma; cell line: MCF-7; ', 'cell type: HER2/ERBB2 amplified cells; tissue: breast adenocarcinoma; cell line: SKBR3; ', 'cell type: normal breast epithelial cells; tissue: breast epithelial; cell line: HBL-100; ' GSE44776 Homo sapiens 10 Genome binding/occupancy profiling by genome tiling array GPL10671; GPL13848; GPL16734 DamID for MBD3 in human breast cancer cell lines 2013-03-01 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE44776 MBD3 localizes at promoters, gene bodies and enhancers of active genes. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1004028 {PLoS genetics (5.224): 10.1371/journal.pgen.1004028} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA191622 https://www.ebi.ac.uk/ena/browser/view/PRJNA191622 None [Overal design]Refer to individual Series; [Treatment]'Not applicable'; [Growth]'Cells were cultured with DMEM/F12 supplemented with 10% fetal bovine serum'; [Extraction]'Genomic DNA was purified and processed for DamID as described in Nature Protocol 2007;2(6):1467-78.'; [Cell type]'Source: ''cell line: MCF-7; replicate: 1; fraction: MBD3-Dam bound DNA; ', 'cell line: MCF-7; replicate: 1; fraction: Dam bound DNA; ', 'cell line: MCF-7; replicate: 2; fraction: MBD3-Dam bound DNA; ', 'cell line: MCF-7; replicate: 2; fraction: Dam bound DNA; ', 'cell line: MDA-231; replicate: 1; fraction: MBD3-Dam bound DNA; ', 'cell line: MDA-231; replicate: 1; fraction: Dam bound DNA; ', 'cell line: MDA-231; replicate: 2; fraction: MBD3-Dam bound DNA; ', 'cell line: MDA-231; replicate: 2; fraction: Dam bound DNA; ', 'cell line: MCF-7; replicate: 3; fraction: MBD3-Dam bound DNA; ', 'cell line: MCF-7; replicate: 3; fraction: Dam bound DNA; ', 'cell line: MDA-231; replicate: 3; fraction: MBD3-Dam bound DNA; ', 'cell line: MDA-231; replicate: 3; fraction: Dam bound DNA; ' GSE115144 Homo sapiens 42 Expression profiling by array GPL17586 Transcriptome analysis of paired luminal breast tumor and para-carcinoma tissues 2018-05-31 With stringent filtering criteria (fold change>2, p<0.001 and False Discovery Rate (FDR) <0.01), we identified 133 lncRNAs and 370 mRNAs that were the most highly differentially expressed. Of all the lncRNAs, 61 were upregulated, and 72 were downregulated. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115144 Transcriptome analysis of luminal breast cancer reveals a role for LOL in tumor progression and tamoxifen resistance. International journal of cancer 4.982 https://doi.org/10.1002/ijc.32185 {International journal of cancer (4.982): 10.1002/ijc.32185} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA473920 https://www.ebi.ac.uk/ena/browser/view/PRJNA473920 None [Overal design]Twenty one paired luminal breast tumor (ER+) and para-carcinoma RNA samples extracted from fresh frozen tissues were analyzed using the Affymetrix Human Transcriptome 2.0 Arrays. Array data was processed by Partak genomic suite software.; [Treatment]'Breast cancer surgery'; [Growth]'Fresh frozon tissue samples were obtained after breast cancer surgery'; [Extraction]"Tissues total RNA were extracted using RNeasy plus Mini Kit (QIAGEN) according to manufacturer's instructions."; [Cell type]'Source: ''disease state: luminal (ER+) breast cancer; tissue: breast; gender: female; ' GSE44408 Homo sapiens 44 Expression profiling by array GPL571 Transcriptomic survey of lymph node-positive vs. - negative ductal breast cancer 2013-02-19 Lymph node involvement is a major prognostic variable in breast cancer. Whether the molecular mechanisms that drive breast cancer cells to colonize lymph nodes are shared with their capacity to form distant metastases is yet to be established. In a transcriptomic survey aimed at identifying molecular factors associated with lymph node involvement of ductal breast cancer, we found that luminal differentiation, assessed by the expression of estrogen receptor (ER) and/or progesterone receptor (PR) and GATA3, was only infrequently lost in node-positive primary tumors and in matched lymph node metastases. The transcription factor GATA3 critically determines luminal lineage specification of mammary epithelium and is widely considered a tumor and metastasis suppressor in breast cancer. Strong expression of GATA3 and ER in a majority of primary node-positive ductal breast cancer was corroborated by quantitative RT-PCR and immunohistochemistry in the initial sample set, and by immunohistochemistry in an additional set from 167 patients diagnosed of node-negative and –positive primary infiltrating ductal breast cancer, including 102 samples from loco-regional lymph node metastases matched to their primary tumors, as well as 37 distant metastases. These observations suggest that loss of luminal differentiation is not a major factor driving the ability of breast cancer cells to colonize regional lymph nodes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE44408 Infrequent loss of luminal differentiation in ductal breast cancer metastasis. PloS one 2.776 https://doi.org/10.1371/journal.pone.0078097 {PloS one (2.776): 10.1371/journal.pone.0078097} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA189786 https://www.ebi.ac.uk/ena/browser/view/PRJNA189786 None [Overal design]The transcriptomic study comprises 16 samples from Lymph node metastasis from infiltrating ductal breast carcinoma, 18 samples from Primary node-positive infiltrating ductal,7 samples from Primary node-negative infiltrating ductal and 3 samples from Unaffected lymph node were included. Their RNA was isolated and prepared for hybridization to human Affymetrix GeneChip arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'For total RNA extraction cryopreserved breast tissue samples were homogenized in TRIzol reagent (Invitrogen, San Diego, CA, USA) using pestle and nuclease-free 1,5ml reaction tubes (Ambion). Total RNA was then extracted following the manufacturers guidelines and quality was assessed with the Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, USA).'; [Cell type]'Source: ''tissue: Unaffected lymph node; ', 'tissue: Lymph node metastasis from infiltrating ductal breast carcinoma; ', 'tissue: Primary node-positive infiltrating ductal breast carcinoma; ', 'tissue: Primary node-negative infiltrating ductal breast carcinoma; ' GSE26134 Homo sapiens 6 Expression profiling by array GPL6244 Expression data from MTDH knockdown in the Hec50co endometrial cancer cell line 2010-12-17 Understanding the molecular underpinnings of chemoresistance is vital to design therapies to restore chemosensitivity. In particular, metadherin (MTDH) has been demonstrated to have a critical role in chemoresistance. Over-expression of MTDH has recently been implicated in poor clinical outcome in breast cancer, neroblastoma, hepatocellular carcinoma and prostate cancer. In this present study, we focused on the therapeutic benefit of MTDH depletion to restore sensitivity to cell death mediated by a combinatorial therapy of tumor necrosis factor-alpha-related apoptosis-inducing ligand (TRAIL), which promotes death of cancerous cells of the human reproductive tract, and histone deacetylase (HDAC) inhibitors, which have been shown to increase sensitivity of cancer cells to TRAIL-induced apoptosis. Our data indicate that depletion of MTDH in endometrial cancer cells results in sensitization of cells that were previously resistant to cell death mediated by combinatorial treatment with TRAIL and HDAC inhibitor LBH589. MTDH was found to be involved in G2/M checkpoint regulation in response to LBH589 alone or LBH589 in combination with TRAIL, suggesting that MTDH functions at the cell cycle checkpoint to accomplish resistance.Using microarray technology, we identified 57 downstream target genes of MTDH, including Calbindin 1 and Galectin 1, which may contribute to MTDH-mediated resistance to combinatorial TRAIL and HDAC inhibitor targeted therapy. Inhibition of PDK1,AKT phosphorylation and increase Bim expression and XIAP degradation may result in sensitivity to cell death induction in MTDH depleted Hec50co cells by TRAIL and LBH 589 combination treatment. These findings indicate that depletion of MTDH is a potentially novel avenue for effective cancer therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26134 Knockdown of MTDH sensitizes endometrial cancer cells to cell death induction by death receptor ligand TRAIL and HDAC inhibitor LBH589 co-treatment. PloS one 2.776 https://doi.org/10.1371/journal.pone.0020920 {PloS one (2.776): 10.1371/journal.pone.0020920} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA135381 https://www.ebi.ac.uk/ena/browser/view/PRJNA135381 None [Overal design]The microarray was performed on three biological triplicates as well as three experimental triplictes of stable knockdown and control cells. MTDH was knocked down using a shRNA.; [Treatment]'We transfected cells with MTDH short hairpin RNA interference constructs provided from ORIGENE (Rockville, MD). Individual cell clones resistant to puromycin were expanded and subjected to screening of the expression of the targeted protein by Western blotting.'; [Growth]'These cell lines were cultured in DMEM medium containing 10% fetal bovine serum and 1% penicillin/streptomycin (Gibco BRL) at 37°C in a humidified atmosphere of 5% CO2 and 95% air.'; [Extraction]"mirVana miRNA Isolation Kit (Ambion, Austin, TX) RNA extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: Hec50co endometrial cancer cell line; cell line traits: Loss of p53, loss of hormone receptors ER and PR; disease state: Grade 3 endometrioid adenocarcinoma; genotype/variation: MTDH knockdown; ', 'cell line: Hec50co endometrial cancer cell line; cell line traits: Loss of p53, loss of hormone receptors ER and PR; disease state: Grade 3 endometrioid adenocarcinoma; genotype/variation: control; ' GSE100687 Homo sapiens 6 Expression profiling by high throughput sequencing GPL16791 RNA-Seq analysis of breast cancer cells after shikonin treatment 2017-06-30 We performed RNA-seq analysis using differnt breast cancer cell lines (MCF-7, SK-BR-3 and MDA-MB-231) after shikonin treatment. We reported that shikonin enhances the expression of DUSP-1 and DUSP-2. Shikonin induces apoptosis and decreases the phosphorylation of JNK1/2 through activationg DUSP-1 and DUSP2. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE100687 RNA-seq transcriptome analysis of breast cancer cell lines under shikonin treatment. Scientific reports 4.011 https://doi.org/10.1038/s41598-018-21065-x {Scientific reports (4.011): 10.1038/s41598-018-21065-x} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA392672 https://www.ebi.ac.uk/ena/browser/view/PRJNA392672 https://www.ncbi.nlm.nih.gov/sra?term=SRP110816 [Overal design]We treated three breast cancer cell lines with 10 μΜ shikonin for 6 hr. The gene expression profiling was performed using RNA-seq. Numbers of significantly differentially expressed (SDE) genes in different human breast cancer cell lines under shikonin treatment had been identified. We analyzed the functional annotation and performed the pathway analysis using 38 common SDE genes.; [Treatment]'MCF-7, SK-BR-3 and MDA-MB-231 cells were treated with 10 μΜ shikonin for 6 hr.'; [Growth]'MCF-7 and MDA-MB-231 cells were maintained in DMEM supplemented with 10% heat-inactivated FBS and 100 μg/mL of penicillin-streptomycin, and SK-BR-3 cells were maintained in DMEM/F12 supplemented with 10% heat-inactivated FBS and 100 μg/mL of penicillin-streptomycin.'; [Extraction]'Total RNA was extracted with TRIzol reagent following the recommendations of the manufacturer.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''cell line: MCF-7; treatment: shikonin 0 μM; ', 'cell line: MCF-7; treatment: shikonin 10 μM; ', 'cell line: SK-BR-3; treatment: shikonin 0 μM; ', 'cell line: SK-BR-3; treatment: shikonin 10 μM; ', 'cell line: MDA-MB-231; treatment: shikonin 0 μM; ', 'cell line: MDA-MB-231; treatment: shikonin 10 μM; ' GSE13914 Homo sapiens 55 Genome variation profiling by array GPL7778; GPL7779; GPL7780; GPL7781; GPL7782; GPL7783; GPL7784 Molecular profiling of breast cancer cell lines defines relevant tumor models (aCGH) 2008-12-11 Breast cancer cell lines have been used widely to investigate breast cancer pathobiology and new therapies. Breast cancer is a molecularly heterogeneous disease, and it is important to understand how well and which cell lines best model that diversity. In particular, microarray studies have identified molecular subtypes - luminal A, luminal B, ERBB2-associated, basal-like and normal-like - with characteristic gene-expression patterns and underlying DNA copy number alterations (CNAs). Here, we studied a collection of breast cancer cell lines to catalog molecular profiles and to assess their relation to breast cancer subtypes. Whole-genome DNA microarrays were used to profile gene expression and CNAs in a collection of 52 widely-used breast cancer cell lines, and comparisons were made to existing profiles of primary breast tumors. Hierarchical clustering was used to identify gene-expression subtypes, and Gene Set Enrichment Analysis (GSEA) to discover biological features of those subtypes. Genomic and transcriptional profiles were integrated to discover within high-amplitude CNAs candidate cancer genes with coordinately altered gene copy number and expression. Transcriptional profiling of breast cancer cell lines identified one luminal and two basal-like (A and B) subtypes. Luminal lines displayed an estrogen receptor (ER) signature and resembled luminal-A/B tumors, basal-A lines were associated with ETS-pathway and BRCA1 signatures and resembled basal-like tumors, and basal-B lines displayed mesenchymal and stem-cell characteristics. Compared to tumors, cell lines exhibited similar patterns of CNA, but an overall higher complexity of CNA (genetically simple luminal-A tumors were not represented), and only partial conservation of subtype-specific CNAs. We identified 80 high-level DNA amplifications and 13 presumptive homozygous deletions, and the resident genes with concomitantly altered gene-expression, highlighting known and novel candidate breast cancer genes. Overall, breast cancer cell lines were genetically more complex than tumors, but retained expression patterns with relevance to the luminal-basal subtype distinction. The compendium of molecular profiles defines cell lines suitable for investigations of subtype-specific pathobiology, biomarkers and therapies, and provides a resource for discovery of new breast cancer genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE13914 Molecular profiling of breast cancer cell lines defines relevant tumor models and provides a resource for cancer gene discovery. PloS one 2.776 https://doi.org/10.1371/journal.pone.0006146 {PloS one (2.776): 10.1371/journal.pone.0006146} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA123169 https://www.ebi.ac.uk/ena/browser/view/PRJNA123169 None [Overal design]cDNA microarrays from the Stanford Functional Genomics Facility were used to carry out array-based Comparative Genomic Hybridization (array CGH) analysis of 52 human breast epithelial cell lines, in comparison to normal female DNA. Three reference arrays of normal male vs. normal female DNA were also done. Map positions for arrayed cDNA clones were assigned using the NCBI genome assembly, accessed through the UCSC genome browser database (NCBI Build 36). The cghFLasso method was used to call DNA gains and losses.; [Treatment]'None'; [Growth]'None'; [Extraction]'not provided'; [Cell type]'Source: ''' GSE104987 Homo sapiens 3 Expression profiling by high throughput sequencing GPL11154 KDM5B links cellular transcriptome heterogeneity to therapy resistance (inDrop) 2017-10-15 The KDM5B histone H3 lysine 4 (H3K4) demethylase has been implicated in therapy resistance in multiple cancer types including breast cancer, but the underlying mechanism is poorly defined. Here we show that inhibition of KDM5B activity increases sensitivity to anti-estrogens by modulating estrogen-receptor (ER) signaling. Conversely, acquired resistance to KDM5 inhibitors leads to gain of ER chromatin binding and estrogen-independent growth. Sequencing of barcoded cell populations and mathematical modeling demonstrate selection for pre-existent genetically distinct endocrine-resistant cells, while resistance to KDM5 inhibitors is a switch to an acquired epigenetic state. Rare resistant cells can already be detected by single cell RNA-seq prior to treatment. Inhibition of KDM5B in luminal ER+ cells increases H3K4me3 broad domains at promoters and decreases cellular transcriptional heterogeneity. Higher transcriptome heterogeneity is associated with higher KDM5B levels and poor prognosis in ER+ luminal breast tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE104987 KDM5 Histone Demethylase Activity Links Cellular Transcriptomic Heterogeneity to Therapeutic Resistance. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2018.10.014 {Cancer cell (23.916): 10.1016/j.ccell.2018.10.014} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA414337 https://www.ebi.ac.uk/ena/browser/view/PRJNA414337 https://www.ncbi.nlm.nih.gov/sra?term=SRP119973 [Overal design]Single cell transcriptome of parental and multiple resistant breast cancer cell lines; [Treatment]'Cells were treated with inhibitors: fulvestrant (1 μM) or KDM5-C70 (10 μM).'; [Growth]'MCF7 and C70R cells were cultured in DMEM supplemented with 10% FBS, 1% penicillin/streptomycin and 10 μg ml−1 insulin. FULVR cells are cultured in RPMI without phenol red supplemented with 10% charcoal-stripped FBS, 1% penicillin/streptomycin and 10 μg ml−1 insulin. SUM159 cells are cultured in DMEM/F12 supplemented with 5% FBS, 10 mM HEPES, 10 μg ml−1 hydrocortisone, 5 μg ml−1 insulin and 1% penicillin/streptomycin.'; [Extraction]'Single-cell RNA-seq was performed using the inDrop protocol on a custom system as described in [https://www.ncbi.nlm.nih.gov/pubmed/27929523]. Hydrogel beads with version 3 oligonucleotide design were purchased from the Harvard Single Cell Core (https://iccb.med.harvard.edu/single-cell-core). Microfluidic encapsulation chips were purchased from 1CellBio (part no. 10080; https://1cell-bio.com/).\nLibrary preparation was performed as described in [https://www.ncbi.nlm.nih.gov/pubmed/27929523].'; [Cell type]'Source: ''cell lines: MCF7; treatment: MCF70 -none, MCF7.C70 - C70, C70R - none; ', 'cell lines: MCF7; treatment: pMCF7 - none, PMCF7.FUL -Fulvestrant, FULR -none, FULR.C70 - C70, SUM159 - none, SUM159.C70 - C70; ', 'cell line: mixed sample (non-demultiplexed); treatment: mixed sample (non-demultiplexed); ' GSE140276 Mus musculus; Homo sapiens 28 Genome binding/occupancy profiling by high throughput sequencing GPL18573; GPL19057; GPL24676 Universal NicE-seq for high resolution accessible chromatin profiling for native and formaldehyde fixed cells and tissues 2019-11-12 Accessible chromatin plays a central role in gene expression and chromatin architecture. Current accessible chromatin approaches depend on limited digestion/cutting and pasting adaptors at the accessible DNA, thus requiring additional materials and time for optimization. Universal NicE-seq (UniNicE-seq) is an improved accessible chromatin profiling method that negate the optimization step and is suited to a variety of mammalian cells and tissues. Addition of 5-methyldeoxycytidine triphosphate during accessible chromatin labeling and an on-bead library making step substantially improved the signal to noise ratio while protecting the accessible regions from repeated nicking in cell lines, mouse T cells, mouse kidney, and human frozen and FFPE tissue sections. These refinements allowed reliable mapping of accessible chromatin for high resolution genomic feature studies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE140276 Universal NicE-seq for high-resolution accessible chromatin profiling for formaldehyde-fixed and FFPE tissues. Clinical epigenetics 5.496 https://doi.org/10.1186/s13148-020-00921-6 {Clinical epigenetics (5.496): 10.1186/s13148-020-00921-6} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA589075 https://www.ebi.ac.uk/ena/browser/view/PRJNA589075 https://www.ncbi.nlm.nih.gov/sra?term=SRP229617 [Overal design]Open-chromatin profile of various samples from cultured cancer cell lines, mouse tissue and human tissue section using nicking enzyme, NtCviPII based NicE-seq library were generated and sequenced. Depending on the experiments some samples were sequenced once, in duplicate or triplicate.; [Treatment]'None'; [Growth]'HCT116 cell line were routinely grown in DMEM media with 10% fetal bovine serum respectively, media being replaced every 3 days. For human tissue section, we purchased it from US Biomax Inc under the agreement of only research purpose. FFPE slides of the liver sample were also custom ordered from BioChain, USA, with 24-48 hrs formalin fixation'; [Extraction]'After we isolated the nuclei from cultured cell or tissue section, the nuclei was labeling with Nt.CviPII, Biotinylated 5mC-dNTP mixture, decroslinked for O/N at 65 degree, and then genomic DNA was extracted using phenol-chloroform method.\nBiotin-labeled open chromatin DNA was captured by streptavidin bead and the beads were washed with high salt buffer for 4 times, and followed the library preparation procedure using NEBNext Ultra II DNA library Prep Kit (E7370S, New England Biolabs, Inc)', '1 ug of genomic DNA was sheared by the standard sonication conditions of UniNicE-seq, pull downed by streptavidin C1 bead, followed the end-repair reaction, adaptor (methylated ) ligation reaction for O/N or 2 hr\nFinally, EM-seq conversion reaction followed as suggested by EM-seq manufacturer (NEB, E7120). The library DNAs were amplified by 11 PCR cylces.'; [Cell type]'Colorectal cancer cells', 'breast cancer', 'myelogenous leukemia', 'T-cell lymphoma', 'Kidney tissue', 'fresh frozen', 'FFPE liver tissue''tissue: Colon; cell type: Colorectal cancer cells; cell line: HCT116; experimental variables: 5mC, onBead, 2.5U, fixed; ', 'tissue: Colon; cell type: Colorectal cancer cells; cell line: HCT116; experimental variables: C, onBead, 2.5U, fixed; ', 'tissue: Colon; cell type: Colorectal cancer cells; cell line: HCT116; experimental variables: 5mC, offBead, 2.5U, fixed; ', 'tissue: Colon; cell type: Colorectal cancer cells; cell line: HCT116; experimental variables: C, offBead, 2.5U, fixed; ', 'tissue: Colon; cell type: Colorectal cancer cells; cell line: HCT116; experimental variables: 5mC, onBead, 25U, fixed; ', 'tissue: Colon; cell type: Colorectal cancer cells; cell line: HCT116; experimental variables: 5mC, onBead, 50U, fixed; ', 'tissue: Breast; cell type: breast cancer; cell line: MCF7; experimental variables: 5mC, onBead, 2.5U, fixed; ', 'tissue: Breast; cell type: breast cancer; cell line: MCF7; experimental variables: C, onBead, 2.5U, fixed; ', 'tissue: Blood; cell type: myelogenous leukemia; cell line: K562; experimental variables: 5mC, onBead, 2.5U, fixed; ', 'tissue: Blood; cell type: myelogenous leukemia; cell line: K562; experimental variables: C, onBead, 2.5U, fixed; ', 'tissue: Lymphocyte; cell type: T-cell lymphoma; experimental variables: 5mC, onBead, 500 cells, fixed; ', 'tissue: Lymphocyte; cell type: T-cell lymphoma; experimental variables: 5mC, onBead, 5K cells, fixed; ', 'tissue: Lymphocyte; cell type: T-cell lymphoma; experimental variables: 5mC, onBead, 25K cells, fixed; ', 'tissue: Kidney; cell type: Kidney tissue; developmental stage: Adult mouse; experimental variables: 5mC, onBead, 250 cells, nonfixed; ', 'tissue: Kidney; cell type: Kidney tissue; developmental stage: Adult mouse; experimental variables: 5mC, onBead, 500 cells, nonfixed; ', 'tissue: Kidney; cell type: Kidney tissue; developmental stage: Adult mouse; experimental variables: 5mC, onBead, 5K cells, nonfixed; ', 'tissue: Kidney; cell type: Kidney tissue; developmental stage: Adult mouse; experimental variables: 5mC, onBead, 10K cells, nonfixed; ', 'tissue: Kidney; cell type: Kidney tissue; developmental stage: Adult mouse; experimental variables: 5mC, onBead, 25K cells, nonfixed; ', 'tissue: Kidney; cell type: Kidney tissue; developmental stage: Adult mouse; experimental variables: 5mC, onBead, 25K cells, fixed; ', 'tissue: Lung; cell type: fresh frozen; developmental stage: Adult Normal lung; experimental variables: 5mC, onBead,fixed; ', 'tissue: Lung; cell type: fresh frozen; developmental stage: Fetal normal; experimental variables: 5mC, onBead,fixed; ', 'tissue: Liver; cell type: fresh frozen; developmental stage: Adult Normal Liver; experimental variables: 5mC, onBead,fixed; ', 'tissue: Liver; cell type: fresh frozen; developmental stage: Fetal normal; experimental variables: 5mC, onBead,fixed; ', 'tissue: Kidney; cell type: fresh frozen; developmental stage: Adult Normal Kidney; experimental variables: 5mC, onBead,fixed; ', 'tissue: Kidney; cell type: fresh frozen; developmental stage: Fetal normal; experimental variables: 5mC, onBead,fixed; ', 'tissue: Colon; cell type: Colorectal cancer cells; cell line: HCT116; experimental variables: 5mC, EM-seq; ', 'tissue: Adult normal liver; cell type: FFPE liver tissue; tissue type: tissue section; experimental variables: 5mC, onBead,fixed; ' GSE149479 Mus musculus 12 Expression profiling by high throughput sequencing GPL19057 Synergism of chemotherapy and PD-1 immune checkpoint blockade in the PyMT mammary carcinoma mouse model 2020-04-27 We studied the impact of a combination of chemotherapy and PD-1 immune checkpoint blockade on tumor progression in the PyMT mammary carcinoma mouse model compared to each treatment as monotherapy. To gain insight into the reasons underlying improved efficacy of combined chemoimmunotherapy, whole transcriptome profiling of tumors of mice receiving either a control antibody, anti-PD-1 antibody, doxorubicin chemotherapy + a control antibody or doxorubicin chemotherapy + anti-PD-1 antibody was performed via next generation mRNA sequencing, in triplicates, on a NextSeq 550 high-throughput bench top sequencer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE149479 Immune Checkpoint Blockade Improves Chemotherapy in the PyMT Mammary Carcinoma Mouse Model. Frontiers in oncology 4.137 https://doi.org/10.3389/fonc.2020.01771 {Frontiers in oncology (4.137): 10.3389/fonc.2020.01771} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA628738 https://www.ebi.ac.uk/ena/browser/view/PRJNA628738 https://www.ncbi.nlm.nih.gov/sra?term=SRP258780 [Overal design]Tumor mRNA profiles of mice bearing polyoma middle T oncogene (PyMT)-induced tumors were generated after treatment with chemotherapy, PD-1 immunotherapy or both for 5 weeks in triplicates.; [Treatment]'PyMT Mice were divided into four groups according to treatment (anti-PD-1 (TWP), IgG1 (TWI), doxorubicin (DOX) + anti-PD-1 (DWP) and DOX + IgG1 (DWI)). For animals receiving immune checkpoint blockade only, treatment was initiated (day 0) once the first tumor reached a size of 0.6 cm in diameter. Antibodies were administrated i.p. at a concentration of 20 mg/kg (on day 0) and 10 mg/kg (on day 6, 12, 18). All mice received either anti-mouse PD-1 antibody (4H2, Ono Pharmaceutical, Osaka, Japan) or anti-mouse IgG1 (BioXcell/Hölzel Diagnostik, Cologne, Germany) diluted in sterile 0.9% NaCl. In the model with the combination of chemotherapy and immune checkpoint blockade treatment started once the first mammary tumor reached a size of 1 cm in diameter. Doxorubicin (Cell Pharm, Bad-Vilbel, Germany) diluted in sterile 0.9% NaCl was administrated i.p. (5 mg/kg) once a week for five weeks. One day after doxorubicin administration, mice were treated with 10 mg/kg of either anti-mouse PD-1 antibody (4H2, Ono Pharmaceutical) or anti-mouse IgG1 (BioXCell). Mice were monitored three times a week for up to five weeks after initial treatment.'; [Growth]'None'; [Extraction]'Total RNA was isolated from snap frozen PyMT tumors using the peqGOLD Total RNA Kit (VWR International, Darmstadt, Germany). RNA samples were analyzed on a 2100 Bioanalyzer using Agilent RNA 6000 Nano chip (both from Agilent Technologies, Santa Clara, USA).\nLibrary preparation was performed using the SMARTer® Stranded Total RNA Sample Prep Kit –HI (Takara Bio Europe, Saint-Germain-en-Laye, France). Quantity and quality of the cDNA libraries were determined by Qubit™ dsDNA HS Assay Kit (Thermo Fisher Scientific, Dreieich, Germany) and Agilent High Sensitivity DNA chip (Agilent Technologies).'; [Cell type]'Source: ''strain: C57BL/6; tissue: tumor; treatment: IgG1; treatment duration: treatment once-weekly for 5 weeks; ', 'strain: C57BL/6; tissue: tumor; treatment: anti-PD-1; treatment duration: treatment once-weekly for 5 weeks; ', 'strain: C57BL/6; tissue: tumor; treatment: DOX + IgG1; treatment duration: treatment once-weekly for 5 weeks; ', 'strain: C57BL/6; tissue: tumor; treatment: DOX + anti-PD-1; treatment duration: treatment once-weekly for 5 weeks; ' GSE67966 Homo sapiens 12 Expression profiling by array GPL570 Antibody-induced CD47 signaling suppresses triple-negative breast cancer stem cells 2015-04-16 Intercellular communication is critical for integrating complex signals in multicellular eukaryotes. Vascular endothelial cells and T lymphocytes closely interact during the recirculation and trans-endothelial migration of T cells. In addition to direct cell-cell contact, we show that T cell derived extracellular vesicles can interact with endothelial cells and modulate their cellular functions. Thrombospondin-1 and its receptor CD47 are expressed on exosomes/ectosomes derived from T cells, and these extracellular vesicles are internalized and modulate signaling in both T cells and endothelial cells. Extracellular vesicles released from cells expressing or lacking CD47 differentially regulate activation of T cells induced by engaging the T cell receptor. Similarly, T cell-derived extracellular vesicles modulate endothelial cell responses to vascular endothelial growth factor and tube formation in a CD47-dependent manner. Uptake of T cell derived extracellular vesicles by recipient endothelial cells globally alters gene expression in a CD47-dependent manner. CD47 also regulates the mRNA content of extracellular vesicles in a manner consistent with some of the resulting alterations in target endothelial cell gene expression. Therefore, the thrombospondin-1 receptor CD47 directly or indirectly regulates intercellular communication mediated by the transfer of extracellular vesicles between vascular cells. Treatment with B6H12 antibody inhibited co-immunoprecipitation of EGFR with CD47 and inhibited EGF-induced EGFR tyrosine phosphorylation. B6H12 treatment of bCSC also suppressed asymmetric cell division and cell proliferation and up-regulated caspase 3/7 activity. Correspondingly, caspase-7 cleavage in human breast cancers correlated with CD47 expression. Our data shows that B6H12 specifically targets bCSCs but not differentiated cancer cells, and this CD47 signaling is independent of SIRPα. Three replicates of each condition were generated. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE67966 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA281386 https://www.ebi.ac.uk/ena/browser/view/PRJNA281386 None [Overal design]Three replicates of each MDA-231 attached cells (differentiated), MDA-231 in suspension cells (bCSC), MDA-231 in suspension cells (bCSC) treated with Control Antibody and MDA-231 in suspension cells (bCSC) treated with B6H12 Antibody.; [Treatment]'differentiated MDA-MB-231 cells and bCSCs (breast cancer stem cells) in the presence of B6H12 (Abcam, Cambridge, MA), or an isotype-matched control IgG (1ug/ml) for 36 h.'; [Growth]'MDA-MB-231 cells were cultured using complete RPM1 medium up to 90% confluence, gently washed with Ix PBS and by gentle shaking, viable, floating single cells were collected by centrifugation at 1,200 rpm for 5 minutes and plated in the RPMI 1640 growth medium with 2%FBS as described in {Cioce, 2010 #23}{Ponti, 2005 #21}. CD44high and CD24low bCSCs were isolated using flow cytometry sorting {Gupta, 2011 #22}. The sorted bCSCs cells were cultured using Premium Cancer Stem Cell Media from ProMab.'; [Extraction]'Total RNAs from cells was extracted using miRNeasy Mini kit (Qiagen). (cat. no. 217004)'; [Cell type]'Triple Negative breast cancer cell line''cell line: MDA-231; cell type: Triple Negative breast cancer cell line; cell subtype: suspension cells (breast cancer stem cells; bCSC); ', 'cell line: MDA-231; cell type: Triple Negative breast cancer cell line; cell subtype: attached cells (differentiated); ', 'cell line: MDA-231; cell type: Triple Negative breast cancer cell line; cell subtype: suspension cells (breast cancer stem cells; bCSC); incubated with: B6H12 antibdody for 36hrs; ', 'cell line: MDA-231; cell type: Triple Negative breast cancer cell line; cell subtype: suspension cells (breast cancer stem cells; bCSC); incubated with: an isotype-matched control IgG (1ug/ml) for 36 h; ' GSE22135 Homo sapiens 60 Methylation profiling by array GPL9183 DNA methylation epigenotypes in Breast Cancer Molecular Subtypes 2010-06-04 Analysis of luminal A, luminal B, cerbB2+ and basal-like breast cancer subtypes' methylation profiles. The hypothesis tested in the present study was that tumor subtype specific aberrant methylation profiles might be inductors of some transcriptional changes taking place in breast cancer molecular subtypes. Results clearly demonstrate the differences in the methylation profiles of basal-like and HER2-overexpressing tumors and provide compelling evidence to support the utilization of this biomarker for prognostication and therapeutic stratification of patients with breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22135 DNA methylation epigenotypes in breast cancer molecular subtypes. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr2721 {Breast cancer research : BCR (5.676): 10.1186/bcr2721} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA127571 https://www.ebi.ac.uk/ena/browser/view/PRJNA127571 None [Overal design]DNA methylation profiling analysis at 1537 CpG loci was performed in 28 paired breast cancer/adjacent tissues representing the four major breast cancer subtypes, plus four more non-affected tissue of which two were peritumoral, i.e. surrounding the tumor, and two corresponded to the adjacent area, i.e. more than 2 cm away from the tumor.; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA was extracted with Phenol:clorophorm:ismoamylalcohol, followed by clean-up and bisulfite modification with EZ DNA methylation kit (Zymo Research, Orange, CA, USA) following the manufacturer’s protocol'; [Cell type]'Source: ''gender: female; tissue: Breast tissue; tissue/tumor subtype: Basal-like peritumoral; ', 'gender: female; tissue: Breast tissue; tissue/tumor subtype: Basal-like adjacent tissue; ', 'gender: female; tissue: Breast cancer tissue; tissue/tumor subtype: Basal-like tumor; ', 'gender: female; tissue: Breast tissue; tissue/tumor subtype: ERBB2+ adjacent tissue; ', 'gender: female; tissue: Breast cancer tissue; tissue/tumor subtype: ERBB2+ tumor; ', 'gender: female; tissue: Breast tissue; tissue/tumor subtype: Luminal A adjacent tissue; ', 'gender: female; tissue: Breast cancer tissue; tissue/tumor subtype: Luminal A tumor; ', 'gender: female; tissue: Breast tissue; tissue/tumor subtype: Luminal B adjacent tissue; ', 'gender: female; tissue: Breast cancer tissue; tissue/tumor subtype: Luminal B tumor; ' GSE74461 Homo sapiens 18 Expression profiling by high throughput sequencing GPL16288 Next Generation Sequencing Quantitative Analysis of steroid receptor RNA activator (SRA1) Transcriptomes 2015-10-29 The steroid receptor RNA activator gene (SRA1) produces both a functional RNA (SRA) and a protein (SRAP), whose exact roles remain unknown. To identify cellular processes regulated by this unusual bi-faceted system, we characterized the transcriptome of two differenct cell lines upon depletion of these molecules. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74461 The steroid receptor RNA activator protein (SRAP) controls cancer cell migration/motility. FEBS letters 2.675 https://doi.org/10.1016/j.febslet.2015.11.007 {FEBS letters (2.675): 10.1016/j.febslet.2015.11.007} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA300491 https://www.ebi.ac.uk/ena/browser/view/PRJNA300491 https://www.ncbi.nlm.nih.gov/sra?term=SRP065472 [Overal design]Two differenct cell lines including breast cancer MBD-MDA-231 and cervical cancer Hela cells upon SRA1 depletion and SRAP overexpression; [Treatment]'Hela cells were plated at 2.5 x105 cells per well in 6-well plates 24 hours prior to siRNA treatment. Each well was then transfected with either 100 nM control siRNA Non-targeting Control Pool (Dharmacon, cat# D-001810-10); human SRA1 Smartpool (Dharmacon, cat# LQ-027192-00) or individual ON-TARGETplus SRA1 siRNA: Si1, Si2, Si3, Si4 (Dharmacon, cat#J-027192-09-0002, cat#J-027192-10-0002 cat#J-027192-11-0002 cat#J-027192-12-0002) for 72 hours using Dharmafect1 (Dharmacon, cat# T-2001) according to the manufacturer’s instructions.'; [Growth]'cells were routinely maintained in high-glucose (4.5 g/L) DMEM (Gibco, cat# 11965-092) supplemented with 10% FBS (Hyclone, cat# SH30396.03) and 2mM L-glutamine (Gibco, cat# 25030). Cells were grown in a 37oC humidified incubator with 5% CO2.'; [Extraction]'cDNA libraries were prepared from rRNA-depleted total RNA (200–500ng) of Hela cells transfected with the various siRNAs, using the SOLiD™ Total RNA-Seq Kit protocol according to the manufacturer’s instructions (Life Technologies).\ncDNA libraries were prepared from rRNA-depleted total RNA (200–500ng) of Hela cells transfected with the various siRNAs, using the SOLiD™ Total RNA-Seq Kit protocol according to the manufacturer’s instructions (Life Technologies). ted only once. For each gene, the raw read data were normalized and expressed as reads per kilobase per million reads (rpkm). Genes with less than 0.5 rpkm in any one sample were not considered for analysis.\nThe SOLiD paired read sequences were mapped onto human reference genome hg19 using LifeScope software package (Life Technologies) with 2-mismatch setting and the best score mapping when multiple mapping occurs. The sequence quality was inspected by Bamstats module. For a given gene the mapped sequence reads were counted against the current gene annotation General Transfer Format (hg19.gtf). Reads that map to overlapping exons or features of a given gene are counted only once. For each gene, the raw read data were normalized and expressed as reads per kilobase per million reads (rpkm). Genes with less than 0.5 rpkm in any one sample were not considered for analysis.'; [Cell type]'Source: ''cell line: Hela; passages: passage number 55-65; provider: ATCC, cat# ATCC-CCL2; sirna treatment conditions: 2.5 x105 hela cells in 6-well plates 100 nM control siRNA Non-targeting Control Pool (Dharmacon, cat# D-001810-10) for 72 h; ', 'cell line: Hela; passages: passage number 55-65; provider: ATCC, cat# ATCC-CCL2; sirna treatment conditions: 2.5 x105 hela cells in 6-well plates 100 nM human SRA1 Smartpool (Dharmacon, cat# LQ-027192-00)for 72 h; ', 'cell line: MBD-MDA-231; passages: passage number 21-31; provider: ATCC, cat# HTB-26; sirna treatment conditions: 2.5 x105 231 cells in 6-well plates 100 nM control siRNA Non-targeting Control Pool (Dharmacon, cat# D-001810-10) for 72 h; ', 'cell line: MBD-MDA-231; passages: passage number 21-31; provider: ATCC, cat# HTB-26; sirna treatment conditions: 2.5 x105 cells in 6-well plates r 100 nM RNAi for 72 h; ', 'cell line: Hela; passages: passage number 55-65; provider: ATCC, cat# ATCC-CCL2; sirna treatment conditions: 2.5 x105 hela cells in 6-well plates 100 nM human SRA1 Smartpool (Dharmacon, cat# LQ-027192-00) for 72 h; ', 'cell line: Hela; passages: passage number 55-65; provider: ATCC, cat# ATCC-CCL2; sirna treatment conditions: 2.5 x105 hela cells in 6-well plates 100 nM human SRA1 siRNA1 (Dharmacon, cat#J-027192-09-0002 for 72 h; ', 'cell line: Hela; passages: passage number 55-65; provider: ATCC, cat# ATCC-CCL2; sirna treatment conditions: 2.5 x105 hela cells in 6-well plates 100 nM human SRA1 siRNA2 (Dharmacon, cat#J-027192-10-0002 ) for 72 h; ', 'cell line: Hela; passages: passage number 55-65; provider: ATCC, cat# ATCC-CCL2; sirna treatment conditions: 2.5 x105 hela cells in 6-well plates 100 nM human SRA1 siRNA3 (Dharmacon,cat#J-027192-11-0002) for 72 h; ', 'cell line: Hela; passages: passage number 55-65; provider: ATCC, cat# ATCC-CCL2; sirna treatment conditions: 2.5 x105 hela cells in 6-well plates 100 nM human SRA1 siRNA4 (Dharmacon, cat#J-027192-12-0002) for 72 h; ', 'cell line: Hela; passages: passage number 55-65; provider: ATCC, cat# ATCC-CCL2; sirna treatment conditions: Hela cells were transfected with an empty GFP vector in 10 cm dishes for 24 hours using Lipofectamin 2000 followed by sorting; ', 'cell line: Hela; passages: passage number 55-65; provider: ATCC, cat# ATCC-CCL2; sirna treatment conditions: Hela cells were transfected with a GFP-SRAP in 10 cm dishes for 24 hours using Lipofectamin 2000 followed by sorting; ' GSE16554 Homo sapiens 19 Expression profiling by array GPL96 Enhancement of metastasis by spontaneous ploidy doubling of breast cancer cell MDA-MB-231. 2009-06-11 MDA-MB-231 bone-metastatic subline 1833 and lung metastatic subline 4175 underwent spontaneous ploidy doubling in culture, i.e. the genome approximately duplicated itself gradually. The modal- and hyper-ploid subpopulations during the ploidy transition were sorted into two separate sublines, 1833-Modal and 1833-Hyper for 1833, 4175-Modal and 4175-Hyper for 4175. Their expresssion patterns were compared to each other as well as to other MDA-MB-231 sublines isolated previously by Kang et al. 2003 and Minn et al. 2005. Keywords: Cell type comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE16554 Organ-specific enhancement of metastasis by spontaneous ploidy duplication and cell size enlargement. Cell research 17.848 https://doi.org/10.1038/cr.2010.93 {Cell research (17.848): 10.1038/cr.2010.93} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA116183 https://www.ebi.ac.uk/ena/browser/view/PRJNA116183 None [Overal design]19 cell lines were analyzed, including the parental line MDA-MB-231, modal-ploid sublines 1833-Modal and 4175-Modal, hyper-ploid sublines 1833-Hyper and 4175-Hyper, strongly bone-metastatic lines 1833 (the original subline after short culture), 2274, 2268 and 2269, weakly bone-metastatic lines 2293, 2295 and 2297, strongly lung-metastaic lines 4142, 4173, 4175 (the original subline after short culture) and 4180, and weakly lung-metastatic lines SCP6, SCP21 and SCP26. Single sample for each line.; [Treatment]'Cells were grown to sub-confluency before harvesting RNA.'; [Growth]'These sublines and their fusion variants were maintained in DMEM with 10% FBS and antibiotics supplemented with appropriate selective drugs.'; [Extraction]"Total RNA was extracted using Qiagen RNAeasy mini kit following manufacturer's instructions."; [Cell type]'breast cancer''cell type: breast cancer; cell line: MDA-MB-231; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: 1833; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: 4175; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: 2293; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: 2295; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: 2297; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: 2274; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: 2268; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: 2269; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: SCP21; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: SCP6; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: SCP26; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: 4142; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: 4173; ', 'cell type: breast cancer; parental cell line: MDA-MB-231; cell line: 4180; ' GSE26370 Homo sapiens 12 Expression profiling by array GPL571 The gene expression response of MCF7 and MDAMB231 to glutamine deprivation 2010-12-30 There are two major subtype of cells in breast cancer. These cancer cells response differently to glutamine deprivation, here we use one luminal type of breast cancer cell (MCF7) and one basal type of breast cancer cell (MDAMB231) to compare the gene expression differences of these two types of cancer cells in glutamine deprivation. Many cancer cells depend on glutamine for survival and oncogenic transformation. Although targeting glutamine metabolism is proposed as novel therapies, their heterogeneity among different tumors is unknown. Here, we found only basal-type, but not luminal-type breast cancer cells, exhibited phenotypes of glutamine dependency and may benefit from glutamine-targeting therapeutics. The glutamine independence of luminal-type cells is caused by the specific expression of glutamine synthetase (GS), a pattern recapitulated in luminal breast cancers. The co-culture of luminal cells partially rescued the basal cells under glutamine deprivation, suggesting glutamine symbiosis. The luminal-specific expression of GS is directly induced GATA3 and down-regulates glutaminase expression to maintain subtype-specific glutamine metabolism. Collectively, these data indicate the distinct glutamine phenotypes among breast cells and enable the rational design of glutamine targeted therapies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26370 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA136895 https://www.ebi.ac.uk/ena/browser/view/PRJNA136895 None [Overal design]Gene expression analysis in MCF7 and MDAMB231 cultured with or without glutamine for 24h; [Treatment]'DMEM with 10%FBS with 4mM glutamine (Q4) or no glutamine (Q0) for 24 hours'; [Growth]'DMEM with 10%FBS'; [Extraction]'RNAs were extracted with Ambion mirVana kit'; [Cell type]'Source: ''treatment: 4mM glutamine; cell line: MCF7; ', 'treatment: no glutamine; cell line: MCF7; ', 'treatment: 4mM glutamine; cell line: MDAMB231; ', 'treatment: no glutamine; cell line: MDAMB231; ' GSE18331 Homo sapiens 14 Expression profiling by array GPL570 A phenotype-based model for rational selection of novel targeted therapies in treating aggressive breast cancer 2009-09-29 Treating unselected cancer patients with new drugs dilutes proof of efficacy when only a fraction of patients respond to therapy. We conducted a meta-analysis on eight primary breast cancer microarray datasets representing diverse breast cancer phenotypes. We present a high-throughput protocol which incorporates drug sensitivity signatures to guide preclinical testing for effective therapeutic agents. Specifically, we focus on drug classes currently undergoing early phase clinical testing. Our genomic and experimental results suggest that the majority of basal-like breast cancers should respond to inhibitors of the phosphatidylinositol-3-kinase pathway, and that a relatively low toxicity histone deacetylase inhibitor, valproic acid, may target aggressive breast cancers. For a subset of drugs, prediction of sensitivity associates with tumor recurrence, suggesting clinical relevance. Preclinical studies using both cell lines and patient tumors grown in 3-dimensional in vitro and orthotopic in vivo preclinical models provide an efficient and highly relevant assessment of drug sensitivity in tumor phenotypes, and validate our genomic analyses. Together, our results show that high-throughput transcriptional profiling can significantly impact drug selection for breast cancer patients. Pre-identification of patient response may not only improve therapeutic response rates, it can also assist in quickly identifying the optimal inclusion criteria for clinical trials. Our model facilitates personalized drug therapy for cancer patients and may be generalized for study of drug efficacy in other diseases. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE18331 A pharmacogenomic method for individualized prediction of drug sensitivity. Molecular systems biology 9.800 https://doi.org/10.1038/msb.2011.47 {Molecular systems biology (9.800): 10.1038/msb.2011.47} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA117991 https://www.ebi.ac.uk/ena/browser/view/PRJNA117991 None [Overal design]Breast cancer pleural effusion samples from triple negative patients. Compared samples that are computationally predicted to be sensitive to valproic acid and those that are not predicted to be sensitive.; [Treatment]'None'; [Growth]'None'; [Extraction]'Standard affymetrix protocol', 'Standard Affymetrix Protocol'; [Cell type]'Source: ''prediction: sensitive to valproic acid; tissue: Pleural Effusion; ', 'prediction: not sensitive to valproic acid; tissue: Pleural Effusion; ', 'tissue: Pleural Effusion; prediction: resistant to valproic acid; ', 'tissue: Pleural Effusion; prediction: intermediate sensitivity to valproic acid; ', 'tissue: Pleural Effusion; prediction: sensitive to valproic acid; ' GSE102436 Homo sapiens 60 Genome binding/occupancy profiling by high throughput sequencing GPL18460 Epigenetic and Expression Profiling of Tissue Selective Estrogen Compounds in Breast Epithelial Cell Lines (ChIP-seq) 2017-08-09 Current approaches to menopausal hormone therapy consist of compounds which provide tissue specific beneficial effects while working to minimize any increase in cancer risk associated with replacement therapy. In this study, an examination of the genomic distribution of histone modification and expression changes in two breast epithelial cell lines, the normal MCF10A cell line and the MCF-7 breast cancer cell line, upon treatment with several of the current therapies used for treating post-menopausal symptoms is presented. Analysis of the observed changes upon treatment with either 17-estradiol (E2), a combined treatment with the top 10 most abundant Premarin chemical equivalents (EC10), the non-steroidal SERM, Bazadoxifene (BZA) and the TSEC; BZA combined with EC10 (Duavee) or BZA combined with E2 provides evidence of expression changes in genes involved in DNA replication, nucleosome assembly, RNA-splicing and processing, biological regulation and cell signaling, and many of the known steroid response genes. There were distinct global changes in chromatin states observed that were specific to each of the breast epithelial cell type normal, basal MCF10A and ESR/PGR positive luminal breast cancer MCF7 cell lines and selective changes observed upon treatment with each of the treatment groups. Specifically, we observed a global loss of H3K4ac upon treatment with BZA. These changes were observed in both ESR1 bound and non-bound regions suggesting modifications in both promoters and enhancer regions. The levels of H3K4ac upon treatment of BZA showed a decrease below basal non-treated H3K4ac levels in MCF7. There was an increase observed with E2 and EC10 treatment in MCF7 that was mitigated by the addition of BZA to either steroid as a combined treatment. This study provides a better understanding of the role of epigenetic modifications in endocrine responsiveness and provides evidence of an improved therapeutic profile for combined TSEC compounds for treating and managing the overall physiological effects of declining estrogen. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE102436 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA397786 https://www.ebi.ac.uk/ena/browser/view/PRJNA397786 https://www.ncbi.nlm.nih.gov/sra?term=SRP115147 [Overal design]6 drug treatments in 2 cell lines with 2 biological replicates; [Treatment]'Prior to treatment cells were plated in serum containing media for 24hrs to establish a monolayer. Media was removed and replaced with 2% charcoal-stripped serum for 48hrs prior to 24hr treatment with each pharmaceutical agent. Cells were harvested for ChIP-seq analysis 24\u200ahrs post-treatment as previously described (Messier, et al. Oncotarget 2016).'; [Growth]'MCF10A cells were grown in DMEM: F12 (Hyclone-SH30272 without phenol red), 5% (v/v) horse serum (Gibco #16050 lot #1075876) + 10ug/ml human insulin (Sigma I-1882)+ 20ng/ml recombinant hEGF (Peprotech AF-100-15) + 100ng/ml Cholera toxin (Sigma C-8052) + 0.5 ug/ml Hydrocortisone (Sigma H-0888) Pen/Strep (Life Technologies) and Glutamine (Life Technologies). MCF7 were grown in DMEM: F12 (Hyclone-SH30272 without phenol red) + 10% (v/v) FBS (Atlanta Biologicals). ) Prior to treatment cells were plated in serum containing media for 24hrs to establish a monolayer. Media was removed and replaced with 2% charcoal-stripped serum for 48hrs prior to 24hr treatment with each pharmaceutical agent. Cells were harvested for ChIP-seq analysis 24\u200ahrs post-treatment as previously described (Messier, et al. Oncotarget 2016).'; [Extraction]'Nuclei extraction was performed using a protocol modified from Dignam et al (Dignam, et al. Nucleic Acids Res 1983). Isolated nuclei were sonicated using a Covaris S-220 Ultrasonic Processor to obtain sheared chromatin with an average peak size of 500 bp. A total of 20 \uf06dg of sheared chromatin was used for ChIP immunoprecipitation with either 6.5 ug of anti-H3K4me3 anti-H3K27ac, or anti-H3K4ac (Abcam, ab1012 lot#GR80367-1) or 8 ug of anti-H3K27me3 (Millipore -07-449 lot#1764447 or 2475696 ) used at a ratio of 3:1 or 2.5:1 chromatin to antibody, respectively. Immunoprecipitated complexes were purified using Protein-G Dynabeads (Life Technologies 10004D lot#123085320). DNA fragments were isolated by uncross-linking the protein-DNA complex overnight at 65°C. The eluted ChIP-DNA were treated with RNase A (0.2mg/ml final concentration-Life Technologies Cat # AM2269), proteinase K treatment (Life Technologies cat # AM2548) and then phenol extracted, precipitated with ethanol, then resuspended in 10mM Tris. DNA was quantified using a Qubit fluorimeter (Life Technologies) prior to the library preparation.\nSequencing libraries were prepared using the TruSeq ChIP sample preparation kit (Illumina cat#9235121 lot #15027084) following instructions provided by the manufacturer. Libraries were then size selected, purified and quantified prior to sequencing by automated DNA sequencing performed in the University of Vermont Cancer Center Advanced Genome Technologies Core (Messier, et al. Oncotarget 2016) .'; [Cell type]'mammary gland/breast epithelial cell''cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: bza; antibody: H3K27AC; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: bza; antibody: H3K27ME3; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: bza; antibody: H3K4AC; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: bza; antibody: H3K4ME3; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: bza; antibody: none; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: control; antibody: H3K27AC; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: control; antibody: H3K27ME3; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: control; antibody: H3K4AC; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: control; antibody: H3K4ME3; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: control; antibody: none; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: e2; antibody: H3K27AC; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: e2; antibody: H3K27ME3; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: e2; antibody: H3K4AC; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: e2; antibody: H3K4ME3; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: e2; antibody: none; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: e2bza; antibody: H3K27AC; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: e2bza; antibody: H3K27ME3; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: e2bza; antibody: H3K4AC; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: e2bza; antibody: H3K4ME3; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: e2bza; antibody: none; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: gc10; antibody: H3K27AC; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: gc10; antibody: H3K27ME3; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: gc10; antibody: H3K4AC; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: gc10; antibody: H3K4ME3; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: gc10; antibody: none; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: gc10bza; antibody: H3K27AC; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: gc10bza; antibody: H3K27ME3; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: gc10bza; antibody: H3K4AC; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: gc10bza; antibody: H3K4ME3; ', 'cell line: MCF10A; cell type: mammary gland/breast epithelial cell; neoplasia type: luminal ductal cells; atcc id: fibrocystic disease;ATCC CRL-10317; treatment: gc10bza; antibody: none; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: bza; antibody: H3K27AC; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: bza; antibody: H3K27ME3; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: bza; antibody: H3K4AC; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: bza; antibody: H3K4ME3; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: bza; antibody: none; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: control; antibody: H3K27AC; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: control; antibody: H3K27ME3; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: control; antibody: H3K4AC; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: control; antibody: H3K4ME3; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: control; antibody: none; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: e2; antibody: H3K27AC; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: e2; antibody: H3K27ME3; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: e2; antibody: H3K4AC; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: e2; antibody: H3K4ME3; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: e2; antibody: none; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: e2bza; antibody: H3K27AC; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: e2bza; antibody: H3K27ME3; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: e2bza; antibody: H3K4AC; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: e2bza; antibody: H3K4ME3; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: e2bza; antibody: none; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: gc10; antibody: H3K27AC; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: gc10; antibody: H3K27ME3; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: gc10; antibody: H3K4AC; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: gc10; antibody: H3K4ME3; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: gc10; antibody: none; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: gc10bza; antibody: H3K27AC; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: gc10bza; antibody: H3K27ME3; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: gc10bza; antibody: H3K4AC; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: gc10bza; antibody: H3K4ME3; ', 'cell line: MCF7; cell type: mammary gland/breast epithelial cell; neoplasia type: metastatic site derived; atcc id: adenocarcinoma; ATCC HTB-22; treatment: gc10bza; antibody: none; ' GSE24506 Homo sapiens 2 Expression profiling by array GPL96 Expression of microRNAs and their gene targets are dysregulated in pre-invasive breast cancer (mRNA) 2010-10-04 Introduction: microRNAs (miRNAs) are short non-coding RNAs that negatively regulate gene expression and may play a causal role in invasive breast cancer. Since many genetic aberrations of invasive disease are detectable in earlier stages, we hypothesized that miRNA expression dysregulation and the predicted changes in gene expression would also be found in early breast neoplasias. Methods: Expression profiling of 365 miRNAs by RT-qPCR was combined with laser-capture microdissection to obtain an epithelial specific miRNA expression signature of normal breast epithelium (n=9) and of paired samples of histologically normal epithelium (HN) and ductal carcinoma in situ (DCIS) (n=16). To determine how miRNAs may control the expression of co-dysregulated mRNAs we also performed gene expression microarray analysis in the same paired HN and DCIS samples and integrated this with miRNA-target prediction. We further validated several target pairs by modulating the expression levels of miRNAs in MCF7 cells and measured the expression of target mRNAs and proteins. Results: Thirty-five miRNAs were aberrantly expressed between RM, HN and DCIS. Twenty-nine miRNAs and 420 mRNAs were aberrantly expressed between HN and DCIS. Combining these two datasets with miRNA-target prediction we identified two established target pairs (miR-195:CCND1 and miR-21:NFIB) and tested several novel miRNA:mRNA target pairs. Over-expression of the putative tumor-suppressor miR-125b, under-expressed in DCIS, repressed the expression of MEMO1, which is required for ErbB2-driven cell motility (also a target of miR-125b); and NRIP1/RIP140, which modulates the transcriptional activity of the estrogen receptor. Knockdown of the putative oncogenic miRNAs miR-182 and miR-183, both highly over-expressed in DCIS, increased the expression of CBX7 (which regulates E-cadherin expression), DOK4, NMT2, and EGR1. Augmentation of CBX7 by knockdown of miR-182 expression, in turn, positively regulated the expression of E-cadherin, a key protein involved in maintaining normal epithelial cell morphology which is commonly lost during neoplastic progression. Conclusions: These data provide the first miRNA expression profile of normal breast epithelium and of pre-invasive breast carcinoma. Further, we demonstrate that altered miRNA expression can modulate gene expression changes that characterize these early cancers. We conclude that miRNA dysregulation likely plays a substantial role in early breast cancer development. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24506 Expression of microRNA and their gene targets are dysregulated in preinvasive breast cancer. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr2839 {Breast cancer research : BCR (5.676): 10.1186/bcr2839} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA133519 https://www.ebi.ac.uk/ena/browser/view/PRJNA133519 None [Overal design]Two total samples were analyzed via Affymetrix U133A. Case numbers correspond to individual patients. Each sample is identified by case number, histologic lesion and corresponding microarray ID.; [Treatment]'Primary patient breast tissue was snap-frozen in liquid nitrogen, embedded in optimal cutting temperature compound and stored at -80C'; [Growth]'None'; [Extraction]"On average, ~50 10 um-thick cryostat sections were prepared for the extraction of total RNA by laser-capture microdissection from normal or DCIS epithelial regions, which were identified by a surgical pathologist (AdlM) using every 7th section stained by Hematoxylin and Eosin. Total RNA was extracted from the captured epithelium using the Picopure RNA Isolation Kit (Arcturus Engineering) according to manufacturer's protocol with additional DNAse treatment step."; [Cell type]'Source: ''sample type: laser capture microdissected human breast; tissue: ductal carcinoma in situ epithelium; gender: female; age: 43 y; ', 'sample type: laser capture microdissected human breast; tissue: ductal carcinoma in situ epithelium; gender: female; age: 54 y; ' GSE131984 Homo sapiens 8 Expression profiling by high throughput sequencing GPL18573 Acquired resistance to combined BET and CDK4/6 inhibition in triple-negative breast cancer [scRNA-Seq] 2019-05-30 BET inhibitors are promising therapeutic agents for the treatment of triple-negative breast cancer (TNBC), but the rapid emergence of resistance necessitates investigation of combination therapies and their effects on tumor evolution. Here, we show that palbociclib, a CDK4/6 inhibitor, and paclitaxel, a microtubule inhibitor, synergize with the BET inhibitor JQ1 in TNBC lines. High-complexity DNA barcoding and mathematical modeling indicate a high rate of de novo acquired resistance to these drugs relative to pre-existing resistance. We demonstrate that the combination of JQ1 and palbociclib induces cell division errors, which can increase the chance of developing aneuploidy. Characterizing acquired resistance to combination treatment at single cell level shows heterogeneous mechanisms including activation of G1-S and senescence pathways. Our results establish a rationale for further investigation of combined BET and CDK4/6 inhibition in TNBC and suggest novel mechanisms of action for these drugs, and new vulnerabilities in cells after emergence of resistance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131984 Acquired resistance to combined BET and CDK4/6 inhibition in triple-negative breast cancer. Nature communications 11.878 https://doi.org/10.1038/s41467-020-16170-3 {Nature communications (11.878): 10.1038/s41467-020-16170-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA545508 https://www.ebi.ac.uk/ena/browser/view/PRJNA545508 https://www.ncbi.nlm.nih.gov/sra?term=SRP199907 [Overal design]RNA-seq of SUM159 breast cancer cell line treated in vitro with JQ1, palbociclib, paclitaxel, and combinations; [Treatment]'Cells were grown in vitro in the presence of DMSO, JQ1 (100 nM), paclitaxel (0.6 nM), palbociclib (160 nM), JQ1+paclitaxel, or JQ1+palbociclib, in triplicates, for up to 18 passages.'; [Growth]'Cells were lentivirally infected with the ClonTracer barcode library (Bhang et al., 2015). Barcoded cells were passaged in vitro in the presence of drug.'; [Extraction]'Equal numbers of cells from triplicates were combined, washed twice in PBS with 0.04% RNase-free BSA, diluted to 700 cells/µL, and filtered through a 35 µm nylon mesh prior to library preparation.\nLibraries were prepared using the Chromium Single Cell 3’ Library & Gel Bead Kit v2 and Single Cell A Chip (10X Genomics).'; [Cell type]'Source: ''cell line: SUM159; treatment: pre-treatment; index: SI-GA-E1; ', 'cell line: SUM159; treatment: DMSO; index: SI-GA-E2; ', 'cell line: SUM159; treatment: paclitaxel; index: SI-GA-E3; ', 'cell line: SUM159; treatment: JQ1; index: SI-GA-E4; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; index: SI-GA-E5; ', 'cell line: SUM159; treatment: palbociclib; index: SI-GA-E6; ', 'cell line: SUM159; treatment: JQ1; index: SI-GA-E7; ', 'cell line: SUM159; treatment: JQ1+palbociclib; index: SI-GA-E8; ' GSE98691 Homo sapiens 8 Expression profiling by array GPL10558 cIAP1 regulates the EGFR/Snai2 axis in triple negative breast cancer cells 2017-05-09 Inhibitor of apoptosis (IAP) proteins constitute a conserved family of molecules which regulate both apoptosis and receptor signaling. They are often deregulated in cancer cells and represent potential targets for therapy. In our work, we investigated the effect of IAP inhibition in vivo to identify novel downstream genes expressed in an IAP-dependent manner that could contribute to cancer aggressiveness. To this end, immunocompromised mice engrafted subcutaneously with the triple negative breast cancer MDA-MB231 cell line were treated with SM83, a pan-IAP inhibitor developed by us, and tumor nodules were profiled for gene expression. Our work suggests that IAP-targeted therapy could contribute to EGFR inhibition and the reduction of its downstream mediators. This approach could be particularly effective in cells characterized by high levels of EGFR and Snai2, such as triple negative breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98691 cIAP1 regulates the EGFR/Snai2 axis in triple-negative breast cancer cells. Cell death and differentiation 8.086 https://doi.org/10.1038/s41418-018-0100-0 {Cell death and differentiation (8.086): 10.1038/s41418-018-0100-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA385920 https://www.ebi.ac.uk/ena/browser/view/PRJNA385920 None [Overal design]Experiments were approved by the Ethics Committee for Animal Experimentation of the Istituto Nazionale Tumori (INT) of Milan according to institutional guidelines and by the Italian Minister of Health. NOD/SCID mice were subcutaneously engrafted with 5x10^6 MDA-MB231 and MDA-MB468 cells and, after two weeks, were treated with 5 mg/Kg SM83 injected intraperitoneally 5 times/week for 2 weeks (MDA-MB231 model).; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with QIAGEN FFPE RNeasy mini kit in accordance with the prescribed protocol provided with the kit.'; [Cell type]'Source: ''sample_id: 1622; treatment: SM; tissue: tumor nodule; ', 'sample_id: 1623; treatment: un; tissue: tumor nodule; ', 'sample_id: 1624; treatment: un; tissue: tumor nodule; ', 'sample_id: 1625; treatment: un; tissue: tumor nodule; ', 'sample_id: 1626; treatment: SM; tissue: tumor nodule; ', 'sample_id: 1627; treatment: SM; tissue: tumor nodule; ', 'sample_id: 1629; treatment: SM; tissue: tumor nodule; ', 'sample_id: 1631; treatment: un; tissue: tumor nodule; ' GSE162347 Mus musculus 17 Genome variation profiling by high throughput sequencing GPL17021 Reproductive history determines ErbB2 locus amplification, WNT signalling and tumor phenotype in a murine breast cancer model [exome sequencing] 2020-11-30 Understanding the mechanisms underlying tumor heterogeneity is key to development of treatments that can target specific tumor subtypes. We have previously targeted CRE recombinase-dependent conditional deletion of the tumor suppressor genes Brca1, Brca2, p53 and/or Pten to basal or luminal ER- cells of the mouse mammary epithelium. We demonstrated that both the cell-of-origin and the tumor-initiating genetic lesions co-operate to influence mammary tumor phenotype. Here, we use a CRE-activated HER2 orthologue to specifically target HER2/ERBB2 oncogenic activity to basal or luminal ER- mammary epithelial cells and carry out a detailed analysis of the tumors which develop. We find that in contrast to our previous studies, basal epithelial cells are refractory to transformation by the activated NeuKI allele, with mammary epithelial tumor formation largely confined to luminal ER- cells. Histologically, the majority of tumors that developed were classified as either adenocarcinomas of no special type or metaplastic adenosquamous tumors. Remarkably, the former were more strongly associated with virgin animals and were typically characterised by amplification of the NeuNT/ErbB2 locus and activation of non-canonical WNT signalling. In contrast, tumors characterised by squamous metaplasia were associated with animals that had been through at least one pregnancy and typically had lower levels of NeuNT/ErbB2 locus amplification but had activated canonical WNT signalling. Squamous changes in these tumors were associated with activation of the Epidermal Differentiation Cluster. Thus, in this model of HER2 breast cancer, cell-of-origin, reproductive history, NeuNT/ErbB2 locus amplification, and the activation of specific branches of the WNT signalling pathway all interact to drive inter-tumor heterogeneity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE162347 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA681573 https://www.ebi.ac.uk/ena/browser/view/PRJNA681573 https://www.ncbi.nlm.nih.gov/sra?term=SRP295151 [Overal design]Mice carrying an engineered active orthologue of the HER2/ERBB2 gene knocked into the endogenous locus but with expression blocked by a FLOX-STOP-FLOX cassette were crossed with mice carrying the Beta-lactoglobulin promoter-driven CRE recombinase transgene, which targets CRE expression to the luminal cells of the mammary gland. Some mice were put through one or more rounds of pregnancy. Ten tumors which developed in the mammary glands of ten mice were snap frozen and processed for gene expression analysis by exome sequencing together with matched spleens. One sample failed QC. Exome sequencing was used to assess point mutations in tumors and also genomic copy number variations.; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA harvested from snap frozen tumor material and matched spleen from a euthanised genetically modified mouse.\nGenomic DNA was extracted from snap-frozen tumor material using the Gentra Puregene Tissue Kit (QIAGEN).\nGenomic DNA (200-600ng) was fragmented to 200bp using a Covaris E Series and the resultant libraries were subjected to DNA Capture using SureSelect XT Mouse All Exon kit (Agilent, Stockport, Cheshire) following manufacturer’s instructions. Final libraries were quantified using qPCR and clustered at a molarity of 14.5 pM, sequencing was performed on an Illumina HiSeq 2500 using 2x76 cycles of version 3 SBS chemistry.'; [Cell type]'Source: ''tissue: Mammary tumor; reproductive history: Virgin; tumor diagnosis: Adenocarcinoma (No Special Type); amplification status of erbb2/neu locus: High Amplification; ', 'tissue: Mammary tumor; reproductive history: Parous; tumor diagnosis: Adenocarcinoma (No Special Type); amplification status of erbb2/neu locus: High Amplification; ', 'tissue: Mammary tumor; reproductive history: Parous; tumor diagnosis: Mammary Sarcoma; amplification status of erbb2/neu locus: Non / low amplification; ', 'tissue: Mammary tumor; reproductive history: Parous; tumor diagnosis: Metaplastic Adenosquamous Carcinoma; amplification status of erbb2/neu locus: Non / low amplification; ', 'tissue: Mammary tumor; reproductive history: Parous; tumor diagnosis: Adenocarcinoma (No Special Type); amplification status of erbb2/neu locus: Non / low amplification; ', 'tissue: Spleen; reproductive history: Virgin; tumor diagnosis: N/A; amplification status of erbb2/neu locus: N/A; ', 'tissue: Spleen; reproductive history: Parous; tumor diagnosis: N/A; amplification status of erbb2/neu locus: N/A; ' GSE117439 Homo sapiens 52 Methylation profiling by genome tiling array GPL13534 DNA Methylation in Breast Cancers: Differences based on Estrogen Receptor Status and Recurrence 2018-07-20 DNA methylation plays a role in the etiology of primary breast cancers. We analyzed paired primary and second breast tumors to elucidate the role of methylation in recurrence. Methylation profiles from paired primary and second breast tumors of 23 women were assessed using the HumanMethylation450 BeadChip. Twelve women had ERpos primary and second tumors, five had estrogen receptor negative (ERneg) primary and second tumors, and six had an ERpos primary tumor but an ERneg second tumor. Stratifying tumors by occurrence revealed that the greater methylation previously associated with ERpos tumors, is more pronounced in primary tumors than in second tumors. Further, ERneg second tumors are more methylated than ERpos second tumors among women who had ERpos primary tumors. Pathway analyses using gene lists generated from comparisons of methylation in ERpos primary tumors from the paired sets with ERpos tumors from 6 women without recurrences, identified differences between groups based on the ER status of the second tumor. Hypermethylated genes of significantly enriched pathways were differentially associated with survival. DNA methylation profiles of ERpos primary breast tumors support the development and use of tumor methylation profiles for stratifying women with breast cancer both for prognosis and therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE117439 DNA methylation in breast cancers: Differences based on estrogen receptor status and recurrence. Journal of cellular biochemistry 3.448 https://doi.org/10.1002/jcb.27431 {Journal of cellular biochemistry (3.448): 10.1002/jcb.27431} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA482117 https://www.ebi.ac.uk/ena/browser/view/PRJNA482117 None [Overal design]Primary tumors (referred to as first tumors) were matched to a second tumor from the same woman in either the ipsilateral or contralateral breast. HumanMethylation450 Bead Chip (HM450 BC) data were obtained for 46 paired tumors and assigned group labels for ease of reading as follows: 12 tumor pairs from women with ERpos first (A1) and ERpos second tumors (A2), 5 tumor pairs from women with ERneg first tumors (B1) and ERneg second tumors (B2), and 6 tumor pairs from women with ERpos first tumors (C1) and ERneg second tumors (C2). Additionally, 6 ERpos tumors from women with no breast cancer recurrence after a 7-year follow up period were included for methylation analysis.; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA was purified from tumor tissue obtained from 10 μm sections of FFPE blocks. Briefly, a pathologist measured and outlined the breast tumor on an H&E stained slide to estimate the number of sections needed to purify a minimum of 500 ng of DNA. For samples exceeding 4 mm x 4 mm, a single section was sufficient. Tumor cells were collected from the sections by placing an unstained slide on top of the H&E stained slide and carefully removing cells within the parameters defined by H&E slide. Cells collected from multiple sections were combined in a single tube and DNA was purified using the BiOstic FFPE tissue DNA isolation kit (Mo Bio, Carlsbad, CA).'; [Cell type]'Source: ''Sex: female; tissue: breast tumor; disease state: cancer; estrogen receptor status: positive; tumor status: primary; ', 'Sex: female; tissue: breast tumor; disease state: cancer; estrogen receptor status: positive; tumor status: second; ', 'Sex: female; tissue: breast tumor; disease state: cancer; estrogen receptor status: negative; tumor status: primary; ', 'Sex: female; tissue: breast tumor; disease state: cancer; estrogen receptor status: negative; tumor status: second; ', 'group: no breast cancer recurrence after a 7-year follow up period; Sex: female; tissue: breast tumor; disease state: cancer; estrogen receptor status: positive; tumor status: primary; ', 'Sex: female; group: no breast cancer recurrence after a 7-year follow up period; tissue: breast tumor; disease state: cancer; estrogen receptor status: positive; tumor status: primary; ', 'group: no breast cancer recurrence after a 7-year follow up period; Sex: female; group: no breast cancer recurrence after a 7-year follow up period; tissue: breast tumor; disease state: cancer; estrogen receptor status: positive; tumor status: primary; ' GSE14244 Homo sapiens 26 Expression profiling by array GPL96 Hybrids assimilate organ-specific metastasis gene signatures from both parental cells 2008-12-30 Spontaneous cell fusion of MDA-MB-231 bone-metastatic subline Bm (i.e., SCP2) and lung metastatic subline Lm (i.e., LM2) gave rise to hybrid lines BLm-FACS or BLm-DRUG, as well as its single clones (#8, #12, #18). The hybrids acquired the metastasis tropisms from both parental cells. Expression profiles of the parental cells, the hybrids and several previously characterized MDA-MB-231 metastatic derivatives were compared. Hierarchical clustering showed the hybrids assimilated the organ-specific metastasis gene signatures from both parental cells. Keywords: Cell type comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE14244 Efficient acquisition of dual metastasis organotropism to bone and lung through stable spontaneous fusion between MDA-MB-231 variants. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.0900108106 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.0900108106} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA111169 https://www.ebi.ac.uk/ena/browser/view/PRJNA111169 None [Overal design]Twenty-six cell lines were analyzed, including the parental line MDA-MB-231; cell fusion partner lines Bm and Lm; self-fused lines BBm and LLm; hetero-fused lines BLm-FACS, BLM-DRUG and clones BLm-DRUG-8, -12 and -18; strongly bone-metastatic lines 1833, SCP14, SCP20, SCP25 and SCP46; strongly lung-metastatic lines 3481, 4142, 4173, 4175 and 4180; and weakly metastatic lines SCP3, SCP4, SCP6, SCP28, SCP32 and SCP43. Single sample for each line.; [Treatment]'Cells were grown to sub-confluency before harvesting RNA.'; [Growth]'The sublines and their fusion variants were maintained in DMEM with 10% FBS and antibiotics supplemented with appropriate selective drugs.'; [Extraction]"Total RNA extracted using Qiagen RNAeasy mini kit following manufacturer's instructions."; [Cell type]'Source: ''Tissue: breast cancer; ' GSE150306 Homo sapiens 6 Expression profiling by high throughput sequencing GPL18573 CDYL2 epigenetically regulates MIR124 to control NF-kB/STAT3-dependent breast cancer cell plasticity [RNA-seq] 2020-05-11 Epigenetic deregulation of gene transcription is central to cancer cell plasticity and malignant progression, but remains poorly understood. We found that the uncharacterized epigenetic factor Chromodomain on Y-like 2 (CDYL2) is commonly over-expressed in breast cancer, and that high CDYL2 levels correlate with poor prognosis. Supporting a functional role for CDYL2 in malignancy, it positively regulated breast cancer cell migration, invasion, stem-like phenotypes, and epithelial-to-mesenchymal transition (EMT). CDYL2 regulation of these plasticity-associated processes depended on signaling via p65/NF-kB and STAT3. This, in turn, was downstream of CDYL2 regulation of MIR124 gene transcription. CDYL2 co-immunoprecipitated with G9a/EHMT2 and GLP/EHMT1, and regulated the chromatin enrichment of G9a and EZH2 at MIR124 genes. We propose that CDYL2 contributes to poor prognosis in breast cancer by recruiting G9a and EZH2 to epigenetically repress MIR124 genes, thereby promoting NF-kB and STAT3 signaling, as well as downstream cancer cell plasticity and malignant progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE150306 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA631744 https://www.ebi.ac.uk/ena/browser/view/PRJNA631744 https://www.ncbi.nlm.nih.gov/sra?term=SRP261131 [Overal design]RNA was extracted from MCF7 cells stably transduced with a CDYL2 expression plasmid (MCF7-CDYL2), or the empty vector (MCF7-Vector), and differentially expressed genes identified.; [Treatment]'CDYL2 cDNA was cloned by PCR from an MCF7 cDNA library and inserted into the Gateway pENTR-D-TOPO vector (Invitrogen, K240020). Sequencing on both strands confirmed that the cDNA corresponded to a published CDYL2 sequence (Genbank, NM_152342.2). The cloned cDNA was then transferred into MSCV plasmid (Addgene # 41033) using LR Clonase (Invitrogen, 11791100), and the resulting expression construct validated by sequencing. MCF7 cells were then stably transduced with MSCV (Vector) or MSCV-CDYL2 retroviruses and selected for 14 days using 2 µg/mL puromycin (Sigma, P8833). Expression was confirmed by western blotting and immunofluorescence using CDYL2 antibody.'; [Growth]'MCF7 cells (ATCC, HTB-22) and their derivatives were grown in DMEM Low Glucose (Gibco, 31885-023) supplemented with 10 % of FBS (Gibco, 10270-106), 40 µg/mL of gentamicin (Gibco, 15710-049) and 0.6 µg/mL of insulin (NovoRapid, 3525909). Cells were grown at 37°C and 5% CO2\xa0in a humidified incubator and passaged every 2 – 4 days by trypsinization. Sustained expression of ER-alpha in MCF7 was validated regularly by western blotting and immunofluorescence. Cells were regularly tested for mycoplasma using a commercial kit (ATCC, 30-1012K), and cultures renewed from low passage stocks every two months or less.'; [Extraction]'RNA was extracted from sub-confluent cells using TRI-reagent (Sigma, T9424).\nRNA libraries were prepared with the TruSeq Stranded Total-RNA kit (Illumina).'; [Cell type]'Source: ''tissue: Breast cancer; transduction: MSCV; ', 'tissue: Breast cancer; transduction: CDYL2; ' GSE124447 Homo sapiens 14 Expression profiling by high throughput sequencing GPL21290 A hypermethylation strategy utilized by enhancer-bound CARM1 to promote estrogen receptor a-dependent transcriptional activation and breast carcinogenesis (RNA-seq) 2018-12-27 While protein arginine methyltransferases (PRMTs) and PRMT-catalyzed protein methylation have been well-known to be involved in a myriad of biological processes, their roles in carcinogenesis, particularly in estrogen receptor alpha (ERa)-positive breast cancers, remain incompletely understood. Here we focused on investigating PRMT4 (also called coactivator associated arginine methyltransferase 1, CARM1) due to its high expression and the associated poor prognosis in ERa-positive breast cancers. We first uncovered the chromatin-binding landscape and transcriptional targets of CARM1 in the presence of estrogen in ERa-positive breast cancer cells employing genomic and transcriptomics approaches. CARM1 was found to be predominantly and specifically recruited to ERa-bound active enhancers and essential for the transcriptional activation of cognate estrogen-induced gene transcriptional activation in response to estrogen. Global mapping of CARM1 substrates revealed that CARM1 methylates a large cohort of proteins with diverse biological functions, including regulation of intracellular estrogen receptor signaling, chromatin organization, chromatin remodeling and others. Intriguingly, a number of proteins were hypermethylated exclusively by CARM1 on a cluster of arginine residues. Exemplified by MED12, hypermethylation of these proteins by CARM1 served as a molecular beacon for recruiting coactivator protein, tudor domain-containing 3 (TDRD3), to ensure the full activation of estrogen/ERa target genes. In consistent with its critical role in estrogen-induced gene transcriptional activation, CARM1 was found to promote cell proliferation of ERa-positive breast cancer cells in vitro and tumor growth in mice. Taken together, our study uncovered a “hypermethylation” strategy utilized by CARM1 in gene transcriptional regulation, and suggested that CARM1 can server as a therapeutic target for breast cancer treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124447 A hypermethylation strategy utilized by enhancer-bound CARM1 to promote estrogen receptor α-dependent transcriptional activation and breast carcinogenesis. Theranostics 8.063 https://doi.org/10.7150/thno.39241 {Theranostics (8.063): 10.7150/thno.39241} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA512031 https://www.ebi.ac.uk/ena/browser/view/PRJNA512031 https://www.ncbi.nlm.nih.gov/sra?term=SRP174618 [Overal design]RNA-seq performed in this study was designed to understand the molecular mechanisms underlying CARM1 regulation of breast cancer; [Treatment]'MCF7 cells were maintained in stripping medium (phenol red free) for three days before treating with or without estrogen (E2, 10-7 M) for 6h.'; [Growth]'MCF7 cells were cultured in DMEM medium supplemented with 10% FBS.'; [Extraction]'Total RNA was isolated using RNeasy Mini Kit (Qiagen) following the manufacturer’s protocol. DNase I in column digestion was included to ensure the RNA quality.\nTotal RNA was isolated using RNeasy Mini Kit (Qiagen) following the manufacturer’s protocol. DNase I in column digestion was included to ensure the RNA quality. RNA library preparation was performed by using NEBNext® Ultra™ Directional RNA Library Prep Kit for Illumina (E7420L). Paired-end sequencing was performed with Illumina HiSeq platform at RiboBio Co., Ltd. or Amogene Biotech Co., Ltd.'; [Cell type]'Source: ''cell line: MCF7; treatment: ethanol+siCTL; ', 'cell line: MCF7; treatment: estrogen+siCTL; ', 'cell line: MCF7; treatment: ethanol+siRNA; ', 'cell line: MCF7; treatment: estrogen+siRNA; ' GSE108984 Homo sapiens 74 Genome variation profiling by genome tiling array GPL9077 Clonality analysis in breast tumour pairs using aCGH data 2018-01-10 Multiple tumours from the same patient were analysed for copy number alterations to assess tumour clonality. Seventy-four tumours corresponding to 37 patients were stratified into four groups based on the anatomic location of the multiple breast cancers (ipsilateral or bilateral) and time interval between the diagnoses (synchronous or metachronous). Ipsilateral was defined as tumours occurring in the same breast while bilateral was defined as the occurrence of tumours in both breasts. Metachronicity was defined as a time interval greater than six months between the diagnoses of the first and second tumours, while synchronicity specified that the two tumours occurred concurrently (BM: bilateral-metachronous; BS: bilateral-synchronous; IM: ipsilateral-metachronous; IS: ipsilateral-synchronous). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE108984 Clonal relatedness in tumour pairs of breast cancer patients. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-018-1022-y {Breast cancer research : BCR (5.676): 10.1186/s13058-018-1022-y} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA429345 https://www.ebi.ac.uk/ena/browser/view/PRJNA429345 None [Overal design]Genomic DNA was isolated from fresh-frozen tissue samples; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was isolated from fresh-frozen tissue specimens using the Wizard Genomic DNA extraction kit, including proteinase K treatment followed by phenol chloroform purification'; [Cell type]'Source: ''gender: female; tissue: Human breast tumor; ', 'gender: female; tissue: Normal female genomic DNA; ' GSE88961 Mus musculus 8 Expression profiling by high throughput sequencing GPL19057 Mechanism of Induction of Mouse Breast Cancer by Non-coding Heterochromatic RNAs 2016-10-19 Heterochromatic non-coding RNAs induce breast tumor formation in mice by interacting with BRCA1-associated proteins functioning in the DNA damage response. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE88961 Heterochromatin-Encoded Satellite RNAs Induce Breast Cancer. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2018.04.023 {Molecular cell (14.548): 10.1016/j.molcel.2018.04.023} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA349194 https://www.ebi.ac.uk/ena/browser/view/PRJNA349194 https://www.ncbi.nlm.nih.gov/sra?term=SRP091793 [Overal design]mouse tumor mRNA profiles using ribosomal mRNA depletion; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was isolated using Trizol reagent (Thermo Fisher Scientific) according to manufacturer’s instructions\nTruSeq Stranded Total RNA Library Prep Kit with Rib-Zero (Illumina) according to manufacturer's provided protocol"; [Cell type]'Source: ''strain: B6D2F1/J; age at injection: 6-8 weeks; genotype/variation: wildtype; injected with: luciferase fragment and shTP53; site of injection: Breast; tissue: Normal Mammary Gland; ', 'strain: B6D2F1/J; age at injection: 6-8 weeks; genotype/variation: wildtype; injected with: murine Major Satellite and shTP53; site of injection: Breast; tissue: Breast Tumor; ', 'strain: B6D2F1/J; age at injection: 6-8 weeks; genotype/variation: wildtype; injected with: human alpha satellite and shTP53; site of injection: Breast; tissue: Breast Tumor; ' GSE181548 Homo sapiens 105 Expression profiling by array GPL17784 Pam50 of a Triple-Negative Breast Cancer Cohort Treated with Neoadjuvant Carboplatin and Docetaxel According to Lehmann's Refined Classification 2021-08-06 Our aims is correlate the data and classification of the subtype breast cancer obtained with the Pam50 assay with the data obtained from the analysis of the same patients RNAseq https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE181548 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA752528 https://www.ebi.ac.uk/ena/browser/view/PRJNA752528 None [Overal design]Total RNA was obtained from breast cancer tissue embedded in parafine (from the surgery) in order to perform the nanostring Pam50 assay.; [Treatment]'None'; [Growth]'None'; [Extraction]'On average, 5 um-thick sections were prepared for the extraction of total RNA from tumor cell-rich areas, which were identified by a surgical pathologist.'; [Cell type]'Source: ''tissue: Breast tumor sample; subtype: Basal; age: 41; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Normal; age: 42; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 67; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 58; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 66; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 64; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 55; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 29; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 42; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Normal; age: 48; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 68; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 71; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 81; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 38; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 44; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 65; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 62; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 59; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 60; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 33; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 56; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 43; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 66; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 73; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 45; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 63; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Normal; age: 54; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 51; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 49; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 70; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 31; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 47; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 54; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 57; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Normal; age: 55; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 44; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 35; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 58; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 30; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 59; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 39; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 40; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 52; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 36; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 74; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 43; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 37; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 62; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 75; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 68; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 72; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 79; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 50; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 77; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 61; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 52; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 73; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 70; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: LumB; age: 53; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 32; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Her2; age: 56; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 34; treatment: Carboplatin and Docetaxel; ', 'tissue: Breast tumor sample; subtype: Basal; age: 46; treatment: Carboplatin and Docetaxel; ' GSE124209 Mus musculus 11 Expression profiling by high throughput sequencing GPL21103 Autophagic turnover of NBR1 restricts metastatic colonization during mammary tumor progression 2018-12-20 Autophagy is implicated in promoting the metastatic potential of tumor cells. Utilizing a mouse model of mammary cancer to temporally delete essential autophagy regulators, ATG12 or ATG5, in tumor cells during distinct stages of carcinoma progression, we determine a stage-specific role for autophagy in suppressing metastatic colonization. In stark contrast to the tumor-promoting role of autophagy in primary mammary tumors, autophagy restricts colonization of disseminated tumor cells (DTCs) and prevents the acquisition of basal epithelial characteristics, effects that are dependent on turnover of the autophagy-specific substrate, Neighbor to BRCA1 (NBR1). Analysis of human breast cancer samples corroborates the importance of NBR1 in overall survival and metastasis, highlighting NBR1 as a potential therapeutic target in preventing DTCs from developing into overt, clinical disease. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124209 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA510992 https://www.ebi.ac.uk/ena/browser/view/PRJNA510992 https://www.ncbi.nlm.nih.gov/sra?term=SRP174075 [Overal design]We inoculated primary GFP+ PyMT mammary tumor cells via lateral tail vein into naïve, 6-week old female C57BL/6 hosts and allowed them to seed the lung for 1 week. We then inducibly deleted the essential autophagy gene, ATG12, exclusively in metastatic tumor cells and allowed overt metastases to develop for an additional 3 weeks. Lungs were dissociated and resulting metastatic ATG12-knockout (ATG12 KO) and ATG12-floxed (control, ATG12 F/F) PyMT tumor cells were sorted by FACS (GFP+/MHC-I+/CD45-/CD31-/Ter119-) and RNA sequencing libraries prepared. Replicates: ATG12-knockout (n=5), ATG12 floxed (Control, n=6); [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen RNeasy Micro was used to extract RNA and DNAseI was used to eliminate residual DNA.\nLibraries were prepared using standard Illumina Nextera XT protocols'; [Cell type]'Source: ''strain: C57BL/6; genotype: ATG12 F/F; age: 6-week old; Sex: female; tissue: Mouse mammary tumor Cells; ', 'strain: C57BL/6; genotype: ATG12 KO; age: 6-week old; Sex: female; tissue: Mouse mammary tumor Cells; ' GSE48161 Homo sapiens 8 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL9115; GPL11154 Mapping ERβ genomic binding sites reveals unique genomic features and identifies EBF1 as an ERβ interactor 2013-06-20 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48161 None None None None None 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA209059 https://www.ebi.ac.uk/ena/browser/view/PRJNA209059 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'On 15-cm plates, C4-12/Flag.ERβ cells were treated with 10nM E2 for 1 hour then crosslinked with 1% formaldehyde. Cells were lysed with 1mL of ChIP-lysis buffer (50mM Tris pH 7.4, 100mM NaCl, 0.1% SDS, 1% Triton-X, 0.5% NP40, PICIII) and sonicated for 10 cycles, each of which was 10 seconds. The lysate was collected and incubated with 30uL Protein G Plus-Agarose (Santa Cruz) preimmuned with 10ug anti-Flag M2 antibodies (Sigma) to capture protein-DNA complex overnight in ChIP-lysis buffer. The Protein G beads were washed once with ChIP-wash buffer I (20mM Tris pH 8.1, 150mM NaCl, 0.1% SDS, 1% Triton X, 2mM EDTA), once with ChIP-wash buffer II (20mM Tris pH 8.1, 500mM NaCl, 0.1% SDS, 1% Triton X, 2mM EDTA), once with ChIP-wash buffer III (10mM Tris pH 8.1, 250mM LiCl, 1% NP40, 1% deoxycholate, 1mM EDTA), and twice with TE buffer. The protein-DNA complexes were eluted with ChIP-elution buffer (100mM NaHCO3, 1% SDS). The crosslinking was reversed by incubating samples at 65oC overnight. After treatment of RNase A and Proteinase K, the inputs and immunoprecipitated samples were extracted once with phenol/chloroform, once with chloroform, and precipitated in ethanol. The genomic DNA precipitate was suspended in 20uL nuclease-free water.\nIllumina ChIP-seq kit', 'After 1 hour of E2 or Vehicle treatment, nuclei from C4-12/Flag-ERβ cells were extracted and processed with nuclear run-on assay.\nRun-on RNA was ligated with adapters and reverse transcribed to generate cDNA library.'; [Cell type]'Source: ''ChIP: anti-Flag M2 (Sigma); treatment: 10nM E2; cell line: C4-12/Flag.ER-beta; ', 'ChIP: anti-Flag M2 (Sigma); treatment: Vehicle; cell line: C4-12/Flag.ER-beta; ', 'ChIP: input; treatment: N/A; cell line: C4-12/Flag.ER-beta; ', 'treatment: Vehicle; replicate: 1; ', 'treatment: Vehicle; replicate: 2; ', 'treatment: 10nM E2; replicate: 1; ', 'treatment: 10nM E2; replicate: 2; ' GSE118812 Mus musculus 58 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL21273 The genome-wide enhancer profiling of breast cancer in the MMTV-PyVT mice 2018-08-20 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE118812 The hyper-activation of transcriptional enhancers in breast cancer. Clinical epigenetics 5.496 https://doi.org/10.1186/s13148-019-0645-x {Clinical epigenetics (5.496): 10.1186/s13148-019-0645-x} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA486844 https://www.ebi.ac.uk/ena/browser/view/PRJNA486844 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'For both normal mammary gland and tumor samples, 20 mg tissue was used for RNA extraction. Total RNA was extracted by using EASYspin RNA Mini Kit (Aidlab RN07).\nRNA-seq libraries were constructed by NEBNext Poly(A) mRNA Magnetic Isolation Module (NEB E7490) and NEBNext Ultra II Non-Directional RNA Second Strand Synthesis Module (NEB E6111).', 'Lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody.\nChIP-seq libraries were constructed by VATHS Universal DNA Library Prep Kit for Illumina (Vazyme ND604).'; [Cell type]'Source: ''strain: FVB wild type; tissue: Normal mammary gland tissue; treatment: No treatment; age: 12 weeks old; ', 'strain: MMTV-PyVT; tissue: Mammary tumor tissue; treatment: No treatment; age: 12 weeks old; ', 'strain: MMTV-PyVT; tissue: Mammary tumor tissue; treatment: 1mg/kg DMSO injection; age: 12 weeks old; ', 'strain: MMTV-PyVT; tissue: Mammary tumor tissue; treatment: 1mg/kg C646 injection; age: 12 weeks old; ', 'strain: FVB wild type; tissue: Normal mammary gland tissue; treatment: No treatment; antibody: H3K27ac; ', 'strain: FVB wild type; tissue: Normal mammary gland tissue; treatment: No treatment; antibody: H3K27me3; ', 'strain: FVB wild type; tissue: Normal mammary gland tissue; treatment: No treatment; antibody: H3K4me3; ', 'strain: FVB wild type; tissue: Normal mammary gland tissue; treatment: No treatment; antibody: H4K8ac; ', 'strain: FVB wild type; tissue: Normal mammary gland tissue; treatment: No treatment; antibody: none; ', 'strain: MMTV-PyVT; tissue: Mammary tumor tissue; treatment: No treatment; antibody: H3K27ac; ', 'strain: MMTV-PyVT; tissue: Mammary tumor tissue; treatment: No treatment; antibody: H3K27me3; ', 'strain: MMTV-PyVT; tissue: Mammary tumor tissue; treatment: No treatment; antibody: H3K4me3; ', 'strain: MMTV-PyVT; tissue: Mammary tumor tissue; treatment: No treatment; antibody: H4K8ac; ', 'strain: MMTV-PyVT; tissue: Mammary tumor tissue; treatment: No treatment; antibody: none; ', 'strain: MMTV-PyVT; tissue: Mammary tumor tissue; treatment: 1mg/kg DMSO injection; antibody: H3K27ac; ', 'strain: MMTV-PyVT; tissue: Mammary tumor tissue; treatment: 1mg/kg DMSO injection; antibody: none; ', 'strain: MMTV-PyVT; tissue: Mammary tumor tissue; treatment: 1mg/kg C646 injection; antibody: H3K27ac; ', 'strain: MMTV-PyVT; tissue: Mammary tumor tissue; treatment: 1mg/kg C646 injection; antibody: none; ' GSE126419 Homo sapiens 3 Non-coding RNA profiling by high throughput sequencing GPL11154 Small RNA sequencing of extracellular vesicles from MDA-MB-231 cells treated with PBS, docetaxel (DTX), or doxorubicin (DOXO) 2019-02-11 To identify the extracellular-vesicle-encapsulated miRNAs that are differentially secreted by the MDA-MB-231 metastatic breast cancer cells following treatment with chemotherapy drugs, we profiled the small RNAs (between 17 and 52 nt) isolated from extracellular vesicles by Illumina sequencing. miRNAs that are significantly induced by chemotherapy drugs are identified. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE126419 Chemotherapy-Induced Extracellular Vesicle miRNAs Promote Breast Cancer Stemness by Targeting ONECUT2. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-18-4055 {Cancer research (8.378): 10.1158/0008-5472.CAN-18-4055} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA521816 https://www.ebi.ac.uk/ena/browser/view/PRJNA521816 https://www.ncbi.nlm.nih.gov/sra?term=SRP185599 [Overal design]Extracellular vesicles were collected by ultracentrifugation of the conditioned medium of MDA-MB-231 cells that had been treated with docetaxel (DTX; 4 nM), doxorubicin (DOXO; 125 nM), or PBS for 48 h. RNA was extracted using TRIZOL LS (Thermo Fisher Scientific), and subjected to library construction and Illumina sequencing.; [Treatment]'Cells were treated with docetaxel (DTX; 4 nM), doxorubicin (DOXO; 125 nM), or PBS for 48 h in growth medium containing EV-depleted FBS.'; [Growth]'MDA-MB-231 cells were grown in DMEM plus 10% fetal bovine serum (FBS). To collect extracellular vesicles (EV), conditioned medium was first prepared by incubating cells grown at sub-confluence in growth medium containing EV-depleted FBS (prepared by overnight ultracentrifugation of medium-diluted sera at 100,000 ×g at 4\u2009°C) for 48\u2009h, and pre-cleared by centrifugation at 500 ×g for 15\u2009min and then at 10,000 ×g for 20\u2009min. EVs were pelleted by ultracentrifugation at 110,000 ×g for 70\u2009min, and washed in PBS under the same ultracentrifugation conditions.'; [Extraction]"TRIZOL LS reagent (Thermo Fisher Scientific) was used to extract total RNA from EVs following the manufacturer’s protocol. RNA pellet was dissolved in RNase-free water, and subjected to library construction and deep sequencing.\nEach sample was independently subjected to library preparation and deep sequencing. All small RNAs of 15–52 nts were selected and sequenced using the Illumina system, following the manufacturer’s protocol (Illumina Inc., San Diego, CA). Library preparation, as well as cluster generation and deep sequencing, was performed according to the 5' ligation-dependent (5′ monophosphate-dependent) manufacturer’s protocol (Digital Gene Expression for small RNA; Illumina). Small RNAs were size-selected between 17 and 52 nt according to the single-stranded DNA marker in the small RNA sequencing kit (Illumina). The library was quantified using picoGreen and qPCR. Sequencing was performed on a Genome Analyzer IIx (Illumina), and image processing and base calling were conducted using Illumina’s pipeline."; [Cell type]'Source: ''cell line: MDA-MB-231; treatment: PBS; sample type: Extracellular vesicles; molecule subtype: miRNA; ', 'cell line: MDA-MB-231; treatment: docetaxel (DTX); sample type: Extracellular vesicles; molecule subtype: miRNA; ', 'cell line: MDA-MB-231; treatment: doxorubicin (DOXO); sample type: Extracellular vesicles; molecule subtype: miRNA; ' GSE47811 Mus musculus 12 Expression profiling by array GPL1261 Pancreatic cancer biomarkers in mouse saliva 2013-06-10 This is a pilot study. We are trying to detect potential salivary biomarkers in mice with a pancreatic tumor. Global gene expression profiling has shown great promise in high-throughput biomarker discovery for early disease detection in body fluids such as saliva, which is accessible, cost-effective, and non-invasive. However, this goal has not been fully realized because saliva, like many clinical samples, contains partially fragmented and degraded RNAs that are difficult to amplify and detect with prevailing technologies. Here, using nanogram scale salivary RNA as a proof-of-principle example, we describe our progress with a novel poly-A tail independent mRNA amplification strategy combined with the Affymetrix GeneChip Exon arrays. We defined a Salivary Exon Core Transcriptome (SECT) with highly similar expression profiles in healthy individuals verified by quantitative PCR. Informatics analysis of SECT provided important mechanistic insight to their potential origin and function. Finally we demonstrated the diagnostic potential of true exon level expression profiling approach with salivary exon biomarkers that accurately discriminated gender in healthy individuals. Recent studies have demonstrated that discriminatory salivary biomarkers can be readily detected upon the development of systemic diseases such as pancreatic cancer, breast cancer, lung cancer and ovarian cancer. However, the utility of salivary biomarkers for the detection of systemic diseases has been undermined due to the absence of biological and mechanistic rationale why distal diseases from the oral cavity would lead to the development of discriminatory biomarkers in saliva. Here, we examine the hypothesis that pancreatic tumor-derived exosomes are mechanistically involved in the development of pancreatic cancer-discriminatory salivary transcriptomic biomarkers. We first developed a pancreatic cancer mouse model that yielded discriminatory salivary biomarkers by implanting the mouse pancreatic cancer cell line Pan02 into the pancreas of the syngeneic host C57BL/6. The role of pancreatic cancer-derived exosomes in the development of discriminatory salivary biomarkers was then tested by engineered a Pan02 cell line that is suppressed for exosome biogenesis, implanted into the C56BL/6 mouse and examine if the discriminatory salivary biomarker profile was ablated or disrupted. Suppression of exosome biogenesis results in the ablation of discriminatory salivary biomarker development. This study supports that tumor-derived exosomes provide a mechanism in the development of discriminatory biomarkers in saliva and distal systemic diseases. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47811 Role of pancreatic cancer-derived exosomes in salivary biomarker development. The Journal of biological chemistry 4.106 https://doi.org/10.1074/jbc.M113.452458 {The Journal of biological chemistry (4.106): 10.1074/jbc.M113.452458} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA208075 https://www.ebi.ac.uk/ena/browser/view/PRJNA208075 None [Overal design]We analyzed saliva from 6 healthy mice and 6 mice with a pancreatic tumor using the Affymetrix Mouse Exon Genome 430 2.0 platform. Array data was processed by dChip. No techinical replicates were performed.; [Treatment]'None'; [Growth]'None'; [Extraction]'For the discovery of candidate pancreatic cancer-discriminatory salivary transcriptomic biomarkers, saliva RNA was isolated using the RNeasy Mini Kit (Qiagen) according to manufacturer?s protocol. There were 30 mice each in the control and tumor group. Samples derived from 5 mice in each group were pooled for RNA extraction. Pooling was necessary to ensure that sufficient salivary mRNA was obtained for microarray analyses. Isolated total RNA was treated with recombinant DNase. For microarray analysis, mRNA from mouse saliva was linearly amplified using the RiboAmp RNA Amplification kit (Molecular Devices). After purification, cDNA were transcribed in vitro and biotinylated using GeneChip Expression 3?-Amplification Reagents for labeling of transcripts (Affymetrix). The labeled RNAs (15 ug each) were subsequently fragmented and sent to the UCLA microarray core facility for array hybridization and scanning.'; [Cell type]'Source: ''strain background: C56BL/6; tissue: saliva supernatant; sample group: healthy mice; ', 'strain background: C56BL/6; tissue: saliva supernatant; sample group: mice with pancreatic tumor; ' GSE23938 Mus musculus 46 Expression profiling by array GPL8321 Comprehensive genomic profiling identified miRNA signatures associated with mammary tumor differentiation and development 2010-09-01 We performed affymetrix gene expression profiling on mammary tumors from eight well-characterized genetically engineered Mouse (GEM) models of human breast cancer. The gene expression data will be combined with the miRNA gene expression data from the corresponding mammary tumors and tissues for integrated miRNA and mRNA gene expression analysis, which are useful in improving the identification of miRNA targets from potential targets identified in silico. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23938 Integrated miRNA and mRNA expression profiling of mouse mammary tumor models identifies miRNA signatures associated with mammary tumor lineage. Genome biology 14.028 https://doi.org/10.1186/gb-2011-12-8-r77 {Genome biology (14.028) doi:10.1186/gb-2011-12-8-r77}; {Clinical epigenetics (5.496) doi:10.1186/s13148-016-0205-6}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA130315 https://www.ebi.ac.uk/ena/browser/view/PRJNA130315 None [Overal design]mRNA expression data for 41 mouse primary mammary tumors and 5 mouse normal mammary glands; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was extracted from tumor and normal tissues using the mirVana miRNA Isolation kit (Ambion) according to the manufacturer's instructions."; [Cell type]'Source: ''genetically engineered mouse model: C3TAg; tissue type: mammary tumor; strain: FVB; ', 'genetically engineered mouse model: MMTV-C-Myc; tissue type: mammary tumor; strain: FVB; ', 'genetically engineered mouse model: MMTV-H2N; tissue type: mammary tumor; strain: FVB; ', 'genetically engineered mouse model: MMTV-Hras; tissue type: mammary tumor; strain: FVB; ', 'genetically engineered mouse model: p53-/-; tissue type: mammary tumor; strain: Balb/C; ', 'genetically engineered mouse model: MMTV-Wnt; tissue type: mammary tumor; strain: FVB; ', 'genetically engineered mouse model: Brca1-/-p53+/-; tissue type: mammary tumor; strain: 129B6/FVB; ', 'genetically engineered mouse model: MMTV-PymT; tissue type: mammary tumor; strain: FVB; ', 'tissue type: normal mammary; strain: FVB; ' GSE13477 Homo sapiens 8 Expression profiling by array GPL570 Gene Expression Analysis of ARC (NSC 188491) Treated MCF7 cells 2008-11-05 ARC (NSC 188491, SMA-491), 4-amino-6-hydrazino-7-beta-d-ribofuranosyl-7H-pyrrolo-(2,3-d)-pyrimidine-5-carboxamide, is a nucleoside analog with profound in vitro anti-cancer activity. First identified in a high-throughput screen for inhibitors of p21 mRNA expression, subsequent experiments showed that ARC also repressed expression of hdm2 and survivin, leading to its classification as a global inhibitor of transcription 1. The following Hu U133 plus 2.0 arrays represent single time point (24 hour) gene expression analysis of transcripts altered by ARC treatment. Arrays for the other compounds (sangivamycin and doxorubicin) are included as comparators. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE13477 ARC (NSC 188491) has identical activity to Sangivamycin (NSC 65346) including inhibition of both P-TEFb and PKC. BMC cancer 2.933 https://doi.org/10.1186/1471-2407-9-63 {BMC cancer (2.933): 10.1186/1471-2407-9-63} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA110155 https://www.ebi.ac.uk/ena/browser/view/PRJNA110155 None [Overal design]MCF7 cells treated with ARC, Sangivamycin or Doxorubicin for 24 hours.; [Treatment]'No Treatment', 'ARC NSC 188491 Treated', 'Sangivamycin Treated', 'Doxorubicin Treated'; [Growth]'RPMI 1640 10% FBS'; [Extraction]'RNeasy (Qiagen)'; [Cell type]'Source: ''' GSE125700 Homo sapiens 31 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL18602 OncoScan analysis of breast carcinomas from the Swedish haemangioma cohort 2019-01-25 The Swedish haemangioma cohort consists of 17,200 women treated with radium-226 for skin haemangioma at an early age (<1.5 years of age) between 1920 and 1965. A total of 877 breast cancer cases were reported by December 2009, estimating an excess relative and absolute risk at the age of 50 years of 0.48 Gy^(−1) and 10.4 (10^4 PYR Gy)^(−1), respectively. We screened 31 primary breast carcinomas for genetic alterations using the OncoScan CNV Plus Assay to assess genomic instability. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE125700 Radiation-induced genomic instability in breast carcinomas of the Swedish hemangioma cohort. Genes, chromosomes & cancer 2.940 https://doi.org/10.1002/gcc.22757 {Genes, chromosomes & cancer (2.940): 10.1002/gcc.22757} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA517197 https://www.ebi.ac.uk/ena/browser/view/PRJNA517197 None [Overal design]Copy number analysis of Affymetrix OncoScan CNV Plus arrays was performed on 31 formamid-fixed paraffin-embedded breast tumours.; [Treatment]'None'; [Growth]'All samples were formalin-fixed paraffin-embedded (FFPE) tumours.'; [Extraction]'Tumour tissues were sectioned and tumour DNA was extracted using the AllPrep DNA/RNA FFPE kit (Qiagen) with overnight Proteinase K treatment. The DNA concentration was determined with the Qubit Fluorometer.'; [Cell type]'Source: ''gender: Female; ' GSE37849 Mus musculus 4 Expression profiling by array GPL1261 Suppressed cytokine and chemokine transcriptional signatures in mammary stem/progenitor cells are associated with dietary protection against Wnt1-driven mammary tumorigenesis 2012-05-08 Maintenance and propagation of breast cancer stem cells (BCSCs) is mediated via cytokine and growth factor networks. Direct in vivo linkage between dietary regulation of mammary stem (MaSC)/progenitor cell numbers and protection from breast cancer has not been reported. Here, we investigated the effect of post-weaning intake of soy protein isolate (SPI) relative to the control casein (CAS) diet on the stem/progenitor population and tumor formation in MMTV-Wnt1-Transgenic (Wnt1-Tg) female mice. Gene expression profile of the basal (MaSC-enriched) sub-population in preneoplastic Wnt1-Tg mice demonstrated a stem cell-like expression pattern and markedly suppressed expression of inflammatory cytokines, C-X-C family chemokines, and metastasis-associated genes with dietary SPI exposure. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37849 Dietary suppression of the mammary CD29(hi)CD24(+) epithelial subpopulation and its cytokine/chemokine transcriptional signatures modifies mammary tumor risk in MMTV-Wnt1 transgenic mice. Stem cell research 3.929 https://doi.org/10.1016/j.scr.2013.08.006 {Stem cell research (3.929): 10.1016/j.scr.2013.08.006} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA163887 https://www.ebi.ac.uk/ena/browser/view/PRJNA163887 None [Overal design]four Samples: two CAS diet, two SPI diet; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was isolated from freshly sorted mammary Basal population using the Arcturus PicoPure RNA isolation kit (Life Technologies Corporation, Carlsbad, CA)'; [Cell type]'Basal (stem cells, myoepithelial cells, myoepithelial progenitors)''strain: B66SJL/HEV/J (mixed background); genotype/variation: MMTV-Wnt1-Transgenic (Wnt1-Tg); tissue: Mammary gland; cell type: Basal (stem cells, myoepithelial cells, myoepithelial progenitors); diet: control casein (CAS) diet; ', 'strain: B66SJL/HEV/J (mixed background); genotype/variation: MMTV-Wnt1-Transgenic (Wnt1-Tg); tissue: Mammary gland; cell type: Basal (stem cells, myoepithelial cells, myoepithelial progenitors); diet: soy protein isolate (SPI) diet; ' GSE16085 Homo sapiens 6 Expression profiling by array GPL570 Networking of differentially expressed genes in human K562 erythtoblastic leukemia cells resistant to methotrexate 2009-05-13 A summary of the work associated to these microarrays is the following: The need for an integrated view of all data obtained from high-throughput technologies gave rise to network analyses. These are especially useful to rationalize phenomena in terms of how external perturbations propagate through the expression of genes. To address this issue in the case of drug resistance, we constructed Biological Association Networks of genes differentially expressed in cell lines resistant to methotrexate (MTX). Seven cell lines representative of different types of cancer including colon cancer (HT29 and Caco2), breast cancer (MCF7 and MDA-MB-468), pancreatic cancer (MIA PaCa-2), erythroblastic leukemia (K562) and osteosarcoma (Saos-2), were used. The differential expression pattern between sensitive and MTX-resistant cells was determined by microarrays covering the whole human genome and analyzed with the GeneSpring GX software package, v.7.3.1. Genes deregulated in common in the two colon cancer cell lines studied, were subject of Biological Association Networks construction. Dikkopf homolog-1 (DKK1) was a clear node of this network, and functional validations of this target using a siRNA showed a chemosensitization toward MTX. Members of the UDP-glucuronosyltransferase 1A (UGT1A) family formed a network of differentially expressed genes in the two breast cancer cell lines studied. siRNA treatment against UGT1A showed also an increase in MTX sensitivity. Eukaryotic translation elongation factor 1 alpha 1 (EEF1A1) was a gene overexpressed in common among the pancreatic cancer, leukemia and osteosarcoma cell lines, and siRNA treatment against EEF1A1 produced a chemosensitization toward MTX. Biological Association Networks identified DKK1, UGT1As and EEF1A1 as important gene nodes in MTX-resistance. Treatments using iRNA technology against these three genes show chemosensitization toward MTX. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE16085 Networking of differentially expressed genes in human cancer cells resistant to methotrexate. Genome medicine 10.886 https://doi.org/10.1186/gm83 {Genome medicine (10.886): 10.1186/gm83} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA123073 https://www.ebi.ac.uk/ena/browser/view/PRJNA123073 None [Overal design]Two cell lines are compared, which are K562 erythroblastic leukemia cells sensitive to methotrexate and K562 cells resistant to 10e-5M methotrexate. Six samples are provided which correspond to triplicates of each cell line. The samples provided were analyzed using the specific software GeneSpring GX.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNeasy Mini Kit from Qiagen'; [Cell type]'erythroblastic leukemia''cell line: K562; cell type: erythroblastic leukemia; methotrexate sensitivity: sensitive; ', 'cell line: K562; cell type: erythroblastic leukemia; methotrexate sensitivity: resistant; ' GSE104967 Mus musculus 6 Expression profiling by high throughput sequencing GPL17021 mRNA Profiling of Murine 4T1 Breast Cancer Cells with Asns knocked down 2017-10-13 Murine 4T1-T Breast cancer cells were infected with retroviral vectors harboring shRNAs for murine or a Renilla, as negative control. After selection cells were harvested and processed with the NuGen Ovation RNAseq system V2. Libraries were sequenced on an Illumina platform and mapped using Bowtie2 to the mm10 genome prior to transcript quantification using HT-Count. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE104967 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA414245 https://www.ebi.ac.uk/ena/browser/view/PRJNA414245 https://www.ncbi.nlm.nih.gov/sra?term=SRP119932 [Overal design]4T1 Breast Cancer Cells with Asns knocked down; [Treatment]'shRNA Knockdown'; [Growth]'Grown in DMEM + Non Essential Amino Acids'; [Extraction]'Trizol\nNugen Ovation RNAseq V2\nmRNA squencing'; [Cell type]'Source: ''treatment: shRNA Infected; ' GSE2860 Mus musculus 84 Expression profiling by array GPL1511; GPL1512 Changes in Gene expression during the development and progression of mammary tumors in MMTV-Wnt-1 and MMTV-Neu TG mice 2005-06-30 Gene expression profiling of samples from normal virgin mammary glands, hyperplastic mammary glands, mamary tumors, and lung metastases from MMTV-Wnt-1 transgenic (TG) mice, and mammary tumors and lung metastases from MMTV-Neu trangenic (TG) mice Keywords: Array analysis, multi-step tumorigenesis, metastasis, MMTV-Wnt-1 trangenic mice, MMTV-Neu transgenic mice https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE2860 Changes in gene expression during the development of mammary tumors in MMTV-Wnt-1 transgenic mice. Genome biology 14.028 https://doi.org/10.1186/gb-2005-6-10-r84 {Genome biology (14.028): 10.1186/gb-2005-6-10-r84} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA92521 https://www.ebi.ac.uk/ena/browser/view/PRJNA92521 None [Overal design]1. We compared expression prifiles among 5 normal virgin mammary glands, 7 hyperplastic mammary glands and 23 mammary tumors from MMTV-Wnt-1 transgenic mice, and 12 mammary tumors from MMTV-Neu transgenic mice. 2. We compared expression profiles between 23 mammary tumors and 10 lung metastases from MMTV-Wnt-1 transgenic mice and 12 mammary tumors and 5 lung metastases from MMTV-Neu transgenic mice. The experiments for the above comparisons were performed in the same time frame using a single array print and the same batch of reference RNA.; [Treatment]'MMTV-Wnt-1Transgenic mouse'; [Growth]'None'; [Extraction]'Trizol'; [Cell type]'Source: ''' GSE152866 Mus musculus 4 Expression profiling by high throughput sequencing GPL21103 Single-Cell RNA-seq Reveals Obesity-Induced Alterations in the BRAC1 Mutant Mammary Tumor Microenvironment 2020-06-19 In this study, we conducted single-cell RNA sequencing (scRNA-seq) studies to investigate the impact of high-fat diet (HFD)-induced obesity on transcriptomic landscapes of stromal and immune cells in mammary glands of Brca1-/-;p53+/- mice, an animal breast cancer model. The scRNA-seq profiling data showed that five different subtypes of stromal fibroblasts existed in mouse mammary glands. HFD-induced obesity led to upregulated expression of extracellular matrix (ECM) genes (Col3a1, Col6a3, Eln, and Sparc) and downregulated expression of immunoregulatory genes (Iigp1, Ccl2, and Cxcl10) in these stromal subtype cells. These findings, taken together, suggest that obesity alters the ECM composition and immune ecosystem through modulating the functionality of mammary stromal cells. Moreover, scRNA-seq analysis of mammary immune cells indicated that HFD-induced obesity promoted the generation and/or recruiting of pro-tumorigenic M2 macrophages in mammary glands. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE152866 Single-Cell RNA-seq Reveals Obesity-Induced Alterations in the Brca1-Mutated Mammary Gland Microenvironment. Cancers 6.162 https://doi.org/10.3390/cancers12082235 {Cancers (6.162): 10.3390/cancers12082235} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA640665 https://www.ebi.ac.uk/ena/browser/view/PRJNA640665 https://www.ncbi.nlm.nih.gov/sra?term=SRP268071 [Overal design]Single-cell RNA-seq profiling analysis of stromal and immune cells in mammary glands isolated from either normal or obese C57BL6 Brca1-/-;p53+/- mice.; [Treatment]'Four two-month-old female C57BL/6 Brca1-/-;p53+/- mice were randomized and fed with either a lean-fat diet (10% kcal from fat) or a high-fat diet (60% kcal from fat) ad libitum for 10 weeks (n = 2 for each diet group).'; [Growth]'None'; [Extraction]"Non-epithelial mammary cells isolated from mammary glands were enriched by removing epithelial cells using the anti-EpCAM antibody and magnetic dynabeads. To isolate viable cells, enriched non-epithelial cells were stained with 7-AAD dye (0.5 µg/ml) and 7-AAD-negative viable cells were sorted using the FACS Aria II cell sorter (BD Biosciences, Franklin Lakes, NJ, USA).\nFACS-sorted viable single cells were processed by using the 10X Genomics Chromium device to prepare scRNA-seq libraries (Single Cell 3' v2) according to the manufacturer’s protocol.\nSingle-cell RNA-seq (scRNA-seq)"; [Cell type]'stromal and immune cells''strain: C57BL/6; tissue: mammary gland; cell type: stromal and immune cells; treatment: regular diets; ', 'strain: C57BL/6; tissue: mammary gland; cell type: stromal and immune cells; treatment: high-fat diets; ' GSE86316 Homo sapiens 12 Expression profiling by high throughput sequencing GPL11154; GPL18573 Messenger RNA expression after silencing or inhibition of MEN1in MCF-7 breast cancer cells 2016-08-31 We performed RNA-seq in MCF-7 cells after silencing of MEN1 using small hairpin RNA's directed at the MEN1 mRNA or chemical inhibition of the MEN1 gene product, menin. We demonstrate that a selected group of transcripts is affected by reduced menin function. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE86316 Enhancer-Mediated Oncogenic Function of the Menin Tumor Suppressor in Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2017.02.025 {Cell reports (7.815): 10.1016/j.celrep.2017.02.025} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA341401 https://www.ebi.ac.uk/ena/browser/view/PRJNA341401 https://www.ncbi.nlm.nih.gov/sra?term=SRP083916 [Overal design]Comparison of mRNA levels using RNA-seq in mCF-7 cells after silencing of MEN1 using small hairpin RNA's directed at the MEN1 mRNA or chemical inhibition of menin.; [Treatment]"Samples 1-8. MCF-7 cells that had been lentivirally infected with constructs for inducible expression of small hairpin RNA's directed against the MEN1 mRNA (ShMEN1#1) or a control sequence (ShCtrl) were synchronized for 72 hrs in phenol red-free medium (DMEM) containing 10% charcoal dextran-treated fetal bovine serum (CDT medium). Expression of small hairpin RNA's was induced by adding 100 ng/ml doxycycline for 72 hrs. 10nM estradiol or vehicle was added to the cells for 45 mins. Samples 9-12. MCF-7 cells were treated with 1mM of the menin inhibitor MI-2 or DMSO for 4 days."; [Growth]'Cells were maintained at 37oC and 5% CO2 in DMEM + 10% FBS and Pen-Strep.'; [Extraction]'RNA was extracted using RNeasy\nLibraries were made from total RNA using the Illumina TruSeq Stranded mRNA Library Prep Kit'; [Cell type]'Source: ''cell line: MCF7; infection: lentivirally infected with constructs against shCtrl; treatment: vehicle; ', 'cell line: MCF7; infection: lentivirally infected with constructs against shCtrl; treatment: 10nM estradiol; ', 'cell line: MCF7; infection: lentivirally infected with constructs against shMEN1; treatment: vehicle; ', 'cell line: MCF7; infection: lentivirally infected with constructs against shMEN1; treatment: 10nM estradiol; ', 'cell line: MCF7; treatment: DMSO; ', 'cell line: MCF7; treatment: 1mM of the menin inhibitor MI-2; ' GSE50105 Homo sapiens 9 Protein profiling by protein array GPL15317 Targeted inhibition of human breast cancer cell line selected as model system of ERBB2-positive/EGFR high breast cancer [RPPA-Shortterm-HCC1954] 2013-08-22 EGFR-inhibition is required for targeted therapies of ERBB2-positive/EGFR high breast cancer. Approximately 30% of human ERBB2-positive breast tumors also express EGFR. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50105 Boolean ErbB network reconstructions and perturbation simulations reveal individual drug response in different breast cancer cell lines. BMC systems biology 2.048 https://doi.org/10.1186/1752-0509-8-75 {BMC systems biology (2.048): 10.1186/1752-0509-8-75} 'protein' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA216097 https://www.ebi.ac.uk/ena/browser/view/PRJNA216097 None [Overal design]Three targeted therapeutics (erlotinib, pertuzumab, trastuzumab) and two ligands (EGF, HRG) were analyzed in all possible combinations. Each experiment involving inhibition with targeted drugs was performed in three, and measurements without inhibitors were performed in five biological replicates. This resulted in 780 samples. Incubation with therapeutics only and dilution series of control lysated were included as controls.; [Treatment]'The inhibitors trastuzumab (10 ng/µL), pertuzumab (10 ng/µL), and erlotinib (1 µM) (Roche, Penzberg, Germany) were added to cells in starvation medium either alone or in combinations 1 h prior to stimulation with EGF or HRG (5 nM) for 0, 4, 8, 12, 16, 20, 30, 40, 50 and 60 min. After stimulation, medium was removed and ice-cold PBS was added to the plates.'; [Growth]'Cells were seeded in 6-well plates, cultivated for 24h, and serum-starved for additional 24h.'; [Extraction]'Medium was replaced by ice-cold PBS, transferred on ice, and cells were harvested manually by scraping in M-PER lysis buffer (Pierce, Bonn, Germany) containing protease inhibitor Complete Mini and phosphatase inhibitor PhosSTOP (Roche, Mannheim, Germany). Cells were lyzed for 20 min on an end-over-end shaker and lysates were cleared at 16,000 x g by centrifugation.'; [Cell type]'Source: ''protein target: phospho-p70S6K; phospho site: T389; antibody id: CST 9206; ', 'protein target: phospho-ERBB1; phospho site: Y1068; antibody id: CST 2236; ', 'protein target: phospho-ERBB2; phospho site: Y1248; antibody id: Millipore 06-229; ', 'protein target: phospho-MEK1/2; phospho site: S217S221; antibody id: Sigma M7683; ', 'protein target: phospho-PLCgamma; phospho site: S1248; antibody id: CST 4510; ', 'protein target: phospho-PKCalpha; phospho site: S657Y658; antibody id: Abcam ab23513; ', 'protein target: phospho-mTOR; phospho site: S2448; antibody id: CST 2971; ', 'protein target: phospho-ERBB3; phospho site: Y1289; antibody id: CST 4791; ', 'protein target: phospho-PDK1; phospho site: S241; antibody id: CST 3438; ' GSE51231 Homo sapiens 3 Expression profiling by array GPL570 Identification of MAF controlled genes in breast cancer cells 2013-09-27 To identify relevant genes transcriptionally controlled by MAF in breast cancer, we focused on genes whose expression changed accordingly to MAF transcriptiion factor overexpression in MCF7. We used comparative RNA hybridization (Affymetrix) to this end. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE51231 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA221779 https://www.ebi.ac.uk/ena/browser/view/PRJNA221779 None [Overal design]Total RNA from parental and MAFshort or long isoform overexpressing MCF7 grown for 48 hours in regular media (see growth protocol) was isolated from in vitro cultured control and MAF expressing MCF7 parental cells. Total RNA was extracted using the TRIzol® Plus RNA Purification Kit (Life Technologies).; [Treatment]'Cells were grown for 2 days following the growth protocol outlined above and RNA extracted'; [Growth]'MCF7 media (Control media): DMEM (Life Technologies), 1X Glutamax (Gibco 35050) and 10% FBS (Biological Industires) when passaging. See growth conditions in Tarragona et al., Journal of Biological Chemistry, 2012), for more details.'; [Extraction]'Total RNA was extracted using the TRIzol® Plus RNA Purification Kit (Life Technologies) and quantified using a Nanodrop spectrophotometer. Quality was assessed using a Bioanalyzer (Agilent) and only high quality samples (RIN ≥9) were used for hybridization.'; [Cell type]'Source: ''cell line: MCF7; ' GSE156144 Homo sapiens 10 Expression profiling by array; Non-coding RNA profiling by array GPL16956 LncRNA expression profile in triple negative breast cancer (TNBC) 2020-08-12 To identify novel TNBC-relevant lncRNAs, we performed lncRNA microarray analysis using 5 TNBC tissues and their matched adjacent non-cancerous tissues by Arraystar Human LncRNA Microarray V3.0. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE156144 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA656835 https://www.ebi.ac.uk/ena/browser/view/PRJNA656835 None [Overal design]LncRNA expression profiling analysis of 10 samples including 5 TNBC tissues and their matched adjacent normal breast tissues by Arraystar Human LncRNA Microarray V3.0.; [Treatment]'TNBC tissues excised from the breast cancer patients during mammectomies were immediately frozen in liquid nitrogen and then stored at -80℃ until used for RNA extraction using the Trizol reagent.'; [Growth]'TNBC and matched non-tumor tissues'; [Extraction]"RNA was extracted using the Trizol reagent (Invitrogen) following the manufacturer's instruction. RNA quantity and quality were measured by NanoDrop ND-1000 and RNA integrity was assessed by standard denaturing agarose gel electrophoresis."; [Cell type]'Source: ''gender: female; tissue: Triple negative breast cancer(TNBC) tumor tissue; matched sample id: 1; ', 'gender: female; tissue: Triple negative breast cancer(TNBC) tumor tissue; matched sample id: 2; ', 'gender: female; tissue: Triple negative breast cancer(TNBC) tumor tissue; matched sample id: 3; ', 'gender: female; tissue: Triple negative breast cancer(TNBC) tumor tissue; matched sample id: 4; ', 'gender: female; tissue: Triple negative breast cancer(TNBC) tumor tissue; matched sample id: 5; ', 'gender: female; tissue: matched non-tumor tissue of Triple negative breast cancer(TNBC); matched sample id: 1; ', 'gender: female; tissue: matched non-tumor tissue of Triple negative breast cancer(TNBC); matched sample id: 2; ', 'gender: female; tissue: matched non-tumor tissue of Triple negative breast cancer(TNBC); matched sample id: 3; ', 'gender: female; tissue: matched non-tumor tissue of Triple negative breast cancer(TNBC); matched sample id: 4; ', 'gender: female; tissue: matched non-tumor tissue of Triple negative breast cancer(TNBC); matched sample id: 5; ' GSE17775 Homo sapiens 23 Non-coding RNA profiling by array GPL9081 microRNA expression profiles in Aromatase Inhibitor-Resistant, Tamoxifen-Resistant and LTED breast cancer cell lines. 2009-08-24 Resistance to endocrine therapy agents has presented a clinical obstacle in the treatment of hormone-dependent breast cancer. Our laboratory has initiated a study of microRNA regulation of signaling pathways that may result in breast cancer progression on aromatase inhibitors (AI). Microarray analysis of microRNA expression identified 115 significantly regulated microRNAs, of which 49 microRNAs were believed to be hormone-responsive. Within the AI-resistant cells, microRNAs were differentially expressed between the steroidal and non-steroidal AI-resistant lines. Also, a group of microRNAs were inversely expressed in the AI-resistant lines versus LTEDaro and tamoxifen-resistant. We focused our work on hsa-miR-128a which was hormone-responsive and up-regulated in the letrozole-resistant cell lines. Human miR-128a was shown to negatively target TGFBRI protein expression by binding to the 3’UTR region of the gene. Loss of TGFBRI resulted in compromised sensitivity to the growth inhibitory effects of TGFB in the letrozole-resistant lines. Inhibition of endogenous miR-128a resulted in re-sensitization of the letrozole-resistant lines to TGFB growth inhibitory effects. This data suggests that the hormone-responsive miR-128a can modulate TGFB signaling and survival of the letrozole-resistant cell lines. To our knowledge, this is the first study to address the role of microRNA regulation as well as TGFB signaling in AI-resistant breast cancer cell lines. We believe that in addition to estrogen-modulation of gene expression, hormone-regulated microRNAs may provide an additional level of post-transcriptional regulation of signaling pathways critically involved in breast cancer progression and AI-resistance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17775 The role of microRNA-128a in regulating TGFbeta signaling in letrozole-resistant breast cancer cells. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-009-0716-3 {Breast cancer research and treatment (3.471): 10.1007/s10549-009-0716-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA118399 https://www.ebi.ac.uk/ena/browser/view/PRJNA118399 None [Overal design]To look at microRNA expression profiles of breast cancer cell lines derived from MCF-7 cells that are resistant to endocrine therapy agents. MCF-7 cells that overexpress aromatase (MCF-7aro) were cultured long-term in the presence of endocrine therapy agents until cells acquired resistance. Three different aromatase inhibitors (letrozole, anastrozole or exemestane) were used, as well as the ER antagonist tamoxifen, or the hormone-free long-term estrogen deprived cells (LTED). Three replicates of the control cells (MCF-7aro) and all resistant cells were used for microarray experiments. Total of 23 samples were analyzed by microarray.; [Treatment]'Cells were grown constantly in the presence of testosterone (where indicated) and inhibitor.'; [Growth]'Cells were grown long-term in the absence and presence of testosterone (T). Where indicated, testosterone is labeled at T+inhibitor. Cells were grown in charcoal-dextran stripped FBS containing MEM.'; [Extraction]"Trizol Extraction for total RNA isolation, according to the maufacturer's recommendation."; [Cell type]'Source: ''cell line: MCF-7; tissue type: breast cancer; ' GSE22386 Homo sapiens 32 Expression profiling by array GPL506 Dynamic changes in gene expression in vivo predict prognosis of tamoxifen-treated patients with breast cancer 2010-06-16 Tamoxifen is the most widely prescribed anti-estrogen treatment for patients with ER-positive breast cancer. However, there is still a need for biomarkers that reliably predict endocrine sensitivity in breast cancers and these may well be expressed in a dynamic manner. In this study we assessed gene expression changes at multiple time points (days 1, 2, 4, 7, 14) after tamoxifen treatment in the ER-positive ZR-75-1 xenograft model that displays significant changes in apoptosis, proliferation and angiogenesis within 2 days of therapy. Hierarchical clustering identified six time-related gene expression patterns, which separated into three groups: two with early/transient responses, two with continuous/late responses and two with variable response patterns. The early/transient response represented reductions in many genes that are involved in cell cycle and proliferation (e.g. BUB1B, CCNA2, CDKN3, MKI67, UBE2C), whereas the continuous/late changed genes represented the more classical estrogen response genes (e.g.TFF1, TFF3, IGFBP5). Genes and the proteins they encode were confirmed to have similar temporal patterns of expression in vitro and in vivo and correlated with reduction in tumour volume in primary breast cancer. The profiles of genes that were most differentially expressed on days 2, 4 and 7 following treatment were able to predict prognosis, whereas those most changed on days 1 and 14 were not, in four tamoxifen treated datasets representing a total of 404 patients. Both early/transient/proliferation response genes and continuous/late/estrogen-response genes are able to predict prognosis of primary breast tumours in a dynamic manner. Temporal expression of therapy-response genes is clearly an important factor in characterising the response to endocrine therapy in breast tumours which has significant implications for the timing of biopsies in neoadjuvant biomarker studies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22386 Dynamic changes in gene expression in vivo predict prognosis of tamoxifen-treated patients with breast cancer. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr2593 {Breast cancer research : BCR (5.676): 10.1186/bcr2593} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA127737 https://www.ebi.ac.uk/ena/browser/view/PRJNA127737 None [Overal design]Tamoxifen treated ZR-75 xenograft samples compared to a pooled control. 5 timepoints, replicates and dye swaps, giving a total of 32 arrays; [Treatment]'All animals received E2. On day 0, animals were randomly allocated to tamoxifen (2.5 mg released over 60 days, Innovative Research of America) or E2 -only control groups'; [Growth]'Total RNA extracted using Qiagen RNeasy kit (Qiagen, Valencia, CA, USA), according to the manufacturer’s instructions'; [Extraction]'Total RNA (100ug), spiked with bacterial-RNA mixture for control was used to prepare direct Cy3- and Cy5-labelled first-strand cDNA probes using a single-base anchored oligo dT17 primer (Sigma) and Superscript II reverse transcriptase (Invitrogen). Unincorporated nucleotides were removed using QIAquick PCR purification kit (QIAGEN)'; [Cell type]'Source: ''cell line: ZR75-1 xenograft; ' GSE123473 Homo sapiens 2 Non-coding RNA profiling by high throughput sequencing GPL20795 Characterization of RNA context tumor associated macrophages and related extracellular vesicles [small RNA-seq] 2018-12-06 Extracellular vesicles (EVs) are membrane vesicles released by all cell types and contain proteins and non-coding RNAs, which are transported into recipient cells to regulate their signal transduction and functions. Increasing evidence has demonstrated that EV shuttling is an effective means of bio-molecule transportation among various cell types in the tumor microenvironment, and thus plays a critical role in regulating cancer cell biology. Previous studies have shown that TAMs are an important source of extracellular vesicles and the extracellular vesicles released by TAMs can promote the invasiveness of breast cancer cells. In this study, we studied the differential expression of TAM EV and the donor cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE123473 Extracellular vesicle-packaged HIF-1α-stabilizing lncRNA from tumour-associated macrophages regulates aerobic glycolysis of breast cancer cells. Nature cell biology 17.728 https://doi.org/10.1038/s41556-019-0299-0 {Nature cell biology (17.728): 10.1038/s41556-019-0299-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA508816 https://www.ebi.ac.uk/ena/browser/view/PRJNA508816 https://www.ncbi.nlm.nih.gov/sra?term=SRP172795 [Overal design]Examination of small RNA-seq in TAMs and TAM EV (mixture from 10 donors).; [Treatment]'Monocytes derived macrophages (MDMs) were as control macrophages, polarized-tumor associated macrophages (TAMs) were stimulated by 30% CM from MDA-MB-231 cells for 6 days.'; [Growth]'Peripheral blood monocytes (PBMs) from healthy donors were isolated by Ficoll density gradient centrifugation as previously described. Monocytes derived macrophages (MDMs) were grown in DMEM (GIBCO) supplemented with 10% fetal bovine serum, 50 U/ml penicillin (GIBCO) and 50 μg/ml streptomycin (GIBCO). To induce tumor associated macrophages (TAMs), MDMs were treated with 30% CM from MDA-MB-231 cells for 6 days.'; [Extraction]"Total RNA was isolated from TAMs or TAM EVs using RNeasy mini kit (Qiagen, Germany) or SeraMir Exosome RNA Purification for Media & Urine (RA806TC-1, System Biosciences, USA).\nAccording to the experimental instructions, the purified total RNA was ligated with a 3'-end linker, a 5'-end linker, reverse transcription, amplification, cDNA library size selection, purification, etc., to complete sequencing sample library construction."; [Cell type]'tumor associated macrophages', 'extracellular vesicles from tumor associated macrophages''cell type: tumor associated macrophages; ', 'cell type: extracellular vesicles from tumor associated macrophages; ' GSE51630 Homo sapiens 139 Expression profiling by RT-PCR GPL17831 Real-time quantitative PCR analysis of hormone-receptor-negative primary breast tumors 2013-10-23 Total RNA was extracted from FFPE samples of 139 chemotherapy-naïve hormone-receptor-negative breast cancers pooled from three sample sources and assayed for the expression of 21 genes within two previously reported microarray-derived prognostic signatures in 6 RT-PCR multiplexes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE51630 An optimized five-gene multi-platform predictor of hormone receptor negative and triple negative breast cancer metastatic risk. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr3567 {Breast cancer research : BCR (5.676): 10.1186/bcr3567} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA224250 https://www.ebi.ac.uk/ena/browser/view/PRJNA224250 None [Overal design]RT-PCR gene expression profiling. Total RNA was extracted from 10 micron FFPE sections, and expression levels of the 21 genes of interest plus two reference genes were quantified with 6 multiplex RT-PCR TaqMan assays.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted from 10 micron FFPE sections using a modified commercially available isolation kit (Zymo Research). The FFPE sections were digested with proteinase K for 18-24 hours at 55°C, spun down and the supernatant treated with a mixture of 100% ethanol and a GuSCN-based extraction buffer. The extracted material was purified on Zymo-Spin II columns, eluted with TE buffer and the RNA reverse transcribed into cDNA using random hexamers and the High Capacity cDNA kit (Life Technologies).'; [Cell type]'Source: ''tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 5.015742642; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.55; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 9.155373032; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.05; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 3.082819986; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.8; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 13.0513347; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 0; tumor size (cm): 1.45; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 14.05886379; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.2; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 14.01232033; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 0.65; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 7.255304586; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.4; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 9.746748802; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 1; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 6.844626968; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.05; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 12.25462012; distant recurrence indicator (1=yes, 0=no): 0; number positive nodes: 0; tumor size (cm): 1.5; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 9.166324435; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.1; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 12.13689254; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 1.5; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 13.78507871; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 0; tumor size (cm): 1.5; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 7.3045859; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.3; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 8.429842574; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 4; number positive nodes: 0; tumor size (cm): 2; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 19.3045859; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.3; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 17.79055441; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.1; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 16.19164956; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.9; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 2.39835729; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.1; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 15.53456537; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 0; tumor size (cm): 1.85; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 10.97330595; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.9; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 14.00958248; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 0; tumor size (cm): 1.7; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 8.588637919; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.5; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 2.447638604; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.1; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 4.136892539; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 7; number positive nodes: 0; tumor size (cm): 2.3; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 10.51882272; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.5; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 6.518822724; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 1.35; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 2.95687885; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.6; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 8.098562628; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.7; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 1.724845996; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.1; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 9.817932923; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.6; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 12.25735797; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 1.1; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 8.813141684; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 0.654346338; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.7; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 8.473648186; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 0.7; ', 'tissue: primary breast tumor; sample source: California Pacific Medical Center; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 8.145106092; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 2.5; ', "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 30.86; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 5.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 14.75; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 4; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 32.12; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 31.66; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 29.15; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 3.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 31.41; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 1.02; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 9; number positive nodes: 2; tumor size (cm): 3.2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 11.17; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 3; tumor size (cm): 5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 28.75; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 4.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 0.44; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 9; number positive nodes: 0; tumor size (cm): 2.2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 28.19; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 2.7; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 30.04; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 0; tumor size (cm): 3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 1.47; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 0; tumor size (cm): 4; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 18.06; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 3; tumor size (cm): 2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 2.03; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 0.62; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 6; number positive nodes: 23; tumor size (cm): 5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 25.65; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 2; tumor size (cm): 6; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 13.65; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 1; tumor size (cm): 5.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 12.67; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 6; tumor size (cm): 3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 27.81; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 26.71; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 0.99; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 11; tumor size (cm): 3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 0.78; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 9; number positive nodes: 2; tumor size (cm): 0; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 5.31; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 0; tumor size (cm): 4; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 26.53; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 0.4; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 9; number positive nodes: 4; tumor size (cm): 5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 0.25; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 11; tumor size (cm): 4.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 5.52; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 26.07; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 2; tumor size (cm): 4.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 7.82; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 5; number positive nodes: 0; tumor size (cm): 3.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 9.74; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 1; tumor size (cm): 4; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 2.15; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 9; number positive nodes: 32; tumor size (cm): 3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 1.86; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 9; number positive nodes: 1; tumor size (cm): 3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 9.81; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 0; tumor size (cm): 2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 7.77; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 0.79; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 6; number positive nodes: 8; tumor size (cm): 4.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 2.19; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 0; tumor size (cm): 2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 18.69; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 0; tumor size (cm): 1.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 18.79; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 0; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 10.75; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 29; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 2.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 26.6; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 4; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 20.18; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 25.06; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 0; tumor size (cm): 1.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 24.53; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 0.756164384; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 9; number positive nodes: 0; tumor size (cm): 4; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 9.093150685; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 2.1; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 5.824657534; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 1; tumor size (cm): 3.2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 0; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 1; tumor size (cm): 4; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 9.326027397; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 1.9; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 9.164383562; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 2.876712329; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 1; tumor size (cm): 1.9; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 1.961643836; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 7; number positive nodes: 0; tumor size (cm): 1.7; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 8.117808219; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.6; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 8.950684932; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 2.2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 2.936986301; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 0; tumor size (cm): 1; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 5.942465753; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 2.3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 8.515068493; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 1; tumor size (cm): 1.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 1.210958904; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 9; number positive nodes: 1; tumor size (cm): 2.3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 0; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 1; tumor size (cm): 7; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 0; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 4.8; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 7.071232877; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 2; tumor size (cm): 0.7; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 3.553424658; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 1.1; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 7.421917808; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 1; tumor size (cm): 1.3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 7.731506849; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 2.7; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 0.619178082; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 9; number positive nodes: 0; tumor size (cm): 5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 3.84109589; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 0; tumor size (cm): 0.9; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 0.254794521; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 7; number positive nodes: 0; tumor size (cm): 10; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 7.156164384; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 2.2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 2.44109589; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.9; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 7.421917808; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 2.1; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 1.073972603; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 2; tumor size (cm): 3.1; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 1.564383562; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 7; number positive nodes: 25; tumor size (cm): 3.2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 0.008219178; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 10; tumor size (cm): 1; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 10.99178082; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 1.8; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 1.731506849; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 6; number positive nodes: 8; tumor size (cm): 6; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 0.008219178; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 1; tumor size (cm): 2.3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 5.238356164; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 2.4; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 0.005479452; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 4.3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 1.753424658; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 0; tumor size (cm): 2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 2.301369863; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 1; tumor size (cm): 2.1; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 2.246575342; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 7; number positive nodes: 14; tumor size (cm): 6.3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 9.189041096; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 1; tumor size (cm): 3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 4.698630137; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 1.4; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 0.550684932; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 9; number positive nodes: 6; tumor size (cm): 7.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 4; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 1; tumor size (cm): 1.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 6.854794521; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 1.2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 0.005479452; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 0.673972603; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 0; tumor size (cm): 4; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 6.504109589; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 11; tumor size (cm): 1.3; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 0; time to distant recurrence (years): 7.347945205; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 1; tumor size (cm): 2.4; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 2.060273973; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: 0; tumor size (cm): 2.2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 7.44109589; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 0; tumor size (cm): 1.2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 11.59452055; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 7; number positive nodes: 0; tumor size (cm): 7; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 4.679452055; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 1.723287671; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 9; number positive nodes: 0; tumor size (cm): 2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 1.808219178; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 6; number positive nodes: 2; tumor size (cm): 1.8; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 3.145205479; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 8; number positive nodes: 11; tumor size (cm): 6; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 10.56712329; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): 1; time to distant recurrence (years): 4.021917808; distant recurrence indicator (1=yes, 0=no): 1; sbr grade: 7; number positive nodes: 2; tumor size (cm): 2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 2.046575342; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 1; tumor size (cm): 2.2; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 9.578082192; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 9; number positive nodes: NA; tumor size (cm): 2.5; ", "tissue: primary breast tumor; sample source: Guy's Hospital; er (0: negative): 0; pr (0: negative): 0; her2 (1: positive, 0: negative or equivocal): NA; time to distant recurrence (years): 9.578082192; distant recurrence indicator (1=yes, 0=no): 0; sbr grade: 8; number positive nodes: 0; tumor size (cm): 1.2; " GSE99225 Homo sapiens 8 Expression profiling by array GPL18451 Gene Expression Profile of Resistant vs Sensitive Breast Cancer Tissues to Taxane Treatment 2017-05-23 The present project aims to evaluate the gene expression profile of breast cancer tissue resistant to treatment with taxanes. Biopsies from tumor tissues were obtained from breast cancer patients without prior treatment. Histopathological analysis and ex vivo exposure to antineoplastic chemotherapeutics were carried out. Alamar Blue and lactate dehydrogenase release assays were performed for quantitative analysis of tumor viability after treatment and to asses the sensibility or resistant behaviour. Sensitive and resistant tumor tissues samples without prior exposure to therapeutic drugs were analyzed by gene expression microarrays. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99225 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA387596 https://www.ebi.ac.uk/ena/browser/view/PRJNA387596 None [Overal design]Two resistant and two sensitive samples were analyzed by duplicated (for a total of 8 microarrays). Total RNA was isolated using the Rneasy Plus mini kit (Qiagen) and converted to doble stranded cDNA by the cDNA synthesis kit system (Roche). Doble stranded DNAs were label with Cy3 and hybridized to Gene expression arrays 12x35k (Roche) which consist of aproximately 132k probes for 42k genes.; [Treatment]'Small tumor explants (4–5 mm in diameter and 250–300 um in thickness) were prepared using the Krumdieck slicing system. Tumor explants were culture in DMEM/F12 medium supplemented with 10% fetal bovine serum, 5 ug/mL bovine insulin, 100 ug/mL gentamicin, insulin-transferrin-selenium, and 25 mM glucose. The treatment of tumor explants with 20 μg/mL paclitaxol was performed after 1 h of preincubation.'; [Growth]'None'; [Extraction]'Biopsies stored at −80°C in RNAlater were used for the isolation of total RNA with the RNeasy Plus Mini kit (QIAGEN) according to the manufacturer’s instructions. RNA was quantified by absorbance at 260/280 nm and quality was evaluated using an Agilent 2100 Bioanalyzer and the RNA 6000 NanoChip kit (Agilent Technologies). Double stranded complementary DNA (ds-cDNA) was generated from 5 µg of RNA using the cDNA Synthesis Kit System (Roche Applied Science), and purified with the GenElute™ PCR Clean-up Kit (Sigma-Aldrich Quimica)'; [Cell type]'T3N4M0', 'T4bN2M0', 'T3N1M0', 'T2N1M0''gender: female; tissue: breast; cell type: T3N4M0; cell type: lobulillar infiltrating; cell type: Luminal A; ', 'gender: female; tissue: breast; cell type: T4bN2M0; cell type: Canalicular Infiltrating; cell type: Basal like; ', 'gender: female; tissue: breast; cell type: T3N1M0; cell type: Ductal Infiltrating; cell type: Luminal B; ', 'gender: female; tissue: breast; cell type: T2N1M0; cell type: Ductal Infiltrating; cell type: HER2+; ' GSE154682 Mus musculus 8 Expression profiling by high throughput sequencing GPL21103 CD95 suppresses immune infiltration in a model of triple negative breast cancer 2020-07-19 CD95 acts as an immune suppressor for TNBC tumors when grown in syngeneic mice. 4T1 cells were grown in two mouse strains. Comparisons included parental, a pool stably expressing vCas9 and two clones in which CD95/Fas was deleted using CRISPR-Cas9 gene editing, clone #54 and clone #69. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE154682 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA647186 https://www.ebi.ac.uk/ena/browser/view/PRJNA647186 https://www.ncbi.nlm.nih.gov/sra?term=SRP272474 [Overal design]Examination of differential gene mRNA expression in tumor with and without CD95 expression in NSG or Balb/c mice.; [Treatment]'4T1 cells were either wt or had CD95 knock out using CRISPR/Cas9'; [Growth]'4T1 cells were grown in either NSG or Balb/c mice (injected into the fat pad) for up to 20 days and tumors were harvested'; [Extraction]'Total RNA was isolated with QIAGEN miRNeasy kit; DNAse digestion was done\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'TNBC Breast cancer''cell type: TNBC Breast cancer; cell line: 4T1; mouse host strain: NSG; cell line genotype: parental; cell line phenotype: WT; ', 'cell type: TNBC Breast cancer; cell line: 4T1; mouse host strain: NSG; cell line genotype: stably expressing vCas9; cell line phenotype: WT; ', 'cell type: TNBC Breast cancer; cell line: 4T1; mouse host strain: NSG; cell line genotype: CD95/Fas knock out clone #54; cell line phenotype: CD95 KO; ', 'cell type: TNBC Breast cancer; cell line: 4T1; mouse host strain: NSG; cell line genotype: CD95 knock out clone #69; cell line phenotype: CD95 KO; ', 'cell type: TNBC Breast cancer; cell line: 4T1; mouse host strain: Balb/c; cell line genotype: parental; cell line phenotype: WT; ', 'cell type: TNBC Breast cancer; cell line: 4T1; mouse host strain: Balb/c; cell line genotype: stably expressing vCas9; cell line phenotype: WT; ', 'cell type: TNBC Breast cancer; cell line: 4T1; mouse host strain: Balb/c; cell line genotype: CD95 knock out clone #54; cell line phenotype: CD95 KO; ', 'cell type: TNBC Breast cancer; cell line: 4T1; mouse host strain: Balb/c; cell line genotype: CD95 knock out clone #69; cell line phenotype: CD95 KO; ' GSE103520 Homo sapiens 27 Expression profiling by high throughput sequencing GPL11154 Transcriptome-wide response to synthetic chromatin protein PcTF: Breast Cancer 2017-09-06 The goal of this study was to identify genes that become upregulated in response to a synthetic transcription factor, PcTF, in a panel of breast cancer model cell lines. PcTF contains a conserved H3K27me3-binding chromodomain expressed in-frame with an mCherry fluorescent tag and a VP64 activation domain. Therefore, we expected genes with H3K27me3-associated promoters to become upregulated upon PcTF expression. We observed that hundreds of genes became up or downregulated. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE103520 The synthetic histone-binding regulator protein PcTF activates interferon genes in breast cancer cells. BMC systems biology 2.048 https://doi.org/10.1186/s12918-018-0608-4 {BMC systems biology (2.048): 10.1186/s12918-018-0608-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA401827 https://www.ebi.ac.uk/ena/browser/view/PRJNA401827 https://www.ncbi.nlm.nih.gov/sra?term=SRP117021 [Overal design]MCF7, BT474, or BT549 cells were transfected with a plasmid that constitutively expressed the PcTF protein. 24, 48, and 72 hrs post-transfection, total mRNA was extracted from treated and untreated cells, as well as from untransfected MCF10A cells.; [Treatment]'Samples 1-6, 9-14, and 17-22 (transfections): DNA/Lipofectamine complexes contained 2 μg of plasmid DNA, 7.5 μl of Lipofectamine LTX (Invitrogen), 2.5 PLUS reagent, and 570 µl OptiMEM. Transfected cells were grown in pen/strep-free growth medium for 18 hrs. The transfection medium was replaced with fresh, pen/strep-supplemented medium and cells were grown for up to 72 hours). Controls (samples 7-8, 15-16, 23-24) were treated with vehicle only (Lipofectamine, PLUS, OptiMEM). Controls (samples 25-27) were not given any treatment.'; [Growth]'Cells were grown up to ~5.0E5 cells in 6-well plates at 37 deg. C in a 5% CO2 humidified incubator in the following media supplemented with 10% Tet-free FBS and 1% penicillin/ streptomycin: BT474 in Hybri-Care supplemented with 1.5 g/L sodium bicarbonate, BT549 in RPMI-1640 supplemented with 0.0008 mg/mL insulin, MCF7 in EMEM supplemented with 0.01 mg/mL insulin, MCF10A in MEGM BulletKit with all provided supplements except GA-1000. Pen/strep was omitted during transient transfections (to reduce toxicity) and replaced after 18 hours.'; [Extraction]'Total messenger RNA was extracted from ~90% confluent cells (~1-2x106). Cells were treated with Trypsin to remove them from the wells, collected into tubes, pelleted by centrifugation at 200 xg for 5 min. at room temperature, separated from the supernatant, and lysed in 500 μl TRIzol. TRIzol cell lysates were extracted with 100 μl chloroform and centrifuged at 12,000 xg for 15 min. at 4°C. RNA was column-purified from the aqueous phase (Qiagen RNeasy Mini kit 74104).\n50 ng of total RNA was used to prepare cDNA via single primer isothermal amplification using the Ovation RNA-Seq System (Nugen 7102-A01) and automated on the Apollo 324 liquid handler (Wafergen). cDNA was sheared to approximately 300 bp fragments using the Covaris M220 ultrasonicator. Libraries were generated using Kapa Biosystem’s library preparation kit (KK8201). In separate reactions, fragments from each replicate sample were end-repaired, A-tailed, and ligated to index and adapter fragments (Bioo, 520999). The adapter-ligated molecules were cleaned using AMPure beads (Agencourt Bioscience/Beckman Coulter, A63883), and amplified with Kapa’s HIFI enzyme. The library was analyzed on an Agilent Bioanalyzer, and quantified by qPCR (KAPA Library Quantification Kit, KK4835) before multiplex pooling and sequencing on a Hiseq 2000 platform (Illumina) at the ASU CLAS Genomics Core facility.'; [Cell type]'Source: ''cell line: BT-474 (ATCC HTB-20); protein: PcTF; treatment: transfection; time: 24 hrs; ', 'cell line: BT-474 (ATCC HTB-20); protein: PcTF; treatment: transfection; time: 48 hrs; ', 'cell line: BT-474 (ATCC HTB-20); protein: PcTF; treatment: transfection; time: 72 hrs; ', 'cell line: BT-474 (ATCC HTB-20); protein: PcTF; treatment: control (vehicle only); time: control; ', 'cell line: BT-549 (ATCC HTB-122); protein: PcTF; treatment: transfection; time: 24 hrs; ', 'cell line: BT-549 (ATCC HTB-122); protein: PcTF; treatment: transfection; time: 48 hrs; ', 'cell line: BT-549 (ATCC HTB-122); protein: PcTF; treatment: transfection; time: 72 hrs; ', 'cell line: BT-549 (ATCC HTB-122); protein: PcTF; treatment: control (vehicle only); time: control; ', 'cell line: MCF7 (ATCC HTB-22); protein: PcTF; treatment: transfection; time: 24 hrs; ', 'cell line: MCF7 (ATCC HTB-22); protein: PcTF; treatment: transfection; time: 48 hrs; ', 'cell line: MCF7 (ATCC HTB-22); protein: PcTF; treatment: transfection; time: 72 hrs; ', 'cell line: MCF7 (ATCC HTB-22); protein: PcTF; treatment: control (vehicle only); time: control; ', 'cell line: MCF 10A (ATCC CRL-10317); protein: PcTF; treatment: control (untreated); time: control; ' GSE66142 Homo sapiens 60 Expression profiling by array GPL6696; GPL9257; GPL19807 BMP-2 response pattern in human lung fibroblasts predicts outcome in lung adenocarcinomas 2015-02-20 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE66142 BMP2 response pattern in human lung fibroblasts predicts outcome in lung adenocarcinomas. BMC medical genomics 2.568 https://doi.org/10.1186/s12920-015-0090-4 {BMC medical genomics (2.568): 10.1186/s12920-015-0090-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA275957 https://www.ebi.ac.uk/ena/browser/view/PRJNA275957 None [Overal design]Refer to individual Series; [Treatment]'None', 'BMP stimulation experiments: For the experiment, 30?000 cells/cm2 were seeded in 3 ml of 5% FBS D-MEM and incubated for 6 h to allow attachment. The cells were washed extensively with phosphate-buffered saline and starved for 48 h in fresh low-serum D-MEM supplemented with 0.2% FBS. The cells were starved to reduce the effects of any stimulation from the regular cell culture medium. The medium was subsequently replaced with fresh low-serum D-MEM with or without 200 ng/ml BMP2 (human recombinant in Escherichia coli; Sigma Aldrich, St. Louis, MO, USA), 24 ng/ml BMP4, 200 ng/ml BMP7, 240 ng/ml Noggin or 1 ug/ml Gremlin. The cells were stimulated for 24 h, and the RNA was harvested to test the effects of BMP and their antagonists on mRNA expression patterns.'; [Growth]'None', "Primary human fibroblasts (CCL-171) and the human breast cancer cell lines MDA-MB-231 and T47D were obtained from the American Type Culture Collection (ATTC, Atlanta, Georgia, USA) on the 15. November 2005. After resuscitation the cells were propagated in Dulbecco's modified Eagle's medium (D-MEM, Invitrogen, Carlsbad, USA) supplemented with 10% heat-inactivated FBS (Invitrogen, Carlsbad, CA, USA), 4.5 g/l glucose, 4 mM L-glutamine, 100 U/ml penicillin and 100 ug/ml streptomycin (Gibco, Carlsbad, CA, USA). The cells were maintained by regular passages when confluence was reached and used for the experiments within 3-4 months. The study was approved by the Ethikkommission beider Basel, Switzerland (approval No. 271/05)."; [Extraction]'not provided', "RNA extraction and amplification: After aspirating the culture medium, the cell monolayer was washed once with phosphate-buffered saline. The cells were lysed in a buffer containing guanidine isothiocyanate (RLT buffer, QIAGEN, CA, USA). The total RNA was extracted with an RNeasy kit (QIAGEN, Valencia, CA, USA) according to the manufacturer?s instructions. The RNA concentration was measured with a NanoDrop system spectrophotometer (ND-1000 Spectrophotometer Technologies, Wilmington, NC, USA). The integrity of extracted RNA was assessed by electrophoresis in a 1% agarose gel in MOPS buffer. For mRNA amplification, an Amino Allyl MasageAmp II aRNA Amplification Kit was used (Ambion, Austin, TX, USA). The amplification of mRNA from 500 ng total RNA, purification of the cDNA, in vitro transcription and purification of aRNA were performed according to the manufacturer's instructions. The integrity and quantity of the amplified RNA were verified as described above."; [Cell type]'Source: ''reference: stratagene universal reference; ', 'cell line: MDA-MB-231; ', 'cell line: T47D; ', 'cell line: CCL171; ', 'cell line: CCL-171; ' GSE114600 Homo sapiens 193 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by genome tiling array GPL13534; GPL18573 TRPS1 is a lineage-specific transcriptional dependency in breast cancer 2018-05-17 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE114600 TRPS1 Is a Lineage-Specific Transcriptional Dependency in Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2018.10.023 {Cell reports (7.815): 10.1016/j.celrep.2018.10.023} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA471878 https://www.ebi.ac.uk/ena/browser/view/PRJNA471878 None [Overal design]Refer to individual Series; [Treatment]'Were indicated as "dox+", cells were treated with 100 ng/ml of doxycycline.'; [Growth]'HCC3153 cells were cultured in RPMI1640 supplemented with 10% FBS and 1% penicillin/streptomycin. MDA-IBC3 and SUM159 cells were cultured in a 1:1 mixture of DMEM/F12 supplemented with 10% FBS and 1% penicillin/streptomycin and Human Mammary Epithelial Cell Medium. For genomic profiling, 59 cell lines were grown in corresponding media described in Table S1.', '59 cell lines were grown in corresponding media described in Table S1'; [Extraction]'For RNA-seq total RNA was extracted using the RNeasy Kit (Qiagen). For ChIP-seq 5-8 × 10^6 cells were fixed by adding 1:20 volume of fixing buffer (11% paraformaldehyde (Electron Microscopy Sciences, cat# 15714), 0.1M NaCl, 1mM EDTA pH 8.0, 50mM HEPES pH 8.0) directly to the tissue culture medium for 10 min at room temperature for histone modification ChIPs or at 37°C for transcription factor ChIPs and subsequently quenched by glycine. Cells were lysed in lysis buffer (50mM HEPES pH 8.0, 140mM NaCl, 1mM EDTA, 10% glycerol, 0.5% NP-40, and 0.25% Triton X-100) for 10 min at 4°C. Nuclei were pelleted and washed in wash buffer (10mM Tris-HCl pH 8.0, 200mM NaCl, 1mM EDTA, 0.5mM EGTA) for 10 min at 4°C and then pelleted and resuspended shearing buffer (10mM Tris-HCl pH 7.4, 1mM EDTA, 0.1% SDS, 1% Triton X-100, 0.1% sodium deoxycholate, 0.25% sarkosyl, 1mM DTT) and sonicated in a Covaris sonicator. Debris was removed by centrifugation (5 min at 10,000g) and 970µl of the lysate was mixed with 30µl of 5M NaCl. Chromatin was pre-cleared for 1 hr at 4°C with 40µl of Dynabeads Protein G (LifeTechnologies, cat# 10003D) washed in 0.5% BSA in PBS. Lysates were then incubated with corresponding primary antibody overnight at 4°C. Complexes were precipitated by incubation with 40µl of washed Dynabeads Protein G for 2 hrs at 4°C, washed with low salt wash buffer (20mM Tris-HCl pH 8.0, 150mM NaCl, 2mM EDTA pH 8.0, 1% Triton X-100, 0.1% SDS), high salt wash buffer (20mM Tris-HCl pH 8.0, 500mM NaCl, 2mM EDTA pH 8.0, 1% Triton X-100, 0.1% SDS), LiCl wash buffer (10mM Tris-HCl pH 8.0, 250mM LiCl, 1mM EDTA pH 8.0, 1% NP40, 1% sodium deoxycholate), and twice with TE pH 8.0. DNA was eluted in elution buffer (100mM NaHCO3, 1% SDS) by incubating overnight at 65°C, followed by 30 min treatment with RNase A at 37°C and 2 hrs treatment with proteinase K at 55°C. DNA was purified with phenol-chloroform extraction and precipitated with isopropanol. For methylation analysis, DNA was isolated using QIAamp DNA Mini kit (QIAGEN, cat# 51304). DNA methylation profiling was carried out on Infinium HumanMethylation450K BeadChip arrays (Illumina, discontinued) at the Harvard Medical School-Partners HealthCare Center for Genetics and Genomics.\nRNA-seq libraries were prepared using Illumina TruSeq Stranded mRNA sample preparation kits from 500 ng of purified total RNA according to the manufacturer’s protocol. The finished dsDNA libraries were quantified by Qubit fluorometer, Agilent TapeStation 2200, and RT-qPCR using the Kapa Biosystems library quantification kit according to manufacturer’s protocols. ChIP-seq libraries were prepared using the Rubicon ThruPLEX DNA-seq Kit from purified ChIP DNA or input DNA according to the manufacturer’s protocol.', 'DNA was isolated using QIAamp DNA Mini kit (QIAGEN, cat# 51304)'; [Cell type]'Source: ''cell line: HCC3153; hairpin: shTRPS1-1; treatment: No Dox; days: 3; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: Dox; days: 3; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: No Dox; days: 4; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: Dox; days: 4; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: No Dox; days: 5; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: Dox; days: 5; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: No Dox; days: 3; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: Dox; days: 3; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: No Dox; days: 4; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: Dox; days: 4; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: No Dox; days: 5; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: Dox; days: 5; ', 'cell line: SUM159; hairpin: shTRPS1-1; treatment: No Dox; days: 3; ', 'cell line: SUM159; hairpin: shTRPS1-1; treatment: Dox; days: 3; ', 'cell line: SUM159; hairpin: shTRPS1-1; treatment: No Dox; days: 4; ', 'cell line: SUM159; hairpin: shTRPS1-1; treatment: Dox; days: 4; ', 'cell line: SUM159; hairpin: shTRPS1-1; treatment: No Dox; days: 5; ', 'cell line: SUM159; hairpin: shTRPS1-1; treatment: Dox; days: 5; ', 'cell line: SUM159; hairpin: shTRPS1-2; treatment: No Dox; days: 3; ', 'cell line: SUM159; hairpin: shTRPS1-2; treatment: Dox; days: 3; ', 'cell line: SUM159; hairpin: shTRPS1-2; treatment: No Dox; days: 4; ', 'cell line: SUM159; hairpin: shTRPS1-2; treatment: Dox; days: 4; ', 'cell line: SUM159; hairpin: shTRPS1-2; treatment: No Dox; days: 5; ', 'cell line: SUM159; hairpin: shTRPS1-2; treatment: Dox; days: 5; ', 'cell line: COG-N-278; ', 'cell line: NLF; ', 'cell line: COG-N-367; ', 'cell line: FC-IBC02; ', 'cell line: COG-N-305; ', 'cell line: LS; ', 'cell line: SMS-KCN; ', 'cell line: Blin1; ', 'cell line: PMC42; ', 'cell line: MHH-NB-11; ', 'cell line: MOLM14; ', 'cell line: UOCB1; ', 'cell line: HCC3153; ', 'cell line: NGP; ', 'cell line: TM87; ', 'cell line: HCA2; ', 'cell line: HCA24; ', 'cell line: HCT116WT; ', 'cell line: HCT116HET; ', 'cell line: HCT116KO; ', 'cell line: KOPT-K1; ', 'cell line: Nalm14; ', 'cell line: CHP-126; ', 'cell line: CHP-134; ', 'cell line: NB69; ', 'cell line: SMS-SAN; ', 'cell line: C4-2; ', 'cell line: C4-2B; ', 'cell line: CWR22Rv1; ', 'cell line: LAPC-4; ', 'cell line: VCaP; ', 'cell line: 2004; ', 'cell line: BT12; ', 'cell line: TTC 549; ', 'cell line: TTC 642; ', 'cell line: TTC 709; ', 'cell line: SUM149R; ', 'cell line: SUM159R; ', 'cell line: LNCaP; ', 'cell line: LNCaP-abl; ', 'cell line: UACC3199; ', 'cell line: MDA-IBC-3; ', 'cell line: C32; ', 'cell line: C80; ', 'cell line: C99; ', 'cell line: HCA-7; ', 'cell line: LIM1899; ', 'cell line: LIM2405; ', 'cell line: LIM2551; ', 'cell line: SW1222; ', 'cell line: BE(2)-C; ', 'cell line: GI-ME-N; ', 'cell line: Kelly; ', 'cell line: 21NT; ', 'cell line: 21PT; ', 'cell line: 21MT1; ', 'cell line: 21MT2; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: No Dox; chip antibody: H3K27me3; chip antibody info: abcam, cat# ab6002, lot GR275911-2; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: Dox; chip antibody: H3K27me3; chip antibody info: abcam, cat# ab6002, lot GR275911-2; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: No Dox; chip antibody: H3K27me3; chip antibody info: abcam, cat# ab6002, lot GR275911-2; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: Dox; chip antibody: H3K27me3; chip antibody info: abcam, cat# ab6002, lot GR275911-2; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: No Dox; chip antibody: GATAD2A; chip antibody info: abcam, cat# ab87663, lot GR252789-14; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: Dox; chip antibody: GATAD2A; chip antibody info: abcam, cat# ab87663, lot GR252789-14; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: No Dox; chip antibody: GATAD2A; chip antibody info: abcam, cat# ab87663, lot GR252789-14; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: Dox; chip antibody: GATAD2A; chip antibody info: abcam, cat# ab87663, lot GR252789-14; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: No Dox; chip antibody: GATAD2B; chip antibody info: Bethyl, cat# A301-283A; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: Dox; chip antibody: GATAD2B; chip antibody info: Bethyl, cat# A301-283A; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: No Dox; chip antibody: GATAD2B; chip antibody info: Bethyl, cat# A301-283A; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: Dox; chip antibody: GATAD2B; chip antibody info: Bethyl, cat# A301-283A; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: No Dox; chip antibody: H3K27ac; chip antibody info: Diagenode, cat# C15410196, lot A1723-0041D; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: Dox; chip antibody: H3K27ac; chip antibody info: Diagenode, cat# C15410196, lot A1723-0041D; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: No Dox; chip antibody: H3K27ac; chip antibody info: Diagenode, cat# C15410196, lot A1723-0041D; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: Dox; chip antibody: H3K27ac; chip antibody info: Diagenode, cat# C15410196, lot A1723-0041D; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: No Dox; chip antibody: TRPS1; chip antibody info: Bethyl, cat# A303-563A; ', 'cell line: HCC3153; hairpin: shTRPS1-1; treatment: Dox; chip antibody: TRPS1; chip antibody info: Bethyl, cat# A303-563A; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: No Dox; chip antibody: TRPS1; chip antibody info: Bethyl, cat# A303-563A; ', 'cell line: HCC3153; hairpin: shTRPS1-2; treatment: Dox; chip antibody: TRPS1; chip antibody info: Bethyl, cat# A303-563A; ', 'cell line: SUM159; chip antibody: TRPS1; chip antibody info: Bethyl, cat# A303-563A; ', 'cell line: MDA-IBC3; chip antibody: TRPS1; chip antibody info: Bethyl, cat# A303-563A; ', 'cell line: X2004; ', 'cell line: X21MT1; ', 'cell line: X21MT2; ', 'cell line: X21NT; ', 'cell line: X21PT; ', 'cell line: BE.2..C; ', 'cell line: C4.2; ', 'cell line: C4.2B; ', 'cell line: CHP.126; ', 'cell line: CHP134; ', 'cell line: COG.N.278; ', 'cell line: COG.N.305; ', 'cell line: COG.N.367; ', 'cell line: CWR_22RV1; ', 'cell line: FC.IBC02; ', 'cell line: GI.ME.N; ', 'cell line: HCA7; ', 'cell line: KOPT.K1; ', 'cell line: LAPC.4; ', 'cell line: LNCaP.abl; ', 'cell line: MDA.IBC.3; ', 'cell line: MHH.NB.11; ', 'cell line: SMS.KCN; ', 'cell line: SMS.SAN; ', 'cell line: SUM.149R_wo_JQ1; ', 'cell line: SUM149; ', 'cell line: SUM159.JQR; ', 'cell line: SUM.159R_wo_JQ1; ', 'cell line: SUM159; ', 'cell line: TTC549; ', 'cell line: TTC642; ', 'cell line: TTC709; ', 'cell line: UACC.3199; ', 'cell line: HCC3153; hairpin: shTRPS1; antibody: HDAC2; antibody info: abcam, cat# ab12169, lot GR319565-3; ', 'cell line: HCC3153; hairpin: shTRPS1; antibody: MTA2; antibody info: abcam, cat# ab8106, lot GR280090-7; ' GSE112094 Mus musculus 9 Expression profiling by high throughput sequencing GPL17021 RNA-seq identifies autophagy as the most prevalent upregulated pathway in dormant breast cancer cells 2018-03-20 Purpose: The goal of this study is to evaluate the transcriptome profiling (RNA-seq) of dormant and proliferating breast cancer cells using an in vitro 3D model Methods: mRNA profiles of D2.0R cells growing either on basal membrane extracts (BME) (dormant phase) or BME + Collagen (COL) (proliferative phase) at days 1 or 5 of culture were generated by deep sequencing in triplicate with Ilumina HiSeq2500 using Illumina TruSeq V4. Aligned reads (BAM files) were analysed using PartekFlow software for differential expression and gene enrichment analysis. Comparisons used Partek Gene Specific Analysis (GSA) algorithm and multiple comparisons were corrected using False Discovery Rate (FDR), which was set at 0.05 Results: Using an optimized data analysis workflow, we mapped about 118 – 133 million reads per sample to the mouse genome (build mm9). Total alignment with reference genome is between 81-90%. RNA-seq identified 5,524 transcripts showing differential expression between the D2.0R cells cultured on BME + COL vs D2.0R cells cultured on BME matrices at day 5, with a fold change ≥1.5 or ≤-1.5 and p value <0.05. On the other hand, only 1,097 were found to be differentially expressed between D2.0R cells growing on BME matrices at day 5 and day 1, with a fold change ≥1.5 or ≤-1.5 and p value <0.05. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to breast cancer dormancy and identifies autophagy as a top biological process activated in dormant D2.0R cells. Conclusions: Our study represents a detailed analysis of the transcriptomes of dormant and proliferating D2.0R cells, with three biologic replicates, generated by RNA-seq technology. RNA-seq based transcriptome characterization identifies autophagy as the most prevalent upregulated pathway in dormant breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112094 Autophagy promotes the survival of dormant breast cancer cells and metastatic tumour recurrence. Nature communications 11.878 https://doi.org/10.1038/s41467-018-04070-6 {Nature communications (11.878): 10.1038/s41467-018-04070-6} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA439284 https://www.ebi.ac.uk/ena/browser/view/PRJNA439284 https://www.ncbi.nlm.nih.gov/sra?term=SRP136107 [Overal design]mRNA profiles of D2.0R cells after culture on BME or BME + COL matrices for 1 or 5 days were generated by deep sequencing in triplicate with Ilumina HiSeq2500 using Illumina TruSeq V4.; [Treatment]'N/A'; [Growth]'Cell culture surfaces were coated with either BME or BME + COL. Cells were resuspended in DMEM low glucose supplemented with 2% FBS and 2% Cultrex or 2% FBS supplemented with Cultrex + COL. Cells were grown for either 1 or 5 days at 37°C and 5% CO2'; [Extraction]'RNA was extracted using the RNeasy kit (Qiagen) following the manufacturer’s instructions. The quality and quantity of extracted total RNA was assessed using TapeStation 2200 (Agilent)\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'D2.0R''cell type: D2.0R; condition: Grown on BME; days in culture: 1; ', 'cell type: D2.0R; condition: Grown on BME; days in culture: 5; ', 'cell type: D2.0R; condition: Grown on BME + COL; days in culture: 5; ' GSE94695 Homo sapiens 3 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL18602 Oncoscan for subclonal analysis in a lobular breast cancer with classical and solid growth pattern mimicking a solid-papillary carcinoma 2017-02-08 Affymetrix Oncoscan arrays were performed according to the manufacturer's directions on DNA extracted from FFPE-breast cancer tissues. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE94695 Subclonal analysis in a lobular breast cancer with classical and solid growth pattern mimicking a solid-papillary carcinoma. The journal of pathology. Clinical research 2.346 https://doi.org/10.1002/cjp2.76 {The journal of pathology. Clinical research (2.346): 10.1002/cjp2.76} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA371830 https://www.ebi.ac.uk/ena/browser/view/PRJNA371830 None [Overal design]Copy number analysis using Affymetrix Oncoscan arrays was performed for 3 parts of the tumor; [Treatment]'none'; [Growth]'primary formalin fixed parafffin embedded tissue'; [Extraction]'genomic DANN was extracted from macrodissected with DNAeasy blood and tissue kit (Qiagen)'; [Cell type]'Source: ''tag: breast tumor tissue; ' GSE112962 Homo sapiens 9 Expression profiling by high throughput sequencing GPL16791 Endogenous interaction profiling identifies DDX5 as an oncogenic coactivator of transcription factor Fra-1 [RNA-seq] 2018-04-11 Fra-1, a member of the activator protein 1 (AP-1) family, is overexpressed in triple-negative breast cancer (TNBC) and plays crucial roles in tumor progression. However, a systematic analysis of the composition of the Fra-1 protein network specifically on chromatin is still missing. Here we performed endogenous purification of Fra-1 transcriptional complex under ChIP conditions, followed by mass spectrometry, to identify chromatin-bound partners of Fra-1 in TNBC cells. This study allowed the identification of 118 interactors, highlighting DDX5 as the high ranking of Fra-1 interacting proteins. DDX5, a previously unrecognized protein in the network, is recruited globally to Fra-1 binding sites and shares a substantial set of Fra-1 target genes required for the TNBC cell growth. We provide evidence that DDX5 expression enhances Fra-1 transcriptional activity, thereby enhancing Fra-1-driven tumorigenesis. By integrating ChIP-seq and RNA-seq, we show that DDX5 target gene signature predicts poor clinical outcome in breast cancer patients. DDX5 protein level was higher in triple-negative basal like tumors than in non-basal like tumors, including luminal A, luminal B and HER2-enriched subtypes. Collectively, this comprehensive Fra-1 interaction profiling provides a broad and deep view of Fra-1 chromatin interaction landscape, which will help in deciphering mechanisms of AP-1 regulation of gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112962 Endogenous interaction profiling identifies DDX5 as an oncogenic coactivator of transcription factor Fra-1. Oncogene 6.634 https://doi.org/10.1038/s41388-019-0824-4 {Oncogene (6.634): 10.1038/s41388-019-0824-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA449623 https://www.ebi.ac.uk/ena/browser/view/PRJNA449623 https://www.ncbi.nlm.nih.gov/sra?term=SRP139509 [Overal design]Examination of genes regulated by knockdown of Fra-1 or DDX5 in BT549 cells; [Treatment]'No treatment'; [Growth]'Cells were maintained in RPMI 1640 supplemented with 10% FBS.'; [Extraction]'Total RNA was extracted using RNeasy Mini Kit (Qiagen, Valencia, CA).\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'ERalpha-negtive breast cancer cells''cell line: BT549; cell type: ERalpha-negtive breast cancer cells; genotype/variation: control; ', 'cell line: BT549; cell type: ERalpha-negtive breast cancer cells; genotype/variation: Fra-1 knockdown; ', 'cell line: BT549; cell type: ERalpha-negtive breast cancer cells; genotype/variation: DDX5 knockdown; ' GSE129111 Homo sapiens 58 Expression profiling by high throughput sequencing GPL18573 Spatial control of oxygen delivery to 3D cultures alters cancer cell growth and gene expression 2019-04-01 Commonly used monolayer cell cultures lack the capacity to provide a physiologically relevant environment for cell culture in terms of cell-cell architecture, extracellular matrix composition, and spatiotemporal delivery of key growth factors and small molecules, such as oxygen. Here, we describe a three-dimensional (3D) approach to cell culture in vitro, utilizing a bioreactor system designed to control oxygenation of 3D cancer cell cultures, in order to better mimic tumor microenvironments observed in vivo. We found transcriptomic differences in breast and ovarian cancer cell cultures grown in traditional monolayer cultures as compared to cultures grown in a Matrigel three-dimensional matrix. We also investigated the transcriptomes of 3D cultures grown in 21% O2, 3% O2, and a gradient of 3% O2 to 0% O2 using our bioreactor system. By controlling oxygen delivery, we observed differences in cell growth morphology and transcriptome regulation under the three conditions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE129111 Spatial control of oxygen delivery to three-dimensional cultures alters cancer cell growth and gene expression. Journal of cellular physiology 4.522 https://doi.org/10.1002/jcp.28665 {Journal of cellular physiology (4.522): 10.1002/jcp.28665} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA530150 https://www.ebi.ac.uk/ena/browser/view/PRJNA530150 https://www.ncbi.nlm.nih.gov/sra?term=SRP189994 [Overal design]Examination of the effects of oxygenation gradients on 3D cancer cell cultures grown in a bioreactor. 3D cell cultures grown in 3% oxygen, 21% oxygen, and gradient oxygen are examined and compared to cells grown in 2D 21% oxygen. MCF-7 and OVCAR-8 cell lines are investigated.; [Treatment]'2D cultures were grown in 21% oxygen. 3D cultures were exposed to one of three oxygen conditions: 3% oxygen, 21% oxygen, or gradient oxygen (bioreactor condition).'; [Growth]'For both cell lines: 2D cultures were grown in T-75 polystyrene culture flasks, allowing cells to reach approximately 80% confluency. Dulbecco’s Modified Eagle Medium (DMEM) 1X was supplemented with 10% fetal bovine serum (FBS) (Atlanta Biologicals, Lawrenceville, GA), penicillin (100 units/mL), streptomycin (100 μg/mL), and L-glutamine (2 mM), which were purchased from Life Technologies (Carlsbad, CA) and used as received. 3D cultures were plated in Matrigel (Corning Life Sciences, Bedford, MA) 3 mg/mL at a density of 6x10^4 per well. The same 10% FBS media was used. 3D cultures were exposed to one of three oxygen conditions: 3% oxygen, 21% oxygen, or gradient oxygen.'; [Extraction]'Total RNA was extracted using Qiagen Rneasy Mini Kit.\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'Source: ''cell line: MCF-7; tissue source: Invasive ductal carcinoma; culture dimension: 2D (polystyrene); culture condition: 21% Oxygen; library prep kit: Illumina NeoPrepTM Library Prep System (Ref: 20003841); ', 'cell line: MCF-7; tissue source: Invasive ductal carcinoma; culture dimension: 3D (Matrigel); culture condition: 3% Oxygen; library prep kit: Illumina NeoPrepTM Library Prep System (Ref: 20003841); ', 'cell line: MCF-7; tissue source: Invasive ductal carcinoma; culture dimension: 3D (Matrigel); culture condition: 21% Oxygen; library prep kit: Illumina NeoPrepTM Library Prep System (Ref: 20003841); ', 'cell line: MCF-7; tissue source: Invasive ductal carcinoma; culture dimension: 3D (Matrigel); culture condition: Gradient Oxygen; library prep kit: Illumina NeoPrepTM Library Prep System (Ref: 20003841); ', 'cell line: OVCAR-8; tissue source: High grade ovarian serous adenocarcinoma; culture dimension: 2D (polystyrene); culture condition: 21% Oxygen; library prep kit: TruSeq Stranded mRNA Library Prep Kit (RS-122-2101); ', 'cell line: OVCAR-8; tissue source: High grade ovarian serous adenocarcinoma; culture dimension: 3D (Matrigel); culture condition: 3% Oxygen; library prep kit: TruSeq Stranded mRNA Library Prep Kit (RS-122-2101); ', 'cell line: OVCAR-8; tissue source: High grade ovarian serous adenocarcinoma; culture dimension: 3D (Matrigel); culture condition: 21% Oxygen; library prep kit: TruSeq Stranded mRNA Library Prep Kit (RS-122-2101); ', 'cell line: OVCAR-8; tissue source: High grade ovarian serous adenocarcinoma; culture dimension: 3D (Matrigel); culture condition: Gradient Oxygen; library prep kit: TruSeq Stranded mRNA Library Prep Kit (RS-122-2101); ', 'cell line: OVCAR-8; tissue source: High grade ovarian serous adenocarcinoma; culture dimension: 2D (polystyrene); culture condition: 21% Oxygen; library prep kit: Illumina NeoPrepTM Library Prep System (Ref: 20003841); ', 'cell line: OVCAR-8; tissue source: High grade ovarian serous adenocarcinoma; culture dimension: 3D (Matrigel); culture condition: 3% Oxygen; library prep kit: Illumina NeoPrepTM Library Prep System (Ref: 20003841); ', 'cell line: OVCAR-8; tissue source: High grade ovarian serous adenocarcinoma; culture dimension: 3D (Matrigel); culture condition: 21% Oxygen; library prep kit: Illumina NeoPrepTM Library Prep System (Ref: 20003841); ', 'cell line: OVCAR-8; tissue source: High grade ovarian serous adenocarcinoma; culture dimension: 3D (Matrigel); culture condition: Gradient Oxygen; library prep kit: Illumina NeoPrepTM Library Prep System (Ref: 20003841); ' GSE106144 Homo sapiens 4 Expression profiling by array GPL6244; GPL17586 Differences of gene expression profiling of breast cancer cells with stable SREBP1 knockdown and the control cells 2017-10-25 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE106144 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA415724 https://www.ebi.ac.uk/ena/browser/view/PRJNA415724 None [Overal design]Refer to individual Series; [Treatment]'MCF-7 cells were stably knocked down of SREBP1 and the control cells', 'MDA-MB-231 cells were stably knocked down of SREBP1 and the control cells'; [Growth]'MCF-7 cells were cultured in DMEM/high glucose supplemented with 10% FBS and streptomycin and penicillin.', 'MDA-MB-231 cells were cultured in DMEM/high glucose supplemented with 10% FBS and streptomycin and penicillin.'; [Extraction]'Total RNA was extracted and purified using miRNeasy Mini Kit and RNase-Free Dnase Set.'; [Cell type]'breast cancer cells', 'Source: ''cell line: MCF-7; cell type: breast cancer cells; genotype/variation: stablely transfected with pLKO.1 vector; ', 'cell line: MCF-7; cell type: breast cancer cells; genotype/variation: stablely transfected with pLKO.1-shSREBP vector; ', 'cell line: MDA-MB-231; genotype: control; ', 'cell line: MDA-MB-231; genotype: SREBP1 KD; ' GSE24117 Homo sapiens 213 Expression profiling by array GPL2986 In Silico ascription of gene expression differences to tumor and stromal cells in a model to study impact on breast cancer outcome 2010-09-14 We present a method for identifying and ascribing differentially expressed genes to tumor epithelial and/or stromal cells, by utilizing pathologic information and weighted t-statistics https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24117 In silico ascription of gene expression differences to tumor and stromal cells in a model to study impact on breast cancer outcome. PloS one 2.776 https://doi.org/10.1371/journal.pone.0014002 {PloS one (2.776) doi:10.1371/journal.pone.0014002}; {Clinical cancer research : an official journal of the American Association for Cancer Research (None) doi:10.1158/1078-0432.CCR-14-0458}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA130051 https://www.ebi.ac.uk/ena/browser/view/PRJNA130051 None [Overal design]Sets of differentially expressed gene-probes were identified in tumors from patients who developed distant metastasis compared with those who did not, by weighing the contribution from each tumor with the relative content of stromal and tumor epithelial cells in their individual tumor specimen. The analyses were performed under various assumptions of mRNA transcription level from tumor epithelial cells compared with stromal cells. Supplementary files: Human_AB1700_Annotations_09_06.txt: This file includes control probes and obsolete probes not listed in GPL2986. Raw_data.txt: This file includes control probes not listed in GPL2986.; [Treatment]'Primary breast tumors were collected after mastectomy. Fresh frozen and kept in storage at minus 80 degrees celcius.'; [Growth]'None'; [Extraction]'Approximately 40 mg of tissue was used for total RNA extraction using the Qiagen Midi kit Extraction column procedure (Qiagen) after homogenisation using the Mixer Mill (MM301, Retsch). RNA quality was assessed using the NanoDrop instrument (concentration and purity), and the Agilent Bioanalyser instrument (degradation). Samples showing a degradation factor > 20 % were excluded from further analyses: the remaining 218 RNA samples of good quality were stored at -80C'; [Cell type]'Source: ''assayname: Signal_HB009HA_7/12/06_9:45_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 65.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009H8_7/20/06_11:41_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 50.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009H7_7/11/06_9:59_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 70.0; tumor-stroma %: 10.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009H6_7/19/06_9:37_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 35.0; adipocyte cells%: 0.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009H5_7/19/06_9:51_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 80.0; tumor-stroma %: 20.0; adipocyte cells%: 0.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009H4_7/19/06_10:39_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 35.0; tumor-stroma %: 45.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009H3_7/11/06_10:15_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 30.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009H2_7/12/06_10:36_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 30.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009H1_7/11/06_11:11_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: NA; tumor-stroma %: NA; adipocyte cells%: NA; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009H0_7/11/06_8:42_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: NA; tumor-stroma %: NA; adipocyte cells%: NA; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009BO_10/24/06_10:38_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: NA; tumor-stroma %: NA; adipocyte cells%: NA; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009GY_7/11/06_9:15_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 12.5; tumor-stroma %: 40.0; adipocyte cells%: 47.5; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009GX_7/19/06_11:28_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 25.0; tumor-stroma %: 55.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009GW_7/19/06_10:58_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 25.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009GV_7/12/06_10:53_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 30.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009GT_7/11/06_10:53_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 20.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009GS_7/11/06_9:36_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 30.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009GR_7/20/06_10:17_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 30.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009GQ_7/12/06_10:20_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 35.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009GP_7/12/06_11:26_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 45.0; tumor-stroma %: 45.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0064K_5/3/06_10:28_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 30.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009GO_7/20/06_10:47_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 30.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009GN_7/19/06_10:21_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 25.0; tumor-stroma %: 40.0; adipocyte cells%: 35.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008N3_2/22/06_2:03_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 25.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009GM_7/19/06_10:05_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 25.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009GL_7/20/06_9:49_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 35.0; tumor-stroma %: 45.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009GK_7/20/06_11:56_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 20.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009GJ_7/20/06_11:26_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 35.0; tumor-stroma %: 40.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009GI_7/12/06_9:31_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 27.5; tumor-stroma %: 37.5; adipocyte cells%: 35.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009GH_7/20/06_11:12_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009GG_7/20/06_10:33_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 25.0; tumor-stroma %: 75.0; adipocyte cells%: 0.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009GF_7/12/06_10:02_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 15.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009GE_7/11/06_10:34_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 45.0; adipocyte cells%: 0.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB009GD_7/19/06_11:42_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 25.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009BQ_10/24/06_10:07_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 25.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB004JN_1/18/06_1:01_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 45.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009BP_10/24/06_10:55_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 45.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB009BM_2/15/06_12:51_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 35.0; tumor-stroma %: 55.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008OD_6/8/06_11:41_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 20.0; tumor-stroma %: 55.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008N6_2/15/06_2:13_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 25.0; tumor-stroma %: 50.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006X6_2/24/06_11:11_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 25.0; tumor-stroma %: 50.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008OB_10/18/06_10:43_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 25.0; tumor-stroma %: 50.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008O9_10/24/06_12:48_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 45.0; tumor-stroma %: 50.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0064I_2/15/06_11:56_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 30.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008O8_10/24/06_12:21_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 30.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008O6_10/18/06_10:14_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 25.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008O3_10/24/06_10:24_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 20.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008O2_10/18/06_10:29_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 25.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008NG_2/15/06_1:58_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 25.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008NZ_10/18/06_11:44_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 25.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008NX_10/18/06_12:04_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008NW_8/16/06_11:31_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 40.0; adipocyte cells%: 30.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008NT_10/18/06_10:58_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 30.0; adipocyte cells%: 30.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008NQ_8/16/06_10:51_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 25.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008NP_10/18/06_12:26_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 75.0; tumor-stroma %: 20.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006X1_2/3/06_12:03_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 70.0; tumor-stroma %: 22.5; adipocyte cells%: 7.5; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008NO_8/16/06_11:51_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 70.0; tumor-stroma %: 22.5; adipocyte cells%: 7.5; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008NJ_2/22/06_12:44_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 35.0; adipocyte cells%: 35.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008NI_5/3/06_12:26_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 70.0; tumor-stroma %: 25.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008NH_8/16/06_9:41_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008NF_5/4/06_12:17_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008NE_8/16/06_9:57_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 70.0; tumor-stroma %: 20.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008ND_2/22/06_12:59_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 30.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061W_3/14/06_1:46_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 30.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008NC_8/16/06_10:12_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 35.0; adipocyte cells%: 0.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008NB_5/3/06_12:41_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 45.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008NA_2/22/06_11:14_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 45.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008N8_5/4/06_10:33_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 25.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008N7_5/4/06_12:01_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 30.0; adipocyte cells%: 40.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008N4_2/22/06_2:18_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 45.0; tumor-stroma %: 25.0; adipocyte cells%: 30.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008N2_2/15/06_1:42_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 20.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008N1_2/15/06_1:27_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 35.0; tumor-stroma %: 25.0; adipocyte cells%: 40.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB008I5_8/15/06_10:28_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 35.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB008HW_8/15/06_10:12_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 40.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006XF_2/3/06_1:57_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 25.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006XE_3/1/06_12:40_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 30.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006XD_3/1/06_1:29_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 20.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0064M_2/22/06_11:33_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 25.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006XC_3/1/06_12:56_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 25.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006XB_6/7/06_10:31_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 20.0; adipocyte cells%: 30.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006XA_2/3/06_10:56_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 35.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006X9_2/24/06_12:52_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 40.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JT_6/15/06_1:25_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 40.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006X7_2/24/06_10:56_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 25.0; tumor-stroma %: 30.0; adipocyte cells%: 45.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006X5_3/1/06_2:09_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 35.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006X4_2/3/06_1:10_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 80.0; tumor-stroma %: 10.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006X3_3/1/06_1:44_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 25.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006X2_3/1/06_1:12_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 45.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006X0_6/7/06_12:07_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 75.0; tumor-stroma %: 20.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006WZ_6/7/06_10:01_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 70.0; tumor-stroma %: 25.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006WY_6/7/06_9:42_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 45.0; tumor-stroma %: 30.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006WX_6/7/06_12:21_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 35.0; tumor-stroma %: 45.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006WV_3/1/06_11:14_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006WU_2/3/06_1:26_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 40.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006T1_5/3/06_11:56_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 40.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006SZ_3/15/06_1:02_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 45.0; tumor-stroma %: 40.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006SV_5/3/06_12:11_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 45.0; adipocyte cells%: 0.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006SP_3/15/06_11:24_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 20.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006SM_3/15/06_1:16_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 85.0; tumor-stroma %: 5.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006JX_6/29/06_11:57_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 80.0; tumor-stroma %: 12.5; adipocyte cells%: 7.5; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JW_6/30/06_10:53_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 70.0; tumor-stroma %: 22.5; adipocyte cells%: 7.5; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JV_6/29/06_10:34_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 35.0; tumor-stroma %: 50.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JU_8/9/06_12:07_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 35.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0060Z_2/24/06_12:21_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 15.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006JS_6/15/06_11:48_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 15.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006JR_8/9/06_11:51_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 45.0; tumor-stroma %: 47.5; adipocyte cells%: 7.5; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JQ_6/15/06_12:05_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 20.0; tumor-stroma %: 40.0; adipocyte cells%: 40.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JP_6/15/06_11:14_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JO_6/30/06_11:52_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 15.0; tumor-stroma %: 70.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JN_6/29/06_9:48_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 5.0; tumor-stroma %: 80.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006JM_6/15/06_10:17_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 60.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JL_6/15/06_12:51_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 30.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006JK_8/9/06_10:17_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 20.0; tumor-stroma %: 55.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JJ_8/9/06_10:33_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 75.0; tumor-stroma %: 15.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JI_6/30/06_10:14_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 25.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JH_8/9/06_10:47_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 0.0; tumor-stroma %: 55.0; adipocyte cells%: 45.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JF_6/30/06_9:22_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 35.0; tumor-stroma %: 45.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JE_8/9/06_11:31_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 25.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006JD_6/30/06_10:00_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 30.0; adipocyte cells%: 30.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB006JC_6/29/06_10:18_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 30.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB006JB_6/15/06_12:36_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 80.0; tumor-stroma %: 20.0; adipocyte cells%: 0.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0067K_1/5/06_2:25_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 45.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0067J_1/13/06_12:05_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 40.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0067I_1/13/06_12:21_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 45.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0067H_1/12/06_1:13_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 80.0; tumor-stroma %: 10.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0067G_1/12/06_11:18_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0067D_1/5/06_1:53_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 45.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0067C_1/12/06_1:47_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 75.0; tumor-stroma %: 10.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0067B_1/5/06_2:41_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 45.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB00679_1/5/06_1:35_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 17.5; tumor-stroma %: 67.5; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00678_1/12/06_12:57_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 20.0; tumor-stroma %: 35.0; adipocyte cells%: 45.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00677_1/13/06_11:18_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 22.5; adipocyte cells%: 12.5; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00676_1/12/06_12:43_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 35.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00673_1/13/06_10:48_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 15.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00672_1/12/06_11:33_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 40.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB00671_1/5/06_2:58_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 30.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0066Y_1/13/06_11:04_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 15.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB004LV_1/18/06_1:16_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 15.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0066X_1/5/06_11:40_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 30.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0066W_1/5/06_2:09_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 45.0; tumor-stroma %: 40.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0066V_1/13/06_11:38_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0064S_5/4/06_10:51_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 30.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0064Q_5/4/06_11:44_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 30.0; adipocyte cells%: 40.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0064P_5/4/06_11:12_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 25.0; tumor-stroma %: 45.0; adipocyte cells%: 30.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0064O_5/4/06_10:11_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 70.0; tumor-stroma %: 30.0; adipocyte cells%: 0.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0064N_2/15/06_12:27_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 40.0; adipocyte cells%: 30.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0064J_2/15/06_12:11_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 25.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0064H_2/22/06_10:46_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 75.0; tumor-stroma %: 15.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0064G_5/4/06_11:28_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 15.0; tumor-stroma %: 85.0; adipocyte cells%: 0.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00625_8/15/06_9:58_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 25.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB00624_3/14/06_11:32_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 35.0; tumor-stroma %: 50.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00623_5/9/06_12:24_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 25.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB00622_2/17/06_1:37_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 35.0; adipocyte cells%: 35.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00621_5/9/06_11:02_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 20.0; tumor-stroma %: 55.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00620_3/14/06_12:56_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 65.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0061Z_3/14/06_12:41_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 30.0; adipocyte cells%: 30.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0061Y_2/17/06_11:23_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 30.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0061X_3/15/06_10:48_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 45.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061V_3/15/06_11:05_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 35.0; tumor-stroma %: 60.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB00613_2/3/06_1:42_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 50.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061U_3/14/06_12:24_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 50.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061T_3/14/06_11:13_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 25.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061S_5/9/06_10:46_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0061R_2/17/06_11:08_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 20.0; tumor-stroma %: 60.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0061Q_5/9/06_12:09_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 30.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0061P_5/9/06_10:00_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 25.0; tumor-stroma %: 60.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061O_2/17/06_1:02_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 35.0; tumor-stroma %: 45.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061M_8/15/06_10:45_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 70.0; tumor-stroma %: 20.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0061L_3/15/06_10:33_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 45.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061K_5/9/06_10:15_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 30.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061J_5/9/06_10:30_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 40.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061I_8/15/06_9:43_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 20.0; tumor-stroma %: 65.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0061H_8/15/06_11:00_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 10.0; adipocyte cells%: 30.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061G_3/14/06_1:11_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 35.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061E_5/9/06_11:54_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: NA; tumor-stroma %: NA; adipocyte cells%: NA; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061D_3/14/06_11:49_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 45.0; tumor-stroma %: 45.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0061C_2/17/06_12:32_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 70.0; tumor-stroma %: 22.5; adipocyte cells%: 7.5; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061B_2/17/06_1:55_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 50.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0061A_2/17/06_11:52_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 27.5; adipocyte cells%: 7.5; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00619_3/15/06_12:46_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 45.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00618_2/17/06_10:52_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 20.0; tumor-stroma %: 70.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB00614_2/24/06_11:36_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 40.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00612_2/24/06_1:07_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 20.0; tumor-stroma %: 50.0; adipocyte cells%: 30.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB00611_3/1/06_11:31_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 20.0; tumor-stroma %: 30.0; adipocyte cells%: 50.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB00610_2/3/06_12:53_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 60.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0060Y_2/24/06_1:27_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 30.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0060X_2/24/06_10:41_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 70.0; tumor-stroma %: 15.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0060W_6/7/06_12:35_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 65.0; tumor-stroma %: 15.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB0060V_6/7/06_9:28_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 35.0; tumor-stroma %: 45.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB0060U_6/7/06_10:16_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: NA; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB005WT_5/3/06_11:39_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 20.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB005WS_5/3/06_10:45_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: NA; tumor-stroma %: NA; adipocyte cells%: NA; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB005WL_3/15/06_12:21_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 45.0; tumor-stroma %: 50.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB005SB_6/30/06_9:45_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 15.0; tumor-stroma %: 70.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB005SA_6/15/06_10:58_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB005S8_6/29/06_11:42_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 30.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB005S7_8/9/06_11:08_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 30.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB005S6_6/30/06_11:27_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB005S5_6/29/06_12:13_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 40.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB005S4_6/29/06_12:35_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 45.0; tumor-stroma %: 35.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB005S2_8/9/06_12:23_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 80.0; tumor-stroma %: 20.0; adipocyte cells%: 0.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB005S1_6/29/06_10:03_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 55.0; tumor-stroma %: 40.0; adipocyte cells%: 5.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB005HS_1/12/06_1:28_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 70.0; tumor-stroma %: 15.0; adipocyte cells%: 15.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB005HR_1/12/06_11:54_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 45.0; adipocyte cells%: 25.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB005HP_1/5/06_12:01_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 40.0; tumor-stroma %: 25.0; adipocyte cells%: 35.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB005HN_1/13/06_12:37_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: NA; tumor-stroma %: NA; adipocyte cells%: NA; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB005HM_1/13/06_12:55_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: NA; tumor-stroma %: NA; adipocyte cells%: NA; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB004LO_1/18/06_1:31_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 30.0; tumor-stroma %: 40.0; adipocyte cells%: 30.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB004JO_1/18/06_11:27_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB004JJ_1/18/06_12:31_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 60.0; tumor-stroma %: 20.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB004JI_1/18/06_12:46_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 45.0; tumor-stroma %: 35.0; adipocyte cells%: 20.0; dm = 1 nodm = -1: 1; ', 'assayname: Signal_HB004JA_1/18/06_11:44_AM; disease state: Mastectomy bulk primary tumor; tumor epi %: NA; tumor-stroma %: NA; adipocyte cells%: NA; dm = 1 nodm = -1: -1; ', 'assayname: Signal_HB004J6_1/18/06_12:16_PM; disease state: Mastectomy bulk primary tumor; tumor epi %: 50.0; tumor-stroma %: 40.0; adipocyte cells%: 10.0; dm = 1 nodm = -1: 1; ' GSE66418 Homo sapiens 124 Expression profiling by array GPL17810 Specific IMPC gene expression signature 2015-03-02 Polarity defects are a hallmark of most carcinomas. Cells from invasive micropapillary carcinomas (IMPCs) of the breast are characterized by a striking cell polarity inversion and represent a good model for the analysis of polarity abnormalities. We have performed an in-depth investigation of polarity alterations in 24 IMPCs, compared with invasive carcinomas of no special type (ICNST). We used microarrays to compared gene expression profilings of IMPC with ICNST in a training set and in validation one. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE66418 LIN7A is a major determinant of cell-polarity defects in breast carcinomas. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-016-0680-x {Breast cancer research : BCR (5.676): 10.1186/s13058-016-0680-x} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA276852 https://www.ebi.ac.uk/ena/browser/view/PRJNA276852 None [Overal design]124 breast cancer samples: 73 IMPC and 51 ICNST (training set: 63 samples and validation set: 61 samples); [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNAs were collected from samples using the miRNeasy kit (Qiagen) according to the manufacturer's instructions"; [Cell type]'Source: ''sample source set: training set; tissue: Breast; tissue subtype: Invasive Micropapillary Carcinoma; ', 'sample source set: validation set; tissue: Breast; tissue subtype: Invasive Micropapillary Carcinoma; ', 'sample source set: validation set; tissue: Breast; tissue subtype: Invasive Carcinoma No Special Type; ', 'sample source set: training set; tissue: Breast; tissue subtype: Invasive Carcinoma No Special Type; ' GSE4767 Mus musculus 2 Genome variation profiling by genome tiling array GPL2884 Genomic aberrations in MMTV-cdc25a;MMTV-neu murine cell line 2006-05-03 CDC25A is a critical target of checkpoint, and its overexpression is observed in various cancers. Here we demonstrate that in vivo levels of Cdc25A expression determine the efficiency of transformation and tumorigenesis. Transgenic expression of CDC25A in murine mammary glands cooperates with tumorigenesis induced by expression of ras or neu. CDC25A- overexpressing tumors display aggressiveness and genomic instability with changes in fragile chromosomal regions, including the region orthologous to human 1p32-36. Keywords: genetic modification, aCGH https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE4767 Deregulated CDC25A expression promotes mammary tumorigenesis with genomic instability. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-06-3927 {Cancer research (8.378): 10.1158/0008-5472.CAN-06-3927} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA95647 https://www.ebi.ac.uk/ena/browser/view/PRJNA95647 None [Overal design]Genomic DNA from a MMTV-cdc25a;MMTV-neu double transgenic murine cell line derived from a mammary tumor was compared to normal mammary tissue DNA from the parental strain. A total of two hybridizations were completed.; [Treatment]'None'; [Growth]'None'; [Extraction]"Dneasy Tissue kit (Qiagen Cat# 69504) per manufacturer's instructions"; [Cell type]'Source: ''Strain: FVB/N , Gender: female , Age: 26 weeks, Tissue: mammary; ', 'Derived from tumor of: Strain: FVB/N , Gender: female , Age: 26 weeks, Tissue: mammary, Tumor Stage: T1 (<1cm, early stage); ' GSE66999 Homo sapiens 76 Expression profiling by array GPL6480 NCIC CTG MA.22 phase I/II trial of epirubicin and docetaxel in locally advanced breast cancer on 2-weekly or 3-weekly schedules 2015-03-17 This phase I/II neoadjuvant trial determined maximally-tolerated doses (MTD), dose-limiting toxicities (DLT), response-to-therapy, and explored the role of new response biomarkers. The combination regimens were delivered with acceptable toxicity, good clinical response, inducing changes in tumor RNA content and integrity. Pre-treatment gene expressions impacted clinical response, including several near 17q12, which with ERBB2, may better identify chemoresponsiveness. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE66999 A phase I/II trial of epirubicin and docetaxel in locally advanced breast cancer (LABC) on 2-weekly or 3-weekly schedules: NCIC CTG MA.22. SpringerPlus 1.78 https://doi.org/10.1186/s40064-015-1392-x {SpringerPlus (1.78): 10.1186/s40064-015-1392-x} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA278663 https://www.ebi.ac.uk/ena/browser/view/PRJNA278663 None [Overal design]The NCIC Clinical Trials Group MA.22 phase I/II clinical trial (ClinicalTrials.gov identifier NCT00066443) sought to determine the optimal dosing regimens for docetaxel/epirubicin combination chemotherapy in women with locally advanced (over 95% of patients) or inflammatory breast cancer. The protocol was approved by Health Canada and local Ethics Review Boards, and patients provided written, informed consent. Various doses of epirubicin and docetaxel were administered to patients in either a standard q3 weekly (Schedule A) or dose dense q2 weekly (Schedule B) regimen. Doses for Schedule A were 75 mg/m2 IV of docetaxel and 75, 90, 105, or 120 mg/m2 IV of epirubicin (with 6 mg of pegfilgrastim per cycle on day 2 to prevent neutropenia). Doses for both docetaxel and epirubicin in Schedule B were 50, 60, and 70 mg/m2 IV (with identical pegfilgrastim support). For each schedule, phase I was dose finding for phase II. Patients were allocated to the various phases and dosing regimens of the trial without randomization. None of the patients received trastuzumab in the initial years of the study and HER2+ patients were not enrolled on study, once trastuzumab funding became available. Six tumor biopsy cores were obtained pre-, mid-, and post-treatment: 3 cores for pathologic assessment; 3 cores for microarray studies. Total RNA was isolated from these cores and RNA integrity was assessed using Agilent Bioanalyzer. One of the RNA samples with the best quality was used for microarray study. One colour microarray of Agilent whole human genome nucleotide arrays was conducted with one array per patient. The current data set represents pre-treatment set. MA.22 clinical trial accrued T3N0, any N2 or N3, and T4 breast cancer patients (according to the classification described at; http://emedicine.medscape.com/article/2007112-overview). However, since the current study does not focus on the tumor grade/stage, the information was not provided in the current records.; [Treatment]'MA.22 clinical trial accrued T3N0, any N2 or N3, and T4 breast cancer patients. Treatment was 3-weekly (Schedule A; N=47) or 2-weekly (Schedule B; N=46) regimens of epirubicin/docetaxel chemotherapy in sequential phase I/II studies, with growth factor support. Toxicity was assessed. In phase I of each schedule, MTDs were determined based on DLT; in phase II, best clinical responses (CR/PR) and pathologic complete responses (pCR) were assessed. Six tumor biopsy cores were obtained pre-, mid-, and post-treatment: 3 cores for pathologic assessment; 3 cores for microarray studies.'; [Growth]'None'; [Extraction]'Total RNA was isolated using RNeasy Mini Kit (Qiagen), and quantity and quality were assessed using Agilent BioAnalyizer. RNA isolations with RIN at or over 5 were used for labelling.'; [Cell type]'Source: ''tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Complete Response (CR); estrogen-receptor: negative; progesterone receptor: negative; her2: positive; topo2: positive; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: negative; progesterone receptor: negative; her2: positive; topo2: positive; experimental batches: E; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; topo2: negative; experimental batches: E; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Complete Response (CR); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: G; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; topo2: positive; experimental batches: E; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: D; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: negative; her2: positive; topo2: positive; experimental batches: D; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; topo2: positive; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Complete Response (CR); estrogen-receptor: negative; progesterone receptor: negative; her2: positive; topo2: positive; experimental batches: E; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: negative; progesterone receptor: negative; her2: positive; topo2: positive; experimental batches: D; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; topo2: negative; experimental batches: D; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Complete Response (CR); estrogen-receptor: negative; progesterone receptor: negative; her2: positive; topo2: positive; experimental batches: D; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: positive; her2: positive; topo2: positive; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Complete Response (CR); estrogen-receptor: positive; progesterone receptor: negative; her2: positive; topo2: positive; experimental batches: D; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: negative; her2: negative; topo2: negative; experimental batches: D; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; topo2: positive; experimental batches: D; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Complete Response (CR); estrogen-receptor: positive; progesterone receptor: negative; her2: positive; topo2: positive; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Stable Disease (SD); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Complete Response (CR); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: D; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Complete Response (CR); estrogen-receptor: negative; progesterone receptor: negative; her2: positive; topo2: negative; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Complete Response (CR); estrogen-receptor: positive; progesterone receptor: positive; her2: positive; topo2: positive; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; topo2: negative; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; experimental batches: E; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: E; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule A; clinical response: Partial Response (PR); estrogen-receptor: negative; progesterone receptor: positive; her2: negative; topo2: positive; experimental batches: E; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: C; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Complete Response (CR); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: C; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Stable Disease (SD); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: C; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: E; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Stable Disease (SD); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Progressive Disease (PD); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: A; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Complete Response (CR); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: A; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); estrogen-receptor: negative; progesterone receptor: negative; her2: positive; topo2: positive; experimental batches: A; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: A; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; topo2: positive; experimental batches: A; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: negative; her2: negative; topo2: positive; experimental batches: F; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; topo2: positive; experimental batches: B; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Complete Response (CR); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; topo2: positive; experimental batches: A; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; topo2: negative; experimental batches: A; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: negative; her2: negative; topo2: negative; experimental batches: A; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); experimental batches: A; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Stable Disease (SD); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; topo2: negative; experimental batches: A; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); estrogen-receptor: positive; progesterone receptor: positive; her2: negative; topo2: negative; experimental batches: B; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Stable Disease (SD); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: negative; experimental batches: B; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); estrogen-receptor: negative; progesterone receptor: negative; her2: negative; topo2: negative; experimental batches: B; ', 'tissue: human breast tumor core biopsy; treatment: pretreatment; schedule: Schedule B; clinical response: Partial Response (PR); experimental batches: B; ' GSE36774 Homo sapiens 256 Expression profiling by array GPL96; GPL570 Expression data from primary breast tumors 2012-03-23 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36774 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA156811 https://www.ebi.ac.uk/ena/browser/view/PRJNA156811 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions.", "Trizol extraction of total RNA was performed according to the manufacturer's instructions"; [Cell type]'Source: ''tumour histological grade: G3; estrogen receptor status: ER+; progesterone receptor status: PgR-; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G3; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G3; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G3; estrogen receptor status: ER-; progesterone receptor status: PgR-; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G3; estrogen receptor status: ER-; progesterone receptor status: PgR-; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G3; estrogen receptor status: ER+; progesterone receptor status: PgR-; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER+; progesterone receptor status: NA; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G1; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G1; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER-; progesterone receptor status: PgR-; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: N/A; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER+; progesterone receptor status: PgR-; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G3; estrogen receptor status: ER-; progesterone receptor status: PgR-; lymph node metastasis: N/A; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER+; progesterone receptor status: PgR-; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tissue: primary breast tumor; disease state: breast cancer; ' GSE12367 Mus musculus 4 Expression profiling by array GPL1261 Deaf-1 regulated genes in the mouse mammary gland 2008-08-07 Microarray analysis was used to compare the gene expression profiles of Deaf-1-transduced mouse mammary epithelial cells (MECs) relative to Deaf-1-deficient MECs. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE12367 Deaf-1 regulates epithelial cell proliferation and side-branching in the mammary gland. BMC developmental biology 2.368 https://doi.org/10.1186/1471-213X-8-94 {BMC developmental biology (2.368): 10.1186/1471-213X-8-94} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA113197 https://www.ebi.ac.uk/ena/browser/view/PRJNA113197 None [Overal design]To investigate potential target genes of Deaf-1, primary mammary epithelial cells (MECs) were isolated from a Deaf-1-null mouse and immortalised by transduction with a retrovirus encoding the human papilloma virus (HPV16) E6/E7 proteins. Two clones were selected and transduced with either an empty retrovirus or one encoding Deaf-1. RNA was subsequently isolated from cells at 24 and 48 hours after transduction for Affymetrix analysis. High levels of Deaf-1 expression were demonstrated in cells transduced with the Deaf-1 retrovirus relative to controls following a 48 hour selection in puromycin. This time-point was therefore selected for further analysis. To compare the gene expression profiles of Deaf-1-transduced MECs relative to Deaf-1-deficient MECs, Affymetrix analysis was performed using the GeneChip® Mouse Expression Set 430 2.0 array which comprises 39,000 transcripts on a single array. Total RNA was harvested from two independent clones (C1 and E1) infected with either control or Deaf-1-expressing retrovirus making 4 samples in total. Clones C1 and E1 were treated as biological replicates in the subsequent analysis.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was harvested from two independent clones (C1 and E1) infected with either control or Deaf-1-expressing retrovirus. RNA was purified using using the QIAGEN RNeasy Kit (Qiagen, Hilden, Germany) \nand quality assessed by spectrophotometry and gel electrophoresis before \nhybridisation to Affymetrix slides.'; [Cell type]'Source: ''' GSE145752 Homo sapiens 114 Other GPL28181 RNA profiling of matched pair samples of primary breast cancer vs. lung and pleura metastasis 2020-02-22 Patient samples were recruited from a series of female patients with metastatic primary breast cancer (PBC) and biopsy-confirmed breast cancer lung or pleural metastasis (BCLPM) at the Department of Thoracic Surgery, Thoraxklinik, Univ. of Heidelberg, Germany. All patients were included who had received lung or pleural metastasis biopsies from 2003 to 2014 and had a prior history of PBC at the Department of Gynaecology and Obstetrics, Univ. Hospital. Formalin-fixed and paraffin-embedded tissue samples were provided by the Tissue Bank at the National Center for Tumor Diseases (NCT, Heidelberg, Germany) in accordance with the regulations of the Tissue Bank and approval of the Ethics Committee at the Medical Faculty of the Univ. of Heidelberg, approval no. S-716/2018. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE145752 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA608129 https://www.ebi.ac.uk/ena/browser/view/PRJNA608129 None [Overal design]Retrospective cohort study; [Treatment]'For selection of tumor tissue for RNA extraction, FFPE tissue blocks from primary breast cancer and metastasis were selected after reviewing all original tissue slides, and re-cut for H&E sections, to be used for reference and to determine tumor cell content (tumor surface area). RNA was extracted using between 5 - 10 unstained FFPE slides for each tumor. Microdissection was performed in most cases to avoid normal breast tissue contamination.'; [Growth]'FFPE tissue'; [Extraction]"The Promega Maxwell 16 Sytem was used to extract total RNA from the samples, according to manufacture's instructions. A minimum of approximately 20 ng of total RNA was used."; [Cell type]'Source: ''age at biopsy: 43.5; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1c; pn: pNX; ', 'age at biopsy: 61.5; Sex: female; ', 'age at biopsy: 67.4; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT1c; pn: pN1; ', 'age at biopsy: 75.7; Sex: female; ', 'age at biopsy: 58.2; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pN2; ', 'age at biopsy: 73.1; Sex: female; ', 'age at biopsy: 66.6; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pN1; ', 'age at biopsy: 70.2; Sex: female; ', 'age at biopsy: 41.9; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1c; pn: pNX; ', 'age at biopsy: 59.6; Sex: female; ', 'age at biopsy: 48.4; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pN0; ', 'age at biopsy: 62.4; Sex: female; ', 'age at biopsy: 57.7; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1c; pn: pN0; ', 'age at biopsy: 59.5; Sex: female; ', 'age at biopsy: 43.0; Sex: female; histology: invasive lobular carcinoma; tumor grade: G2; pt: pT2; pn: pN0; ', 'age at biopsy: 64.3; Sex: female; ', 'age at biopsy: 68.7; Sex: female; histology: invasive lobular carcinoma; tumor grade: G2; pt: pT3; pn: pN3; ', 'age at biopsy: 75.6; Sex: female; ', 'age at biopsy: 54.4; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1c; pn: pN0; ', 'age at biopsy: 64.0; Sex: female; ', 'age at biopsy: 52.2; Sex: female; histology: NA; tumor grade: NA; pt: pTX; pn: pNX; ', 'age at biopsy: 72.1; Sex: female; ', 'age at biopsy: 49.1; Sex: female; histology: NA; tumor grade: NA; pt: pTX; pn: pNX; ', 'age at biopsy: 70.5; Sex: female; ', 'age at biopsy: 56.2; Sex: female; histology: invasive lobular carcinoma; tumor grade: G2; pt: pT3; pn: pN2; ', 'age at biopsy: 56.3; Sex: female; ', 'age at biopsy: 47.3; Sex: female; histology: invasive mucinous carcinoma; tumor grade: NA; pt: pT1c; pn: pN1; ', 'age at biopsy: 48.8; Sex: female; ', 'age at biopsy: 60.5; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pN0; ', 'age at biopsy: 71.1; Sex: female; ', 'age at biopsy: 68.4; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1b; pn: pN0; ', 'age at biopsy: 81.2; Sex: female; ', 'age at biopsy: 62.5; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1c; pn: pN1; ', 'age at biopsy: 74.0; Sex: female; ', 'age at biopsy: 65.9; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1b; pn: pN0; ', 'age at biopsy: 71.5; Sex: female; ', 'age at biopsy: 62.9; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1c; pn: pN3; ', 'age at biopsy: 69.7; Sex: female; ', 'age at biopsy: 58.5; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT1c; pn: pN0; ', 'age at biopsy: 61.8; Sex: female; ', 'age at biopsy: 46.9; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pN2; ', 'age at biopsy: 45.7; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT2; pn: pN0; ', 'age at biopsy: 54.7; Sex: female; ', 'age at biopsy: 48.4; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1c; pn: pN0; ', 'age at biopsy: 52.0; Sex: female; ', 'age at biopsy: 43.2; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pN0; ', 'age at biopsy: 51.3; Sex: female; ', 'age at biopsy: 41.0; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1c; pn: pN0; ', 'age at biopsy: 50.5; Sex: female; ', 'age at biopsy: 32.6; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT3; pn: pN0; ', 'age at biopsy: 32.7; Sex: female; ', 'age at biopsy: 60.2; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1c; pn: pN1; ', 'age at biopsy: 65.0; Sex: female; ', 'age at biopsy: 47.2; Sex: female; histology: invasive lobular carcinoma; tumor grade: G3; pt: rpT2; pn: pN0; ', 'age at biopsy: 71.3; Sex: female; ', 'age at biopsy: 43.4; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1c; pn: pN0; ', 'age at biopsy: 57.2; Sex: female; ', 'age at biopsy: 51.8; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT2; pn: pN0; ', 'age at biopsy: 54.9; Sex: female; ', 'age at biopsy: 53.6; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT4b; pn: pN2; ', 'age at biopsy: 59.4; Sex: female; ', 'age at biopsy: 53.6; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pN3; ', 'age at biopsy: 56.9; Sex: female; ', 'age at biopsy: 47.1; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT4d; pn: pN1; ', 'age at biopsy: 49.0; Sex: female; ', 'age at biopsy: 62.6; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT2; pn: pN2; ', 'age at biopsy: 74.7; Sex: female; ', 'age at biopsy: 54.0; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: rpT2; pn: pN0; ', 'age at biopsy: 55.9; Sex: female; ', 'age at biopsy: 41.1; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT2; pn: pN0; ', 'age at biopsy: 43.0; Sex: female; ', 'age at biopsy: 48.4; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pNX; ', 'age at biopsy: 63.2; Sex: female; ', 'age at biopsy: 59.4; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT1c; pn: pN0; ', 'age at biopsy: 66.9; Sex: female; ', 'age at biopsy: 44.0; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: rpT1c; pn: pN0; ', 'age at biopsy: 62.9; Sex: female; ', 'age at biopsy: 73.4; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pNX; ', 'age at biopsy: 76.7; Sex: female; ', 'age at biopsy: 52.1; Sex: female; histology: invasive lobular carcinoma; tumor grade: G2; pt: pT2; pn: pN3; ', 'age at biopsy: 52.5; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT3; pn: pN3; ', 'age at biopsy: 56.0; Sex: female; ', 'age at biopsy: 56.4; Sex: female; histology: invasive ductal carcinoma; tumor grade: G1; pt: pT2; pn: pN2; ', 'age at biopsy: 67.0; Sex: female; ', 'age at biopsy: 67.9; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pN2; ', 'age at biopsy: 42.8; Sex: female; histology: invasive lobular carcinoma; tumor grade: G3; pt: pT2; pn: pN2; ', 'age at biopsy: 46.3; Sex: female; ', 'age at biopsy: 67.5; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pN3; ', 'age at biopsy: 67.9; Sex: female; ', 'age at biopsy: 65.0; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT1c; pn: pN3; ', 'age at biopsy: 69.9; Sex: female; ', 'age at biopsy: 39.6; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pN3; ', 'age at biopsy: 47.7; Sex: female; ', 'age at biopsy: 58.3; Sex: female; histology: invasive lobular carcinoma; tumor grade: G2; pt: pT1c; pn: pN0; ', 'age at biopsy: 66.5; Sex: female; ', 'age at biopsy: 61.9; Sex: female; histology: invasive lobular carcinoma; tumor grade: G2; pt: pT2; pn: pN1; ', 'age at biopsy: 76.0; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT2; pn: pN0; ', 'age at biopsy: 79.7; Sex: female; ', 'age at biopsy: 43.6; Sex: female; histology: invasive ductal carcinoma; tumor grade: G2; pt: pT2; pn: pN2; ', 'age at biopsy: 50.1; Sex: female; ', 'age at biopsy: 47.8; Sex: female; histology: invasive ductal carcinoma; tumor grade: G1; pt: pTX; pn: pNX; ', 'age at biopsy: 57.3; Sex: female; ', 'age at biopsy: 76.8; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT4b; pn: pN3; ', 'age at biopsy: 77.3; Sex: female; ', 'age at biopsy: 33.4; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT1b; pn: pN3; ', 'age at biopsy: 39.9; Sex: female; ', 'age at biopsy: 27.3; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT4b; pn: pN2; ', 'age at biopsy: 27.3; Sex: female; ', 'age at biopsy: 39.8; Sex: female; histology: invasive ductal carcinoma; tumor grade: G3; pt: pT1c; pn: pNX; ', 'age at biopsy: 44.3; Sex: female; ' GSE159353 Homo sapiens 6 Expression profiling by high throughput sequencing GPL11154 EphA2-SE-KO RNA-seq 2020-10-10 We used Crispr/Cas9 technology to establish a homozygous clone of EphA2-SE deletion in tumor cells. Wild-type cells (WT) and homozygous cloned cells (EphA2-SE-/-) were selected for high-throughput data detection. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE159353 EphA2 super-enhancer promotes tumor progression by recruiting FOSL2 and TCF7L2 to activate the target gene EphA2. Cell death & disease 5.959 https://doi.org/10.1038/s41419-021-03538-6 {Cell death & disease (5.959): 10.1038/s41419-021-03538-6} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA668532 https://www.ebi.ac.uk/ena/browser/view/PRJNA668532 https://www.ncbi.nlm.nih.gov/sra?term=SRP286990 [Overal design]mRNA profiles of WT and EphA2-SE-/- cells.; [Treatment]'None'; [Growth]'Cells were cultured in DMEM (GIBCO, USA) containing 10% fetal bovine serum (FBS) with penicillin/streptomycin.'; [Extraction]'Cells from cell culture were used for RNA extraction. RNA was harvested using Trizol reagent.\nVazyme VAHTS mRNA-seq V2 Library Prep Kit for Illumina kit (NR601) is used to construct the sequencing library.'; [Cell type]'cervix cancer', 'colon cancer', 'breast cancer''cell line: HeLa; cell type: cervix cancer; genotype: Wild type; ', 'cell line: HeLa; cell type: cervix cancer; genotype: EphA2-SE -/-; ', 'cell line: HCT-116; cell type: colon cancer; genotype: Wild type; ', 'cell line: HCT-116; cell type: colon cancer; genotype: EphA2-SE -/-; ', 'cell line: MCF-7; cell type: breast cancer; genotype: Wild type; ', 'cell line: MCF-7; cell type: breast cancer; genotype: EphA2-SE -/-; ' GSE121662 Homo sapiens 22 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Role of iron in the regulation of the epithelial-to-mesenchymal transition (ChIP-seq) 2018-10-23 The biological process termed Epithelial-to-Mesenchymal Transition (EMT) plays a central role in cancer cell invasion, metastasis, self-renewal and resistance to therapy1,2. Here, we characterize using chromatin immunoprecipitation and Next Generation Sequencing the genome-wide H3K9me2 distribution occurring during EMT induced by epidermal growth factor in breast cancer MDA-MB-468 cells. 1. Nieto, M. A., Huang, R. Y., Jackson, R. A. & Thiery, J. P. EMT: 2016. Cell 166, 21–45 (2016). 2. Puisieux, A. & Brabletz, T. & Caramel, J. Oncogenic roles of EMT-inducing transcription factors. Nat. Cell Biol. 16, 488–494 (2014). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE121662 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA498059 https://www.ebi.ac.uk/ena/browser/view/PRJNA498059 https://www.ncbi.nlm.nih.gov/sra?term=SRP166453 [Overal design]Analysis of 9 samples: (i)Input DNA to normalize samples; (ii) H3K9me2 Immunoprecipitated in untreated cells and (iii) H3K9me2 immunoprecipitated in EGF-treated cells. Experiment was performed in 3 independent biological replicates.; [Treatment]'Cells were harvested by trypsinization. After adding media to stop trypsin, cells were centrifuged at 500 x g for 5 min at room temperature. The pelleted cells were resuspended in media, counted and crosslinked with 37% formaldehyde (final concentration 1%) for 10 min at room temperature. The crosslinking was stopped by addition of 2.5 M glycine (final concentration 0.125 M) for 5 min at room temperature followed by centrifugation at 500 x g for 5 min at 4°C.'; [Growth]'MDA-MB-468 cells grown in 145 mm2 dishes until ~ 70% confluence were treated with EGF (100 ng mL-1) for 72h in biological triplicate and untreated cells were used as an appropriate control.'; [Extraction]'The pelleted cells were washed twice with ice-cold PBS1x by centrifuging at 500 x g for 5 min at 4°C. For lysis of crosslinked chromatin, the pellet was resuspended in lysis buffer A (50 mM Tris HCl pH8, 10 mM EDTA, 1% SDS, 50 x protease inhibitor cocktail) at room temperature and incubated for 5 min on rotating wheel. Next, lysate was centrifuged at 300 x g for 10 min at 8°C to prevent SDS precipitation and the supernatant was discarded. For chromatin shearing, the pellet was sheared in buffer B (25 mM Tris HCl pH8, 3 mM EDTA, 0.1% SDS, 1% Triton X-100, 150 mM NaCl, 50 x protease inhibitor cocktail) to approximatively 200-600 base-pair average size using the Bioruptor Pico (Diagenode). After centrifugation at 20\xa0000 x g, 4ºC for 15 min, the supernatant containing sheared chromatin was used for immunoprecipitation. 25 µL (10%) of sheared chromatin was used as input DNA to normalize sequencing data. As supplement control for normalization, we used spike-in chromatin Drosophila and spike-in antibody (Active motif). For chromatin immunoprecipitation (1 million cells per ChIP), it was carried out using sheared chromatin and antibody H3K9me2 complexed to Dynal Protein G magnetic beads (Thermo Fisher). Briefly, 6 µL of H3K9me2 antibody was mixed with 1 µg of spike-in antibody. 23 µL of magnetic beads were washed three times in ice-cold buffer C (20 mM Tris HCl pH8, 2 mM EDTA, 0.1% SDS, 1% Triton X-100, 150 mM NaCl, 50 x protease inhibitor cocktail) and incubated with the mix of H3K9me2 and spike-in antibody for 4h at room temperature on rotating wheel in buffer C (494 µL). After the quick-spin and the removal of supernatant, the beads were resuspended in 100 µL buffer C. Each 50 µL of the latter was incubated with 250 µL of sheared chromatin mixed previously with 50 ng of spike-in chromatin Drosophila (250 µL chromatin of interest: 2,5 µL of spike-in chromatin, v:v) at 4°C on rotating wheel, overnight (~ 16h). After quick-spin, the supernatant was discarded and the beads were successively washed in buffer C, buffer D (20 mM Tris-HCl pH8, 2 mM EDTA, 0.1% SDS, 1% Triton X-100, 500 mM NaCl), buffer E (10 mM Tris-HCl pH8, 0.25 M LiCl, 0.5% NP-40, 0.5% Sodium Deoxycholate, 1 mM EDTA) and buffer F (10 mM Tris-HCl pH8, 1 mM EDTA, 50 mM NaCl). Finally, input and immunoprecipitated chromatin samples were resuspended in solution containing TE buffer/ 1% SDS, decrosslinked by heating at 65°C overnight and subjected to both RNase A and Proteinase K treatments.\nIllumina compatible libraries were prepared from input and immunoprecipitated DNAs using the Illumina TruSeq ChIP library preparation kit according to the manufacturer’s protocol. Briefly, 4 to 10ng of DNA were subjected to subsequent steps of end-repair, dA-tailing and ligation of TruSeq indexed Illumina adapters. After a final PCR amplification step, the 24 resulting barcoded libraries were equimolarly pooled in 2 groups quantified using a qPCR method (KAPA library quantification kit, Roche) before sequencing on the Illumina HiSeq2500 instrument. Each pool was loaded on 1 rapid flow cell (11pM) and sequenced using a single read mode (SR50). This sequencing configuration was set to reach an average of 25 million reads (50-base long) per sample.'; [Cell type]'Source: ''cell line: MDA-MB-468; tissue: Basal breast cancer cells; passages used: From 6 to 14; chip antibody: H3K9me2 ( cell signaling, Cat # 4658S; Rabbit monoclonal [D85B4]); ', 'cell line: MDA-MB-468; tissue: Basal breast cancer cells; passages used: From 6 to 14; chip antibody: none (input); ', 'cell line: MDA-MB-468 cells; passages used: From 6 to 14; chip antibody: H3K4me3; ', 'cell line: MDA-MB-468 cells; passages used: From 6 to 14; chip antibody: H3K9me3; ' GSE76924 Homo sapiens 8 Non-coding RNA profiling by array GPL15517 The miRNA profiling in MDA-MB-231, MDA-MB-231/E1A and knockdown of Dicer in MDA-MB-231/E1A cells 2016-01-15 Dicer, RNase III endonuclease, is an essential enzyme in miRNA biogenesis that regulates target gene expression, and it has been reported that aberrant expressions of Dicer associate with the clinical outcomes of patients in various cancers. To explore the miRNA differencial expression regulated by Dicer in MDA-MB-231/E1A cells, the microarray profiling analysis was employed to conduct differentially expressed miRNAs in stable MDA-MB-231/vector, MDA-MB-231/E1A, and MDA-MB-231/E1A/shDicer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76924 Dicer Elicits Paclitaxel Chemosensitization and Suppresses Cancer Stemness in Breast Cancer by Repressing AXL. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-15-2555 {Cancer research (8.378): 10.1158/0008-5472.CAN-15-2555} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA308943 https://www.ebi.ac.uk/ena/browser/view/PRJNA308943 None [Overal design]The four groups including vector control, E1A-expressing and Dicer knockdown in E1A-expressing MDA-MB-231 cells were harvested and RNA were isolated. Two independent experiments were performed for each group.; [Treatment]'None'; [Growth]"MDA-MB-231 cells were grown in Dulbecco's modified Eagle's medium (DMEM/F12) containing 10% fetal bovine serum in 37℃ with 5% CO2."; [Extraction]"Total RNA extracted using Trizol following manufacturer's instructions"; [Cell type]'Source: ''cell line: MDA-MB-231 (HTB-26); ' GSE23177 Homo sapiens 116 Expression profiling by array GPL570 Prediction of lymph node involvement in breast cancer from primary tumor tissue using gene expression profiling and miRNAs. 2010-07-27 Lymph node involvement is the most important prognostic factor in breast cancer, but little is known about the underlying molecular changes. First, to identify a molecular signature associated with nodal metastasis, gene expression analysis was performed on a homogeneous group of 96 primary breast tumors, balanced for lymph node involvement. Each tumor was diagnosed as a poorly differentiated, estrogen positive, her2-neu negative invasive ductal cancer. (Affymetrix Human U133 Plus 2.0 microarray chips). A model, including 241 genes was built and validated on an internal and external dataset performed with Affymetrix technology. All samples used for validation had the same characteristics as the initial tumors. The area under the ROC curve (AUC) for the internal dataset was 0.646 and 0.651 for the external datasets. Thus, the molecular profile of a breast tumor reveals information about lymph node involvement, even in a homogeneous group of tumors. However, an AUC of 0.65 indicates only a weak correlation. Our model includes multiple kinases, apoptosis related and zinc ion binding genes. Pathway analysis using the Molecular Signatures Database revealed relevant gene sets (BAF57, Van 't Veer). Next, miRNA profiling was performed on 82/96 tumors using Human MiRNA microarray chips (Illumina). Eight miRNAs were significantly differentially expressed according to lymph node status at a significance level of 0.05, without correcting for multiple testing. The analysis of the inverse correlation between a miRNA and its computationally predicted targets point to general deregulation of the miRNA machinery potentially responsible for lymph node invasion. In conclusion, our results provide evidence that lymph node involvement in breast cancer is not a random process. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23177 Prediction of lymph node involvement in breast cancer from primary tumor tissue using gene expression profiling and miRNAs. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-010-1265-5 {Breast cancer research and treatment (3.471): 10.1007/s10549-010-1265-5} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA131649 https://www.ebi.ac.uk/ena/browser/view/PRJNA131649 None [Overal design]Gene expression profiling: A training set of 96 patients and an independent internal dataset of 20 patients balanced for lymph node involvement was selected from the multidisciplinary breast centre database miRNA profiling not provided in this Series.; [Treatment]'None'; [Growth]'Each tumor is snap-frozen in liquid nitrogen within 30 minutes after surgical extirpation and stored at -80°C', 'Each tumor is snap-frozen in liquid nitrogen within 30 minutes after surgical extirpation and stored at -80°C'; [Extraction]'8-10 sections from frozen blocks, 10 µm thick, were homogenized and total bulk RNA extracted by the trizol method was further purified using RNAeasy columns (Qiagen, Valencia, CA, USA). RNA concentration and purity were determined spectrophotometrically using the Nanodrop ND-1000 (Nanodrop Technolgies) and RNA integrity was assessed using a Bioanalyser 2100 (Agilent).'; [Cell type]'Source: ''patient type: internal dataset balanced for lymph node involvement; disease state: Primary breast tumor; ln: neg; lnratio: 0; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: internal dataset balanced for lymph node involvement; disease state: Primary breast tumor; ln: pos; lnratio: 0.50; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: internal dataset balanced for lymph node involvement; disease state: Primary breast tumor; ln: pos; lnratio: 0.87; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: internal dataset balanced for lymph node involvement; disease state: Primary breast tumor; ln: pos; lnratio: 0.65; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: internal dataset balanced for lymph node involvement; disease state: Primary breast tumor; ln: pos; lnratio: 0.2; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: internal dataset balanced for lymph node involvement; disease state: Primary breast tumor; ln: pos; lnratio: 0.56; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: internal dataset balanced for lymph node involvement; disease state: Primary breast tumor; ln: pos; lnratio: 0.57; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: internal dataset balanced for lymph node involvement; disease state: Primary breast tumor; ln: pos; lnratio: 0.05; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: internal dataset balanced for lymph node involvement; disease state: Primary breast tumor; ln: pos; lnratio: 0.4; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: internal dataset balanced for lymph node involvement; disease state: Primary breast tumor; ln: pos; lnratio: 0.94; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: internal dataset balanced for lymph node involvement; disease state: Primary breast tumor; ln: pos; lnratio: 0.16; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: internal dataset balanced for lymph node involvement; disease state: Primary breast tumor; ln: pos; lnratio: 0.13; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: neg; lnratio: 0; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.27; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.14; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.05; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.06; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.09; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.08; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.10; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.38; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.29; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.17; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.31; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.41; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.65; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.07; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.15; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.25; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.22; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.13; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.11; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.20; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.57; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.96; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.48; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.42; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.12; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ', 'patient type: training set; disease state: Primary breast tumor; ln: pos; lnratio: 0.04; er: pos; her2-: neg; grade: III; menopause: postmenopausal; histology: ID; ' GSE39783 Homo sapiens 2 Methylation profiling by genome tiling array GPL5082 Estrogen deprivation alters epigenetic modifications in breast cancer cells - HOXC10 loss in endocrine resistance 2012-07-31 Postmenopausal breast cancer patients benefit from aromatase inhibitors (AIs) that reduce the levels of estrogens critical for the growth of estrogen receptor (ER)-positive tumors. Unfortunately, many tumors are resistant to AI, and we are only beginning to understand the complex mechanisms underlying treatment resistance. Here we set out to determine whether epigenetic changes could contribute to therapy resistance. For AI-resistance models, we used previously established MCF-7 cell clones, termed C4-12 and long-term estrogen deprivation (LTED), that were isolated after being cultured in estrogen-free media for 9 months and 18–24 months, respectively. Methyl CpG Binding Domain (MBD) - pull down followed by affymetrix promoter array was used to detect promoter methylation patterns in these cell lines. These studies identified widespread genomic hyper- and hypomethylation events, with a significant enrichment of promoter hypermethylation of development-associated genes in both cell lines. A developmentally regulated gene that was heavily methylated and lost expression in both cell-line systems was HOXC10. Moreover, we found that HOXC10 is an estrogen-regulated gene and lack of ER regulation is associated with progressive epigenetic silencing through EZH2/H3K27me3 and DNA hypermethylation. Stable knockdown of HOXC10 in MCF-7 cells resulted in increased cell growth, reduced cell apoptosis, and increased cell motility. A preliminary study using AI-treated breast tumors did not show significant associations, however, the numbers were small. We identified HOXC10 methylation as a novel determinant of endocrine resistance. Also, we revealed that epigenetic reprogramming of genes involved in development may be a fundamental phenomenon in hormone resistance. Therefore, our study might provide the basis for the expansion of clinical markers for endocrine resistance and future clinical trials such as combination of endocrine and epigenetic therapies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39783 Epigenetic reprogramming of HOXC10 in endocrine-resistant breast cancer. Science translational medicine 17.161 https://doi.org/10.1126/scitranslmed.3008326 {Science translational medicine (17.161): 10.1126/scitranslmed.3008326} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA171707 https://www.ebi.ac.uk/ena/browser/view/PRJNA171707 None [Overal design]Long-term estrogen deprived previously established MCF-7 cell clones termed C4-12 and LTED genomic DNA subjected to Methyl CpG Binding Domain (MBD) - pull down followed by affymetrix promoter array to detect promoter methylation patterns; [Treatment]'None'; [Growth]'C4-12 cells were routinely maintained in αMEM (Invitrogen Life Technologies) without phenol red supplemented with 5% charcoal/dextran-treated fetal bovine serum (Hyclone), 2 mM glutamine, 100 IU/ml penicillin, 100 μg/ml streptomycin, 10 mM HEPES (Gibco) and 10 μg/ml Insulin. LTED cells were maintained in Improved MEM that was supplemented with 5% charcoal-dextran treated fetal bovine serum (HyClone), 2mM glutamine, 100 IU/ml penicillin, and 100 μg/ml streptomycin. The cells were cultured at 37°C with 5% CO2 in the air.'; [Extraction]'Genomic DNA from ~2×106 cells was prepared from cells lysed in guanidine thiocyanate buffer (3.6M guanidine thiocyanate, 0.05% SDS, 50mM Tris, pH 8), the lysate was extracted with phenol/chloroform and then precipitated twice with ethanol.'; [Cell type]'Source: ''cell line: MCF7 C4-12; ', 'cell line: MCF7; ', 'cell line: MCF7 LTED; ' GSE161360 Fusobacterium periodonticum 2_1_31; Fusobacterium nucleatum subsp. polymorphum ATCC 10953; Fusobacterium nucleatum subsp. nucleatum ATCC 25586; Fusobacterium nucleatum subsp. vincentii 3_1_36A2; Fusobacterium nucleatum subsp. animalis 7_1 90 Expression profiling by high throughput sequencing GPL29408; GPL29409; GPL29942; GPL29943; GPL29944 RNA landscape of the emerging cancer-bug Fusobacterium nucleatum 2020-11-12 Fusobacterium nucleatum, long known as a constituent of the oral microflora, has recently garnered much attention for its newly discovered prevalence in colorectal and breast cancer tissue. The growing interest in this emerging cancer-associated bacterium sharply contrasts with a paucity of knowledge about its basic gene expression features and physiological responses. Post-transcriptional networks are also unknown, for fusobacteria lack all established small RNA-associated proteins. Here, we present high-resolution global RNA maps for two clinically relevant F. nucleatum subspecies for different growth conditions, and use these to uncover fundamental aspects of fusobacterial gene expression architecture and a previously unknown suite of noncoding RNAs. Developing a new vector for functional analysis of fusobacterial genes, we identify a conserved oxygen-induced small RNA as a post-transcriptional repressor of major porin FomA. Our findings provide a crucial step towards delineating the regulatory networks enabling F. nucleatum to colonize different compartments of the human body. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE161360 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA677955 https://www.ebi.ac.uk/ena/browser/view/PRJNA677955 https://www.ncbi.nlm.nih.gov/sra?term=SRP292349 [Overal design]Samples of different growth stages were taken for RNA extraction. Isolated RNA was used for cDNA library generation following the dRNA-seq protocol.; [Treatment]'see description of samples'; [Growth]'Growth was performed in Columbia broth at 37°C inside an anaerobic chamber. Pre-cultures were inoculated with a signel colony. After 24h, the working cultures were inoculated at a dilution 1:50 and samples taken at the indicated growth stages.'; [Extraction]'Total RNA was extracted using the hot phenol protocol. Bacterial cultures were grown to the desired OD600, mixed with 0.2 volumes of STOP solution (95\xa0% ethanol, 5\xa0% phenol) and snap-frozen at –\xa080\xa0°C if not directly processed. The bacterial solution was centrifuged for 20\xa0min, 4500\xa0rpm at 4\xa0°C and the supernatant was completely discarded. Cells were suspended in 600\xa0μl of 10\xa0mg/ml lysozyme in TE buffer (pH\xa08.0) and incubated at 37\xa0°C for 10\xa0min. Next, 60\xa0μl of 10\xa0% w/v SDS was added and everything mixed by inversion. Samples were incubated in a water bath at 64\xa0°C, 1-2\xa0min before adding 66\xa0μl 3\xa0M\xa0NaOAc, pH\xa05.2. Next, 750\xa0μl acid phenol (Roti-Aqua phenol) was added, followed by incubation for 5\xa0min. at 64\xa0°C. Samples were briefly placed on ice to cool before centrifugation for 15\xa0min, 13,000\xa0rpm at 4\xa0°C. The aqueous layer was transferred into a 2\xa0ml phase lock gel tube (Eppendorf), 750\xa0μl chloroform (Roth, #Y015.2) was added, and everything centrifuged for 12\xa0min, 13,000\xa0rpm at room temperature. For ethanol precipitation, the aqueous layer was transferred to a fresh tube, 2 volumes of 30:1 mix (EtOH:3\xa0M\xa0NaOAc, pH\xa06.5) was added and incubated overnight at -20\xa0°C. Precipitated RNA was harvested by centrifugation, washed with cold 75\xa0% v/v ethanol and air-dried. Purified RNA was resuspended in 50\xa0µl RNase-free water and stored at -80\xa0°C.\nLibrary preparation for dRNA-seq was accomplished by Vertis Biotechnology AG. In brief, total RNA was analyzed on a Shimadzu MultiNA microchip electrophoresis system. 23S/16S ratio for all samples was 1.3. RNA was fragmented via ultrasound (4 pulses a 30 sec, 4 °C) and subsequently treated with T4 Polynucleotide Kinase (NEB). Half of the samples were then treated with terminator exonuclease (TEX) for dRNA-seq. For the cDNA synthesis, the RNA fragments were poly(A)-tailed and 5’PPP structures were removed with RNA 5’ Polyphosphatase (Epicentre). The RNA sequencing adapter with the barcodes were ligated to the 5’-monophosphate of the fragments. First strand cDNA was synthesized with an oligo(dT)-adapter primer and M-MLV reverse transcriptase. Amplification of cDNA was done via PCR to an approximate amount of 10 20 ng/µl. cDNA was purified with the Agencourt AMPure XP kit (Beckman Coulter Genomics) and analyzed with Shimadzu MultiNA microchip electrophoresis. Equimolar amounts of the samples were pooled for sequencing. cDNAs had a size between 200 and 550 bp. The library pool was fractionated via differential clean-up with the Agencourt AMPure kit. The cDNA pool was checked with capillary electrophoresis as stated above. Libraries were sequenced on an Illumina NextSeq 500 system using 75 bp read length.'; [Cell type]'Source: ''treatment: untreated; ', 'treatment: TEX treated; ' GSE104985 Homo sapiens 118 Expression profiling by high throughput sequencing GPL11154 KDM5B links cellular transcriptome heterogeneity to therapy resistance (RNA-Seq) 2017-10-15 The KDM5B histone H3 lysine 4 (H3K4) demethylase has been implicated in therapy resistance in multiple cancer types including breast cancer, but the underlying mechanism is poorly defined. Here we show that inhibition of KDM5B activity increases sensitivity to anti-estrogens by modulating estrogen-receptor (ER) signaling. Conversely, acquired resistance to KDM5 inhibitors leads to gain of ER chromatin binding and estrogen-independent growth. Sequencing of barcoded cell populations and mathematical modeling demonstrate selection for pre-existent genetically distinct endocrine-resistant cells, while resistance to KDM5 inhibitors is a switch to an acquired epigenetic state. Rare resistant cells can already be detected by single cell RNA-seq prior to treatment. Inhibition of KDM5B in luminal ER+ cells increases H3K4me3 broad domains at promoters and decreases cellular transcriptional heterogeneity. Higher transcriptome heterogeneity is associated with higher KDM5B levels and poor prognosis in ER+ luminal breast tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE104985 KDM5 Histone Demethylase Activity Links Cellular Transcriptomic Heterogeneity to Therapeutic Resistance. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2018.10.014 {Cancer cell (23.916): 10.1016/j.ccell.2018.10.014} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA414329 https://www.ebi.ac.uk/ena/browser/view/PRJNA414329 https://www.ncbi.nlm.nih.gov/sra?term=SRP119970 [Overal design]RNA-Seq of parental and multiple resistant breast cancer cell lines; [Treatment]'MCF7, C70R, C49R, FULVR and TAMR cells were treated with E2 (100 nM) or three different inhibitors: fulvestrant (1 μM), KDM5-C70 (10 μM) and KDM5-C49 (10 μM).'; [Growth]'MCF7, C70R and C49R cells were cultured in DMEM supplemented with 10% FBS, 1% penicillin/streptomycin and 10 μg ml−1 insulin. FULVR and TAMR cells are cultured in RPMI without phenol red supplemented with 10% charcoal-stripped FBS, 1% penicillin/streptomycin and 10 μg ml−1 insulin. For the analysis between MCF7, FULVR and TAMR, MCF7 cells are cultured in RPMI without phenol red supplemented with 10% charcoal-stripped FBS, 1% penicillin/streptomycin and 10 μg ml−1 insulin. Cells were cultured in RPMI without phenol red supplemented with 10% charcoal-stripped FBS, 1% penicillin/streptomycin for E2 and its corresponding control.'; [Extraction]'Total RNA was extracted using the RNeasy Mini Kit (Qiagen).\nRNA-seq libraries were prepared using Illumina TruSeq Stranded mRNA sample preparation kits from 500 ng of purified total RNA according to the manufacturer’s protocol. The finished dsDNA libraries were quantified by Qubit fluorometer, Agilent TapeStation 2200, and RT-qPCR using the Kapa Biosystems library quantification kit according to manufacturer’s protocols.'; [Cell type]'Source: ''cell line: MCF7; treatment time: None; ', 'cell line: MCF7; treatment time: C49 14day; ', 'cell line: MCF7; treatment time: C49 2day; ', 'cell line: MCF7; treatment time: C49 7day; ', 'cell line: MCF7; treatment time: C70 14day; ', 'cell line: MCF7; treatment time: C70 2day; ', 'cell line: MCF7; treatment time: C70 7day; ', 'cell line: C49R; treatment time: None; ', 'cell line: C49R; treatment time: C49 2day; ', 'cell line: C49R; treatment time: C70 2day; ', 'cell line: C70R; treatment time: None; ', 'cell line: C70R; treatment time: C49 2day; ', 'cell line: C70R; treatment time: C70 2day; ', 'cell line: C49R; treatment time: E2 3hour; ', 'cell line: C49R; treatment time: E2 6hour; ', 'cell line: C70R; treatment time: E2 3hour; ', 'cell line: C70R; treatment time: E2 6hour; ', 'cell line: MCF7; treatment time: E2 3hour; ', 'cell line: MCF7; treatment time: E2 6hour; ', 'cell line: FULR; treatment time: None; ', 'cell line: TAMR; treatment time: None; ', 'cell line: MCF7; treatment: None; time: control; ', 'cell line: MCF7; treatment: FULV; time: 7day; ', 'cell line: FULVR; treatment: None; time: control; ', 'cell line: FULVR; treatment: FULV; time: 2day; ', 'cell line: BT474; treatment: None; time: control; ', 'cell line: BT474; treatment: C70; time: 7day; ', 'cell line: FULVR; treatment: C70; time: 7day; ', 'cell line: SUM159; treatment: None; time: control; ', 'cell line: SUM159; treatment: C70; time: 7day; ', 'cell line: T47D; treatment: None; time: control; ', 'cell line: T47D; treatment: C70; time: 7day; ', 'cell line: ZR75; treatment: None; time: control; ', 'cell line: ZR75; treatment: C70; time: 7day; ' GSE58887 Homo sapiens 17 Expression profiling by array; Genome variation profiling by genome tiling array GPL9128; GPL18850 Drug screening and genomic analyses of HER2 positive breast cancer cell lines reveal predictors for treatment response 2014-06-27 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58887 None None None None None 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA253811 https://www.ebi.ac.uk/ena/browser/view/PRJNA253811 None [Overal design]Refer to individual Series; [Treatment]'None', 'No treatment'; [Growth]'All cells were grown according to protocol provided by manufacturer.'; [Extraction]'Total RNA was isolated from all cell lines using the Rneasy kit by Qiagen, and isolated according to the protocol provided by Qiagen.', 'TriZOL'; [Cell type]'Source: ''gender: female; cell line: AU565; ', 'gender: female; cell line: BT474; ', 'gender: female; cell line: EFM-192A; ', 'gender: female; cell line: HCC1419; ', 'gender: female; cell line: HCC1569; ', 'gender: female; cell line: HCC1954; ', 'gender: female; cell line: HCC202; ', 'gender: female; cell line: JIMT1; ', 'gender: female; cell line: KPL4; ', 'gender: female; cell line: MDA-MB-453; ', 'gender: female; cell line: SKBR3; ', 'gender: female; cell line: SUM190PT; ', 'gender: female; cell line: SUM225; ', 'gender: female; her2 status: positive; ', 'gender: female; ' GSE23978 Mus musculus 46 Non-coding RNA profiling by array GPL10880 Genomic Profiling of mouse mammary tumor models identifies miRNA signatures associated with mammary tumor lineage (primary tumors and normal mammary glands) 2010-09-03 MicroRNAs (miRNAs) are small, non-coding, endogenous RNAs involved in many human diseases including breast cancer. miRNA expression profiling of human breast cancers has identified miRNAs related to the clinical diversity of the disease and potentially provides novel diagnostic and prognostic tools for breast cancer therapy. In order to further understand the roles of miRNAs in association with oncogenic drivers and in specifying sub-types of breast cancer, we performed miRNAexpression profiling on mammary tumors from eight well-characterized genetically -engineered Mouse (GEM) models of human breast cancer including MMTV–H-Ras, -Her2/neu, -c-Myc, -PymT, –Wnt1 and C3(1)/SV40 T/t-antigen transgenic mice, BRCA1fl/fl;p53+/-;MMTV-cre and the p53fl/fl ;MMTV-cre transplant model. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23978 Integrated miRNA and mRNA expression profiling of mouse mammary tumor models identifies miRNA signatures associated with mammary tumor lineage. Genome biology 14.028 https://doi.org/10.1186/gb-2011-12-8-r77 {Genome biology (14.028): 10.1186/gb-2011-12-8-r77} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA130467 https://www.ebi.ac.uk/ena/browser/view/PRJNA130467 None [Overal design]miRNA expression data for 41 mouse primary mammary tumors and 5 mouse normal mammary glands; [Treatment]'None'; [Growth]'None'; [Extraction]'The total RNA containing the microRNA species were extracted from tumor and tissue samples using mirVana miRNA Isolation kit (Ambion).'; [Cell type]'Source: ''strain: FVB; ', 'strain: Balb/C; ', 'strain: 129B6/FVB; ' GSE78758 Homo sapiens 116 Methylation profiling by array; Methylation profiling by high throughput sequencing; Third-party reanalysis GPL10999; GPL13534 DNA methylation profile of triple negative breast cancer specific genes 2016-02-29 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE78758 DNA methylation profile of triple negative breast cancer-specific genes comparing lymph node positive patients to lymph node negative patients. Scientific reports 4.011 https://doi.org/10.1038/srep33435 {Scientific reports (4.011): 10.1038/srep33435} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA313436 https://www.ebi.ac.uk/ena/browser/view/PRJNA313436 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None', 'DNA was extracted from cells microdissected from human tissue samples representing normal breast and tumor breast tissue.'; [Extraction]'genomic DNA was extracted from FFPE samples using Qiagen Gentra Puregene Tissue Kit', 'The MethylMinerTM Methylated DNA Enrichment Kit (Invitrogen) was used to isolate methylated DNA from 500 ng – 1 μg of genomic FFPET DNA.\n10ng DNA of MBDCap enriched DNA was prepared for Ilumina sequencing using the Illumina ChIP-Seq DNA sample prep kit (IP-102-1001) according to the manufacturer’s instructions. The library preparation was analyzed on Agilent High Sensitivity DNA 1000 Chip.'; [Cell type]'Source: ''gender: female; tumour grade: 3; tissue type: IDC; ', 'gender: female; tumour grade: 3; tissue type: LN; ', 'gender: female; tumour grade: 3; tissue type: NAT; ', 'gender: female; tumour grade: 1; age at diagnosis: 51.94; survival: dead; disease specific death: FALSE; month of follow up/to death: 186; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 52.1; survival: dead; disease specific death: TRUE; month of follow up/to death: 44; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 37; survival: dead; disease specific death: TRUE; month of follow up/to death: 16; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 66; survival: dead; disease specific death: TRUE; month of follow up/to death: 82; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 76; survival: alive; disease specific death: FALSE; month of follow up/to death: 113; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 45; survival: dead; disease specific death: TRUE; month of follow up/to death: 40; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 71; survival: alive; disease specific death: FALSE; month of follow up/to death: 68; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 62; survival: alive; disease specific death: FALSE; month of follow up/to death: 52; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 81; survival: dead; disease specific death: FALSE; month of follow up/to death: 8; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 75; survival: NA; disease specific death: NA; month of follow up/to death: 17; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 45; survival: dead; disease specific death: FALSE; month of follow up/to death: 35; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 42; survival: alive; disease specific death: FALSE; month of follow up/to death: 140; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 41; survival: dead; disease specific death: TRUE; month of follow up/to death: 39; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 37; survival: alive; disease specific death: FALSE; month of follow up/to death: 172; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 52.55; survival: dead; disease specific death: TRUE; month of follow up/to death: 61; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 68.26; survival: dead; disease specific death: FALSE; month of follow up/to death: NA; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 70; survival: dead; disease specific death: TRUE; month of follow up/to death: 33; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 37; survival: alive; disease specific death: FALSE; month of follow up/to death: 7; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 71; survival: dead; disease specific death: TRUE; month of follow up/to death: 17; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 74; survival: alive; disease specific death: FALSE; month of follow up/to death: 170; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 41; survival: dead; disease specific death: TRUE; month of follow up/to death: 23; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 59; survival: alive; disease specific death: FALSE; month of follow up/to death: 66; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 59; survival: dead; disease specific death: TRUE; month of follow up/to death: 21; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 83; survival: alive; disease specific death: FALSE; month of follow up/to death: 46; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 42; survival: dead; disease specific death: FALSE; month of follow up/to death: 37; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 32; survival: alive; disease specific death: FALSE; month of follow up/to death: 66; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 44; survival: dead; disease specific death: FALSE; month of follow up/to death: 29; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 35; survival: alive; disease specific death: FALSE; month of follow up/to death: 46; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 43; survival: dead; disease specific death: FALSE; month of follow up/to death: 62; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 61; survival: alive; disease specific death: FALSE; month of follow up/to death: 48; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 39; survival: dead; disease specific death: FALSE; month of follow up/to death: 40; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 55.46; survival: dead; disease specific death: FALSE; month of follow up/to death: 188; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 29.09; survival: dead; disease specific death: TRUE; month of follow up/to death: NA; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 32; survival: alive; disease specific death: FALSE; month of follow up/to death: 49; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 74; survival: dead; disease specific death: TRUE; month of follow up/to death: 24; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 45; survival: alive; disease specific death: FALSE; month of follow up/to death: 169; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 55.9; survival: dead; disease specific death: FALSE; month of follow up/to death: 131; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 30; survival: dead; disease specific death: TRUE; month of follow up/to death: 43; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 62; survival: dead; disease specific death: TRUE; month of follow up/to death: 7; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 45.64; survival: dead; disease specific death: TRUE; month of follow up/to death: 32; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 44; survival: dead; disease specific death: TRUE; month of follow up/to death: 38; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: NA; survival: alive; disease specific death: FALSE; month of follow up/to death: NA; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 47; survival: dead; disease specific death: TRUE; month of follow up/to death: 27; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 62; survival: alive; disease specific death: FALSE; month of follow up/to death: 35; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 67; survival: alive; disease specific death: FALSE; month of follow up/to death: 28; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 56.59; survival: dead; disease specific death: TRUE; month of follow up/to death: 30; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 47; survival: dead; disease specific death: TRUE; month of follow up/to death: 8; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 79; survival: dead; disease specific death: TRUE; month of follow up/to death: 103; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 69; survival: NA; disease specific death: NA; month of follow up/to death: 34; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 39; survival: dead; disease specific death: FALSE; month of follow up/to death: 62; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 54.58; survival: dead; disease specific death: TRUE; month of follow up/to death: 23; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 78; survival: alive; disease specific death: FALSE; month of follow up/to death: 49; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 60; survival: dead; disease specific death: TRUE; month of follow up/to death: 24; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 44; survival: dead; disease specific death: TRUE; month of follow up/to death: 81; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 39; survival: alive; disease specific death: FALSE; month of follow up/to death: 46; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 38.84; survival: dead; disease specific death: TRUE; month of follow up/to death: 44; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 46; survival: alive; disease specific death: FALSE; month of follow up/to death: 43; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 45.38; survival: alive; disease specific death: FALSE; month of follow up/to death: 194; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 66.18; survival: dead; disease specific death: TRUE; month of follow up/to death: 69; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 68; survival: dead; disease specific death: FALSE; month of follow up/to death: 59; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 38; survival: dead; disease specific death: TRUE; month of follow up/to death: 18; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 39; survival: dead; disease specific death: FALSE; month of follow up/to death: 168; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 62; survival: dead; disease specific death: TRUE; month of follow up/to death: 9; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 62; survival: dead; disease specific death: FALSE; month of follow up/to death: 148; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 78; survival: dead; disease specific death: TRUE; month of follow up/to death: 15; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 60; survival: dead; disease specific death: TRUE; month of follow up/to death: 195; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 62; survival: dead; disease specific death: TRUE; month of follow up/to death: 102; tissue type: IDC; ', 'gender: female; tumour grade: 3; age at diagnosis: 58; survival: dead; disease specific death: TRUE; month of follow up/to death: 45; tissue type: IDC; ', 'tissue: lymph node metastatic breast tumour tissue; ' GSE32052 Homo sapiens 2 Expression profiling by array GPL570 Role of S100A7 in regulating inflammatory pathways during mammary tumorigenesis 2011-09-12 Psoriasin (S100A7) has been shown to be highly expressed in invasive estrogen receptor negative breast cancers. Expression of S100A7 in human breast tumors represents a poor prognostic marker and correlates with lymphocyte infiltration in high-grade morphology. Recent studies have shown that S100A7 downregulation in ERα- cells lines inhibits tumor growth in in vivo mouse model systems. However, not much is known about its mechanisms in regulating breast cancers. We used microarrays to determine the global differential gene expression in S100A7 overexpressing breast cells and vector control cells and found out that most of the genes involved in inflammatory pathways were differentially regulated. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32052 S100A7 enhances mammary tumorigenesis through upregulation of inflammatory pathways. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-11-0669 {Cancer research (8.378): 10.1158/0008-5472.CAN-11-0669} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA147669 https://www.ebi.ac.uk/ena/browser/view/PRJNA147669 None [Overal design]S100A7 was sub-cloned into pIRES2-EGFP plasmid which was then transfected into MDA-MB 231 breast cancers cells to select stable cells. Cells transfected with into pIRES2-EGFP only served as vector control. Then microarray analysis was done on these cells to determine the genes which were regulated by S100A7.; [Treatment]'None'; [Growth]'The cells were cultured in Dulbecco’s modified Eagle Medium (DMEM) with 10% fetal bovine serum and 1% Pencillin-streptomyocin at 37°C and 5% CO2. Characteristic features of cultured lines (morphology, doubling time, and so on) were continually monitored for detection of potential cross-contamination by light microscopy'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MDA-MB 231; transfection: pIRES2-EGFP; ', 'cell line: MDA-MB 231; transfection: S100A7 sub-cloned into pIRES2-EGFP; ' GSE83818 Homo sapiens 2 Expression profiling by array GPL570 Expression data from KDM3A knockdown MDA-MB-231 cells 2016-06-28 Breast cancer invasive growth, metastasis and therapeutic resistance affects the clinical ourcome. We explored the epigenetic mechanisms that control these process in breast cancer cell line, MDA-MB-231 by knocking down a lysine specific demethylase KDM3A We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE83818 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA327095 https://www.ebi.ac.uk/ena/browser/view/PRJNA327095 None [Overal design]Human breast cancer cell line MDA-MB-231 was infected with scramble or KDM3A shRNA. After selection, the cells were used for microarray analysis.; [Treatment]'The cells were transfected with scramble or KDM3A shRNA. After puromycin (1 mcg/ml) selection, cells were used.'; [Growth]'Hunam breast cancer cell line, MDA-MB-231 was cultured by standard protocl using DMEM with 10% FBS and antibiotics'; [Extraction]'RNA was extracted using RNeasy kit (quagen) following manufacturers protocol'; [Cell type]'Epithelial''cell line: MDA-MB-231; infection: scramble shRNA; tissue: Mammary gland/breast; derived from metastatic site: pleural effusion; cell type: Epithelial; age: Derived from 51 years old female; ', 'cell line: MDA-MB-231; infection: KDM3A shRNA; tissue: mammary gland/breast; derived from metastatic site: pleural effusion; cell type: Epithelial; age: Derived from 51 years old female; ' GSE125117 Homo sapiens 18 Genome binding/occupancy profiling by high throughput sequencing GPL16791 ChIP-seq analysis of genome-edited MCF7 and T47D ESR1 mutant cell models 2019-01-15 This study is designed to comprehensively characterize the cistromes of Y537S and D538G mutated ER versus WT ER in breast cancer cells. Genome-edited MCF7 and T47D cells were hormone deprived and treated with or without E2 for 45 minuts. Chromatin DNA was then extracted from each sample. The immunoprecipitation was performed using ERα (Santa Cruz Biotechnologies, sc543) antibody. Pooled DNA samples from individual clones were sent to sequencing with Illumina Hiseq 2500 Platform. ChIP-seq reads were aligned to either hg38 genome assembly using Bowtie 2.0, and peaks were called using MACS2.0 with p value below 10E-5. DiffBind was used to perform principle component analysis, identify differentially expressed binding sites and analyze intersection ratios with other data sets. Genomic feature distribution were called using ChIPseeker. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE125117 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA515270 https://www.ebi.ac.uk/ena/browser/view/PRJNA515270 https://www.ncbi.nlm.nih.gov/sra?term=SRP179616 [Overal design]Individual clones of genome-eidted MCF7 and T47D cell lines with knock-in of WT/Y537S/D538G ER were hromone deprived and treated with veh or 1 nM E2 for 45 minutes. Chromatin DNA was then extracted from each sample. The immunoprecipitation was performed using ERα (sc543) antibody (Santa Cruz Biotechnologies). Pooled DNA samples from individual clones were sent to sequencing with Illumina Hiseq 2500 Platform.; [Treatment]'Cells were washed with pheno-red-free CSS with 5% (MCF7) or 10% (T47D) CSS for 3 days, then treated with 1 nM E2 or 1% Ethanol for 45 minutes.'; [Growth]'Individual clones were maintained in RPMI 1640 (T47D) and DMEM (MCF7) respectively, supplemented with 10 % FBS, 100 μg/mL penicillin and 100 mg/mL streptomycin, at 37 °C in a humidified incubator with 5% CO2.'; [Extraction]'Lysates were clarified from sonicated nuclei and ER-bound DNA complexes were isolated with antibody (Santa Cruz, sc-543).\nChIP was performed according to our in-house protocols. A minimum of 10ng DNA was sent to McGill University sequencing core. The library was prepared using TruSeq ChIP Library Preperation kit (Illumina) and was sequenced on Hiseq 2500 (Illumina). Over 16M single end 50bp reads were allocated for each sample.'; [Cell type]'Source: ''esr1 genotype: Wild-type; treatments: None; chip antibody: None; ', 'esr1 genotype: Wild-type; treatments: Vehicle; chip antibody: ERα (Santa Cruz Biotechnologies, sc543); ', 'esr1 genotype: Wild-type; treatments: 1 nM E2; chip antibody: ERα (Santa Cruz Biotechnologies, sc543); ', 'esr1 genotype: Y537S; treatments: None; chip antibody: None; ', 'esr1 genotype: Y537S; treatments: Vehicle; chip antibody: ERα (Santa Cruz Biotechnologies, sc543); ', 'esr1 genotype: Y537S; treatments: 1 nM E2; chip antibody: ERα (Santa Cruz Biotechnologies, sc543); ', 'esr1 genotype: D538G; treatments: None; chip antibody: None; ', 'esr1 genotype: D538G; treatments: Vehicle; chip antibody: ERα (Santa Cruz Biotechnologies, sc543); ', 'esr1 genotype: D538G; treatments: 1 nM E2; chip antibody: ERα (Santa Cruz Biotechnologies, sc543); ' GSE36102 Homo sapiens 8 Expression profiling by array GPL10558 Cancer stem cells from lobular infiltrating breast tumor metastasize to bone and acquire a gene signature associated to bone tropism 2012-02-27 We investigated the role of breast cancer stem-like cells (CSCs-like), isolated from primary tumor, in promoting bone metastases in a human-in-mice model. Luciferase-transduced CD44+CD24- breast CSCs-like were injected through subcutaneous (SC) and intracardiac (IC) route in nonobese/severe combined immunodeficient (NOD/SCID) mice carrying subcutaneous human bone implants. The implanted bone was viable, active and human neo-vascularization was present. By in vivo luciferase imaging, we monitored tumor growth and detected bone-localized breast CSCs-like, both after SC and IC injection. Bone metastatic lesions were histologically evident, and tumor cells expressed epithelial markers and vimentin. Bone metastatic cells isolated from bone implants showed a CD44-CD24+ phenotype and re-created tumors and bone metastases after injection in secondary mice. A “bone tropism” expression signature was found to distinguish bone-colonizing cells from parental CSCs-like and to persist at subsequent passages also in the absence of surrounding bone tissue. The bone tropism signature displayed significant enrichment in genes discriminating bone metastases of breast cancer from metastases at other organs. Our results demonstrate the ability of breast CSCs-like to promote bone metastasis and provide a CSCs-like bone tropism signature, with potential prognostic value. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36102 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA152975 https://www.ebi.ac.uk/ena/browser/view/PRJNA152975 None [Overal design]C10 breast cancer stem-like cells (CSCs-like) were derived as mammospheres from a lobular-infiltrating breast carcinoma (ER+, HER2-). Samples are organized in the following groups: (i) Breast CSCs-like (C10, duplicate); (ii) Luciferase-transduced CSCs-like (C10L, simplicate); (iii) Bone-isolated C10L metastatic cells (C10-bone, duplicate) and subsequently (iv) grown in vitro as spheroids (C10-CSC, simplicate) or (v) re-grown in subcutaneous implants (C10-SC, duplicate).; [Treatment]'Cells were grown as mammospheres before harvesting RNA.'; [Growth]'Breast CSCs-like and the bone metastatic cells were grown in DMEM F12 with 10ng/ml b-FGF, 20 ng/ml EGF, 5mg/ml insulin and 0,4% bovine serum albumine'; [Extraction]'RNA extraction was performed using Trizol plus RNA purification kit (Invitrogen). RNA qualitative and quantitative assessment was performed using the Bioanalyzer 2100 (Agilent Tecnologies).'; [Cell type]'breast cancer stem-like cells (CSCs-like)''cell line: C10; cell type: breast cancer stem-like cells (CSCs-like); cell hystology: CD44+CD24-; cell description: CSCs-like isolated from primary lobular infiltrating breast carcinoma (ER+, HER2-); ', 'cell line: C10; cell type: breast cancer stem-like cells (CSCs-like); cell hystology: CD44+CD24-; cell description: breast CSCs-like transduced with a luciferase-lentiviral expression vector; ', 'cell line: C10; cell type: breast cancer stem-like cells (CSCs-like); cell hystology: CD44-CD24+; cell description: metastatic cells isolated from the human implanted bone; ', 'cell line: C10; cell type: breast cancer stem-like cells (CSCs-like); cell hystology: CD44-CD24+; cell description: metastatic cells isolated from the human implanted bone and cultured in vitro as spheroids; ', 'cell line: C10; cell type: breast cancer stem-like cells (CSCs-like); cell hystology: CD44+CD24-; cell description: CSCs-like isolated from tumor masses in secondary mice; ' GSE101562 Homo sapiens 14 Genome binding/occupancy profiling by high throughput sequencing; Other GPL11154 JMJD6 licenses estrogen receptor alpha-dependent enhancer RNA and coding gene activation by modulating CARM1/MED12 co-activator complex in breast cancer 2017-07-18 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE101562 JMJD6 Licenses ERα-Dependent Enhancer and Coding Gene Activation by Modulating the Recruitment of the CARM1/MED12 Co-activator Complex. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2018.03.006 {Molecular cell (14.548): 10.1016/j.molcel.2018.03.006} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA394829 https://www.ebi.ac.uk/ena/browser/view/PRJNA394829 None [Overal design]Refer to individual Series; [Treatment]'MCF7 cells were maintained in stripping medium (phenol red free) for three days before treating with or without estrogen (E2, 10-7 M) for 1h.'; [Growth]'MCF7 cells were cultured in DMEM medium supplemented with 10% FBS.'; [Extraction]'Cells were then fixed with 1% formaldehyde (Sigma) for 10 mins at room temperature (RT) (for MED12 and Pol II ChIP), or fixed with disuccinimidyl glutarate (DSG) (2mM) (Proteochem) for 45 min at RT, washed twice with PBS and then double-fixed with 1% formaldehyde for another 10 min at RT (for JMJD6 ChIP). Fixation was stopped by adding glycine (0.125M) and incubated for 5 mins at RT, followed by washing with PBS twice. Chromatin DNA was sheared to 300~500 bp average in size through sonication. Resultant was immunoprecipitated with anti-MED12, anti-Pol II or anti-JMJD6 antibody overnight at 4°C, followed by incubation with protein G magnetic beads (Invitrogen) for an additional 2 hrs. After washing and elution, the protein-DNA complex was reversed by heating at 65°C overnight. Immunoprecipitated DNA was purified by using QIAquick spin columns (Qiagen) and subjected to high throughput sequencing.\nThe libraries were constructed following Illumina’s Chip-Seq Sample prep kit. Briefly, Chip DNA was end-blunted and added with an ‘A’ base so the adaptors from Illumina with a ‘T’ can ligate on the ends. Then 200–400 bp fragments are gel-isolated and purified. The library was amplified by 18 cycles of PCR.', 'MCF7 cells were washed 3 times with cold 1X phosphate buffered saline (PBS) buffer and then incubated in swelling buffer (10mM Tris-Cl pH7.5, 2mM MgCl2, 3mM CaCl2) for 5min on ice and harvested. Cells were first re-suspended and lysed in lysis buffer (swelling buffer with 0.5% IGEPAL and 10% glycerol). The resultant nuclei were washed once again with 10 ml lysis buffer and then re-suspended in 100ml of freezing buffer (50mM Tris-Cl pH 8.3, 40% glycerol, 5mM MgCl2, 0.1mM EDTA).\nFor run-on assay, resuspended nuclei were mixed with an equal volume of reaction buffer (10mM Tris-Cl pH 8.0, 5mM MgCl2, 1mM DTT, 300mM KCl, 20 units of SUPERase In, 1% sarkosyl, 500mM ATP, GTP, and Br-UTP, 2mM CTP) and incubated for 5 min at 30°C. The nuclear-run-on RNA (NRO-RNA) was then extracted with TRIzol LS reagent (Invitogen) following manufacturer’s instructions. NRO-RNA was then subjected to base hydrolysis on ice for 40 min and followed by treatment with DNase I and antarctic phosphatase. To purify the Br-UTP labeled nascent RNA, the NRO-RNA was immunoprecipitated with an anti-BrdU agarose beads (Santa Cruz Biotech) in binding buffer (0.5XSSPE, 1mM EDTA, 0.05% tween-20) for 1h at 4°C while rotating. To repair the end, the immunoprecipitated BrU-RNA was re-suspended in 50mL reaction (43mL DEPC water, 5.2mL T4 PNK buffer, 1mL SUPERase In and 1mL T4 PNK (New England BioLabs)) and incubated at 37°C for 1h. RNA was then extracted, precipitated using acidic phenol-chloroform (Ambion) and subjected to poly-A tailing reaction by using poly-A polymerase (New England BioLabs) for 30 min at 37°C. Subsequently, reverse transcription was performed using oNTI223- primers (5’- pGATCGTCGGACTGTAGAACTCT; CAAGCAGAAGACGGCATACGATTTTTTTTTTTTTTTTTTTTVN-3’) where the p indicates 5’ phosphorylation, ‘;’ indicates the abasic dSpacer furan and VN indicates degenerate nucleotides. Specifically, tailed RNA (8.0mL) was subjected to reverse transcription using superscript III (Invitrogen), after which the cDNA products were separated on a 10% polyacrylamide TBE-urea gel. The extended first-strand product (100-500bp) was excised and recovered by gel extraction. After that, the first-strand cDNA was circularized by CircLigase (Epicentre) and re-linearized by Ape1 (New England BioLabs). Re-linearized single strand cDNA (sscDNA) was separated in a 10% polyacrylamide TBE gel as described above and the product of needed size was excised (~170-400bp) for gel extraction. Finally, sscDNA template was amplified by PCR using the Phusion High-Fidelity enzyme (NEB) according to the manufacturer’s instructions. Primers oNTI200 (5’-CAAGCAGAAGACGGCATA-3’) and oNTI201 (5’- AATGATACGGCGACCACCGACAGGTTCAGAGTTCTACAGTCCGACG-3’) were used to generate DNAs for deep sequencing.'; [Cell type]'Source: ''antibody: JMJD6; treatment: none; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); antibody catalog/vendor: ab10526(Abcam); ', 'antibody: JMJD6; treatment: E2; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); antibody catalog/vendor: ab10526(Abcam); ', 'antibody: PolII; sirna: siCTL; treatment: none; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); antibody catalog/vendor: SC-899(Santa Cruz Biotechnology); ', 'antibody: PolII; sirna: siCTL; treatment: E2; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); antibody catalog/vendor: SC-899(Santa Cruz Biotechnology); ', 'antibody: PolII; sirna: siJMJD6; treatment: none; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); antibody catalog/vendor: SC-899(Santa Cruz Biotechnology); ', 'antibody: PolII; sirna: siJMJD6; treatment: E2; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); antibody catalog/vendor: SC-899(Santa Cruz Biotechnology); ', 'antibody: Med12; sirna: siCTL; treatment: none; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); antibody catalog/vendor: A300-774A(Bethyl Laboratory); ', 'antibody: Med12; sirna: siCTL; treatment: E2; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); antibody catalog/vendor: A300-774A(Bethyl Laboratory); ', 'antibody: Med12; sirna: siJMJD6; treatment: none; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); antibody catalog/vendor: A300-774A(Bethyl Laboratory); ', 'antibody: Med12; sirna: siJMJD6; treatment: E2; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); antibody catalog/vendor: A300-774A(Bethyl Laboratory); ', 'sirna: siCTL; treatment: none; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); ', 'sirna: siCTL; treatment: E2; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); ', 'sirna: siJMJD6; treatment: none; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); ', 'sirna: siJMJD6; treatment: E2; cell line: Michigan Cancer Foundation-7 cells(MCF-7 cells); ' GSE25429 Homo sapiens 129 Expression profiling by array GPL570; GPL3921 Gene expression profiles of primary cultured ovarian cells and ovarian cancer cell lines in the presence and absence of a DNA methyltransferase inhibitor 2010-11-16 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE25429 Epigenetic suppression of the TGF-beta pathway revealed by transcriptome profiling in ovarian cancer. Genome research 9.944 https://doi.org/10.1101/gr.108803.110 {Genome research (9.944) doi:10.1101/gr.108803.110}; {Frontiers in oncology (4.137) doi:10.3389/fonc.2013.00269}; {Frontiers in oncology (4.137) doi:10.3389/fonc.2013.00131}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA133783 https://www.ebi.ac.uk/ena/browser/view/PRJNA133783 None [Overal design]Refer to individual Series; [Treatment]'When confluent, cells underwent selective trypsinization to remove fibroblasts and were divided into two dishes and grown until ~70% confluent, at which time they were mock treated or treated with 5 µM 5-azacytidine (5-azaC) for 72 hours. Normal OSE (NO) cells were similarly treated, but due to small numbers of cells, we pooled specimens from five individuals to use for each of the arrays. All specimen cultures were analyzed by immunocytochemical staining using anti-cytokeratin antibodies; only cultures with >90% epithelial content were used for the microarrays.', "At ~70% confluence, cells were either mock treated with tissue culture media (Mock) or with 5 µM 5-aza-2'-deoxxycytidine (Decitabine) for 72 hours."; [Growth]'Cells were grown in a 1:1 mixture of Medium 199 and MCDB 105 medium with 15% FBS in a humidifed incubator maintained at 37 degrees Celsius with 5% CO2 until confluent.', 'All cells, including sorted CD133+ and CD133- A2780 and PEO1 cells, were grown in RPMI1640 media with 10% FBS in a humidifed incubator maintained at 37 degrees Celsius with 5% CO2 until ~70% confluent.'; [Extraction]'RNA Stat-60.'; [Cell type]'normal ovarian surface epithelium', 'serous borderline ovarian cells', 'serous epithelial ovarian cancer cells', 'endometrioid ovarian cancer cells', 'ovarian cancer cells', 'breast cancer cells', 'cervical cancer cells''tissue: ovary; cell type: normal ovarian surface epithelium; gender: female; treatment: mock; ', 'tissue: ovary; cell type: serous borderline ovarian cells; gender: female; treatment: mock; ', 'tissue: ovary; cell type: serous epithelial ovarian cancer cells; gender: female; treatment: mock; ', 'tissue: ovary; cell type: endometrioid ovarian cancer cells; gender: female; treatment: mock; ', 'tissue: ovary; cell type: normal ovarian surface epithelium; gender: female; treatment: 5-azacytidine (5-AzaC); ', 'tissue: ovary; cell type: serous borderline ovarian cells; gender: female; treatment: 5-azacytidine (5-AzaC); ', 'tissue: ovary; cell type: serous epithelial ovarian cancer cells; gender: female; treatment: 5-azacytidine (5-AzaC); ', 'tissue: ovary; cell type: endometrioid ovarian cancer cells; gender: female; treatment: 5-azacytidine (5-AzaC); ', 'cell line: 41M-cisR; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: HEY; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: HEYA8; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: HEYC2; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: PEO1; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: PEO4; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: MCF7; cell type: breast cancer cells; gender: female; treatment: mock; ', 'cell line: OVCAR-2; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCAR-3; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCAR-5; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCAR-8; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCAR-10; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: SKOV-3; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: SKOV-4; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: SKOV-6; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: SKOV-8; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCA420; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCA429; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCA432; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCA433; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVARY1847; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: PA-1; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: DOV13A; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: DOV13B; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: DOV13; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: CAOV-2; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: CAOV-3; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: CH1; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: CH1-cisR; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: TOV-112D; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: Tyk-nu; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: Tyk-nu-cisR; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: A2780; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: A2780-cisR; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: FUOV1; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OV90; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: ME-180; cell type: cervical cancer cells; gender: female; treatment: mock; ', 'cell line: IGROV1; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: ME-180A; cell type: cervical cancer cells; gender: female; treatment: mock; ', 'cell line: 41M; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: TOV-21G; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: ME-180C; cell type: cervical cancer cells; gender: female; treatment: mock; ', 'cell line: MCAS; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: 41M-cisR; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: HEY; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: HEYA8; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: HEYC2; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: PEO1; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: PEO4; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: MCF7; cell type: breast cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCAR-2; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCAR-3; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCAR-5; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCAR-8; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCAR-10; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: SKOV-3; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: SKOV-4; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: SKOV-6; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: SKOV-8; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCA420; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCA429; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCA432; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCA433; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVARY1847; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: PA-1; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: DOV13A; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: DOV13B; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: DOV13; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: CAOV-2; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: CAOV-3; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: CH1; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: CH1-cisR; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: TOV-112D; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: Tyk-nu; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: Tyk-nu-cisR; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: A2780; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: A2780-cisR; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: FUOV1; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OV90; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: ME-180; cell type: cervical cancer cells; gender: female; treatment: decitabine; ', 'cell line: IGROV1; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: ME-180A; cell type: cervical cancer cells; gender: female; treatment: decitabine; ', 'cell line: 41M; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: TOV-21G; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: ME-180C; cell type: cervical cancer cells; gender: female; treatment: decitabine; ', 'cell line: MCAS; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: A2780; cell type: ovarian cancer cells; cell population: CD133+; gender: female; treatment: mock; ', 'cell line: A2780; cell type: ovarian cancer cells; cell population: CD133+; gender: female; treatment: decitabine; ', 'cell line: A2780; cell type: ovarian cancer cells; cell population: CD133-; gender: female; treatment: mock; ', 'cell line: A2780; cell type: ovarian cancer cells; cell population: CD133-; gender: female; treatment: decitabine; ', 'cell line: PEO1; cell type: ovarian cancer cells; cell population: CD133+; gender: female; treatment: mock; ', 'cell line: PEO1; cell type: ovarian cancer cells; cell population: CD133+; gender: female; treatment: decitabine; ', 'cell line: PEO1; cell type: ovarian cancer cells; cell population: CD133-; gender: female; treatment: mock; ', 'cell line: PEO1; cell type: ovarian cancer cells; cell population: CD133-; gender: female; treatment: decitabine; ' GSE49119 Homo sapiens 9 Expression profiling by array GPL6947 Histone demethylase RBP2 is critical for breast cancer progression and metastasis 2013-07-23 To determine the roles of RBP2 in breast cancer metastasis, MDA-MD-231 cells were transfected with siRNAs against RBP2 or luciferase control, followed with gene expression microarray analysis and gene set enrichment analysis. These analyses revealed that RBP2 knockdown significantly decreased expression of genes linked to breast cancer metastasis to lung. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE49119 Histone demethylase RBP2 is critical for breast cancer progression and metastasis. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2014.02.004 {Cell reports (7.815): 10.1016/j.celrep.2014.02.004} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA213069 https://www.ebi.ac.uk/ena/browser/view/PRJNA213069 None [Overal design]Total RNA obtained from the breast cancer cell line MDA-MB231 72 hours after transfection with siRNA targeting KDM5A/RBP2/JARID1A, and targeting Luceferase gene as a control.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed by electrophoresis in agarose gel.'; [Cell type]'Source: ''cell line: breast cancer cell line MDA-MB231; genotype/variation: control; ', 'cell line: breast cancer cell line MDA-MB231; genotype/variation: KD2; ', 'cell line: breast cancer cell line MDA-MB231; genotype/variation: KD1; ' GSE80297 Homo sapiens 87 Expression profiling by high throughput sequencing GPL16791 mRNA expression of breast cancer cell lines across different densities [SCRB-Seq] 2016-04-14 mRNA expression profiles for 3 breast cancer cell lines seeded at different density and grown for different duration https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80297 Growth rate inhibition metrics correct for confounders in measuring sensitivity to cancer drugs. Nature methods 28.467 https://doi.org/10.1038/nmeth.3853 {Nature methods (28.467): 10.1038/nmeth.3853} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA318513 https://www.ebi.ac.uk/ena/browser/view/PRJNA318513 https://www.ncbi.nlm.nih.gov/sra?term=SRP073318 [Overal design]This experiment is part of a study fo the effect of cell density on drug sensitivity [1]. Cells plated at different densities in 384-well plates were harvested at the indicated times and RNA was extracted using the RNeasy mini kit (Qiagen). To ensure sufficient RNA amounts wells with low cell numbers were pooled. Some conditions have been tested in biollogical replicates grown at the same time. Libraries were prepared by the Broad Technology Labs (BTL) following the protocol for SCRB-Seq described in [2]. Transcripts were quantified by the BTL computational pipeline using Cuffquant version 2.2.1 [3]. [1] Hafner, M., Niepel, M., Chung, M., Sorger, P.K., Growth rate inhibition metrics correct for confounders in measuring sensitivity to cancer drugs. DOI:10.1038/NMETH.3853 [2] Soumillon, M., Cacchiarelli, D., Semrau, S., van Oudenaarden, A. & Mikkelsen, T.S. Characterization of directed differentiation by high-throughput single-cell RNA-Seq http://biorxiv.org/content/early/2014/03/05/003236 [3] Trapnell, C., Roberts, A., Goff, L., Pertea, G., Kim, D., Kelley, D.R., Pimentel, H., Salzberg, S.L., Rinn, J.L. & Pachter, L. Differential gene and transcript expression analysis of RNA-seq experiments with TopHat and Cufflinks, Nat. Protoc. 7, 562-578 (2012).; [Treatment]'No treatment'; [Growth]'All cells lines were obtained from the ATCC and grown according to their recommendations.'; [Extraction]'RNA was extracted using the RNeasy mini kit (Qiagen).\nThe 3’-DGE libraries were prepared from total RNA according to the Single Cell RNA Barcoding and Sequencing method originally developed for single cell RNA-seq (SCRB-seq, Soumillon et al., 2014) and adapted to extracted total RNA. Briefly, Poly(A)+ mRNA from extracted total RNA are converted to cDNA decorated with universal adapters, sample-specific barcodes and unique molecular identifiers (UMIs) using a template-switching reverse transcriptase. Decorated cDNA from multiple samples are then pooled, amplified and prepared for multiplexed sequencing using a modified transposon-based fragmentation approach that enriches for 3’ ends and preserves strand information.'; [Cell type]'Source: ''growth time (days): 1; seeding density (cell/well): 625; ', 'growth time (days): 1; seeding density (cell/well): 1250; ', 'growth time (days): 1; seeding density (cell/well): 2500; ', 'growth time (days): 1; seeding density (cell/well): 5000; ', 'growth time (days): 2; seeding density (cell/well): 156; ', 'growth time (days): 2; seeding density (cell/well): 313; ', 'growth time (days): 2; seeding density (cell/well): 625; ', 'growth time (days): 2; seeding density (cell/well): 1250; ', 'growth time (days): 2; seeding density (cell/well): 2500; ', 'growth time (days): 2; seeding density (cell/well): 5000; ', 'growth time (days): 3; seeding density (cell/well): 313; ', 'growth time (days): 3; seeding density (cell/well): 625; ', 'growth time (days): 3; seeding density (cell/well): 1250; ', 'growth time (days): 3; seeding density (cell/well): 2500; ', 'growth time (days): 3; seeding density (cell/well): 5000; ' GSE47079 Homo sapiens 7 Expression profiling by array GPL570 Expression data of patient-derived triple negative breast cancer xenograft tumors 2013-05-18 Triple negative breast cancer (TNBC) is an aggressive subtype that lack targeted clinical therapies. In addition, TNBC is heterogeneous and was recently further sub-classified into seven TNBC subtypes that displayed unique gene expression patterns. To develop therapeutic treatment regimens, we established seven patient-derived xenograft models from TNBC tumors. These xenograft models not only retained the histology and clinical markers of the corresponding patient tumors, but also bearing the same mutations and deletions identified in the patient tumors. Moreover, as part of evaluation of these models, we performed microarrays on the xenograft tumors to assess their TNBC subtypes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47079 Patient-derived xenografts of triple-negative breast cancer reproduce molecular features of patient tumors and respond to mTOR inhibition. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr3640 {Breast cancer research : BCR (5.676): 10.1186/bcr3640} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA204463 https://www.ebi.ac.uk/ena/browser/view/PRJNA204463 None [Overal design]After obtaining IRB-approved informed written patient consent, breast cancer tissues were obtained fresh from Stanford Hospital and transplanted into the number 2 mammary fat pads of female NOD SCID mice (NOD.CB17-Prkdcscid/J, Jackson Laboratory West, Sacramento, CA, USA). Mice were maintained in pathogen-free animal housing. The established xenografts were subsequently passaged from mouse to mouse. Xenograft tumor tissues were frozen on dry ice for RNA isolation and microarray analysis.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted using RNeasy Plus Mini Kit (Qiagen, Valencia, CA, USA) following the manufacturer’s instructions. The quantity and purity of the RNA sample was measured using Agilent 2100 bioanalyzer (Agilent Technologies, Santa Clara, CA, USA).'; [Cell type]'Source: ''tissue: Patient-derived xenograft tumor from primary TNBC; ', 'tissue: Patient-derived xenograft tumor from soft tissue metastasis of TNBC; ' GSE86923 Mus musculus 10 Expression profiling by array GPL6887 Preferential Epigenetic Programming of Estrogen Response after in utero xenoestrogen (bisphenol-A) exposure [Illumina] 2016-09-14 Bisphenol-A (BPA) is an environmentally ubiquitous estrogen-like endocrine-disrupting compound. Exposure toBPAin utero hasbeen linked to female reproductive disorders, including endometrial hyperplasia and breast cancer. Estrogens are an etiological factor in many of these conditions. We sought to determine whether in utero exposure to BPA altered the global CpG methylation pattern of the uterine genome, subsequent gene expression, and estrogen response. Pregnant mice were exposed to an environmentally relevant dose of BPA or DMSO control. Uterine DNA and RNA were examined by using methylated DNA immunoprecipitation methylation microarray, expression microarray, and quantitative PCR. In utero BPA exposure altered the global CpG methylation profile of the uterine genome and subsequent gene expression. The effect on gene expression was not apparent until sexual maturation, which suggested that estrogen response was the primary alteration. Indeed, prenatal BPA exposure preferentially altered adult estrogen-responsive gene expression. Changes in estrogen response were accompanied by altered methylation that preferentially affected estrogen receptor-a (ERa)–binding genes. The majority of genes that demonstrated both altered expression and ERa binding had decreased methylation. BPA selectively altered the normal developmental programming of estrogen-responsive genes via modification of the genes that bind ERa. Gene– environment interactions driven by early life xenoestrogen exposure likely contributes to increased risk of estrogen related disease in adults.—Jorgensen, E. M.,Alderman,M.H., III,Taylor, H. S. Preferential epigenetic programmingof estrogen response after in utero xenoestrogen (bisphenol-A) exposure. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE86923 Preferential epigenetic programming of estrogen response after in utero xenoestrogen (bisphenol-A) exposure. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 5.391 https://doi.org/10.1096/fj.201500089R {FASEB journal : official publication of the Federation of American Societies for Experimental Biology (5.391): 10.1096/fj.201500089R} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA343002 https://www.ebi.ac.uk/ena/browser/view/PRJNA343002 None [Overal design]Dams were exposed to 5mg/kg/day of BPA or DMSO (CTL) for day 9-21 of gestation. Offspring were oopherectomized at 6 weeks. At 8 weeks mice were given 300ng E2 or DMSO and uteri were harvested 6h later. Total RNA was analyzed. Samples were pooled by litter.; [Treatment]'Pregnant dams were either exposed to 5/mg/kg/day of BPA IP or DMSO control. At 6 weeks offspring were oopherectomized. At 8 weeks offspring were either injected with 300ng estradiol or DMSO control.'; [Growth]'None'; [Extraction]'Each sample was placed in 1 ml TRIzol solution (Thermo Fisher Scientific,Waltham, MA, USA), and total RNA was purified by using the Qiagen RNeasy Plus Mini kit according to manufacturer instructions.'; [Cell type]'Source: ''strain: CD-1; in utero exposure: DMSO; 8wk treatment: Estradiol; age: 8 weeks; tissue: uterus; ', 'strain: CD-1; in utero exposure: DMSO; 8wk treatment: DMSO; age: 8 weeks; tissue: uterus; ', 'strain: CD-1; in utero exposure: BPA; 8wk treatment: Estradiol; age: 8 weeks; tissue: uterus; ', 'strain: CD-1; in utero exposure: BPA; 8wk treatment: DMSO; age: 8 weeks; tissue: uterus; ' GSE64101 Homo sapiens 4 Expression profiling by array GPL6244 Pit-1 overexpression in the human breast adenocarcinoma MCF-7 cell line 2014-12-11 The aim of the study is to evaluate Pit-1-induced genes in the MCF-7 cell line The Pit-1 transcription factor (also known as POU1F1) plays a critical role in cell differentiation during organogenesis of the anterior pituitary in mammals and is a transcriptional activator for pituitary gene transcription. Increased expression of Pit-1 has been reported in human tumorigenic breast cells. Here, we found that Pit-1 overexpression or knockdown in human breast cancer cell lines induced profound phenotypic changes in the expression of proteins involved in cell proliferation, apoptosis, and invasion. In immunodeficient mice, Pit-1 overexpression induced tumoral growth and promoted metastasis in lung. In patients with invasive ductal carcinoma of the breast and node-positive tumors elevated expression of Pit-1 was significantly and independently associated with the occurrence of distant metastasis. These findings suggest that Pit-1 could help to make a more accurate prognosis in patients with node positive breast cancer and may represent a new therapeutic target (Journal of Clinical Investigation 2010, 120:4289-4302) https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64101 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA270118 https://www.ebi.ac.uk/ena/browser/view/PRJNA270118 None [Overal design]MCF-7 cells were transfected with the pcDNA3 (control, two samples as condition, named C1 and C2) or the pcDNA3-Pit-1 overexpression vector (two samples as condition, named 1+ and 2+) for 48 hours.; [Treatment]'When cells were 80% confluent, cells were transfected with the pcDNA3 (control) or the pcDNA3-Pit-1 overexpression vector for 48 hours.'; [Growth]'MCF-7 cells were grown in DMEM with 10% of FBS,100 mU/mL penicillin, 100 μg/mL streptomycin, and 2 mM l-glutamine in a 5% CO2 atmosphere at 37°C.'; [Extraction]'Total RNA was extracted and purified using the PureLink Micro-to-Midi kit (Invitrogen).'; [Cell type]'Breast tumor cell line''cell line: MCF-7; cell type: Breast tumor cell line; transfected with: pcDNA3 (control vector); ', 'cell line: MCF-7; cell type: Breast tumor cell line; transfected with: pcDNA3-Pit-1 overexpression vector; ' GSE43486 Mus musculus 18 Non-coding RNA profiling by array GPL16502 miRNA expression analysis in AKXD RI strain mammary tumors 2013-01-14 Transcriptional profiling of miRNA levels in mammary tumors from 18 [PyMT x AKXD]F1 sublines. The PyMT strain was FVB/N-TgN(MMTV-PyVT)634Mul. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43486 Inherited variation in miR-290 expression suppresses breast cancer progression by targeting the metastasis susceptibility gene Arid4b. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-12-3513 {Cancer research (8.378): 10.1158/0008-5472.CAN-12-3513} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA186560 https://www.ebi.ac.uk/ena/browser/view/PRJNA186560 None [Overal design]Mammary tumor total RNA from mice representing one of 18 AKXD RI strains were pooled to represent each strain and expression profiled using a custom miRNA microarray.; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was extracted using the mirVana Isolation Kit (Ambion) following manufacturer's instructions."; [Cell type]'Source: ''strain: [FVB/N-TgN(MMTV-PyVT)634Mul x AKXD R1]F1 sublines; tissue: mammary tumor; ', 'strain: Swiss Webster mice; tissue: various; ' GSE152345 Homo sapiens 18 Expression profiling by high throughput sequencing GPL23227 Impact of chronic extracellular acidosis on gene expression in mammary and pancreatic cancer cell lines 2020-06-12 The study aim was to determine whether the microenvironmental acidosis in solid tumors contributes to cancer aggressiveness via changes in gene expression. RNA seq was carried out in parallel to a large array of phenotypical analyses of proliferation, growth, and invasiveness. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE152345 Cancer Cell Acid Adaptation Gene Expression Response Is Correlated to Tumor-Specific Tissue Expression Profiles and Patient Survival. Cancers 6.162 https://doi.org/10.3390/cancers12082183 {Cancers (6.162): 10.3390/cancers12082183} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA639069 https://www.ebi.ac.uk/ena/browser/view/PRJNA639069 https://www.ncbi.nlm.nih.gov/sra?term=SRP267051 [Overal design]3 human cancer cell lines (2 mammary, 1 pancreatic) adapted for 1-2 months to growth at extracellular pH 7.6 and 6.5, respectively, were subjected to RNA sequencing (BGI Hongkong), each in triplicates.; [Treatment]'To adjust pH to 7.6 or 6.5 while maintaining osmolarity, medium was prepared with 0 or 35 mM NaCl and 38 or 3 mM NaHCO3-, respectively.'; [Growth]'MDA-MB-231, MCF-7 S9, and Panc-1 cells were cultured in RPMI medium supplemented with 10 mM Glucose, 5% fetal bovine serum (FBS, Sigma-Aldrich, F9665) and 1% Penicillin/Streptomycin. Cells were cultured at 37 °C, 5% CO2 and passaged at a confluence of ~70-80%.'; [Extraction]"Total RNA was isolated using NucleoSpin® RNA II (Macherey-Nagel, Germany) according to the manufacturer's instructions\nRNA libraries were prepared for sequencing using standard Illumina protocols"; [Cell type]'Source: ''treatment: Grown at pH 6.5 for 1-2 months; ', 'treatment: Grown at pH 7.6 for 1-2 months; ' GSE131876 Homo sapiens 6 Expression profiling by high throughput sequencing GPL11154 miR-146 connects stem cell identity with metabolism and pharmacological resistance in breast cancer 2019-05-28 Although ectopic overexpression of miRNAs can influence mammary normal and cancer stem cells (SCs/CSCs), their physiological relevance remains uncertain. Here, we found that the miR-146 family is linked to SC identity, since: i) their expression is very high in SCs/CSCs from human/mouse primary mammary tissues; correlates with the basal-like breast cancer subtype, which typically has a high CSC content; and specifically distinguishes cells with SC/CSC identity; ii) miR-146 depletion reduces SC/CSC self-renewal in vitro and the number of tumor-initiating cells in vivo. Analysis of the transcriptional effects of miR-146 in breast SC-like cells revealed a complex network of highly connected miR-146 targets related to quiescence, transcription and metabolic pathways (one-carbon pool, purine synthesis and folate metabolism). As predicted by our analysis, SCs/CSCs display innate resistance to anti-folate therapy that can be reversed by miR-146 depletion, unmasking a “hidden vulnerability” that could be exploited for the development of anti-CSC therapies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131876 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA545160 https://www.ebi.ac.uk/ena/browser/view/PRJNA545160 https://www.ncbi.nlm.nih.gov/sra?term=SRP199685 [Overal design]total RNA expression by deep-sequencing in HMLE sorted for different levels of miR-146 activity; [Treatment]'HMLE cells infected with lentiviral miR-146 sensor were FACS-sorted according to different endogenous levels of miR-146. miR-146high and miR-146 low cells were plated in adhesion. miR-146high cells were treated with 100 nM power family inhibitor to KD miR-146 , then all the samples were collected 24hs after transfection. Two independent infections, sorting and transfection procedures were performed.'; [Growth]"HMLE cells were grown in MEGM medium, according to manufacturer's protocol."; [Extraction]'Total RNA was isolated through the miRNeasy micro kit (Qiagen).\n500 nanograms of total RNA were used to prepare total RNA libraries following the Illumina TruSeqTM Stranded RNA kit instructions'; [Cell type]'Source: ''infection: miR-146 sensor; levels of mir-146: low; tissue: breast normal; cell line: Human Mammary Epithelial cell line (HMLE) cell line; ', 'infection: miR-146 sensor; levels of mir-146: high; tissue: breast normal; cell line: Human Mammary Epithelial cell line (HMLE) cell line; ', 'infection: miR-146 sensor; levels of mir-146: high; treatment: power family inhibitor to KD miR-146; tissue: breast normal; cell line: Human Mammary Epithelial cell line (HMLE) cell line; ' GSE99384 Homo sapiens 4 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Analysis of the DNA accessibility upon multiple histone H1 variants by ATAC-seq 2017-05-29 Combined depletion of H1.2 and H1.4 has a strong deleterious effect in the cancer cells examined, and induces a strong interferon (IFN) response with up-regulation of many IFN-stimulated genes (ISGs), which is not seen in individual H1 knock-downs. Although H1 participates to repress ISG promoters, its activation upon H1 KD is mainly generated by the activation of the IFN response through cytosolic nucleic acids receptors, IFN synthesis and JAK-STAT pathway activation. The IFN response may be triggered by the expression of noncoding dsRNAs generated from heterochromatic repeats or endogenous retroviruses upon H1 KD. H1 KD promotes the appearance of accessibility sites genome wide and, particularly, at satellites and other repeats. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99384 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA388343 https://www.ebi.ac.uk/ena/browser/view/PRJNA388343 https://www.ncbi.nlm.nih.gov/sra?term=SRP108224 [Overal design]4 samples; [Treatment]'None'; [Growth]'Breast cancer T47D-MTVL cells (carrying one stably integrated copy of luciferase reporter gene driven by the MMTV promoter) or derivative cells, were grown at 37ºC with 5% CO2 in RPMI 1640 medium'; [Extraction]'75.000 cells were harvested and treated with transposase Tn5 (Nextera DNA Library Preparation Kit, Illumina). DNA was purified using MinElute PCR Purification Kit (Qiagen).\nAll samples were then amplified by PCR using NEBNextHigh-Fidelity 2x PCR Master Mix (New Englands Labs.) and primers containing a barcode to generate the libraries. DNA was again purified using MinElute PCR Purification Kit and samples were sequenced using Illumina HiSeq 2500 system.'; [Cell type]'Source: ''cell line: T47D; phenotype: Knock-down; replicate: Replicate 1; shRNA: shRNA multiH1 variants; ', 'cell line: T47D; phenotype: Knock-down; replicate: Replicate 2; shRNA: shRNA multiH1 variants; ', 'cell line: T47D; phenotype: Control; replicate: Replicate 1; shRNA: shRNA random; ', 'cell line: T47D; phenotype: Control; replicate: Replicate 2; shRNA: shRNA random; ' GSE68836 Homo sapiens 27 Expression profiling by high throughput sequencing GPL11154 BRCA1, R-loops and Recombination defects in Ewing's sarcoma (RNA-seq) 2015-05-13 Ewing’s sarcoma family of tumors (ESFT) is an aggressive pediatric bone and soft tissue cancer. It is the prototypical example of mesenchymal tumors driven by a fusion oncogene involving the ewing sarcoma break point region 1 (EWSR1) gene, most frequently– EWS-FLI1. We have discovered that loss of EWSR1 leads to accumulation of R-loops, replication stress and impaired homologous recombination, recapitulating breast cancer 1, early onset (BRCA1) deficiency. EWS-FLI1 acts dominant negatively in ESFT to impart the same phenotypes. Further we demonstrate that in ESFT, BRCA1 predominantly associates with the elongating transcription machinery and is unavailable for DNA strand break repair. Gene expression profiling identified upregulated compensatory mechanisms in ESFT cells to process increased R-loops (RNASEH2 and FEN1) and replication stress (Fanconi Anemia). Taken together, our data identifies BRCA1 sequestration due to transcription stress as the mechanistic basis for ESFT chemosensitivity and suggests potential targets for the much lacking second-line therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE68836 EWS-FLI1 increases transcription to cause R-loops and block BRCA1 repair in Ewing sarcoma. Nature 43.070 https://doi.org/10.1038/nature25748 {Nature (43.070): 10.1038/nature25748} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA283885 https://www.ebi.ac.uk/ena/browser/view/PRJNA283885 https://www.ncbi.nlm.nih.gov/sra?term=SRP058310 [Overal design]Examination of gene expression of four ESFT cell lines and two control cell lines. Cells were treated to LD65 dose of etoposideand samples collected at 6 hour intervals over 24 hours; [Treatment]'Samples were treated with either vehicle (DMSO) or indicated doses of etoposide for indicated amout of time before extraction of RNA'; [Growth]'Cells were passaged in 10cm corningware dishes using media described in Samples section in a 37°C humidified incubator'; [Extraction]'Total RNA was extracted from sub-confluent 10cm dishes using Qiagen RNeasy kit\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]"Ewing's sarcoma", 'Human fetal lung fibroblasts', 'Osteosarcoma'"cell line: TC32; cell type: Ewing's sarcoma; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; treatment prototcol: DMSO (NT: No Treatment); ", "cell line: TC32; cell type: Ewing's sarcoma; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; treatment prototcol: 0.05μM Etoposide for 6 hours; ", "cell line: TC32; cell type: Ewing's sarcoma; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; treatment prototcol: 0.05μM Etoposide for 12 hours; ", "cell line: TC32; cell type: Ewing's sarcoma; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; treatment prototcol: 0.05μM Etoposide for 18 hours; ", "cell line: TC32; cell type: Ewing's sarcoma; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; treatment prototcol: 0.05μM Etoposide for 24 hours; ", "cell line: EWS502; cell type: Ewing's sarcoma; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; treatment prototcol: DMSO (NT: No Treatment); ", "cell line: EWS502; cell type: Ewing's sarcoma; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; treatment prototcol: 0.25μM Etoposide for 6 hours; ", "cell line: EWS502; cell type: Ewing's sarcoma; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; treatment prototcol: 0.25μM Etoposide for 12 hours; ", "cell line: EWS502; cell type: Ewing's sarcoma; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; treatment prototcol: 0.25μM Etoposide for 18 hours; ", "cell line: EWS502; cell type: Ewing's sarcoma; growth protocol: Cells were grown in RPMI-40 supplemented with 10%FBS; treatment prototcol: 0.25μM Etoposide for 24 hours; ", "cell line: CHLA258; cell type: Ewing's sarcoma; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; treatment prototcol: DMSO (NT: No Treatment); ", "cell line: CHLA258; cell type: Ewing's sarcoma; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; treatment prototcol: 0.1μM Etoposide for 6 hours; ", "cell line: CHLA258; cell type: Ewing's sarcoma; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; treatment prototcol: 0.1μM Etoposide for 12 hours; ", "cell line: CHLA258; cell type: Ewing's sarcoma; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; treatment prototcol: 0.1μM Etoposide for 18 hours; ", "cell line: CHLA258; cell type: Ewing's sarcoma; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; treatment prototcol: 0.1μM Etoposide for 24 hours; ", "cell line: CHLA10; cell type: Ewing's sarcoma; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; treatment prototcol: DMSO (NT: No Treatment); ", "cell line: CHLA10; cell type: Ewing's sarcoma; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; treatment prototcol: 0.15μM Etoposide for 6 hours; ", "cell line: CHLA10; cell type: Ewing's sarcoma; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; treatment prototcol: 0.15μM Etoposide for 12 hours; ", "cell line: CHLA10; cell type: Ewing's sarcoma; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; treatment prototcol: 0.15μM Etoposide for 18 hours; ", "cell line: CHLA10; cell type: Ewing's sarcoma; growth protocol: Cells were grown in IMDM supplemented with 10%FBS; treatment prototcol: 0.15μM Etoposide for 24 hours; ", 'cell line: IMR90; cell type: Human fetal lung fibroblasts; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: DMSO (NT: No Treatment); ', 'cell line: IMR90; cell type: Human fetal lung fibroblasts; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: 6μM Etoposide for 6 hours; ', 'cell line: IMR90; cell type: Human fetal lung fibroblasts; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: 6μM Etoposide for 12 hours; ', 'cell line: IMR90; cell type: Human fetal lung fibroblasts; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: 6μM Etoposide for 18 hours; ', 'cell line: IMR90; cell type: Human fetal lung fibroblasts; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: 6μM Etoposide for 24 hours; ', 'cell type: Osteosarcoma; cell line: U2OS; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: DMSO (NT: No Treatment); ', 'cell type: Osteosarcoma; cell line: U2OS; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: 6μM Etoposide for 6 hours; ' GSE50567 Homo sapiens 41 Expression profiling by array GPL570 BRCA1-related gene signature in breast cancer: the role of ER status and molecular type 2013-09-04 We have analyzed, using DNA microarrays, putative differences in gene-expression level between hereditary BRCA1 mutation-linked and sporadic breast cancer. Our results show that a previously reported marked difference between BRCA1-mutation linked and sporadic breast cancer was probably due to uneven stratification of samples with different ER status and basal-like versus luminal-like subtype. We observed that apparent difference between BRCA1-linked and other types of breast cancer found in univariate analysis was diminished when data were corrected for ER status and molecular subtype in multivariate analyses. In fact, the difference in gene expression pattern of BRCA1-mutated and sporadic cancer is very discrete. These conclusions were supported by the results of Q-PCR validation. We also found that BRCA1 gene inactivation due to promoter hypermethylation had similar effect on general gene expression profile as mutation-induced protein truncation. This suggests that in the molecular studies of hereditary breast cancer, BRCA1 gene methylation should be recognized and considered together with gene mutation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50567 BRCA1-related gene signature in breast cancer: the role of ER status and molecular type. Frontiers in bioscience (Elite edition) 1.94 https://doi.org/10.2741/e227 {Frontiers in bioscience (Elite edition) (1.94): 10.2741/e227} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA217957 https://www.ebi.ac.uk/ena/browser/view/PRJNA217957 None [Overal design]We analyzed 35 breast cancer specimens. Surgical samples obtained during mastectomy were flash-frozen in liquid nitrogen and stored at -80°C. Only samples from patients without neoadjuvant chemotherapy were used in this study as chemotherapy may seriously affect gene expression profile. All tissue samples were collected at the Pomeranian Medical University in Szczecin. Seventeen tumor samples were collected from patients with hereditary breast cancer: 12 were derived from tumors affecting women with hereditary BRCA1 mutation, the only one from a woman with BRCA2 mutation, while another eight cases had familial history of breast/ovarian cancer, but were negative for the BRCA1/2 mutations (so called BRCAx cases). Proportion of BRCA1 and BRCA2 mutated tumors was typical for the Polish population. Ten samples were derived from patients with apparently sporadic disease (no familial history of cancer) while 4 patients had a history of familial cancer aggregation (FCA) but without prevalence of breast/ovarian cancers. Thus, these samples were merged with sporadic samples in most of the analyses. All BRCA1 mutation-linked tumors in our study were negative for estrogen receptor (by immunohistochemistry, standard procedures for ER, PGR and HER2 staining were applied), while the only BRCA2-mutated tumor was ER-positive. There were 26 ductal and 5 medullary carcinomas within the study group, which is consistent with the distribution of histopathological types in BRCA1 mutation carriers. Patients were diagnosed at stage T1-2, N0-1 and M0. Caution: this submission contains the data from 6 microarrays done on the normal/pathologically unchanged breast tissue from breast cancer patiets. The data from normal tissues was not analyzed in the paper BRCA1-related gene signature in breast cancer is strongly influenced by ER status and molecular type by Lisowska et al., 2011, Front Biosci (Elite Ed). 2011 Jan 1;3:125-36; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was isolated using Rneasy Mini Kit (Qiagen) according to the manufacturer's instructions."; [Cell type]'Source: ''clinical sample: surgical tumor sample; histopathology: medullary breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: BRCA1 5382insC Ex20; brca1 promoter methylation: unmethylated; age: 42; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: BRCA1 5382insC Ex20; brca1 promoter methylation: unmethylated; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: BRCA1 5382insC Ex20; brca1 promoter methylation: unmethylated; age: 51; ', 'clinical sample: surgical tumor sample; histopathology: medullary breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: BRCA1 5382insC Ex20; brca1 promoter methylation: unmethylated; age: 55; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: BRCA1 4153delA Ex11; brca1 promoter methylation: unmethylated; age: 49; ', 'clinical sample: surgical tumor sample; histopathology: medullary breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: BRCA1 5382insC Ex20; brca1 promoter methylation: unmethylated; age: 52; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: BRCA1 5382insC Ex20; brca1 promoter methylation: unmethylated; age: 41; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: BRCA1 C61G Ex5; brca1 promoter methylation: unmethylated; age: 48; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: BRCA1 5382insC Ex20; brca1 promoter methylation: unmethylated; age: 62; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(+); brca1/2 mutation: BRCA2 9631delC Ex25; brca1 promoter methylation: unmethylated; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 56; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: methylated; age: 58; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 50; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 50; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(+); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(+); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 50; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(+); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 76; ', 'clinical sample: surgical tumor sample; histopathology: medullary breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: methylated; age: 45; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: methylated; age: 39; ', 'clinical sample: surgical tumor sample; histopathology: medullary breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 70; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 27; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 74; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 59; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 57; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: methylated; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(+); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 48; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 61; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): luminal-like; estrogen receptor status (by immunohistochemistry): ER(+); brca1/2 mutation: No mutation; brca1 promoter methylation: unmethylated; age: 51; ', 'clinical sample: surgical tumor sample; histopathology: ductal breast ca.; molecular subtype (according to sorlie et al., pnas 100, 8418-23 (2003): basal-like; estrogen receptor status (by immunohistochemistry): ER(-); brca1/2 mutation: No mutation; brca1 promoter methylation: methylated; age: 52; ', 'clinical sample: surgical sample of pathologically unchanged breast tissue, adjacent to the tumor; histopathology: normal breast; estrogen receptor status (by immunohistochemistry): not analyzed; brca1/2 mutation: No mutation; brca1 promoter methylation: not analyzed; ', 'clinical sample: surgical sample of pathologically unchanged breast tissue, adjacent to the tumor; histopathology: normal breast; estrogen receptor status (by immunohistochemistry): not analyzed; brca1/2 mutation: No mutation; brca1 promoter methylation: not analyzed; age: 39; ', 'clinical sample: surgical sample of pathologically unchanged breast tissue, adjacent to the tumor; histopathology: normal breast; estrogen receptor status (by immunohistochemistry): not analyzed; brca1/2 mutation: No mutation; brca1 promoter methylation: not analyzed; age: 55; ', 'clinical sample: surgical sample of pathologically unchanged breast tissue, adjacent to the tumor; histopathology: normal breast; estrogen receptor status (by immunohistochemistry): not analyzed; brca1/2 mutation: No mutation; brca1 promoter methylation: not analyzed; age: 49; ', 'clinical sample: surgical sample of pathologically unchanged breast tissue, adjacent to the tumor; histopathology: normal breast; estrogen receptor status (by immunohistochemistry): not analyzed; brca1/2 mutation: No mutation; brca1 promoter methylation: not analyzed; age: 48; ' GSE131091 Homo sapiens 44 Other GPL11154 Synthetic lethal and resistance interactions with BET bromodomain inhibitors [CRISPR screen] 2019-05-13 BET bromodomain inhibitors (BBDI) are promising therapeutic agents in triple-negative breast cancer (TNBC). However, not all tumors respond and acquired resistance emerges rapidly even in the responders. Using CRISPR and small molecule inhibitor screens combined with comprehensive molecular profiling of BBDI response and resistance in TNBC cell lines, we identified numerous synthetic lethal interactions with BBDIs as well as genes that when deleted confer resistance. The most prominent and consistent synergy was observed with CDK4/6 inhibitors and paclitaxel. We also uncovered functional similarities and differences between BBD proteins BRD2, BRD4, and BRD7, whereas deletion of BRD2 and BRD4 enhances sensitivity to BBDIs, BRD7 loss leads to resistance. Lastly, single cell RNA-seq and cellular barcoding analysis of BBDI responses in sensitive and resistant cell lines highlight heterogeneity among samples and demonstrate that BBDI resistance can be both pre-existing and acquired. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131091 Synthetic Lethal and Resistance Interactions with BET Bromodomain Inhibitors in Triple-Negative Breast Cancer. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2020.04.027 {Molecular cell (14.548): 10.1016/j.molcel.2020.04.027} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA542642 https://www.ebi.ac.uk/ena/browser/view/PRJNA542642 https://www.ncbi.nlm.nih.gov/sra?term=SRP198246 [Overal design]CRISPR screen of parental and JQ1 resistant breast cancer cell lines; [Treatment]'SUM149, SUM159, SUM149R, SUM159R cells were continously treated with JQ1 or DMSO treatment.'; [Growth]'SUM149, SUM159, SUM149R, SUM159R cells were grown in SUM Medium'; [Extraction]'For the pooled genome-wide CRISPR screen, 100 million SUM149 and SUM159 Parental and resistant cells were infected with the pooled lentiviral H1 and H2 libraries essentially as described (Jeselsohn et al., 2018) at a multiplicity of infection of 0.3. After 3 d of puromycin selection, half of the surviving cells were stored as 0-d control samples, and the rest of cells were cultured for an additional 5 passages with or without different concentrations of JQ1 treatment.\nPCR was performed on genomic DNA to construct the sequencing library.'; [Cell type]'Source: ''cell line: SUM149; agent: DMSO; dose: -; passage: 0; crispr library: H1; ', 'cell line: SUM149; agent: DMSO; dose: -; passage: 5; crispr library: H1; ', 'cell line: SUM149; agent: JQ1; dose: 100nM; passage: 5; crispr library: H1; ', 'cell line: SUM149; agent: JQ1; dose: 200nM; passage: 5; crispr library: H1; ', 'cell line: SUM149; agent: DMSO; dose: -; passage: 0; crispr library: H2; ', 'cell line: SUM149; agent: DMSO; dose: -; passage: 5; crispr library: H2; ', 'cell line: SUM149; agent: JQ1; dose: 100nM; passage: 5; crispr library: H2; ', 'cell line: SUM149; agent: JQ1; dose: 200nM; passage: 5; crispr library: H2; ', 'cell line: SUM149; agent: DMSO; dose: -; passage: 0; replicate: Replicate; crispr library: H1; ', 'cell line: SUM149; agent: DMSO; dose: -; passage: 5; replicate: Replicate; crispr library: H1; ', 'cell line: SUM149; agent: JQ1; dose: 400nM; passage: 5; replicate: Replicate; crispr library: H1; ', 'cell line: SUM149; agent: JQ1; dose: 800nM; passage: 5; replicate: Replicate; crispr library: H1; ', 'cell line: SUM149; agent: DMSO; dose: -; passage: 0; replicate: Replicate; crispr library: H2; ', 'cell line: SUM149; agent: DMSO; dose: -; passage: 5; replicate: Replicate; crispr library: H2; ', 'cell line: SUM149; agent: JQ1; dose: 400nM; passage: 5; replicate: Replicate; crispr library: H2; ', 'cell line: SUM149; agent: JQ1; dose: 800nM; passage: 5; replicate: Replicate; crispr library: H2; ', 'cell line: SUM149R; agent: DMSO; dose: -; passage: 0; crispr library: H1; ', 'cell line: SUM149R; agent: DMSO; dose: -; passage: 5; crispr library: H1; ', 'cell line: SUM149R; agent: JQ1; dose: 10uM; passage: 5; crispr library: H1; ', 'cell line: SUM149R; agent: DMSO; dose: -; passage: 0; crispr library: H2; ', 'cell line: SUM149R; agent: DMSO; dose: -; passage: 5; crispr library: H2; ', 'cell line: SUM149R; agent: JQ1; dose: 10uM; passage: 5; crispr library: H2; ', 'cell line: SUM159; agent: DMSO; dose: -; passage: 0; crispr library: H1; ', 'cell line: SUM159; agent: DMSO; dose: -; passage: 5; crispr library: H1; ', 'cell line: SUM159; agent: JQ1; dose: 500nM; passage: 5; crispr library: H1; ', 'cell line: SUM159; agent: JQ1; dose: 1uM; passage: 5; crispr library: H1; ', 'cell line: SUM159; agent: DMSO; dose: -; passage: 0; crispr library: H2; ', 'cell line: SUM159; agent: DMSO; dose: -; passage: 5; crispr library: H2; ', 'cell line: SUM159; agent: JQ1; dose: 500nM; passage: 5; crispr library: H2; ', 'cell line: SUM159; agent: JQ1; dose: 1uM; passage: 5; crispr library: H2; ', 'cell line: SUM159; agent: DMSO; dose: -; passage: 0; replicate: Replicate; crispr library: H1; ', 'cell line: SUM159; agent: DMSO; dose: -; passage: 5; replicate: Replicate; crispr library: H1; ', 'cell line: SUM159; agent: JQ1; dose: 500nM; passage: 5; replicate: Replicate; crispr library: H1; ', 'cell line: SUM159; agent: JQ1; dose: 1uM; passage: 5; replicate: Replicate; crispr library: H1; ', 'cell line: SUM159; agent: DMSO; dose: -; passage: 0; replicate: Replicate; crispr library: H2; ', 'cell line: SUM159; agent: DMSO; dose: -; passage: 5; replicate: Replicate; crispr library: H2; ', 'cell line: SUM159; agent: JQ1; dose: 500nM; passage: 5; replicate: Replicate; crispr library: H2; ', 'cell line: SUM159; agent: JQ1; dose: 1uM; passage: 5; replicate: Replicate; crispr library: H2; ', 'cell line: SUM159R; agent: DMSO; dose: -; passage: 0; crispr library: H1; ', 'cell line: SUM159R; agent: DMSO; dose: -; passage: 5; crispr library: H1; ', 'cell line: SUM159R; agent: JQ1; dose: 10uM; passage: 5; crispr library: H1; ', 'cell line: SUM159R; agent: DMSO; dose: -; passage: 0; crispr library: H2; ', 'cell line: SUM159R; agent: DMSO; dose: -; passage: 5; crispr library: H2; ', 'cell line: SUM159R; agent: JQ1; dose: 10uM; passage: 5; crispr library: H2; ' GSE12863 Mus musculus 4 Expression profiling by array GPL8321 An Ets2-specific transcriptional program in tumor-associated macrophages promotes metastasis 2008-09-19 Macrophages have been implicated in breast cancer progression and metastasis, but relatively little is known about the genes and pathways that are involved. Using a conditional allele of Ets2 in the mouse, we have identified Ets2 as a critical gene in tumor associated macrophages (TAMs) that specifically promotes mammary tumor metastasis. Loss of Ets2 in TAMs decreased the frequency and size of lung metastases without impacting primary tumor burden. Expression profiling of isolated tumor macrophages established that Ets2 deficiency resulted in the de-repression of a defined set of anti-angiogenic genes. Activation of this transcriptional program correlated with decreased angiogenesis in metastatic tumors and decreased metastatic growth. Comparison of this Ets2-specific TAM expression profile with human breast cancer profiles revealed a macrophage gene expression signature that could predict overall survival of estrogen receptor negative patients. In summary, we have identified a critical factor, Ets2, in TAMs that represses a transcriptional program to promote the growth of mammary tumor metastases in the lung. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE12863 An ets2-driven transcriptional program in tumor-associated macrophages promotes tumor metastasis. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-09-1474 {Cancer research (8.378): 10.1158/0008-5472.CAN-09-1474} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA111101 https://www.ebi.ac.uk/ena/browser/view/PRJNA111101 None [Overal design]Breast TAMs were isolated from early-stage PyMT-induced mammary tumors expressing Ets2 and also from the tumors with Ets2-deficient TAMs. Since macrophages have also been implicated in normal mammary gland remodeling, normal remeodeling macrophages were also purified from females expressing Ets2 and the ones where Ets2 is deleted in the macrophages. One RNA sample was extracted from each genetic group for gene-expression profiling.; [Treatment]'YFP-positive macrophages isolated by FACS were eluted in DMEM media with 3% FBS. For RNA preparation, the eluant was centrifuged at 1200rpm for 5minutes at 4C to obtain pellet containing the macrophages.'; [Growth]'Mice used in the experiment endogenously expressed YFP in macrophages. YFP positive macrophages from each genetic group were isolated by digital high-speed fluorescence activated cell sorting (FACS).'; [Extraction]'RNA was extracted using the RNeasy Stratagene micro-prep column (Stratagene) as per the manufacturer’s instructions.'; [Cell type]'Source: ''Strain: FVBN; Gender: female; age: 50days; Tissue: mammary gland; Tumor stage: n/a; ', 'Strain: FVBN; Gender: female; age: 65days; Tissue: mammary gland; Tumor stage: early; ' GSE114459 Homo sapiens 4 Expression profiling by high throughput sequencing GPL16791 Genetic and transcriptional variation alters cancer cell line drug response [MCF7] 2018-05-15 10X Genomics single cell RNAseq of MCF7 cells Human cancer cell lines are the workhorse of cancer research. While cell lines are known to evolve in culture, the extent of the resultant genetic and transcriptional heterogeneity and its functional consequences remain understudied. Here, genomic analyses of 106 cell lines grown in two laboratories revealed extensive clonal diversity. Follow-up comprehensive genomic characterization of 27 strains of the common breast cancer cell line MCF7 uncovered rapid genetic diversification. Similar results were obtained with multiple strains of 13 additional cell lines. Importantly, genetic changes were associated with differential activation of gene expression programs and marked differences in cell morphology and proliferation. Barcoding experiments showed that cell line evolution occurs as a result of positive clonal selection that is highly sensitive to culture conditions. Analyses of single cell-derived clones showed that ongoing instability quickly translates into cell line heterogeneity. Testing of the 27 MCF7 strains against 321 anti-cancer compounds uncovered strikingly disparate drug response: at least 75% of compounds that strongly inhibited some strains were completely inactive in others. This study documents the extent, origin and consequence of genetic variation within cell lines, and provides a framework for researchers to measure such variation in efforts to support maximally reproducible cancer research. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE114459 Genetic and transcriptional evolution alters cancer cell line drug response. Nature 43.070 https://doi.org/10.1038/s41586-018-0409-3 {Nature (43.070): 10.1038/s41586-018-0409-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA471584 https://www.ebi.ac.uk/ena/browser/view/PRJNA471584 https://www.ncbi.nlm.nih.gov/sra?term=SRP147451 [Overal design]Single cell clones were derived from MCF7 cells and cultured.; [Treatment]'Single cell clones were then isolated by single cell sorting. Single cells were sorted into individual wells of 96-well plates, using BD FACSAriaII SORP Cell Sorter.'; [Growth]'MCF7 cells were cultured in RPMI-1640 (Life Technologies), with 10% Fetal Bovine Serum (Sigma-Aldrich) and 1% Penicillin-Streptomycin-Glutamine (Life Technologies).'; [Extraction]'DissociateCells were washed, trypsinized, passed through a 40μM cell strainer, centrifuged at 400g, and resuspended at a concentration of 1,000 cells/μL in PBS + 0.5% BSA.\nSingle cells were processed through the Chromium Single Cell 3′ Solution platform using the Chromium Single Cell 3’ Gel Bead, Chip and Library Kits (10X Genomics), as per the manufacturer’s protocol.'; [Cell type]'human cancer cell line''cell line background: MCF7; cell type: human cancer cell line; clone: parental; ', 'cell line background: MCF7; cell type: human cancer cell line; clone: subclone; ' GSE45341 Mus musculus; Homo sapiens 8 Methylation profiling by high throughput sequencing GPL10999; GPL11002; GPL13112 Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer [RRBS] 2013-03-20 Genetic and epigenetic alterations are essential for the initiation and progression of human cancer. We previously reported that primary human medulloblastomas showed extensive cancer-specific CpG island DNA hypermethylation in critical developmental pathways. To determine whether genetically engineered mouse models (GEMMs) of medulloblastoma have comparable epigenetic changes, we assessed genome-wide DNA methylation in three mouse models of medulloblastoma. In contrast to human samples, very few loci with cancer-specific DNA hypermethylation were detected, and in almost all cases the degree of methylation was relatively modest compared to the dense hypermethylation in the human cancers. To determine if this finding was common to other GEMMs, we examined a Burkitt lymphoma and breast cancer model and did not detect promoter CpG island DNA hypermethylation, suggesting that human cancers and at least some GEMMs are fundamentally different with respect to this epigenetic modification. These findings provide an opportunity to both better understand the mechanism of aberrant DNA methylation in human cancer and construct better GEMMs to serve as preclinical platforms for therapy development. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE45341 Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer. Epigenetics 4.173 https://doi.org/10.4161/epi.26486 {Epigenetics (4.173): 10.4161/epi.26486} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA193503 https://www.ebi.ac.uk/ena/browser/view/PRJNA193503 https://www.ncbi.nlm.nih.gov/sra?term=SRP019827 [Overal design]Examination of DNA methylation in one representative human medulloblastoma patient sample and three different mouse models of medulloblastoma using RRBS; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA from all sources was isolated using the DNeasy Blood and Tissue Kit (Qiagen).\nEpiQuest libraries were prepared from 500 ng genomic DNA. The DNA was digested with 60 units of TaqI and 30 units of MspI (NEB) sequentially. Size-selected TaqI-MspI fragments (40–120bp and 120–350bp) were filled-in and 30-terminal-A extended, extracted with Zymo Research DNA Clean and Concentrator(tm) kit. Ligation to pre-annealed adaptors containing 50-methyl-cytosine instead of cytosine (Illumina) was performed using the Illumina DNA preparation kit and protocol. Purified, adaptor-ligated fragments were bisulphite treated using the EZ DNA Methylation-Direct(tm) Kit (Zymo Research). Preparative-scale PCR was performed and DNA Clean and Concentrator-purified PCR products were subjected to a final size selection on a 4% NuSieve 3:1 agarose gel. SYBR-green-stained gel slices containing adaptor-ligated fragments of 130–210 or 210–460bp in size were excised. Library material was recovered from the gel (Zymoclean(tm) Gel DNA Recovery Kit) and sequenced on an Illumina GAIIx genome analyzer.'; [Cell type]'Source: ''background strain: C57BL/6; tissue: medulloblastoma; genotype: SmoA1 -/+; ', 'background strain: C57BL/6; tissue: medulloblastoma; genotype: SmoA2 -/+; ', 'background strain: C57BL/6; tissue: normal cerebellum; genotype: wild type; ', 'tissue: medulloblastoma; ', 'tissue: normal cerebellum; ', 'background strain: C57BL/6; tissue: medulloblastoma; genotype: Glt1-tTA:TRE-MYCN/Luc; ' GSE12917 Homo sapiens 12 Expression profiling by array GPL570 Gene expression profile of normal and RhoA immortal cells 2008-09-24 Rho family small GTPases serve as molecular switches in the regulation of diverse cellular functions including actin cytoskeleton remodeling, cell migration, gene transcription, and cell proliferation. Importantly, Rho overexpression is frequently seen in many carcinomas. However, published studies have almost invariably utilized immortal or tumorigenic cell lines to study Rho GTPase functions and there are no studies on the potential of Rho small GTPase to overcome senescence checkpoints and induce preneoplastic transformation of human mammary epithelial cells (hMECs). We found that ectopic expression of wild-type RhoA as well as a constitutively-active RhoA mutant (G14V) in primary hMEC strains led to their immortalization and preneoplastic transformation. Significantly, RhoA-T37A mutant, known to be incapable of interacting with many well known Rho-effectors ,was also capable of immortalizing hMECs.Our results demonstrate that RhoA can induce the preneoplastic transformation of hMECs by altering multiple pathways linked cellular transformation and breast cancer. Through microarray analysis, we want to identify genes and pathways linked to RhoA induced hMECs immortalization. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE12917 Overexpression of RhoA induces preneoplastic transformation of primary mammary epithelial cells. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-08-2907 {Cancer research (8.378): 10.1158/0008-5472.CAN-08-2907} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA110827 https://www.ebi.ac.uk/ena/browser/view/PRJNA110827 None [Overal design]4 samples, in triplicate analyses per sample.; [Treatment]'No treatment. Logarithmically growing cells were collected for RNA extraction.'; [Growth]'Reduction mammoplasty-derived human mammary epithelial cell strains, 76N and RhoA immortalized 76N cells were grown in the DFCI-1 medium'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions.For each cell line, RNA was isolated in three independent experiments."; [Cell type]'Source: ''' GSE60324 Homo sapiens 12 Expression profiling by array GPL6244; GPL16686 Effect of knock down of LASP-1 on human breast cancer cells 2014-08-11 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60324 LASP-1: a nuclear hub for the UHRF1-DNMT1-G9a-Snail1 complex. Oncogene 6.634 https://doi.org/10.1038/onc.2015.166 {Oncogene (6.634): 10.1038/onc.2015.166} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA258027 https://www.ebi.ac.uk/ena/browser/view/PRJNA258027 None [Overal design]Refer to individual Series; [Treatment]'Not applicable'; [Growth]'MCF cells (Non-silencing and LASP-1 knock down) were cultured on growth factor reduced Matrigel for 3 days to form spheroids.', 'MDA-MB-231S and MDA-Bone-Un breast cancer cells (Non-silencing and LASP-1 knock down) were cultured on growth factor reduced Matrigel for 3 days to form stellate clusters.'; [Extraction]'Total RNA was quantitated from MCF7 spheroids using the QuBit RNA assay and were run on the Agilent Bioanalyzer.', 'Total RNA from MDA-MB-231S and MDA-Bone-Un stellate clusters was quantitated using the QuBit RNA assay and were run on the Agilent Bioanalyzer.'; [Cell type]'Luminal breast cells', 'Basal-like breast cells''cell line: MCF7; cell type: Luminal breast cells; ', 'cell line: MDA-MB-231-S; cell type: Basal-like breast cells; ', 'cell line: MDA-Bone-Un; cell type: Basal-like breast cells; ' GSE36240 Mus musculus 7 Expression profiling by array GPL11383 Nf1 deletion and recurrent copy number alterations in mammary tumorigenesis 2012-03-02 Breast cancer is the most prevalent cancer in women, and most cases are believed to have a sporadic, rather than heritable basis. Therefore, a major challenge in cancer research is to determine the underlying genomic alterations leading to carcinogenesis and malignancy, and then use this information for personalized therapies. Genomic studies of human cancers that aim to identify causative mutations are complicated by the prevalence of passenger mutations, genetic heterogeneity, and the diversity of breast cancer etiologies and tumor subtypes. Mouse cancer models are powerful for untangling the genomic basis of cancers because genetic and phenotypic variation can be eliminated or controlled. To identify genes contributing to mammary tumorigenesis, we exploited the C3H-Mcm4Chaos3/Chaos3 (“Chaos3”) mouse model that, by virtue of bearing a defective DNA replicative helicase subunit that causes elevated genomic instability (GIN), sustains somatic alterations ultimately causing mammary adenocarcinomas. Genomic analysis of Chaos3 mammary tumors revealed recurrent copy number alterations (CNAs) of specific genomic regions, most notably deletion of the Neurofibromin 1 (Nf1) tumor suppressor gene in all cases. NF1, a negative regulator of RAS, is traditionally recognized for its role in driving the development of neurofibromas in the context of the human disease Neurofibromitosis but not breast cancer. We observed elevated RAS activation and increased sensitivity of both Chaos3 and human Nf1-mutated breast cancer lines to MAPK and/or PI3K/AKT pathway inhibitors. We also found striking overlap between Chaos3 CNAs and human breast cancer CNA data curated in public genomic databases, including Nf1 deletion. Together, our results indicate that spontaneous NF1 loss can drive breast cancer and suggests a potential therapeutic strategy in that subset of patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36240 Comparative oncogenomics implicates the neurofibromin 1 gene (NF1) as a breast cancer driver. Genetics 3.564 https://doi.org/10.1534/genetics.112.142802 {Genetics (3.564): 10.1534/genetics.112.142802} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA153159 https://www.ebi.ac.uk/ena/browser/view/PRJNA153159 None [Overal design]reference x sample; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA isolated using Qiagen RNeasy Kit', 'Total RNA isolated using Qiagen Rneasy Kit'; [Cell type]'Source: ''reference: common reference RNA sample for these experiments consisted of total RNA harvested from equal numbers of C57Bl6/J and 129 male and female Day1 pups; ', 'tumor: Untreated mammary tumor from Chaos3 mouse model; ' GSE58879 Homo sapiens 18 Expression profiling by array GPL6244 Coordinated epigenetic remodelling occurs during early breast carcinogenesis [Expression profiling] 2014-06-27 Dysregulation of the epigenome is a common event in malignancy. However, deciphering the earliest cancer associated epigenetic events remains a challenge. Cancer epigenome studies to date have primarily utilised cancer cell lines or clinical samples, where it is difficult to identify the initial epigenetic lesions from those that occur over time. Here, we analysed the epigenome of normal Human Mammary Epithelial Cells (HMEC) and a matched variant cell population (vHMEC) that has escaped senescence and undergone partial carcinogenic transformation. Using this model system we sought to identify the earliest epigenetic changes that potentially occur during carcinogenesis. First we show that the transcriptome of vHMEC resembles that of basal-like breast cancer. Moreover, in vHMEC there is significant deregulation of MYC, p53, EZH2/polycomb, the Aryl Hydrocarbon Receptor (AHR) and miRNAs-143, 145, 199a and 519a at the transcriptional level. Second, we find that vHMEC exhibit genome-wide changes in DNA methylation affecting key cancer-associated pathways. Hypermethylation predominately impacted gene promoters (particularly those targeted by AHR and TP53) and polycomb associated loci, whereas hypomethylation frequently affected enhancers. Next we show that long range epigenetic deregulation occurred in vHMEC involving concordant change in chromatin modification and gene expression across ~0.5-1Mb regions. Finally, we demonstrate that the DNA methylation changes we observe in vHMECs, occur in basal-like breast cancer (notably FOXA1 hypermethylation).. Overall our results suggest that the first steps of carcinogenesis are associated with a co-ordinated deregulation of DNA methylation and chromatin modification spanning a range of genomic loci potentially targeted by key transcription factors and a corresponding deregulation of transcriptional networks. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58879 Coordinated epigenetic remodelling of transcriptional networks occurs during early breast carcinogenesis. Clinical epigenetics 5.496 https://doi.org/10.1186/s13148-015-0086-0 {Clinical epigenetics (5.496): 10.1186/s13148-015-0086-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA253807 https://www.ebi.ac.uk/ena/browser/view/PRJNA253807 None [Overal design]We sought to compare the differences in gene expression in vHMEC when compared to isogenic HMEC cells. Two time points in the vHMEC growth phase were used to assess if continual passage of vHMEC contributed to expression differences. RNA was extracted from a total of 4 HMEC (and matched vHMEC) lines.; [Treatment]'Cells were cultured under normal conditions'; [Growth]'HMEC lines were generated from tissue taken from healthy women with informed donor consent as part of breast reduction mammoplasty (institutional ethics approval provided by the Sydney Adventist Hospital Ethics Committee, Project ID 06/03). At the time of surgery, all donors were aged between 23 and 43 years of age. Breast tissue was diced and then digested with collagenase to generate organoids. To establish HMEC lines, organoids were allowed to expand in MBD170 serum free basal medium (Life Technologies, Carlsbad CA, USA) until large colonies (1-2 cm) were observed (5-10 days). Organoid colonies were partially trypsinised to remove stromal cells and the remaining epithelial cells were transferred into a new tissue culture flask to generate passage 1 HMEC. vHMEC lines were then generated by serial passage of HMEC until proliferation slowed and the cells entered the selection phase. Selection phase HMEC were maintained with twice-weekly media changes until large, actively growing colonies (1-2 cm) were observed. Growing cells were trypsinised and transferred to a new culture vessel, generating the vHMEC lines.'; [Extraction]'Total RNA was extracted using TRIzol (invitrogen) according to the manufactureres protocol'; [Cell type]'Source: ''tissue: Breast; passage: 10; ', 'tissue: Breast; passage: 16; ', 'tissue: Breast; passage: 3; ', 'tissue: Breast; passage: 11; ', 'tissue: Breast; passage: 14; ', 'tissue: Breast; passage: 5; ', 'tissue: Breast; passage: 2; ', 'tissue: Breast; passage: 7; ', 'tissue: Breast; passage: 8; ' GSE46184 Homo sapiens 74 Expression profiling by array GPL96 Breast Cancer Gene Expression Data from Hamburg Series 2013-04-18 Gene expression profiling of surgical biopsies from 74 breast cancer patients of different subtypes from Hamburg dataset. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE46184 Dynamic classification using case-specific training cohorts outperforms static gene expression signatures in breast cancer. International journal of cancer 4.982 https://doi.org/10.1002/ijc.29247 {Breast cancer research and treatment (3.471) doi:10.1007/s10549-014-2949-z}; {International journal of cancer (4.982) doi:10.1002/ijc.29247}; {Breast cancer research and treatment (3.471) doi:10.1007/s10549-012-2296-x}; {European journal of cancer (Oxford, England : 1990) (None) doi:10.1016/j.ejca.2008.10.016}; {Breast cancer research and treatment (3.471) doi:10.1007/s10549-008-9964-x}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA197524 https://www.ebi.ac.uk/ena/browser/view/PRJNA197524 None [Overal design]Fresh frozen pre-treatment surgical biopsy samples from breast cancer patients were analyzed on Affymetrix HGU133A.; [Treatment]'samples were snap frozen and stored at -80°C'; [Growth]'None'; [Extraction]"RNeasy kit, Qiagen. according to the manufacturer's instructions"; [Cell type]'Source: ''gender: female; tissue: pretreatment surgical biopsy; cohort: HH; ' GSE136151 Homo sapiens 48 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL16791; GPL18573 Opposing functions of BRD4 isoforms in breast cancer 2019-08-21 Bromodomain-containing protein 4 (BRD4) is a cancer therapeutic target in many ongoing clinical trials disrupting primarily BRD4-regulated transcription programs. A critical role of BRD4 in cancer development has been reported and attributed mainly to the abundant long isoform (BRD4-L). Here we show, by isoform-specific knockdown and endogenous protein detection along with transgene expression, the less abundant BRD4 short isoform (BRD4-S) is oncogenic while BRD4-L is tumor-suppressive in breast cancer cell proliferation and migration as well as mammary tumor formation and metastasis. Through integrated RNA-seq transcriptome and genome-wide ChIP-seq and CUT&RUN association profiling, we identify Engrailed-1 (EN1) homeobox transcription factor as a key BRD4-S coregulator particularly in triple-negative breast cancer. BRD4-S and EN1 co-modulate the extracellular matrix (ECM)-associated matrisome network, including type II cystatin gene cluster, mucin 5 and cathepsin loci, via enhancer regulation of cancer-associated genes and pathways. Our work highlights the importance of targeted therapy for the oncogenic but not tumor-suppressive activity of BRD4. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE136151 Opposing Functions of BRD4 Isoforms in Breast Cancer. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2020.04.034 {Molecular cell (14.548): 10.1016/j.molcel.2020.04.034} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA561383 https://www.ebi.ac.uk/ena/browser/view/PRJNA561383 https://www.ncbi.nlm.nih.gov/sra?term=SRP219026 [Overal design]Whole-genome expression profiling by RNA-seq with BRD4 pan or isoform-specific siRNA knockdown in MCF-7 and MDA-MB-231 cells and genome-wide binding profilling of BRD4 isoforms and EN1 by ChiP-seq and CUT&RUN in MDA-MB-231 and also in its derived line (named 3f:S) ecopotically expressing three FLAG-tagged BRD4-S with or without JQ1 treatment; [Treatment]'Cells were transfected by BRD4 pan or isoform-specific siRNA or universal negative control siRNA (Sigma cat# SIC001) twice with 48-hour treatment each time.', 'Cells were either untreated (unt) or treated with 1 µM inactive JQ1(-) (i.e., JQ1-neg) or active JQ1(+) (i.e., JQ1-pos) for 4 hours.', 'no treatment'; [Growth]'Cells were maintained in high-glucose DMEM + 10% heat-inactivated FBS + Penicillin (100 units/ml) & Streptomycin (0.1 mg/ml).', 'MDA-MB-231 and its derived 3F:BRD4-S(a) line were maintained in high-glucose DMEM + 10% heat-inactivated FBS + Penicillin (100 units/ml) & Streptomycin (0.1 mg/ml).'; [Extraction]"RNA was harvested using miRNeasy Mini Kit (Qiagen #217004) following the manufacturer's instructions. Integrity was verified using the Agilent 2100 Bioanalyzer. All samples had a RIN score of 9 or higher.\nOne microgram of total DNase-treated RNA was prepared by using the TruSeq Stranded Total RNA LT Sample Prep Kit from Illumina (Illumina #RS-122). Total RNA was depleted of its rRNA and fragmented before strand-specific cDNA synthesis. cDNA was A-tailed and then ligated with indexed adapters. After adapter ligation, samples were PCR-amplified and purified with AmpureXP beads, then validated again on the Agilent 2100 Bioanalyzer. Samples were quantified by Qubit before being normalized and pooled for sequencing.", 'Lysates were clarified from sonicated nuclei and protein-DNA complexes were isolated by IP with anti-BRD4-L or BRD4-S [i.e., S(a)] antibody or with Abcam EN1 antibody (Cat# ab108598).\nSequencing libraries were constructed using NEBNext Ultra II DNA Library Prep Kit for Illumina (NEB) following manufacturer’s protocol.', 'Unfixed cells were immobilized on Concanavalin A-coated magnetic beads and permeablized with 0.05% digitonin. After antibody binding and pA-Mnase digestions, antibody-bound DNA fragments were released into solution, purified, and used for library construction.\nSequencing libraries were constructed using NEBNext Ultra II DNA Library Prep Kit for Illumina (NEB) with modification for shorter DNA fragments (< 100 bp).'; [Cell type]'Source: ''cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; sirna treatment: universal negative control siRNA (Sigma cat# SIC001); bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; sirna treatment: siRNA for all BRD4 isoforms (pan); bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; sirna treatment: siRNA for BRD4-L isoform (L); bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; sirna treatment: siRNA for BRD4-S(a) isoform (S); bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MCF-7; er/pr/her2 statue: ER+; PR+; sirna treatment: universal negative control siRNA (Sigma cat# SIC001); bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MCF-7; er/pr/her2 statue: ER+; PR+; sirna treatment: siRNA for all BRD4 isoforms (pan); bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MCF-7; er/pr/her2 statue: ER+; PR+; sirna treatment: siRNA for BRD4-L isoform (L); bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MCF-7; er/pr/her2 statue: ER+; PR+; sirna treatment: siRNA for BRD4-S(a) isoform (S); bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: anti-BRD4-S(a); bet inhibitor jq1 treatment: inactive enantiomer JQ1, i.e. JQ1_neg or JQ1(-); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: anti-BRD4-S(a); bet inhibitor jq1 treatment: active JQ1, i.e. JQ1_pos or JQ1(+); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: anti-BRD4-L; bet inhibitor jq1 treatment: inactive enantiomer JQ1, i.e. JQ1_neg or JQ1(-); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: anti-BRD4-L; bet inhibitor jq1 treatment: active JQ1, i.e. JQ1_pos or JQ1(+); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: input; bet inhibitor jq1 treatment: inactive enantiomer JQ1, i.e. JQ1_neg or JQ1(-); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: input; bet inhibitor jq1 treatment: active JQ1, i.e. JQ1_pos or JQ1(+); ', 'cell line: breast cancer cell line MDA-MB-231 ectopic 3f:BRD4-S(a) expression; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: anti-BRD4-S(a); bet inhibitor jq1 treatment: inactive enantiomer JQ1, i.e. JQ1_neg or JQ1(-); ', 'cell line: breast cancer cell line MDA-MB-231 ectopic 3f:BRD4-S(a) expression; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: anti-BRD4-S(a); bet inhibitor jq1 treatment: active JQ1, i.e. JQ1_pos or JQ1(+); ', 'cell line: breast cancer cell line MDA-MB-231 ectopic 3f:BRD4-S(a) expression; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: anti-EN1; bet inhibitor jq1 treatment: inactive enantiomer JQ1, i.e. JQ1_neg or JQ1(-); ', 'cell line: breast cancer cell line MDA-MB-231 ectopic 3f:BRD4-S(a) expression; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: input; bet inhibitor jq1 treatment: inactive enantiomer JQ1, i.e. JQ1_neg or JQ1(-); ', 'cell line: breast cancer cell line MDA-MB-231 ectopic 3f:BRD4-S(a) expression; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: input; bet inhibitor jq1 treatment: active JQ1, i.e. JQ1_pos or JQ1(+); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: anti-EN1; bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: input; bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: anti-BRD4-S(a); bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: anti-BRD4-L; bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MDA-MB-231; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: IgG; bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MDA-MB-231 ectopic 3f:BRD4-S(a) expression; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: anti-BRD4-S(a); bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MDA-MB-231 ectopic 3f:BRD4-S(a) expression; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: anti-BRD4-L; bet inhibitor jq1 treatment: untreated (unt); ', 'cell line: breast cancer cell line MDA-MB-231 ectopic 3f:BRD4-S(a) expression; er/pr/her2 statue: triple negative – ER-; PR-; HER2-; chip antibody: IgG; bet inhibitor jq1 treatment: untreated (unt); ' GSE146237 Homo sapiens 8 Genome binding/occupancy profiling by high throughput sequencing GPL20301 GLI1 ChIP-Seq in non-irradiated versus irradiated SUM1315 cells 2020-03-02 Changes in the GLI1 cistrome following ionizing radiation were investigated using ChIP-Seq in SUM1315 triple-negative breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE146237 Hedgehog signaling enables repair of ribosomal DNA double-strand breaks. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkaa733 {Nucleic acids research (11.147): 10.1093/nar/gkaa733} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA609752 https://www.ebi.ac.uk/ena/browser/view/PRJNA609752 https://www.ncbi.nlm.nih.gov/sra?term=SRP251291 [Overal design]8 samples analyzed in total, 2 conditions with paired 2% input controls done in duplicate, SUM1315 cells 4 hours after 4 Gy ionizing radiation or nonirradiated; [Treatment]'Dishes were exposed to 4 Gy ionizing radiation as indicated using an X-ray irradiator and chromatin was crosslinked and harvested 4 hours later for ChIP. GLI1 pull-down was done using 3 ug of C-1 antibody (Santa Cruz).'; [Growth]'SUM1315 cells were grown in complete media prior to irradiation or mock irradiation.'; [Extraction]"ChIP done and DNA extracted using SimpleChIP Plus kit (Cell Signaling Technologies, 9005S)\nDone by external vendor (GENEWIZ). Library was constructed with NEBNext Ultra DNA Library Prep with Beads Size Selection following manufacturer’s recommendations. Briefly, the ChIP DNA was end repaired and adapters were ligated after adenylation of the 3’ends. Adapter-ligated DNA was size selected, followed by clean up, and limited cycle PCR enrichment. The ChIP library was validated using Agilent TapeStation and quantified using Qubit 2.0 Fluorometer as well as real time PCR (Applied Biosystems, Carlsbad, CA, USA).\nChIP-Seq done by external vendor (GENEWIZ). The sequencing libraries were multiplexed and clustered on one lane of a flowcell. After clustering, the flowcell was loaded on the Illumina HiSeq instrument according to manufacturer’s instructions (Illumina, San Diego, CA, USA). Sequencing was performed using a 2x150 Paired End (PE) configuration. Image analysis and base calling were conducted by the HiSeq Control Software (HCS). Raw sequence data (.bcl files) generated from Illumina HiSeq was converted into fastq files and de-multiplexed using Illumina's bcl2fastq 2.17 software. One mis-match was allowed for index sequence identification."; [Cell type]'Source: ''4 gy ionizing radiation: Yes; gli1 antibody (c-1, santa cruz): No; 2% input control: Yes; ', '4 gy ionizing radiation: Yes; gli1 antibody (c-1, santa cruz): Yes; 2% input control: No; ', '4 gy ionizing radiation: No; gli1 antibody (c-1, santa cruz): No; 2% input control: Yes; ', '4 gy ionizing radiation: No; gli1 antibody (c-1, santa cruz): Yes; 2% input control: No; ' GSE127887 Homo sapiens 6 Expression profiling by high throughput sequencing GPL20301 Breast tumor stiffness instructs bone metastasis via mechanical memory 2019-03-05 The mechanical microenvironment of primary breast tumors plays a substantial role in promoting tumor progression. While the transitory response of cancer cells to pathological stiffness in their native microenvironment has been well described, it is unclear whether mechanical stimuli in the primary tumor influence distant, late-stage metastatic phenotypes in absentia. Here, we show that primary tumor stiffness promotes stable yet non-genetically heritable phenotypes in breast cancer cells. This “mechanical memory” instructs cancer cells to adopt and maintain increased cytoskeletal dynamics, traction force, and 3D invasion in vitro, in addition to promoting osteolytic bone metastasis in vivo. We established a “mechanical conditioning score” comprised of mechanically-regulated genes as a proxy measurement of tumor stiffness response, and we show that it is associated with bone metastasis in patients. Using a discovery approach, we mechanistically traced mechanical memory in part to ERK-mediated mechanotransductive activation of RUNX2, an osteogenic gene bookmarker and bone metastasis driver. This combination of traits allows for the stable transactivation of osteolytic target genes which persists after cancer cells disseminate from their activating microenvironment. Using genetic, epigenetic, and functional approaches, RUNX2-mediated mechanical memory can be stimulated, repressed, selected, or extended. In concert with previous studies detailing how biochemical properties of the primary tumor stroma influence distinct metastatic phenotypes, the impact of local biomechanical properties we present here support a generalized model of cancer progression in which the integrated properties of the primary tumor microenvironment govern cell behavior in the metastatic microenvironment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE127887 Breast tumor stiffness instructs bone metastasis via maintenance of mechanical conditioning. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2021.109293 {Cell reports (7.815): 10.1016/j.celrep.2021.109293} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA525698 https://www.ebi.ac.uk/ena/browser/view/PRJNA525698 https://www.ncbi.nlm.nih.gov/sra?term=SRP187598 [Overal design]Two mechanical conditions were used to grow SUM159 cells: soft (0.5 kPa) and stiff (8.0 kPa) with three biological replicates.; [Treatment]'Continuous mechanical preconditioning'; [Growth]'SUM159 cells were cultured for 2 weeks on collagen I-conjugated hydrogels that reflect native human breast tumor stiffness corresponding to regions of high cellularity/low matrix deposition (0.5 kPa; Petrisoft, Matrigen), versus low cellularity/high matrix deposition (8.0 kPa; Petrisoft, Matrigen). Cells were fed every 2 days and were split or analyzed when ~80% confluent.'; [Extraction]'Lysates were processed for RNA extraction using Isolate II RNA kit (Bioline), and 1µg from each sample was used for polyA selection with [Oligo d(T) Magnetic Beads,New England BioLabs #S1419S]\nFor RNA-seq, cDNA was synthesized using the SuperScript III system from Invitrogen, followed by second strand synthesis, ds End Repair and UDG treatment to recover strand-specific libraries. Libraries were barcoded with BioO Nextflex adapters and amplified prior to sequencing'; [Cell type]'Source: ''tissue: SUM159 cells; treatment: grown on collagen-coated soft hydrogel (0.5 kPa); ', 'tissue: SUM159 cells; treatment: grown on collagen-coated stiff hydrogel (8.0 kPa); ' GSE28844 Homo sapiens 61 Expression profiling by array GPL570 Differentially expressed genes after treatment with chemotherapy in breast cancer and their correlation with pathologic response 2011-04-25 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28844 Transcriptional shift identifies a set of genes driving breast cancer chemoresistance. PloS one 2.776 https://doi.org/10.1371/journal.pone.0053983 {PloS one (2.776): 10.1371/journal.pone.0053983} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA140625 https://www.ebi.ac.uk/ena/browser/view/PRJNA140625 None [Overal design]Refer to individual Series; [Treatment]'RNA processing: snap frozen in liquid nitrogen and preserved at -80ºC. Before RNA extraction protocol, samples were sectioned in a cryostat to evalute the celularity', 'RNA processing: snap frozen in liquid nitrogen and preserved at -80ºC. Before RNA extraction protocol, samples were sectioned in a cryostat to evalute the celularity.'; [Growth]'None'; [Extraction]'Total RNA was extracted using using an RNeasy minikit from Qiagen. Quality and quantity was assessed by agarose electrophoresis and spectrophotometric analysis (Absorbance 260/280 nm)'; [Cell type]'Source: ''age: 39; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE128; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 70; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE134; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 58; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE140; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 69; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE152; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 42; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE158; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 55; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE170; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 48; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE172; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 58; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE178; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 53; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE188; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 53; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE275; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 39; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: C; sample_id: 08SE129; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 70; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE135; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 58; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE141; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 69; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: C; sample_id: 08SE153; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 42; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: C; sample_id: 08SE159; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 55; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE171; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 48; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: B; sample_id: 08SE173; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 58; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: C; sample_id: 08SE179; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 53; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE189; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 53; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE276+08SE277; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 49; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE132; pathologic response to chemotherapy (miller & payne grade): 5; ', 'age: 39; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE144; pathologic response to chemotherapy (miller & payne grade): 5; ', 'age: 59; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE156; pathologic response to chemotherapy (miller & payne grade): 4; ', 'age: 45; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE176; pathologic response to chemotherapy (miller & payne grade): 4; ', 'age: 63; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE180; pathologic response to chemotherapy (miller & payne grade): 4; ', 'age: 38; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE186; pathologic response to chemotherapy (miller & payne grade): 5; ', 'age: 47; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE190; pathologic response to chemotherapy (miller & payne grade): 4; ', 'age: 39; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE278; pathologic response to chemotherapy (miller & payne grade): 5; ', 'age: 49; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE133; pathologic response to chemotherapy (miller & payne grade): 5; ', 'age: 59; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: C; sample_id: 08SE157; pathologic response to chemotherapy (miller & payne grade): 4; ', 'age: 45; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE177; pathologic response to chemotherapy (miller & payne grade): 4; ', 'age: 63; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: C; sample_id: 08SE181; pathologic response to chemotherapy (miller & payne grade): 4; ', 'age: 39; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE279+08SE280; pathologic response to chemotherapy (miller & payne grade): 5; ', 'age: 42; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE130; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 70; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE136; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 51; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE138; pathologic response to chemotherapy (miller & payne grade): 1; ', 'age: 73; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE142; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 58; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE146; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 57; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE154; pathologic response to chemotherapy (miller & payne grade): 1; ', 'age: 73; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE160; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 42; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE162; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 72; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE164; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 58; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE166; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 71; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE168; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 43; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE174; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 45; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE182; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 29; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none(Prechemotherapy); sample_id: 08SE273; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 70; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE137; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 51; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE139; pathologic response to chemotherapy (miller & payne grade): 1; ', 'age: 73; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE143; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 58; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: B; sample_id: 08SE147; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 57; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: B; sample_id: 08SE155; pathologic response to chemotherapy (miller & payne grade): 1; ', 'age: 73; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE161; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 42; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: B; sample_id: 08SE163; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 72; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE165; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 58; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE167; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 71; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE169; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 43; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: B; sample_id: 08SE175; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 45; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE183; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 74; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE185; pathologic response to chemotherapy (miller & payne grade): 2; ', 'age: 29; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: C; sample_id: 08SE274; pathologic response to chemotherapy (miller & payne grade): 2; ' GSE87048 Homo sapiens 200 Genome variation profiling by SNP array GPL6801 Analysis of somatic DNA copy number alterations and frequency of breast cancer intrinsic subtypes from Mexican women [copy number] 2016-09-17 Breast cancer is a heterogeneous disease described in well-recognized biological subtypes. Particularly, gene expression profiling has revealed 5 intrinsic subtypes of breast cancer characterized by different biological and clinical features. The diversity of the intrinsic subtypes across human population has been limited described, and there is few information about the genomic architecture of breast tumors in Mexican or Hispanic populations. In this study, we performed PAM50 assay, based in Affymetrix microarray profiling of 128 fresh frozen tumors from Mexican Latino Hispanic population, to describe the overall distribution of subtypes, and characterize the relation to clinicopathologic characteristics. As well, we correlated the mRNA expression patterns with specific copy number alterations (CPA), in order to analyze their role in breast tumors. A total of 100 blood-tumor samples were assayed using Affymetrix 6.0 SNP arrays; segmentation analysis and GISTIC were performed to identify focal amplifications or deletions. The distribution of PAM50 intrinsic subtypes in our cohort was computed to be 44% luminal A, 20% luminal B, 12.0% HER2-enriched, 12% basal-like, and 12% normal-like. Study comparison with the literature mainly TCGA and METABRIC (most of the patients came from Caucasian population), as well as LACE (which describe a population study) show a similar distribution of the intrinsic subtypes within Hispanic and Caucasian populations. Interestingly, basal-like subtype is less represented than in African-American race. The sum of sensitivity and specificity between the clinicopathologic and intrinsic subtype categories across 4 groups (excluding normal-like) was 50% and 87.5%, respectively. Differentially expression profiles within the subtypes reveal a set of genes altered in each group with biological relevance to stablish the phenotypical characteristics of each subtype. Our analyses confirmed the already reported copy number data. Importantly, many of the copy number profiles correlated with mRNA subtype. With this analysis we can conclude that breast cancer intrinsic subtypes have been reproduced in Mexican population contributing to the description of the PAM50 subtypes among multiple ethnic groups based on a gene expression assay. Our observation based in the integrative genomic analysis of mRNA expression and CPA allowed us to define gene circuits and phenotypic characteristics that can explain the heterogeneity of breast cancer subtypes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE87048 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA343312 https://www.ebi.ac.uk/ena/browser/view/PRJNA343312 None [Overal design]Breast cancer tumors were collected at the Fundación Mexicana de Fomento para la Prevención Oportuna del Cáncer de Mama, A.C., (FUCAM) during the surgical procedure in adjuvant, togehetr with 5ml of blood. Two training pathologist carefully performed a histopathological review to define percentage of tumoral cells. Also, immunochemistry markers (ER-, PR- and Her2-) were analyzed. Thus tumors with at least 70% of tumoral cells were processed (N=124). Genomic DNA was extracted and hybridize on Affymetrix SNP6 microarrays. To define SCNAs GISTIC algorithm was computed. SNP markers were used to define ancestry; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA from peripheral blood lymphocytes was extracted with the QIAamp DNA Blood Maxi Kit (Qiagen, Valencia, CA), according to manufacturer’s instructions'; [Cell type]'Germinal cell fraction', 'Somatic cell fraction''tissue: Buffy coat from peripheral blood; cell type: Germinal cell fraction; population: Mexican hispanic; ', 'tissue: Breast cancer tissue; cell type: Somatic cell fraction; population: Mexican hispanic; ' GSE28860 Homo sapiens 53 Expression profiling by array GPL6480 WU-BC 3, 4, and 5 PAM50 Subtypes with Passage and Gene Expression Comparison Between Xenografts and Primary Tumors 2011-04-26 Whole genome expression studies were performed on Xenograft panels with multiple passages from 3 different patient tumors. We assessed the global gene expression concordance from passages to passage and from passage to primary tumor when available and performed PAM50 subtype classification. These results were examined within the context of 40 PAM50 prototype experiments. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28860 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA140693 https://www.ebi.ac.uk/ena/browser/view/PRJNA140693 None [Overal design]Thirteen experiments representing different tumor passages from WU-BC 3, 4, and 5 were compared using unsupervised hierarchical clustering and PAM50 Subtype Classification. These experiments were analyzed within the context of previously published PAM50 Prototypes (GSE26082).; [Treatment]'None'; [Growth]'patient biopsies were frozen and stored in oct compound'; [Extraction]'Trizol extractions followed by Dnase treatment and column purification.'; [Cell type]'Source: ''reference: Stratagene Human Reference total RNA from 10 human cell lines: 1_Adenocarcinoma, mammary gland 2_Hepatoblastoma, liver 3_Adenocarcinoma, cervix 4_Embryonal carcinoma, testis 5_Glioblastoma, brain 6_Melanoma 7_Liposarcoma 8_Histiocytic Lymphoma; macrophage; histocyte 9_ Lymphoblastic leukemia, T lymphoblast 10_Plasmacytoma; myeloma; B lymphocyte. Also, mRNA spiked in from MCF7 and ME16C.; ', 'patient id: 15928; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMB; ', 'patient id: 10752; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: BASAL; ', 'patient id: 11726; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: BASAL; ', 'patient id: 119B-0Tumor; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: Normal; ', 'patient id: 13774; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: BASAL; ', 'patient id: 17033; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: Normal; ', 'patient id: 17034; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: Normal; ', 'patient id: 17035; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: Normal; ', 'patient id: 19640; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: HER2; ', 'patient id: 201B-0Tumor; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: Normal; ', 'patient id: 2388; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: BASAL; ', 'patient id: 2851; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: HER2; ', 'patient id: 4584; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: HER2; ', 'patient id: 4646; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: HER2; ', 'patient id: 4773; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: BASAL; ', 'patient id: 8679; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: BASAL; ', 'patient id: 8681; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: HER2; ', 'patient id: 8682; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: BASAL; ', 'patient id: 8699; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: HER2; ', 'patient id: 8997; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: BASAL; ', 'patient id: ES105; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: HER2; ', 'patient id: ES106; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: BASAL; ', 'patient id: 304; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMA; ', 'patient id: 15616_S; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMA; ', 'patient id: 15913_S; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMA; ', 'patient id: 15921_S; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMA; ', 'patient id: 15991_S; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMA; ', 'patient id: 15997_M; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMA; ', 'patient id: 16064_M; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMA; ', 'patient id: 16170_M; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMA; ', 'patient id: 16170_M_NR; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMA; ', 'patient id: 15879; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMB; ', 'patient id: 15945; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMB; ', 'patient id: 16002; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMB; ', 'patient id: 16025; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMB; ', 'patient id: 16035; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMB; ', 'patient id: 16140; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMB; ', 'patient id: 15469; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMA; ', 'patient id: 15694; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMA; ', 'patient id: 15995; sample type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; prototype: LUMA; ', 'tissue type: primary breast tumor; sample type: oct block from human:mouse xenograft which contained at least 50% tumor cellularity; clinical er: Negative; clinical pgr: Negative; clinical her2: Negative; ', 'tissue type: primary breast tumor; sample type: oct blocks from biopsy which contained at least 50% tumor cellularity; clinical er: Negative; clinical pgr: Negative; clinical her2: Negative; ', 'tissue type: ovary metastasis; sample type: oct block from human:mouse xenograft which contained at least 50% tumor cellularity; clinical er: Negative; clinical pgr: Negative; clinical her2: Negative; ' GSE71142 Homo sapiens 10 Non-coding RNA profiling by array GPL20717 Identification of differentially expressed miRNAs in drug resistant and drug sensitive breast cancer tissues 2015-07-21 To identify miRNAs involved in drug resistance of human breast cancer, a miRNA microarray was performed on 5 cases of drug resistant tissues and 5 cases of drug sensitive tissues.The expression levels of totally 2019 miRNAs in 5 pairs of matched, drug resistant and drug sensitive tissues were examined by microarray. There were 27 differentially expressed miRNAs between drug resistant and drug sensitive tissues were identified of which there were 11 significantly up-regulated while the other 16 were down-regulated in drug resistant tissues compared to drug sensitive tissues. It was found that miR-489 was one of the most downregulated miRNAs in drug resistant tissues. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE71142 Suppression of SPIN1-mediated PI3K-Akt pathway by miR-489 increases chemosensitivity in breast cancer. The Journal of pathology 5.942 https://doi.org/10.1002/path.4743 {The Journal of pathology (5.942): 10.1002/path.4743} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA290448 https://www.ebi.ac.uk/ena/browser/view/PRJNA290448 None [Overal design]Group 1: Examination of miRNAs in drug resistant tissues (5 cases), including C100, C17, C28, C22 and C115. Group 2: Examination of miRNAs in drug sensitive tissues (5 cases), including H801, H31, H19, H20, and H32.; [Treatment]'None'; [Growth]'None'; [Extraction]"MiRNAs were isolated from breast cancer tissues using a miRNeasy FFPE Kit (Bioteke, Beijing, China) according to the manufacturer's instructions."; [Cell type]'Source: ''drug sensitivity status: drug resistant tissue; tissue: human breast cancer tissue; ', 'drug sensitivity status: drug sensitive tissue; tissue: human breast cancer tissue; ' GSE72254 Homo sapiens 58 Methylation profiling by array GPL13534 DNA methylation-based immune response signature improves patient diagnosis in multiple cancers (TOP Cohort) 2015-08-20 Breast cancer (BC) is one of the most common and deadliest malignancies in women worldwide. Tumor immune response is increasingly recognized to be associated with better clinical outcome in breast and other cancers. However, the quantitative evaluation of the tumor immune response by measuring tumor-infiltrating lymphocytes (TILs) remains challenging, since it relies on subjective measurements, which are limited in accuracy and reproducibility. In this study, we sought to identify a set of DNA methylation markers (MeTIL signature) that better recapitulate the evaluation of TILs and their impact on long-term outcome in BC. We showed that the MeTIL score measures TIL distributions in a more robust and sensitive manner than conventional pathological TIL counts and that this translates into better prediction of survival and response to chemotherapy in BC. We demonstrated that the MeTIL score can be determined in low amounts of DNA from FFPE tumor tissue by bisulfite pyrosequencing allowing for the fast and cost-efficient evaluation of TILs in the clinical setting. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72254 DNA methylation-based immune response signature improves patient diagnosis in multiple cancers. The Journal of clinical investigation 12.282 https://doi.org/10.1172/JCI91095 {The Journal of clinical investigation (12.282): 10.1172/JCI91095} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA293702 https://www.ebi.ac.uk/ena/browser/view/PRJNA293702 None [Overal design]Bisulphite converted DNA of 58 samples from the TOP Cohort were hybridized to the Illumina Infinium 450k Human Methylation Beadchip; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was extracted with the Qiagen-DNeasy Blood &Tissue Kit (Qiagen, Hilden, Germany) or the QIAamp DNA Mini Kit (Qiagen, Hilden, Germany)'; [Cell type]'Source: ''tissue: breast tumor; cohort id: 1109; geo_accn_gse16446: GSM411332; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.13; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 693; dmfs_event: 0; dmfs_time (days): 693; pcr: 0; ', 'tissue: breast tumor; cohort id: 123; geo_accn_gse16446: GSM411364; grade: 3; t: T1; n: N0; esr1bimod: 0; her2_fish: 2.34; her2_fish_bin: 1; erbb2bimod: 0; age_bin: 1; os_event: null; os_time (days): null; dmfs_event: null; dmfs_time (days): null; pcr: 0; ', 'tissue: breast tumor; cohort id: 1312; geo_accn_gse16446: GSM411363; grade: 3; t: T1; n: N0; esr1bimod: 0; her2_fish: 6.37; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 860; dmfs_event: 0; dmfs_time (days): 860; pcr: 0; ', 'tissue: breast tumor; cohort id: 1366; geo_accn_gse16446: GSM411346; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.18; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 1404; dmfs_event: 0; dmfs_time (days): 1404; pcr: 0; ', 'tissue: breast tumor; cohort id: 1391; geo_accn_gse16446: GSM411300; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 6.96; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 1; os_event: 0; os_time (days): 1082; dmfs_event: 0; dmfs_time (days): 1082; pcr: 0; ', 'tissue: breast tumor; cohort id: 1536; geo_accn_gse16446: GSM411407; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 11.56; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 620; dmfs_event: 0; dmfs_time (days): 620; pcr: 1; ', 'tissue: breast tumor; cohort id: 1674; geo_accn_gse16446: GSM411371; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 1852; dmfs_event: 0; dmfs_time (days): 1852; pcr: 0; ', 'tissue: breast tumor; cohort id: 1767; geo_accn_gse16446: GSM411402; grade: 2; t: T2; n: N0; esr1bimod: 0; her2_fish: 2.25; her2_fish_bin: 1; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 2011; dmfs_event: 0; dmfs_time (days): 2011; pcr: 1; ', 'tissue: breast tumor; cohort id: 2090; geo_accn_gse16446: GSM411360; grade: 3; t: T4; n: N1; esr1bimod: 0; her2_fish: 1.76; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 1; os_time (days): null; dmfs_event: 1; dmfs_time (days): null; pcr: 0; ', 'tissue: breast tumor; cohort id: 2165; geo_accn_gse16446: GSM411366; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 4.55; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 991; dmfs_event: 0; dmfs_time (days): 991; pcr: 0; ', 'tissue: breast tumor; cohort id: 220; geo_accn_gse16446: GSM411324; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.05; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1358; dmfs_event: 0; dmfs_time (days): 1358; pcr: 0; ', 'tissue: breast tumor; cohort id: 2325; geo_accn_gse16446: GSM411293; grade: 3; t: T4; n: N1; esr1bimod: 0; her2_fish: 4.29; her2_fish_bin: 1; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 675; dmfs_event: 0; dmfs_time (days): 675; pcr: 0; ', 'tissue: breast tumor; cohort id: 2337; geo_accn_gse16446: GSM411326; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.06; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 710; dmfs_event: 0; dmfs_time (days): 710; pcr: 0; ', 'tissue: breast tumor; cohort id: 2744; geo_accn_gse16446: GSM411369; grade: 3; t: T1; n: N3; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 2069; dmfs_event: 0; dmfs_time (days): 2069; pcr: 0; ', 'tissue: breast tumor; cohort id: 3276; geo_accn_gse16446: GSM411333; grade: 3; t: T1; n: N0; esr1bimod: 0; her2_fish: 1.07; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1041; dmfs_event: 0; dmfs_time (days): 1041; pcr: 0; ', 'tissue: breast tumor; cohort id: 3414; geo_accn_gse16446: GSM411351; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 7.5; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 1; os_event: 0; os_time (days): 2187; dmfs_event: 1; dmfs_time (days): 254; pcr: 0; ', 'tissue: breast tumor; cohort id: 3731; geo_accn_gse16446: GSM411294; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 4.67; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 845; dmfs_event: 0; dmfs_time (days): 845; pcr: 0; ', 'tissue: breast tumor; cohort id: 4082; geo_accn_gse16446: GSM411354; grade: 3; t: T4; n: N1; esr1bimod: 0; her2_fish: 1.34; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 1; os_time (days): 314; dmfs_event: 1; dmfs_time (days): 314; pcr: 0; ', 'tissue: breast tumor; cohort id: 4270; geo_accn_gse16446: GSM411387; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 0; age_bin: 1; os_event: 1; os_time (days): 359; dmfs_event: 1; dmfs_time (days): 63; pcr: 0; ', 'tissue: breast tumor; cohort id: 4291; geo_accn_gse16446: GSM411337; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.09; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 1; os_time (days): 1932; dmfs_event: 1; dmfs_time (days): 1414; pcr: 0; ', 'tissue: breast tumor; cohort id: 4511; geo_accn_gse16446: GSM411353; grade: 3; t: T3; n: N0; esr1bimod: 0; her2_fish: 1.34; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1839; dmfs_event: 0; dmfs_time (days): 1839; pcr: 0; ', 'tissue: breast tumor; cohort id: 4864; geo_accn_gse16446: GSM411331; grade: 3; t: T1; n: N0; esr1bimod: 0; her2_fish: 1.07; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1211; dmfs_event: 1; dmfs_time (days): 627; pcr: 0; ', 'tissue: breast tumor; cohort id: 4917; geo_accn_gse16446: GSM411312; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.15; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 771; dmfs_event: 0; dmfs_time (days): 771; pcr: 0; ', 'tissue: breast tumor; cohort id: 4938; geo_accn_gse16446: GSM411379; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 449; dmfs_event: 0; dmfs_time (days): 449; pcr: 0; ', 'tissue: breast tumor; cohort id: 4984; geo_accn_gse16446: GSM411295; grade: 3; t: T2; n: N3; esr1bimod: 0; her2_fish: 3.96; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 1856; dmfs_event: 0; dmfs_time (days): 1856; pcr: 0; ', 'tissue: breast tumor; cohort id: 5180; geo_accn_gse16446: GSM411347; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.22; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 1; os_time (days): 431; dmfs_event: 1; dmfs_time (days): 223; pcr: 0; ', 'tissue: breast tumor; cohort id: 5328; geo_accn_gse16446: GSM411398; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.05; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1132; dmfs_event: 0; dmfs_time (days): 1132; pcr: 1; ', 'tissue: breast tumor; cohort id: 5437; geo_accn_gse16446: GSM411352; grade: 3; t: T1; n: N0; esr1bimod: 0; her2_fish: 1.33; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 669; dmfs_event: 0; dmfs_time (days): 669; pcr: 0; ', 'tissue: breast tumor; cohort id: 5622; geo_accn_gse16446: GSM411305; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 7.23; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 794; dmfs_event: 0; dmfs_time (days): 794; pcr: 0; ', 'tissue: breast tumor; cohort id: 5706; geo_accn_gse16446: GSM411362; grade: 2; t: T2; n: N0; esr1bimod: 0; her2_fish: 2.3; her2_fish_bin: 1; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1524; dmfs_event: 1; dmfs_time (days): 1072; pcr: 0; ', 'tissue: breast tumor; cohort id: 5751; geo_accn_gse16446: GSM411376; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 919; dmfs_event: 0; dmfs_time (days): 919; pcr: 0; ', 'tissue: breast tumor; cohort id: 5783; geo_accn_gse16446: GSM411399; grade: 3; t: T2; n: N0; esr1bimod: 1; her2_fish: 1.1; her2_fish_bin: 0; erbb2bimod: null; age_bin: 1; os_event: null; os_time (days): null; dmfs_event: null; dmfs_time (days): null; pcr: 1; ', 'tissue: breast tumor; cohort id: 5920; geo_accn_gse16446: GSM411340; grade: 3; t: T2; n: N2; esr1bimod: 0; her2_fish: 1.13; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): null; dmfs_event: 0; dmfs_time (days): null; pcr: 0; ', 'tissue: breast tumor; cohort id: 6181; geo_accn_gse16446: GSM411322; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.03; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 777; dmfs_event: 0; dmfs_time (days): 777; pcr: 0; ', 'tissue: breast tumor; cohort id: 6198; geo_accn_gse16446: GSM411314; grade: 2; t: T2; n: N1; esr1bimod: 0; her2_fish: 1; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1259; dmfs_event: 0; dmfs_time (days): 1259; pcr: 0; ', 'tissue: breast tumor; cohort id: 6276; geo_accn_gse16446: GSM411318; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.09; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 748; dmfs_event: 0; dmfs_time (days): 748; pcr: 0; ', 'tissue: breast tumor; cohort id: 6754; geo_accn_gse16446: GSM411320; grade: 2; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.06; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1376; dmfs_event: 0; dmfs_time (days): 1376; pcr: 0; ', 'tissue: breast tumor; cohort id: 6767; geo_accn_gse16446: GSM411317; grade: 3; t: T4; n: N1; esr1bimod: 0; her2_fish: 0.98; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 1; os_time (days): 464; dmfs_event: 1; dmfs_time (days): 464; pcr: 0; ', 'tissue: breast tumor; cohort id: 682; geo_accn_gse16446: GSM411339; grade: 2; t: T4; n: N2; esr1bimod: 0; her2_fish: 1.12; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 1; os_time (days): 732; dmfs_event: 1; dmfs_time (days): 732; pcr: 0; ', 'tissue: breast tumor; cohort id: 6839; geo_accn_gse16446: GSM411359; grade: 3; t: T1; n: N1; esr1bimod: 0; her2_fish: 1.7; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1390; dmfs_event: 0; dmfs_time (days): 1390; pcr: 0; ', 'tissue: breast tumor; cohort id: 6951; geo_accn_gse16446: GSM411325; grade: 2; t: T4; n: N1; esr1bimod: 0; her2_fish: 1.03; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 725; dmfs_event: 0; dmfs_time (days): 725; pcr: 0; ', 'tissue: breast tumor; cohort id: 7173; geo_accn_gse16446: GSM411406; grade: 3; t: T2; n: N2; esr1bimod: 0; her2_fish: 7.18; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 1; os_event: 0; os_time (days): 1130; dmfs_event: 0; dmfs_time (days): 1130; pcr: 1; ', 'tissue: breast tumor; cohort id: 7182; geo_accn_gse16446: null; grade: null; t: null; n: null; esr1bimod: null; her2_fish: null; her2_fish_bin: null; erbb2bimod: null; age_bin: null; os_event: null; os_time (days): null; dmfs_event: null; dmfs_time (days): null; pcr: 0; ', 'tissue: breast tumor; cohort id: 7469; geo_accn_gse16446: GSM411309; grade: 3; t: T3; n: N1; esr1bimod: 0; her2_fish: 1.08; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 1; os_time (days): 858; dmfs_event: 1; dmfs_time (days): 291; pcr: 0; ', 'tissue: breast tumor; cohort id: 7500; geo_accn_gse16446: GSM411377; grade: 3; t: T3; n: N1; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 726; dmfs_event: 1; dmfs_time (days): 558; pcr: 0; ', 'tissue: breast tumor; cohort id: 7634; geo_accn_gse16446: GSM411396; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 1208; dmfs_event: 0; dmfs_time (days): 1208; pcr: 1; ', 'tissue: breast tumor; cohort id: 8319; geo_accn_gse16446: GSM411323; grade: 2; t: T4; n: N1; esr1bimod: 0; her2_fish: 1018; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 1772; dmfs_event: 0; dmfs_time (days): 1772; pcr: 0; ', 'tissue: breast tumor; cohort id: 845; geo_accn_gse16446: GSM411365; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 4.4; her2_fish_bin: 1; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1647; dmfs_event: 0; dmfs_time (days): 1647; pcr: 0; ', 'tissue: breast tumor; cohort id: 8660; geo_accn_gse16446: GSM411297; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 1; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): null; dmfs_event: 0; dmfs_time (days): null; pcr: 0; ', 'tissue: breast tumor; cohort id: 8739; geo_accn_gse16446: GSM411296; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 0.71; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: null; os_time (days): null; dmfs_event: null; dmfs_time (days): null; pcr: 0; ', 'tissue: breast tumor; cohort id: 8999; geo_accn_gse16446: GSM411373; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 0; age_bin: 0; os_event: 1; os_time (days): 547; dmfs_event: 1; dmfs_time (days): 249; pcr: 0; ', 'tissue: breast tumor; cohort id: 9049; geo_accn_gse16446: GSM411345; grade: 1; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.2; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 599; dmfs_event: 0; dmfs_time (days): 599; pcr: 0; ', 'tissue: breast tumor; cohort id: 9064; geo_accn_gse16446: GSM411348; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.22; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 1408; dmfs_event: 0; dmfs_time (days): 1408; pcr: 0; ', 'tissue: breast tumor; cohort id: 9171; geo_accn_gse16446: GSM411299; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 4.81; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 1719; dmfs_event: 0; dmfs_time (days): 1719; pcr: 0; ', 'tissue: breast tumor; cohort id: 9386; geo_accn_gse16446: GSM411343; grade: 2; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.16; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 956; dmfs_event: 0; dmfs_time (days): 956; pcr: 0; ', 'tissue: breast tumor; cohort id: 9434; geo_accn_gse16446: GSM411374; grade: 3; t: T4; n: N1; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 737; dmfs_event: 1; dmfs_time (days): 160; pcr: 0; ', 'tissue: breast tumor; cohort id: 9576; geo_accn_gse16446: GSM411400; grade: 3; t: T4; n: N1; esr1bimod: 0; her2_fish: 1.11; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 1748; dmfs_event: 0; dmfs_time (days): 1748; pcr: 1; ', 'tissue: breast tumor; cohort id: 9665; geo_accn_gse16446: GSM411338; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 6.67; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 1008; dmfs_event: 0; dmfs_time (days): 1008; pcr: 0; ' GSE43415 Mus musculus 2 Genome binding/occupancy profiling by high throughput sequencing GPL13112 Estrogen Receptor alpha ChIP-Seq in mouse mammary gland 2013-01-10 Estrogen Receptor is a key transcriptional regulator in mammary gland development and breast cancer. In this study, we have mapped the Estrogen Receptor chromatin binding patterns in healthy mouse mammary gland https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43415 The transcriptional co-factor RIP140 regulates mammary gland development by promoting the generation of key mitogenic signals. Development (Cambridge, England) 5.763 https://doi.org/10.1242/dev.085720 {Development (Cambridge, England) (5.763): 10.1242/dev.085720} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA186027 https://www.ebi.ac.uk/ena/browser/view/PRJNA186027 https://www.ncbi.nlm.nih.gov/sra?term=SRP017873 [Overal design]A minimum of 6 pairs of mouse mammary gland pads from mice at 5-6 weeks of age were excised and Estrogen Receptor ChIp-seq was performed.; [Treatment]'None'; [Growth]'The mice used in this study were backcrossed several generations to the C57BL/6J background. All animal studies were carried out in accordance with the United Kingdom Home Office guidelines. A minimum of 6 pairs of mouse mammary gland pads from mice at 5-6 weeks of age were excised washed with phosphate buffered saline (PBS) and minced.'; [Extraction]"After tissue fixation and cell lysis, lysates were clarified from sonicated nuclei.Lysate was immunoprecipitated for Estrogen Receptor and protein-DNA complexes were isolated with antibody.\nLibraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit (Part# 0801-0303). Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation DNA was PCR amplified with Illumina primers for 15 cycles and library fragments of ~250 bp (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the Genome Analyzer following the manufacturer's protocols."; [Cell type]'Source: ''chip antibody: ERalpha; chip antibody catalog #: sc-543; chip antibody manufacturer: Santa Cruz; genetic background: C57BL/6J; tissue: mammary gland; ', 'genetic background: C57BL/6J; tissue: mammary gland; ' GSE152559 Homo sapiens 16 Genome binding/occupancy profiling by high throughput sequencing GPL16791 PTEN-dependent regulation of genome-wide transcription during metabolic stress [ChIP-Seq] 2020-06-16 PTEN is implicated in a wide variety of pathophysiological conditions and traditionally studied in the context of the PIK3-AKT-mTOR axis. Recent studies from our group and others have reported a novel role of PTEN in the regulation of transcription at the genome-wide scale. This emerging role of PTEN on global transcriptional regulation is providing a better understanding of various diseases, including cancer. Since cancer progression is an energy-demanding process and PTEN is known to regulate metabolic processes, we sought to understand the role of PTEN in transcriptional regulation under metabolic stress, a condition often developing in the tumor microenvironment. In the present study, we demonstrate that PTEN modulates genome-wide RNA Polymerase II (Pol II) occupancy in cells undergoing glucose deprivation. The glucose-deprived PTEN null cells were found to continue global gene transcription, which may activate a survival mode. However, cells with constitutive PTEN expression slow transcription, an evolutionary mechanism that may save cellular energy and activate programmed cell death pathways, in the absence of glucose. Interestingly, alternative exon usage by PTEN null cells is increased under metabolic stress compared to PTEN expressing cells. Overall, our study comprehensively demonstrates distinct mechanisms involved in PTEN-dependent genome-wide transcriptional control under metabolic stress. Our findings provide a new insight in understanding the tumor microenvironment and how PTEN loss of function, whether by genetic or non-genetic mechanisms, can contribute to a favorable transcriptional program employed by tumor cells to escape apoptosis, hence developing more aggressive and metastatic phenotypes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE152559 Metabolic stress regulates genome-wide transcription in a PTEN-dependent manner. Human molecular genetics 4.544 https://doi.org/10.1093/hmg/ddaa168 {Human molecular genetics (4.544): 10.1093/hmg/ddaa168} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA639718 https://www.ebi.ac.uk/ena/browser/view/PRJNA639718 https://www.ncbi.nlm.nih.gov/sra?term=SRP267476 [Overal design]RNA Pol II ChIP-seq was performed on BT-549 control and PTEN over-expressing BT-549_PTEN cell.; [Treatment]'Three hours of glucose deprivation'; [Growth]'Cells were cultured in DMEM/F-12 medium (Life Technologies, Grand Island, NY) supplemented with 10% FBS (Thermo Scientific Gibco, Waltham, MA) at 37°C with 5% CO2.'; [Extraction]'Chromatin was immunoprecipitated using RNA Pol II antibody, washed, reverse-crosslinked, and DNA isolated using the phenol-chloroform method. Input DNA isolated using the phenol-chloroform method\n10ng precipitated DNA was used to prepare library using Illumina TruSeq ChIP library preparation kit.'; [Cell type]'Source: ''cell line: BT-549; genotype: WT; treatment: 3 hrs Glucose deprivation; chip antibody: none; ', 'cell line: BT-549; genotype: WT; treatment: 3 hrs Glucose deprivation; chip antibody: RNA Pol II antibody; ', 'cell line: BT-549; genotype: PTEN over-expressed; treatment: 3 hrs Glucose deprivation; chip antibody: none; ', 'cell line: BT-549; genotype: PTEN over-expressed; treatment: 3 hrs Glucose deprivation; chip antibody: RNA Pol II antibody; ', 'cell line: BT-549; genotype: WT; treatment: control; chip antibody: none; ', 'cell line: BT-549; genotype: WT; treatment: control; chip antibody: Rpb1 (D8L4Y) (Cell Signaling cat# 14958); ', 'cell line: BT-549; genotype: PTEN over-expressed; treatment: control; chip antibody: none; ', 'cell line: BT-549; genotype: PTEN over-expressed; treatment: control; chip antibody: Rpb1 (D8L4Y) (Cell Signaling cat# 14958); ' GSE129530 Homo sapiens 8 Expression profiling by high throughput sequencing; Other GPL16791 Transcriptome-wide binding profile of RNA-binding protein HuR and its inhibitor in MDA-MB-231 cells 2019-04-09 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE129530 Targeting the interaction between RNA-binding protein HuR and FOXQ1 suppresses breast cancer invasion and metastasis. Communications biology 0.12 https://doi.org/10.1038/s42003-020-0933-1 {Communications biology (0.12): 10.1038/s42003-020-0933-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA531659 https://www.ebi.ac.uk/ena/browser/view/PRJNA531659 None [Overal design]Refer to individual Series; [Treatment]'None', 'Cells in 6-well plate were treated with DMSO or KH-3 for 24 hours.'; [Growth]'MDA-MB-231 cells were routinely cultured in DMEM supplemented with 10% fetal bovine serum and 1% antibiotics.'; [Extraction]"HuR-RNA complex in the cell lysate was isolated by antibody, and RNA was harvested by Trizol reagent.\nLibraries were prepared according to Illumina's instructions accompanying the TruSeq RNA Library Prep Kit v2 (Cat#RS-121-2001) without poly A selection.", "Total RNA was harvested by Trizol reagent.\nLibraries were prepared according to Illumina's instructions accompanying the TruSeq Standard mRNA (Cat#RS-122-2101)."; [Cell type]'Source: ''cell line: MDA-MB-231; tissue: breast cancer cell; rip antibody: mouse anti-HuR antibody; ', 'cell line: MDA-MB-231; tissue: breast cancer cell; rip antibody: mouse IgG; ', 'cell line: MDA-MB-231; tissue: breast cancer cell; treatment: DMSO; ', 'cell line: MDA-MB-231; tissue: breast cancer cell; treatment: 10uM KH-3; ' GSE88715 Homo sapiens 76 Expression profiling by array GPL14550 Gene expression profiles of microdissected tumor epithelium and stroma from TN breast tumors 2016-10-13 Engaging the immune system promises to be key for optimal cancer therapy, especially in hard-to-treat disease such as triple-negative breast cancer (TNBC). However, the immune microenvironment remains poorly understood. Using gene expression based on laser capture microdissection, we identify three distinct tumor microenvironments associated with CD8+ T cell localization patterns and outcome in TNBC. An immunoreactive microenvironment is defined by granzyme B-positive CD8+ T cell infiltration, a type I interferon signature, tumor expression of PD-L1 and good outcome. In contrast, tumors with an immune-cold microenvironment display restriction of CD8+ T cells to tumor margins, elevated tumor expression of the immunosuppressive marker B7-H4, a signature of desmoplastic stroma and poor outcome. A third distinct immunomodulatory microenvironment associated with poor outcome is enriched for IL-17-producing cells and neutrophils, as well as stroma-restricted localisation of CD8+ T cells. These distinct immune microenvironments have implications for TNBC patient stratification for current and future therapies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE88715 Spatially distinct tumor immune microenvironments stratify triple-negative breast cancers. The Journal of clinical investigation 12.282 https://doi.org/10.1172/JCI96313 {The Journal of clinical investigation (12.282): 10.1172/JCI96313} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA348764 https://www.ebi.ac.uk/ena/browser/view/PRJNA348764 None [Overal design]38 patient samples, tissue compartments isolated by laser capture microdissection to yield 38 samples of tumor epithelium, 38 samples of tumor stroma; each subjected to gene expression profiling in a common reference design using Agilent whole human genome oligonucleotide arrays.; [Treatment]"Tissue compartments isolated from OCT-embedded frozen human tissue samples by laser capture microscopy following HistoGene staining and pathologist's evaluation"; [Growth]'None'; [Extraction]'Tumor epithelium and stroma were separately microdissected from tissue samples using a PixCell IIe LCM system (Arcturus). All microdissections were performed within three hours of tissue staining. Total RNA was extracted from each population of microdissected cells using an Arcturus PicoPure RNA Isolation Kit (Cat# 12204-01).'; [Cell type]'Source: ''compartment: Tumor Epithelium; ', 'sample type: reference; ', 'compartment: Tumor Stroma; ' GSE97972 Homo sapiens 2 Genome binding/occupancy profiling by high throughput sequencing GPL16791 ChIP-seq analysis of MCF10A cells exressing active mutant YAP-5SA 2017-04-19 To understand the direct target genes YAP transcription co-activator invovled with in gonome-wide levels, next generation sequencing was conducted in Flag-YAP-5SA overexpressing MCF10A cells using Flag (sigma) antibody. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE97972 Mechanical cue-induced YAP instructs Skp2-dependent cell cycle exit and oncogenic signaling. The EMBO journal 11.227 https://doi.org/10.15252/embj.201696089 {The EMBO journal (11.227): 10.15252/embj.201696089} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA383543 https://www.ebi.ac.uk/ena/browser/view/PRJNA383543 https://www.ncbi.nlm.nih.gov/sra?term=SRP104266 [Overal design]Genomic profiles bound by YAP was generated in MCF10A expressing Flag-YAP-5SA using Illumina's Hi-Seq; [Treatment]'None'; [Growth]'Cells were growin in DMEM/F12 supplemented with 5% horse serum (Invitrogen), 20 ng/ml EGF (Peprotech), 10 mg/ml insulin (Sigma), 0.5 mg/ml hydrocortisone (Sigma), 100 ng/ml cholera toxin (Sigma) and penicillin/streptomycin (Invitrogen).'; [Extraction]'Cells were fixed with 1% formaldehyde for 15 min and quenched with 0.125 M glycine. Lysates were sonicated with a microtip sonicator to shear the DNA. Genomic DNA (Input) was prepared by treating aliquots of chromatin with RNase, proteinase K and heat for de-crosslinking, followed by ethanol precipitation. Starting with 50 ug of chromatin, genomic DNA regions of interest were isolated using Flag-M2 affinity beads. Immune complexes were washed, eluted from the beads with SDS buffer, and subjected to RNase and proteinase K treatment. Crosslinks were reversed by incubation overnight at 65 C, and ChIP DNA was purified by phenol-chloroform extraction and ethanol precipitation.\nIllumina sequencing libraries were prepared from the ChIP and Input DNAs by the standard consecutive enzymatic steps of end-polishing, dA-addition, and adaptor ligation. After a final PCR amplification step, the resulting DNA libraries were quantified and sequenced on HiSeq 2500.'; [Cell type]'breast cancer cell line''cell line: MCF10A; cell type: breast cancer cell line; chip antibody: Flag-M2 (Sigma, A2220); ', 'cell line: MCF10A; cell type: breast cancer cell line; chip antibody: none (input); ' GSE46581 Homo sapiens 90 Expression profiling by array GPL8432 Yale Triple Negative Breast Cancer Cohort 2013-05-02 Triple negative breast cancer (TNBC) is characterized by high proliferation, poor differentiation and a poor prognosis due to high rates of recurrence. Despite lower overall incidence African American (AA) patients suffer from higher breast cancer mortality in part due to the higher proportion of TNBC cases among AA patients compared to European Americans (EA). It was recently shown that the clinical heterogeneity of TNBC is reflected by distinct transcriptional programs with distinct drug response profiles in preclinical models. In this study, we used gene expression profiling and immunohistochemistry to eluicidate potential differences between TNBC tumors of EA and AA patients on a molecular level. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE46581 Molecular phenotypes in triple negative breast cancer from African American patients suggest targets for therapy. PloS one 2.776 https://doi.org/10.1371/journal.pone.0071915 {PloS one (2.776): 10.1371/journal.pone.0071915} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA201430 https://www.ebi.ac.uk/ena/browser/view/PRJNA201430 None [Overal design]WG-DASL experiment of 90 FFPE samples of ER, PR and HER2 (triple) negative breast cancer samples diagnosed between 1987 and 2007. Invasive disease was identified on H&E sections by the study pathologist and one to three 1.5 mm cores were punched from the top down in the designated tumor areas of each FFPE block. The cores were deparaffinized with xylene at 50°C for 3 minutes. RNA was extracted using the RecoverAll Total Nucleic Acid Isolation kit (Applied Biosystems) following the manufacturer's protocol. The isolated RNA was hybridized to Whole-Genome DASL (HumanRef8 V 3.0, Illumina) at the Yale Center for Genome Analysis. 90 primary tumor RNA samples from 90 patients were adequate for analysis and passed Quality control.; [Treatment]'None'; [Growth]'None'; [Extraction]"1.5mm core from FFPE block, area of invasive disease indicated by study pathologist based on H&E staining. RecoverAll Total Nucleic Acid Isolation kit (Applied Biosystems) following the manufacturer's protocol"; [Cell type]'Source: ''race: African American; diagnosis age: 54; Stage: 2; nodes: Positive; mva: 0.412876705; ', 'race: African American; diagnosis age: 42; Stage: 2; nodes: Positive; mva: 2.927163929; ', 'race: European American; diagnosis age: 50; Stage: 1; nodes: Negative; mva: NA; ', 'race: Hispanic; diagnosis age: 39; Stage: 3; nodes: Positive; mva: 1.085153604; ', 'race: African American; diagnosis age: 53; Stage: 2; nodes: Negative; mva: 5.458596219; ', 'race: African American; diagnosis age: 53; Stage: 2; nodes: Positive; mva: 3.687001737; ', 'race: Hispanic; diagnosis age: 70; Stage: 3; nodes: Positive; mva: 2.671889361; ', 'race: African American; diagnosis age: 47; Stage: 2; nodes: Positive; mva: 2.7833767; ', 'race: African American; diagnosis age: 39; Stage: 2; nodes: NA; mva: NA; ', 'race: Hispanic; diagnosis age: 47; Stage: 3; nodes: Negative; mva: 0.129757785; ', 'race: African American; diagnosis age: 56; Stage: 2; nodes: NA; mva: NA; ', 'race: Hispanic; diagnosis age: 39; Stage: 3; nodes: Positive; mva: 2.872358269; ', 'race: African American; diagnosis age: 45; Stage: 2; nodes: NA; mva: 0.469100626; ', 'race: African American; diagnosis age: 39; Stage: 2; nodes: NA; mva: 0.180011756; ', 'race: African American; diagnosis age: 49; Stage: 2; nodes: NA; mva: NA; ', 'race: NA; diagnosis age: 41; Stage: 4; nodes: Positive; mva: NA; ', 'race: European American; diagnosis age: 65; Stage: 1; nodes: NA; mva: 2.329003649; ', 'race: African American; diagnosis age: 64; Stage: 2; nodes: NA; mva: 3.490080157; ', 'race: African American; diagnosis age: 57; Stage: 2; nodes: NA; mva: 5.010414048; ', 'race: European American; diagnosis age: 56; Stage: 1; nodes: NA; mva: 1.127046995; ', 'race: European American; diagnosis age: 46; Stage: 1; nodes: NA; mva: 0.4291204; ', 'race: European American; diagnosis age: 59; Stage: 1; nodes: NA; mva: 1.340759549; ', 'race: African American; diagnosis age: 45; Stage: 2; nodes: NA; mva: 3.924957103; ', 'race: European American; diagnosis age: 49; Stage: 1; nodes: NA; mva: 2.208974804; ', 'race: Hispanic; diagnosis age: 36; Stage: 3; nodes: NA; mva: 1.446670643; ', 'race: African American; diagnosis age: 39; Stage: 2; nodes: NA; mva: 1.448641439; ', 'race: Hispanic; diagnosis age: 45; Stage: 3; nodes: NA; mva: 1.007293961; ', 'race: NA; diagnosis age: 59; Stage: NA; nodes: Positive; mva: NA; ', 'race: African American; diagnosis age: 55; Stage: 2; nodes: Positive; mva: 0.232070335; ', 'race: African American; diagnosis age: 49; Stage: 2; nodes: Negative; mva: NA; ', 'race: European American; diagnosis age: 34; Stage: 1; nodes: NA; mva: 0.16394902; ', 'race: African American; diagnosis age: 59; Stage: 2; nodes: Positive; mva: 2.435320892; ', 'race: NA; diagnosis age: 44; Stage: 4; nodes: Positive; mva: 2.815534566; ', 'race: African American; diagnosis age: 42; Stage: 2; nodes: Negative; mva: 0.322379526; ', 'race: European American; diagnosis age: 56; Stage: 1; nodes: Negative; mva: 1.279787411; ', 'race: African American; diagnosis age: 54; Stage: 2; nodes: Negative; mva: 0.390556369; ', 'race: European American; diagnosis age: 43; Stage: 1; nodes: Negative; mva: 0.663625641; ', 'race: African American; diagnosis age: 54; Stage: 2; nodes: Positive; mva: 1.146281395; ', 'race: African American; diagnosis age: 39; Stage: 2; nodes: Negative; mva: NA; ', 'race: NA; diagnosis age: 49; Stage: 4; nodes: Negative; mva: 0.481067463; ', 'race: African American; diagnosis age: 75; Stage: 2; nodes: Negative; mva: 0.020176242; ', 'race: Hispanic; diagnosis age: 57; Stage: 3; nodes: Positive; mva: NA; ', 'race: European American; diagnosis age: 67; Stage: 1; nodes: Negative; mva: 0.624330243; ', 'race: NA; diagnosis age: 90; Stage: 4; nodes: Positive; mva: 0.16359007; ', 'race: African American; diagnosis age: 60; Stage: 2; nodes: Negative; mva: 0.417820114; ', 'race: African American; diagnosis age: 51; Stage: 2; nodes: NA; mva: 0.401529254; ', 'race: African American; diagnosis age: 40; Stage: 2; nodes: Positive; mva: 0.501526385; ', 'race: NA; diagnosis age: NA; Stage: NA; nodes: NA; mva: 0.074857706; ', 'race: European American; diagnosis age: 52; Stage: 1; nodes: Negative; mva: NA; ', 'race: African American; diagnosis age: 84; Stage: 2; nodes: Negative; mva: 1.584511097; ', 'race: African American; diagnosis age: 71; Stage: 2; nodes: Negative; mva: 1.175211076; ', 'race: European American; diagnosis age: 47; Stage: 1; nodes: NA; mva: 0.084014002; ', 'race: European American; diagnosis age: 74; Stage: 1; nodes: Negative; mva: 0.043439726; ', 'race: African American; diagnosis age: 45; Stage: 2; nodes: NA; mva: 0.982746354; ', 'race: NA; diagnosis age: 38; Stage: 4; nodes: NA; mva: 2.02517938; ', 'race: NA; diagnosis age: 39; Stage: NA; nodes: NA; mva: 0.409714444; ', 'race: African American; diagnosis age: 76; Stage: 2; nodes: Negative; mva: NA; ', 'race: NA; diagnosis age: 39; Stage: 4; nodes: NA; mva: 0.031379209; ', 'race: African American; diagnosis age: 61; Stage: 2; nodes: Positive; mva: 2.8996418; ', 'race: African American; diagnosis age: 79; Stage: 2; nodes: Negative; mva: 2.552813083; ', 'race: African American; diagnosis age: 34; Stage: 2; nodes: Negative; mva: 0.09590402; ', 'race: European American; diagnosis age: 45; Stage: 1; nodes: Negative; mva: 0.086054253; ', 'race: European American; diagnosis age: 33; Stage: 1; nodes: Positive; mva: 0.873091351; ', 'race: NA; diagnosis age: NA; Stage: NA; nodes: NA; mva: 1.242491834; ', 'race: European American; diagnosis age: 65; Stage: 1; nodes: Negative; mva: 0.287234043; ', 'race: NA; diagnosis age: 41; Stage: NA; nodes: NA; mva: 0.066478081; ', 'race: African American; diagnosis age: 44; Stage: 2; nodes: Negative; mva: 0.09978395; ', 'race: African American; diagnosis age: 55; Stage: 2; nodes: Negative; mva: 0.152082358; ', 'race: NA; diagnosis age: NA; Stage: NA; nodes: NA; mva: 1.012092203; ', 'race: European American; diagnosis age: 60; Stage: 1; nodes: Negative; mva: 0.20062613; ', 'race: NA; diagnosis age: 50; Stage: 4; nodes: Negative; mva: 1.217493655; ', 'race: European American; diagnosis age: 77; Stage: 1; nodes: Negative; mva: 0.425990556; ', 'race: European American; diagnosis age: 45; Stage: 1; nodes: Negative; mva: NA; ', 'race: African American; diagnosis age: 50; Stage: 2; nodes: Positive; mva: 0.340217778; ', 'race: NA; diagnosis age: 47; Stage: 4; nodes: NA; mva: 0.953238816; ', 'race: European American; diagnosis age: 39; Stage: 1; nodes: Positive; mva: 0.824052787; ', 'race: European American; diagnosis age: 52; Stage: 1; nodes: Negative; mva: 0.505653245; ', 'race: European American; diagnosis age: 61; Stage: 1; nodes: Negative; mva: 0.385397709; ', 'race: African American; diagnosis age: 35; Stage: 2; nodes: Positive; mva: NA; ', 'race: African American; diagnosis age: 51; Stage: 2; nodes: Negative; mva: 0.826716784; ', 'race: African American; diagnosis age: 64; Stage: 2; nodes: Negative; mva: 7.142694311; ', 'race: Hispanic; diagnosis age: 51; Stage: 3; nodes: Negative; mva: 0.903227323; ', 'race: African American; diagnosis age: 64; Stage: 2; nodes: Negative; mva: 15.73596358; ', 'race: European American; diagnosis age: 54; Stage: 1; nodes: Negative; mva: 2.602045181; ', 'race: African American; diagnosis age: 62; Stage: 2; nodes: Negative; mva: 0.095945871; ', 'race: European American; diagnosis age: 81; Stage: 1; nodes: Negative; mva: 0.219696246; ', 'race: European American; diagnosis age: 74; Stage: 1; nodes: Negative; mva: 2.033437258; ', 'race: African American; diagnosis age: 55; Stage: 2; nodes: NA; mva: 0.03152811; ', 'race: African American; diagnosis age: 48; Stage: 2; nodes: NA; mva: 0.221183735; ', 'race: African American; diagnosis age: 52; Stage: 2; nodes: Negative; mva: 0.315471283; ' GSE7377 Homo sapiens 16 Expression profiling by array GPL1352 Expression data from premalignant breast cancers 2007-03-27 Enlargement of normal terminal duct lobular units (TDLUs) by hyperplastic columnar epithelial cells is one of the most common abnormalities of growth in the adult female human breast. These hyperplastic enlarged lobular units (HELUs) are important clinically as the earliest histologically identifiable potential precursor of breast cancer. The causes of the hyperplasia are unknown but may include estrogen-simulated growth mediated by estrogen receptor alpha, which is highly elevated in HELUs and may be fundamental to their development. This study used DNA microarray technology and RNA from microdissected pure epithelial cells to learn more about changes in gene expression and molecular pathways associated with the development of HELUs from TDLUs Keywords: Identification of early cancer precursors https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7377 Alterations of gene expression in the development of early hyperplastic precursors of breast cancer. The American journal of pathology 3.762 https://doi.org/10.2353/ajpath.2007.061010 {The American journal of pathology (3.762): 10.2353/ajpath.2007.061010} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA100411 https://www.ebi.ac.uk/ena/browser/view/PRJNA100411 None [Overal design]Samples for the microarray studies were derived from 8 formalin-fixed paraffin-embedded tissue (FFPET) biopsies containing paired normal TDLUs and well-developed HELUs from non-cancerous adult female human breasts obtained within the past 3 years. Populations of nearly pure (>95%) epithelial cells were isolated from the TDLUs and HELUs in each biopsy (approximately 25,000 cells/sample) by laser capture microdissection (LCM); [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA extracted using the Optimum Kit, which is based on proteinase K digestion followed by phase separation in a proprietary micro-filter cartridge and incubation with DNase to remove contaminating genomic DNA.'; [Cell type]'Source: ''' GSE121279 Mus musculus 29 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL17021 RNA-seq and ChIP-seq to study how transcription factor Foxp1 regulates Foxp3 binding to chromatin and coordinates regulatory T cell function 2018-10-15 Regulatory T (Treg) cells, whose differentiation and function are controlled by transcription factor Foxp3, express high amounts of a closely related family member Foxp1, which is also expressed in quiescent naive T cells. Here we explored Foxp1 function in Treg cells. We found that a large number of Foxp3-bound genomic sites in Treg cells were occupied by Foxp1 in both Treg and conventional T cells. In Treg cells, Foxp1 markedly increased Foxp3 binding to these sites, which were enriched for canonic forkhead and Ets binding motifs. Foxp1 deficiency in Treg cells resulted in their impaired function and competitive fitness associated with markedly reduced CD25 expression and interleukin-2 (IL-2) responsiveness, diminished CTLA-4 and increased SATB1 expression. The characteristic patterns of CD25, Foxp3, and CTLA-4 expression in Treg cells were rescued, at least in part, upon strong IL-2 signaling. Our studies suggest that in addition to the Foxp1-mediated regulation of quiescence that is common to Treg and conventional T cells, Foxp1 has an essential non-redundant function in Treg cells by enforcing Foxp3-mediated regulation of gene expression and enabling efficient IL-2 signaling in these cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE121279 Transcription factor Foxp1 regulates Foxp3 chromatin binding and coordinates regulatory T cell function. Nature immunology 23.530 https://doi.org/10.1038/s41590-018-0291-z {Nature immunology (23.530): 10.1038/s41590-018-0291-z} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA496510 https://www.ebi.ac.uk/ena/browser/view/PRJNA496510 https://www.ncbi.nlm.nih.gov/sra?term=SRP165789 [Overal design]Foxp1 ChIP-seq in Treg (triplicates) and conventional T cells (duplicates), with genetic controls; Foxp3 ChIP-seq in wildtype (duplicates) and Foxp1-deficient (triplicates) Treg cells, with genetic controls; RNA-seq in naïve and activated wildtype and Foxp1-deficient Treg cell (triplicates); [Treatment]'None'; [Growth]'Mice were bred and housed in the pathogen-free animal facility at Memorial Sloan-Kettering Cancer Center and were used in accordance with institutional guidelines. Mouse experiments were approved by the Institutional Animal Care and Use Committee of Memorial Sloan-Kettering Cancer Center. Unless otherwise noted, 8- to 10-week-old male and female sex-matched mice were used for all experiments. The Foxp1 conditional targeting construct was designed to use 2 site-specific recombinations in vivo: (1) Flp recombinase to delete the neo marker from the mouse germline, and (2) Cre recombinase to conditionally delete Foxp1 exon 11 flanked by 2 loxP sites. Foxp1f/+ mice (C57Bl/6/129 mixed background) were backcrossed with C57BL/6 mice for at least 5 generations. Genotypes of Foxp1fl/+, Foxp1fl/fl mice were determined by polymerase chain reaction (PCR) amplification. The wild-type allele was identified by the production of a 376–base pair PCR product and mutated Foxp1 allele was identified by the production of a 257–base pair PCR product (Supplementary Table 6). Foxp1fl/fl mice were crossed with Foxp3YFP-Cre transgenic mice to generate Foxp3YFP-Cre/+Foxp1fl/+ female mice. These mice were bred to Foxp3+Foxp1fl/+ male mice. Foxp3YFP-Cre/+Foxp1fl/fl and Foxp3YFP- Cre/+Foxp1+/+ female offspring and Foxp3YFP-CreFoxp1fl/fl and Foxp3YFP-CreFoxp1+/+ male offspring were used in experiments. In mammary tumor experiments, Foxp3YFP-Cre/YFP-CreFoxp1fl/fl mice were used as experimental mice and Foxp3YFP-Cre/+Foxp1fl/fl mice were used as control mice. Foxp1fl/fl mice were crossed with CD4Cre transgenic mice to generate CD4CreFoxp1fl/+ mice. These mice were crossed to generate CD4CreFoxp1fl/fl experimental and CD4CreFoxp1+/+ control mice. Tcrb/Tcrd−/− mice and C57Bl/6 Ly5.1 mice were purchased from Jackson Laboratories and bred in-house. No blinding was performed during the mouse experiments.'; [Extraction]'Single cell suspensions of cells were prepared from spleen and lymph nodes. For exclusion of dead cells, samples were first stained with Ghost Dye (Tonbo) cell viability reagent for 10 min in PBS on ice. Cells were then stained for 30 min on ice in FACS buffer (PBS, 2% FBS, 2 mM EDTA) with antibodies against cell surface proteins. For downstream in vitro assays, cells were sorted into fetal bovine serum (FBS). For intracellular staining, cells were washed and fixed with Fix/Perm buffer (BD Biosciences) for 20 min on ice or with Foxp3 staining buffer (eBioscience) for 45 min on ice, washed and stained with antibodies against intracellular proteins. Stained cells were either analyzed on a LSRII flow cytometer (BD) or sorted using a FACSAria II (BD). Flow cytometry data were analyzed with FlowJo software (TreeStar).\nRNA-seq: CD44hi or CD62Lhi YFP+ Foxp1+ or Foxp1- Treg cell populations were FACS- sorted from Foxp3YFP-Cre/+Foxp1+/+ and Foxp3YFP-Cre/+Foxp1fl/fl mice directly into Trizol-LS (ThermoFisher) and volume was adjusted post-sort. Samples were stored at −80°C prior to RNA extraction. Total RNA was extracted and assessed for nucleic acid quantity and quality on the Agilent BioAnalyzer. SMARTer amplification with 12-16 cycles of PCR was followed by Illumina TruSeq paired- end library preparation following manufacturer’s protocols. Samples were sequenced on the Illumina HiSeq 2500 to an average depth of 30 million 50-bp read pairs per sample. ChIP-seq: FACS-sorted cell populations (2x106 cells for Foxp3-ChIP-seq; 6x106 cells for Foxp1-ChIP-seq) were crosslinked in 1% paraformaldehyde I PBS for 10 minutes at RT. The reaction was quenched by addition of 125mM glycine. Crosslinked cells were lysed and digested nuclei were resuspended in nuclear lysis buffer containing 1% SDS. Cells were sonicated for three rounds of 10x30s with a Bioruptor (Diagenode) on high setting. Following sonication, chromatin was diluted with nuclear lysis buffer to final SDS concentration of 0.1% and pre- cleared for 1h at 4°C with rotation with protein A/G magnetic beads (Pierce). 5% of pre-cleared DNA was saved as input. Chromatin was incubated overnight at 4°C with rotation with polyclonal antibodies against Foxp3 (Rudensky lab) or Foxp1 (EMD Millipore ABE68). Immunocomplexes were incubated with protein A/G magnetic beads for 1h at 4°C with rotation. Immunocomplexes were precipitated and washed. After washing, precipitated chromatin and input DNA was decrosslinked overnight at 65°C in the presence of proteinase K and DNA fragments were isolated using Qiagen PCR-purification kit. Purified DNA was processed for sequencing on Illumina Hiseq 2500 to an average depth of 30 million 50-bp read pairs per sample.'; [Cell type]'Treg', 'Tconv''cell type: Treg; genotype: Foxp3YFP-Cre Foxp1+/+; activation status: pooled; ', 'cell type: Treg; genotype: Foxp3YFP-Cre Foxp1f/f; activation status: pooled; ', 'cell type: Tconv; genotype: Foxp3YFP-Cre Foxp1+/+; activation status: CD62Lhi; ', 'cell type: Tconv; genotype: Foxp3YFP-Cre Foxp1f/f; activation status: CD62Lhi; ', 'cell type: Treg; genotype: Foxp3YFP-Cre Foxp1+/+; activation status: CD62Lhi; ', 'cell type: Treg; genotype: Foxp3YFP-Cre Foxp1f/f; activation status: CD62Lhi; ', 'cell type: Treg; genotype: Foxp3YFP-Cre Foxp1+/+; activation status: CD44hi; ', 'cell type: Treg; genotype: Foxp3YFP-Cre Foxp1f/f; activation status: CD44hi; ' GSE24727 Mus musculus 8 Expression profiling by array GPL11062 The transcription factor ZNF217 is a prognostic biomarker and therapeutic target during breast cancer progression 2010-10-15 The transcription factor ZNF217 is a candidate oncogene in the amplicon on chromosome 20q13 that occurs in 20-30% of primary human breast cancers and that correlates with poor prognosis. We show Znf217 overexpression drives aberrant differentiation and signaling events, promotes increased self-renewal capacity, mesenchymal marker expression, motility and metastasis, and represses an adult tissue stem cell gene signature downregulated in cancers. By in silico screening, we identified candidate therapeutics that at low concentrations inhibit growth of cancer cells expressing high ZNF217. We demonstrate that the nucleoside analog triciribine inhibits ZNF217-induced tumor growth and chemotherapy resistance, and inhibits signaling events (e.g., P-AKT, P-MAPK) in vivo. Our data suggest ZNF217 is a biomarker of poor prognosis and a therapeutic target in breast cancer patients, and triciribine may be part of a personalized treatment strategy in patients overexpressing ZNF217. Since ZNF217 is amplified in numerous cancers, these results have implications for other cancers. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24727 The transcription factor ZNF217 is a prognostic biomarker and therapeutic target during breast cancer progression. Cancer discovery 26.370 https://doi.org/10.1158/2159-8290.CD-12-0093 {Cancer discovery (26.370): 10.1158/2159-8290.CD-12-0093} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA132345 https://www.ebi.ac.uk/ena/browser/view/PRJNA132345 None [Overal design]Total RNA was isolated from samples overexpressing ZNF217 (3 Primary and 5 SCp2). RNA was also harvested from each cell line expressing a vector control to use as a reference for each microarray sample analyzed. Total RNA was hybridized to mouse MEEBO arrays as described (http://www.microarray.org/sfgf/meebo.do). Samples were verified to have strong overexpression of ZNF217 by qRT-PCR or Western analysis.; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen RNeasy kit'; [Cell type]'primary mammary epithelial cells', 'Source: ''expression: vector control; cell type: primary mammary epithelial cells; ', 'expression: ZNF217 overexpression; cell type: primary mammary epithelial cells; ', 'expression: vector control; cell line: SCp2; ', 'expression: ZNF217 overexpression; cell line: SCp2; ' GSE27463 Homo sapiens 8 Expression profiling by high throughput sequencing GPL9052 Global Analysis of the Immediate Transcriptional Effects of Estrogen Signaling Reveals a Rapid, Extensive, and Transient Response 2011-02-23 We report the immediate effects of estrogen signaling on the transcriptome of breast cancer cells using Global Run-On and sequencing (GRO-seq). We found that estrogen signaling directly regulates a strikingly large fraction of the transcriptome in a rapid, robust, and unexpectedly transient manner. In addition to protein-coding genes, estrogen regulates the distribution and activity of all three RNA polymerases, and virtually every class of non-coding RNA that has been described to date. This data submission covers >95% of mapped reads comprising nearly all transcript classes described. Reads mapping to intergenic and enhancer transcripts were removed from this data submission and will be reported separately (manuscripts in preparation). Bed files are tab-separated text files in which columns represent: chrom, chromStart (5' End of the read), chromEnd (chromStart+1), name (unused always 'n'), score (the number of mismatches), and strand. Note that because of the inclusion of reads mapping to the rRNA chromosome, bed files cannot be uploaded to the UCSC genome browser directly. Instead, use the wiggle files (coming soon!) for this purpose. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE27463 A rapid, extensive, and transient transcriptional response to estrogen signaling in breast cancer cells. Cell 36.216 https://doi.org/10.1016/j.cell.2011.03.042 {Cell (36.216): 10.1016/j.cell.2011.03.042} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA138459 https://www.ebi.ac.uk/ena/browser/view/PRJNA138459 https://www.ncbi.nlm.nih.gov/sra?term=SRP013239 [Overal design]Using GRO-seq over a time course (0, 10, 40, 160 min) of estrogen signaling in ER-alpha positive MCF-7 human breast cancer cells.; [Treatment]'MCF-7 cells were plated at a density of 1 x 106 cells per 15 cm diameter dish in phenol-red free MEM + 5% CDCS, using one dish per experimental condition. After three days, the cells were treated with 100 nM E2 as indicated and washed three times with ice cold PBS.'; [Growth]'MCF-7 human breast adenocarcinoma cells were kindly provided by Dr. Benita Katzenellenbogen (University of Illinois, Urbana-Champaign). The cells were maintained in minimal essential medium (MEM) with Hank’s salts (Sigma) supplemented with 5% calf serum (CS), sodium bicarbonate, penicillin/streptomycin and gentamicin. Cells were plated for experiments in phenol red-free MEM (Sigma) supplemented with 5% charcoal-dextran treated calf serum (CDCS) prior to 17-b estradiol (E2) treatment.'; [Extraction]'Nuclear run-on reactions were performed for 5 minutes at 30°C in the presence of NTPs and 0.5% Sarkosyl in run-on buffer to allow a run-on of ~100 nucleotides. The reaction was stopped by incubation with DNase I, followed by incubation with proteinase K. Newly synthesized nascent RNAs were isolated by acid phenol-chloroform extraction, followed by ethanol precipitation. After re-dissolving, the isolated RNAs were base-hydrolyzed with 0.2 N NaOH and the reaction was neutralized by the addition of 500 mM Tris×HCl, pH 6.8. The base-hydrolyzed RNAs were subjected to BioRad P-30 chromatography for buffer exchange. The isolated and base hydrolyzed RNAs were subjected to three bead binding steps where the bromo-UTP incorporated nascent RNAs (BrU-RNAs) were enriched using anti-bromo-deoxy-U antibody conjugated beads. After each binding step, the BrU-RNAs were eluted, acid phenol-chloroform extracted, and precipitated. Each of the three bead binding steps also contained additional manipulations. After the first binding step, the BrU-RNAs were treated with tobacco acid pyrophosphatase to remove 5’-methyl guanosine caps, then with T4 polynucelotide kiase to remove 3’-phosphate group at low pH. The BrU-RNAs were treated with T4 PNK again at high pH in the presence of ATP to add 5’-phosphate group. 5’-adaptors were added to the end-repaired BrU-RNAs by T4 RNA ligase. After the addition of the 5’-adaptors, the BrU-RNAs were subjected to the second bead binding step to remove excessive adaptors and further enrich the BrU-RNAs. After the second bead binding step, 3’ adaptors were ligated by T4 RNA ligase, followed by the third bead binding. The affinity purified 5’- and 3’-adaptor-ligated BrU-RNAs were reverse transcribed into cDNAs usining annealed RT-oligo and Super Scripts III reverse transcriptase. The RNAs were then degraded by incubation with RNase cocktail. The cDNAs were then subjected to PCR-amplification using Phusion DNA Polymerase with small RNA PCR primers. Samples of the amplified cDNAs were analyzed on a 2% agarose gel to assess yield and size. The remaining samples were extracted by phenol:chloroform:isoamyl alcohol (25:24:1). The purified cDNAs were run on a 6% native PAGE gel for further purification. The gel was stained with SYBRE gold and the cDNAs were visualized using a Dark Reader transilluminator. The bands between size 100 bp to 250 bp were cut out and the cDNAs were eluted from the gel by incubating overnight in elution buffer. The eluted cDNA were extracted again with phenol-chloroform, resuspended in water, and quantified using a Nanodrop. The final libraries were then sequenced using an Illumina Genome Analyzer.'; [Cell type]'Source: ''cell line: MCF7; ', 'cell line: MCF7; treatment time: 10; ', 'cell line: MCF7; treatment time: 40; ', 'cell line: MCF7; treatment time: 160; ' GSE73527 Homo sapiens 12 Expression profiling by high throughput sequencing GPL11154 Modulation of Indoleamine 2, 3-dioxygenase 1 Expression by Activated Human T cells in Breast Cancer Cells is Controlled by DNA Promoter Methylation 2015-09-28 Tumor infiltrating lymphocytes (TILs) play a critical role in modulating the immunoediting features in certain malignancies like triple negative breast cancer (TNBC). Nevertheless, much is still unknown concerning the specific responses of tumors when challenged by lymphocyte infiltration. Based on this void, we conducted a immuno-phenotype comparison using mRNA sequencing between the TNBC cell line MDA-MB-231 and the luminal breast cancer cell line MCF7 after both were co-cultured with activated human T-cells. We found that, though the cytokine-induced immune signature of the two cell lines was similar, MDA-MD-231 cells were able to transcribe IDO1 at a significantly higher level than MCF7 cells. Though no differences occurred in upstream JAK/STAT1 signaling or IDO1 mRNA stability between the two cell lines, stimulation with IFNγ was able to differentially induce IDO protein expression and enzymatic activity in ER- cell lines compared to ER+ cell lines. Further experiments show that 5-aza-deoxycytidine treatment was able to reverse suppression of IDO1 expression in MCF7 cells, suggesting DNA methylation as a potential determinant in IDO1 induction. By analyzing TCGA breast cancer datasets, we discovered subtype-specific mRNA and promoter methylation differences in IDO1, with TNBC/basal subtypes exhibiting lower methylation/higher expression and ER+/luminal subtypes exhibiting higher methylation/lower expression. We confirmed this trend of IDO1 methylation by bisulfite pyrosequencing breast cancer cell lines and an independent cohort of primary breast tumors. Taken together, these findings suggest that IDO1 methylation regulates anti-immune responses in breast cancer subtypes and could be used as a predictive biomarker for IDO inhibitor-based immunotherapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE73527 Promoter Methylation Modulates Indoleamine 2,3-Dioxygenase 1 Induction by Activated T Cells in Human Breast Cancers. Cancer immunology research 8.619 https://doi.org/10.1158/2326-6066.CIR-16-0182 {Cancer immunology research (8.619): 10.1158/2326-6066.CIR-16-0182} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA297215 https://www.ebi.ac.uk/ena/browser/view/PRJNA297215 https://www.ncbi.nlm.nih.gov/sra?term=SRP064258 [Overal design]To determine the immunomodulatory effects of cytokines secreted by activated human T-cells on breast cancer cells, we performed RNAseq analysis in MCF7 and MDA-MB-231 cells, after co-culturing them with normal PBMCs activated with anti-CD3/CD28 antibodies in a contact-independent manner. MDA-MB-231 or MCF7 cells were co-cultured with PBMCs alone or the conditioned-media or a combination of both for 24 hrs, and then total RNA was harvest for RNA-seq analysis.; [Treatment]'No treatment invovled.'; [Growth]'Blood samples from healthy donors were purchased from a local blood bank. Peripheral blood mononuclear cells (PBMCs) were isolated using Ficoll-Paque (GE Healthcare) density gradient separation. To activate T cells, a total of 3 million PBMCs were treated with immobilized anti-CD3 and soluble anti-CD28 antibodies (eBioscience) in 1ml of RPMI-1640 media supplemented with 10% FBS. After 48 hrs, PBMCs and the conditioned-media were harvested. PBMCs were transferred into 0.4µm Transwell Insert (Corning) and placed into 6-well plates with pre-seeded MDA-MB-231 and MCF7 cells, respectively. MDA-MB-231 or MCF7 cells were co-cultured with PBMCs alone or the conditioned-media or a combination of both for 24 hrs, and then harvested for further analysis. Control experiments were performed in the same manner except that isotype control antibodies were used.'; [Extraction]'RNA was extracted using Qiagen Qiazal reagents\nLibraries for stranded mRNA sequencing were prepared using KAPA Stranded mRNAseq Kit Illumina platform (Kapa Biosystems) following manufacturer’s instructions.'; [Cell type]'Source: ''cell line: MCF7; cell types: Breast Cancer Cell line, ER(+); tumorgenecity: Tumor; treatment: Isotype SP; ', 'cell line: MCF7; cell types: Breast Cancer Cell line, ER(+); tumorgenecity: Tumor; treatment: Isotype PBMC; ', 'cell line: MCF7; cell types: Breast Cancer Cell line, ER(+); tumorgenecity: Tumor; treatment: Isotype PBMC+SP; ', 'cell line: MCF7; cell types: Breast Cancer Cell line, ER(+); tumorgenecity: Tumor; treatment: CD3-CD28 SP; ', 'cell line: MCF7; cell types: Breast Cancer Cell line, ER(+); tumorgenecity: Tumor; treatment: CD3-CD28 PBMC; ', 'cell line: MCF7; cell types: Breast Cancer Cell line, ER(+); tumorgenecity: Tumor; treatment: CD3-CD28 PBMC+SP; ', 'cell line: MDA-MB-231; cell types: Breast Cancer Cell line, ER(-); tumorgenecity: Tumor; treatment: Isotype SP; ', 'cell line: MDA-MB-231; cell types: Breast Cancer Cell line, ER(-); tumorgenecity: Tumor; treatment: Isotype PBMC; ', 'cell line: MDA-MB-231; cell types: Breast Cancer Cell line, ER(-); tumorgenecity: Tumor; treatment: Isotype PBMC+SP; ', 'cell line: MDA-MB-231; cell types: Breast Cancer Cell line, ER(-); tumorgenecity: Tumor; treatment: CD3-CD28 SP; ', 'cell line: MDA-MB-231; cell types: Breast Cancer Cell line, ER(-); tumorgenecity: Tumor; treatment: CD3-CD28 PBMC; ', 'cell line: MDA-MB-231; cell types: Breast Cancer Cell line, ER(-); tumorgenecity: Tumor; treatment: CD3-CD28 PBMC+SP; ' GSE17768 Homo sapiens 10 Expression profiling by array; Third-party reanalysis GPL570 An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: gene expression 2009-08-23 10 Breast cancer cell lines profiled on the Affymetrix U133 Plus 2.0 platform used in conjunction with matched DNA copy number and DNA methylation data for integrative analysis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17768 An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer. BMC systems biology 2.048 https://doi.org/10.1186/1752-0509-4-67 {BMC systems biology (2.048): 10.1186/1752-0509-4-67} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA129037 https://www.ebi.ac.uk/ena/browser/view/PRJNA129037 None [Overal design]In total, 10 samples were used. The MCF10A profile used as normal was obtained from GSM254525 and the remaining 2 cell lines were obtained from caBIG. Full RMA normalized expression profile is attached.; [Treatment]'None'; [Growth]'None', 'Normal growth media for MCF10As is DMEM:F12 (Cellgro) w/ 2mM glutamine, containing 5% horse serum, insulin (10 µg ml-1) (Gibco), hydrocortisone (0.5 µg ml-1) (Sigma), EGF (20 ng ml-1) (Upstate) and 1 I.U. ml-1 penicillin, 0.1 µg ml-1 streptomysin, 0.25 µg ml-1 amphotericin B (Cellgro).'; [Extraction]'Qiagen Mini prep', 'Total RNA from cells grown in monolayer and Transwell® cultures were extracted using Tri reagent (MRC, Cincinnati, OH) and cleaned using DNaseI (Promega, Madison, WI) followed by standard phenol/chloroform precipitation and extraction method.', 'standard Affymetrix protocol'; [Cell type]'Source: ''cell line: HCC38; catalog number: ATCC# CRL-2314; ', 'cell line: HCC1008; catalog number: ATCC# CRL-2320; ', 'cell line: HCC1143; catalog number: ATCC# CRL-2321; ', 'cell line: HCC1395; catalog number: ATCC# CRL-2324; ', 'cell line: HCC1599; catalog number: ATCC# CRL-2331; ', 'cell line: HCC1937; catalog number: ATCC# CRL-2336; ', 'cell line: HCC2218; catalog number: ATCC# CRL-2343; ', 'cell line: MCF10A; catalog number: ATCC# CRL-10317; ', 'cell line: BT474; catalog number: ATCC# HTB-20; ', 'cell line: MCF7; catalog number: ATCC# HTB-22; ' GSE51336 Mus musculus; Homo sapiens 266 Genome binding/occupancy profiling by high throughput sequencing GPL9052; GPL9115; GPL9185; GPL10999; GPL11154 Mouse regulatory DNA landscapes reveal global principles of cis-regulatory evolution 2013-10-02 To study the evolutionary dynamics of regulatory DNA, we mapped >1.3 million deoxyribonuclease I–hypersensitive sites (DHSs) in 45 mouse cell and tissue types, and systematically compared these with human DHS maps from orthologous compartments. We found that the mouse and human genomes have undergone extensive cis-regulatory rewiring that combines branch-specific evolutionary innovation and loss with widespread repurposing of conserved DHSs to alternative cell fates, and that this process is mediated by turnover of transcription factor (TF) recognition elements. Despite pervasive evolutionary remodeling of the location and content of individual cis-regulatory regions, within orthologous mouse and human cell types the global fraction of regulatory DNA bases encoding recognition sites for each TF has been strictly conserved. Our findings provide new insights into the evolutionary forces shaping mammalian regulatory DNA landscapes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE51336 Mouse regulatory DNA landscapes reveal global principles of cis-regulatory evolution. Science (New York, N.Y.) 41.037 https://doi.org/10.1126/science.1246426 {Science (New York, N.Y.) (41.037): 10.1126/science.1246426} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA267839 https://www.ebi.ac.uk/ena/browser/view/PRJNA267839 None [Overal design]To study the evolutionary dynamics of regulatory DNA, we mapped >1.3 million deoxyribonuclease I–hypersensitive sites (DHSs) in 45 mouse cell and tissue types, and systematically compared these with human DHS maps from orthologous compartments.; [Treatment]'None'; [Growth]'None', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HCFaa_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:WERI-Rb-1_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/GM12878_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:NHDF-neo_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HRGEC_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:Stam_15_protocols.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/HudsonAlpha:Jurkat_protocol.pdf UW_Stam:Jurkat_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HMVEC-LLy_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/HudsonAlpha:BE2-C_Myers_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HBMEC_Myers_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:GM12865_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:MonoCD14_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:AG04450_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HCM_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/HudsonAlpha:PANC-1_Myers_protocol.pdf UW_Stam:PANC-1_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:BJ-tert_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/HudsonAlpha:SK-N-MC_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HFFMyc_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:GM12864_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HRE_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/Broad_Histone:HSMMtube_Bernstein_protocol.pdf Duke/UNC/UTA/EBI_Open_Chromatin:HSMM_HSMMtube_Crawford_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:AG09319_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HVMF_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HA-sp_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HMVEC-Lbl_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:RPTEC_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/Broad:NH-A_Bernstein_protocol.pdf UW_Stam: NH-A_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/Keratinocyte_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HConF_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HRCEpiC_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:AG09309_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HPAF_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/Broad_Histone:HSMM_Bernstein_protocol.pdf Duke/UNC/UTA/EBI_Open_Chromatin:HSMM_HSMMtube_Crawford_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:AG04449_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/HeLa-S3:HeLa-S3_protocol.pdf HeLa-S3_IFN_Crawford:HeLa-S3_IFN_Crawford_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/Duke/UNC/UTA/EBI_Open_Chromatin:LNCaP_Crawford_protocol.pdf Yale_TFBS(Farnham):LNCaP_protocol.pdf UW_Stam:LNCaP_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:NHDF-Ad_Stam_protocol.pdf Broad_Histone:NHDF-Ad_Bernstein_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HCF_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HCPEpiC_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HMVEC-dBl-Neo_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HPF_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/HUVEC_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HMVEC-dLy-Neo_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HGF_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/HudsonAlpha:A549_protocol.pdf Duke/UNC/UTA/EBI_Open_Chromatin:A549_Crawford_protocol.pdf UW_Stam:A549_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/Duke/UNC/UTA/EBI_Open_Chromatin:MCF-7_Crawford_protocol.pdf Yale_TFBS(Farnham):MCF-7_Farnham_protocol.pdf UW_Stam:Stam_15_protocols.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/H1_ES_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:AoAF_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HEEpiC_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HAc_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HIPEpiC_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:SkMC_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HAh_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:AG10803_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HMVEC-dLy-Ad_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/Yale_TFBS:HCT-116_protocol.pdf UW_Stam:HCT116_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HFF_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/Yale_TFBS:NB4_protocol.pdf UW_Stam:NB4_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:CMK_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:SAEC_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HMVEC-dBl-Ad_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HMVEC-dNeo_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/Broad_Histone:NHLF_Bernstein_protocol.pdf UW_Stam:NHLF_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:WI38_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HNPCEpiC_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HL-60_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HMF_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/K562_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HRPEpiC_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HAEpiC_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:HPdLF_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/Broad_Histone:HMEC_Bernstein_protocol.pdf Duke/UNC/UTA/EBI_Open_Chromatin:HMEC_Crawford_protocol.pdf UW_Stam:HMEC_Stam_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/HepG2_protocol.pdf', 'Cells were grown according to ENCODE cell culture protocols: http://genome.ucsc.edu/ENCODE/protocols/cells/human/UW_Stam:H7-hESC_Stam_protocol.pdf', 'TReg_Stam_protocol.pdf', 'THelper-Activated_Stam_protocol.pdf', 'Tissue_Stam_protocol.pdf', 'ES-E14_Stam_protocol.pdf', 'ES-WW6_Stam_protocol.pdf', '416B_Stam_protocol.pdf', 'A20_Stam_protocol.pdf', 'ZhBTc4_Stam_protocol.pdf', 'bCellCd43_Stam_protocol.pdf', 'Patski_Stam_protocol.pdf', 'HeadlessEmbryo_Stam_protocol.pdf', 'GenitalFatPad_Stam_protocol.pdf', 'ForelimbBuds_Stam_protocol.pdf', 'Retina_Stam_protocol.pdf', 'NIH-3T3_Stam_protocol.pdf', 'Mesoderm_Stam_protocol.pdf', 'HindlimbBuds_Stam_protocol.pdf', 'Spleen_Stam_protocol.pdf', 'Thymus_Stam_protocol.pdf', 'LargeIntestine_Stam_protocol.pdf', 'ES-CJ7_Stam_protocol.pdf', 'SkeletalMuscle_Stam_protocol.pdf', 'bCellCd19_Stam_protocol.pdf', 'MEL_Stam_protocol.pdf', '3134_Stam_protocol.pdf', 'Fibroblast_Stam_protocol.pdf', 'TReg-Activated_Stam_protocol.pdf', 'AdultCD4naiveTcell_Crawford.v2_PlusStam.v1_SOP.pdf', 'PrEC_Stam_protocol.pdf', 'HMVECdAd_Stam_protocol.pdf', 'HBVP_Stam_protocol.pdf', 'NT2-D1_protocol.pdf', 'HPAEC_Stam_protocol.pdf', 'CD20+_Stam_protocol.pdf', 'HBVSMC_Stam_protocol.pdf', 'CD34+Mobilized_Stam_protocol.pdf', 'M059J_Stam_protocol.pdf', 'GM04504A_Stam_protocol.pdf', 'GM04503D_Stam_protocol.pdf', 'RPMI7951_Stam_protocol.pdf'; [Extraction]'Library construction protocol: Single read - Illumina', 'For extraction protocol details see: http://genome.ucsc.edu/cgi-bin/hgTrackUi?db=hg19&g=wgEncodeUwDnase', 'Instrument model unknown. ("Illumina Genome Analyzer" specified by default). For more information, see http://genome.ucsc.edu/cgi-bin/hgTrackUi?db=mm9&g=wgEncodeUwDnase', 'Instrument model unknown. ("Illumina Genome Analyzer" specified by default). For more information, see http://genome.ucsc.edu/cgi-bin/hgTrackUi?db=hg19&g=wgEncodeUwDnase'; [Cell type]'Source: ''molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal brain; tissue_depot: UW; collection_method: fetal; donor_id: H-22510; donor_age: 122 days; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal adrenal; tissue_depot: UW; collection_method: fetal; donor_id: H-22662; donor_age: 96 days; donor_health_status: NA; donor_sex: Unknown; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal heart; tissue_depot: UW; collection_method: fetal; donor_id: H-22662; donor_age: 96 days; donor_health_status: NA; donor_sex: Unknown; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal kidney; tissue_depot: UW; collection_method: fetal; donor_id: H-22676; donor_age: 122 days; donor_health_status: NA; donor_sex: Unknown; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal lung; tissue_depot: UW; collection_method: fetal; donor_id: H-22676; donor_age: 122 days; donor_health_status: NA; donor_sex: Unknown; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: FHCRC HEIMFELD; biomaterial_type: Primary Cell; cell_type: CD34 Primary Cells; markers: CD34+; donor_id: RO 01549; donor_age: 33 years; donor_health_status: NA; donor_sex: Female; donor_ethnicity: Caucasian; passage_if_expanded: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal heart; tissue_depot: UW; collection_method: fetal; donor_id: H-22727; donor_age: 101 days; donor_health_status: NA; donor_sex: Unknown; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal lung; tissue_depot: UW; collection_method: fetal; donor_id: H-22727; donor_age: 101 days; donor_health_status: NA; donor_sex: Unknown; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal lung; tissue_depot: UW; collection_method: fetal; donor_id: H-23090; donor_age: day 103; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal brain; tissue_depot: UW; collection_method: fetal; donor_id: H-22911; donor_age: day 117; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal lung; tissue_depot: UW; collection_method: fetal; donor_id: H-23247; donor_age: day 67; donor_health_status: NA; donor_sex: Unknown; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal brain; tissue_depot: UW; collection_method: fetal; donor_id: H-23266; donor_age: day 85; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal lung; tissue_depot: UW; collection_method: fetal; donor_id: H-23266; donor_age: day 85; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal lung; tissue_depot: UW; collection_method: fetal; donor_id: H-23284; donor_age: day 96; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: fetal brain; tissue_depot: UW; collection_method: fetal; donor_id: H-23284; donor_age: day 96; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol; ', 'sample alias: fAdrenal.H-23327d85; sample common name: Fetal Adrenal Gland; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Adrenal Gland; tissue_depot: UW; collection_method: fetal; donor_id: H-23327; donor_age: day 85; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fBrain.H-23399d112; sample common name: Fetal Brain; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Brain; tissue_depot: UW; collection_method: fetal; donor_id: H-23399; donor_age: day 112; donor_health_status: NA; donor_sex: Unknown; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fLung.H-23399d112; sample common name: Fetal Lung; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Lung; tissue_depot: UW; collection_method: fetal; donor_id: H-23399; donor_age: day 112; donor_health_status: NA; donor_sex: Unknown; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fLung.H-23419d82; sample common name: Fetal Lung; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Lung; tissue_depot: UW; collection_method: fetal; donor_id: H-23419; donor_age: day 82; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fLung_Right.H-23435d117; sample common name: Fetal Lung, Right; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Lung, Right; tissue_depot: UW; collection_method: fetal; donor_id: H-23435; donor_age: day 117; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fHeart.H-23435d117; sample common name: Fetal Heart; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Heart; tissue_depot: UW; collection_method: fetal; donor_id: H-23435; donor_age: day 117; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fKidney_Right.H-23435d117; sample common name: Fetal Kidney, Right; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Kidney, Right; tissue_depot: UW; collection_method: fetal; donor_id: H-23435; donor_age: day 117; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fHeart.H-23500d103; sample common name: Fetal Heart; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Heart; tissue_depot: UW; collection_method: fetal; donor_id: H-23500; donor_age: day 103; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Large.H-23500d103; sample common name: Fetal Intestine, Large; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Large; tissue_depot: UW; collection_method: fetal; donor_id: H-23500; donor_age: day 103; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Large.H-23524d105; sample common name: Fetal Intestine, Large; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Large; tissue_depot: UW; collection_method: fetal; donor_id: H-23524; donor_age: day 105; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fBrain.H-23548d142; sample common name: Fetal Brain; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Brain; tissue_depot: UW; collection_method: fetal; donor_id: H-23548; donor_age: day 142; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fKidney_Left.H-23589d147; sample common name: Fetal Kidney, Left; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Kidney, Left; tissue_depot: UW; collection_method: fetal; donor_id: H-23589; donor_age: day 147; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fThymus.H-23589d147; sample common name: Fetal Thymus; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Thymus; tissue_depot: UW; collection_method: fetal; donor_id: H-23589; donor_age: day 147; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fHeart.H-23589d147; sample common name: Fetal Heart; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Heart; tissue_depot: UW; collection_method: fetal; donor_id: H-23589; donor_age: day 147; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Small.H-23604d110; sample common name: Fetal Intestine, Small; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Small; tissue_depot: UW; collection_method: fetal; donor_id: H-23604; donor_age: day 110; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Large.H-23604d110; sample common name: Fetal Intestine, Large; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Large; tissue_depot: UW; collection_method: fetal; donor_id: H-23604; donor_age: day 110; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fLung_Left.H-23604d110; sample common name: Fetal Lung, Left; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Lung, Left; tissue_depot: UW; collection_method: fetal; donor_id: H-23604; donor_age: day 110; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fKidney_Left.H-23604d110; sample common name: Fetal Kidney, Left; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Kidney, Left; tissue_depot: UW; collection_method: fetal; donor_id: H-23604; donor_age: day 110; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fHeart.H-23604d110; sample common name: Fetal Heart; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Heart; tissue_depot: UW; collection_method: fetal; donor_id: H-23604; donor_age: day 110; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fKidney_Left.H-23640d115; sample common name: Fetal Kidney, Left; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Kidney, Left; tissue_depot: UW; collection_method: fetal; donor_id: H-23640; donor_age: day 115; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Small.H-23663d105; sample common name: Fetal Intestine, Small; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Small; tissue_depot: UW; collection_method: fetal; donor_id: H-23663; donor_age: day 105; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Small.H-23640d115; sample common name: Fetal Intestine, Small; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Small; tissue_depot: UW; collection_method: fetal; donor_id: H-23640; donor_age: day 115; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Large.H-23758d107; sample common name: Fetal Intestine, Large; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Large; tissue_depot: UW; collection_method: fetal; donor_id: H-23758; donor_age: day 107; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: CD19.RO_01727; sample common name: CD19 Primary Cells; molecule: genomic DNA; disease: None; biomaterial_provider: FHCRC HEIMFELD; biomaterial_type: Primary Cell; cell_type: CD19 Primary Cells; markers: CD19+; donor_id: RO 01689; donor_age: year 34; donor_health_status: NA; donor_sex: Female; donor_ethnicity: Caucasian; passage_if_expanded: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Large.H-23769d108; sample common name: Fetal Intestine, Large; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Large; tissue_depot: UW; collection_method: fetal; donor_id: H-23769; donor_age: day 108; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Small.H-23769d108; sample common name: Fetal Intestine, Small; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Small; tissue_depot: UW; collection_method: fetal; donor_id: H-23769; donor_age: day 108; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fKidney_renal_cortex.H-23790d108; sample common name: Fetal Renal Cortex; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Renal Cortex; tissue_depot: UW; collection_method: fetal; donor_id: H-23790; donor_age: day 108; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fMuscle_Arm.H-23808d115; sample common name: Fetal Muscle, Arm; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Arm; tissue_depot: UW; collection_method: fetal; donor_id: H-23808; donor_age: day 115; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fSpleen.H-23399d112; sample common name: Fetal Spleen; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Spleen; tissue_depot: UW; collection_method: fetal; donor_id: H-23399; donor_age: day 112; donor_health_status: NA; donor_sex: Unknown; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fKidney_renal_cortex.H-23833d113; sample common name: Fetal Renal Cortex; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Renal Cortex; tissue_depot: UW; collection_method: fetal; donor_id: H-23833; donor_age: day 113; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fLung_Left.H-23833d113; sample common name: Fetal Lung, Left; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Lung, Left; tissue_depot: UW; collection_method: fetal; donor_id: H-23833; donor_age: day 113; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fLung_Left.H-23887d108; sample common name: Fetal Lung, Left; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Lung, Left; tissue_depot: UW; collection_method: fetal; donor_id: H-23887; donor_age: day 108; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fStomach.H-23914d91; sample common name: Fetal Stomach; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Stomach; tissue_depot: UW; collection_method: fetal; donor_id: H-23914; donor_age: day 91; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Large.H-23941d120; sample common name: Fetal Intestine, Large; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Large; tissue_depot: UW; collection_method: fetal; donor_id: H-23941; donor_age: day 120; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fKidney_renal_cortex.H-23941d120; sample common name: Fetal Renal Cortex; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Renal Cortex; tissue_depot: UW; collection_method: fetal; donor_id: H-23941; donor_age: day 120; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fMuscle_Trunk.H-23941d120; sample common name: Fetal Muscle, Trunk; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Trunk; tissue_depot: UW; collection_method: fetal; donor_id: H-23941; donor_age: day 120; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fMuscle_Back.H-23964d98; sample common name: Fetal Muscle, Back; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Back; tissue_depot: UW; collection_method: fetal; donor_id: H-23964; donor_age: day 98; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fStomach.H-23964d98; sample common name: Fetal Stomach; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Stomach; tissue_depot: UW; collection_method: fetal; donor_id: H-23964; donor_age: day 98; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: CD4.RO_01736; sample common name: CD4 Primary Cells; molecule: genomic DNA; disease: None; biomaterial_provider: FHCRC HEIMFELD; biomaterial_type: Primary Cell; cell_type: CD4 Primary Cells; markers: CD4+; donor_id: RO 01701; donor_age: year 37; donor_health_status: NA; donor_sex: Male; donor_ethnicity: Hispanic; passage_if_expanded: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'cell: HCFaa; cell organism: Human; cell description: Human Cardiac Fibroblasts-Adult Atrial; cell sex: F; replicate: 1; ', 'cell: WERI-Rb-1; cell organism: Human; cell description: retinoblastoma (PMID: 844036); cell sex: F; replicate: 1; ', 'cell: GM12878; cell organism: Human; cell description: lymphoblastoid; cell karyotype: relatively normal; cell lineage: International HapMap Project - CEPH/Utah - European Caucasion; Epstein-Barr Virus; cell sex: F; replicate: 1; ', 'cell: NHDF-neo; cell organism: Human; cell description: Neonatal Human Dermal Fibroblasts; cell lineage: mesoderm; cell sex: U; replicate: 1; ', 'cell: HRGEC; cell organism: human; cell description: Human Renal Glomerular Endothelial Cells; cell karyotype: Normal; cell lineage: Endothelial; cell sex: U; replicate: 1; ', 'cell: Caco-2; cell organism: Human; cell description: colorectal adenocarcinoma. (PMID: 1939345); cell karyotype: cancer; cell sex: M; replicate: 1; ', 'cell: Jurkat; cell organism: Human; cell description: T lymphoblastoid derived from an acute T cell leukemia, "The Jurkat cell line was established from the peripheral blood of a 14 year old boy by Schneider et al., and was originally designated JM." - ATCC. (PMID: 68013); cell karyotype: cancer; cell lineage: mesoderm; cell sex: M; replicate: 1; ', 'cell: HMVEC-LLy; cell organism: Human; cell description: Normal Human Lymphatic Microvascular Endothelial Cells, Lung-Derived; cell sex: F; replicate: 1; ', 'cell: BE2_C; cell organism: Human; cell description: Human neuroblastoma; cell lineage: ectoderm; cell sex: M; replicate: 1; ', 'cell: HBMEC; cell organism: Human; cell description: Human Brain Microvascular Endothelial Cells; cell sex: U; replicate: 1; ', 'cell: GM12865; cell organism: Human; cell description: B-Lymphocyte, Lymphoblastoid, International HapMap Project, CEPH/Utah pedigree 1459, Treatment: Epstein-Barr Virus transformed; cell karyotype: unknown; cell lineage: mesoderm; cell sex: F; replicate: 1; ', 'cell: Monocytes-CD14+; cell organism: human; cell description: Monocytes-CD14+ are CD14-positive cells from human leukapheresis product; cell karyotype: Normal; cell lineage: Monocytic; cell sex: F; replicate: 1; ', 'cell: AG04450; cell organism: Human; cell description: Fetal lung fibroblast; cell lineage: mesoderm; cell sex: M; replicate: 1; ', 'cell: HCM; cell organism: Human; cell description: Human Cardiac Myocytes; cell lineage: mesoderm; cell sex: U; replicate: 1; ', 'cell: PANC-1; cell organism: Human; cell description: pancreatic carcinoma. (PMID: 1140870); cell karyotype: cancer; cell sex: M; replicate: 1; ', 'cell: BJ; cell organism: Human; cell description: Skin fibroblast "The line was established from skin taken from normal foreskin." - ATCC. (PMID: 9916803); cell karyotype: normal; cell lineage: mesoderm; cell sex: M; replicate: 1; ', 'cell: SK-N-MC; cell organism: Human; cell description: neuroepithelioma cell line derived from a metastatic supra-orbital human brain tumor, "SK-N-MC was isolated in September of l971 and was found to have moderate dopamine - beta - hydroxylase activity as well as formaldehyde induced fluorescence indicative of intracellular catecholamines." - ATCC. (Biedler, et al. Morphology and Growth, Tumorigenicity, and Cytogenetics of Human Neuroblastoma Cells in Continuous Culture. Cancer Research 33, 2643-2652, November 1973.); cell karyotype: cancer; cell lineage: ectoderm; cell sex: F; replicate: 1; ', 'cell: HFF-Myc; cell organism: human; cell description: Human Foreskin Fibroblast Cells Expressing Canine cMyc; cell karyotype: Normal (cMyc); cell lineage: Fibroblast; cell sex: M; replicate: 1; ', 'cell: GM12864; cell organism: Human; cell description: B-Lymphocyte, Lymphoblastoid, International HapMap Project, CEPH/Utah pedigree 1459, Treatment: Epstein-Barr Virus transformed; cell karyotype: unknown; cell lineage: mesoderm; cell sex: M; replicate: 1; ', 'cell: HRE; cell organism: Human; cell description: Human Renal Epithelial cells (normal); cell karyotype: normal; cell lineage: mesoderm; cell sex: U; replicate: 1; ', 'cell: HSMMtube; cell organism: Human; cell description: Normal Human Skeletal Muscle Myotubes; cell karyotype: normal; cell lineage: mesoderm; cell sex: U; replicate: 1; ', 'cell: AG09319; cell organism: Human; cell description: Adult human gum tissue fibroblasts; cell lineage: mesoderm; cell sex: F; replicate: 1; ', 'cell: HVMF; cell organism: Human; cell description: Human Villous Mesenchymal Fibroblast Cells; cell sex: U; replicate: 1; ', 'cell: HA-sp; cell organism: human; cell description: Human astrocytes spinal cord; cell karyotype: Normal; cell lineage: Astrocytic; cell sex: U; replicate: 1; ', 'cell: HMVEC-LBl; cell organism: Human; cell description: Normal Human Blood Microvascular Endothelial Cells, Lung-Derived; cell sex: F; replicate: 1; ', 'cell: RPTEC; cell organism: Human; cell description: Renal Proximal Tubule Epithelial Cells; cell sex: U; replicate: 1; ', 'cell: NH-A; cell organism: Human; cell description: normal human astrocytes; cell sex: U; replicate: 1; ', 'cell: NHEK; cell organism: Human; cell description: Normal Human Epidermal Keratinocytes; cell karyotype: normal; cell lineage: ectoderm; cell sex: F; replicate: 1; ', 'cell: HConF; cell organism: Human; cell description: Human Conjunctival Fibroblast; cell sex: U; replicate: 1; ', 'cell: HRCEpiC; cell organism: Human; cell description: Human Renal Cortical Epithelial cells (normal); cell karyotype: normal; cell lineage: mesoderm; cell sex: U; replicate: 1; ', 'cell: AG09309; cell organism: Human; cell description: Adult human toe fibroblast; cell lineage: mesoderm; cell sex: F; replicate: 1; ', 'cell: HPAF; cell organism: Human; cell description: Human Pulmonary Artery Fibroblasts; cell sex: U; replicate: 1; ', 'cell: GM06990; cell organism: Human; cell description: Lymphoblastoid, International HapMap Project, CEPH/Utah, Treatment: Epstein-Barr Virus transformed; cell karyotype: normal; cell lineage: mesoderm; cell sex: F; replicate: 1; ', 'cell: SK-N-SH_RA; cell organism: Human; cell description: neuroblastoma cell line, treatment: differentiated with retinoic acid. (Biedler, et al. Morphology and Growth, Tumorigenicity, and Cytogenetics of Human Neuroblastoma Cells in Continuous Culture. Cancer Research 33, 2643-2652, November 1973.); cell karyotype: cancer; cell lineage: ectoderm; cell sex: F; replicate: 1; ', 'cell: HSMM; cell organism: Human; cell description: Normal Human Skeletal Muscle Myoblasts; cell karyotype: normal; cell lineage: mesoderm; cell sex: U; replicate: 1; ', 'cell: AG04449; cell organism: Human; cell description: Fetal buttock/thigh fibroblast; cell lin eage: mesoderm; cell sex: M; replicate: 1; ', 'biomaterial_type: immortalized cell line; line: HeLa-S3; cell: HeLa-S3; cell organism: Human; cell description: cervical carcinoma; cell karyotype: cancer; cell lineage: ectoderm; cell sex: F; replicate: 1; ', 'cell: LNCaP; cell organism: Human; cell description: prostate adenocarcinoma, "LNCaP clone FGC was isolated in 1977 by J.S. Horoszewicz, et al., from a needle aspiration biopsy of the left supraclavicular lymph node of a 50-year-old Caucasian male (blood type B+) with confirmed diagnosis of metastatic prostate carcinoma." - ATCC. (Horoszewicz et al. LNCaP Model of Human Prostatic Carcinoma. Cancer Research 43, 1809-1818, April 1983.); cell karyotype: cancer; cell lineage: endoderm; cell sex: M; replicate: 1; ', 'cell: NHDF-Ad; cell organism: Human; cell description: Adult Normal Human Dermal Fibroblasts; cell sex: F; replicate: 1; ', 'cell: HCF; cell organism: Human; cell description: Human Cardiac Fibroblasts; cell lineage: mesoderm; cell sex: U; replicate: 1; ', 'cell: HCPEpiC; cell organism: Human; cell description: Human Choroid Plexus Epithelial Cells; cell sex: U; replicate: 1; ', 'cell: HMVEC-dBl-Neo; cell organism: Human; cell description: Normal Neonatal Human Blood Microvascular Endothelial Cells, Dermal-Derived; cell sex: M; replicate: 1; ', 'cell: HPF; cell organism: Human; cell description: Human Pulmonary Fibroblasts isolated from lung tissue; cell sex: U; replicate: 1; ', 'cell: HUVEC; cell organism: Human; cell description: Human Umbilical Vein Endothelial Cell; cell karyotype: normal; cell lineage: mesoderm; cell sex: U; replicate: 1; ', 'cell: HMVEC-dLy-Neo; cell organism: Human; cell description: Normal Neonatal Human Lymphatic Microvascular Endothelial Cells, Dermal-Derived; cell sex: M; replicate: 1; ', 'cell: HGF; cell organism: Human; cell description: Human Gingival Fibroblasts; cell karyotype: normal; cell sex: U; replicate: 1; ', 'cell: A549; cell organism: Human; cell description: epithelial cell line "This line was initiated in 1972 by D.J. Giard, et al. through explant culture of lung carcinomatous tissue from a 58-year-old Caucasian male." - ATCC, derived from a lung carcinoma tissue. (PMID: 175022); cell karyotype: cancer; cell lineage: endoderm; cell sex: M; replicate: 1; ', 'cell: MCF-7; cell organism: Human; cell description: mammary gland, adenocarcinoma. (PMID: 4357757); cell karyotype: cancer; cell sex: F; replicate: 1; ', 'biomaterial_type: stem cell; line: H1-hESC; cell organism: Human; cell description: Human Embryonic Stem Cells; cell karyotype: normal; cell lineage: embryonic stem cells; cell sex: M; replicate: 1; ', 'cell: AoAF; cell organism: Human; cell description: Normal Human Aortic Adventitial Fibroblast Cells; cell sex: F; replicate: 1; ', 'cell: HEEpiC; cell organism: Human; cell description: Human Esophageal Epithelial Cells; cell lineage: endoderm; cell sex: U; replicate: 1; ', 'cell: HAc; cell organism: human; cell description: Human Astrocytes-cerebellar; cell karyotype: Normal; cell lineage: Astrocytic; cell sex: U; replicate: 1; ', 'cell: HIPEpiC; cell organism: Human; cell description: Human Iris Pigment Epithelial Cells; cell lineage: ectoderm; cell sex: U; replicate: 1; ', 'cell: SKMC; cell organism: Human; cell description: Human Skeletal Muscle Cells; cell karyotype: unknown; cell lineage: mesoderm; cell sex: U; replicate: 1; ', 'cell: HA-h; cell organism: human; cell description: Human Astrocytes-hippocampal; cell karyotype: Normal; cell lineage: Astrocytic; cell sex: U; replicate: 1; ', 'cell: AG10803; cell organism: Human; cell description: Adult human abdominal skin fibroblasts; cell lineage: mesoderm; cell sex: M; replicate: 1; ', 'cell: HMVEC-dLy-Ad; cell organism: Human; cell description: Normal Adult Human Blood Microvascular Endothelial Cells, Dermal-Derived; cell sex: F; replicate: 1; ', 'biomaterial_type: immortalized cell line; line: HCT-116; cell organism: Human; cell description: colorectal carcinoma (PMID: 7214343); cell karyotype: cancer; cell lineage: endoderm; cell sex: M; replicate: 1; ', 'cell: HFF; cell organism: human; cell description: Human Foreskin Fibroblast; cell karyotype: Normal; cell lineage: Fibroblast; cell sex: M; replicate: 1; ', 'cell: NB4; cell organism: Human; cell description: acute promyelocytic leukemia cell line. (PMID: 1995093); cell karyotype: cancer; cell sex: U; replicate: 1; ', 'cell: CMK; cell organism: Human; cell description: human acute megakaryocytic leukemia cells, "established from the peripheral blood of a 10-month-old boy with Down\'s syndrome and acute megakaryocytic leukemia (AML M7) at relapse in 1985" - DSMZ. (PMID: 3016165); cell sex: M; replicate: 1; ', 'cell: SAEC; cell organism: Human; cell description: Small Airway Epithelial Cells; cell karyotype: normal; cell sex: U; replicate: 1; ', 'cell: HMVEC-dBl-Ad; cell organism: Human; cell description: Normal Adult Human Blood Microvascular Endothelial Cells, Dermal-Derived; cell sex: F; replicate: 1; ', 'cell: HMVEC-dNeo; cell organism: Human; cell description: Normal Neonatal Human Microvascular Endothelial Cells (single Donnor), Dermal-Derived; cell sex: M; replicate: 1; ', 'cell: NHLF; cell organism: Human; cell description: Normal Human Lung Fibroblasts; cell sex: U; replicate: 1; ', 'cell: WI-38; cell organism: human; cell description: Embryonic Lung Fibroblast Cells, hTERT immortalized, includes Raf1 construct; cell karyotype: Normal (RAF); cell lineage: Fibroblast; cell sex: F; replicate: 1; ', 'cell: HNPCEpiC; cell organism: Human; cell description: Human Non-Pigment Ciliary Epithelial Cells; cell sex: U; replicate: 1; ', 'cell: HL-60; cell organism: Human; cell description: Human promyelocytic leukemia cells. (PMID: 276884); cell karyotype: cancer; cell sex: F; replicate: 1; ', 'cell: HMF; cell organism: Human; cell description: human mammary fibroblasts; cell sex: F; replicate: 1; ', 'cell: K562; cell organism: Human; cell description: leukemia; cell karyotype: cancer; cell lineage: "The continuous cell line K-562 was established by Lozzio and Lozzio from the pleural effusion of a 53-year-old female with chronic myelogenous leukemia in terminal blast crises." - ATCC; cell sex: F; replicate: 1; ', 'cell: HRPEpiC; cell organism: Human; cell description: Human Retinal Pigment Epithelial Cells; cell lineage: ectoderm; cell sex: U; replicate: 1; ', 'cell: HAEpiC; cell organism: Human; cell description: Human Amniotic Epithelial Cells; cell sex: U; replicate: 1; ', 'cell: HPdLF; cell organism: Human; cell description: Normal Human Periodontal Ligament Fibroblasts; cell sex: M; replicate: 1; ', 'cell: HMEC; cell organism: Human; cell description: Human Mammary Epithelial Cells; cell sex: U; replicate: 1; ', 'cell: HepG2; cell organism: Human; cell description: liver carcinoma; cell karyotype: cancer; cell lineage: endoderm; cell sex: M; replicate: 1; ', 'cell: H7-hESC; cell organism: Human; cell description: Undifferentiated human embryonic stem cells; cell karyotype: unknown; cell sex: U; replicate: 1; ', 'sample alias: fStomach.H-23589d147; sample common name: Fetal Stomach; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Stomach; tissue_depot: UW; collection_method: fetal; donor_id: H-23589; donor_age: day 147; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fHeart.H-23663d105; sample common name: Fetal Heart; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Heart; tissue_depot: UW; collection_method: fetal; donor_id: H-23663; donor_age: day 105; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fThymus.H-23663d105; sample common name: Fetal Thymus; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Thymus; tissue_depot: UW; collection_method: fetal; donor_id: H-23663; donor_age: day 105; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Small.H-23744d91; sample common name: Fetal Intestine, Small; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Small; tissue_depot: UW; collection_method: fetal; donor_id: H-23744; donor_age: day 91; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fLung_Right.H-23744d91; sample common name: Fetal Lung, Right; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Lung, Right; tissue_depot: UW; collection_method: fetal; donor_id: H-23744; donor_age: day 91; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Small.H-23758d107; sample common name: Fetal Intestine, Small; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Small; tissue_depot: UW; collection_method: fetal; donor_id: H-23758; donor_age: day 107; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fStomach.H-23758d107; sample common name: Fetal Stomach; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Stomach; tissue_depot: UW; collection_method: fetal; donor_id: H-23758; donor_age: day 107; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Large.H-23808d115; sample common name: Fetal Intestine, Large; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Large; tissue_depot: UW; collection_method: fetal; donor_id: H-23808; donor_age: day 115; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Large.H-23833d113; sample common name: Fetal Intestine, Large; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Large; tissue_depot: UW; collection_method: fetal; donor_id: H-23833; donor_age: day 113; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fPlacenta.H-23887d108; sample common name: Fetal Placenta; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Placenta; tissue_depot: UW; collection_method: fetal; donor_id: H-23887; donor_age: day 108; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fPlacenta.H-23914d91; sample common name: Fetal Placenta; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Placenta; tissue_depot: UW; collection_method: fetal; donor_id: H-23914; donor_age: day 91; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Large.H-23914d91; sample common name: Fetal Intestine, Large; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Large; tissue_depot: UW; collection_method: fetal; donor_id: H-23914; donor_age: day 91; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fKidney_renal_pelvis.H-23914d91; sample common name: Fetal Renal Pelvis; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Renal Pelvis; tissue_depot: UW; collection_method: fetal; donor_id: H-23914; donor_age: day 91; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fMuscle_Arm.H-23914d91; sample common name: Fetal Muscle, Arm; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Arm; tissue_depot: UW; collection_method: fetal; donor_id: H-23914; donor_age: day 91; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Small.H-23941d120; sample common name: Fetal Intestine, Small; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Small; tissue_depot: UW; collection_method: fetal; donor_id: H-23941; donor_age: day 120; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fLung_Right.H-23964d98; sample common name: Fetal Lung, Right; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Lung, Right; tissue_depot: UW; collection_method: fetal; donor_id: H-23964; donor_age: day 98; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Large.H-23964d98; sample common name: Fetal Intestine, Large; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Large; tissue_depot: UW; collection_method: fetal; donor_id: H-23964; donor_age: day 98; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Small.H-23864d98; sample common name: Fetal Intestine, Small; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Small; tissue_depot: UW; collection_method: fetal; donor_id: H-23864; donor_age: day 98; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fThymus.H-23964d98; sample common name: Fetal Thymus; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Thymus; tissue_depot: UW; collection_method: fetal; donor_id: H-23964; donor_age: day 98; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fLung_Right.H-24005d105; sample common name: Fetal Lung, Right; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Lung, Right; tissue_depot: UW; collection_method: fetal; donor_id: H-24005; donor_age: day 105; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fStomach.H-24005d105; sample common name: Fetal Stomach; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Stomach; tissue_depot: UW; collection_method: fetal; donor_id: H-24005; donor_age: day 105; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fMuscle_Back.H-24005d105; sample common name: Fetal Muscle, Back; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Back; tissue_depot: UW; collection_method: fetal; donor_id: H-24005; donor_age: day 105; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fLung_Left.H-23640d115; sample common name: Fetal Lung, Left; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Lung, Left; tissue_depot: UW; collection_method: fetal; donor_id: H-23640; donor_age: day 115; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fMuscle_Leg.H-24078d127; sample common name: Fetal Muscle, Leg; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Leg; tissue_depot: UW; collection_method: fetal; donor_id: H-24078; donor_age: day 127; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fIntestine_Small.H-23724d87; sample common name: Fetal Intestine, Small; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Intestine, Small; tissue_depot: UW; collection_method: fetal; donor_id: H-23724; donor_age: day 87; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fKidney_Right.H-23758d107; sample common name: Fetal Kidney, Right; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Kidney, Right; tissue_depot: UW; collection_method: fetal; donor_id: H-23758; donor_age: day 107; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fLung_Right.H-23758d107; sample common name: Fetal Lung, Right; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Lung, Right; tissue_depot: UW; collection_method: fetal; donor_id: H-23758; donor_age: day 107; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fAdrenal.H-23887d108; sample common name: Fetal Adrenal Gland; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Adrenal Gland; tissue_depot: UW; collection_method: fetal; donor_id: H-23887; donor_age: day 108; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fThymus.H-24078d127; sample common name: Fetal Thymus; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Thymus; tissue_depot: UW; collection_method: fetal; donor_id: H-24078; donor_age: day 127; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fStomach.H-24078d127; sample common name: Fetal Stomach; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Stomach; tissue_depot: UW; collection_method: fetal; donor_id: H-24078; donor_age: day 127; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fKidney_renal_pelvis.H-24078d127; sample common name: Fetal Renal Pelvis; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Renal Pelvis; tissue_depot: UW; collection_method: fetal; donor_id: H-24078; donor_age: day 127; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fSpinal_Cord.H-24111d105; sample common name: Fetal Spinal Cord; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Spinal Cord; tissue_depot: UW; collection_method: fetal; donor_id: H-24111; donor_age: day 105; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fStomach.H-24125d101; sample common name: Fetal Stomach; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Stomach; tissue_depot: UW; collection_method: fetal; donor_id: H-24125; donor_age: day 101; donor_health_status: NA; donor_sex: Unknown; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fMuscle_Leg.H-24259d97; sample common name: Fetal Muscle, Leg; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Leg; tissue_depot: UW; collection_method: fetal; donor_id: H-24259; donor_age: day 97; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fMuscle_Back.H-24272d85; sample common name: Fetal Muscle, Back; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Back; tissue_depot: UW; collection_method: fetal; donor_id: H-24272; donor_age: day 85; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fPlacenta.H-24272d85; sample common name: Fetal Placenta; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Placenta; tissue_depot: UW; collection_method: fetal; donor_id: H-24272; donor_age: day 85; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fHeart.H-23744d91; sample common name: Fetal Heart; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Heart; tissue_depot: UW; collection_method: fetal; donor_id: H-23744; donor_age: day 91; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: Stamlab DNase Protocol, Sabo, P. J. et al. Nat Methods 3, 511-518 (2006); ', 'sample alias: fMuscle_Leg.H-24244d96; sample common name: Fetal Muscle, Leg; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Leg; tissue_depot: UW; collection_method: fetal; donor_id: H-24244; donor_age: day 96; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fKidney_renal_cortex.H-24259d97; sample common name: Fetal Renal Cortex; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Renal Cortex; tissue_depot: UW; collection_method: fetal; donor_id: H-24259; donor_age: day 97; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fHeart.H-24042d120; sample common name: Fetal Heart; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Heart; tissue_depot: UW; collection_method: fetal; donor_id: H-24042; donor_age: day 120; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fMuscle_Leg.H-24279d101; sample common name: Fetal Muscle, Leg; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Leg; tissue_depot: UW; collection_method: fetal; donor_id: H-24279; donor_age: day 101; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fMuscle_Back.H-24297d104; sample common name: Fetal Muscle, Back; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Back; tissue_depot: UW; collection_method: fetal; donor_id: H-24297; donor_age: day 104; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fBrain.H-24279d101; sample common name: Fetal Brain; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Brain; tissue_depot: UW; collection_method: fetal; donor_id: H-24279; donor_age: day 101; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fBrain.H-24297d104; sample common name: Fetal Brain; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Brain; tissue_depot: UW; collection_method: fetal; donor_id: H-24297; donor_age: day 104; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fBrain.H-24381d109; sample common name: Fetal Brain; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Brain; tissue_depot: UW; collection_method: fetal; donor_id: H-24381; donor_age: day 109; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fMuscle_Leg.H-24409d113; sample common name: Fetal Muscle, Leg; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Leg; tissue_depot: UW; collection_method: fetal; donor_id: H-24409; donor_age: day 113; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fThymus.H-24401d108; sample common name: Fetal Thymus; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Thymus; tissue_depot: UW; collection_method: fetal; donor_id: H-24401; donor_age: day 108; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fThymus.H-24409d113; sample common name: Fetal Thymus; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Thymus; tissue_depot: UW; collection_method: fetal; donor_id: H-24409; donor_age: day 113; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fAdrenal.H-24409d113; sample common name: Fetal Adrenal Gland; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Adrenal Gland; tissue_depot: UW; collection_method: fetal; donor_id: H-24409; donor_age: day 113; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fPlacenta.H-24409d113; sample common name: Fetal Placenta; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Placenta; tissue_depot: UW; collection_method: fetal; donor_id: H-24409; donor_age: day 113; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fStomach.H-24401d108; sample common name: Fetal Stomach; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Stomach; tissue_depot: UW; collection_method: fetal; donor_id: H-24401; donor_age: day 108; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fSpinal_Cord.H-24409d113; sample common name: Fetal Spinal Cord; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Spinal Cord; tissue_depot: UW; collection_method: fetal; donor_id: H-24409; donor_age: day 113; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fKidney_renal_pelvis.H-24477d103; sample common name: Fetal Renal Pelvis; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Renal Pelvis; tissue_depot: UW; collection_method: fetal; donor_id: H-24477; donor_age: day 103; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fSpinal_Cord.H-24493d89; sample common name: Fetal Spinal Cord; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Spinal Cord; tissue_depot: UW; collection_method: fetal; donor_id: H-24493; donor_age: day 89; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fMuscle_Trunk.H-24507d121; sample common name: Fetal Muscle, Trunk; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Muscle, Trunk; tissue_depot: UW; collection_method: fetal; donor_id: H-24507; donor_age: day 121; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fStomach.H-24507d121; sample common name: Fetal Stomach; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Stomach; tissue_depot: UW; collection_method: fetal; donor_id: H-24507; donor_age: day 121; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fKidney.H-24507d121; sample common name: Fetal Kidney; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Kidney; tissue_depot: UW; collection_method: fetal; donor_id: H-24507; donor_age: day 121; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fKidney_renal_cortex.H-24493d89; sample common name: Fetal Renal Cortex; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Renal Cortex; tissue_depot: UW; collection_method: fetal; donor_id: H-24493; donor_age: day 89; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: TReg; cell organism: mouse; cell description: Regulatory T cells CD4+,CD25+; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS16358; labversion: 1,Hotspot-v5.2,Hotspot-v5.1,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,3,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: THelper-Activated; cell organism: mouse; cell description: Activated primary CD4 effector cells, isolated ex vivo; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS17070,DS18848; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: WholeBrain; cell organism: mouse; cell description: Whole Brain; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labversion: 1,Hotspot-v5.1,lmax-v1.0,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,3,2,5,4,7,6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; line: CH12; cell organism: mouse; cell description: B-cell lymphoma (GM12878 analog); cell sex: F; age: immortalized; biomaterial_type: immortalized cell line; strain: B10.H-2aH-4bp/Wts; strain description: Derived by inbreeding from selected F2 progeny of B10.A X B10.129; age: immortalized; biomaterial_type: immortalized cell line; labexpid: DS22536,DS22542; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: Derived by inbreeding from selected F2 progeny of B10.A X B10.129; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; line: ES-E14; cell organism: mouse; biomaterial_type: mouse embryonic stem cells; cell sex: M; age: E0; age description: Embryonic day 0 (stem cell); strain: 129/Ola; strain description: The mice have yellow coats and late onset severe vacuolation in brain (700+ days). Inbred strain used as a control group to compare with null PrP mice.; age: E0; age description: Embryonic day 0 (stem cell); labexpid: DS21450,DS18505; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: The mice have yellow coats and late onset severe vacuolation in brain (700+ days). Inbred strain used as a control group to compare with null PrP mice.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: EPC_(CD117+,CD71-,TER119-); cell organism: mouse; cell description: liver fraction CD117+,CD71-,TER119-; cell sex: M; age: E14.5; age description: Embryonic day 14.5; strain: CD-1; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; age: E14.5; age description: Embryonic day 14.5; labexpid: DS20991; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: EPC_(CD117-,CD71+,TER119+); cell organism: mouse; cell description: liver fraction CD117-,CD71+,TER119+; cell sex: M; age: E14.5; age description: Embryonic day 14.5; strain: CD-1; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; age: E14.5; age description: Embryonic day 14.5; labexpid: DS20937; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: EPC_(CD117+,CD71+,TER119+); cell organism: mouse; cell description: liver fraction CD117+,CD71+,TER119+; cell sex: M; age: E14.5; age description: Embryonic day 14.5; strain: CD-1; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; age: E14.5; age description: Embryonic day 14.5; labexpid: DS20999; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: EPC_(CD117+,CD71+,TER119-); cell organism: mouse; cell description: liver fraction CD117+,CD71+,TER119-; cell sex: M; age: E14.5; age description: Embryonic day 14.5; strain: CD-1; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; age: E14.5; age description: Embryonic day 14.5; labexpid: DS20994; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: ES-WW6; cell organism: mouse; cell description: ES-cells isolated from mix of ~20% C57/B6J, ~75% 129/Sv and ~5% SJL strains; cell sex: M; age: E0; age description: Embryonic day 0 (stem cell); strain: Unknown; strain description: Unknown strain origin; age: E0; age description: Embryonic day 0 (stem cell); labexpid: DS17060,DS17613; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: Unknown strain origin; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Liver; cell organism: mouse; cell description: Liver; cell sex: M; age: E14.5; age description: Embryonic day 14.5; strain: 129; strain description: Strain 129, has widely available embryonic stem cells; age: E14.5; age description: Embryonic day 14.5; labexpid: DS19246; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1; strain description: Strain 129, has widely available embryonic stem cells; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: 416B; cell organism: mouse; cell description: myeloid progenitor cells, CD34+; cell sex: M; age: immortalized; age description: Immortal cells; strain: B6D2F1/J; strain description: Derived from cross between C57BL/6J Female x DBA/2J Male (C57BL/6xDBA/2)F1.; age: immortalized; age description: Immortal cells; labversion: 1,Hotspot-v5.1,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: Derived from cross between C57BL/6J Female x DBA/2J Male (C57BL/6xDBA/2)F1.; ', 'biomaterial_type: tissue; donor_id: ENCDO072AAA; tissue_type: cerebellum; lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Cerebellum; cell organism: mouse; cell description: Cerebellum; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS19087; labversion: Hotspot-v5.2,Hotspot-v5.1,1,lmax-v1.1,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1,3,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: FatPad; cell organism: mouse; cell description: Adipose tissue; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labversion: 1,Hotspot-v5.1,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Heart; cell organism: mouse; cell description: Heart; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS18138; labversion: 1,Hotspot-v5.2,Hotspot-v5.1,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: A20; cell organism: mouse; cell description: B cell lymphoma line derived from a spontaneous reticulum cell neoplasm; cell sex: M; age: immortalized; age description: Immortal cells; strain: BALB/cAnN; strain description: ccMyeloma high incidence H2d; age: immortalized; age description: Immortal cells; labversion: 1,Hotspot-v5.1,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: ccMyeloma high incidence H2d; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Cerebrum; cell organism: mouse; cell description: Cerebrum; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labversion: 1,Hotspot-v5.1,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1,3,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: ZhBTc4; cell organism: mouse; cell description: Undifferentiated mouse embryonic stem cells; cell sex: M; age: E0; age description: Embryonic day 0 (stem cell); strain: 129/Ola; strain description: The mice have yellow coats and late onset severe vacuolation in brain (700+ days). Inbred strain used as a control group to compare with null PrP mice.; age: E0; age description: Embryonic day 0 (stem cell); labexpid: DS17616; labversion: 1,Hotspot-v5.2,Hotspot-v5.1,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: The mice have yellow coats and late onset severe vacuolation in brain (700+ days). Inbred strain used as a control group to compare with null PrP mice.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: B-cell_(CD43-); cell organism: mouse; cell description: mouse spleen B cells, CD43-,CD11b-; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS18865; labversion: 1,Hotspot-v5.2,Hotspot-v5.1,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,3,2,4; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Patski; cell organism: mouse; cell description: Mouse Embryonic Kidney Fibroblast. As described in Lingenfelter et al., 1998 (Nat Genet. 1998 18:212-3) and Yang et al., 2010 (Genome Res. 2010 20:614-22), PATSKI is a female interspecific mouse fibroblast that was derived from the embryonic kidney of an M.spretus x C57BL/6J hybrid mouse such that the C57Bl/6J X chromosome (maternal) is always the inactive X. This is an adherent cell line.; cell sex: M; age: immortalized; age description: Immortal cells; strain: Spretus.BL6-Xist; strain description: M.spretus x C57BL/6J hybrid mouse such that the C57Bl/6J X chromosome (maternal) is always the inactive X.; age: immortalized; age description: Immortal cells; labversion: 1,Hotspot-v5.1,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: M.spretus x C57BL/6J hybrid mouse such that the C57Bl/6J X chromosome (maternal) is always the inactive X.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: HeadlessEmbryo; cell organism: mouse; cell description: Whole embryos with heads removed; cell sex: M; age: E11.5; age description: Embryonic day 11.5; strain: CD-1; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; age: E11.5; age description: Embryonic day 11.5; labexpid: DS17129; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: GenitalFatPad; cell organism: mouse; cell description: Genital Adipose tissue; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: ForelimbBud; cell organism: mouse; cell description: embryo forelimb buds; cell sex: M; age: E11.5; age description: Embryonic day 11.5; strain: CD-1; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; age: E11.5; age description: Embryonic day 11.5; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Retina; cell organism: mouse; cell description: Retina; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS19060; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: NIH-3T3; cell organism: mouse; cell description: fibroblast; cell sex: M; age: immortalized; age description: Immortal cells; strain: NIH/Swiss; strain description: An outbred Swiss mouse used as a general-purpose stock. Used extensively for pertussis HSF testing.; age: immortalized; age description: Immortal cells; labexpid: DS16900; labversion: 1,Hotspot-v5.2,Hotspot-v5.1,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: An outbred Swiss mouse used as a general-purpose stock. Used extensively for pertussis HSF testing.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Mesoderm; cell organism: mouse; cell description: axial somatic and lateral plate mesoderm from eviscerated headless, limbless embryos; cell sex: M; age: E11.5; age description: Embryonic day 11.5; strain: CD-1; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; age: E11.5; age description: Embryonic day 11.5; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: HindlimbBud; cell organism: mouse; cell description: embryo hindlimb buds; cell sex: M; age: E11.5; age description: Embryonic day 11.5; strain: CD-1; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; age: E11.5; age description: Embryonic day 11.5; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: Multipurpose mouse used for safety testing, aging studies, surgical models and pseudopregnancy.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; biomaterial_type: tissue; donor_id: ENCDO072AAA; cell organism: mouse; tissue_type: Spleen; Sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS18870,DS18884; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; biomaterial_type: tissue; donor_id: ENCDO088AAA; cell organism: mouse; tissue_type: liver; Sex: M; age: E14.5; age description: Embryonic day 14.5; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: E14.5; age description: Embryonic day 14.5; labexpid: DS20666; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; biomaterial_type: tissue; donor_id: ENCDO072AAA; cell organism: mouse; tissue_type: thymus; Sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS18890,DS18819; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: LgIntestine; cell organism: mouse; cell description: Large Intestine; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS18784,DS19140; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: ES-CJ7; cell organism: mouse; cell description: ES-cells were originally isolated from 129S1/SVImJ mice by Swiatek PJ et al. in 1993 ("Perinatal lethality and defects in hindbrain development in mice homozygous for a targeted mutation of the zinc finger gene Krox20". Swiatek PJ, Gridley T. Genes Dev. 1993 Nov,7(11):2071-84.); cell sex: M; age: E0; age description: Embryonic day 0 (stem cell); strain: 129S1/SVImJ; strain description: Control inbred strain of the steel-derived ES cells.; age: E0; age description: Embryonic day 0 (stem cell); labversion: 1,Hotspot-v5.1,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: Control inbred strain of the steel-derived ES cells.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: SkMuscle; cell organism: mouse; cell description: Skeletal Muscle; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS18892,DS18130; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: B-cell_(CD19+); cell organism: mouse; cell description: B Cell , CD19+; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labversion: Hotspot-v5.1,1,lmax-v1.1,2,WindowDensity-bin20-win+/-75,lmax-v1.0; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; line: MEL; cell organism: mouse; cell description: Leukemia (K562 analog); cell sex: M; age: immortalized; biomaterial_type: immortalized cell line; strain: Unknown; strain description: Unknown strain origin; age: immortalized; biomaterial_type: immortalized cell line; labversion: 1,Hotspot-v5.1,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1,3,2; strain description: Unknown strain origin; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: T-Naive; cell organism: mouse; cell description: Naive T cells: CD4+, CD25-; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS17082,DS17080; labversion: Hotspot-v5.2,Hotspot-v5.1,1,lmax-v1.1,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1,3,2,4; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Kidney; cell organism: mouse; cell description: Kidney; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labversion: 1,Hotspot-v5.1,lmax-v1.0,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Lung; cell organism: mouse; cell description: Lung; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labversion: 1,Hotspot-v5.1,lmax-v1.0,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,3,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; biomaterial_type: tissue; donor_id: ENCDO072AAA; cell organism: mouse; tissue_type: liver; Sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS16853,DS16858,DS19375,DS19636; labversion: Hotspot-v5.2,Hotspot-v5.1,1,lmax-v1.1,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 11,10,13,12,14,1,3,2,5,4,7,6,9,8; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: 3134; cell organism: mouse; cell description: Mammary; cell sex: M; age: immortalized; age description: Immortal cells; strain: RIII; strain description: High mammary tumor incidence in unfostered substrains.; age: immortalized; age description: Immortal cells; labversion: 1,Hotspot-v5.1,lmax-v1.0,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: High mammary tumor incidence in unfostered substrains.; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; biomaterial_type: tissue; donor_id: ENCDO088AAA; cell organism: mouse; tissue_type: Whole Brain; Sex: M; age: E14.5; age description: Embryonic day 14.5; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: E14.5; age description: Embryonic day 14.5; labversion: 1,Hotspot-v5.1,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Retina; cell organism: mouse; cell description: Retina; cell sex: M; age: adult-1wks; age description: Adult 1 week; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-1wks; age description: Adult 1 week; labexpid: DS20000; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Fibroblast; cell organism: mouse; cell description: Fibroblast; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labversion: 1,Hotspot-v5.1,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW-m; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: TReg-Activated; cell organism: mouse; cell description: Activated primary T regulatory cells, isolated ex vivo; cell sex: M; age: adult-8wks; age description: Adult 8 weeks; strain: C57BL/6; strain description: C57 black 6, the most common inbred strain of laboratory mouse; age: adult-8wks; age description: Adult 8 weeks; labexpid: DS17077,DS20149; labversion: 1,Hotspot-v5.2,lmax-v1.1,WindowDensity-bin20-win+/-75; replicate: 1,2; strain description: C57 black 6, the most common inbred strain of laboratory mouse; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Th2_Wb54553204; cell organism: human; cell description: Th2 cells in vivo isolation, donor is Caucasian, male 33 year old, primary pheresis of single normal subject; cell karyotype: normal; cell lineage: mesoderm; cell sex: M; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS17597; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: PrEC; cell organism: human; cell description: prostate epithelial cell line; cell karyotype: normal; cell lineage: epithelial; cell sex: U; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS12098; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Treg_Wb78495824; cell organism: human; cell description: T regulatory cells in vivo isolation; cell karyotype: normal donor is Causasian, female 35 year old, primary pheresis of single normal subject; cell lineage: mesoderm; cell sex: F; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS14702; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: HMVEC-dAd; cell organism: human; cell description: adult dermal microvascular endothelial cells.; cell karyotype: normal; cell sex: F; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS12957; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: HBVP; cell organism: human; cell description: brain vascular pericytes; cell karyotype: normal; cell lineage: mesoderm; cell sex: U; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS14834; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: NT2-D1; cell organism: human; cell description: malignant pluripotent embryonal carcinoma (NTera-2), "The NTERA-2 cl.D1 cell line is a pluripotent human testicular embryonal carcinoma cell line derived by cloning the NTERA-2 cell line." - ATCC. (PMID: 6694356); cell karyotype: cancer; cell lineage: inner cell mass; cell sex: M; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS14575; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Th1_Wb54553204; cell organism: human; cell description: Th1 cells in vivo isolation, donor is Caucasian, male 33 year old, primary pheresis of single normal subject; cell karyotype: normal; cell lineage: mesoderm; cell sex: M; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS17593; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: T-47D; cell organism: human; cell description: epithelial cell line derived from a mammary ductal carcinoma.; cell karyotype: cancer; cell sex: F; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS19794; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: HPAEC; cell organism: human; cell description: pulmonary artery endothelial cells.; cell karyotype: normal; cell lineage: mesoderm; cell sex: F; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS12916; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: CD20+_RO01778; cell organism: human; cell description: B cells, caucasian, draw number 1, newly promoted to tier 2: not in 2011 analysis; cell karyotype: normal; cell lineage: mesoderm; cell sex: F; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS18208; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: HBVSMC; cell organism: human; cell description: brain vascular smooth muscle cells.; cell karyotype: normal; cell lineage: mesoderm; cell sex: F; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS14860; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: CD34+_Mobilized; cell organism: human; cell description: hematopoietic progenitor cells- mobilized, from donor RO01679.; cell sex: M; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS16814; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: M059J; cell organism: human; cell description: malignant glioblastoma, glioma, lack DNA-dependent protein kinase activity, deficient in repair of DNA double strand breaks, the cells are negative for glial fibrillary acidic protein (GFAP), tumor specimen taken from a 33 year old; cell karyotype: cancer; cell lineage: ectoderm; cell sex: M; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS20493; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: GM04504; cell organism: human; cell description: adult twin pair fibroblasts, monozygotic twin of GM04503, 13% of the cells examined show random chromosome loss; cell karyotype: normal; cell sex: F; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS18973; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: GM04503; cell organism: human; cell description: adult twin pair fibroblasts, monozygotic twin of GM04504; cell karyotype: normal; cell sex: F; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS18637; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: RPMI-7951; cell organism: human; cell description: Human Skin Malignant Melanoma Cells, This is a hyperdiploid human cell line with the modal chromosome number of 49, occurring in 24% of cells. Polyploid cells occurred at 22%, which is high.; cell karyotype: cancer; cell lineage: ectoderm; cell sex: F; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS20909; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: NHBE_RA; cell organism: human; cell description: bronchial epithelial cells with retinoic acid; cell karyotype: normal; cell sex: F; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS11969; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: LHCN-M2; cell organism: human; cell description: skeletal myoblasts derived from satellite cells from the pectoralis major muscle of a 41 year old caucasian heart transplant donor, immortalized with lox-hygro-hTERT ("LH"), and Cdk4-neo ("CN"), Zhu et al. (2007) in Aging Cell, vol. 6, pp 515-523, newly promoted to tier 2: not in 2011 analysis.; cell lineage: mesoderm; cell sex: M; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS20548; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: CD4+_Naive_Wb11970640; cell organism: human; cell description: CD4+ naive sorted cells, donor is Caucasian, male 26 year old, primary pheresis of single normal subject; cell karyotype: normal; cell lineage: mesoderm; cell sex: M; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS14108; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'lab: UW; lab description: Stamatoyannopoulous - University of Washington; datatype: DnaseSeq; datatype description: DNaseI HS Sequencing; cell: Th17; cell organism: human; cell description: T helper cells expressing IL-17, primary pheresis of single normal subject; cell karyotype: normal; cell lineage: mesoderm; cell sex: B; treatment: None; treatment description: No special treatment or protocol applies; labexpid: DS11039; labversion: Hotspot-v5.2,lmax-v1.0,WindowDensity-bin20-win+/-75; replicate: 1; ', 'sample alias: fOvary.H23758_H23604pool; sample common name: Fetal Ovary; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Ovary; tissue_depot: UW; collection_method: fetal; donor_id: H23758_H23604; donor_age: pool; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fSpinal_Cord.H-24244d96; sample common name: Fetal Spinal Cord; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Spinal Cord; tissue_depot: UW; collection_method: fetal; donor_id: H-24244; donor_age: day 96; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fAdrenal.H-24279d101; sample common name: Fetal Adrenal Gland; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Adrenal Gland; tissue_depot: UW; collection_method: fetal; donor_id: H-24279; donor_age: day 101; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fThymus.H-24297d104; sample common name: Fetal Thymus; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Thymus; tissue_depot: UW; collection_method: fetal; donor_id: H-24297; donor_age: day 104; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fKidney_renal_cortex.H-24365d96; sample common name: Fetal Renal Cortex; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Renal Cortex; tissue_depot: UW; collection_method: fetal; donor_id: H-24365; donor_age: day 96; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fStomach.H-24365d96; sample common name: Fetal Stomach; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Stomach; tissue_depot: UW; collection_method: fetal; donor_id: H-24365; donor_age: day 96; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fBrain.H-24510d105; sample common name: Fetal Brain; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Brain; tissue_depot: UW; collection_method: fetal; donor_id: H-24510; donor_age: day 105; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fKidney.H-24510d105; sample common name: Fetal Kidney; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Kidney; tissue_depot: UW; collection_method: fetal; donor_id: H-24510; donor_age: day 105; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fPlacenta.H-24510d105; sample common name: Fetal Placenta; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Placenta; tissue_depot: UW; collection_method: fetal; donor_id: H-24510; donor_age: day 105; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fKidney_Left.H-24568d98; sample common name: Fetal Kidney, Left; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Kidney, Left; tissue_depot: UW; collection_method: fetal; donor_id: H-24568; donor_age: day 98; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fSpinal_Cord.H-24582d87; sample common name: Fetal Spinal Cord; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Spinal Cord; tissue_depot: UW; collection_method: fetal; donor_id: H-24582; donor_age: day 87; donor_health_status: NA; donor_sex: Female; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fKidney.H-24608d85; sample common name: Fetal Kidney; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Kidney; tissue_depot: UW; collection_method: fetal; donor_id: H-24608; donor_age: day 85; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fLung_Left.H-24626d87; sample common name: Fetal Lung, Left; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Lung, Left; tissue_depot: UW; collection_method: fetal; donor_id: H-24626; donor_age: day 87; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ', 'sample alias: fKidney_Right.H-24626d87; sample common name: Fetal Kidney, Right; molecule: genomic DNA; disease: None; biomaterial_provider: University of Washington, Congenital Defects Lab. Ian Glass; biomaterial_type: Primary Tissue; tissue_type: Fetal Kidney, Right; tissue_depot: UW; collection_method: fetal; donor_id: H-24626; donor_age: day 87; donor_health_status: NA; donor_sex: Male; donor_ethnicity: NA; experiment_type: Chromatin Accessibility; extraction_protocol: Qiagen minElut; dnase_protocol: http://www.roadmapepigenomics.org/protocols/type/experimental/; ' GSE139951 Homo sapiens 10 Genome binding/occupancy profiling by high throughput sequencing GPL16791 TEAD1 ChIP-seq on on MDA-MB-231 and Detroit X1 562 cells 2019-11-05 The Hippo Pathway is a critical signaling network that regulates organ size and cellular proliferation in metazoans. The transcriptional enhanced associate domain (TEAD) family of transcription factors serve as the receptors for the downstream effectors of the Hippo pathway, YAP and TAZ, to upregulate expression of multiple genes involved in proliferation, cell-fate determination, polarity, and survival1. Recent work revealed that TEAD proteins are palmitoylated at a conserved cysteine with the lipid tail extending into the hydrophobic core of the protein2. Mutagenic and covalent modulation of the palmitoylation site disrupts Hippo signaling2,3; however, an understanding of why TEAD proteins require this seemingly essential modification and the therapeutic implications of modulating TEAD palmitoylation has remained elusive. Here we report the identification and optimization of a potent pan-TEAD small molecule that binds the TEAD lipid pocket (LP), blocks palmitoylation, and dysregulates TEAD activity in multiple cancer cell lines. Cellular and biochemical data interrogating the mechanism of action for our compound reveal TEAD palmitoylation to function as a checkpoint that regulates TEAD homeostasis. We show that bypassing this checkpoint with a small molecule increases TEAD protein levels thereby decreasing the ability of YAP/TAZ to activate downstream target gene transcription in a dominant-negative manner. Our study demonstrates a new role for lipidation in protein signaling and establishes the TEAD LP as a bona fide therapeutic site for modulation of the Hippo Pathway. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE139951 Small Molecule Dysregulation of TEAD Lipidation Induces a Dominant-Negative Inhibition of Hippo Pathway Signaling. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2020.107809 {Cell reports (7.815): 10.1016/j.celrep.2020.107809} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA587718 https://www.ebi.ac.uk/ena/browser/view/PRJNA587718 https://www.ncbi.nlm.nih.gov/sra?term=SRP228603 [Overal design]ChIP-seq of TEAD1 was performed on the following cells in two replicates: MDA-MB-231 and Detroit X1 562 cells. We had one input sample as control for each cell type.; [Treatment]'None'; [Growth]'None'; [Extraction]'Cells were plated and dosed with either DMSO or small molecular (Compound 2) at 10 mM for 24 hrs. For dual cross-linking, cells were first incubated with 2 mM disuccinimidyl glutarate (ThermoFisher, 20593) for 20 min and then with formaldehyde at 1% (v/v) for an additional 10 min. Nuclei were extracted and sheared to an average length of 300-600 bp using truChIP Chromatin Shearing Kit (Covaris, 520154) following the manufacturer’s guidelines. All chromatin immunoprecipitation samples were supplemented with 20 ng of Drosophila chromatin (Active Motif, 53083) and 2 µg of a Drosophila-specific antibody (Active Motif, 61686) for normalization of ChIP-seq samples. For immunoprecipitations, 20 µg of sheared chromatin was incubated with 3-5 µg of antibody at 4 °C overnight. Complexes were captured by incubating with 40 mL Protein A Dynabeads (ThermoFisher, 10002D) for 2 hr at 4 °C. ChIP’d DNA was purified using ChIP DNA Clean & Concentrator (Zymo Research, D5205) following elution from magnetic beads, digestion with RNase and proteinase K, and reversal of crosslink by heating at 65 °C. 10 ng of purified DNA was used to generate libraries with the Ovation Ultra Low Library Prep Kit (NuGEN, 0344NB-32). Sequencing was performed on an Illumina HiSeq 2500 platform.\nLibraries were prepared using standard protocols for the Ovation Ultralow System. Briefly, samples were PCR-amplified and sized using the Agilent 2100Bioanalyzer. Barcoded libraries were sequenced 50 bp single end on HiSeq 2500 (Illumina).'; [Cell type]'Source: ''age: 51 years; chip antibody: none; ', 'age: 51 years; chip antibody: anti TEF1/TEAD-1 (Abcam, ab133533); treatment: DMSO; ', 'age: 51 years; chip antibody: anti TEF1/TEAD-1 (Abcam, ab133533); treatment: small molecular (Compound 2) at 10 mM; ', 'age: Adult; chip antibody: none; ', 'age: Adult; chip antibody: anti TEF1/TEAD-1 (Abcam, ab133533); treatment: DMSO; ', 'age: Adult; chip antibody: anti TEF1/TEAD-1 (Abcam, ab133533); treatment: small molecular (Compound 2) at 10 mM; ' GSE127067 Homo sapiens 42 Expression profiling by array GPL23126 Clariom D expression in breast cancer samples 2019-02-25 We analysed expression using Clariom D array in 42 breast cancer FFPE samples https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE127067 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA524163 https://www.ebi.ac.uk/ena/browser/view/PRJNA524163 None [Overal design]The RNA for the Clariom™ D study was extracted from tissue fixed in formaldehyde and embedded in paraffin, preserved at room temperature. Four sections of 20 μm from breast cancer tumour paraffin embedded were used. The extraction of the RNA material was carried out using the commercial kit RecoverAll ™ Total Nucleic Acid Isolation Kit from ambion® (Applied Biosystems ™ by Life Technologies ™, Carlsbad, California, USA). RNA was quantified by Qubit® 3.0 (InvitrogenTM by Termo Fisher Scientific, Waltham, MA, USA) y Qubit® RNA HS Assay Kit (Molecular Probes® by Life Technologies Carlsbad, California, USA). Before hybridization RNA quality was assessed using Real Time PCR (qRT-PCR).; [Treatment]'None'; [Growth]'None'; [Extraction]'The RNA for the Clariom™ D study was extracted from tissue fixed in formaldehyde and embedded in paraffin, preserved at room temperature. Four sections of 20 μm from breast cancer tumour paraffin embedded were used. The extraction of the RNA material was carried out using the commercial kit RecoverAll ™ Total Nucleic Acid Isolation Kit from ambion® (Applied Biosystems ™ by Life Technologies ™, Carlsbad, California, USA)'; [Cell type]'Source: ''tissue: breast cancer; ' GSE50220 Homo sapiens 48 Methylation profiling by array GPL8490 Epigenome analysis of irradiated and non-irradiated breast tumor tissue samples and normal controls 2013-08-27 Genome wide DNA methylation profiling of irradiated and non-irradiated breast tumor samples and normal control tissue. The Illumina Infinium 27k Human DNA methylation Beadchip, Genome Build 36 was used to obtain DNA methylation profiles across approximately 27,000 CpGs in breast tumor samples. Samples included 20 non-irradiated tumor samples, 19 irradiated tumor samples and 9 normal controls. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50220 Differential DNA methylation analysis of breast cancer reveals the impact of immune signaling in radiation therapy. International journal of cancer 4.982 https://doi.org/10.1002/ijc.28862 {International journal of cancer (4.982): 10.1002/ijc.28862} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA217315 https://www.ebi.ac.uk/ena/browser/view/PRJNA217315 None [Overal design]Bisulphite converted DNA from the 48 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2; [Treatment]'None'; [Growth]'None'; [Extraction]'genomic DNA was extracted and purified from tumor and normal samples using Maxwell 16 DNA Purification Kit according to standard instructions'; [Cell type]'Source: ''gender: Female; irradiation status: Non-irradiated; disease state: breast cancer; ', 'gender: Female; irradiation status: Irradiated; disease state: breast cancer; ', 'gender: Female; irradiation status: Non-irradiated; disease state: normal; ' GSE60609 Mus musculus 12 Expression profiling by array GPL19103 In vivo isolated HER2/neu-Prim1 Primary, Residual, and Recurrent Tumor Cells, and Recurrent Tumor Stromal Cells 2014-08-21 Residual disease represents a major obstacle to the successful treatment of breast cancer, however little is known about the biology of residual tumor cells in vivo. To identify genes differentially expressed in vivo in residual tumor cells compared to primary tumor cells or recurrent tumor cells, we used flow cytometry to isolate GFP-labeled tumor cells from primary, residual, or recurrent tumors grown orthotopically in nu/nu mice. WTA was used to amplify RNA from all tumor cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60609 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA258648 https://www.ebi.ac.uk/ena/browser/view/PRJNA258648 None [Overal design]Three timepoints (Primary tumor, residual disease, recurrent tumor) were taken with 3-4 replicates per timepoint.; [Treatment]'Doxycycline withdrawal was used in order to inactivate oncogene and lead to tumor regression'; [Growth]'H2B-eGFP-labeled tumor cells were grown orthotopically in nu/nu mice on doxycycline'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions"; [Cell type]'Source: ''strain: nu/nu; gender: Female; tissue: Isolated Orthotopic Primary Tumor Tumor Cells; cell genotype: MMTV-rtTA;TetO-HER2/neu; treatment: Untreated; time point: Primary Tumor; ', 'strain: nu/nu; gender: Female; tissue: Isolated Orthotopic Residual Lesion Tumor Cells; cell genotype: MMTV-rtTA;TetO-HER2/neu; treatment: HER2/neu inhibition; time point: 28d after doxycycline withdrawal; ', 'strain: nu/nu; gender: Female; tissue: Isolated Orthotopic Recurrent Tumor Tumor Cells; cell genotype: MMTV-rtTA;TetO-HER2/neu; treatment: HER2/neu inhibition; time point: Recurrent Tumor; ', 'strain: nu/nu; gender: Female; tissue: Isolated Orthotopic Recurrent Tumor Stromal Cells; cell genotype: MMTV-rtTA;TetO-HER2/neu; treatment: HER2/neu inhibition; time point: Recurrent Tumor; ' GSE33658 Homo sapiens 22 Expression profiling by array GPL570 A phase II neoadjuvant trial of anastrozole (A), fulvestrant (F) and gefitinib (I - iressa) in patients with newly diagnosed estrogen receptor positive breast cancer 2011-11-14 Endocrine therapy in patients with breast cancer can be limited by the problem of resistance. Preclinical studies suggest that complete blockade of the estrogen receptor (ER) combined with inhibition of the epidermal growth factor receptor (EGFR) can overcome endocrine resistance. We tested this hypothesis in a phase II neoadjuvant trial of anastrozole and fulvestrant combined with gefitinib in postmenopausal women with newly diagnosed ER-positive breast cancer. After a baseline tumor core biopsy, patients were randomized to receive anastrozole and fulvestrant (AF) or anastrozole, fulvestrant, and gefitinib (AFG) for 3 weeks. After a second biopsy at 3 weeks, all patients received AFG for 4 months and surgery was done if the tumor was operable. The primary endpoint was best clinical response by RECIST criteria and secondary endpoints were toxicity and change in biomarkers. The study closed after 15 patients were enrolled because of slow accrual. Median patient age was 67 years and median clinical tumor size was 7 cm. Four patients had metastatic disease present. Three patients withdrew before response was assessed. In the remaining twelve patients, there were two complete clinical responses (17%), three partial responses (25%), five had stable disease (41%), and two (17%) had progressive disease. Most common adverse events were rash in four patients, diarrhea in four, joint symptoms in three, and abnormal liver function tests in three. There were no grade 4 toxicities and all toxicities were reversible. At 3 weeks, cell proliferation as measured by Ki-67 was significantly reduced in the AFG group (p value= 0.01) with a parallel reduction in the expression of the Cyclin D1 (p value=0.02). RNA microarray data showed a corresponding decrease in the expression of cell cycle genes. These results suggest that AFG was an effective neoadjuvant therapy and consistently reduced proliferation in ER-positive tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE33658 A phase II neoadjuvant trial of anastrozole, fulvestrant, and gefitinib in patients with newly diagnosed estrogen receptor positive breast cancer. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-011-1679-8 {Breast cancer research and treatment (3.471): 10.1007/s10549-011-1679-8} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA148645 https://www.ebi.ac.uk/ena/browser/view/PRJNA148645 None [Overal design]We tested this hypothesis in a phase II neoadjuvant trial of anastrozole and fulvestrant combined with gefitinib in postmenopausal women with newly diagnosed ER-positive breast cancer. After a baseline tumor core biopsy, patients were randomized to receive anastrozole and fulvestrant (AF) or anastrozole, fulvestrant, and gefitinib (AFG, also known as AFI) for 3 weeks. After a second biopsy at 3 weeks, all patients received AFG for 4 months and surgery was done if the tumor was operable. The primary endpoint was best clinical response by RECIST criteria and secondary endpoints were toxicity and change in biomarkers. The study closed after 15 patients were enrolled because of slow accrual. Median patient age was 67 years and median clinical tumor size was 7 cm. Four patients had metastatic disease present. Three patients withdrew before response was assessed. In the remaining twelve patients, there were two complete clinical responses (17%), three partial responses (25%), five had stable disease (41%), and two (17%) had progressive disease. Most common adverse events were rash in four patients, diarrhea in four, joint symptoms in three, and abnormal liver function tests in three. There were no grade 4 toxicities and all toxicities were reversible. At 3 weeks, cell proliferation as measured by Ki-67 was significantly reduced in the AFG group (p value= 0.01) with a parallel reduction in the expression of the Cyclin D1 (p value=0.02). RNA microarray data showed a corresponding decrease in the expression of cell cycle genes. These results suggest that AFG was an effective neoadjuvant therapy and consistently reduced proliferation in ER-positive tumors.; [Treatment]'After a baseline tumor biopsy, patients were randomized to receive Anastrazole/fulvestrant(AF) or anastrazole/Fulvestrant/Gefitinib (AFG) for 3 weeks, then a second biopsy was obtained. After that all patients received the AFG treatment.'; [Growth]'N/A'; [Extraction]'Trizol extraction'; [Cell type]'Source: ''type_of_rx: AF; pre_or_post_treatment: pre; response: PD; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 76; baseline tumor size (cm): 7x8; patient id (to identify the 2 chips from the same patient): 13491389; ', 'type_of_rx: AF; pre_or_post_treatment: post; response: PD; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 76; baseline tumor size (cm): 7x8; patient id (to identify the 2 chips from the same patient): 13491389; ', 'type_of_rx: AF; pre_or_post_treatment: pre; response: PR; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 72; baseline tumor size (cm): 6x5; patient id (to identify the 2 chips from the same patient): 16821717; ', 'type_of_rx: AF; pre_or_post_treatment: post; response: PR; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 72; baseline tumor size (cm): 6x5; patient id (to identify the 2 chips from the same patient): 16821717; ', 'type_of_rx: AF; pre_or_post_treatment: pre; response: SD; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 68; baseline tumor size (cm): 8x8; patient id (to identify the 2 chips from the same patient): 12781328; ', 'type_of_rx: AF; pre_or_post_treatment: post; response: SD; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 68; baseline tumor size (cm): 8x8; patient id (to identify the 2 chips from the same patient): 12781328; ', 'type_of_rx: AF; pre_or_post_treatment: pre; response: SD; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 56; baseline tumor size (cm): 8x7; patient id (to identify the 2 chips from the same patient): 16281659; ', 'type_of_rx: AF; pre_or_post_treatment: post; response: SD; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 56; baseline tumor size (cm): 8x7; patient id (to identify the 2 chips from the same patient): 16281659; ', 'type_of_rx: AF; pre_or_post_treatment: pre; response: SD; er_status: pos; pgr_status_: neg; her_2_status: neg; baseline age (years): 50; baseline tumor size (cm): missing; patient id (to identify the 2 chips from the same patient): 22332259; ', 'type_of_rx: AF; pre_or_post_treatment: post; response: SD; er_status: pos; pgr_status_: neg; her_2_status: neg; baseline age (years): 50; baseline tumor size (cm): missing; patient id (to identify the 2 chips from the same patient): 22332259; ', 'type_of_rx: AFG; pre_or_post_treatment: pre; response: CR; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 72; baseline tumor size (cm): 3x3; patient id (to identify the 2 chips from the same patient): 12961346; ', 'type_of_rx: AFG; pre_or_post_treatment: post; response: CR; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 72; baseline tumor size (cm): 3x3; patient id (to identify the 2 chips from the same patient): 12961346; ', 'type_of_rx: AFG; pre_or_post_treatment: pre; response: CR; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 59; baseline tumor size (cm): 3x3; patient id (to identify the 2 chips from the same patient): 16101647; ', 'type_of_rx: AFG; pre_or_post_treatment: post; response: CR; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 59; baseline tumor size (cm): 3x3; patient id (to identify the 2 chips from the same patient): 16101647; ', 'type_of_rx: AFG; pre_or_post_treatment: pre; response: PD; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 73; baseline tumor size (cm): 7x6; patient id (to identify the 2 chips from the same patient): 15751594; ', 'type_of_rx: AFG; pre_or_post_treatment: post; response: PD; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 73; baseline tumor size (cm): 7x6; patient id (to identify the 2 chips from the same patient): 15751594; ', 'type_of_rx: AFG; pre_or_post_treatment: pre; response: PR; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 67; baseline tumor size (cm): 9x7; patient id (to identify the 2 chips from the same patient): 12791332; ', 'type_of_rx: AFG; pre_or_post_treatment: post; response: PR; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 67; baseline tumor size (cm): 9x7; patient id (to identify the 2 chips from the same patient): 12791332; ', 'type_of_rx: AFG; pre_or_post_treatment: pre; response: PR; er_status: pos; pgr_status_: neg; her_2_status: neg; baseline age (years): 87; baseline tumor size (cm): 5x3; patient id (to identify the 2 chips from the same patient): 19301950; ', 'type_of_rx: AFG; pre_or_post_treatment: post; response: PR; er_status: pos; pgr_status_: neg; her_2_status: neg; baseline age (years): 87; baseline tumor size (cm): 5x3; patient id (to identify the 2 chips from the same patient): 19301950; ', 'type_of_rx: AFG; pre_or_post_treatment: pre; response: SD; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 57; baseline tumor size (cm): 5x5; patient id (to identify the 2 chips from the same patient): 19101935; ', 'type_of_rx: AFG; pre_or_post_treatment: post; response: SD; er_status: pos; pgr_status_: pos; her_2_status: neg; baseline age (years): 57; baseline tumor size (cm): 5x5; patient id (to identify the 2 chips from the same patient): 19101935; ' GSE113573 Homo sapiens 12 Expression profiling by high throughput sequencing GPL18573 DHX15 regulates CMTR1-dependent gene expression and cell proliferation 2018-04-24 We discovered that the RNA helicase DHX15 is a regulator of the methyltransferase CMTR1. To determine the biological consequences of this interaction we overexpressed CMTR1 or a mutated CMTR1 (2LA)that does not bind DHX15, in the human breast cancer cell line HCC1806. To assess the effects of the DHX15-CMTR1 interaction on translation, polysomes were separated on a sucrose gradient and sequencing libraries generated from the polysomal and input RNA. We found that the DHX15-CMTR1 interaction controls ribosome loading of a subset of mRNAs and impacts on cell proliferation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113573 DHX15 regulates CMTR1-dependent gene expression and cell proliferation. Life science alliance 3.448 https://doi.org/10.26508/lsa.201800092 {Life science alliance (3.448): 10.26508/lsa.201800092} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA453131 https://www.ebi.ac.uk/ena/browser/view/PRJNA453131 https://www.ncbi.nlm.nih.gov/sra?term=SRP142438 [Overal design]Polysome and input RNA samples were sequenced from two replicate experiments. In each experiment HCC1806 cells were transfected with either pcDNA5 (vector control), pcDNA 5 HA-CMTR1 WT (wildtype CMTR1) or pcDNA 5 HA-CMTR1 2L/A mutant (mutant CMTR1 that does not interact with DHX15).; [Treatment]'Cells in 10 cm dishes were transfected with either pcDNA5 (vector control), pcDNA 5 HA-CMTR1 WT (wildtype CMTR1) or pcDNA 5 HA-CMTR1 2L/A mutant (mutant CMTR1 that does not interact with DHX15) using polyethylenimine (Polysciences). Cells were cultured for 36 hours before harvesting.'; [Growth]'Cultured in RPMI with 10% (v/v) Foetal Bovine Serum, 100U/ml penicillin, 0.1mg/ml streptomycin and 2mM L-glutamine.'; [Extraction]'Cells were incubated in 100 μg/ml cycloheximide for 10 min, washed in ice cold PBS supplemented with 100 μg/ml cycloheximide and extracts collected in polysome lysis buffer (15mM Tris (pH7.5), 15mM MgCl2, 0.3 M NaCl, 1 mM DTT, 1% Triton X-100, 100 mg/ml cycloheximide, 100 U/ml RNasin). 10% of the extracts were retained as input and 90% resolved by centrifugation through a 10 ml 10%–50% sucrose gradient at 18 000 x g for 2 hr at 4oC. Fractions were collected on FoxyR1 fractionator (Teledyne ISCO) with OD259 nm monitoring. Polysomal fractions 16-20 were purified by Phenol:Chloroform:Isoamyl Alcohol (25:24:1). RNA was precipitated overnight with 2M of LiCl, 20mM Tris pH 7.5, EDTA 10mM. Input RNA was purified using Trizol Reagent. RNA was quality checked using a TapeStation (Agilent Technologies).\nTruSeq Stranded Total RNA with Ribo-Zero-Gold kit (Illumina). Sequencing was performed using NextSeq Series High Output Kit 2 × 75 bp (Illumina).'; [Cell type]'Breast carcinoma''cell harvest date: 2016-08-11; transfected with: Empty vector; cell type: Breast carcinoma; cell line: HCC1806; ', 'cell harvest date: 2016-08-11; transfected with: HA CMTR1 WT; cell type: Breast carcinoma; cell line: HCC1806; ', 'cell harvest date: 2016-08-11; transfected with: HA CMTR1 2L/A; cell type: Breast carcinoma; cell line: HCC1806; ', 'cell harvest date: 2016-08-12; transfected with: Empty vector; cell type: Breast carcinoma; cell line: HCC1806; ', 'cell harvest date: 2016-08-12; transfected with: HA CMTR1 WT; cell type: Breast carcinoma; cell line: HCC1806; ', 'cell harvest date: 2016-08-12; transfected with: HA CMTR1 2L/A; cell type: Breast carcinoma; cell line: HCC1806; ' GSE55886 Mus musculus 8 Expression profiling by array GPL11533 Effect of Spot14 Loss on Gene Expression Profile of MMTV-PyMT Mouse Tumors 2014-03-13 The objective of this study was to determine the effect of Thyroid Hormone Responsive Protein Spot14 (Spot14) loss on the gene expression profiles of tumors from MMTV-Polyomavirus middle-T antigen (PyMT) mice. MMTV-PyMT/S14-heterozygous mice were crossed with S14-heterozygous mice and 1 cm tumors from MMTV-PyMT control (wild-type S14) or MMTV-PyMT/S14-null offspring were profiled using Affymetrix gene arrays. Tumor latency was not different between groups; however, tumors lacking S14 grew significantly slower than control tumors. Loss of S14 also decreased the levels of de novo synthesized fatty acids in mammary tumors. In additional studies, performed on MMTV-Neu mice, we found that S14 overexpression was associated with increased tumor cell proliferation and elevated levels of tumor fatty acids. Gene expression profiling revealed that S14 loss and overexpression in mouse mammary tumors altered pathways associated with proliferation and metabolism. This study provides important information about the role of S14 in mammary tumorigenesis and tumor metabolism. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55886 Modulation of tumor fatty acids, through overexpression or loss of thyroid hormone responsive protein spot 14 is associated with altered growth and metastasis. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-014-0481-z {Breast cancer research : BCR (5.676): 10.1186/s13058-014-0481-z} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA241245 https://www.ebi.ac.uk/ena/browser/view/PRJNA241245 None [Overal design]Microarray analysis was performed on 4 mammary tumors from MMTV-PyMT mice and 4 tumors from MMTV-PyMT/S14-null mice.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted using Trizol (Invitrogen) and the RNEasy mini kit (Qiagen) with on-column DNAse digestion was used following Trizol extraction. 100ng total RNA per sample was used for array analysis.'; [Cell type]'Source: ''strain: FVB/N; genotype: PyMT; ', 'strain: FVB/N; genotype: PyMT/S14-null; ' GSE62327 Homo sapiens 24 Expression profiling by array GPL14951 Gene expression profiling of primary HER2-positive breast cancers treated with neoadjuvant trastuzumab 2014-10-14 Trastuzumab, a humanized monoclonal antibody directed to the HER2 protein, is the standard-of-care treatment for patients with HER2 positive breast cancer, reducing the risk of relapse and death in patients. Nonetheless, some patients do not benefit from this treatment, underscoring the need to identify patients for whom chemotherapy + trastuzumab is adequate versus patients requiring additional drugs. The series comprised 24 incisional biopsies of breast carcinomas derived from patients that received neoadjuvant trastuzumab based therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE62327 Whole-transcriptome analysis links trastuzumab sensitivity of breast tumors to both HER2 dependence and immune cell infiltration. Oncotarget None https://doi.org/10.18632/oncotarget.4405 {Oncotarget (None): 10.18632/oncotarget.4405} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA263833 https://www.ebi.ac.uk/ena/browser/view/PRJNA263833 None [Overal design]Gene expression profiling was performed using RNA from frozen core biopsies from 24 patients with primary HER2-positive (HER2+) tumors treated with neoadjuvant chemotherapy and trastuzumab.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''tumor size: T2; lymph node status: NA; grade: III; response: PR; tissue: breast cancer tumor; ', 'tumor size: T2; lymph node status: neg; grade: III; response: PR; tissue: breast cancer tumor; ', 'tumor size: T2; lymph node status: neg; grade: III; response: CR; tissue: breast cancer tumor; ', 'tumor size: T2; lymph node status: pos; grade: III; response: CR; tissue: breast cancer tumor; ', 'tumor size: T2; lymph node status: pos; grade: III; response: PR; tissue: breast cancer tumor; ', 'tumor size: T3; lymph node status: pos; grade: III; response: PR; tissue: breast cancer tumor; ', 'tumor size: T4; lymph node status: NA; grade: III; response: PR; tissue: breast cancer tumor; ', 'tumor size: T3; lymph node status: NA; grade: II; response: CR; tissue: breast cancer tumor; ', 'tumor size: T2; lymph node status: neg; grade: I; response: PR; tissue: breast cancer tumor; ', 'tumor size: T2; lymph node status: NA; grade: III; response: CR; tissue: breast cancer tumor; ', 'tumor size: T2; lymph node status: neg; grade: II; response: PR; tissue: breast cancer tumor; ', 'tumor size: T1; lymph node status: neg; grade: II; response: PR; tissue: breast cancer tumor; ', 'tumor size: T3; lymph node status: neg; grade: III; response: PR; tissue: breast cancer tumor; ', 'tumor size: T2; lymph node status: pos; grade: II; response: PR; tissue: breast cancer tumor; ', 'tumor size: T1; lymph node status: neg; grade: III; response: PR; tissue: breast cancer tumor; ' GSE37405 Homo sapiens 153 Non-coding RNA profiling by array GPL13703; GPL14149; GPL15462 Global microRNA expression profiling of high-risk ER+ breast cancers from patients receiving adjuvant Tamoxifen mono-therapy: a DBCG study 2012-04-18 Purpose: Despite the benefits of estrogen receptor (ER)-targeted endocrine therapies in breast cancer, many tumors develop resistance. MicroRNAs (miRNAs) have been suggested as promising biomarkers and we here evaluated whether a miRNA profile could be identified, sub-grouping ER+ breast cancer patients treated with adjuvant Tamoxifen with regards to probability of recurrence. Experimental design: Global miRNA analysis was performed on 152 ER+ primary tumors from high-risk breast cancer patients with an initial discovery set of 52 patients, followed by 2 independent test sets (N=60 and N=40). All patients had received adjuvant Tamoxifen as mono-therapy (median clinical follow-up: 4.6 years) and half had developed distant recurrence (median time-to-recurrence: 3.5 years). MiRNA expression was examined by unsupervised hierarchical clustering and supervised analysis, including clinical parameters as co-variables. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37405 Global microRNA expression profiling of high-risk ER+ breast cancers from patients receiving adjuvant tamoxifen mono-therapy: a DBCG study. PloS one 2.776 https://doi.org/10.1371/journal.pone.0036170 {PloS one (2.776) doi:10.1371/journal.pone.0036170}; {Oncotarget (None) doi:10.18632/oncotarget.11136}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA159897 https://www.ebi.ac.uk/ena/browser/view/PRJNA159897 None [Overal design]3 parts of microRNA profiling of ER+ breast cancer samples; [Treatment]'All patients had archival formalin-fixed, paraffin-embedded, (FFPE) tumor tissue stored in the dark'; [Growth]'None'; [Extraction]'Five sections of 10 μm were de-paraffinized and total RNA was extracted with Roche high pure kit according to the manufacturer’s protocol (Roche, Basel, Switzerland).'; [Cell type]'Source: ''slide id: 13854627; age at op: 74; size (mm): 32; er-status: 90; pgr-status: 5; nodal-status, positive: 0; nodal-status, total removed: 12; duration of tamoxifen (years): 0.91; time.to.ok: 0.91; time.to.recurrence (years): .; time.to.death (years): 1.6; ', 'slide id: 13854628; age at op: 57; size (mm): 25; er-status: 100; pgr-status: 95; nodal-status, positive: 1; nodal-status, total removed: 10; duration of tamoxifen (years): 1.87; time.to.ok: 10.11; time.to.recurrence (years): .; time.to.death (years): .; ', 'slide id: 13854630; age at op: 53; size (mm): 20; er-status: NA; pgr-status: NA; nodal-status, positive: 1; nodal-status, total removed: 16; duration of tamoxifen (years): 0.94; time.to.ok: 5.20; time.to.recurrence (years): .; time.to.death (years): 5.7; ', 'slide id: 13854631; age at op: 51; size (mm): 25; er-status: 60; pgr-status: 1; nodal-status, positive: 1; nodal-status, total removed: 24; duration of tamoxifen (years): 4.99; time.to.ok: 4.99; time.to.recurrence (years): .; ', 'slide id: 13854632; age at op: 67; size (mm): 38; er-status: 100; pgr-status: 0; nodal-status, positive: 1; nodal-status, total removed: 7; duration of tamoxifen (years): 0.82; time.to.ok: 3.88; time.to.recurrence (years): .; ', 'slide id: 13854633; age at op: 73; size (mm): 40; er-status: IHC+; pgr-status: 90; nodal-status, positive: 1; nodal-status, total removed: 9; duration of tamoxifen (years): 0.84; time.to.ok: 7.50; time.to.recurrence (years): .; ', 'slide id: 13854634; age at op: 73; size (mm): 28; er-status: 100; pgr-status: 100; nodal-status, positive: 2; nodal-status, total removed: 19; duration of tamoxifen (years): 4.38; time.to.ok: 4.38; time.to.recurrence (years): .; ', 'slide id: 13854635; age at op: 58; size (mm): 22; er-status: 90; pgr-status: 90; nodal-status, positive: 2; nodal-status, total removed: 9; duration of tamoxifen (years): 0.83; time.to.ok: 5.68; time.to.recurrence (years): .; ', 'slide id: 13854636; age at op: 50; size (mm): 28; er-status: 15; pgr-status: 90; nodal-status, positive: 8; nodal-status, total removed: 15; duration of tamoxifen (years): 1.86; time.to.ok: 10.16; time.to.recurrence (years): .; ', 'slide id: 13854637; age at op: 67; size (mm): 29; er-status: 95; pgr-status: 25; nodal-status, positive: 9; nodal-status, total removed: 15; duration of tamoxifen (years): 4.92; time.to.ok: 4.92; time.to.recurrence (years): .; ', 'slide id: 13854638; age at op: 54; size (mm): 21; er-status: 100; pgr-status: 100; nodal-status, positive: 10; nodal-status, total removed: 24; duration of tamoxifen (years): 1.98; time.to.ok: 5.23; time.to.recurrence (years): .; ', 'slide id: 13854730; age at op: 64; size (mm): 60; er-status: 100; pgr-status: 90; nodal-status, positive: 10; nodal-status, total removed: 14; time.to.ok: 0.95; time.to.recurrence (years): .; time.to.death (years): 4.47123287671233; ', 'slide id: 13854731; age at op: 71; size (mm): 40; er-status: 95; pgr-status: 0; nodal-status, positive: 13; nodal-status, total removed: 20; duration of tamoxifen (years): 1.90; time.to.ok: 7.07; time.to.recurrence (years): .; ', 'slide id: 13854732; age at op: 61; size (mm): 40; er-status: B+; pgr-status: B+; nodal-status, positive: 13; nodal-status, total removed: 18; duration of tamoxifen (years): 1.90; time.to.ok: 6.25; time.to.recurrence (years): .; time.to.death (years): 7.35068493150685; ', 'slide id: 13854733; age at op: 64; size (mm): 27; er-status: 100; pgr-status: 95; nodal-status, positive: 1; nodal-status, total removed: 17; duration of tamoxifen (years): 0.85; time.to.ok: 4.61; time.to.recurrence (years): .; ', 'slide id: 13854734; age at op: 56; size (mm): 22; er-status: 100; pgr-status: 50; nodal-status, positive: 12; nodal-status, total removed: 14; duration of tamoxifen (years): 0.86; time.to.ok: 9.25; time.to.recurrence (years): .; time.to.death (years): 10.5068493150685; ', 'slide id: 13854735; age at op: 71; size (mm): 20; er-status: 50; pgr-status: 100; nodal-status, positive: 5; nodal-status, total removed: 14; duration of tamoxifen (years): 4.61; time.to.ok: 5.12; time.to.recurrence (years): .; ', 'slide id: 13854748; age at op: 65; size (mm): 26; er-status: 100; pgr-status: 0; nodal-status, positive: 5; nodal-status, total removed: 7; duration of tamoxifen (years): 0.85; time.to.ok: 10.33; time.to.recurrence (years): .; ', 'slide id: 13854751; age at op: 57; size (mm): 25; er-status: 100; pgr-status: 45; nodal-status, positive: 2; nodal-status, total removed: 13; duration of tamoxifen (years): 0.92; time.to.ok: 1.44; time.to.recurrence (years): .; ', 'slide id: 13854737; age at op: 57; nodal-status, positive: 1; time.to.recurrence (years): .; ', 'slide id: 13854738; age at op: 55; size (mm): 25; er-status: 100; pgr-status: 100; nodal-status, positive: 7; nodal-status, total removed: 12; duration of tamoxifen (years): 3.97; time.to.ok: 3.97; time.to.recurrence (years): .; ', 'slide id: 13854739; age at op: 64; size (mm): 95; er-status: 90; pgr-status: IHC-; nodal-status, positive: 1; nodal-status, total removed: 18; duration of tamoxifen (years): 0.85; time.to.ok: 6.48; time.to.recurrence (years): .; ', 'slide id: 13854740; age at op: 66; size (mm): 15; er-status: NA; pgr-status: NA; nodal-status, positive: 1; nodal-status, total removed: 14; duration of tamoxifen (years): 0.83; time.to.ok: 0.83; time.to.recurrence (years): .; ', 'slide id: 13854741; age at op: 49; size (mm): 15; er-status: 90; pgr-status: 100; nodal-status, positive: 4; nodal-status, total removed: 18; duration of tamoxifen (years): 0.73; time.to.ok: 6.01; time.to.recurrence (years): .; ', 'slide id: 13854744; age at op: 73; size (mm): 14; er-status: 100; pgr-status: 50; nodal-status, positive: 6; nodal-status, total removed: 21; duration of tamoxifen (years): 4.62; time.to.ok: 5.14; time.to.recurrence (years): .; ', 'slide id: 13854746; age at op: 74; size (mm): 25; er-status: 28; pgr-status: 0; nodal-status, total removed: 16; duration of tamoxifen (years): 0.81; time.to.ok: 6.09; time.to.recurrence (years): .; ', 'slide id: 13854707; age at op: 66; size (mm): 80; er-status: 90; pgr-status: 7; nodal-status, positive: 0; nodal-status, total removed: 13; duration of tamoxifen (years): 0.84; time.to.ok: .; time.to.recurrence (years): 1.53; time.to.death (years): 2.67; ', 'slide id: 13854708; age at op: 69; size (mm): 25; er-status: 95; pgr-status: 0; nodal-status, positive: 1; nodal-status, total removed: 12; duration of tamoxifen (years): 2.03; time.to.ok: .; time.to.recurrence (years): 2.16; time.to.death (years): 2.44; ', 'slide id: 13854709; age at op: 54; size (mm): 22; er-status: 90; pgr-status: 65; nodal-status, positive: 1; nodal-status, total removed: 13; duration of tamoxifen (years): 2.84; time.to.ok: .; time.to.recurrence (years): 3.72; time.to.death (years): 4.50; ', 'slide id: 13854721; age at op: 61; size (mm): 20; er-status: IHC+; pgr-status: IHC+; nodal-status, positive: 1; nodal-status, total removed: 9; duration of tamoxifen (years): 2.31; time.to.ok: .; time.to.recurrence (years): 2.83; time.to.death (years): 3.41; ', 'slide id: 13854722; age at op: 51; size (mm): 28; er-status: 95; pgr-status: 80; nodal-status, positive: 1; nodal-status, total removed: 13; duration of tamoxifen (years): 5.09; time.to.ok: .; time.to.recurrence (years): 5.54; time.to.death (years): 6.10; ', 'slide id: 13854723; age at op: 59; size (mm): 40; er-status: 100; pgr-status: 85; nodal-status, positive: 1; nodal-status, total removed: 30; duration of tamoxifen (years): 1.87; time.to.ok: .; time.to.recurrence (years): 2.78; time.to.death (years): 3.93; ', 'slide id: 13854724; age at op: 73; size (mm): 32; er-status: 95; pgr-status: 95; nodal-status, positive: 1; nodal-status, total removed: 7; duration of tamoxifen (years): 1.08; time.to.ok: .; time.to.recurrence (years): 1.51; time.to.death (years): 3.45; ', 'slide id: 13854752; age at op: 48; size (mm): 80; er-status: 90; pgr-status: 25; nodal-status, positive: 2; nodal-status, total removed: 15; duration of tamoxifen (years): 3.04; time.to.ok: .; time.to.recurrence (years): 3.17; ', 'slide id: 13854753; age at op: 59; size (mm): 24; er-status: B+; pgr-status: B+; nodal-status, positive: 2; nodal-status, total removed: 18; duration of tamoxifen (years): 1.07; time.to.ok: .; time.to.recurrence (years): 2.08; time.to.death (years): 2.78; ', 'slide id: 13854727; age at op: 48; size (mm): 28; er-status: 100; pgr-status: 80; nodal-status, positive: 6; nodal-status, total removed: 15; duration of tamoxifen (years): 1.84; time.to.ok: .; time.to.recurrence (years): 2.40; ', 'slide id: 13854728; age at op: 52; size (mm): 32; er-status: 100; pgr-status: 70; nodal-status, positive: 7; nodal-status, total removed: 16; duration of tamoxifen (years): 4.92; time.to.ok: .; time.to.recurrence (years): 8.66; ', 'slide id: 13854729; age at op: 48; size (mm): 18; er-status: 85; pgr-status: 100; nodal-status, positive: 12; nodal-status, total removed: 22; duration of tamoxifen (years): 1.03; time.to.ok: .; time.to.recurrence (years): 1.16; time.to.death (years): 2.64; ', 'slide id: 13854614; age at op: 62; size (mm): 24; er-status: 0; pgr-status: 90; nodal-status, positive: 10; nodal-status, total removed: 13; duration of tamoxifen (years): 1.84; time.to.ok: .; time.to.recurrence (years): 6.05; time.to.death (years): 8.45; ', 'slide id: 13854747; age at op: 63; size (mm): 30; er-status: 100; pgr-status: 0; nodal-status, positive: 12; nodal-status, total removed: 27; duration of tamoxifen (years): 1.60; time.to.ok: .; time.to.recurrence (years): 1.65; time.to.death (years): 2.79; ', 'slide id: 13854615; time.to.ok: .; ', 'slide id: 13854616; age at op: 70; size (mm): 80; er-status: 90; pgr-status: 10; nodal-status, positive: 11; nodal-status, total removed: 16; duration of tamoxifen (years): 2.85; time.to.ok: .; time.to.recurrence (years): 3.23; time.to.death (years): 5.35; ', 'slide id: 13854617; age at op: 63; size (mm): 35; er-status: 100; pgr-status: 100; nodal-status, positive: 1; nodal-status, total removed: 14; duration of tamoxifen (years): 1.10; time.to.ok: .; time.to.recurrence (years): 8.70; ', 'slide id: 13854618; age at op: 57; size (mm): 85; er-status: 75; pgr-status: 5; nodal-status, positive: 13; nodal-status, total removed: 18; duration of tamoxifen (years): 0.59; time.to.ok: .; time.to.recurrence (years): 0.67; time.to.death (years): 2.34; ', 'slide id: 13854620; age at op: 56; size (mm): 21; er-status: 50; pgr-status: 0; nodal-status, positive: 7; nodal-status, total removed: 12; duration of tamoxifen (years): 1.58; time.to.ok: .; time.to.recurrence (years): 2.01; time.to.death (years): 4.32; ', 'slide id: 13854755; age at op: 72; size (mm): 22; er-status: 100; pgr-status: 100; nodal-status, positive: 7; nodal-status, total removed: 21; duration of tamoxifen (years): 0.82; time.to.ok: .; time.to.recurrence (years): 1.82; time.to.death (years): 5.22; ', 'slide id: 13854622; age at op: 54; size (mm): 35; er-status: 100; pgr-status: 25; nodal-status, positive: 2; nodal-status, total removed: 25; duration of tamoxifen (years): 0.87; time.to.ok: .; time.to.recurrence (years): 2.17; ', 'slide id: 13854623; age at op: 70; size (mm): 24; er-status: 95; pgr-status: 85; nodal-status, positive: 1; nodal-status, total removed: 22; duration of tamoxifen (years): 4.60; time.to.ok: .; time.to.recurrence (years): 3.48; ', 'slide id: 13854624; age at op: 56; size (mm): 35; er-status: IHC+; pgr-status: IHC-; nodal-status, positive: 8; nodal-status, total removed: 17; duration of tamoxifen (years): 0.82; time.to.ok: .; time.to.recurrence (years): 1.37; time.to.death (years): 2.99; ', 'slide id: 13854625; age at op: 52; size (mm): 18; er-status: B+; pgr-status: B+; nodal-status, positive: 1; nodal-status, total removed: 19; duration of tamoxifen (years): 0.58; time.to.ok: .; time.to.recurrence (years): 2.90; time.to.death (years): 3.91; ', 'slide id: 13854626; age at op: 61; size (mm): 12; er-status: 100; pgr-status: 75; nodal-status, positive: 1; nodal-status, total removed: 11; duration of tamoxifen (years): 0.82; time.to.ok: .; time.to.recurrence (years): 7.52; ', 'slide id: 13854742; age at op: 56; size (mm): 12; er-status: 90; pgr-status: 90; nodal-status, positive: 4; nodal-status, total removed: 15; duration of tamoxifen (years): 0.33; time.to.ok: .; time.to.recurrence (years): 3.97; ', 'slide id: 13854743; age at op: 58; size (mm): 20; er-status: 80; pgr-status: 70; nodal-status, positive: 9; nodal-status, total removed: 10; duration of tamoxifen (years): 0.81; time.to.recurrence (years): 5.13; time.to.death (years): 5.98; ', 'age at op: 63; size (mm): 35; er-status: 100; pgr-status: 70; nodal-status, positive: 0; nodal-status, total removed: 7; duration of tamoxifen (years): 2.34; time.to.ok: 5.22; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 52; size (mm): 20; er-status: B+; pgr-status: B+; nodal-status, positive: 3; nodal-status, total removed: 19; duration of tamoxifen (years): 0.85; time.to.ok: 11.00; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 68; size (mm): 50; er-status: IHC+; pgr-status: IHC+; nodal-status, positive: 1; nodal-status, total removed: 19; duration of tamoxifen (years): 1.80; time.to.ok: 2.31; time.to.recurrence (years): .; time.to.death (years): 2.58; data set (out of 3): 2; ', 'age at op: 57; size (mm): 24; er-status: IHC+; pgr-status: IHC+; nodal-status, positive: 1; nodal-status, total removed: 16; duration of tamoxifen (years): 0.96; time.to.ok: 6.07; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 62; size (mm): 29; er-status: B+; pgr-status: B-; nodal-status, positive: 1; nodal-status, total removed: 12; duration of tamoxifen (years): 0.86; time.to.ok: 9.63; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 64; size (mm): 14; er-status: B+; pgr-status: B+; nodal-status, positive: 1; nodal-status, total removed: 20; duration of tamoxifen (years): 0.91; time.to.ok: 4.35; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 62; size (mm): 20; er-status: 95; pgr-status: 85; nodal-status, positive: 2; nodal-status, total removed: 11; duration of tamoxifen (years): 5.27; time.to.ok: 5.27; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 65; size (mm): 29; er-status: B+; pgr-status: B+; nodal-status, positive: 1; nodal-status, total removed: 4; duration of tamoxifen (years): 1.87; time.to.ok: 2.14; time.to.recurrence (years): .; time.to.death (years): 10.78; data set (out of 3): 2; ', 'age at op: 53; size (mm): 25; er-status: 80; pgr-status: 10; nodal-status, positive: 1; nodal-status, total removed: 18; duration of tamoxifen (years): 1.33; time.to.ok: 5.30; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 52; size (mm): 20; er-status: 90; pgr-status: 90; nodal-status, positive: 1; nodal-status, total removed: 8; duration of tamoxifen (years): 0.83; time.to.ok: 5.11; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 63; size (mm): 55; er-status: B+; pgr-status: B+; nodal-status, positive: 1; nodal-status, total removed: 14; duration of tamoxifen (years): 0.84; time.to.ok: 11.28; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 62; size (mm): 8; er-status: 95; pgr-status: 60; nodal-status, positive: 1; nodal-status, total removed: 15; duration of tamoxifen (years): 0.83; time.to.ok: 3.35; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 58; size (mm): 15; er-status: IHC+; pgr-status: IHC-; nodal-status, positive: 2; nodal-status, total removed: 11; duration of tamoxifen (years): 1.95; time.to.ok: 5.16; time.to.recurrence (years): .; time.to.death (years): 6.82; data set (out of 3): 2; ', 'age at op: 63; size (mm): 38; er-status: 80; pgr-status: 50; nodal-status, positive: 7; nodal-status, total removed: 16; duration of tamoxifen (years): 1.82; time.to.ok: 5.19; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 72; size (mm): 26; er-status: 80; pgr-status: 60; nodal-status, positive: 6; nodal-status, total removed: 16; duration of tamoxifen (years): 4.30; time.to.ok: 5.05; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 64; size (mm): 20; er-status: IHC-; pgr-status: 50; nodal-status, positive: 8; nodal-status, total removed: 15; duration of tamoxifen (years): 1.84; time.to.ok: 4.28; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 57; size (mm): 22; er-status: IHC-; pgr-status: 90; nodal-status, positive: 1; nodal-status, total removed: 10; duration of tamoxifen (years): 0.92; time.to.ok: 5.30; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 67; size (mm): 58; er-status: IHC-; pgr-status: 80; nodal-status, positive: 3; nodal-status, total removed: 18; duration of tamoxifen (years): 0.83; time.to.ok: 5.16; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 67; size (mm): 20; er-status: 80; pgr-status: 0; nodal-status, positive: 1; nodal-status, total removed: 14; duration of tamoxifen (years): 0.88; time.to.ok: 2.16; time.to.recurrence (years): .; time.to.death (years): 4.68; data set (out of 3): 2; ', 'age at op: 54; size (mm): 20; er-status: 90; pgr-status: 90; nodal-status, positive: 7; nodal-status, total removed: 14; duration of tamoxifen (years): 1.08; time.to.ok: 7.01; time.to.recurrence (years): .; time.to.death (years): 7.54; data set (out of 3): 2; ', 'age at op: 60; size (mm): 25; er-status: 70; pgr-status: IHC-; nodal-status, positive: 5; nodal-status, total removed: 13; duration of tamoxifen (years): 4.57; time.to.ok: 5.10; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 72; size (mm): 19; er-status: 90; pgr-status: 0; nodal-status, positive: 4; nodal-status, total removed: 9; duration of tamoxifen (years): 1.78; time.to.ok: 3.33; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 65; size (mm): 15; er-status: B+; pgr-status: B+; nodal-status, positive: 2; nodal-status, total removed: 12; duration of tamoxifen (years): 1.07; time.to.ok: NA; time.to.recurrence (years): .; time.to.death (years): 5.36; data set (out of 3): 2; ', 'age at op: 68; size (mm): 25; er-status: B+; pgr-status: NA; nodal-status, positive: 1; nodal-status, total removed: 13; duration of tamoxifen (years): 1.98; time.to.ok: 8.70; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 65; size (mm): 18; er-status: 80; pgr-status: 90; nodal-status, positive: 1; nodal-status, total removed: 20; duration of tamoxifen (years): 1.69; time.to.ok: 4.99; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 67; size (mm): 27; er-status: 90; pgr-status: 90; nodal-status, positive: 1; nodal-status, total removed: 9; duration of tamoxifen (years): 0.85; time.to.ok: 1.63; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 69; size (mm): 20; er-status: 55; pgr-status: 55; nodal-status, positive: 1; nodal-status, total removed: 13; duration of tamoxifen (years): 0.85; time.to.ok: 5.29; time.to.recurrence (years): .; time.to.death (years): 5.85; data set (out of 3): 2; ', 'age at op: 67; size (mm): 20; er-status: IHC+; pgr-status: IHC+; nodal-status, positive: 5; nodal-status, total removed: 20; duration of tamoxifen (years): 0.96; time.to.ok: 7.27; time.to.recurrence (years): .; time.to.death (years): 9.21; data set (out of 3): 2; ', 'age at op: 61; size (mm): 20; er-status: 83; pgr-status: 83; nodal-status, positive: 6; nodal-status, total removed: 16; duration of tamoxifen (years): 0.94; time.to.ok: 5.09; time.to.recurrence (years): .; time.to.death (years): 5.69; data set (out of 3): 2; ', 'age at op: 63; size (mm): 50; er-status: B+; pgr-status: B+; nodal-status, positive: 14; nodal-status, total removed: 31; duration of tamoxifen (years): 0.86; time.to.ok: 7.67; time.to.recurrence (years): .; data set (out of 3): 2; ', 'age at op: 68; size (mm): 14; er-status: B+; pgr-status: B-; nodal-status, positive: 11; nodal-status, total removed: 17; duration of tamoxifen (years): 0.84; time.to.ok: .; time.to.recurrence (years): 5.08; time.to.death (years): 9.90; data set (out of 3): 2; ', 'age at op: 65; size (mm): 45; er-status: 93; pgr-status: IHC-; nodal-status, positive: 19; nodal-status, total removed: 21; duration of tamoxifen (years): 0.83; time.to.ok: .; time.to.recurrence (years): 3.40; time.to.death (years): 4.27; data set (out of 3): 2; ', 'age at op: 63; size (mm): 20; er-status: 75; pgr-status: 0; nodal-status, positive: 2; nodal-status, total removed: 8; duration of tamoxifen (years): 2.20; time.to.ok: .; time.to.recurrence (years): 1.73; time.to.death (years): 2.63; data set (out of 3): 2; ', 'age at op: 51; size (mm): 22; er-status: 60; pgr-status: 5; nodal-status, positive: 14; nodal-status, total removed: 25; duration of tamoxifen (years): 0.83; time.to.ok: .; time.to.recurrence (years): 1.55; time.to.death (years): 4.67; data set (out of 3): 2; ', 'age at op: 57; size (mm): 34; er-status: NA; pgr-status: NA; nodal-status, positive: 18; nodal-status, total removed: 28; duration of tamoxifen (years): 1.25; time.to.ok: .; time.to.recurrence (years): 1.34; time.to.death (years): 2.43; data set (out of 3): 2; ', 'age at op: 53; size (mm): 24; er-status: 90; pgr-status: 90; nodal-status, positive: 2; nodal-status, total removed: 21; duration of tamoxifen (years): 1.11; time.to.ok: .; time.to.recurrence (years): 1.11; data set (out of 3): 2; ', 'age at op: 62; size (mm): 20; er-status: 80; pgr-status: 5; nodal-status, positive: 12; nodal-status, total removed: 19; duration of tamoxifen (years): 1.07; time.to.ok: .; time.to.recurrence (years): 1.30; time.to.death (years): 3.83; data set (out of 3): 2; ', 'age at op: 54; size (mm): 60; er-status: 50; pgr-status: 20; nodal-status, positive: 2; nodal-status, total removed: 20; duration of tamoxifen (years): 1.96; time.to.ok: .; time.to.recurrence (years): 4.52; time.to.death (years): 6.19; data set (out of 3): 2; ', 'age at op: 66; size (mm): 27; er-status: 80; pgr-status: 2; nodal-status, positive: 9; nodal-status, total removed: 23; duration of tamoxifen (years): 2.07; time.to.ok: .; time.to.recurrence (years): 2.07; time.to.death (years): 3.04; data set (out of 3): 2; ', 'age at op: 65; size (mm): 28; er-status: IHC+; pgr-status: IHC+; nodal-status, positive: 10; nodal-status, total removed: 20; duration of tamoxifen (years): 0.89; time.to.ok: .; time.to.recurrence (years): 2.16; time.to.death (years): 5.09; data set (out of 3): 2; ', 'age at op: 51; size (mm): 40; er-status: 95; pgr-status: 95; nodal-status, positive: 3; nodal-status, total removed: 24; duration of tamoxifen (years): 4.80; time.to.ok: .; time.to.recurrence (years): 8.21; data set (out of 3): 2; ', 'age at op: 66; size (mm): 40; er-status: B+; pgr-status: B+; nodal-status, positive: 2; nodal-status, total removed: 13; duration of tamoxifen (years): 0.91; time.to.ok: .; time.to.recurrence (years): 7.03; time.to.death (years): 10.46; data set (out of 3): 2; ', 'age at op: 62; size (mm): 60; er-status: 95; pgr-status: 2; nodal-status, positive: 3; nodal-status, total removed: 14; duration of tamoxifen (years): 1.58; time.to.ok: .; time.to.recurrence (years): 2.08; time.to.death (years): 3.42; data set (out of 3): 2; ', 'age at op: 56; size (mm): 22; er-status: 95; pgr-status: 10; nodal-status, positive: 9; nodal-status, total removed: 16; duration of tamoxifen (years): 1.55; time.to.ok: .; time.to.recurrence (years): 1.62; time.to.death (years): 3.65; data set (out of 3): 2; ', 'age at op: 49; size (mm): 28; er-status: 20; pgr-status: 2; nodal-status, positive: 1; nodal-status, total removed: 18; duration of tamoxifen (years): 4.57; time.to.ok: .; time.to.recurrence (years): 4.57; data set (out of 3): 2; ', 'age at op: 61; size (mm): 19; er-status: 65; pgr-status: 65; nodal-status, positive: 29; nodal-status, total removed: 37; duration of tamoxifen (years): 0.86; time.to.ok: .; time.to.recurrence (years): 4.88; time.to.death (years): 5.37; data set (out of 3): 2; ', 'age at op: 63; size (mm): 34; er-status: 100; pgr-status: 95; nodal-status, positive: 6; nodal-status, total removed: 10; duration of tamoxifen (years): 4.36; time.to.ok: .; time.to.recurrence (years): 4.36; data set (out of 3): 2; ', 'age at op: 63; size (mm): 31; er-status: B+; pgr-status: B+; nodal-status, positive: 11; nodal-status, total removed: 20; duration of tamoxifen (years): 1.04; time.to.ok: .; time.to.recurrence (years): 1.31; time.to.death (years): 2.38; data set (out of 3): 2; ', 'age at op: 68; size (mm): 18; er-status: 25; pgr-status: 0; nodal-status, positive: 12; nodal-status, total removed: 20; duration of tamoxifen (years): 1.87; time.to.ok: .; time.to.recurrence (years): 5.76; time.to.death (years): 6.09; data set (out of 3): 2; ', 'age at op: 63; size (mm): 14; er-status: 75; pgr-status: 75; nodal-status, positive: 9; nodal-status, total removed: 14; duration of tamoxifen (years): 1.87; time.to.ok: .; time.to.recurrence (years): 2.19; data set (out of 3): 2; ', 'age at op: 69; size (mm): 60; er-status: IHC+; pgr-status: IHC+; nodal-status, positive: 3; nodal-status, total removed: 16; duration of tamoxifen (years): 1.81; time.to.ok: .; time.to.recurrence (years): 6.08; time.to.death (years): 8.56; data set (out of 3): 2; ', 'age at op: 66; size (mm): 20; er-status: B+; pgr-status: B+; nodal-status, positive: 11; nodal-status, total removed: 26; duration of tamoxifen (years): 0.84; time.to.ok: .; time.to.recurrence (years): 3.62; time.to.death (years): 6.92; data set (out of 3): 2; ', 'age at op: 70; size (mm): 27; er-status: 90; pgr-status: IHC-; nodal-status, positive: 3; nodal-status, total removed: 8; duration of tamoxifen (years): 1.02; time.to.ok: .; time.to.recurrence (years): 4.41; time.to.death (years): 5.36; data set (out of 3): 2; ', 'age at op: 60; size (mm): 80; er-status: IHC-; pgr-status: IHC+; nodal-status, positive: 1; nodal-status, total removed: 17; duration of tamoxifen (years): 0.83; time.to.ok: .; time.to.recurrence (years): 0.83; data set (out of 3): 2; ', 'age at op: 62; size (mm): 40; er-status: B+; pgr-status: B+; nodal-status, positive: 14; nodal-status, total removed: 31; duration of tamoxifen (years): 1.07; time.to.ok: .; time.to.recurrence (years): 14.93; data set (out of 3): 2; ', 'age at op: 67; size (mm): 16; er-status: 90; pgr-status: 0; nodal-status, positive: 2; nodal-status, total removed: 19; duration of tamoxifen (years): 0.85; time.to.ok: .; time.to.recurrence (years): 0.85; data set (out of 3): 2; ', 'age at op: 61; size (mm): 45; er-status: B+; pgr-status: B+; nodal-status, positive: 11; nodal-status, total removed: 11; duration of tamoxifen (years): 1.04; time.to.ok: .; time.to.recurrence (years): 2.36; time.to.death (years): 4.73; data set (out of 3): 2; ', 'age at op: 64; size (mm): 7; er-status: 100; pgr-status: 70; nodal-status, positive: 6; nodal-status, total removed: 9; duration of tamoxifen (years): 5.23; time.to.ok: .; time.to.recurrence (years): 6.57; time.to.death (years): 7.20; data set (out of 3): 2; ', 'age at op: 59; size (mm): 35; er-status: B+; pgr-status: B+; nodal-status, positive: 19; nodal-status, total removed: 32; duration of tamoxifen (years): 0.86; time.to.ok: .; time.to.recurrence (years): 3.44; time.to.death (years): 5.36; data set (out of 3): 2; ', 'age at op: 62; size (mm): 14; er-status: 100; pgr-status: NA; nodal-status, positive: 5; nodal-status, total removed: 11; duration of tamoxifen (years): 1.86; time.to.ok: .; time.to.recurrence (years): 1.86; data set (out of 3): 2; ', 'slide id: Slide 5; imagene id: 14210080; age at op: 54; size (mm): 20; er-status: IHC+; pgr-status: NA; nodal-status, positive: 1; nodal-status, total removed: 14; duration of tamoxifen (years): 4.62; time.to.ok: 5.07; time.to.recurrence (years): .; ', 'slide id: Slide 6; imagene id: 14210081; age at op: 54; size (mm): 32; er-status: IHC+; pgr-status: NA; nodal-status, positive: 8; nodal-status, total removed: 24; duration of tamoxifen (years): 4.66; time.to.ok: 7.26; time.to.recurrence (years): .; ', 'slide id: Slide 7; imagene id: 14210082; age at op: 55; size (mm): 21; er-status: IHC+; pgr-status: NA; nodal-status, positive: 0; nodal-status, total removed: 14; duration of tamoxifen (years): 4.49; time.to.ok: 4.56; time.to.recurrence (years): .; ', 'slide id: Slide 8; imagene id: 14210083; age at op: 72; size (mm): 35; er-status: IHC+; pgr-status: NA; nodal-status, positive: 0; nodal-status, total removed: 20; duration of tamoxifen (years): 4.60; time.to.ok: 4.66; time.to.recurrence (years): .; ', 'slide id: Slide 9; imagene id: 14210084; age at op: 65; size (mm): 22; er-status: IHC+; pgr-status: NA; nodal-status, positive: 1; nodal-status, total removed: 19; duration of tamoxifen (years): 4.43; time.to.ok: 6.02; time.to.recurrence (years): .; ', 'slide id: Slide 14; imagene id: 14210168; age at op: 65; size (mm): 30; er-status: 100; pgr-status: 90; nodal-status, positive: 4; nodal-status, total removed: 22; duration of tamoxifen (years): 4.08; time.to.ok: 5.07; time.to.recurrence (years): .; ', 'slide id: Slide 15; imagene id: 14210171; age at op: 62; size (mm): 20; er-status: 50; pgr-status: 0; nodal-status, positive: 2; nodal-status, total removed: 15; duration of tamoxifen (years): 5.00; time.to.ok: 6.10; time.to.recurrence (years): .; ', 'slide id: Slide 16; imagene id: 14210172; age at op: 56; size (mm): 10; er-status: 90; pgr-status: 90; nodal-status, positive: 1; nodal-status, total removed: 13; duration of tamoxifen (years): 4.65; time.to.ok: 5.33; time.to.recurrence (years): .; ', 'slide id: Slide 18; imagene id: 14210175; age at op: 51; size (mm): 10; er-status: 50; pgr-status: 90; nodal-status, positive: 1; nodal-status, total removed: 12; duration of tamoxifen (years): 4.11; time.to.ok: 5.02; time.to.recurrence (years): .; ', 'slide id: Slide 19; imagene id: 14210176; age at op: 65; size (mm): 14; er-status: 99; pgr-status: 2; nodal-status, positive: 6; nodal-status, total removed: 16; duration of tamoxifen (years): 4.72; time.to.ok: 6.39; time.to.recurrence (years): .; time.to.death (years): 9.09; ', 'slide id: Slide 20; imagene id: 14210178; age at op: 52; size (mm): 21; er-status: 10; pgr-status: 0; nodal-status, positive: 4; nodal-status, total removed: 25; duration of tamoxifen (years): 5.00; time.to.ok: 3.04; time.to.recurrence (years): .; ', 'slide id: Slide 21; imagene id: 14210179; age at op: 69; size (mm): 14; er-status: 85; pgr-status: 0; nodal-status, positive: 1; nodal-status, total removed: 12; duration of tamoxifen (years): 4.79; time.to.ok: 4.99; time.to.recurrence (years): .; time.to.death (years): 7.58; ', 'slide id: Slide 22; imagene id: 14210180; age at op: 70; size (mm): 14; er-status: 90; pgr-status: 0; nodal-status, positive: 0; nodal-status, total removed: 11; duration of tamoxifen (years): 2.74; time.to.ok: 2.81; time.to.recurrence (years): .; time.to.death (years): 3.95; ', 'slide id: Slide 23; imagene id: 14210181; age at op: 60; size (mm): 12; er-status: 100; pgr-status: 10; nodal-status, positive: 0; nodal-status, total removed: 22; duration of tamoxifen (years): 4.77; time.to.ok: 4.95; time.to.recurrence (years): .; ', 'slide id: Slide 24; imagene id: 14210183; age at op: 61; size (mm): 45; er-status: 90; pgr-status: 75; nodal-status, positive: 0; nodal-status, total removed: 20; duration of tamoxifen (years): 4.67; time.to.ok: 5.39; time.to.recurrence (years): .; ', 'slide id: Slide 25; imagene id: 14210184; age at op: 55; size (mm): 26; er-status: 95; pgr-status: 75; nodal-status, positive: 4; nodal-status, total removed: 19; duration of tamoxifen (years): 3.11; time.to.ok: 5.26; time.to.recurrence (years): .; ', 'slide id: Slide 27; imagene id: 14210186; age at op: 64; size (mm): 22; er-status: 80; pgr-status: NA; nodal-status, positive: 0; nodal-status, total removed: 17; duration of tamoxifen (years): 4.67; time.to.ok: 5.28; time.to.recurrence (years): .; ', 'slide id: Slide 29; imagene id: 14210188; age at op: 61; size (mm): 11; er-status: 90; pgr-status: 90; nodal-status, positive: 0; nodal-status, total removed: 13; duration of tamoxifen (years): 5.00; time.to.ok: 5.01; time.to.recurrence (years): .; ', 'slide id: Slide 33; imagene id: 14210194; age at op: 65; size (mm): 23; er-status: 100; pgr-status: 0; nodal-status, positive: 0; nodal-status, total removed: 0; duration of tamoxifen (years): 4.84; time.to.ok: 5.08; time.to.recurrence (years): .; ', 'slide id: Slide 37; imagene id: 14210232; age at op: 55; size (mm): 13; er-status: 100; pgr-status: 0; nodal-status, positive: 1; nodal-status, total removed: 10; duration of tamoxifen (years): 4.67; time.to.ok: 5.31; time.to.recurrence (years): .; ', 'slide id: Slide 39; imagene id: 14210234; age at op: 49; size (mm): 16; er-status: 100; pgr-status: 30; nodal-status, positive: 0; nodal-status, total removed: 1; duration of tamoxifen (years): 4.78; time.to.ok: 5.94; time.to.recurrence (years): .; ', 'slide id: Slide 34; imagene id: 14210196; age at op: 50; size (mm): 30; er-status: 100; pgr-status: IHC-; nodal-status, positive: 2; nodal-status, total removed: 16; duration of tamoxifen (years): 5.00; time.to.ok: .; time.to.recurrence (years): 7.22; time.to.death (years): 7.94; ', 'slide id: Slide 1; imagene id: 14209976; age at op: 61; size (mm): 32; er-status: IHC+; pgr-status: NA; nodal-status, positive: 11; nodal-status, total removed: 15; duration of tamoxifen (years): 3.11; time.to.ok: .; time.to.recurrence (years): 3.55; time.to.death (years): 6.36; ', 'slide id: Slide 2; imagene id: 14209977; age at op: 58; size (mm): 22; er-status: IHC+; pgr-status: NA; nodal-status, positive: 5; nodal-status, total removed: 14; duration of tamoxifen (years): 3.44; time.to.ok: .; time.to.recurrence (years): 4.21; time.to.death (years): 8.38; ', 'slide id: Slide 3; imagene id: 14209978; age at op: 51; size (mm): 60; er-status: IHC+; pgr-status: NA; nodal-status, positive: 5; nodal-status, total removed: 30; duration of tamoxifen (years): 3.02; time.to.ok: .; time.to.recurrence (years): 3.77; time.to.death (years): 8.23; ', 'slide id: Slide 4; imagene id: 14210079; age at op: 61; size (mm): 55; er-status: IHC+; pgr-status: NA; nodal-status, positive: 2; nodal-status, total removed: 15; duration of tamoxifen (years): 3.82; time.to.ok: .; time.to.recurrence (years): 4.04; time.to.death (years): 7.56; ', 'slide id: Slide 10; imagene id: 14210085; age at op: 53; size (mm): 40; er-status: B+; pgr-status: B-; nodal-status, positive: 3; nodal-status, total removed: 17; duration of tamoxifen (years): NA; time.to.ok: .; time.to.recurrence (years): 0.83; time.to.death (years): 2.09; ', 'slide id: Slide 11; imagene id: 14210086; age at op: 67; size (mm): 29; er-status: B+; pgr-status: B+; nodal-status, positive: 7; nodal-status, total removed: 14; duration of tamoxifen (years): 1.78; time.to.ok: .; time.to.recurrence (years): 5.12; time.to.death (years): 10.91; ', 'slide id: Slide 12; imagene id: 14210087; age at op: 67; size (mm): 65; er-status: 70; pgr-status: 20; nodal-status, positive: 2; nodal-status, total removed: 24; duration of tamoxifen (years): 2.55; time.to.ok: .; time.to.recurrence (years): 3.02; time.to.death (years): 7.16; ', 'slide id: Slide 13; imagene id: 14210088; age at op: 64; size (mm): 18; er-status: 100; pgr-status: 90; nodal-status, positive: 1; nodal-status, total removed: 15; duration of tamoxifen (years): 4.05; time.to.ok: .; time.to.recurrence (years): 4.35; ', 'slide id: Slide 17; imagene id: 14210174; age at op: 64; size (mm): 26; er-status: 95; pgr-status: 90; nodal-status, positive: 5; nodal-status, total removed: 19; duration of tamoxifen (years): 5.00; time.to.ok: .; time.to.recurrence (years): 6.21; time.to.death (years): 8.70; ', 'slide id: Slide 26; imagene id: 14210185; age at op: 70; size (mm): 14; er-status: 95; pgr-status: 95; nodal-status, positive: 0; nodal-status, total removed: 32; duration of tamoxifen (years): 3.39; time.to.ok: .; time.to.recurrence (years): 4.13; time.to.death (years): 4.33; ', 'slide id: Slide 28; imagene id: 14210187; age at op: 51; size (mm): 11; er-status: 90; pgr-status: 30; nodal-status, positive: 0; nodal-status, total removed: 19; duration of tamoxifen (years): 5.00; time.to.ok: .; time.to.recurrence (years): 8.73; ', 'slide id: Slide 30; imagene id: 14210189; age at op: 64; size (mm): 17; er-status: 50; pgr-status: 0; nodal-status, positive: 3; nodal-status, total removed: 22; duration of tamoxifen (years): 1.74; time.to.ok: .; time.to.recurrence (years): 2.54; time.to.death (years): 3.93; ', 'slide id: Slide 31; imagene id: 14210190; age at op: 50; size (mm): 26; er-status: 90; pgr-status: 5; nodal-status, positive: 2; nodal-status, total removed: 10; duration of tamoxifen (years): 2.34; time.to.ok: .; time.to.recurrence (years): 2.76; time.to.death (years): 4.79; ', 'slide id: Slide 32; imagene id: 14210191; age at op: 72; size (mm): 32; er-status: 100; pgr-status: 50; nodal-status, positive: 5; nodal-status, total removed: 16; duration of tamoxifen (years): 2.60; time.to.ok: .; time.to.recurrence (years): 2.75; time.to.death (years): 2.98; ', 'slide id: Slide 35; imagene id: 14210197; age at op: 54; size (mm): 25; er-status: 80; pgr-status: 10; nodal-status, positive: 0; nodal-status, total removed: 18; duration of tamoxifen (years): NA; time.to.ok: .; time.to.recurrence (years): 1.70; ', 'slide id: Slide 36; imagene id: 14210200; age at op: 51; size (mm): 20; er-status: 95; pgr-status: 5; nodal-status, positive: 0; nodal-status, total removed: 10; duration of tamoxifen (years): 3.50; time.to.ok: .; time.to.recurrence (years): 3.52; ', 'slide id: Slide 38; imagene id: 14210233; age at op: 61; size (mm): 9; er-status: 25; pgr-status: 0; nodal-status, positive: 6; nodal-status, total removed: 16; duration of tamoxifen (years): 1.72; time.to.ok: .; time.to.recurrence (years): 1.82; ', 'slide id: Slide 40; imagene id: 14210235; age at op: 54; size (mm): 8; er-status: NA; pgr-status: NA; nodal-status, positive: 3; nodal-status, total removed: 14; duration of tamoxifen (years): 2.14; time.to.ok: .; time.to.recurrence (years): 2.52; time.to.death (years): 3.71; ' GSE45827 Homo sapiens 155 Expression profiling by array GPL570 Expression data from Breast cancer subtypes 2013-04-05 Expression data from Breast cancer subtypes https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE45827 Chronic oxidative stress promotes H2AX protein degradation and enhances chemosensitivity in breast cancer patients. EMBO molecular medicine 10.624 https://doi.org/10.15252/emmm.201505891 {EMBO molecular medicine (10.624): 10.15252/emmm.201505891} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA196431 https://www.ebi.ac.uk/ena/browser/view/PRJNA196431 None [Overal design]In a cohort study of primary invasive breast cancer (41 TN, 30 HER2, 29 Luminal A and 30 Luminal B) as well as 11 normal tissues samples and 14 cell lines , we obtained a tumor specimen at surgery before any patient treatment. Total RNA was extracted from all samples and the whole transcriptome was quantified with Affymetrix U133 Plus 2.0 Chips.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted and purified from tumor samples by using the Rneasy Mini Kit (Qiagen) and then, the RNA clean up kit (Macherey Nagel) according to the manufacturers’ instructions'; [Cell type]'Source: ''diagnosis: Breast cancer; tumor subtype: Basal; batch: 8; hybridation: -1; ', 'diagnosis: Breast cancer; tumor subtype: Her2; batch: 8; hybridation: -1; ', 'diagnosis: Breast cancer; tumor subtype: Basal; batch: 9; hybridation: -1; ', 'diagnosis: Breast cancer; tumor subtype: Her2; batch: 9; hybridation: -1; ', 'diagnosis: Breast cancer; tumor subtype: Basal; batch: 10; hybridation: -1; ', 'diagnosis: Breast cancer; tumor subtype: Her2; batch: 10; hybridation: -1; ', 'cell line: BT20; cell origin: Breast carcinoma; batch: 2; hybridation: 2; ', 'cell line: HCC70; cell origin: Breast carcinoma; batch: 5; hybridation: 1; ', 'cell line: HCC1143; cell origin: Breast carcinoma; batch: 1; hybridation: 3; ', 'cell line: HCC1187; cell origin: Breast carcinoma; batch: 2; hybridation: 1; ', 'cell line: HCC1937; cell origin: Breast carcinoma; batch: 2; hybridation: 3; ', 'cell line: MDA-MB-468; cell origin: Breast carcinoma; batch: 4; hybridation: 2; ', 'cell line: HCC38; cell origin: Breast carcinoma; batch: 3; hybridation: 2; ', 'cell line: MDA-MB-231; cell origin: Breast carcinoma; batch: 5; hybridation: 3; ', 'cell line: MDA-MB-436; cell origin: Breast carcinoma; batch: 1; hybridation: 2; ', 'cell line: MDA-MB-157; cell origin: Breast carcinoma; batch: 5; hybridation: 2; ', 'cell line: BT-549; cell origin: Breast carcinoma; batch: 4; hybridation: 3; ', 'cell line: Hs 578T; cell origin: Breast carcinoma; batch: 3; hybridation: 3; ', 'cell line: MCF-12A; cell origin: Breast mammary gland; batch: 3; hybridation: 1; ', 'cell line: 184B5; cell origin: Breast mammary gland; batch: 1; hybridation: 1; ', 'diagnosis: None (normal); tumor subtype: N/A; batch: 1; hybridation: 2; ', 'diagnosis: None (normal); tumor subtype: N/A; batch: 5; hybridation: 1; ', 'diagnosis: None (normal); tumor subtype: N/A; batch: 5; hybridation: 2; ', 'diagnosis: None (normal); tumor subtype: N/A; batch: 2; hybridation: 1; ', 'diagnosis: None (normal); tumor subtype: N/A; batch: 2; hybridation: 2; ', 'diagnosis: None (normal); tumor subtype: N/A; batch: 4; hybridation: 1; ', 'diagnosis: None (normal); tumor subtype: N/A; batch: 3; hybridation: 3; ', 'diagnosis: None (normal); tumor subtype: N/A; batch: 1; hybridation: 3; ', 'diagnosis: None (normal); tumor subtype: N/A; batch: 2; hybridation: 3; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 1; hybridation: 1; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 1; hybridation: 1; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 1; hybridation: 2; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 1; hybridation: 2; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 1; hybridation: 3; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 1; hybridation: 3; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 2; hybridation: 1; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 2; hybridation: 1; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 2; hybridation: 2; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 2; hybridation: 2; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 2; hybridation: 3; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 2; hybridation: 3; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 3; hybridation: 1; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 3; hybridation: 1; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 3; hybridation: 2; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 3; hybridation: 2; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 3; hybridation: 3; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 3; hybridation: 3; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 4; hybridation: 1; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 4; hybridation: 1; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 4; hybridation: 2; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 4; hybridation: 3; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 4; hybridation: 3; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 5; hybridation: 1; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 5; hybridation: 1; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 5; hybridation: 2; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 5; hybridation: 2; ', 'diagnosis: Breast cancer; tumor subtype: Luminal A; batch: 5; hybridation: 3; ', 'diagnosis: Breast cancer; tumor subtype: Luminal B; batch: 5; hybridation: 3; ' GSE59361 Homo sapiens 4 Expression profiling by array GPL570 Gene expression of SUM159-mir100 ALDH+ and ALDH- cells from CTRL or mir100-overexpressing group 2014-07-11 Emerging evidence suggest that miRNAs play an essential role in self-renewal and differentiation of normal and malignant stem cells by regulating the expression of key stem cell regulatory genes. Here we demonstrate that mir-100 expression is related to cellular differentiation state with lowest expression in cells displaying stem cell markers. Utilizing a tetracycline inducible lentivirus driving mir-100 expression, we found that mir-100 overexpression decreased breast cancer stem cells (BCSCs) and inhibited cancer cell proliferation in vitro and in mouse xenografts by targeting SMARCA5, SMARCD1 and BMPR2. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59361 MicroRNA100 inhibits self-renewal of breast cancer stem-like cells and breast tumor development. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-13-3710 {Cancer research (8.378): 10.1158/0008-5472.CAN-13-3710} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA255137 https://www.ebi.ac.uk/ena/browser/view/PRJNA255137 None [Overal design]In order to determine the cellular targets of mir-100 in BCSCs and non-BCSCs, ALDH-positive and -negative populations of pTRIPZ-SUM159-mir-100 cells were separated and cultured in suspension for ten hours in the presence or absence of DOX. Gene expression profiles of the four populations were determined utilizing Affymetrix microarrays; [Treatment]'ALDH-positive and -negative populations of pTRIPZ-SUM159-mir-100 cells were separated and cultured in suspension for ten hours in the presence or absence of DOXYCYLINE(DOX)'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: SUM-159; aldh status: ALDH+; treatment: control; ', 'cell line: SUM-159; aldh status: ALDH+; treatment: Doxycycline(DOX), 10hrs; ', 'cell line: SUM-159; aldh status: ALDH-; treatment: control; ', 'cell line: SUM-159; aldh status: ALDH-; treatment: Doxycycline(DOX), 10hrs; ' GSE125677 Homo sapiens 6 Non-coding RNA profiling by array GPL23178 All the regulated lncRNAs in breast cancer tissues compared to adjacent normal breast tissues 2019-01-25 Circulating transcriptional landscapes between breast cancer tissues and adjacent normal tissues were compared using the Affymetrix Human OE LncRNA Microarray with probes for profiling of 63542 human lncRNAs. Goal was to investigate potential lncRNAs involved in breast cancer progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE125677 LncCCAT1 Promotes Breast Cancer Stem Cell Function through Activating WNT/β-catenin Signaling. Theranostics 8.063 https://doi.org/10.7150/thno.37892 {Theranostics (8.063): 10.7150/thno.37892} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA517149 https://www.ebi.ac.uk/ena/browser/view/PRJNA517149 None [Overal design]The total RNAs of 3 paired breast cancer and adjacent normal tissues were extracted, and the global expression profile of lncRNAs was detected with Affymetrix Human OE LncRNA Microarray.; [Treatment]'None of the patients received radiotherapy and chemotherapy before the surgery.'; [Growth]'None'; [Extraction]'The total RNA was extracted from fresh tissues using TRIzol reagent (Invitrogen, CA, USA). The quantity of RNA was assessed by NanoDrop ND-2000 (Thermo Scientific) and the RNA integrity was tested by standard denaturing agarose gel electrophoresis. RNA from the 3 paired tissues was used for microarray analysis by Affymetrix Human OE LncRNA Microarray.'; [Cell type]'Source: ''tissue: breast tissue; disease state: tumor; gender: Female; ', 'tissue: breast tissue; disease state: adjacent normal; gender: Female; ' GSE46715 Homo sapiens 12 Expression profiling by array GPL10904 Progesterone Receptor–Cyclin D1 Complexes Induce Cell Cycle–Dependent Transcriptional Programs in Breast Cancer Cells 2013-05-07 The progesterone receptor (PR) and its coactivators are direct targets of activated cyclin-dependent kinases (CDKs) in response to peptide growth factors, progesterone, and deregulation of cell cycle inhibitors. Herein, using the T47D breast cancer model, we probed mechanisms of cell cycle-dependent PR action. In the absence of exogenous progestin, the PR is specifically phosphorylated during the G2/M phase. Accordingly, numerous PR target genes are cell cycle regulated, including HSPB8, a heat-shock protein whose high expression is associated with tamoxifen resistance. Progestin-induced HSPB8 expression required cyclin D1 and was insensitive to antiestrogens but blocked by antiprogestins or inhibition of specificity factor 1 (SP1). HSPB8 expression increased with or without ligand when cells were G2/M synchronized or contained high levels of cyclin D1. Knockdown of PRs abrogated ligand-independent HSPB8 expression in synchronized cells. Notably, PRs and cyclin D1 copurified in whole-cell lysates of transiently transfected COS-1 cells and in PR-positive T47D breast cancer cells expressing endogenous cyclin D1. PRs, cyclin D1, and SP1 were recruited to the HSPB8 promoter in progestin-treated T47D breast cancer cells. Mutation of PR Ser345 to Ala (S345A) or inhibition of CDK2 activity using roscovitine disrupted PR/cyclin D1 interactions with DNA and blocked HSPB8 mRNA expression. Interaction of phosphorylated PRs with SP1 and cyclin D1 provides a mechanism for targeting transcriptionally active PRs to selected gene promoters relevant to breast cancer progression. Understanding the functional linkage between PRs and cell cycle regulatory proteins will provide keys to targeting novel PR/cyclin D1 cross talk in both hormone-responsive disease and HSPB8-high refractory disease with high HSPB8 expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE46715 Progesterone receptor-cyclin D1 complexes induce cell cycle-dependent transcriptional programs in breast cancer cells. Molecular endocrinology (Baltimore, Md.) 3.628 https://doi.org/10.1210/me.2013-1196 {Molecular endocrinology (Baltimore, Md.) (3.628): 10.1210/me.2013-1196} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA202065 https://www.ebi.ac.uk/ena/browser/view/PRJNA202065 None [Overal design]The study contains 4 different sample groups measured in triplicate, for a total of 12 individual samples (12 arrays). In T47D human breast cancer cell lines stably expressing PR-B, cells were synchronized (or not synchronized) before G2/M phase using nocodazole. These cell lines (synchronized or not synchronized) were treated with either (1) vehicle control (ethanol) or (2) PR ligand R5020 10e-8 M for 6 hours before total RNA harvest. Thus, the experiment contains two cell lines, and two treatments (4 sample groups) treated and analyzed in triplicate (12 microarrays). Standard Illumina HT-12v4 chip controls were used during hybridization.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with the QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''parental cell line: T47D-YB; tissue derivation: breast cancer; stable vector integration: pSG5-PR-B; cell synchronization: vehicle; treatment: ethanol vehicle; time point: 6 hr; ', 'parental cell line: T47D-YB; tissue derivation: breast cancer; stable vector integration: pSG5-PR-B; cell synchronization: nocodazole; treatment: R5020 10e-8 M; time point: 6 hr; ' GSE32651 Homo sapiens 1003 Expression profiling by array GPL8432 Expression profiling of archival tissues for long-term health studies 2011-10-05 Over 20 million archival tissue samples are stored annually in the United States as formalin-fixed, paraffin-embedded (FFPE) tissue blocks, but only recently has whole-genome expression profiling from these samples become technically feasible. Here, we introduce novel general methods for assessing, summarizing, and visualizing expression data quality from archival samples. We validated these methods in technical study of 144 clinical breast cancer and autopsy samples and in an overview of all current publicly available FFPE whole-genome expression data. We additionally performed a case study incorporating over 1,000 colorectal cancer (CRC) samples collected from patients across the United States over a period of more than 25 years, integrating clinicopathological information, tumor molecular data, and archival tissue gene expression on an unparalleled scale. Both large-scale clinical studies presented a much greater range of data quality than previous smaller studies, emphasizing the need for rigorous quality control in translational applications of archival tissue gene expression profiling. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32651 Expression profiling of archival tumors for long-term health studies. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-12-1915 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-12-1915} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA146961 https://www.ebi.ac.uk/ena/browser/view/PRJNA146961 None [Overal design]This series includes 1,003 FFPE-preserved CRC tumors, assayed by Illumina HumanRef-v3 WG-DASL microarray.; [Treatment]'None'; [Growth]'None'; [Extraction]'Using formalin-fixed, paraffin-embedded CRC tissues, total RNA was extracted using TRIzol (Invitrogen).'; [Cell type]'Source: ''tumor id: 1848; tumor location: rectum; sample age: 12.5; rna (ng/ul): 40; sample_well: A01; sentrix_id: 4642203001; sentrix_position: A; plate: 1; ', 'tumor id: 1874; tumor location: colon; sample age: 12.8333333333333; rna (ng/ul): 40; sample_well: A02; sentrix_id: 4642203003; sentrix_position: A; plate: 1; ', 'tumor id: 483; tumor location: colon; sample age: 18.9166666666667; rna (ng/ul): 40; sample_well: A03; sentrix_id: 4642203017; sentrix_position: A; plate: 1; ', 'tumor id: 1289; tumor location: rectum; sample age: 11.25; rna (ng/ul): 40; sample_well: A04; sentrix_id: 4642203025; sentrix_position: A; plate: 1; ', 'tumor id: 2642; tumor location: colon; sample age: 26.0833333333333; rna (ng/ul): 11; sample_well: A05; sentrix_id: 4642203026; sentrix_position: A; plate: 1; ', 'tumor id: 100; tumor location: colon; sample age: 17.0833333333333; rna (ng/ul): 40; sample_well: A06; sentrix_id: 4642203027; sentrix_position: A; plate: 1; ', 'tumor id: null; tumor location: null; sample age: null; rna (ng/ul): null; sample_well: null; sentrix_id: null; sentrix_position: null; plate: null; ', 'tumor id: 3152; tumor location: rectum; sample age: 7.08333333333333; rna (ng/ul): 40; sample_well: A09; sentrix_id: 4642203038; sentrix_position: A; plate: 1; ', 'tumor id: 449; tumor location: rectum; sample age: 13.1666666666667; rna (ng/ul): 13; sample_well: A10; sentrix_id: 4642203049; sentrix_position: A; plate: 1; ', 'tumor id: 613; tumor location: rectum; sample age: 15.3333333333333; rna (ng/ul): 40; sample_well: A11; sentrix_id: 4642203055; sentrix_position: A; plate: 1; ', 'tumor id: 642; tumor location: rectum; sample age: 13; rna (ng/ul): 40; sample_well: A12; sentrix_id: 4642203062; sentrix_position: A; plate: 1; ', 'tumor id: 1871; tumor location: rectum; sample age: 10.3333333333333; rna (ng/ul): 19; sample_well: B01; sentrix_id: 4642203001; sentrix_position: B; plate: 1; ', 'tumor id: 2603; tumor location: colon; sample age: 12.3333333333333; rna (ng/ul): 35; sample_well: B02; sentrix_id: 4642203003; sentrix_position: B; plate: 1; ', 'tumor id: 506; tumor location: colon; sample age: 20.6666666666667; rna (ng/ul): 40; sample_well: B03; sentrix_id: 4642203017; sentrix_position: B; plate: 1; ', 'tumor id: 1741; tumor location: colon; sample age: 10.25; rna (ng/ul): 37; sample_well: B04; sentrix_id: 4642203025; sentrix_position: B; plate: 1; ', 'tumor id: 487; tumor location: rectum; sample age: 20.3333333333333; rna (ng/ul): 20; sample_well: B06; sentrix_id: 4642203027; sentrix_position: B; plate: 1; ', 'tumor id: 1771; tumor location: rectum; sample age: 11.5833333333333; rna (ng/ul): 40; sample_well: B07; sentrix_id: 4642203032; sentrix_position: B; plate: 1; ', 'tumor id: 1258; tumor location: colon; sample age: 12.1666666666667; rna (ng/ul): 22; sample_well: B08; sentrix_id: 4642203034; sentrix_position: B; plate: 1; ', 'tumor id: 1841; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: B09; sentrix_id: 4642203038; sentrix_position: B; plate: 1; ', 'tumor id: 464; tumor location: rectum; sample age: 14.5833333333333; rna (ng/ul): 30; sample_well: B10; sentrix_id: 4642203049; sentrix_position: B; plate: 1; ', 'tumor id: 615; tumor location: rectum; sample age: 15.5; rna (ng/ul): 40; sample_well: B11; sentrix_id: 4642203055; sentrix_position: B; plate: 1; ', 'tumor id: 670; tumor location: rectum; sample age: 16.75; rna (ng/ul): 40; sample_well: B12; sentrix_id: 4642203062; sentrix_position: B; plate: 1; ', 'tumor id: 2183; tumor location: rectum; sample age: 12.9166666666667; rna (ng/ul): 40; sample_well: C01; sentrix_id: 4642203001; sentrix_position: C; plate: 1; ', 'tumor id: 2667; tumor location: colon; sample age: 8.33333333333333; rna (ng/ul): 40; sample_well: C02; sentrix_id: 4642203003; sentrix_position: C; plate: 1; ', 'tumor id: 2674; tumor location: rectum; sample age: 7.58333333333333; rna (ng/ul): 21; sample_well: C04; sentrix_id: 4642203025; sentrix_position: C; plate: 1; ', 'tumor id: 298; tumor location: rectum; sample age: 9.08333333333333; rna (ng/ul): 40; sample_well: C05; sentrix_id: 4642203026; sentrix_position: C; plate: 1; ', 'tumor id: 3144; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: C06; sentrix_id: 4642203027; sentrix_position: C; plate: 1; ', 'tumor id: 1791; tumor location: rectum; sample age: 10.9166666666667; rna (ng/ul): 40; sample_well: C07; sentrix_id: 4642203032; sentrix_position: C; plate: 1; ', 'tumor id: 1748; tumor location: rectum; sample age: 11; rna (ng/ul): 28; sample_well: C08; sentrix_id: 4642203034; sentrix_position: C; plate: 1; ', 'tumor id: 1845; tumor location: colon; sample age: 11.4166666666667; rna (ng/ul): 40; sample_well: C09; sentrix_id: 4642203038; sentrix_position: C; plate: 1; ', 'tumor id: 466; tumor location: rectum; sample age: 13.0833333333333; rna (ng/ul): 40; sample_well: C10; sentrix_id: 4642203049; sentrix_position: C; plate: 1; ', 'tumor id: 618; tumor location: colon; sample age: 16; rna (ng/ul): 40; sample_well: C11; sentrix_id: 4642203055; sentrix_position: C; plate: 1; ', 'tumor id: 673; tumor location: colon; sample age: 16.8333333333333; rna (ng/ul): 40; sample_well: C12; sentrix_id: 4642203062; sentrix_position: C; plate: 1; ', 'tumor id: 2251; tumor location: colon; sample age: 8.16666666666667; rna (ng/ul): 40; sample_well: D01; sentrix_id: 4642203001; sentrix_position: D; plate: 1; ', 'tumor id: 182; tumor location: colon; sample age: 18.1666666666667; rna (ng/ul): 29; sample_well: D02; sentrix_id: 4642203003; sentrix_position: D; plate: 1; ', 'tumor id: 2195; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: D03; sentrix_id: 4642203017; sentrix_position: D; plate: 1; ', 'tumor id: 517; tumor location: rectum; sample age: 17.4166666666667; rna (ng/ul): 40; sample_well: D04; sentrix_id: 4642203025; sentrix_position: D; plate: 1; ', 'tumor id: 555; tumor location: colon; sample age: 20.6666666666667; rna (ng/ul): 40; sample_well: D05; sentrix_id: 4642203026; sentrix_position: D; plate: 1; ', 'tumor id: 2568; tumor location: rectum; sample age: 27.4166666666667; rna (ng/ul): 40; sample_well: D06; sentrix_id: 4642203027; sentrix_position: D; plate: 1; ', 'tumor id: 1800; tumor location: rectum; sample age: 12.3333333333333; rna (ng/ul): 14; sample_well: D07; sentrix_id: 4642203032; sentrix_position: D; plate: 1; ', 'tumor id: 2217; tumor location: rectum; sample age: 11; rna (ng/ul): 40; sample_well: D08; sentrix_id: 4642203034; sentrix_position: D; plate: 1; ', 'tumor id: 1803; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: D09; sentrix_id: 4642203038; sentrix_position: D; plate: 1; ', 'tumor id: 545; tumor location: colon; sample age: 16.5; rna (ng/ul): 19; sample_well: D10; sentrix_id: 4642203049; sentrix_position: D; plate: 1; ', 'tumor id: 1743; tumor location: colon; sample age: 11.3333333333333; rna (ng/ul): 40; sample_well: D12; sentrix_id: 4642203062; sentrix_position: D; plate: 1; ', 'tumor id: 2668; tumor location: colon; sample age: 7.91666666666667; rna (ng/ul): 40; sample_well: E01; sentrix_id: 4642203001; sentrix_position: E; plate: 1; ', 'tumor id: 222; tumor location: colon; sample age: 17.3333333333333; rna (ng/ul): 40; sample_well: E02; sentrix_id: 4642203003; sentrix_position: E; plate: 1; ', 'tumor id: 228; tumor location: rectum; sample age: 15.9166666666667; rna (ng/ul): 40; sample_well: E03; sentrix_id: 4642203017; sentrix_position: E; plate: 1; ', 'tumor id: 477; tumor location: colon; sample age: 20.6666666666667; rna (ng/ul): 40; sample_well: E04; sentrix_id: 4642203025; sentrix_position: E; plate: 1; ', 'tumor id: 3149; tumor location: colon; sample age: 8.58333333333333; rna (ng/ul): 40; sample_well: E05; sentrix_id: 4642203026; sentrix_position: E; plate: 1; ', 'tumor id: 2921; tumor location: colon; sample age: 7.91666666666667; rna (ng/ul): 40; sample_well: E06; sentrix_id: 4642203027; sentrix_position: E; plate: 1; ', 'tumor id: 539; tumor location: colon; sample age: 17; rna (ng/ul): 40; sample_well: E07; sentrix_id: 4642203032; sentrix_position: E; plate: 1; ', 'tumor id: 70; tumor location: colon; sample age: 17.1666666666667; rna (ng/ul): 40; sample_well: E08; sentrix_id: 4642203034; sentrix_position: E; plate: 1; ', 'tumor id: 1772; tumor location: colon; sample age: 12; rna (ng/ul): 40; sample_well: E09; sentrix_id: 4642203038; sentrix_position: E; plate: 1; ', 'tumor id: 554; tumor location: colon; sample age: 15.1666666666667; rna (ng/ul): 40; sample_well: E10; sentrix_id: 4642203049; sentrix_position: E; plate: 1; ', 'tumor id: 3339; tumor location: colon; sample age: 6.25; rna (ng/ul): 11; sample_well: E11; sentrix_id: 4642203055; sentrix_position: E; plate: 1; ', 'tumor id: 3145; tumor location: rectum; sample age: 7.5; rna (ng/ul): 40; sample_well: E12; sentrix_id: 4642203062; sentrix_position: E; plate: 1; ', 'tumor id: 96; tumor location: colon; sample age: 20.75; rna (ng/ul): 40; sample_well: F01; sentrix_id: 4642203001; sentrix_position: F; plate: 1; ', 'tumor id: 301; tumor location: rectum; sample age: 12.9166666666667; rna (ng/ul): 40; sample_well: F02; sentrix_id: 4642203003; sentrix_position: F; plate: 1; ', 'tumor id: 256; tumor location: rectum; sample age: 19; rna (ng/ul): 40; sample_well: F03; sentrix_id: 4642203017; sentrix_position: F; plate: 1; ', 'tumor id: 559; tumor location: colon; sample age: 19.1666666666667; rna (ng/ul): 40; sample_well: F04; sentrix_id: 4642203025; sentrix_position: F; plate: 1; ', 'tumor id: 472; tumor location: rectum; sample age: 13.25; rna (ng/ul): 40; sample_well: F05; sentrix_id: 4642203026; sentrix_position: F; plate: 1; ', 'tumor id: 2583; tumor location: colon; sample age: 26.8333333333333; rna (ng/ul): 40; sample_well: F06; sentrix_id: 4642203027; sentrix_position: F; plate: 1; ', 'tumor id: 2293; tumor location: colon; sample age: 7; rna (ng/ul): 28; sample_well: F07; sentrix_id: 4642203032; sentrix_position: F; plate: 1; ', 'tumor id: 3151; tumor location: colon; sample age: 6.91666666666667; rna (ng/ul): 40; sample_well: F08; sentrix_id: 4642203034; sentrix_position: F; plate: 1; ', 'tumor id: 423; tumor location: colon; sample age: 14.25; rna (ng/ul): 40; sample_well: F09; sentrix_id: 4642203038; sentrix_position: F; plate: 1; ', 'tumor id: 578; tumor location: rectum; sample age: 16.9166666666667; rna (ng/ul): 40; sample_well: F10; sentrix_id: 4642203049; sentrix_position: F; plate: 1; ', 'tumor id: 612; tumor location: colon; sample age: 15.9166666666667; rna (ng/ul): 14; sample_well: F11; sentrix_id: 4642203055; sentrix_position: F; plate: 1; ', 'tumor id: 3158; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: F12; sentrix_id: 4642203062; sentrix_position: F; plate: 1; ', 'tumor id: 176; tumor location: colon; sample age: 16.8333333333333; rna (ng/ul): 40; sample_well: G01; sentrix_id: 4642203001; sentrix_position: G; plate: 1; ', 'tumor id: 2564; tumor location: rectum; sample age: 16.3333333333333; rna (ng/ul): 40; sample_well: G02; sentrix_id: 4642203003; sentrix_position: G; plate: 1; ', 'tumor id: 429; tumor location: colon; sample age: 14; rna (ng/ul): 40; sample_well: G03; sentrix_id: 4642203017; sentrix_position: G; plate: 1; ', 'tumor id: 521; tumor location: colon; sample age: 22.1666666666667; rna (ng/ul): 14; sample_well: G04; sentrix_id: 4642203025; sentrix_position: G; plate: 1; ', 'tumor id: 424; tumor location: rectum; sample age: 12.9166666666667; rna (ng/ul): 28; sample_well: G06; sentrix_id: 4642203027; sentrix_position: G; plate: 1; ', 'tumor id: 1798; tumor location: colon; sample age: 11.3333333333333; rna (ng/ul): 40; sample_well: G08; sentrix_id: 4642203034; sentrix_position: G; plate: 1; ', 'tumor id: 430; tumor location: colon; sample age: 16.25; rna (ng/ul): 40; sample_well: G09; sentrix_id: 4642203038; sentrix_position: G; plate: 1; ', 'tumor id: 595; tumor location: colon; sample age: 16.1666666666667; rna (ng/ul): 40; sample_well: G10; sentrix_id: 4642203049; sentrix_position: G; plate: 1; ', 'tumor id: 614; tumor location: rectum; sample age: 15.4166666666667; rna (ng/ul): 40; sample_well: G11; sentrix_id: 4642203055; sentrix_position: G; plate: 1; ', 'tumor id: 2384; tumor location: colon; sample age: 11.5833333333333; rna (ng/ul): 40; sample_well: G12; sentrix_id: 4642203062; sentrix_position: G; plate: 1; ', 'tumor id: 664; tumor location: colon; sample age: 16.0833333333333; rna (ng/ul): 40; sample_well: H01; sentrix_id: 4642203001; sentrix_position: H; plate: 1; ', 'tumor id: 2643; tumor location: rectum; sample age: 14.6666666666667; rna (ng/ul): 40; sample_well: H02; sentrix_id: 4642203003; sentrix_position: H; plate: 1; ', 'tumor id: 475; tumor location: colon; sample age: 13.5833333333333; rna (ng/ul): 40; sample_well: H03; sentrix_id: 4642203017; sentrix_position: H; plate: 1; ', 'tumor id: 627; tumor location: colon; sample age: 16.9166666666667; rna (ng/ul): 40; sample_well: H04; sentrix_id: 4642203025; sentrix_position: H; plate: 1; ', 'tumor id: 1749; tumor location: rectum; sample age: 11.25; rna (ng/ul): 40; sample_well: H05; sentrix_id: 4642203026; sentrix_position: H; plate: 1; ', 'tumor id: 1760; tumor location: colon; sample age: 12.75; rna (ng/ul): 27; sample_well: H06; sentrix_id: 4642203027; sentrix_position: H; plate: 1; ', 'tumor id: 1739; tumor location: colon; sample age: 9.58333333333333; rna (ng/ul): 40; sample_well: H07; sentrix_id: 4642203032; sentrix_position: H; plate: 1; ', 'tumor id: 1742; tumor location: colon; sample age: 12.1666666666667; rna (ng/ul): 40; sample_well: H08; sentrix_id: 4642203034; sentrix_position: H; plate: 1; ', 'tumor id: 431; tumor location: rectum; sample age: 13.4166666666667; rna (ng/ul): 40; sample_well: H09; sentrix_id: 4642203038; sentrix_position: H; plate: 1; ', 'tumor id: 605; tumor location: colon; sample age: 16.25; rna (ng/ul): 40; sample_well: H10; sentrix_id: 4642203049; sentrix_position: H; plate: 1; ', 'tumor id: 629; tumor location: colon; sample age: 15.4166666666667; rna (ng/ul): 40; sample_well: H11; sentrix_id: 4642203055; sentrix_position: H; plate: 1; ', 'tumor id: 3340; tumor location: rectum; sample age: 12.5; rna (ng/ul): 40; sample_well: H12; sentrix_id: 4642203062; sentrix_position: H; plate: 1; ', 'tumor id: 1764; tumor location: colon; sample age: 12.3333333333333; rna (ng/ul): 40; sample_well: A01; sentrix_id: 4642203064; sentrix_position: A; plate: 2; ', 'tumor id: 2282; tumor location: colon; sample age: 8.08333333333333; rna (ng/ul): 40; sample_well: A02; sentrix_id: 4642203065; sentrix_position: A; plate: 2; ', 'tumor id: 226; tumor location: colon; sample age: 17.0833333333333; rna (ng/ul): 40; sample_well: A03; sentrix_id: 4642203083; sentrix_position: A; plate: 2; ', 'tumor id: 3001; tumor location: rectum; sample age: 3.33333333333333; rna (ng/ul): 40; sample_well: A05; sentrix_id: 4642203085; sentrix_position: A; plate: 2; ', 'tumor id: 3020; tumor location: rectum; sample age: 6.75; rna (ng/ul): 40; sample_well: A06; sentrix_id: 4642203101; sentrix_position: A; plate: 2; ', 'tumor id: 3266; tumor location: colon; sample age: 6.5; rna (ng/ul): 40; sample_well: A07; sentrix_id: 4642203102; sentrix_position: A; plate: 2; ', 'tumor id: 3244; tumor location: rectum; sample age: 5.75; rna (ng/ul): 40; sample_well: A08; sentrix_id: 4642203103; sentrix_position: A; plate: 2; ', 'tumor id: 3246; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: A09; sentrix_id: 4642203115; sentrix_position: A; plate: 2; ', 'tumor id: 2760; tumor location: colon; sample age: 7.25; rna (ng/ul): 40; sample_well: A10; sentrix_id: 4642203116; sentrix_position: A; plate: 2; ', 'tumor id: 3033; tumor location: rectum; sample age: 4.25; rna (ng/ul): 40; sample_well: A11; sentrix_id: 4642203120; sentrix_position: A; plate: 2; ', 'tumor id: 1209; tumor location: colon; sample age: 8.58333333333333; rna (ng/ul): 40; sample_well: A12; sentrix_id: 4424556043; sentrix_position: A; plate: 2; ', 'tumor id: 660; tumor location: rectum; sample age: 15.4166666666667; rna (ng/ul): 40; sample_well: B01; sentrix_id: 4642203064; sentrix_position: B; plate: 2; ', 'tumor id: 2284; tumor location: colon; sample age: 7.5; rna (ng/ul): 40; sample_well: B02; sentrix_id: 4642203065; sentrix_position: B; plate: 2; ', 'tumor id: 351; tumor location: colon; sample age: 27.8333333333333; rna (ng/ul): 31; sample_well: B03; sentrix_id: 4642203083; sentrix_position: B; plate: 2; ', 'tumor id: 2940; tumor location: rectum; sample age: 6.75; rna (ng/ul): 40; sample_well: B05; sentrix_id: 4642203085; sentrix_position: B; plate: 2; ', 'tumor id: 3034; tumor location: colon; sample age: 6.41666666666667; rna (ng/ul): 40; sample_well: B06; sentrix_id: 4642203101; sentrix_position: B; plate: 2; ', 'tumor id: 3178; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: B07; sentrix_id: 4642203102; sentrix_position: B; plate: 2; ', 'tumor id: 3188; tumor location: colon; sample age: 5.08333333333333; rna (ng/ul): 40; sample_well: B08; sentrix_id: 4642203103; sentrix_position: B; plate: 2; ', 'tumor id: 3249; tumor location: rectum; sample age: 6.08333333333333; rna (ng/ul): 40; sample_well: B09; sentrix_id: 4642203115; sentrix_position: B; plate: 2; ', 'tumor id: 2936; tumor location: rectum; sample age: 7.5; rna (ng/ul): 40; sample_well: B10; sentrix_id: 4642203116; sentrix_position: B; plate: 2; ', 'tumor id: 3110; tumor location: colon; sample age: 6.58333333333333; rna (ng/ul): 40; sample_well: B11; sentrix_id: 4642203120; sentrix_position: B; plate: 2; ', 'tumor id: 2224; tumor location: rectum; sample age: 12.6666666666667; rna (ng/ul): 40; sample_well: C01; sentrix_id: 4642203064; sentrix_position: C; plate: 2; ', 'tumor id: 20; tumor location: rectum; sample age: 20.4166666666667; rna (ng/ul): 40; sample_well: C02; sentrix_id: 4642203065; sentrix_position: C; plate: 2; ', 'tumor id: 373; tumor location: colon; sample age: 20.1666666666667; rna (ng/ul): 40; sample_well: C03; sentrix_id: 4642203083; sentrix_position: C; plate: 2; ', 'tumor id: 3024; tumor location: rectum; sample age: 5.33333333333333; rna (ng/ul): 40; sample_well: C04; sentrix_id: 4642203084; sentrix_position: C; plate: 2; ', 'tumor id: 2953; tumor location: rectum; sample age: 5.16666666666667; rna (ng/ul): 40; sample_well: C05; sentrix_id: 4642203085; sentrix_position: C; plate: 2; ', 'tumor id: 3255; tumor location: rectum; sample age: 4.08333333333333; rna (ng/ul): 40; sample_well: C07; sentrix_id: 4642203102; sentrix_position: C; plate: 2; ', 'tumor id: 3233; tumor location: colon; sample age: 4.66666666666667; rna (ng/ul): 40; sample_well: C09; sentrix_id: 4642203115; sentrix_position: C; plate: 2; ', 'tumor id: 2967; tumor location: colon; sample age: 6.83333333333333; rna (ng/ul): 40; sample_well: C10; sentrix_id: 4642203116; sentrix_position: C; plate: 2; ', 'tumor id: 3267; tumor location: rectum; sample age: 5.66666666666667; rna (ng/ul): 40; sample_well: C11; sentrix_id: 4642203120; sentrix_position: C; plate: 2; ', 'tumor id: 3331; tumor location: colon; sample age: 4.58333333333333; rna (ng/ul): 36; sample_well: C12; sentrix_id: 4424556043; sentrix_position: C; plate: 2; ', 'tumor id: 2345; tumor location: colon; sample age: 22.3333333333333; rna (ng/ul): 40; sample_well: D01; sentrix_id: 4642203064; sentrix_position: D; plate: 2; ', 'tumor id: 3052; tumor location: rectum; sample age: 4.58333333333333; rna (ng/ul): 40; sample_well: D04; sentrix_id: 4642203084; sentrix_position: D; plate: 2; ', 'tumor id: 2973; tumor location: rectum; sample age: 6.91666666666667; rna (ng/ul): 40; sample_well: D05; sentrix_id: 4642203085; sentrix_position: D; plate: 2; ', 'tumor id: 3037; tumor location: rectum; sample age: 6.75; rna (ng/ul): 40; sample_well: D06; sentrix_id: 4642203101; sentrix_position: D; plate: 2; ', 'tumor id: 3241; tumor location: rectum; sample age: 3.58333333333333; rna (ng/ul): 40; sample_well: D07; sentrix_id: 4642203102; sentrix_position: D; plate: 2; ', 'tumor id: 3182; tumor location: rectum; sample age: 9.16666666666667; rna (ng/ul): 40; sample_well: D08; sentrix_id: 4642203103; sentrix_position: D; plate: 2; ', 'tumor id: 3174; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: D09; sentrix_id: 4642203115; sentrix_position: D; plate: 2; ', 'tumor id: 3014; tumor location: rectum; sample age: 4.25; rna (ng/ul): 40; sample_well: D10; sentrix_id: 4642203116; sentrix_position: D; plate: 2; ', 'tumor id: 3227; tumor location: colon; sample age: 5.91666666666667; rna (ng/ul): 40; sample_well: D11; sentrix_id: 4642203120; sentrix_position: D; plate: 2; ', 'tumor id: 3205; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: D12; sentrix_id: 4424556043; sentrix_position: D; plate: 2; ', 'tumor id: 1844; tumor location: rectum; sample age: 9.5; rna (ng/ul): 40; sample_well: E01; sentrix_id: 4642203064; sentrix_position: E; plate: 2; ', 'tumor id: 2949; tumor location: colon; sample age: 6.83333333333333; rna (ng/ul): 40; sample_well: E02; sentrix_id: 4642203065; sentrix_position: E; plate: 2; ', 'tumor id: 3398; tumor location: colon; sample age: 6.75; rna (ng/ul): 40; sample_well: E03; sentrix_id: 4642203083; sentrix_position: E; plate: 2; ', 'tumor id: 3155; tumor location: rectum; sample age: null; rna (ng/ul): 35; sample_well: E04; sentrix_id: 4642203084; sentrix_position: E; plate: 2; ', 'tumor id: 2974; tumor location: rectum; sample age: 4.58333333333333; rna (ng/ul): 40; sample_well: E05; sentrix_id: 4642203085; sentrix_position: E; plate: 2; ', 'tumor id: 3038; tumor location: colon; sample age: 7.58333333333333; rna (ng/ul): 40; sample_well: E06; sentrix_id: 4642203101; sentrix_position: E; plate: 2; ', 'tumor id: 3318; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: E07; sentrix_id: 4642203102; sentrix_position: E; plate: 2; ', 'tumor id: 3325; tumor location: rectum; sample age: 5.25; rna (ng/ul): 37; sample_well: E08; sentrix_id: 4642203103; sentrix_position: E; plate: 2; ', 'tumor id: 2947; tumor location: colon; sample age: 8.08333333333333; rna (ng/ul): 40; sample_well: E09; sentrix_id: 4642203115; sentrix_position: E; plate: 2; ', 'tumor id: 2458; tumor location: colon; sample age: 8.91666666666667; rna (ng/ul): 40; sample_well: E10; sentrix_id: 4642203116; sentrix_position: E; plate: 2; ', 'tumor id: 3323; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: E11; sentrix_id: 4642203120; sentrix_position: E; plate: 2; ', 'tumor id: 1854; tumor location: colon; sample age: 11.5; rna (ng/ul): 40; sample_well: F01; sentrix_id: 4642203064; sentrix_position: F; plate: 2; ', 'tumor id: 110; tumor location: colon; sample age: 24.5833333333333; rna (ng/ul): 40; sample_well: F02; sentrix_id: 4642203065; sentrix_position: F; plate: 2; ', 'tumor id: 392; tumor location: colon; sample age: 28.25; rna (ng/ul): 40; sample_well: F03; sentrix_id: 4642203083; sentrix_position: F; plate: 2; ', 'tumor id: 2269; tumor location: colon; sample age: 11.25; rna (ng/ul): 40; sample_well: F04; sentrix_id: 4642203084; sentrix_position: F; plate: 2; ', 'tumor id: 2955; tumor location: rectum; sample age: 5.33333333333333; rna (ng/ul): 40; sample_well: F05; sentrix_id: 4642203085; sentrix_position: F; plate: 2; ', 'tumor id: 2929; tumor location: colon; sample age: 8.08333333333333; rna (ng/ul): 40; sample_well: F06; sentrix_id: 4642203101; sentrix_position: F; plate: 2; ', 'tumor id: 3204; tumor location: rectum; sample age: 6.16666666666667; rna (ng/ul): 39; sample_well: F07; sentrix_id: 4642203102; sentrix_position: F; plate: 2; ', 'tumor id: 3190; tumor location: colon; sample age: 5.16666666666667; rna (ng/ul): 40; sample_well: F08; sentrix_id: 4642203103; sentrix_position: F; plate: 2; ', 'tumor id: 3226; tumor location: colon; sample age: 5.5; rna (ng/ul): 40; sample_well: F09; sentrix_id: 4642203115; sentrix_position: F; plate: 2; ', 'tumor id: 3005; tumor location: rectum; sample age: 4.5; rna (ng/ul): 40; sample_well: F10; sentrix_id: 4642203116; sentrix_position: F; plate: 2; ', 'tumor id: 3273; tumor location: rectum; sample age: 5.5; rna (ng/ul): 40; sample_well: F11; sentrix_id: 4642203120; sentrix_position: F; plate: 2; ', 'tumor id: 3298; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: F12; sentrix_id: 4424556043; sentrix_position: F; plate: 2; ', 'tumor id: 2225; tumor location: rectum; sample age: 9.91666666666667; rna (ng/ul): 40; sample_well: G01; sentrix_id: 4642203064; sentrix_position: G; plate: 2; ', 'tumor id: 132; tumor location: colon; sample age: 16.75; rna (ng/ul): 40; sample_well: G02; sentrix_id: 4642203065; sentrix_position: G; plate: 2; ', 'tumor id: 631; tumor location: colon; sample age: 15.1666666666667; rna (ng/ul): 29; sample_well: G03; sentrix_id: 4642203083; sentrix_position: G; plate: 2; ', 'tumor id: 41; tumor location: rectum; sample age: 27.5; rna (ng/ul): 40; sample_well: G04; sentrix_id: 4642203084; sentrix_position: G; plate: 2; ', 'tumor id: 2987; tumor location: rectum; sample age: 5.66666666666667; rna (ng/ul): 40; sample_well: G05; sentrix_id: 4642203085; sentrix_position: G; plate: 2; ', 'tumor id: 2932; tumor location: rectum; sample age: 5.16666666666667; rna (ng/ul): 40; sample_well: G06; sentrix_id: 4642203101; sentrix_position: G; plate: 2; ', 'tumor id: 3142; tumor location: colon; sample age: 7.08333333333333; rna (ng/ul): 40; sample_well: G07; sentrix_id: 4642203102; sentrix_position: G; plate: 2; ', 'tumor id: 3299; tumor location: colon; sample age: 8.75; rna (ng/ul): 40; sample_well: G08; sentrix_id: 4642203103; sentrix_position: G; plate: 2; ', 'tumor id: 3262; tumor location: rectum; sample age: 6.33333333333333; rna (ng/ul): 40; sample_well: G09; sentrix_id: 4642203115; sentrix_position: G; plate: 2; ', 'tumor id: 3261; tumor location: colon; sample age: 8.16666666666667; rna (ng/ul): 17; sample_well: G10; sentrix_id: 4642203116; sentrix_position: G; plate: 2; ', 'tumor id: 3238; tumor location: rectum; sample age: 6.5; rna (ng/ul): 40; sample_well: G11; sentrix_id: 4642203120; sentrix_position: G; plate: 2; ', 'tumor id: 2941; tumor location: rectum; sample age: 5.41666666666667; rna (ng/ul): 40; sample_well: G12; sentrix_id: 4424556043; sentrix_position: G; plate: 2; ', 'tumor id: 2272; tumor location: rectum; sample age: 7.66666666666667; rna (ng/ul): 40; sample_well: H01; sentrix_id: 4642203064; sentrix_position: H; plate: 2; ', 'tumor id: 137; tumor location: colon; sample age: 23.25; rna (ng/ul): 40; sample_well: H02; sentrix_id: 4642203065; sentrix_position: H; plate: 2; ', 'tumor id: 676; tumor location: colon; sample age: 14.8333333333333; rna (ng/ul): 40; sample_well: H03; sentrix_id: 4642203083; sentrix_position: H; plate: 2; ', 'tumor id: 191; tumor location: rectum; sample age: 11.6666666666667; rna (ng/ul): 40; sample_well: H04; sentrix_id: 4642203084; sentrix_position: H; plate: 2; ', 'tumor id: 3004; tumor location: colon; sample age: 6.41666666666667; rna (ng/ul): 40; sample_well: H05; sentrix_id: 4642203085; sentrix_position: H; plate: 2; ', 'tumor id: 3224; tumor location: rectum; sample age: 6.25; rna (ng/ul): 40; sample_well: H06; sentrix_id: 4642203101; sentrix_position: H; plate: 2; ', 'tumor id: 3330; tumor location: rectum; sample age: 6.16666666666667; rna (ng/ul): 40; sample_well: H07; sentrix_id: 4642203102; sentrix_position: H; plate: 2; ', 'tumor id: 3169; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: H09; sentrix_id: 4642203115; sentrix_position: H; plate: 2; ', 'tumor id: 2959; tumor location: colon; sample age: 8.25; rna (ng/ul): 40; sample_well: H10; sentrix_id: 4642203116; sentrix_position: H; plate: 2; ', 'tumor id: 3016; tumor location: rectum; sample age: 5.25; rna (ng/ul): 40; sample_well: H11; sentrix_id: 4642203120; sentrix_position: H; plate: 2; ', 'tumor id: 3321; tumor location: rectum; sample age: 6.75; rna (ng/ul): 40; sample_well: H12; sentrix_id: 4424556043; sentrix_position: H; plate: 2; ', 'tumor id: 3147; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: A01; sentrix_id: 4642203013; sentrix_position: A; plate: 3; ', 'tumor id: 3336; tumor location: rectum; sample age: 10.5; rna (ng/ul): 40; sample_well: A02; sentrix_id: 4642203014; sentrix_position: A; plate: 3; ', 'tumor id: 2992; tumor location: rectum; sample age: 8.16666666666667; rna (ng/ul): 40; sample_well: A03; sentrix_id: 4642203015; sentrix_position: A; plate: 3; ', 'tumor id: 3084; tumor location: rectum; sample age: 4.16666666666667; rna (ng/ul): 40; sample_well: A04; sentrix_id: 4642203028; sentrix_position: A; plate: 3; ', 'tumor id: 2441; tumor location: colon; sample age: 9.91666666666667; rna (ng/ul): 40; sample_well: A05; sentrix_id: 4642203029; sentrix_position: A; plate: 3; ', 'tumor id: 3247; tumor location: rectum; sample age: 6.25; rna (ng/ul): 29; sample_well: A06; sentrix_id: 4642203051; sentrix_position: A; plate: 3; ', 'tumor id: 2565; tumor location: colon; sample age: 11.8333333333333; rna (ng/ul): 40; sample_well: A07; sentrix_id: 4642203069; sentrix_position: A; plate: 3; ', 'tumor id: 50; tumor location: colon; sample age: 24; rna (ng/ul): 40; sample_well: A08; sentrix_id: 4642203080; sentrix_position: A; plate: 3; ', 'tumor id: 195; tumor location: rectum; sample age: 12.4166666666667; rna (ng/ul): 40; sample_well: A09; sentrix_id: 4642203088; sentrix_position: A; plate: 3; ', 'tumor id: 37; tumor location: colon; sample age: 15.6666666666667; rna (ng/ul): 31; sample_well: A10; sentrix_id: 4642203114; sentrix_position: A; plate: 3; ', 'tumor id: 3404; tumor location: rectum; sample age: null; rna (ng/ul): 29; sample_well: A11; sentrix_id: 4646298009; sentrix_position: A; plate: 3; ', 'tumor id: 2383; tumor location: colon; sample age: 23.9166666666667; rna (ng/ul): 40; sample_well: A12; sentrix_id: 4646298010; sentrix_position: A; plate: 3; ', 'tumor id: 3167; tumor location: colon; sample age: 6.83333333333333; rna (ng/ul): 40; sample_well: B01; sentrix_id: 4642203013; sentrix_position: B; plate: 3; ', 'tumor id: 3337; tumor location: colon; sample age: 7; rna (ng/ul): 33; sample_well: B02; sentrix_id: 4642203014; sentrix_position: B; plate: 3; ', 'tumor id: 2763; tumor location: colon; sample age: 9.41666666666667; rna (ng/ul): 40; sample_well: B03; sentrix_id: 4642203015; sentrix_position: B; plate: 3; ', 'tumor id: 2976; tumor location: rectum; sample age: 6.41666666666667; rna (ng/ul): 40; sample_well: B04; sentrix_id: 4642203028; sentrix_position: B; plate: 3; ', 'tumor id: 231; tumor location: rectum; sample age: 12.75; rna (ng/ul): 40; sample_well: B05; sentrix_id: 4642203029; sentrix_position: B; plate: 3; ', 'tumor id: 3184; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: B06; sentrix_id: 4642203051; sentrix_position: B; plate: 3; ', 'tumor id: 45; tumor location: colon; sample age: 24.6666666666667; rna (ng/ul): 40; sample_well: B08; sentrix_id: 4642203080; sentrix_position: B; plate: 3; ', 'tumor id: 2354; tumor location: colon; sample age: 14.25; rna (ng/ul): 40; sample_well: B09; sentrix_id: 4642203088; sentrix_position: B; plate: 3; ', 'tumor id: 32; tumor location: rectum; sample age: 14.3333333333333; rna (ng/ul): 40; sample_well: B10; sentrix_id: 4642203114; sentrix_position: B; plate: 3; ', 'tumor id: 3400; tumor location: colon; sample age: 6.58333333333333; rna (ng/ul): 40; sample_well: B11; sentrix_id: 4646298009; sentrix_position: B; plate: 3; ', 'tumor id: 63; tumor location: rectum; sample age: 14.5833333333333; rna (ng/ul): 40; sample_well: B12; sentrix_id: 4646298010; sentrix_position: B; plate: 3; ', 'tumor id: 3170; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: C01; sentrix_id: 4642203013; sentrix_position: C; plate: 3; ', 'tumor id: 3036; tumor location: rectum; sample age: 6.25; rna (ng/ul): 40; sample_well: C02; sentrix_id: 4642203014; sentrix_position: C; plate: 3; ', 'tumor id: 2999; tumor location: colon; sample age: 6.75; rna (ng/ul): 40; sample_well: C03; sentrix_id: 4642203015; sentrix_position: C; plate: 3; ', 'tumor id: 2944; tumor location: rectum; sample age: 8.25; rna (ng/ul): 40; sample_well: C04; sentrix_id: 4642203028; sentrix_position: C; plate: 3; ', 'tumor id: 2647; tumor location: colon; sample age: 9.16666666666667; rna (ng/ul): 40; sample_well: C05; sentrix_id: 4642203029; sentrix_position: C; plate: 3; ', 'tumor id: 2637; tumor location: colon; sample age: 6.75; rna (ng/ul): 40; sample_well: C06; sentrix_id: 4642203051; sentrix_position: C; plate: 3; ', 'tumor id: 76; tumor location: rectum; sample age: 11.5833333333333; rna (ng/ul): 40; sample_well: C07; sentrix_id: 4642203069; sentrix_position: C; plate: 3; ', 'tumor id: 347; tumor location: rectum; sample age: 11.4166666666667; rna (ng/ul): 40; sample_well: C08; sentrix_id: 4642203080; sentrix_position: C; plate: 3; ', 'tumor id: 253; tumor location: rectum; sample age: 13.4166666666667; rna (ng/ul): 40; sample_well: C09; sentrix_id: 4642203088; sentrix_position: C; plate: 3; ', 'tumor id: 30; tumor location: rectum; sample age: 11.6666666666667; rna (ng/ul): 40; sample_well: C10; sentrix_id: 4642203114; sentrix_position: C; plate: 3; ', 'tumor id: 60; tumor location: rectum; sample age: 18.9166666666667; rna (ng/ul): 40; sample_well: C11; sentrix_id: 4646298009; sentrix_position: C; plate: 3; ', 'tumor id: 3288; tumor location: colon; sample age: 6.58333333333333; rna (ng/ul): 40; sample_well: C12; sentrix_id: 4646298010; sentrix_position: C; plate: 3; ', 'tumor id: 3172; tumor location: rectum; sample age: null; rna (ng/ul): 26; sample_well: D01; sentrix_id: 4642203013; sentrix_position: D; plate: 3; ', 'tumor id: 2956; tumor location: colon; sample age: 7.41666666666667; rna (ng/ul): 40; sample_well: D02; sentrix_id: 4642203014; sentrix_position: D; plate: 3; ', 'tumor id: 3025; tumor location: rectum; sample age: 6.41666666666667; rna (ng/ul): 40; sample_well: D03; sentrix_id: 4642203015; sentrix_position: D; plate: 3; ', 'tumor id: 2768; tumor location: colon; sample age: 7; rna (ng/ul): 40; sample_well: D04; sentrix_id: 4642203028; sentrix_position: D; plate: 3; ', 'tumor id: 186; tumor location: colon; sample age: 12.4166666666667; rna (ng/ul): 40; sample_well: D05; sentrix_id: 4642203029; sentrix_position: D; plate: 3; ', 'tumor id: 61; tumor location: colon; sample age: 12.25; rna (ng/ul): 40; sample_well: D06; sentrix_id: 4642203051; sentrix_position: D; plate: 3; ', 'tumor id: 311; tumor location: colon; sample age: 14.0833333333333; rna (ng/ul): 40; sample_well: D07; sentrix_id: 4642203069; sentrix_position: D; plate: 3; ', 'tumor id: 38; tumor location: colon; sample age: 9.66666666666667; rna (ng/ul): 40; sample_well: D08; sentrix_id: 4642203080; sentrix_position: D; plate: 3; ', 'tumor id: 1180; tumor location: rectum; sample age: 12.3333333333333; rna (ng/ul): 40; sample_well: D09; sentrix_id: 4642203088; sentrix_position: D; plate: 3; ', 'tumor id: 24; tumor location: colon; sample age: 13.9166666666667; rna (ng/ul): 40; sample_well: D10; sentrix_id: 4642203114; sentrix_position: D; plate: 3; ', 'tumor id: 2372; tumor location: rectum; sample age: 13.75; rna (ng/ul): 40; sample_well: D11; sentrix_id: 4646298009; sentrix_position: D; plate: 3; ', 'tumor id: 71; tumor location: rectum; sample age: 11.8333333333333; rna (ng/ul): 40; sample_well: D12; sentrix_id: 4646298010; sentrix_position: D; plate: 3; ', 'tumor id: 2969; tumor location: rectum; sample age: 8.33333333333333; rna (ng/ul): 40; sample_well: E01; sentrix_id: 4642203013; sentrix_position: E; plate: 3; ', 'tumor id: 2963; tumor location: rectum; sample age: 6.16666666666667; rna (ng/ul): 40; sample_well: E02; sentrix_id: 4642203014; sentrix_position: E; plate: 3; ', 'tumor id: 3265; tumor location: colon; sample age: 5.58333333333333; rna (ng/ul): 40; sample_well: E03; sentrix_id: 4642203015; sentrix_position: E; plate: 3; ', 'tumor id: 3002; tumor location: colon; sample age: 5.5; rna (ng/ul): 40; sample_well: E04; sentrix_id: 4642203028; sentrix_position: E; plate: 3; ', 'tumor id: 263; tumor location: rectum; sample age: 11.4166666666667; rna (ng/ul): 40; sample_well: E05; sentrix_id: 4642203029; sentrix_position: E; plate: 3; ', 'tumor id: 66; tumor location: colon; sample age: 16.75; rna (ng/ul): 40; sample_well: E06; sentrix_id: 4642203051; sentrix_position: E; plate: 3; ', 'tumor id: 18; tumor location: colon; sample age: 11.8333333333333; rna (ng/ul): 40; sample_well: E07; sentrix_id: 4642203069; sentrix_position: E; plate: 3; ', 'tumor id: 348; tumor location: colon; sample age: 17.8333333333333; rna (ng/ul): 40; sample_well: E08; sentrix_id: 4642203080; sentrix_position: E; plate: 3; ', 'tumor id: 527; tumor location: rectum; sample age: 18.4166666666667; rna (ng/ul): 40; sample_well: E09; sentrix_id: 4642203088; sentrix_position: E; plate: 3; ', 'tumor id: 33; tumor location: rectum; sample age: 12.1666666666667; rna (ng/ul): 40; sample_well: E10; sentrix_id: 4642203114; sentrix_position: E; plate: 3; ', 'tumor id: 2388; tumor location: colon; sample age: 16.9166666666667; rna (ng/ul): 40; sample_well: E11; sentrix_id: 4646298009; sentrix_position: E; plate: 3; ', 'tumor id: 322; tumor location: rectum; sample age: 17.0833333333333; rna (ng/ul): 40; sample_well: E12; sentrix_id: 4646298010; sentrix_position: E; plate: 3; ', 'tumor id: 3305; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: F01; sentrix_id: 4642203013; sentrix_position: F; plate: 3; ', 'tumor id: 2938; tumor location: colon; sample age: 6.83333333333333; rna (ng/ul): 40; sample_well: F02; sentrix_id: 4642203014; sentrix_position: F; plate: 3; ', 'tumor id: 2939; tumor location: colon; sample age: 6.33333333333333; rna (ng/ul): 40; sample_well: F03; sentrix_id: 4642203015; sentrix_position: F; plate: 3; ', 'tumor id: 3018; tumor location: rectum; sample age: 5.91666666666667; rna (ng/ul): 40; sample_well: F04; sentrix_id: 4642203028; sentrix_position: F; plate: 3; ', 'tumor id: 284; tumor location: colon; sample age: 12; rna (ng/ul): 40; sample_well: F05; sentrix_id: 4642203029; sentrix_position: F; plate: 3; ', 'tumor id: 335; tumor location: rectum; sample age: 12.25; rna (ng/ul): 40; sample_well: F06; sentrix_id: 4642203051; sentrix_position: F; plate: 3; ', 'tumor id: 2380; tumor location: colon; sample age: 14.75; rna (ng/ul): 40; sample_well: F07; sentrix_id: 4642203069; sentrix_position: F; plate: 3; ', 'tumor id: 225; tumor location: colon; sample age: 15.3333333333333; rna (ng/ul): 40; sample_well: F08; sentrix_id: 4642203080; sentrix_position: F; plate: 3; ', 'tumor id: 304; tumor location: colon; sample age: 15.6666666666667; rna (ng/ul): 40; sample_well: F09; sentrix_id: 4642203088; sentrix_position: F; plate: 3; ', 'tumor id: 19; tumor location: colon; sample age: 16.25; rna (ng/ul): 40; sample_well: F10; sentrix_id: 4642203114; sentrix_position: F; plate: 3; ', 'tumor id: 2950; tumor location: colon; sample age: 5.16666666666667; rna (ng/ul): 40; sample_well: F11; sentrix_id: 4646298009; sentrix_position: F; plate: 3; ', 'tumor id: 196; tumor location: colon; sample age: 16.8333333333333; rna (ng/ul): 40; sample_well: F12; sentrix_id: 4646298010; sentrix_position: F; plate: 3; ', 'tumor id: 2948; tumor location: colon; sample age: 4.58333333333333; rna (ng/ul): 40; sample_well: G02; sentrix_id: 4642203014; sentrix_position: G; plate: 3; ', 'tumor id: 2951; tumor location: colon; sample age: 5.66666666666667; rna (ng/ul): 40; sample_well: G03; sentrix_id: 4642203015; sentrix_position: G; plate: 3; ', 'tumor id: 2767; tumor location: colon; sample age: 9.5; rna (ng/ul): 40; sample_well: G04; sentrix_id: 4642203028; sentrix_position: G; plate: 3; ', 'tumor id: 407; tumor location: rectum; sample age: 18.5; rna (ng/ul): 40; sample_well: G05; sentrix_id: 4642203029; sentrix_position: G; plate: 3; ', 'tumor id: 248; tumor location: rectum; sample age: 14.5833333333333; rna (ng/ul): 40; sample_well: G06; sentrix_id: 4642203051; sentrix_position: G; plate: 3; ', 'tumor id: 42; tumor location: colon; sample age: 15.5833333333333; rna (ng/ul): 40; sample_well: G07; sentrix_id: 4642203069; sentrix_position: G; plate: 3; ', 'tumor id: 53; tumor location: colon; sample age: 23.3333333333333; rna (ng/ul): 40; sample_well: G08; sentrix_id: 4642203080; sentrix_position: G; plate: 3; ', 'tumor id: 27; tumor location: colon; sample age: 20.5833333333333; rna (ng/ul): 40; sample_well: G11; sentrix_id: 4646298009; sentrix_position: G; plate: 3; ', 'tumor id: 3225; tumor location: colon; sample age: 5.75; rna (ng/ul): 40; sample_well: G12; sentrix_id: 4646298010; sentrix_position: G; plate: 3; ', 'tumor id: 3308; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: H01; sentrix_id: 4642203013; sentrix_position: H; plate: 3; ', 'tumor id: 3008; tumor location: rectum; sample age: 7.41666666666667; rna (ng/ul): 40; sample_well: H02; sentrix_id: 4642203014; sentrix_position: H; plate: 3; ', 'tumor id: 2991; tumor location: rectum; sample age: 9.5; rna (ng/ul): 40; sample_well: H03; sentrix_id: 4642203015; sentrix_position: H; plate: 3; ', 'tumor id: 2769; tumor location: rectum; sample age: 7.08333333333333; rna (ng/ul): 40; sample_well: H04; sentrix_id: 4642203028; sentrix_position: H; plate: 3; ', 'tumor id: 446; tumor location: colon; sample age: 18.0833333333333; rna (ng/ul): 29; sample_well: H05; sentrix_id: 4642203029; sentrix_position: H; plate: 3; ', 'tumor id: 215; tumor location: colon; sample age: 21.5; rna (ng/ul): 40; sample_well: H06; sentrix_id: 4642203051; sentrix_position: H; plate: 3; ', 'tumor id: 46; tumor location: colon; sample age: 18; rna (ng/ul): 40; sample_well: H07; sentrix_id: 4642203069; sentrix_position: H; plate: 3; ', 'tumor id: 250; tumor location: rectum; sample age: 9.41666666666667; rna (ng/ul): 40; sample_well: H08; sentrix_id: 4642203080; sentrix_position: H; plate: 3; ', 'tumor id: 2954; tumor location: rectum; sample age: 6.33333333333333; rna (ng/ul): 40; sample_well: H09; sentrix_id: 4642203088; sentrix_position: H; plate: 3; ', 'tumor id: 285; tumor location: colon; sample age: 21.4166666666667; rna (ng/ul): 40; sample_well: H10; sentrix_id: 4642203114; sentrix_position: H; plate: 3; ', 'tumor id: 25; tumor location: colon; sample age: 22.1666666666667; rna (ng/ul): 40; sample_well: H11; sentrix_id: 4646298009; sentrix_position: H; plate: 3; ', 'tumor id: 62; tumor location: rectum; sample age: 14; rna (ng/ul): 40; sample_well: H12; sentrix_id: 4646298010; sentrix_position: H; plate: 3; ', 'tumor id: 2946; tumor location: rectum; sample age: 6; rna (ng/ul): 40; sample_well: A02; sentrix_id: 4646298015; sentrix_position: A; plate: 4; ', 'tumor id: 2997; tumor location: colon; sample age: 5.58333333333333; rna (ng/ul): 40; sample_well: A03; sentrix_id: 4646298016; sentrix_position: A; plate: 4; ', 'tumor id: 2933; tumor location: rectum; sample age: 6.25; rna (ng/ul): 40; sample_well: A04; sentrix_id: 4646298017; sentrix_position: A; plate: 4; ', 'tumor id: 2418; tumor location: colon; sample age: 11.0833333333333; rna (ng/ul): 40; sample_well: A05; sentrix_id: 4646298018; sentrix_position: A; plate: 4; ', 'tumor id: 2984; tumor location: rectum; sample age: 7.25; rna (ng/ul): 40; sample_well: A06; sentrix_id: 4646298020; sentrix_position: A; plate: 4; ', 'tumor id: 2614; tumor location: rectum; sample age: 16.9166666666667; rna (ng/ul): 40; sample_well: A07; sentrix_id: 4646298021; sentrix_position: A; plate: 4; ', 'tumor id: 264; tumor location: colon; sample age: 12; rna (ng/ul): 40; sample_well: A08; sentrix_id: 4646298023; sentrix_position: A; plate: 4; ', 'tumor id: 109; tumor location: colon; sample age: 16.4166666666667; rna (ng/ul): 40; sample_well: A10; sentrix_id: 4646298033; sentrix_position: A; plate: 4; ', 'tumor id: 326; tumor location: rectum; sample age: 11.25; rna (ng/ul): 32; sample_well: A11; sentrix_id: 4646298034; sentrix_position: A; plate: 4; ', 'tumor id: 251; tumor location: rectum; sample age: 13.3333333333333; rna (ng/ul): 40; sample_well: A12; sentrix_id: 4654538045; sentrix_position: A; plate: 4; ', 'tumor id: 197; tumor location: rectum; sample age: 18.6666666666667; rna (ng/ul): 40; sample_well: B01; sentrix_id: 4646298011; sentrix_position: B; plate: 4; ', 'tumor id: 3000; tumor location: rectum; sample age: 5.25; rna (ng/ul): 40; sample_well: B02; sentrix_id: 4646298015; sentrix_position: B; plate: 4; ', 'tumor id: 3021; tumor location: rectum; sample age: 7.25; rna (ng/ul): 40; sample_well: B03; sentrix_id: 4646298016; sentrix_position: B; plate: 4; ', 'tumor id: 2982; tumor location: rectum; sample age: 4.91666666666667; rna (ng/ul): 22; sample_well: B06; sentrix_id: 4646298020; sentrix_position: B; plate: 4; ', 'tumor id: 3319; tumor location: rectum; sample age: 6.66666666666667; rna (ng/ul): 40; sample_well: B07; sentrix_id: 4646298021; sentrix_position: B; plate: 4; ', 'tumor id: 93; tumor location: colon; sample age: 12.0833333333333; rna (ng/ul): 40; sample_well: B08; sentrix_id: 4646298023; sentrix_position: B; plate: 4; ', 'tumor id: 119; tumor location: rectum; sample age: 12.0833333333333; rna (ng/ul): 40; sample_well: B09; sentrix_id: 4646298032; sentrix_position: B; plate: 4; ', 'tumor id: 92; tumor location: rectum; sample age: 12.6666666666667; rna (ng/ul): 40; sample_well: B10; sentrix_id: 4646298033; sentrix_position: B; plate: 4; ', 'tumor id: 292; tumor location: rectum; sample age: 12.75; rna (ng/ul): 40; sample_well: B11; sentrix_id: 4646298034; sentrix_position: B; plate: 4; ', 'tumor id: 123; tumor location: colon; sample age: 12.5; rna (ng/ul): 40; sample_well: B12; sentrix_id: 4654538045; sentrix_position: B; plate: 4; ', 'tumor id: 2998; tumor location: colon; sample age: 5.58333333333333; rna (ng/ul): 40; sample_well: C02; sentrix_id: 4646298015; sentrix_position: C; plate: 4; ', 'tumor id: 2993; tumor location: rectum; sample age: 7.66666666666667; rna (ng/ul): 25; sample_well: C03; sentrix_id: 4646298016; sentrix_position: C; plate: 4; ', 'tumor id: 1221; tumor location: rectum; sample age: 9.08333333333333; rna (ng/ul): 40; sample_well: C04; sentrix_id: 4646298017; sentrix_position: C; plate: 4; ', 'tumor id: 2765; tumor location: rectum; sample age: 6.66666666666667; rna (ng/ul): 40; sample_well: C05; sentrix_id: 4646298018; sentrix_position: C; plate: 4; ', 'tumor id: 2957; tumor location: rectum; sample age: 7.33333333333333; rna (ng/ul): 40; sample_well: C07; sentrix_id: 4646298021; sentrix_position: C; plate: 4; ', 'tumor id: 280; tumor location: colon; sample age: 14.5; rna (ng/ul): 40; sample_well: C08; sentrix_id: 4646298023; sentrix_position: C; plate: 4; ', 'tumor id: 2367; tumor location: rectum; sample age: 20.4166666666667; rna (ng/ul): 40; sample_well: C09; sentrix_id: 4646298032; sentrix_position: C; plate: 4; ', 'tumor id: 88; tumor location: rectum; sample age: 15.3333333333333; rna (ng/ul): 40; sample_well: C11; sentrix_id: 4646298034; sentrix_position: C; plate: 4; ', 'tumor id: 277; tumor location: rectum; sample age: 11.0833333333333; rna (ng/ul): 40; sample_well: C12; sentrix_id: 4654538045; sentrix_position: C; plate: 4; ', 'tumor id: 43; tumor location: colon; sample age: 23; rna (ng/ul): 40; sample_well: D01; sentrix_id: 4646298011; sentrix_position: D; plate: 4; ', 'tumor id: 3240; tumor location: colon; sample age: 6.66666666666667; rna (ng/ul): 40; sample_well: D02; sentrix_id: 4646298015; sentrix_position: D; plate: 4; ', 'tumor id: 2994; tumor location: colon; sample age: 3.83333333333333; rna (ng/ul): 40; sample_well: D03; sentrix_id: 4646298016; sentrix_position: D; plate: 4; ', 'tumor id: 2621; tumor location: colon; sample age: 7.91666666666667; rna (ng/ul): 40; sample_well: D04; sentrix_id: 4646298017; sentrix_position: D; plate: 4; ', 'tumor id: 2971; tumor location: rectum; sample age: 7.66666666666667; rna (ng/ul): 36; sample_well: D05; sentrix_id: 4646298018; sentrix_position: D; plate: 4; ', 'tumor id: 3269; tumor location: rectum; sample age: 5.41666666666667; rna (ng/ul): 40; sample_well: D06; sentrix_id: 4646298020; sentrix_position: D; plate: 4; ', 'tumor id: 10; tumor location: colon; sample age: 13.6666666666667; rna (ng/ul): 40; sample_well: D07; sentrix_id: 4646298021; sentrix_position: D; plate: 4; ', 'tumor id: 287; tumor location: rectum; sample age: 12.4166666666667; rna (ng/ul): 40; sample_well: D08; sentrix_id: 4646298023; sentrix_position: D; plate: 4; ', 'tumor id: 89; tumor location: colon; sample age: 12.1666666666667; rna (ng/ul): 40; sample_well: D09; sentrix_id: 4646298032; sentrix_position: D; plate: 4; ', 'tumor id: 117; tumor location: colon; sample age: 14.5; rna (ng/ul): 40; sample_well: D10; sentrix_id: 4646298033; sentrix_position: D; plate: 4; ', 'tumor id: 2979; tumor location: rectum; sample age: 6.33333333333333; rna (ng/ul): 25; sample_well: D11; sentrix_id: 4646298034; sentrix_position: D; plate: 4; ', 'tumor id: 120; tumor location: colon; sample age: 18.5; rna (ng/ul): 40; sample_well: D12; sentrix_id: 4654538045; sentrix_position: D; plate: 4; ', 'tumor id: 57; tumor location: colon; sample age: 17; rna (ng/ul): 40; sample_well: E01; sentrix_id: 4646298011; sentrix_position: E; plate: 4; ', 'tumor id: 3030; tumor location: colon; sample age: 7.25; rna (ng/ul): 40; sample_well: E02; sentrix_id: 4646298015; sentrix_position: E; plate: 4; ', 'tumor id: 2927; tumor location: rectum; sample age: 6.33333333333333; rna (ng/ul): 27; sample_well: E03; sentrix_id: 4646298016; sentrix_position: E; plate: 4; ', 'tumor id: 2966; tumor location: rectum; sample age: 6.41666666666667; rna (ng/ul): 40; sample_well: E04; sen trix_id: 4646298017; sentrix_position: E; plate: 4; ', 'tumor id: 3099; tumor location: rectum; sample age: 10.25; rna (ng/ul): 40; sample_well: E05; sentrix_id: 4646298018; sentrix_position: E; plate: 4; ', 'tumor id: 640; tumor location: colon; sample age: 13.25; rna (ng/ul): 13; sample_well: E06; sentrix_id: 4646298020; sentrix_position: E; plate: 4; ', 'tumor id: 687; tumor location: rectum; sample age: 16.8333333333333; rna (ng/ul): 17; sample_well: E07; sentrix_id: 4646298021; sentrix_position: E; plate: 4; ', 'tumor id: 2419; tumor location: rectum; sample age: 8.83333333333333; rna (ng/ul): 40; sample_well: E08; sentrix_id: 4646298023; sentrix_position: E; plate: 4; ', 'tumor id: 3232; tumor location: colon; sample age: 12.6666666666667; rna (ng/ul): 40; sample_well: E09; sentrix_id: 4646298032; sentrix_position: E; plate: 4; ', 'tumor id: 98; tumor location: rectum; sample age: 12.5; rna (ng/ul): 40; sample_well: E11; sentrix_id: 4646298034; sentrix_position: E; plate: 4; ', 'tumor id: 401; tumor location: colon; sample age: 11.9166666666667; rna (ng/ul): 40; sample_well: E12; sentrix_id: 4654538045; sentrix_position: E; plate: 4; ', 'tumor id: 3399; tumor location: colon; sample age: 8.41666666666667; rna (ng/ul): 30; sample_well: F01; sentrix_id: 4646298011; sentrix_position: F; plate: 4; ', 'tumor id: 2931; tumor location: rectum; sample age: 4.41666666666667; rna (ng/ul): 40; sample_well: F02; sentrix_id: 4646298015; sentrix_position: F; plate: 4; ', 'tumor id: 3271; tumor location: rectum; sample age: 5.83333333333333; rna (ng/ul): 40; sample_well: F03; sentrix_id: 4646298016; sentrix_position: F; plate: 4; ', 'tumor id: 1223; tumor location: colon; sample age: 9.16666666666667; rna (ng/ul): 40; sample_well: F04; sentrix_id: 4646298017; sentrix_position: F; plate: 4; ', 'tumor id: 241; tumor location: colon; sample age: 12.3333333333333; rna (ng/ul): 40; sample_well: F06; sentrix_id: 4646298020; sentrix_position: F; plate: 4; ', 'tumor id: 325; tumor location: colon; sample age: 22.75; rna (ng/ul): 16; sample_well: F07; sentrix_id: 4646298021; sentrix_position: F; plate: 4; ', 'tumor id: 3202; tumor location: rectum; sample age: 5.58333333333333; rna (ng/ul): 40; sample_well: F09; sentrix_id: 4646298032; sentrix_position: F; plate: 4; ', 'tumor id: 341; tumor location: colon; sample age: 8.83333333333333; rna (ng/ul): 40; sample_well: F10; sentrix_id: 4646298033; sentrix_position: F; plate: 4; ', 'tumor id: 345; tumor location: rectum; sample age: 10.75; rna (ng/ul): 40; sample_well: F11; sentrix_id: 4646298034; sentrix_position: F; plate: 4; ', 'tumor id: 131; tumor location: colon; sample age: 11.6666666666667; rna (ng/ul): 40; sample_well: F12; sentrix_id: 4654538045; sentrix_position: F; plate: 4; ', 'tumor id: 58; tumor location: rectum; sample age: 13.1666666666667; rna (ng/ul): 40; sample_well: G01; sentrix_id: 4646298011; sentrix_position: G; plate: 4; ', 'tumor id: 1204; tumor location: colon; sample age: 9.58333333333333; rna (ng/ul): 40; sample_well: G02; sentrix_id: 4646298015; sentrix_position: G; plate: 4; ', 'tumor id: 3253; tumor location: rectum; sample age: 6.58333333333333; rna (ng/ul): 18; sample_well: G03; sentrix_id: 4646298016; sentrix_position: G; plate: 4; ', 'tumor id: 3405; tumor location: rectum; sample age: 6.16666666666667; rna (ng/ul): 30; sample_well: G04; sentrix_id: 4646298017; sentrix_position: G; plate: 4; ', 'tumor id: 2762; tumor location: rectum; sample age: 9.91666666666667; rna (ng/ul): 40; sample_well: G05; sentrix_id: 4646298018; sentrix_position: G; plate: 4; ', 'tumor id: 2774; tumor location: rectum; sample age: 7.75; rna (ng/ul): 40; sample_well: G06; sentrix_id: 4646298020; sentrix_position: G; plate: 4; ', 'tumor id: 346; tumor location: colon; sample age: 11.8333333333333; rna (ng/ul): 10; sample_well: G07; sentrix_id: 4646298021; sentrix_position: G; plate: 4; ', 'tumor id: 412; tumor location: rectum; sample age: 16.8333333333333; rna (ng/ul): 40; sample_well: G08; sentrix_id: 4646298023; sentrix_position: G; plate: 4; ', 'tumor id: 74; tumor location: rectum; sample age: 13.5; rna (ng/ul): 40; sample_well: G09; sentrix_id: 4646298032; sentrix_position: G; plate: 4; ', 'tumor id: 399; tumor location: colon; sample age: 22.9166666666667; rna (ng/ul): 40; sample_well: G10; sentrix_id: 4646298033; sentrix_position: G; plate: 4; ', 'tumor id: 82; tumor location: rectum; sample age: 13.4166666666667; rna (ng/ul): 40; sample_well: G11; sentrix_id: 4646298034; sentrix_position: G; plate: 4; ', 'tumor id: 496; tumor location: colon; sample age: 20.0833333333333; rna (ng/ul): 40; sample_well: G12; sentrix_id: 4654538045; sentrix_position: G; plate: 4; ', 'tumor id: 1207; tumor location: rectum; sample age: 9; rna (ng/ul): 40; sample_well: H01; sentrix_id: 4646298011; sentrix_position: H; plate: 4; ', 'tumor id: 2990; tumor location: colon; sample age: 6.66666666666667; rna (ng/ul): 24; sample_well: H02; sentrix_id: 4646298015; sentrix_position: H; plate: 4; ', 'tumor id: 3163; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: H03; sentrix_id: 4646298016; sentrix_position: H; plate: 4; ', 'tumor id: 684; tumor location: rectum; sample age: 16.25; rna (ng/ul): 40; sample_well: H04; sentrix_id: 4646298017; sentrix_position: H; plate: 4; ', 'tumor id: 2926; tumor location: colon; sample age: 8; rna (ng/ul): 12; sample_well: H05; sentrix_id: 4646298018; sentrix_position: H; plate: 4; ', 'tumor id: 454; tumor location: colon; sample age: 14.5833333333333; rna (ng/ul): 40; sample_well: H06; sentrix_id: 4646298020; sentrix_position: H; plate: 4; ', 'tumor id: 551; tumor location: colon; sample age: 16.5; rna (ng/ul): 40; sample_well: H07; sentrix_id: 4646298021; sentrix_position: H; plate: 4; ', 'tumor id: 339; tumor location: rectum; sample age: 15.1666666666667; rna (ng/ul): 40; sample_well: H08; sentrix_id: 4646298023; sentrix_position: H; plate: 4; ', 'tumor id: 327; tumor location: rectum; sample age: 16.25; rna (ng/ul): 40; sample_well: H10; sentrix_id: 4646298033; sentrix_position: H; plate: 4; ', 'tumor id: 2412; tumor location: colon; sample age: 19.5; rna (ng/ul): 40; sample_well: H11; sentrix_id: 4646298034; sentrix_position: H; plate: 4; ', 'tumor id: 2258; tumor location: rectum; sample age: 7.91666666666667; rna (ng/ul): 17; sample_well: H12; sentrix_id: 4654538045; sentrix_position: H; plate: 4; ', 'tumor id: 2342; tumor location: colon; sample age: 16.3333333333333; rna (ng/ul): 40; sample_well: A01; sentrix_id: 4642203031; sentrix_position: A; plate: 5; ', 'tumor id: 2582; tumor location: rectum; sample age: 15.6666666666667; rna (ng/ul): 40; sample_well: A02; sentrix_id: 4642203033; sentrix_position: A; plate: 5; ', 'tumor id: 607; tumor location: colon; sample age: 15.6666666666667; rna (ng/ul): 40; sample_well: A03; sentrix_id: 4642203035; sentrix_position: A; plate: 5; ', 'tumor id: 658; tumor location: rectum; sample age: 12.9166666666667; rna (ng/ul): 40; sample_well: A04; sentrix_id: 4642203036; sentrix_position: A; plate: 5; ', 'tumor id: 573; tumor location: rectum; sample age: 18.6666666666667; rna (ng/ul): 40; sample_well: A05; sentrix_id: 4642203040; sentrix_position: A; plate: 5; ', 'tumor id: 562; tumor location: rectum; sample age: 17.9166666666667; rna (ng/ul): 40; sample_well: A06; sentrix_id: 4642203046; sentrix_position: A; plate: 5; ', 'tumor id: 1202; tumor location: rectum; sample age: 9.33333333333333; rna (ng/ul): 40; sample_well: A08; sentrix_id: 4642203068; sentrix_position: A; plate: 5; ', 'tumor id: 1226; tumor location: colon; sample age: 7.66666666666667; rna (ng/ul): 40; sample_well: A10; sentrix_id: 4642203111; sentrix_position: A; plate: 5; ', 'tumor id: 1177; tumor location: colon; sample age: 12.1666666666667; rna (ng/ul): 40; sample_well: A11; sentrix_id: 4642203112; sentrix_position: A; plate: 5; ', 'tumor id: 101; tumor location: colon; sample age: 14.1666666666667; rna (ng/ul): 40; sample_well: A12; sentrix_id: 4646298004; sentrix_position: A; plate: 5; ', 'tumor id: 104; tumor location: rectum; sample age: 22.5; rna (ng/ul): 40; sample_well: B01; sentrix_id: 4642203031; sentrix_position: B; plate: 5; ', 'tumor id: 495; tumor location: rectum; sample age: 22.5; rna (ng/ul): 40; sample_well: B03; sentrix_id: 4642203035; sentrix_position: B; plate: 5; ', 'tumor id: 2197; tumor location: rectum; sample age: 12.5; rna (ng/ul): 40; sample_well: B04; sentrix_id: 4642203036; sentrix_position: B; plate: 5; ', 'tumor id: 486; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: B05; sentrix_id: 4642203040; sentrix_position: B; plate: 5; ', 'tumor id: 503; tumor location: rectum; sample age: 21.8333333333333; rna (ng/ul): 40; sample_well: B06; sentrix_id: 4642203046; sentrix_position: B; plate: 5; ', 'tumor id: 1165; tumor location: colon; sample age: 9.16666666666667; rna (ng/ul): 40; sample_well: B07; sentrix_id: 4642203047; sentrix_position: B; plate: 5; ', 'tumor id: 1237; tumor location: rectum; sample age: 9.75; rna (ng/ul): 40; sample_well: B08; sentrix_id: 4642203068; sentrix_position: B; plate: 5; ', 'tumor id: 1208; tumor location: rectum; sample age: 10; rna (ng/ul): 40; sample_well: B09; sentrix_id: 4642203070; sentrix_position: B; plate: 5; ', 'tumor id: 1211; tumor location: rectum; sample age: 9.08333333333333; rna (ng/ul): 40; sample_well: B10; sentrix_id: 4642203111; sentrix_position: B; plate: 5; ', 'tumor id: 379; tumor location: colon; sample age: 13.4166666666667; rna (ng/ul): 40; sample_well: B11; sentrix_id: 4642203112; sentrix_position: B; plate: 5; ', 'tumor id: 122; tumor location: rectum; sample age: 14.3333333333333; rna (ng/ul): 40; sample_well: B12; sentrix_id: 4646298004; sentrix_position: B; plate: 5; ', 'tumor id: 2370; tumor location: rectum; sample age: 15.4166666666667; rna (ng/ul): 30; sample_well: C01; sentrix_id: 4642203031; sentrix_position: C; plate: 5; ', 'tumor id: 2578; tumor location: colon; sample age: 10.5833333333333; rna (ng/ul): 40; sample_well: C02; sentrix_id: 4642203033; sentrix_position: C; plate: 5; ', 'tumor id: 433; tumor location: rectum; sample age: 14.1666666666667; rna (ng/ul): 40; sample_well: C03; sentrix_id: 4642203035; sentrix_position: C; plate: 5; ', 'tumor id: 1872; tumor location: colon; sample age: 12.1666666666667; rna (ng/ul): 30; sample_well: C04; sentrix_id: 4642203036; sentrix_position: C; plate: 5; ', 'tumor id: 2366; tumor location: colon; sample age: 17.4166666666667; rna (ng/ul): 40; sample_well: C05; sentrix_id: 4642203040; sentrix_position: C; plate: 5; ', 'tumor id: 557; tumor location: rectum; sample age: 20.8333333333333; rna (ng/ul): 40; sample_well: C06; sentrix_id: 4642203046; sentrix_position: C; plate: 5; ', 'tumor id: 1163; tumor location: colon; sample age: 10.25; rna (ng/ul): 40; sample_well: C07; sentrix_id: 4642203047; sentrix_position: C; plate: 5; ', 'tumor id: 1236; tumor location: colon; sample age: 7.66666666666667; rna (ng/ul): 40; sample_well: C08; sentrix_id: 4642203068; sentrix_position: C; plate: 5; ', 'tumor id: 229; tumor location: colon; sample age: 11.0833333333333; rna (ng/ul): 40; sample_well: C09; sentrix_id: 4642203070; sentrix_position: C; plate: 5; ', 'tumor id: 1212; tumor location: rectum; sample age: 7.75; rna (ng/ul): 40; sample_well: C10; sentrix_id: 4642203111; sentrix_position: C; plate: 5; ', 'tumor id: 1183; tumor location: colon; sample age: 9.58333333333333; rna (ng/ul): 40; sample_well: C11; sentrix_id: 4642203112; sentrix_position: C; plate: 5; ', 'tumor id: 113; tumor location: colon; sample age: 16.6666666666667; rna (ng/ul): 40; sample_well: C12; sentrix_id: 4646298004; sentrix_position: C; plate: 5; ', 'tumor id: 611; tumor location: rectum; sample age: 16.0833333333333; rna (ng/ul): 40; sample_well: D01; sentrix_id: 4642203031; sentrix_position: D; plate: 5; ', 'tumor id: 688; tumor location: colon; sample age: 16.25; rna (ng/ul): 40; sample_well: D03; sentrix_id: 4642203035; sentrix_position: D; plate: 5; ', 'tumor id: 84; tumor location: colon; sample age: 13; rna (ng/ul): 40; sample_well: D04; sentrix_id: 4642203036; sentrix_position: D; plate: 5; ', 'tumor id: 570; tumor location: colon; sample age: 21.3333333333333; rna (ng/ul): 40; sample_well: D05; sentrix_id: 4642203040; sentrix_position: D; plate: 5; ', 'tumor id: 542; tumor location: colon; sample age: 22.0833333333333; rna (ng/ul): 40; sample_well: D06; sentrix_id: 4642203046; sentrix_position: D; plate: 5; ', 'tumor id: 1161; tumor location: colon; sample age: 8.5; rna (ng/ul): 40; sample_well: D07; sentrix_id: 4642203047; sentrix_position: D; plate: 5; ', 'tumor id: 1254; tumor location: colon; sample age: 9.91666666666667; rna (ng/ul): 40; sample_well: D08; sentrix_id: 4642203068; sentrix_position: D; plate: 5; ', 'tumor id: 1224; tumor location: colon; sample age: 9.33333333333333; rna (ng/ul): 40; sample_well: D09; sentrix_id: 4642203070; sentrix_position: D; plate: 5; ', 'tumor id: 2368; tumor location: rectum; sample age: 18.0833333333333; rna (ng/ul): 40; sample_well: D10; sentrix_id: 4642203111; sentrix_position: D; plate: 5; ', 'tumor id: 328; tumor location: rectum; sample age: 13.4166666666667; rna (ng/ul): 40; sample_well: D11; sentrix_id: 4642203112; sentrix_position: D; plate: 5; ', 'tumor id: 683; tumor location: colon; sample age: 14.4166666666667; rna (ng/ul): 40; sample_well: D12; sentrix_id: 4646298004; sentrix_position: D; plate: 5; ', 'tumor id: 2422; tumor location: colon; sample age: 11.1666666666667; rna (ng/ul): 40; sample_well: E01; sentrix_id: 4642203031; sentrix_position: E; plate: 5; ', 'tumor id: 694; tumor location: colon; sample age: 19.9166666666667; rna (ng/ul): 40; sample_well: E02; sentrix_id: 4642203033; sentrix_position: E; plate: 5; ', 'tumor id: 502; tumor location: colon; sample age: 19.1666666666667; rna (ng/ul): 40; sample_well: E03; sentrix_id: 4642203035; sentrix_position: E; plate: 5; ', 'tumor id: 604; tumor location: colon; sample age: 16.6666666666667; rna (ng/ul): 40; sample_well: E04; sentrix_id: 4642203036; sentrix_position: E; plate: 5; ', 'tumor id: 560; tumor location: colon; sample age: 19; rna (ng/ul): 40; sample_well: E05; sentrix_id: 4642203040; sentrix_position: E; plate: 5; ', 'tumor id: 592; tumor location: colon; sample age: 19.5; rna (ng/ul): 40; sample_well: E06; sentrix_id: 4642203046; sentrix_position: E; plate: 5; ', 'tumor id: 1160; tumor location: colon; sample age: 9.83333333333333; rna (ng/ul): 40; sample_well: E07; sentrix_id: 4642203047; sentrix_position: E; plate: 5; ', 'tumor id: 2378; tumor location: colon; sample age: 18.75; rna (ng/ul): 17; sample_well: E08; sentrix_id: 4642203068; sentrix_position: E; plate: 5; ', 'tumor id: 1229; tumor location: rectum; sample age: 8.58333333333333; rna (ng/ul): 40; sample_well: E09; sentrix_id: 4642203070; sentrix_position: E; plate: 5; ', 'tumor id: 193; tumor location: rectum; sample age: 10.5833333333333; rna (ng/ul): 32; sample_well: E10; sentrix_id: 4642203111; sentrix_position: E; plate: 5; ', 'tumor id: 2390; tumor location: colon; sample age: 16.4166666666667; rna (ng/ul): 40; sample_well: E11; sentrix_id: 4642203112; sentrix_position: E; plate: 5; ', 'tumor id: 112; tumor location: colon; sample age: 16.75; rna (ng/ul): 40; sample_well: E12; sentrix_id: 4646298004; sentrix_position: E; plate: 5; ', 'tumor id: 593; tumor location: colon; sample age: 21.3333333333333; rna (ng/ul): 40; sample_well: F01; sentrix_id: 4642203031; sentrix_position: F; plate: 5; ', 'tumor id: 525; tumor location: colon; sample age: 17.0833333333333; rna (ng/ul): 40; sample_well: F02; sentrix_id: 4642203033; sentrix_position: F; plate: 5; ', 'tumor id: 655; tumor location: rectum; sample age: 14.5; rna (ng/ul): 40; sample_well: F03; sentrix_id: 4642203035; sentrix_position: F; plate: 5; ', 'tumor id: 2392; tumor location: colon; sample age: 15.1666666666667; rna (ng/ul): 40; sample_well: F04; sentrix_id: 4642203036; sentrix_position: F; plate: 5; ', 'tumor id: 686; tumor location: colon; sample age: 20.1666666666667; rna (ng/ul): 40; sample_well: F05; sentrix_id: 4642203040; sentrix_position: F; plate: 5; ', 'tumor id: 587; tumor location: colon; sample age: 19.0833333333333; rna (ng/ul): 40; sample_well: F06; sentrix_id: 4642203046; sentrix_position: F; plate: 5; ', 'tumor id: 1190; tumor location: rectum; sample age: 9.83333333333333; rna (ng/ul): 40; sample_well: F07; sentrix_id: 4642203047; sentrix_position: F; plate: 5; ', 'tumor id: 1244; tumor location: rectum; sample age: 9.66666666666667; rna (ng/ul): 40; sample_well: F08; sentrix_id: 4642203068; sentrix_position: F; plate: 5; ', 'tumor id: 1227; tumor location: colon; sample age: 9.75; rna (ng/ul): 40; sample_well: F09; sentrix_id: 4642203070; sentrix_position: F; plate: 5; ', 'tumor id: 2945; tumor location: rectum; sample age: 4.41666666666667; rna (ng/ul): 40; sample_well: F10; sentrix_id: 4642203111; sentrix_position: F; plate: 5; ', 'tumor id: 1222; tumor location: rectum; sample age: 9.66666666666667; rna (ng/ul): 40; sample_well: F11; sentrix_id: 4642203112; sentrix_position: F; plate: 5; ', 'tumor id: 321; tumor location: rectum; sample age: 13; rna (ng/ul): 40; sample_well: F12; sentrix_id: 4646298004; sentrix_position: F; plate: 5; ', 'tumor id: 2379; tumor location: rectum; sample age: 14.3333333333333; rna (ng/ul): 40; sample_well: G01; sentrix_id: 4642203031; sentrix_position: G; plate: 5; ', 'tumor id: 513; tumor location: colon; sample age: 18.4166666666667; rna (ng/ul): 40; sample_well: G02; sentrix_id: 4642203033; sentrix_position: G; plate: 5; ', 'tumor id: 102; tumor location: rectum; sample age: 10.5; rna (ng/ul): 40; sample_well: G03; sentrix_id: 4642203035; sentrix_position: G; plate: 5; ', 'tumor id: 530; tumor location: null; sample age: null; rna (ng/ul): 40; sample_well: G04; sentrix_id: 4642203036; sentrix_position: G; plate: 5; ', 'tumor id: 73; tumor location: rectum; sample age: 21; rna (ng/ul): 11; sample_well: G05; sentrix_id: 4642203040; sentrix_position: G; plate: 5; ', 'tumor id: 340; tumor location: rectum; sample age: 21.5; rna (ng/ul): 40; sample_well: G06; sentrix_id: 4642203046; sentrix_position: G; plate: 5; ', 'tumor id: 1197; tumor location: colon; sample age: 10.5; rna (ng/ul): 40; sample_well: G07; sentrix_id: 4642203047; sentrix_position: G; plate: 5; ', 'tumor id: 1243; tumor location: colon; sample age: 9.16666666666667; rna (ng/ul): 31; sample_well: G08; sentrix_id: 4642203068; sentrix_position: G; plate: 5; ', 'tumor id: 1216; tumor location: colon; sample age: 8.08333333333333; rna (ng/ul): 40; sample_well: G09; sentrix_id: 4642203070; sentrix_position: G; plate: 5; ', 'tumor id: 115; tumor location: rectum; sample age: 16.0833333333333; rna (ng/ul): 40; sample_well: G10; sentrix_id: 4642203111; sentrix_position: G; plate: 5; ', 'tumor id: 2340; tumor location: colon; sample age: 13.9166666666667; rna (ng/ul): 40; sample_well: G11; sentrix_id: 4642203112; sentrix_position: G; plate: 5; ', 'tumor id: 108; tumor location: colon; sample age: 20.5833333333333; rna (ng/ul): 40; sample_well: G12; sentrix_id: 4646298004; sentrix_position: G; plate: 5; ', 'tumor id: 2410; tumor location: rectum; sample age: 22.6666666666667; rna (ng/ul): 40; sample_well: H01; sentrix_id: 4642203031; sentrix_position: H; plate: 5; ', 'tumor id: 561; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: H02; sentrix_id: 4642203033; sentrix_position: H; plate: 5; ', 'tumor id: 606; tumor location: rectum; sample age: 17; rna (ng/ul): 40; sample_well: H03; sentrix_id: 4642203035; sentrix_position: H; plate: 5; ', 'tumor id: 541; tumor location: colon; sample age: 17.5833333333333; rna (ng/ul): 40; sample_well: H04; sentrix_id: 4642203036; sentrix_position: H; plate: 5; ', 'tumor id: 2271; tumor location: rectum; sample age: 7.25; rna (ng/ul): 40; sample_well: H05; sentrix_id: 4642203040; sentrix_position: H; plate: 5; ', 'tumor id: 402; tumor location: colon; sample age: 20; rna (ng/ul): 40; sample_well: H06; sentrix_id: 4642203046; sentrix_position: H; plate: 5; ', 'tumor id: 1206; tumor location: colon; sample age: 8.75; rna (ng/ul): 40; sample_well: H08; sentrix_id: 4642203068; sentrix_position: H; plate: 5; ', 'tumor id: 270; tumor location: colon; sample age: 22.6666666666667; rna (ng/ul): 40; sample_well: H09; sentrix_id: 4642203070; sentrix_position: H; plate: 5; ', 'tumor id: 114; tumor location: rectum; sample age: 11.3333333333333; rna (ng/ul): 40; sample_well: H10; sentrix_id: 4642203111; sentrix_position: H; plate: 5; ', 'tumor id: 281; tumor location: colon; sample age: 17.8333333333333; rna (ng/ul): 40; sample_well: H11; sentrix_id: 4642203112; sentrix_position: H; plate: 5; ', 'tumor id: 198; tumor location: colon; sample age: 16.5833333333333; rna (ng/ul): 40; sample_well: H12; sentrix_id: 4646298004; sentrix_position: H; plate: 5; ', 'tumor id: 2341; tumor location: colon; sample age: 13.1666666666667; rna (ng/ul): 40; sample_well: A01; sentrix_id: 4646298005; sentrix_position: A; plate: 6; ', 'tumor id: 124; tumor location: colon; sample age: 21.8333333333333; rna (ng/ul): 40; sample_well: A02; sentrix_id: 4646298006; sentrix_position: A; plate: 6; ', 'tumor id: 421; tumor location: rectum; sample age: 17.4166666666667; rna (ng/ul): 25; sample_well: A03; sentrix_id: 4646298007; sentrix_position: A; plate: 6; ', 'tumor id: 488; tumor location: colon; sample age: 21; rna (ng/ul): 40; sample_well: A04; sentrix_id: 4646298012; sentrix_position: A; plate: 6; ', 'tumor id: 589; tumor location: rectum; sample age: 17.75; rna (ng/ul): 40; sample_well: A05; sentrix_id: 4646298024; sentrix_position: A; plate: 6; ', 'tumor id: 3056; tumor location: rectum; sample age: 6.66666666666667; rna (ng/ul): 40; sample_well: A06; sentrix_id: 4646298025; sentrix_position: A; plate: 6; ', 'tumor id: 3105; tumor location: rectum; sample age: 3.33333333333333; rna (ng/ul): 40; sample_well: A07; sentrix_id: 4646298026; sentrix_position: A; plate: 6; ', 'tumor id: 3092; tumor location: rectum; sample age: 7.5; rna (ng/ul): 40; sample_well: A08; sentrix_id: 4646298030; sentrix_position: A; plate: 6; ', 'tumor id: 461; tumor location: colon; sample age: 14.3333333333333; rna (ng/ul): 40; sample_well: A09; sentrix_id: 4646298031; sentrix_position: A; plate: 6; ', 'tumor id: 549; tumor location: colon; sample age: 18.4166666666667; rna (ng/ul): 40; sample_well: A10; sentrix_id: 4646298036; sentrix_position: A; plate: 6; ', 'tumor id: 581; tumor location: colon; sample age: 19.6666666666667; rna (ng/ul): 40; sample_well: A11; sentrix_id: 4646298037; sentrix_position: A; plate: 6; ', 'tumor id: 2215; tumor location: rectum; sample age: 9.33333333333333; rna (ng/ul): 31; sample_well: A12; sentrix_id: 4646298038; sentrix_position: A; plate: 6; ', 'tumor id: 400; tumor location: rectum; sample age: 21.8333333333333; rna (ng/ul): 40; sample_well: B01; sentrix_id: 4646298005; sentrix_position: B; plate: 6; ', 'tumor id: 343; tumor location: rectum; sample age: 11.0833333333333; rna (ng/ul): 40; sample_well: B02; sentrix_id: 4646298006; sentrix_position: B; plate: 6; ', 'tumor id: 491; tumor location: colon; sample age: 17; rna (ng/ul): 40; sample_well: B04; sentrix_id: 4646298012; sentrix_position: B; plate: 6; ', 'tumor id: 516; tumor location: rectum; sample age: 19.8333333333333; rna (ng/ul): 32; sample_well: B05; sentrix_id: 4646298024; sentrix_position: B; plate: 6; ', 'tumor id: 3059; tumor location: colon; sample age: 5.41666666666667; rna (ng/ul): 40; sample_well: B06; sentrix_id: 4646298025; sentrix_position: B; plate: 6; ', 'tumor id: 3118; tumor location: colon; sample age: 4.91666666666667; rna (ng/ul): 40; sample_well: B07; sentrix_id: 4646298026; sentrix_position: B; plate: 6; ', 'tumor id: 3094; tumor location: rectum; sample age: 7.41666666666667; rna (ng/ul): 40; sample_well: B08; sentrix_id: 4646298030; sentrix_position: B; plate: 6; ', 'tumor id: 462; tumor location: rectum; sample age: 13.9166666666667; rna (ng/ul): 19; sample_well: B09; sentrix_id: 4646298031; sentrix_position: B; plate: 6; ', 'tumor id: 553; tumor location: rectum; sample age: 17; rna (ng/ul): 40; sample_well: B10; sentrix_id: 4646298036; sentrix_position: B; plate: 6; ', 'tumor id: 659; tumor location: colon; sample age: 14.9166666666667; rna (ng/ul): 40; sample_well: B11; sentrix_id: 4646298037; sentrix_position: B; plate: 6; ', 'tumor id: 2220; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: B12; sentrix_id: 4646298038; sentrix_position: B; plate: 6; ', 'tumor id: 2429; tumor location: colon; sample age: 15.3333333333333; rna (ng/ul): 40; sample_well: C01; sentrix_id: 4646298005; sentrix_position: C; plate: 6; ', 'tumor id: 2361; tumor location: rectum; sample age: 15.6666666666667; rna (ng/ul): 40; sample_well: C02; sentrix_id: 4646298006; sentrix_position: C; plate: 6; ', 'tumor id: 441; tumor location: colon; sample age: 17.1666666666667; rna (ng/ul): 40; sample_well: C03; sentrix_id: 4646298007; sentrix_position: C; plate: 6; ', 'tumor id: 501; tumor location: rectum; sample age: 19.0833333333333; rna (ng/ul): 40; sample_well: C04; sentrix_id: 4646298012; sentrix_position: C; plate: 6; ', 'tumor id: 591; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: C05; sentrix_id: 4646298024; sentrix_position: C; plate: 6; ', 'tumor id: 3062; tumor location: colon; sample age: 5.5; rna (ng/ul): 40; sample_well: C06; sentrix_id: 4646298025; sentrix_position: C; plate: 6; ', 'tumor id: 3049; tumor location: rectum; sample age: 7.91666666666667; rna (ng/ul): 40; sample_well: C07; sentrix_id: 4646298026; sentrix_position: C; plate: 6; ', 'tumor id: 419; tumor location: rectum; sample age: 21.3333333333333; rna (ng/ul): 32; sample_well: C08; sentrix_id: 4646298030; sentrix_position: C; plate: 6; ', 'tumor id: 563; tumor location: colon; sample age: 18.8333333333333; rna (ng/ul): 40; sample_well: C10; sentrix_id: 4646298036; sentrix_position: C; plate: 6; ', 'tumor id: 2279; tumor location: colon; sample age: 7.41666666666667; rna (ng/ul): 40; sample_well: C11; sentrix_id: 4646298037; sentrix_position: C; plate: 6; ', 'tumor id: 691; tumor location: colon; sample age: 18.0833333333333; rna (ng/ul): 40; sample_well: C12; sentrix_id: 4646298038; sentrix_position: C; plate: 6; ', 'tumor id: 85; tumor location: rectum; sample age: 15.3333333333333; rna (ng/ul): 40; sample_well: D01; sentrix_id: 4646298005; sentrix_position: D; plate: 6; ', 'tumor id: 2270; tumor location: rectum; sample age: 8.25; rna (ng/ul): 40; sample_well: D02; sentrix_id: 4646298006; sentrix_position: D; plate: 6; ', 'tumor id: 445; tumor location: rectum; sample age: 19.4166666666667; rna (ng/ul): 40; sample_well: D03; sentrix_id: 4646298007; sentrix_position: D; plate: 6; ', 'tumor id: 520; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: D04; sentrix_id: 4646298012; sentrix_position: D; plate: 6; ', 'tumor id: 634; tumor location: colon; sample age: 21.3333333333333; rna (ng/ul): 40; sample_well: D05; sentrix_id: 4646298024; sentrix_position: D; plate: 6; ', 'tumor id: 3083; tumor location: colon; sample age: 5.25; rna (ng/ul): 40; sample_well: D06; sentrix_id: 4646298025; sentrix_position: D; plate: 6; ', 'tumor id: 675; tumor location: rectum; sample age: 20.6666666666667; rna (ng/ul): 28; sample_well: D07; sentrix_id: 4646298026; sentrix_position: D; plate: 6; ', 'tumor id: 425; tumor location: colon; sample age: 13.9166666666667; rna (ng/ul): 40; sample_well: D08; sentrix_id: 4646298030; sentrix_position: D; plate: 6; ', 'tumor id: 476; tumor location: rectum; sample age: 20.75; rna (ng/ul): 40; sample_well: D09; sentrix_id: 4646298031; sentrix_position: D; plate: 6; ', 'tumor id: 567; tumor location: colon; sample age: 21.8333333333333; rna (ng/ul): 40; sample_well: D10; sentrix_id: 4646298036; sentrix_position: D; plate: 6; ', 'tumor id: 662; tumor location: colon; sample age: 19.6666666666667; rna (ng/ul): 40; sample_well: D11; sentrix_id: 4646298037; sentrix_position: D; plate: 6; ', 'tumor id: 1782; tumor location: colon; sample age: 12; rna (ng/ul): 40; sample_well: D12; sentrix_id: 4646298038; sentrix_position: D; plate: 6; ', 'tumor id: 2359; tumor location: rectum; sample age: 12.9166666666667; rna (ng/ul): 40; sample_well: E01; sentrix_id: 4646298005; sentrix_position: E; plate: 6; ', 'tumor id: 299; tumor location: rectum; sample age: 12.75; rna (ng/ul): 40; sample_well: E02; sentrix_id: 4646298006; sentrix_position: E; plate: 6; ', 'tumor id: 2304; tumor location: rectum; sample age: 7.91666666666667; rna (ng/ul): 40; sample_well: E03; sentrix_id: 4646298007; sentrix_position: E; plate: 6; ', 'tumor id: 528; tumor location: rectum; sample age: 17.0833333333333; rna (ng/ul): 40; sample_well: E04; sentrix_id: 4646298012; sentrix_position: E; plate: 6; ', 'tumor id: 681; tumor location: colon; sample age: 18.0833333333333; rna (ng/ul): 22; sample_well: E05; sentrix_id: 4646298024; sentrix_position: E; plate: 6; ', 'tumor id: 3096; tumor location: colon; sample age: 4.5; rna (ng/ul): 40; sample_well: E06; sentrix_id: 4646298025; sentrix_position: E; plate: 6; ', 'tumor id: 695; tumor location: rectum; sample age: 17.75; rna (ng/ul): 40; sample_well: E07; sentrix_id: 4646298026; sentrix_position: E; plate: 6; ', 'tumor id: 481; tumor location: rectum; sample age: 18.9166666666667; rna (ng/ul): 40; sample_well: E09; sentrix_id: 4646298031; sentrix_position: E; plate: 6; ', 'tumor id: 572; tumor location: rectum; sample age: 19.1666666666667; rna (ng/ul): 40; sample_well: E10; sentrix_id: 4646298036; sentrix_position: E; plate: 6; ', 'tumor id: 668; tumor location: rectum; sample age: 16; rna (ng/ul): 40; sample_well: E11; sentrix_id: 4646298037; sentrix_position: E; plate: 6; ', 'tumor id: 1850; tumor location: colon; sample age: 9.83333333333333; rna (ng/ul): 40; sample_well: E12; sentrix_id: 4646298038; sentrix_position: E; plate: 6; ', 'tumor id: 2214; tumor location: rectum; sample age: 11.6666666666667; rna (ng/ul): 40; sample_well: F01; sentrix_id: 4646298005; sentrix_position: F; plate: 6; ', 'tumor id: 451; tumor location: rectum; sample age: 14.5833333333333; rna (ng/ul): 40; sample_well: F03; sentrix_id: 4646298007; sentrix_position: F; plate: 6; ', 'tumor id: 492; tumor location: rectum; sample age: 18.4166666666667; rna (ng/ul): 40; sample_well: F04; sentrix_id: 4646298012; sentrix_position: F; plate: 6; ', 'tumor id: 1849; tumor location: rectum; sample age: 9.41666666666667; rna (ng/ul): 40; sample_well: F05; sentrix_id: 4646298024; sentrix_position: F; plate: 6; ', 'tumor id: 3061; tumor location: rectum; sample age: 6.25; rna (ng/ul): 40; sample_well: F06; sentrix_id: 4646298025; sentrix_position: F; plate: 6; ', 'tumor id: 544; tumor location: rectum; sample age: 19; rna (ng/ul): 18; sample_well: F07; sentrix_id: 4646298026; sentrix_position: F; plate: 6; ', 'tumor id: 438; tumor location: rectum; sample age: 14.1666666666667; rna (ng/ul): 30; sample_well: F08; sentrix_id: 4646298030; sentrix_position: F; plate: 6; ', 'tumor id: 2246; tumor location: rectum; sample age: 11; rna (ng/ul): 33; sample_well: F09; sentrix_id: 4646298031; sentrix_position: F; plate: 6; ', 'tumor id: 519; tumor location: rectum; sample age: 16.9166666666667; rna (ng/ul): 40; sample_well: F10; sentrix_id: 4646298036; sentrix_position: F; plate: 6; ', 'tumor id: 3157; tumor location: rectum; sample age: 8.83333333333333; rna (ng/ul): 40; sample_well: F11; sentrix_id: 4646298037; sentrix_position: F; plate: 6; ', 'tumor id: 2202; tumor location: colon; sample age: 12.0833333333333; rna (ng/ul): 40; sample_well: F12; sentrix_id: 4646298038; sentrix_position: F; plate: 6; ', 'tumor id: 97; tumor location: rectum; sample age: 13; rna (ng/ul): 40; sample_well: G02; sentrix_id: 4646298006; sentrix_position: G; plate: 6; ', 'tumor id: 467; tumor location: colon; sample age: 14.0833333333333; rna (ng/ul): 39; sample_well: G03; sentrix_id: 4646298007; sentrix_position: G; plate: 6; ', 'tumor id: 546; tumor location: rectum; sample age: 18.1666666666667; rna (ng/ul): 40; sample_well: G04; sentrix_id: 4646298012; sentrix_position: G; plate: 6; ', 'tumor id: 635; tumor location: rectum; sample age: 21; rna (ng/ul): 24; sample_well: G05; sentrix_id: 4646298024; sentrix_position: G; plate: 6; ', 'tumor id: 3088; tumor location: rectum; sample age: 6.5; rna (ng/ul): 40; sample_well: G06; sentrix_id: 4646298025; sentrix_position: G; plate: 6; ', 'tumor id: 3050; tumor location: rectum; sample age: 7.16666666666667; rna (ng/ul): 17; sample_well: G07; sentrix_id: 4646298026; sentrix_position: G; plate: 6; ', 'tumor id: 453; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: G08; sentrix_id: 4646298030; sentrix_position: G; plate: 6; ', 'tumor id: 2303; tumor location: rectum; sample age: 7.41666666666667; rna (ng/ul): 40; sample_well: G09; sentrix_id: 4646298031; sentrix_position: G; plate: 6; ', 'tumor id: 617; tumor location: colon; sample age: 16.3333333333333; rna (ng/ul): 40; sample_well: G10; sentrix_id: 4646298036; sentrix_position: G; plate: 6; ', 'tumor id: 678; tumor location: colon; sample age: 15.6666666666667; rna (ng/ul): 40; sample_well: G11; sentrix_id: 4646298037; sentrix_position: G; plate: 6; ', 'tumor id: 3011; tumor location: rectum; sample age: 6.66666666666667; rna (ng/ul): 40; sample_well: G12; sentrix_id: 4646298038; sentrix_position: G; plate: 6; ', 'tumor id: 380; tumor location: rectum; sample age: 26.8333333333333; rna (ng/ul): 40; sample_well: H01; sentrix_id: 4646298005; sentrix_position: H; plate: 6; ', 'tumor id: 418; tumor location: colon; sample age: 17.5833333333333; rna (ng/ul): 40; sample_well: H02; sentrix_id: 4646298006; sentrix_position: H; plate: 6; ', 'tumor id: 485; tumor location: colon; sample age: 16.5; rna (ng/ul): 40; sample_well: H03; sentrix_id: 4646298007; sentrix_position: H; plate: 6; ', 'tumor id: 576; tumor location: colon; sample age: 17.25; rna (ng/ul): 40; sample_well: H04; sentrix_id: 4646298012; sentrix_position: H; plate: 6; ', 'tumor id: 648; tumor location: colon; sample age: 14; rna (ng/ul): 40; sample_well: H05; sentrix_id: 4646298024; sentrix_position: H; plate: 6; ', 'tumor id: 3101; tumor location: colon; sample age: 8.25; rna (ng/ul): 40; sample_well: H06; sentrix_id: 4646298025; sentrix_position: H; plate: 6; ', 'tumor id: 3053; tumor location: rectum; sample age: 7.41666666666667; rna (ng/ul): 40; sample_well: H07; sentrix_id: 4646298026; sentrix_position: H; plate: 6; ', 'tumor id: 455; tumor location: rectum; sample age: 14.5833333333333; rna (ng/ul): 40; sample_well: H08; sentrix_id: 4646298030; sentrix_position: H; plate: 6; ', 'tumor id: 533; tumor location: colon; sample age: 19.6666666666667; rna (ng/ul): 40; sample_well: H09; sentrix_id: 4646298031; sentrix_position: H; plate: 6; ', 'tumor id: 580; tumor location: colon; sample age: 19.9166666666667; rna (ng/ul): 22; sample_well: H10; sentrix_id: 4646298036; sentrix_position: H; plate: 6; ', 'tumor id: 478; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: H11; sentrix_id: 4646298037; sentrix_position: H; plate: 6; ', 'tumor id: 86; tumor location: rectum; sample age: 27.5; rna (ng/ul): 40; sample_well: A01; sentrix_id: 4642203098; sentrix_position: A; plate: 7; ', 'tumor id: 313; tumor location: colon; sample age: 24.75; rna (ng/ul): 40; sample_well: A02; sentrix_id: 4642203099; sentrix_position: A; plate: 7; ', 'tumor id: 3048; tumor location: rectum; sample age: 8; rna (ng/ul): 40; sample_well: A03; sentrix_id: 4642203100; sentrix_position: A; plate: 7; ', 'tumor id: 3022; tumor location: rectum; sample age: 7.41666666666667; rna (ng/ul): 40; sample_well: A04; sentrix_id: 4642203104; sentrix_position: A; plate: 7; ', 'tumor id: 2942; tumor location: rectum; sample age: 7.58333333333333; rna (ng/ul): 40; sample_well: A05; sentrix_id: 4642203105; sentrix_position: A; plate: 7; ', 'tumor id: 2427; tumor location: colon; sample age: 9.58333333333333; rna (ng/ul): 11; sample_well: A06; sentrix_id: 4642203106; sentrix_position: A; plate: 7; ', 'tumor id: 2405; tumor location: rectum; sample age: 10.3333333333333; rna (ng/ul): 18; sample_well: A07; sentrix_id: 4646298008; sentrix_position: A; plate: 7; ', 'tumor id: 2403; tumor location: rectum; sample age: 9.41666666666667; rna (ng/ul): 17; sample_well: A08; sentrix_id: 4646298022; sentrix_position: A; plate: 7; ', 'tumor id: 3260; tumor location: rectum; sample age: 6.41666666666667; rna (ng/ul): 40; sample_well: A09; sentrix_id: 4646298027; sentrix_position: A; plate: 7; ', 'tumor id: 2641; tumor location: colon; sample age: 11.25; rna (ng/ul): 40; sample_well: A10; sentrix_id: 4646298028; sentrix_position: A; plate: 7; ', 'tumor id: 2440; tumor location: rectum; sample age: 9.83333333333333; rna (ng/ul): 26; sample_well: A11; sentrix_id: 4646298029; sentrix_position: A; plate: 7; ', 'tumor id: 2448; tumor location: rectum; sample age: 10.9166666666667; rna (ng/ul): 40; sample_well: A12; sentrix_id: 4646298035; sentrix_position: A; plate: 7; ', 'tumor id: 368; tumor location: rectum; sample age: 18.6666666666667; rna (ng/ul): 17; sample_well: B01; sentrix_id: 4642203098; sentrix_position: B; plate: 7; ', 'tumor id: 246; tumor location: colon; sample age: 18.3333333333333; rna (ng/ul): 40; sample_well: B02; sentrix_id: 4642203099; sentrix_position: B; plate: 7; ', 'tumor id: 3064; tumor location: rectum; sample age: 7.08333333333333; rna (ng/ul): 40; sample_well: B03; sentrix_id: 4642203100; sentrix_position: B; plate: 7; ', 'tumor id: 3047; tumor location: rectum; sample age: 7.66666666666667; rna (ng/ul): 40; sample_well: B04; sentrix_id: 4642203104; sentrix_position: B; plate: 7; ', 'tumor id: 3010; tumor location: rectum; sample age: 8.25; rna (ng/ul): 40; sample_well: B05; sentrix_id: 4642203105; sentrix_position: B; plate: 7; ', 'tumor id: 1157; tumor location: rectum; sample age: 7.83333333333333; rna (ng/ul): 32; sample_well: B06; sentrix_id: 4642203106; sentrix_position: B; plate: 7; ', 'tumor id: 1241; tumor location: rectum; sample age: 9.33333333333333; rna (ng/ul): 40; sample_well: B07; sentrix_id: 4646298008; sentrix_position: B; plate: 7; ', 'tumor id: 2376; tumor location: colon; sample age: 22.5; rna (ng/ul): 31; sample_well: B08; sentrix_id: 4646298022; sentrix_position: B; plate: 7; ', 'tumor id: 2406; tumor location: colon; sample age: 12; rna (ng/ul): 17; sample_well: B09; sentrix_id: 4646298027; sentrix_position: B; plate: 7; ', 'tumor id: 3126; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: B10; sentrix_id: 4646298028; sentrix_position: B; plate: 7; ', 'tumor id: 1795; tumor location: colon; sample age: 9.08333333333333; rna (ng/ul): 40; sample_well: B11; sentrix_id: 4646298029; sentrix_position: B; plate: 7; ', 'tumor id: 166; tumor location: rectum; sample age: 13.9166666666667; rna (ng/ul): 40; sample_well: B12; sentrix_id: 4646298035; sentrix_position: B; plate: 7; ', 'tumor id: 207; tumor location: rectum; sample age: 11; rna (ng/ul): 40; sample_well: C01; sentrix_id: 4642203098; sentrix_position: C; plate: 7; ', 'tumor id: 2397; tumor location: rectum; sample age: 19; rna (ng/ul): 40; sample_well: C02; sentrix_id: 4642203099; sentrix_position: C; plate: 7; ', 'tumor id: 3068; tumor location: rectum; sample age: 7.66666666666667; rna (ng/ul): 40; sample_well: C03; sentrix_id: 4642203100; sentrix_position: C; plate: 7; ', 'tumor id: 3058; tumor location: colon; sample age: 4.5; rna (ng/ul): 40; sample_well: C04; sentrix_id: 4642203104; sentrix_position: C; plate: 7; ', 'tumor id: 3091; tumor location: rectum; sample age: 7.83333333333333; rna (ng/ul): 40; sample_well: C05; sentrix_id: 4642203105; sentrix_position: C; plate: 7; ', 'tumor id: 2439; tumor location: colon; sample age: 10.3333333333333; rna (ng/ul): 40; sample_well: C06; sentrix_id: 4642203106; sentrix_position: C; plate: 7; ', 'tumor id: 1240; tumor location: rectum; sample age: 9.33333333333333; rna (ng/ul): 40; sample_well: C07; sentrix_id: 4646298008; sentrix_position: C; plate: 7; ', 'tumor id: 1219; tumor location: colon; sample age: 8.83333333333333; rna (ng/ul): 40; sample_well: C08; sentrix_id: 4646298022; sentrix_position: C; plate: 7; ', 'tumor id: 3263; tumor location: rectum; sample age: 7.91666666666667; rna (ng/ul): 40; sample_well: C09; sentrix_id: 4646298027; sentrix_position: C; plate: 7; ', 'tumor id: 3270; tumor location: colon; sample age: 5.58333333333333; rna (ng/ul): 40; sample_well: C10; sentrix_id: 4646298028; sentrix_position: C; plate: 7; ', 'tumor id: 2455; tumor location: colon; sample age: 7.83333333333333; rna (ng/ul): 40; sample_well: C11; sentrix_id: 4646298029; sentrix_position: C; plate: 7; ', 'tumor id: 2445; tumor location: colon; sample age: 8.66666666666667; rna (ng/ul): 40; sample_well: C12; sentrix_id: 4646298035; sentrix_position: C; plate: 7; ', 'tumor id: 40; tumor location: rectum; sample age: 26.4166666666667; rna (ng/ul): 16; sample_well: D01; sentrix_id: 4642203098; sentrix_position: D; plate: 7; ', 'tumor id: 2983; tumor location: rectum; sample age: 7.91666666666667; rna (ng/ul): 36; sample_well: D03; sentrix_id: 4642203100; sentrix_position: D; plate: 7; ', 'tumor id: 3080; tumor location: rectum; sample age: 5.41666666666667; rna (ng/ul): 40; sample_well: D04; sentrix_id: 4642203104; sentrix_position: D; plate: 7; ', 'tumor id: 3085; tumor location: rectum; sample age: 10.0833333333333; rna (ng/ul): 32; sample_well: D05; sentrix_id: 4642203105; sentrix_position: D; plate: 7; ', 'tumor id: 2775; tumor location: rectum; sample age: 7.66666666666667; rna (ng/ul): 40; sample_well: D06; sentrix_id: 4642203106; sentrix_position: D; plate: 7; ', 'tumor id: 2764; tumor location: colon; sample age: 5.5; rna (ng/ul): 40; sample_well: D07; sentrix_id: 4646298008; sentrix_position: D; plate: 7; ', 'tumor id: 134; tumor location: colon; sample age: 12.6666666666667; rna (ng/ul): 40; sample_well: D08; sentrix_id: 4646298022; sentrix_position: D; plate: 7; ', 'tumor id: 3194; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: D09; sentrix_id: 4646298027; sentrix_position: D; plate: 7; ', 'tumor id: 2943; tumor location: rectum; sample age: 6.41666666666667; rna (ng/ul): 40; sample_well: D10; sentrix_id: 4646298028; sentrix_position: D; plate: 7; ', 'tumor id: 2407; tumor location: rectum; sample age: 9.58333333333333; rna (ng/ul): 39; sample_well: D11; sentrix_id: 4646298029; sentrix_position: D; plate: 7; ', 'tumor id: 2371; tumor location: rectum; sample age: 9; rna (ng/ul): 40; sample_well: D12; sentrix_id: 4646298035; sentrix_position: D; plate: 7; ', 'tumor id: 36; tumor location: rectum; sample age: 14.3333333333333; rna (ng/ul): 40; sample_well: E01; sentrix_id: 4642203098; sentrix_position: E; plate: 7; ', 'tumor id: 272; tumor location: colon; sample age: 16.6666666666667; rna (ng/ul): 40; sample_well: E02; sentrix_id: 4642203099; sentrix_position: E; plate: 7; ', 'tumor id: 3112; tumor location: colon; sample age: 5.83333333333333; rna (ng/ul): 40; sample_well: E03; sentrix_id: 4642203100; sentrix_position: E; plate: 7; ', 'tumor id: 3082; tumor location: rectum; sample age: 7.08333333333333; rna (ng/ul): 40; sample_well: E04; sentrix_id: 4642203104; sentrix_position: E; plate: 7; ', 'tumor id: 3408; tumor location: colon; sample age: 5.16666666666667; rna (ng/ul): 40; sample_well: E05; sentrix_id: 4642203105; sentrix_position: E; plate: 7; ', 'tumor id: 1179; tumor location: colon; sample age: 8.91666666666667; rna (ng/ul): 40; sample_well: E06; sentrix_id: 4642203106; sentrix_position: E; plate: 7; ', 'tumor id: 2635; tumor location: colon; sample age: 7.41666666666667; rna (ng/ul): 32; sample_well: E07; sentrix_id: 4646298008; sentrix_position: E; plate: 7; ', 'tumor id: 139; tumor location: rectum; sample age: 12; rna (ng/ul): 40; sample_well: E08; sentrix_id: 4646298022; sentrix_position: E; plate: 7; ', 'tumor id: 3221; tumor location: colon; sample age: 5.5; rna (ng/ul): 40; sample_well: E09; sentrix_id: 4646298027; sentrix_position: E; plate: 7; ', 'tumor id: 2438; tumor location: colon; sample age: 8.75; rna (ng/ul): 40; sample_well: E10; sentrix_id: 4646298028; sentrix_position: E; plate: 7; ', 'tumor id: 2435; tumor location: colon; sample age: 8.5; rna (ng/ul): 15; sample_well: E11; sentrix_id: 4646298029; sentrix_position: E; plate: 7; ', 'tumor id: 2434; tumor location: colon; sample age: 13.8333333333333; rna (ng/ul): 40; sample_well: E12; sentrix_id: 4646298035; sentrix_position: E; plate: 7; ', 'tumor id: 200; tumor location: rectum; sample age: 22.5833333333333; rna (ng/ul): 40; sample_well: F01; sentrix_id: 4642203098; sentrix_position: F; plate: 7; ', 'tumor id: 2400; tumor location: colon; sample age: 17.75; rna (ng/ul): 40; sample_well: F02; sentrix_id: 4642203099; sentrix_position: F; plate: 7; ', 'tumor id: 2934; tumor location: colon; sample age: 5.08333333333333; rna (ng/ul): 40; sample_well: F03; sentrix_id: 4642203100; sentrix_position: F; plate: 7; ', 'tumor id: 2995; tumor location: colon; sample age: 6; rna (ng/ul): 40; sample_well: F04; sentrix_id: 4642203104; sentrix_position: F; plate: 7; ', 'tumor id: 3079; tumor location: colon; sample age: 4.83333333333333; rna (ng/ul): 39; sample_well: F05; sentrix_id: 4642203105; sentrix_position: F; plate: 7; ', 'tumor id: 2624; tumor location: rectum; sample age: 8.08333333333333; rna (ng/ul): 40; sample_well: F06; sentrix_id: 4642203106; sentrix_position: F; plate: 7; ', 'tumor id: 2759; tumor location: colon; sample age: 7.16666666666667; rna (ng/ul): 24; sample_well: F07; sentrix_id: 4646298008; sentrix_position: F; plate: 7; ', 'tumor id: 405; tumor location: colon; sample age: 17.0833333333333; rna (ng/ul): 40; sample_well: F08; sentrix_id: 4646298022; sentrix_position: F; plate: 7; ', 'tumor id: 276; tumor location: rectum; sample age: 12.1666666666667; rna (ng/ul): 40; sample_well: F09; sentrix_id: 4646298027; sentrix_position: F; plate: 7; ', 'tumor id: 2446; tumor location: colon; sample age: 9.41666666666667; rna (ng/ul): 40; sample_well: F10; sentrix_id: 4646298028; sentrix_position: F; plate: 7; ', 'tumor id: 2430; tumor location: rectum; sample age: 8.25; rna (ng/ul): 20; sample_well: F11; sentrix_id: 4646298029; sentrix_position: F; plate: 7; ', 'tumor id: 2457; tumor location: rectum; sample age: 9.41666666666667; rna (ng/ul): 40; sample_well: F12; sentrix_id: 4646298035; sentrix_position: F; plate: 7; ', 'tumor id: 87; tumor location: colon; sample age: 17.6666666666667; rna (ng/ul): 40; sample_well: G01; sentrix_id: 4642203098; sentrix_position: G; plate: 7; ', 'tumor id: 3045; tumor location: rectum; sample age: 5.75; rna (ng/ul): 11; sample_well: G02; sentrix_id: 4642203099; sentrix_position: G; plate: 7; ', 'tumor id: 3116; tumor location: colon; sample age: 5.33333333333333; rna (ng/ul): 40; sample_well: G03; sentrix_id: 4642203100; sentrix_position: G; plate: 7; ', 'tumor id: 3108; tumor location: rectum; sample age: 5.58333333333333; rna (ng/ul): 40; sample_well: G04; sentrix_id: 4642203104; sentrix_position: G; plate: 7; ', 'tumor id: 3060; tumor location: colon; sample age: 6.25; rna (ng/ul): 40; sample_well: G05; sentrix_id: 4642203105; sentrix_position: G; plate: 7; ', 'tumor id: 1187; tumor location: rectum; sample age: 10.25; rna (ng/ul): 13; sample_well: G06; sentrix_id: 4642203106; sentrix_position: G; plate: 7; ', 'tumor id: 2444; tumor location: colon; sample age: 21.1666666666667; rna (ng/ul): 13; sample_well: G07; sentrix_id: 4646298008; sentrix_position: G; plate: 7; ', 'tumor id: 262; tumor location: colon; sample age: 19.6666666666667; rna (ng/ul): 40; sample_well: G08; sentrix_id: 4646298022; sentrix_position: G; plate: 7; ', 'tumor id: 2766; tumor location: rectum; sample age: 5.33333333333333; rna (ng/ul): 40; sample_well: G09; sentrix_id: 4646298027; sentrix_position: G; plate: 7; ', 'tumor id: 2423; tumor location: colon; sample age: 10.25; rna (ng/ul): 40; sample_well: G10; sentrix_id: 4646298028; sentrix_position: G; plate: 7; ', 'tumor id: 1156; tumor location: colon; sample age: 9.33333333333333; rna (ng/ul): 40; sample_well: G11; sentrix_id: 4646298029; sentrix_position: G; plate: 7; ', 'tumor id: 3537; tumor location: colon; sample age: 7.83333333333333; rna (ng/ul): 40; sample_well: G12; sentrix_id: 4646298035; sentrix_position: G; plate: 7; ', 'tumor id: 183; tumor location: rectum; sample age: 14; rna (ng/ul): 35; sample_well: H01; sentrix_id: 4642203098; sentrix_position: H; plate: 7; ', 'tumor id: 3046; tumor location: colon; sample age: 5; rna (ng/ul): 40; sample_well: H02; sentrix_id: 4642203099; sentrix_position: H; plate: 7; ', 'tumor id: 3067; tumor location: colon; sample age: 7.08333333333333; rna (ng/ul): 35; sample_well: H03; sentrix_id: 4642203100; sentrix_position: H; plate: 7; ', 'tumor id: 3111; tumor location: colon; sample age: 5.16666666666667; rna (ng/ul): 40; sample_well: H04; sentrix_id: 4642203104; sentrix_position: H; plate: 7; ', 'tumor id: 2812; tumor location: rectum; sample age: 9.66666666666667; rna (ng/ul): 40; sample_well: H06; sentrix_id: 4642203106; sentrix_position: H; plate: 7; ', 'tumor id: 1246; tumor location: colon; sample age: 9.5; rna (ng/ul): 29; sample_well: H07; sentrix_id: 4646298008; sentrix_position: H; plate: 7; ', 'tumor id: 3309; tumor location: rectum; sample age: 8.66666666666667; rna (ng/ul): 40; sample_well: H08; sentrix_id: 4646298022; sentrix_position: H; plate: 7; ', 'tumor id: 3301; tumor location: rectum; sample age: 6.41666666666667; rna (ng/ul): 40; sample_well: H09; sentrix_id: 4646298027; sentrix_position: H; plate: 7; ', 'tumor id: 388; tumor location: colon; sample age: 12.6666666666667; rna (ng/ul): 40; sample_well: H10; sentrix_id: 4646298028; sentrix_position: H; plate: 7; ', 'tumor id: 2416; tumor location: rectum; sample age: 10.4166666666667; rna (ng/ul): 40; sample_well: H11; sentrix_id: 4646298029; sentrix_position: H; plate: 7; ', 'tu mor id: 3424; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: H12; sentrix_id: 4646298035; sentrix_position: H; plate: 7; ', 'tumor id: 1174; tumor location: colon; sample age: 8.58333333333333; rna (ng/ul): 40; sample_well: A01; sentrix_id: 4642203007; sentrix_position: A; plate: 8; ', 'tumor id: 1192; tumor location: colon; sample age: 9.58333333333333; rna (ng/ul): 40; sample_well: A02; sentrix_id: 4642203008; sentrix_position: A; plate: 8; ', 'tumor id: 224; tumor location: rectum; sample age: 12.1666666666667; rna (ng/ul): 28; sample_well: A03; sentrix_id: 4642203009; sentrix_position: A; plate: 8; ', 'tumor id: 293; tumor location: rectum; sample age: 12.4166666666667; rna (ng/ul): 40; sample_well: A04; sentrix_id: 4642203022; sentrix_position: A; plate: 8; ', 'tumor id: 1175; tumor location: rectum; sample age: 12.0833333333333; rna (ng/ul): 40; sample_well: A05; sentrix_id: 4642203024; sentrix_position: A; plate: 8; ', 'tumor id: 1182; tumor location: rectum; sample age: 8.33333333333333; rna (ng/ul): 40; sample_well: A06; sentrix_id: 4642203030; sentrix_position: A; plate: 8; ', 'tumor id: 125; tumor location: colon; sample age: 11.25; rna (ng/ul): 40; sample_well: A07; sentrix_id: 4642203044; sentrix_position: A; plate: 8; ', 'tumor id: 3102; tumor location: rectum; sample age: 7.58333333333333; rna (ng/ul): 40; sample_well: A08; sentrix_id: 4642203056; sentrix_position: A; plate: 8; ', 'tumor id: 1804; tumor location: colon; sample age: 9.83333333333333; rna (ng/ul): 40; sample_well: A09; sentrix_id: 4642203074; sentrix_position: A; plate: 8; ', 'tumor id: 2289; tumor location: rectum; sample age: 6.91666666666667; rna (ng/ul): 40; sample_well: A10; sentrix_id: 4642203075; sentrix_position: A; plate: 8; ', 'tumor id: 2281; tumor location: rectum; sample age: 6.91666666666667; rna (ng/ul): 40; sample_well: A11; sentrix_id: 4642203076; sentrix_position: A; plate: 8; ', 'tumor id: 2259; tumor location: rectum; sample age: 7.41666666666667; rna (ng/ul): 40; sample_well: A12; sentrix_id: 4642203096; sentrix_position: A; plate: 8; ', 'tumor id: 1193; tumor location: rectum; sample age: 10.0833333333333; rna (ng/ul): 40; sample_well: B02; sentrix_id: 4642203008; sentrix_position: B; plate: 8; ', 'tumor id: 1233; tumor location: colon; sample age: 9.5; rna (ng/ul): 35; sample_well: B03; sentrix_id: 4642203009; sentrix_position: B; plate: 8; ', 'tumor id: 305; tumor location: colon; sample age: 14.9166666666667; rna (ng/ul): 40; sample_well: B04; sentrix_id: 4642203022; sentrix_position: B; plate: 8; ', 'tumor id: 1247; tumor location: colon; sample age: 11; rna (ng/ul): 40; sample_well: B05; sentrix_id: 4642203024; sentrix_position: B; plate: 8; ', 'tumor id: 133; tumor location: rectum; sample age: 14.25; rna (ng/ul): 40; sample_well: B06; sentrix_id: 4642203030; sentrix_position: B; plate: 8; ', 'tumor id: 463; tumor location: rectum; sample age: 13.25; rna (ng/ul): 40; sample_well: B09; sentrix_id: 4642203074; sentrix_position: B; plate: 8; ', 'tumor id: 3069; tumor location: rectum; sample age: 8.25; rna (ng/ul): 40; sample_well: B10; sentrix_id: 4642203075; sentrix_position: B; plate: 8; ', 'tumor id: 2297; tumor location: rectum; sample age: 8; rna (ng/ul): 40; sample_well: B11; sentrix_id: 4642203076; sentrix_position: B; plate: 8; ', 'tumor id: 2323; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: B12; sentrix_id: 4642203096; sentrix_position: B; plate: 8; ', 'tumor id: 1170; tumor location: colon; sample age: 8.58333333333333; rna (ng/ul): 40; sample_well: C01; sentrix_id: 4642203007; sentrix_position: C; plate: 8; ', 'tumor id: 1199; tumor location: colon; sample age: 8.33333333333333; rna (ng/ul): 40; sample_well: C02; sentrix_id: 4642203008; sentrix_position: C; plate: 8; ', 'tumor id: 1232; tumor location: colon; sample age: 8.16666666666667; rna (ng/ul): 40; sample_well: C03; sentrix_id: 4642203009; sentrix_position: C; plate: 8; ', 'tumor id: 296; tumor location: colon; sample age: 13.75; rna (ng/ul): 40; sample_well: C04; sentrix_id: 4642203022; sentrix_position: C; plate: 8; ', 'tumor id: 1184; tumor location: colon; sample age: 10.3333333333333; rna (ng/ul): 40; sample_well: C05; sentrix_id: 4642203024; sentrix_position: C; plate: 8; ', 'tumor id: 138; tumor location: rectum; sample age: 21.0833333333333; rna (ng/ul): 40; sample_well: C06; sentrix_id: 4642203030; sentrix_position: C; plate: 8; ', 'tumor id: 2364; tumor location: colon; sample age: 13.1666666666667; rna (ng/ul): 40; sample_well: C07; sentrix_id: 4642203044; sentrix_position: C; plate: 8; ', 'tumor id: 2249; tumor location: colon; sample age: 8.33333333333333; rna (ng/ul): 40; sample_well: C08; sentrix_id: 4642203056; sentrix_position: C; plate: 8; ', 'tumor id: 2671; tumor location: colon; sample age: 7.83333333333333; rna (ng/ul): 40; sample_well: C09; sentrix_id: 4642203074; sentrix_position: C; plate: 8; ', 'tumor id: 3140; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: C10; sentrix_id: 4642203075; sentrix_position: C; plate: 8; ', 'tumor id: 1875; tumor location: rectum; sample age: 11.8333333333333; rna (ng/ul): 40; sample_well: C11; sentrix_id: 4642203076; sentrix_position: C; plate: 8; ', 'tumor id: 3312; tumor location: colon; sample age: 6.66666666666667; rna (ng/ul): 40; sample_well: C12; sentrix_id: 4642203096; sentrix_position: C; plate: 8; ', 'tumor id: 1167; tumor location: rectum; sample age: 10.25; rna (ng/ul): 40; sample_well: D01; sentrix_id: 4642203007; sentrix_position: D; plate: 8; ', 'tumor id: 1200; tumor location: colon; sample age: 10; rna (ng/ul): 40; sample_well: D02; sentrix_id: 4642203008; sentrix_position: D; plate: 8; ', 'tumor id: 588; tumor location: colon; sample age: 20.5; rna (ng/ul): 32; sample_well: D03; sentrix_id: 4642203009; sentrix_position: D; plate: 8; ', 'tumor id: 314; tumor location: rectum; sample age: 15.9166666666667; rna (ng/ul): 40; sample_well: D04; sentrix_id: 4642203022; sentrix_position: D; plate: 8; ', 'tumor id: 1185; tumor location: colon; sample age: 9.83333333333333; rna (ng/ul): 40; sample_well: D05; sentrix_id: 4642203024; sentrix_position: D; plate: 8; ', 'tumor id: 474; tumor location: colon; sample age: 14.25; rna (ng/ul): 40; sample_well: D07; sentrix_id: 4642203044; sentrix_position: D; plate: 8; ', 'tumor id: 1262; tumor location: colon; sample age: 9.83333333333333; rna (ng/ul): 40; sample_well: D08; sentrix_id: 4642203056; sentrix_position: D; plate: 8; ', 'tumor id: 2260; tumor location: rectum; sample age: 7.91666666666667; rna (ng/ul): 40; sample_well: D09; sentrix_id: 4642203074; sentrix_position: D; plate: 8; ', 'tumor id: 3124; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: D10; sentrix_id: 4642203075; sentrix_position: D; plate: 8; ', 'tumor id: 1794; tumor location: rectum; sample age: 9.66666666666667; rna (ng/ul): 40; sample_well: D11; sentrix_id: 4642203076; sentrix_position: D; plate: 8; ', 'tumor id: 1806; tumor location: rectum; sample age: 9.25; rna (ng/ul): 40; sample_well: D12; sentrix_id: 4642203096; sentrix_position: D; plate: 8; ', 'tumor id: 649; tumor location: rectum; sample age: 13.8333333333333; rna (ng/ul): 22; sample_well: E02; sentrix_id: 4642203008; sentrix_position: E; plate: 8; ', 'tumor id: 2411; tumor location: colon; sample age: 27; rna (ng/ul): 22; sample_well: E03; sentrix_id: 4642203009; sentrix_position: E; plate: 8; ', 'tumor id: 1205; tumor location: rectum; sample age: 9.16666666666667; rna (ng/ul): 26; sample_well: E04; sentrix_id: 4642203022; sentrix_position: E; plate: 8; ', 'tumor id: 2417; tumor location: rectum; sample age: 8.75; rna (ng/ul): 40; sample_well: E05; sentrix_id: 4642203024; sentrix_position: E; plate: 8; ', 'tumor id: 261; tumor location: rectum; sample age: 11.6666666666667; rna (ng/ul): 40; sample_well: E06; sentrix_id: 4642203030; sentrix_position: E; plate: 8; ', 'tumor id: 213; tumor location: rectum; sample age: 15.3333333333333; rna (ng/ul): 40; sample_well: E07; sentrix_id: 4642203044; sentrix_position: E; plate: 8; ', 'tumor id: 2261; tumor location: colon; sample age: 8.83333333333333; rna (ng/ul): 18; sample_well: E08; sentrix_id: 4642203056; sentrix_position: E; plate: 8; ', 'tumor id: 3220; tumor location: colon; sample age: 5.75; rna (ng/ul): 40; sample_well: E09; sentrix_id: 4642203074; sentrix_position: E; plate: 8; ', 'tumor id: 3153; tumor location: colon; sample age: 13.5833333333333; rna (ng/ul): 40; sample_well: E10; sentrix_id: 4642203075; sentrix_position: E; plate: 8; ', 'tumor id: 3128; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: E11; sentrix_id: 4642203076; sentrix_position: E; plate: 8; ', 'tumor id: 3191; tumor location: colon; sample age: 4.91666666666667; rna (ng/ul): 40; sample_well: E12; sentrix_id: 4642203096; sentrix_position: E; plate: 8; ', 'tumor id: 1154; tumor location: rectum; sample age: 9.5; rna (ng/ul): 40; sample_well: F01; sentrix_id: 4642203007; sentrix_position: F; plate: 8; ', 'tumor id: 1231; tumor location: rectum; sample age: 10; rna (ng/ul): 40; sample_well: F03; sentrix_id: 4642203009; sentrix_position: F; plate: 8; ', 'tumor id: 257; tumor location: rectum; sample age: 16.75; rna (ng/ul): 40; sample_well: F04; sentrix_id: 4642203022; sentrix_position: F; plate: 8; ', 'tumor id: 2420; tumor location: rectum; sample age: 8.66666666666667; rna (ng/ul): 40; sample_well: F05; sentrix_id: 4642203024; sentrix_position: F; plate: 8; ', 'tumor id: 184; tumor location: colon; sample age: 19.5; rna (ng/ul): 19; sample_well: F06; sentrix_id: 4642203030; sentrix_position: F; plate: 8; ', 'tumor id: 406; tumor location: rectum; sample age: 22.1666666666667; rna (ng/ul): 40; sample_well: F07; sentrix_id: 4642203044; sentrix_position: F; plate: 8; ', 'tumor id: 3131; tumor location: colon; sample age: 6.08333333333333; rna (ng/ul): 40; sample_well: F08; sentrix_id: 4642203056; sentrix_position: F; plate: 8; ', 'tumor id: 3326; tumor location: rectum; sample age: 4.41666666666667; rna (ng/ul): 40; sample_well: F09; sentrix_id: 4642203074; sentrix_position: F; plate: 8; ', 'tumor id: 3217; tumor location: colon; sample age: 6.08333333333333; rna (ng/ul): 40; sample_well: F10; sentrix_id: 4642203075; sentrix_position: F; plate: 8; ', 'tumor id: 3074; tumor location: colon; sample age: 5.08333333333333; rna (ng/ul): 40; sample_well: F11; sentrix_id: 4642203076; sentrix_position: F; plate: 8; ', 'tumor id: 2257; tumor location: rectum; sample age: 8; rna (ng/ul): 40; sample_well: F12; sentrix_id: 4642203096; sentrix_position: F; plate: 8; ', 'tumor id: 223; tumor location: colon; sample age: 18; rna (ng/ul): 40; sample_well: G01; sentrix_id: 4642203007; sentrix_position: G; plate: 8; ', 'tumor id: 1239; tumor location: rectum; sample age: 11; rna (ng/ul): 40; sample_well: G02; sentrix_id: 4642203008; sentrix_position: G; plate: 8; ', 'tumor id: 1250; tumor location: colon; sample age: 8.75; rna (ng/ul): 40; sample_well: G03; sentrix_id: 4642203009; sentrix_position: G; plate: 8; ', 'tumor id: 1230; tumor location: colon; sample age: 10.4166666666667; rna (ng/ul): 40; sample_well: G04; sentrix_id: 4642203022; sentrix_position: G; plate: 8; ', 'tumor id: 55; tumor location: rectum; sample age: 11.0833333333333; rna (ng/ul): 40; sample_well: G05; sentrix_id: 4642203024; sentrix_position: G; plate: 8; ', 'tumor id: 206; tumor location: colon; sample age: 20.6666666666667; rna (ng/ul): 40; sample_well: G06; sentrix_id: 4642203030; sentrix_position: G; plate: 8; ', 'tumor id: 204; tumor location: colon; sample age: 20.6666666666667; rna (ng/ul): 40; sample_well: G07; sentrix_id: 4642203044; sentrix_position: G; plate: 8; ', 'tumor id: 2275; tumor location: rectum; sample age: 7.41666666666667; rna (ng/ul): 40; sample_well: G08; sentrix_id: 4642203056; sentrix_position: G; plate: 8; ', 'tumor id: 3237; tumor location: rectum; sample age: 4.75; rna (ng/ul): 40; sample_well: G09; sentrix_id: 4642203074; sentrix_position: G; plate: 8; ', 'tumor id: 3304; tumor location: colon; sample age: 6.33333333333333; rna (ng/ul): 25; sample_well: G10; sentrix_id: 4642203075; sentrix_position: G; plate: 8; ', 'tumor id: 1765; tumor location: rectum; sample age: 10.1666666666667; rna (ng/ul): 40; sample_well: G11; sentrix_id: 4642203076; sentrix_position: G; plate: 8; ', 'tumor id: 3139; tumor location: rectum; sample age: 7.5; rna (ng/ul): 40; sample_well: G12; sentrix_id: 4642203096; sentrix_position: G; plate: 8; ', 'tumor id: 1191; tumor location: colon; sample age: 8.75; rna (ng/ul): 40; sample_well: H01; sentrix_id: 4642203007; sentrix_position: H; plate: 8; ', 'tumor id: 286; tumor location: rectum; sample age: 10.5833333333333; rna (ng/ul): 40; sample_well: H02; sentrix_id: 4642203008; sentrix_position: H; plate: 8; ', 'tumor id: 652; tumor location: colon; sample age: 14.25; rna (ng/ul): 40; sample_well: H03; sentrix_id: 4642203009; sentrix_position: H; plate: 8; ', 'tumor id: 1195; tumor location: rectum; sample age: 8.08333333333333; rna (ng/ul): 40; sample_well: H04; sentrix_id: 4642203022; sentrix_position: H; plate: 8; ', 'tumor id: 95; tumor location: colon; sample age: 15.4166666666667; rna (ng/ul): 40; sample_well: H05; sentrix_id: 4642203024; sentrix_position: H; plate: 8; ', 'tumor id: 2432; tumor location: colon; sample age: 17.75; rna (ng/ul): 40; sample_well: H06; sentrix_id: 4642203030; sentrix_position: H; plate: 8; ', 'tumor id: 586; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: H07; sentrix_id: 4642203044; sentrix_position: H; plate: 8; ', 'tumor id: 3409; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: H08; sentrix_id: 4642203056; sentrix_position: H; plate: 8; ', 'tumor id: 597; tumor location: colon; sample age: 18.5833333333333; rna (ng/ul): 40; sample_well: H10; sentrix_id: 4642203075; sentrix_position: H; plate: 8; ', 'tumor id: 2247; tumor location: rectum; sample age: 8.66666666666667; rna (ng/ul): 40; sample_well: H11; sentrix_id: 4642203076; sentrix_position: H; plate: 8; ', 'tumor id: 2264; tumor location: colon; sample age: 7.33333333333333; rna (ng/ul): 40; sample_well: H12; sentrix_id: 4642203096; sentrix_position: H; plate: 8; ', 'tumor id: 3168; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: A01; sentrix_id: 4953108016; sentrix_position: A; plate: 9; ', 'tumor id: 3208; tumor location: colon; sample age: 5.5; rna (ng/ul): 40; sample_well: A02; sentrix_id: 4953108017; sentrix_position: A; plate: 9; ', 'tumor id: 3496; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: A03; sentrix_id: 4953108018; sentrix_position: A; plate: 9; ', 'tumor id: 3211; tumor location: rectum; sample age: 5.25; rna (ng/ul): 11; sample_well: A04; sentrix_id: 4953108040; sentrix_position: A; plate: 9; ', 'tumor id: 3527; tumor location: colon; sample age: 3.83333333333333; rna (ng/ul): 40; sample_well: A05; sentrix_id: 4953108041; sentrix_position: A; plate: 9; ', 'tumor id: 3538; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: A06; sentrix_id: 4953108043; sentrix_position: A; plate: 9; ', 'tumor id: 2387; tumor location: rectum; sample age: 16.4166666666667; rna (ng/ul): 40; sample_well: A08; sentrix_id: 4953108052; sentrix_position: A; plate: 9; ', 'tumor id: 3443; tumor location: colon; sample age: 1.91666666666667; rna (ng/ul): 40; sample_well: A09; sentrix_id: 4953108053; sentrix_position: A; plate: 9; ', 'tumor id: 3534; tumor location: rectum; sample age: 5.5; rna (ng/ul): 40; sample_well: A10; sentrix_id: 4953108054; sentrix_position: A; plate: 9; ', 'tumor id: 1797; tumor location: colon; sample age: 9; rna (ng/ul): 40; sample_well: A11; sentrix_id: 4953108055; sentrix_position: A; plate: 9; ', 'tumor id: 2640; tumor location: colon; sample age: 20.8333333333333; rna (ng/ul): 40; sample_well: A12; sentrix_id: 4953108057; sentrix_position: A; plate: 9; ', 'tumor id: 1260; tumor location: colon; sample age: 9.33333333333333; rna (ng/ul): 40; sample_well: B01; sentrix_id: 4953108016; sentrix_position: B; plate: 9; ', 'tumor id: 2266; tumor location: rectum; sample age: 7.58333333333333; rna (ng/ul): 40; sample_well: B02; sentrix_id: 4953108017; sentrix_position: B; plate: 9; ', 'tumor id: 628; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: B04; sentrix_id: 4953108040; sentrix_position: B; plate: 9; ', 'tumor id: 3451; tumor location: rectum; sample age: 3.33333333333333; rna (ng/ul): 40; sample_well: B05; sentrix_id: 4953108041; sentrix_position: B; plate: 9; ', 'tumor id: 3503; tumor location: rectum; sample age: 1.83333333333333; rna (ng/ul): 40; sample_well: B06; sentrix_id: 4953108043; sentrix_position: B; plate: 9; ', 'tumor id: 3029; tumor location: rectum; sample age: 5.41666666666667; rna (ng/ul): 40; sample_well: B07; sentrix_id: 4953108044; sentrix_position: B; plate: 9; ', 'tumor id: 657; tumor location: colon; sample age: 13.3333333333333; rna (ng/ul): 40; sample_well: B08; sentrix_id: 4953108052; sentrix_position: B; plate: 9; ', 'tumor id: 1178; tumor location: colon; sample age: 10.1666666666667; rna (ng/ul): 40; sample_well: B09; sentrix_id: 4953108053; sentrix_position: B; plate: 9; ', 'tumor id: 3450; tumor location: colon; sample age: 3.5; rna (ng/ul): 40; sample_well: B10; sentrix_id: 4953108054; sentrix_position: B; plate: 9; ', 'tumor id: 2421; tumor location: colon; sample age: 8.83333333333333; rna (ng/ul): 40; sample_well: B11; sentrix_id: 4953108055; sentrix_position: B; plate: 9; ', 'tumor id: 199; tumor location: colon; sample age: 14.25; rna (ng/ul): 40; sample_well: B12; sentrix_id: 4953108057; sentrix_position: B; plate: 9; ', 'tumor id: 2252; tumor location: colon; sample age: 8; rna (ng/ul): 40; sample_well: C01; sentrix_id: 4953108016; sentrix_position: C; plate: 9; ', 'tumor id: 2296; tumor location: rectum; sample age: 7.41666666666667; rna (ng/ul): 24; sample_well: C02; sentrix_id: 4953108017; sentrix_position: C; plate: 9; ', 'tumor id: 2930; tumor location: colon; sample age: 8.25; rna (ng/ul): 40; sample_well: C03; sentrix_id: 4953108018; sentrix_position: C; plate: 9; ', 'tumor id: 3119; tumor location: colon; sample age: 6.91666666666667; rna (ng/ul): 40; sample_well: C04; sentrix_id: 4953108040; sentrix_position: C; plate: 9; ', 'tumor id: 3542; tumor location: rectum; sample age: 3.5; rna (ng/ul): 40; sample_well: C05; sentrix_id: 4953108041; sentrix_position: C; plate: 9; ', 'tumor id: 3535; tumor location: rectum; sample age: 4.08333333333333; rna (ng/ul): 40; sample_well: C06; sentrix_id: 4953108043; sentrix_position: C; plate: 9; ', 'tumor id: 1169; tumor location: colon; sample age: 9.83333333333333; rna (ng/ul): 40; sample_well: C07; sentrix_id: 4953108044; sentrix_position: C; plate: 9; ', 'tumor id: 3187; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: C08; sentrix_id: 4953108052; sentrix_position: C; plate: 9; ', 'tumor id: 1249; tumor location: colon; sample age: 8.58333333333333; rna (ng/ul): 40; sample_well: C09; sentrix_id: 4953108053; sentrix_position: C; plate: 9; ', 'tumor id: 458; tumor location: rectum; sample age: 13.5833333333333; rna (ng/ul): 40; sample_well: C10; sentrix_id: 4953108054; sentrix_position: C; plate: 9; ', 'tumor id: 504; tumor location: rectum; sample age: 18.25; rna (ng/ul): 40; sample_well: C11; sentrix_id: 4953108055; sentrix_position: C; plate: 9; ', 'tumor id: 3256; tumor location: colon; sample age: 9.16666666666667; rna (ng/ul): 37; sample_well: C12; sentrix_id: 4953108057; sentrix_position: C; plate: 9; ', 'tumor id: 2250; tumor location: rectum; sample age: 18.6666666666667; rna (ng/ul): 26; sample_well: D01; sentrix_id: 4953108016; sentrix_position: D; plate: 9; ', 'tumor id: 1288; tumor location: rectum; sample age: 12.0833333333333; rna (ng/ul): 40; sample_well: D03; sentrix_id: 4953108018; sentrix_position: D; plate: 9; ', 'tumor id: 1755; tumor location: rectum; sample age: 9; rna (ng/ul): 40; sample_well: D04; sentrix_id: 4953108040; sentrix_position: D; plate: 9; ', 'tumor id: 3543; tumor location: rectum; sample age: 3.66666666666667; rna (ng/ul): 40; sample_well: D05; sentrix_id: 4953108041; sentrix_position: D; plate: 9; ', 'tumor id: 3512; tumor location: rectum; sample age: 2.75; rna (ng/ul): 40; sample_well: D06; sentrix_id: 4953108043; sentrix_position: D; plate: 9; ', 'tumor id: 3442; tumor location: colon; sample age: 3.08333333333333; rna (ng/ul): 40; sample_well: D07; sentrix_id: 4953108044; sentrix_position: D; plate: 9; ', 'tumor id: 3502; tumor location: colon; sample age: 1.25; rna (ng/ul): 40; sample_well: D08; sentrix_id: 4953108052; sentrix_position: D; plate: 9; ', 'tumor id: 2644; tumor location: rectum; sample age: 25; rna (ng/ul): 40; sample_well: D09; sentrix_id: 4953108053; sentrix_position: D; plate: 9; ', 'tumor id: 1745; tumor location: rectum; sample age: 9.25; rna (ng/ul): 40; sample_well: D10; sentrix_id: 4953108054; sentrix_position: D; plate: 9; ', 'tumor id: 3480; tumor location: colon; sample age: 1.91666666666667; rna (ng/ul): 40; sample_well: D11; sentrix_id: 4953108055; sentrix_position: D; plate: 9; ', 'tumor id: 677; tumor location: colon; sample age: 16.8333333333333; rna (ng/ul): 40; sample_well: E01; sentrix_id: 4953108016; sentrix_position: E; plate: 9; ', 'tumor id: 2666; tumor location: colon; sample age: 7.25; rna (ng/ul): 40; sample_well: E02; sentrix_id: 4953108017; sentrix_position: E; plate: 9; ', 'tumor id: 1761; tumor location: colon; sample age: 10.0833333333333; rna (ng/ul): 40; sample_well: E03; sentrix_id: 4953108018; sentrix_position: E; plate: 9; ', 'tumor id: 3479; tumor location: rectum; sample age: 2.25; rna (ng/ul): 40; sample_well: E04; sentrix_id: 4953108040; sentrix_position: E; plate: 9; ', 'tumor id: 3477; tumor location: rectum; sample age: 2.41666666666667; rna (ng/ul): 27; sample_well: E05; sentrix_id: 4953108041; sentrix_position: E; plate: 9; ', 'tumor id: 3446; tumor location: rectum; sample age: 1.91666666666667; rna (ng/ul): 40; sample_well: E06; sentrix_id: 4953108043; sentrix_position: E; plate: 9; ', 'tumor id: 2664; tumor location: rectum; sample age: 8.41666666666667; rna (ng/ul): 40; sample_well: E07; sentrix_id: 4953108044; sentrix_position: E; plate: 9; ', 'tumor id: 3189; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: E08; sentrix_id: 4953108052; sentrix_position: E; plate: 9; ', 'tumor id: 291; tumor location: rectum; sample age: 12.8333333333333; rna (ng/ul): 40; sample_well: E09; sentrix_id: 4953108053; sentrix_position: E; plate: 9; ', 'tumor id: 2267; tumor location: colon; sample age: 7.58333333333333; rna (ng/ul): 40; sample_well: E10; sentrix_id: 4953108054; sentrix_position: E; plate: 9; ', 'tumor id: 3441; tumor location: rectum; sample age: 3.16666666666667; rna (ng/ul): 40; sample_well: E11; sentrix_id: 4953108055; sentrix_position: E; plate: 9; ', 'tumor id: 3078; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: F01; sentrix_id: 4953108016; sentrix_position: F; plate: 9; ', 'tumor id: 3315; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: F02; sentrix_id: 4953108017; sentrix_position: F; plate: 9; ', 'tumor id: 1762; tumor location: colon; sample age: 10; rna (ng/ul): 40; sample_well: F03; sentrix_id: 4953108018; sentrix_position: F; plate: 9; ', 'tumor id: 3421; tumor location: rectum; sample age: 3.5; rna (ng/ul): 40; sample_well: F04; sentrix_id: 4953108040; sentrix_position: F; plate: 9; ', 'tumor id: 3523; tumor location: rectum; sample age: 1.91666666666667; rna (ng/ul): 40; sample_well: F05; sentrix_id: 4953108041; sentrix_position: F; plate: 9; ', 'tumor id: 3436; tumor location: rectum; sample age: 3.33333333333333; rna (ng/ul): 40; sample_well: F06; sentrix_id: 4953108043; sentrix_position: F; plate: 9; ', 'tumor id: 44; tumor location: colon; sample age: 14.75; rna (ng/ul): 40; sample_well: F07; sentrix_id: 4953108044; sentrix_position: F; plate: 9; ', 'tumor id: 3254; tumor location: colon; sample age: 8; rna (ng/ul): 40; sample_well: F08; sentrix_id: 4953108052; sentrix_position: F; plate: 9; ', 'tumor id: 3505; tumor location: rectum; sample age: 1.58333333333333; rna (ng/ul): 40; sample_well: F09; sentrix_id: 4953108053; sentrix_position: F; plate: 9; ', 'tumor id: 585; tumor location: colon; sample age: 20.3333333333333; rna (ng/ul): 40; sample_well: F10; sentrix_id: 4953108054; sentrix_position: F; plate: 9; ', 'tumor id: 3498; tumor location: rectum; sample age: 1.41666666666667; rna (ng/ul): 40; sample_well: F11; sentrix_id: 4953108055; sentrix_position: F; plate: 9; ', 'tumor id: 3311; tumor location: colon; sample age: 6.75; rna (ng/ul): 40; sample_well: G01; sentrix_id: 4953108016; sentrix_position: G; plate: 9; ', 'tumor id: 3427; tumor location: colon; sample age: 3.5; rna (ng/ul): 40; sample_well: G02; sentrix_id: 4953108017; sentrix_position: G; plate: 9; ', 'tumor id: 2227; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: G03; sentrix_id: 4953108018; sentrix_position: G; plate: 9; ', 'tumor id: 3540; tumor location: rectum; sample age: 2.91666666666667; rna (ng/ul): 40; sample_well: G04; sentrix_id: 4953108040; sentrix_position: G; plate: 9; ', 'tumor id: 3510; tumor location: rectum; sample age: 1.66666666666667; rna (ng/ul): 40; sample_well: G05; sentrix_id: 4953108041; sentrix_position: G; plate: 9; ', 'tumor id: 3414; tumor location: colon; sample age: 4.33333333333333; rna (ng/ul): 40; sample_well: G06; sentrix_id: 4953108043; sentrix_position: G; plate: 9; ', 'tumor id: 2935; tumor location: colon; sample age: 10.1666666666667; rna (ng/ul): 40; sample_well: G07; sentrix_id: 4953108044; sentrix_position: G; plate: 9; ', 'tumor id: 3235; tumor location: rectum; sample age: 4.66666666666667; rna (ng/ul): 40; sample_well: G08; sentrix_id: 4953108052; sentrix_position: G; plate: 9; ', 'tumor id: 1245; tumor location: colon; sample age: 7.16666666666667; rna (ng/ul): 18; sample_well: G09; sentrix_id: 4953108053; sentrix_position: G; plate: 9; ', 'tumor id: 1770; tumor location: rectum; sample age: null; rna (ng/ul): 40; sample_well: G10; sentrix_id: 4953108054; sentrix_position: G; plate: 9; ', 'tumor id: 3483; tumor location: colon; sample age: 2.08333333333333; rna (ng/ul): 30; sample_well: G11; sentrix_id: 4953108055; sentrix_position: G; plate: 9; ', 'tumor id: 3428; tumor location: colon; sample age: 4.58333333333333; rna (ng/ul): 40; sample_well: H02; sentrix_id: 4953108017; sentrix_position: H; plate: 9; ', 'tumor id: 3165; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: H03; sentrix_id: 4953108018; sentrix_position: H; plate: 9; ', 'tumor id: 3529; tumor location: colon; sample age: null; rna (ng/ul): 40; sample_well: H04; sentrix_id: 4953108040; sentrix_position: H; plate: 9; ', 'tumor id: 3422; tumor location: rectum; sample age: 3.83333333333333; rna (ng/ul): 40; sample_well: H05; sentrix_id: 4953108041; sentrix_position: H; plate: 9; ', 'tumor id: 2980; tumor location: colon; sample age: 5.08333333333333; rna (ng/ul): 26; sample_well: H07; sentrix_id: 4953108044; sentrix_position: H; plate: 9; ', 'tumor id: 1153; tumor location: colon; sample age: 8.5; rna (ng/ul): 40; sample_well: H08; sentrix_id: 4953108052; sentrix_position: H; plate: 9; ', 'tumor id: 3415; tumor location: colon; sample age: 3.41666666666667; rna (ng/ul): 40; sample_well: H09; sentrix_id: 4953108053; sentrix_position: H; plate: 9; ', 'tumor id: 3504; tumor location: rectum; sample age: 1.91666666666667; rna (ng/ul): 33; sample_well: H10; sentrix_id: 4953108054; sentrix_position: H; plate: 9; ', 'tumor id: 3528; tumor location: colon; sample age: 3; rna (ng/ul): 40; sample_well: H11; sentrix_id: 4953108055; sentrix_position: H; plate: 9; ', 'tumor id: 3644; tumor location: colon; sample age: 3.91666666666667; rna (ng/ul): null; sample_well: A01; sentrix_id: 5370975012; sentrix_position: A; plate: 10; ', 'tumor id: 3651; tumor location: colon; sample age: 1.75; rna (ng/ul): null; sample_well: A02; sentrix_id: 5370975015; sentrix_position: A; plate: 10; ', 'tumor id: 3643; tumor location: rectum; sample age: 3.16666666666667; rna (ng/ul): null; sample_well: A03; sentrix_id: 5370975034; sentrix_position: A; plate: 10; ', 'tumor id: 3648; tumor location: rectum; sample age: 3.66666666666667; rna (ng/ul): null; sample_well: A04; sentrix_id: 5394951055; sentrix_position: A; plate: 10; ', 'tumor id: 3641; tumor location: rectum; sample age: 2.58333333333333; rna (ng/ul): null; sample_well: A06; sentrix_id: 5394951058; sentrix_position: A; plate: 10; ', 'tumor id: 3640; tumor location: rectum; sample age: 3; rna (ng/ul): null; sample_well: A07; sentrix_id: 5394951076; sentrix_position: A; plate: 10; ', 'tumor id: 3645; tumor location: rectum; sample age: 3.16666666666667; rna (ng/ul): null; sample_well: A08; sentrix_id: 5394951078; sentrix_position: A; plate: 10; ', 'tumor id: 3647; tumor location: rectum; sample age: 3.66666666666667; rna (ng/ul): null; sample_well: A09; sentrix_id: 5394951082; sentrix_position: A; plate: 10; ', 'tumor id: 3646; tumor location: rectum; sample age: 2.75; rna (ng/ul): null; sample_well: A10; sentrix_id: 5394951083; sentrix_position: A; plate: 10; ', 'tumor id: 3642; tumor location: colon; sample age: 2.5; rna (ng/ul): null; sample_well: A11; sentrix_id: 5394951084; sentrix_position: A; plate: 10; ', 'tumor id: 3563; tumor location: colon; sample age: 6.91666666666667; rna (ng/ul): null; sample_well: A12; sentrix_id: 5406051008; sentrix_position: A; plate: 10; ', 'tumor id: 3720; tumor location: rectum; sample age: 3.66666666666667; rna (ng/ul): null; sample_well: A01; sentrix_id: 5406051053; sentrix_position: A; plate: 11; ', 'tumor id: 3717; tumor location: colon; sample age: null; rna (ng/ul): null; sample_well: A02; sentrix_id: 5406051055; sentrix_position: A; plate: 11; ', 'tumor id: 3721; tumor location: rectum; sample age: 4.16666666666667; rna (ng/ul): null; sample_well: A03; sentrix_id: 5406051056; sentrix_position: A; plate: 11; ', 'tumor id: 3718; tumor location: colon; sample age: 3.66666666666667; rna (ng/ul): null; sample_well: A05; sentrix_id: 5406051077; sentrix_position: A; plate: 11; ', 'tumor id: 2263; tumor location: rectum; sample age: 10; rna (ng/ul): null; sample_well: A06; sentrix_id: 5406051085; sentrix_position: A; plate: 11; ', 'tumor id: 3447; tumor location: colon; sample age: 2.83333333333333; rna (ng/ul): null; sample_well: B01; sentrix_id: 5370975012; sentrix_position: B; plate: 10; ', 'tumor id: 3658; tumor location: rectum; sample age: 3.25; rna (ng/ul): null; sample_well: B02; sentrix_id: 5370975015; sentrix_position: B; plate: 10; ', 'tumor id: 3659; tumor location: rectum; sample age: 3.08333333333333; rna (ng/ul): null; sample_well: B03; sentrix_id: 5370975034; sentrix_position: B; plate: 10; ', 'tumor id: 3431; tumor location: colon; sample age: 4; rna (ng/ul): null; sample_well: B05; sentrix_id: 5394951057; sentrix_position: B; plate: 10; ', 'tumor id: 3417; tumor location: colon; sample age: 2.91666666666667; rna (ng/ul): null; sample_well: B06; sentrix_id: 5394951058; sentrix_position: B; plate: 10; ', 'tumor id: 3485; tumor location: colon; sample age: 1.66666666666667; rna (ng/ul): null; sample_well: B07; sentrix_id: 5394951076; sentrix_position: B; plate: 10; ', 'tumor id: 636; tumor location: rectum; sample age: 13.5; rna (ng/ul): null; sample_well: B08; sentrix_id: 5394951078; sentrix_position: B; plate: 10; ', 'tumor id: 278; tumor location: colon; sample age: 14.8333333333333; rna (ng/ul): null; sample_well: B09; sentrix_id: 5394951082; sentrix_position: B; plate: 10; ', 'tumor id: 3620; tumor location: colon; sample age: 6.08333333333333; rna (ng/ul): null; sample_well: B10; sentrix_id: 5394951083; sentrix_position: B; plate: 10; ', 'tumor id: 3603; tumor location: rectum; sample age: null; rna (ng/ul): null; sample_well: B12; sentrix_id: 5406051008; sentrix_position: B; plate: 10; ', 'tumor id: 3697; tumor location: rectum; sample age: 1.5; rna (ng/ul): null; sample_well: B01; sentrix_id: 5406051053; sentrix_position: B; plate: 11; ', 'tumor id: 3708; tumor location: rectum; sample age: 0.75; rna (ng/ul): null; sample_well: B02; sentrix_id: 5406051055; sentrix_position: B; plate: 11; ', 'tumor id: 3704; tumor location: rectum; sample age: 1.41666666666667; rna (ng/ul): null; sample_well: B03; sentrix_id: 5406051056; sentrix_position: B; plate: 11; ', 'tumor id: 3709; tumor location: colon; sample age: 3.41666666666667; rna (ng/ul): null; sample_well: B04; sentrix_id: 5406051057; sentrix_position: B; plate: 11; ', 'tumor id: 3698; tumor location: colon; sample age: 4.33333333333333; rna (ng/ul): null; sample_well: B05; sentrix_id: 5406051077; sentrix_position: B; plate: 11; ', 'tumor id: 3430; tumor location: colon; sample age: 4.41666666666667; rna (ng/ul): null; sample_well: B06; sentrix_id: 5406051085; sentrix_position: B; plate: 11; ', 'tumor id: 3604; tumor location: rectum; sample age: 3.75; rna (ng/ul): null; sample_well: C01; sentrix_id: 5370975012; sentrix_position: C; plate: 10; ', 'tumor id: 3454; tumor location: colon; sample age: 4.08333333333333; rna (ng/ul): null; sample_well: C02; sentrix_id: 5370975015; sentrix_position: C; plate: 10; ', 'tumor id: 3497; tumor location: rectum; sample age: 8.75; rna (ng/ul): null; sample_well: C03; sentrix_id: 5370975034; sentrix_position: C; plate: 10; ', 'tumor id: 3489; tumor location: colon; sample age: 2.5; rna (ng/ul): null; sample_well: C05; sentrix_id: 5394951057; sentrix_position: C; plate: 10; ', 'tumor id: 3601; tumor location: colon; sample age: 1.33333333333333; rna (ng/ul): null; sample_well: C06; sentrix_id: 5394951058; sentrix_position: C; plate: 10; ', 'tumor id: 3637; tumor location: rectum; sample age: 2.16666666666667; rna (ng/ul): null; sample_well: C07; sentrix_id: 5394951076; sentrix_position: C; plate: 10; ', 'tumor id: 3610; tumor location: rectum; sample age: null; rna (ng/ul): null; sample_well: C08; sentrix_id: 5394951078; sentrix_position: C; plate: 10; ', 'tumor id: 3351; tumor location: rectum; sample age: null; rna (ng/ul): null; sample_well: C09; sentrix_id: 5394951082; sentrix_position: C; plate: 10; ', 'tumor id: 3621; tumor location: colon; sample age: null; rna (ng/ul): null; sample_well: C10; sentrix_id: 5394951083; sentrix_position: C; plate: 10; ', 'tumor id: 3632; tumor location: rectum; sample age: 2.66666666666667; rna (ng/ul): null; sample_well: C12; sentrix_id: 5406051008; sentrix_position: C; plate: 10; ', 'tumor id: 2670; tumor location: rectum; sample age: 9.91666666666667; rna (ng/ul): null; sample_well: C01; sentrix_id: 5406051053; sentrix_position: C; plate: 11; ', 'tumor id: 2287; tumor location: rectum; sample age: 6.08333333333333; rna (ng/ul): null; sample_well: C02; sentrix_id: 5406051055; sentrix_position: C; plate: 11; ', 'tumor id: 608; tumor location: rectum; sample age: 16.1666666666667; rna (ng/ul): null; sample_well: C03; sentrix_id: 5406051056; sentrix_position: C; plate: 11; ', 'tumor id: 603; tumor location: rectum; sample age: 15; rna (ng/ul): null; sample_well: C04; sentrix_id: 5406051057; sentrix_position: C; plate: 11; ', 'tumor id: 547; tumor location: colon; sample age: 17.25; rna (ng/ul): null; sample_well: C05; sentrix_id: 5406051077; sentrix_position: C; plate: 11; ', 'tumor id: 3481; tumor location: colon; sample age: 2.41666666666667; rna (ng/ul): null; sample_well: C06; sentrix_id: 5406051085; sentrix_position: C; plate: 11; ', 'tumor id: 3660; tumor location: colon; sample age: 3.5; rna (ng/ul): null; sample_well: D01; sentrix_id: 5370975012; sentrix_position: D; plate: 10; ', 'tumor id: 3654; tumor location: colon; sample age: 3.83333333333333; rna (ng/ul): null; sample_well: D03; sentrix_id: 5370975034; sentrix_position: D; plate: 10; ', 'tumor id: 3656; tumor location: rectum; sample age: 2.5; rna (ng/ul): null; sample_well: D04; sentrix_id: 5394951055; sentrix_position: D; plate: 10; ', 'tumor id: 3665; tumor location: rectum; sample age: 4.08333333333333; rna (ng/ul): null; sample_well: D05; sentrix_id: 5394951057; sentrix_position: D; plate: 10; ', 'tumor id: 3671; tumor location: rectum; sample age: 3.5; rna (ng/ul): null; sample_well: D06; sentrix_id: 5394951058; sentrix_position: D; plate: 10; ', 'tumor id: 3668; tumor location: colon; sample age: 4.16666666666667; rna (ng/ul): null; sample_well: D07; sentrix_id: 5394951076; sentrix_position: D; plate: 10; ', 'tumor id: 644; tumor location: colon; sample age: 13.5833333333333; rna (ng/ul): null; sample_well: D08; sentrix_id: 5394951078; sentrix_position: D; plate: 10; ', 'tumor id: 3666; tumor location: rectum; sample age: 2.41666666666667; rna (ng/ul): null; sample_well: D09; sentrix_id: 5394951082; sentrix_position: D; plate: 10; ', 'tumor id: 3667; tumor location: colon; sample age: 3.91666666666667; rna (ng/ul): null; sample_well: D10; sentrix_id: 5394951083; sentrix_position: D; plate: 10; ', 'tumor id: 3682; tumor location: rectum; sample age: null; rna (ng/ul): null; sample_well: D11; sentrix_id: 5394951084; sentrix_position: D; plate: 10; ', 'tumor id: 3692; tumor location: colon; sample age: 1.66666666666667; rna (ng/ul): null; sample_well: D12; sentrix_id: 5406051008; sentrix_position: D; plate: 10; ', 'tumor id: 3138; tumor location: rectum; sample age: null; rna (ng/ul): null; sample_well: D01.; sentrix_id: 5406051053; sentrix_position: D; plate: 11; ', 'tumor id: 645; tumor location: colon; sample age: 14; rna (ng/ul): null; sample_well: D02; sentrix_id: 5406051055; sentrix_position: D; plate: 11; ', 'tumor id: 2604; tumor location: colon; sample age: 6.83333333333333; rna (ng/ul): null; sample_well: D03; sentrix_id: 5406051056; sentrix_position: D; plate: 11; ', 'tumor id: 2277; tumor location: colon; sample age: 7.41666666666667; rna (ng/ul): null; sample_well: D04; sentrix_id: 5406051057; sentrix_position: D; plate: 11; ', 'tumor id: 3115; tumor location: colon; sample age: 4.91666666666667; rna (ng/ul): null; sample_well: D05; sentrix_id: 5406051077; sentrix_position: D; plate: 11; ', 'tumor id: 3476; tumor location: colon; sample age: 1.5; rna (ng/ul): null; sample_well: D06; sentrix_id: 5406051085; sentrix_position: D; plate: 11; ', 'tumor id: 3688; tumor location: colon; sample age: 2.33333333333333; rna (ng/ul): null; sample_well: E01; sentrix_id: 5370975012; sentrix_position: E; plate: 10; ', 'tumor id: 3633; tumor location: rectum; sample age: null; rna (ng/ul): null; sample_well: E02; sentrix_id: 5370975015; sentrix_position: E; plate: 10; ', 'tumor id: 3678; tumor location: colon; sample age: 3; rna (ng/ul): null; sample_well: E03; sentrix_id: 5370975034; sentrix_position: E; plate: 10; ', 'tumor id: 3690; tumor location: rectum; sample age: 2.33333333333333; rna (ng/ul): null; sample_well: E04; sentrix_id: 5394951055; sentrix_position: E; plate: 10; ', 'tumor id: 3674; tumor location: rectum; sample age: 2.5; rna (ng/ul): null; sample_well: E05; sentrix_id: 5394951057; sentrix_position: E; plate: 10; ', 'tumor id: 3672; tumor location: colon; sample age: 3.25; rna (ng/ul): null; sample_well: E06; sentrix_id: 5394951058; sentrix_position: E; plate: 10; ', 'tumor id: 3677; tumor location: colon; sample age: 0.75; rna (ng/ul): null; sample_well: E07; sentrix_id: 5394951076; sentrix_position: E; plate: 10; ', 'tumor id: 3650; tumor location: colon; sample age: 2.91666666666667; rna (ng/ul): null; sample_well: E08; sentrix_id: 5394951078; sentrix_position: E; plate: 10; ', 'tumor id: 3684; tumor location: colon; sample age: 8.08333333333333; rna (ng/ul): null; sample_well: E09; sentrix_id: 5394951082; sentrix_position: E; plate: 10; ', 'tumor id: 3676; tumor location: rectum; sample age: 2.83333333333333; rna (ng/ul): null; sample_well: E10; sentrix_id: 5394951083; sentrix_position: E; plate: 10; ', 'tumor id: 3669; tumor location: rectum; sample age: 3; rna (ng/ul): null; sample_well: E11; sentrix_id: 5394951084; sentrix_position: E; plate: 10; ', 'tumor id: 3653; tumor location: rectum; sample age: 2.5; rna (ng/ul): null; sample_well: E12; sentrix_id: 5406051008; sentrix_position: E; plate: 10; ', 'tumor id: 2255; tumor location: rectum; sample age: 7.33333333333333; rna (ng/ul): null; sample_well: E01; sentrix_id: 5406051053; sentrix_position: E; plate: 11; ', 'tumor id: 3132; tumor location: colon; sample age: null; rna (ng/ul): null; sample_well: E02; sentrix_id: 5406051055; sentrix_position: E; plate: 11; ', 'tumor id: 3705; tumor location: rectum; sample age: 3.91666666666667; rna (ng/ul): null; sample_well: E03; sentrix_id: 5406051056; sentrix_position: E; plate: 11; ', 'tumor id: 1263; tumor location: rectum; sample age: 10.5833333333333; rna (ng/ul): null; sample_well: E04; sentrix_id: 5406051057; sentrix_position: E; plate: 11; ', 'tumor id: 1214; tumor location: colon; sample age: 8.83333333333333; rna (ng/ul): null; sample_well: E05; sentrix_id: 5406051077; sentrix_position: E; plate: 11; ', 'tumor id: 3501; tumor location: rectum; sample age: 1.58333333333333; rna (ng/ul): null; sample_well: E06; sentrix_id: 5406051085; sentrix_position: E; plate: 11; ', 'tumor id: 3343; tumor location: rectum; sample age: 4.75; rna (ng/ul): null; sample_well: F01; sentrix_id: 5370975012; sentrix_position: F; plate: 10; ', 'tumor id: 3508; tumor location: rectum; sample age: null; rna (ng/ul): null; sample_well: F02; sentrix_id: 5370975015; sentrix_position: F; plate: 10; ', 'tumor id: 3689; tumor location: rectum; sample age: 4.16666666666667; rna (ng/ul): null; sample_well: F03; sentrix_id: 5370975034; sentrix_position: F; plate: 10; ', 'tumor id: 3673; tumor location: rectum; sample age: 1.58333333333333; rna (ng/ul): null; sample_well: F04; sentrix_id: 5394951055; sentrix_position: F; plate: 10; ', 'tumor id: 3680; tumor location: rectum; sample age: 1.08333333333333; rna (ng/ul): null; sample_well: F05; sentrix_id: 5394951057; sentrix_position: F; plate: 10; ', 'tumor id: 3661; tumor location: rectum; sample age: 2.66666666666667; rna (ng/ul): null; sample_well: F06; sentrix_id: 5394951058; sentrix_position: F; plate: 10; ', 'tumor id: 3683; tumor location: colon; sample age: 4.16666666666667; rna (ng/ul): null; sample_well: F07; sentrix_id: 5394951076; sentrix_position: F; plate: 10; ', 'tumor id: 3675; tumor location: rectum; sample age: 1.75; rna (ng/ul): null; sample_well: F08; sentrix_id: 5394951078; sentrix_position: F; plate: 10; ', 'tumor id: 1259; tumor location: colon; sample age: null; rna (ng/ul): null; sample_well: F09; sentrix_id: 5394951082; sentrix_position: F; plate: 10; ', 'tumor id: 641; tumor location: colon; sample age: 13; rna (ng/ul): null; sample_well: F10; sentrix_id: 5394951083; sentrix_position: F; plate: 10; ', 'tumor id: 625; tumor location: colon; sample age: 14.8333333333333; rna (ng/ul): null; sample_well: F11; sentrix_id: 5394951084; sentrix_position: F; plate: 10; ', 'tumor id: 2268; tumor location: colon; sample age: 7.16666666666667; rna (ng/ul): null; sample_well: F12; sentrix_id: 5406051008; sentrix_position: F; plate: 10; ', 'tumor id: 3701; tumor location: rectum; sample age: 1.16666666666667; rna (ng/ul): null; sample_well: F01; sentrix_id: 5406051053; sentrix_position: F; plate: 11; ', 'tumor id: 2298; tumor location: colon; sample age: 8.08333333333333; rna (ng/ul): null; sample_well: F02; sentrix_id: 5406051055; sentrix_position: F; plate: 11; ', 'tumor id: 650; tumor location: colon; sample age: 15.5833333333333; rna (ng/ul): null; sample_well: F03; sentrix_id: 5406051056; sentrix_position: F; plate: 11; ', 'tumor id: 3706; tumor location: colon; sample age: 3; rna (ng/ul): null; sample_well: F05; sentrix_id: 5406051077; sentrix_position: F; plate: 11; ', 'tumor id: 3484; tumor location: colon; sample age: null; rna (ng/ul): null; sample_well: F06; sentrix_id: 5406051085; sentrix_position: F; plate: 11; ', 'tumor id: 350; tumor location: colon; sample age: 22.5; rna (ng/ul): null; sample_well: G02; sentrix_id: 5370975015; sentrix_position: G; plate: 10; ', 'tumor id: 1225; tumor location: rectum; sample age: 9.66666666666667; rna (ng/ul): null; sample_well: G04; sentrix_id: 5394951055; sentrix_position: G; plate: 10; ', 'tumor id: 1155; tumor location: rectum; sample age: 9.08333333333333; rna (ng/ul): null; sample_well: G05; sentrix_id: 5394951057; sentrix_position: G; plate: 10; ', 'tumor id: 1194; tumor location: rectum; sample age: 9.16666666666667; rna (ng/ul): null; sample_well: G06; sentrix_id: 5394951058; sentrix_position: G; plate: 10; ', 'tumor id: 306; tumor location: colon; sample age: 14.0833333333333; rna (ng/ul): null; sample_well: G07; sentrix_id: 5394951076; sentrix_position: G; plate: 10; ', 'tumor id: 2413; tumor location: colon; sample age: 22.5; rna (ng/ul): null; sample_well: G08; sentrix_id: 5394951078; sentrix_position: G; plate: 10; ', 'tumor id: 80; tumor location: colon; sample age: 11.6666666666667; rna (ng/ul): null; sample_well: G09; sentrix_id: 5394951082; sentrix_position: G; plate: 10; ', 'tumor id: 357; tumor location: colon; sample age: 27.75; rna (ng/ul): null; sample_well: G10; sentrix_id: 5394951083; sentrix_position: G; plate: 10; ', 'tumor id: 2336; tumor location: rectum; sample age: 12.8333333333333; rna (ng/ul): null; sample_well: G11; sentrix_id: 5394951084; sentrix_position: G; plate: 10; ', 'tumor id: 665; tumor location: colon; sample age: 15.5; rna (ng/ul): null; sample_well: G12; sentrix_id: 5406051008; sentrix_position: G; plate: 10; ', 'tumor id: 3123; tumor location: colon; sample age: null; rna (ng/ul): null; sample_well: G01; sentrix_id: 5406051053; sentrix_position: G; plate: 11; ', 'tumor id: 2274; tumor location: colon; sample age: null; rna (ng/ul): null; sample_well: G02; sentrix_id: 5406051055; sentrix_position: G; plate: 11; ', 'tumor id: 3712; tumor location: colon; sample age: 1.08333333333333; rna (ng/ul): null; sample_well: G03; sentrix_id: 5406051056; sentrix_position: G; plate: 11; ', 'tumor id: 1805; tumor location: colon; sample age: 12.5833333333333; rna (ng/ul): null; sample_well: G05; sentrix_id: 5406051077; sentrix_position: G; plate: 11; ', 'tumor id: 1751; tumor location: colon; sample age: 9.83333333333333; rna (ng/ul): null; sample_well: G06; sentrix_id: 5406051085; sentrix_position: G; plate: 11; ', 'tumor id: 336; tumor location: colon; sample age: 11.5; rna (ng/ul): null; sample_well: H01; sentrix_id: 5370975012; sentrix_position: H; plate: 10; ', 'tumor id: 2351; tumor location: colon; sample age: 14.5833333333333; rna (ng/ul): null; sample_well: H02; sentrix_id: 5370975015; sentrix_position: H; plate: 10; ', 'tumor id: 2356; tumor location: rectum; sample age: 16.9166666666667; rna (ng/ul): null; sample_well: H03; sentrix_id: 5370975034; sentrix_position: H; plate: 10; ', 'tumor id: 240; tumor location: colon; sample age: 14.75; rna (ng/ul): null; sample_well: H04; sentrix_id: 5394951055; sentrix_position: H; plate: 10; ', 'tumor id: 2394; tumor location: colon; sample age: 15.4166666666667; rna (ng/ul): null; sample_well: H05; sentrix_id: 5394951057; sentrix_position: H; plate: 10; ', 'tumor id: 2639; tumor location: rectum; sample age: 12.1666666666667; rna (ng/ul): null; sample_well: H06; sentrix_id: 5394951058; sentrix_position: H; plate: 10; ', 'tumor id: 354; tumor location: rectum; sample age: 10.1666666666667; rna (ng/ul): null; sample_well: H07; sentrix_id: 5394951076; sentrix_position: H; plate: 10; ', 'tumor id: 2415; tumor location: colon; sample age: 11.9166666666667; rna (ng/ul): null; sample_well: H08; sentrix_id: 5394951078; sentrix_position: H; plate: 10; ', 'tumor id: 375; tumor location: colon; sample age: 15.6666666666667; rna (ng/ul): null; sample_well: H09; sentrix_id: 5394951082; sentrix_position: H; plate: 10; ', 'tumor id: 330; tumor location: colon; sample age: 13.6666666666667; rna (ng/ul): null; sample_well: H10; sentrix_id: 5394951083; sentrix_position: H; plate: 10; ', 'tumor id: 252; tumor location: colon; sample age: 10.5; rna (ng/ul): null; sample_well: H11; sentrix_id: 5394951084; sentrix_position: H; plate: 10; ', 'tumor id: 230; tumor location: colon; sample age: 11.9166666666667; rna (ng/ul): null; sample_well: H12; sentrix_id: 5406051008; sentrix_position: H; plate: 10; ', 'tumor id: 1802; tumor location: colon; sample age: 11.5; rna (ng/ul): null; sample_well: H01; sentrix_id: 5406051053; sentrix_position: H; plate: 11; ', 'tumor id: 3699; tumor location: rectum; sample age: 2.83333333333333; rna (ng/ul): null; sample_well: H03; sentrix_id: 5406051056; sentrix_position: H; plate: 11; ', 'tumor id: 2404; tumor location: colon; sample age: 17.25; rna (ng/ul): null; sample_well: H04; sentrix_id: 5406051057; sentrix_position: H; plate: 11; ', 'tumor id: 3506; tumor location: colon; sample age: 1.91666666666667; rna (ng/ul): null; sample_well: H05; sentrix_id: 5406051077; sentrix_position: H; plate: 11; ', 'tumor id: 3432; tumor location: rectum; sample age: 2.75; rna (ng/ul): null; sample_well: H06; sentrix_id: 5406051085; sentrix_position: H; plate: 11; ', 'tumor id: 3714; tumor location: colon; sample age: 2.41666666666667; rna (ng/ul): null; sample_well: B01; sentrix_id: 5406051012; sentrix_position: B; plate: 12; ', 'tumor id: 443; tumor location: rectum; sample age: 13.4166666666667; rna (ng/ul): null; sample_well: C01; sentrix_id: 5406051012; sentrix_position: C; plate: 12; ', 'tumor id: 3639; tumor location: rectum; sample age: 3.58333333333333; rna (ng/ul): null; sample_well: D01; sentrix_id: 5406051012; sentrix_position: D; plate: 12; ', 'tumor id: 3509; tumor location: colon; sample age: 2.16666666666667; rna (ng/ul): null; sample_well: E01; sentrix_id: 5406051012; sentrix_position: E; plate: 12; ', 'tumor id: 3630; tumor location: colon; sample age: null; rna (ng/ul): null; sample_well: F01; sentrix_id: 5406051012; sentrix_position: F; plate: 12; ', 'tumor id: 3710; tumor location: colon; sample age: 0.75; rna (ng/ul): null; samp le_well: G01; sentrix_id: 5406051012; sentrix_position: G; plate: 12; ' GSE72308 Homo sapiens 295 Methylation profiling by array GPL13534 DNA methylation-based immune response signature improves patient diagnosis in multiple cancers 2015-08-24 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72308 DNA methylation-based immune response signature improves patient diagnosis in multiple cancers. The Journal of clinical investigation 12.282 https://doi.org/10.1172/JCI91095 {The Journal of clinical investigation (12.282): 10.1172/JCI91095} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA293700 https://www.ebi.ac.uk/ena/browser/view/PRJNA293700 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was extracted with the Qiagen-DNeasy Blood &Tissue Kit (Qiagen, Hilden, Germany) or the QIAamp DNA Mini Kit (Qiagen, Hilden, Germany)'; [Cell type]'Source: ''tissue: breast tumor; cohort id: BC1; geo_accn_gse20713_27k: GSM519817; geo_accn_gse20713_expr: GSM519722; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 1; size_cm: 2.2; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 74.94; age_bin: 1; rfs_event: 1; rfs_time (years): 0.93; rfs_event_censored: 1; rfs_time_censored (years): 0.93; relapse_5years: 1; os_event: 0; os_time (years): 8.28; ', 'tissue: breast tumor; cohort id: BC3; geo_accn_gse20713_27k: GSM519864; geo_accn_gse20713_expr: GSM519724; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 0; str-ly: 70; grade: 3; size_bin: 0; size_cm: 1.8; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 52.58; age_bin: 1; rfs_event: 0; rfs_time (years): 8.64; rfs_event_censored: 0; rfs_time_censored (years): 8.64; relapse_5years: 0; os_event: 0; os_time (years): 8.64; ', 'tissue: breast tumor; cohort id: BC4; geo_accn_gse20713_27k: GSM519875; geo_accn_gse20713_expr: GSM519725; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 1; size_cm: 4.5; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 44.06; age_bin: 0; rfs_event: 0; rfs_time (years): 8.4; rfs_event_censored: 0; rfs_time_censored (years): 8.4; relapse_5years: 0; os_event: 0; os_time (years): 8.4; ', 'tissue: breast tumor; cohort id: BC5; geo_accn_gse20713_27k: GSM519886; geo_accn_gse20713_expr: null; subtype_ihc: LumB; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 0; size_cm: 1.7; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 77.34; age_bin: 1; rfs_event: 0; rfs_time (years): 6.53; rfs_event_censored: 0; rfs_time_censored (years): 6.53; relapse_5years: 0; os_event: 0; os_time (years): 6.53; ', 'tissue: breast tumor; cohort id: BC6; geo_accn_gse20713_27k: GSM519895; geo_accn_gse20713_expr: GSM519726; subtype_ihc: HER2; subtype_pam50: Basal; itu-ly: null; str-ly: null; grade: 3; size_bin: 0; size_cm: 1.5; nodal_status: 0; er_ihc_status: 0; her2_status: 1; age_diagnosis: 35.86; age_bin: 0; rfs_event: 0; rfs_time (years): 7.21; rfs_event_censored: 0; rfs_time_censored (years): 7.21; relapse_5years: 0; os_event: 0; os_time (years): 7.21; ', 'tissue: breast tumor; cohort id: BC7; geo_accn_gse20713_27k: GSM519906; geo_accn_gse20713_expr: GSM519727; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 40; str-ly: 80; grade: 3; size_bin: 1; size_cm: 2.2; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 65.42; age_bin: 1; rfs_event: 1; rfs_time (years): 7.01; rfs_event_censored: 1; rfs_time_censored (years): 7.01; relapse_5years: 0; os_event: 0; os_time (years): 8.19; ', 'tissue: breast tumor; cohort id: BC8; geo_accn_gse20713_27k: GSM519916; geo_accn_gse20713_expr: null; subtype_ihc: LumA; subtype_pam50: null; itu-ly: 0; str-ly: 10; grade: 1; size_bin: 0; size_cm: 1.3; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 36.2; age_bin: 0; rfs_event: 0; rfs_time (years): 8.79; rfs_event_censored: 0; rfs_time_censored (years): 8.79; relapse_5years: 0; os_event: 0; os_time (years): 8.79; ', 'tissue: breast tumor; cohort id: BC9; geo_accn_gse20713_27k: GSM519926; geo_accn_gse20713_expr: null; subtype_ihc: HER2; subtype_pam50: null; itu-ly: 0; str-ly: 2; grade: 3; size_bin: 1; size_cm: 2.7; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 28.64; age_bin: 0; rfs_event: 0; rfs_time (years): 9.02; rfs_event_censored: 0; rfs_time_censored (years): 9.02; relapse_5years: 0; os_event: 0; os_time (years): 9.02; ', 'tissue: breast tumor; cohort id: BC10; geo_accn_gse20713_27k: GSM519818; geo_accn_gse20713_expr: GSM519728; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 5; str-ly: 20; grade: 3; size_bin: 1; size_cm: 5.1; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 50.12; age_bin: 1; rfs_event: 0; rfs_time (years): 2.12; rfs_event_censored: 0; rfs_time_censored (years): 2.12; relapse_5years: 0; os_event: 1; os_time (years): 2.52; ', 'tissue: breast tumor; cohort id: BC11; geo_accn_gse20713_27k: GSM519828; geo_accn_gse20713_expr: GSM519729; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 1; str-ly: 5; grade: 3; size_bin: 1; size_cm: 2.2; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 52.64; age_bin: 1; rfs_event: 0; rfs_time (years): 8.32; rfs_event_censored: 0; rfs_time_censored (years): 8.32; relapse_5years: 0; os_event: 0; os_time (years): 8.32; ', 'tissue: breast tumor; cohort id: BC12; geo_accn_gse20713_27k: GSM519837; geo_accn_gse20713_expr: GSM519730; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 1; size_cm: 3.8; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 46.58; age_bin: 0; rfs_event: 0; rfs_time (years): 8.82; rfs_event_censored: 0; rfs_time_censored (years): 8.82; relapse_5years: 0; os_event: 0; os_time (years): 8.82; ', 'tissue: breast tumor; cohort id: BC13; geo_accn_gse20713_27k: GSM519846; geo_accn_gse20713_expr: GSM519731; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 5; str-ly: 40; grade: 3; size_bin: 0; size_cm: 1.3; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 63.54; age_bin: 1; rfs_event: 0; rfs_time (years): 9.03; rfs_event_censored: 0; rfs_time_censored (years): 9.03; relapse_5years: 0; os_event: 0; os_time (years): 9.03; ', 'tissue: breast tumor; cohort id: BC14; geo_accn_gse20713_27k: GSM519847; geo_accn_gse20713_expr: null; subtype_ihc: Basal; subtype_pam50: null; itu-ly: null; str-ly: null; grade: 2; size_bin: 1; size_cm: 3.2; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 75.86; age_bin: 1; rfs_event: 1; rfs_time (years): 2.85; rfs_event_censored: 1; rfs_time_censored (years): 2.85; relapse_5years: 1; os_event: 1; os_time (years): 3.43; ', 'tissue: breast tumor; cohort id: BC15; geo_accn_gse20713_27k: GSM519848; geo_accn_gse20713_expr: GSM519732; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 5; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.7; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 45.07; age_bin: 0; rfs_event: 0; rfs_time (years): 8.98; rfs_event_censored: 0; rfs_time_censored (years): 8.98; relapse_5years: 0; os_event: 0; os_time (years): 8.98; ', 'tissue: breast tumor; cohort id: BC16; geo_accn_gse20713_27k: GSM519849; geo_accn_gse20713_expr: GSM519733; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 5; str-ly: 90; grade: 3; size_bin: 0; size_cm: 1.7+0.7 BIFOCAL; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 60.57; age_bin: 1; rfs_event: 0; rfs_time (years): 7.61; rfs_event_censored: 0; rfs_time_censored (years): 7.61; relapse_5years: 0; os_event: 0; os_time (years): 7.61; ', 'tissue: breast tumor; cohort id: BC17; geo_accn_gse20713_27k: GSM519850; geo_accn_gse20713_expr: null; subtype_ihc: LumB; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 3.8; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 57.72; age_bin: 1; rfs_event: 1; rfs_time (years): 4.93; rfs_event_censored: 1; rfs_time_censored (years): 4.93; relapse_5years: 1; os_event: 1; os_time (years): 8.9; ', 'tissue: breast tumor; cohort id: BC18; geo_accn_gse20713_27k: GSM519851; geo_accn_gse20713_expr: GSM519734; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 5; str-ly: 60; grade: 3; size_bin: 1; size_cm: 2.8+1.5; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 59.56; age_bin: 1; rfs_event: 0; rfs_time (years): 9.45; rfs_event_censored: 0; rfs_time_censored (years): 9.45; relapse_5years: 0; os_event: 0; os_time (years): 9.45; ', 'tissue: breast tumor; cohort id: BC19; geo_accn_gse20713_27k: GSM519852; geo_accn_gse20713_expr: GSM519735; subtype_ihc: LumB; subtype_pam50: LumA; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 2.6+0.6; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 59.1; age_bin: 1; rfs_event: 1; rfs_time (years): 4.28; rfs_event_censored: 1; rfs_time_censored (years): 4.28; relapse_5years: 1; os_event: 0; os_time (years): 9.32; ', 'tissue: breast tumor; cohort id: BC20; geo_accn_gse20713_27k: GSM519854; geo_accn_gse20713_expr: GSM519736; subtype_ihc: LumA; subtype_pam50: LumA; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 1; size_cm: 2.7; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 68.03; age_bin: 1; rfs_event: 0; rfs_time (years): 6.07; rfs_event_censored: 0; rfs_time_censored (years): 6.07; relapse_5years: 0; os_event: 0; os_time (years): 6.07; ', 'tissue: breast tumor; cohort id: BC21; geo_accn_gse20713_27k: GSM519855; geo_accn_gse20713_expr: null; subtype_ihc: LumB; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 3.4; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 52.76; age_bin: 1; rfs_event: 1; rfs_time (years): 8.19; rfs_event_censored: 1; rfs_time_censored (years): 8.19; relapse_5years: 0; os_event: 0; os_time (years): 9.3; ', 'tissue: breast tumor; cohort id: BC22; geo_accn_gse20713_27k: GSM519856; geo_accn_gse20713_expr: null; subtype_ihc: LumA; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 0; size_cm: 1.3; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 69.83; age_bin: 1; rfs_event: 0; rfs_time (years): 9.68; rfs_event_censored: 0; rfs_time_censored (years): 9.68; relapse_5years: 0; os_event: 0; os_time (years): 9.68; ', 'tissue: breast tumor; cohort id: BC23; geo_accn_gse20713_27k: GSM519857; geo_accn_gse20713_expr: GSM519737; subtype_ihc: Basal; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 0; size_cm: 1.2; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 74.24; age_bin: 1; rfs_event: 1; rfs_time (years): 2.56; rfs_event_censored: 1; rfs_time_censored (years): 2.56; relapse_5years: 1; os_event: 1; os_time (years): 4.07; ', 'tissue: breast tumor; cohort id: BC24; geo_accn_gse20713_27k: GSM519858; geo_accn_gse20713_expr: GSM519738; subtype_ihc: LumB; subtype_pam50: Basal; itu-ly: 50; str-ly: 20; grade: 3; size_bin: 1; size_cm: 3.4; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 53.78; age_bin: 1; rfs_event: 0; rfs_time (years): 8.84; rfs_event_censored: 0; rfs_time_censored (years): 8.84; relapse_5years: 0; os_event: 0; os_time (years): 8.84; ', 'tissue: breast tumor; cohort id: BC25; geo_accn_gse20713_27k: GSM519859; geo_accn_gse20713_expr: GSM519739; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 5; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.8; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 49.04; age_bin: 0; rfs_event: 0; rfs_time (years): 8.03; rfs_event_censored: 0; rfs_time_censored (years): 8.03; relapse_5years: 0; os_event: 0; os_time (years): 8.03; ', 'tissue: breast tumor; cohort id: BC26; geo_accn_gse20713_27k: GSM519860; geo_accn_gse20713_expr: null; subtype_ihc: LumA; subtype_pam50: null; itu-ly: 0; str-ly: 5; grade: 1; size_bin: 1; size_cm: 3.2; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 40.59; age_bin: 0; rfs_event: 0; rfs_time (years): 7.63; rfs_event_censored: 0; rfs_time_censored (years): 7.63; relapse_5years: 0; os_event: 0; os_time (years): 7.63; ', 'tissue: breast tumor; cohort id: BC27; geo_accn_gse20713_27k: GSM519861; geo_accn_gse20713_expr: GSM519740; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 20; str-ly: 30; grade: 3; size_bin: 1; size_cm: 2.1; nodal_status: 1; er_ihc_status: 1; her2_status: 1; age_diagnosis: 53.66; age_bin: 1; rfs_event: 0; rfs_time (years): 1.85; rfs_event_censored: 0; rfs_time_censored (years): 1.85; relapse_5years: 0; os_event: 0; os_time (years): 1.85; ', 'tissue: breast tumor; cohort id: BC28; geo_accn_gse20713_27k: GSM519862; geo_accn_gse20713_expr: GSM519741; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 40; str-ly: 20; grade: 3; size_bin: 1; size_cm: 2.9; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 49.61; age_bin: 0; rfs_event: 1; rfs_time (years): 0.51; rfs_event_censored: 1; rfs_time_censored (years): 0.51; relapse_5years: 1; os_event: 1; os_time (years): 4.99; ', 'tissue: breast tumor; cohort id: BC29; geo_accn_gse20713_27k: GSM519863; geo_accn_gse20713_expr: null; subtype_ihc: LumA; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 0; size_cm: 1.8; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 57.08; age_bin: 1; rfs_event: 0; rfs_time (years): 8.01; rfs_event_censored: 0; rfs_time_censored (years): 8.01; relapse_5years: 0; os_event: 0; os_time (years): 8.01; ', 'tissue: breast tumor; cohort id: BC30; geo_accn_gse20713_27k: GSM519865; geo_accn_gse20713_expr: GSM519742; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 1; size_cm: 2.1; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 51.36; age_bin: 1; rfs_event: 0; rfs_time (years): 5.72; rfs_event_censored: 0; rfs_time_censored (years): 5.72; relapse_5years: 0; os_event: 0; os_time (years): 5.72; ', 'tissue: breast tumor; cohort id: BC31; geo_accn_gse20713_27k: GSM519866; geo_accn_gse20713_expr: GSM519743; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 0; size_cm: 1.2; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 60.34; age_bin: 1; rfs_event: 0; rfs_time (years): 7.44; rfs_event_censored: 0; rfs_time_censored (years): 7.44; relapse_5years: 0; os_event: 0; os_time (years): 7.44; ', 'tissue: breast tumor; cohort id: BC32; geo_accn_gse20713_27k: GSM519867; geo_accn_gse20713_expr: GSM519744; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 5; str-ly: 10; grade: 3; size_bin: 1; size_cm: 2.7; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 51.61; age_bin: 1; rfs_event: 0; rfs_time (years): 4.48; rfs_event_censored: 0; rfs_time_censored (years): 4.48; relapse_5years: 0; os_event: 0; os_time (years): 4.48; ', 'tissue: breast tumor; cohort id: BC33; geo_accn_gse20713_27k: GSM519868; geo_accn_gse20713_expr: null; subtype_ihc: LumB; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 3.2; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 51.87; age_bin: 1; rfs_event: 1; rfs_time (years): 0.13; rfs_event_censored: 1; rfs_time_censored (years): 0.13; relapse_5years: 1; os_event: 0; os_time (years): 7.64; ', 'tissue: breast tumor; cohort id: BC34; geo_accn_gse20713_27k: GSM519869; geo_accn_gse20713_expr: GSM519745; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 2; str-ly: 5; grade: 3; size_bin: 0; size_cm: 1.5; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 37.66; age_bin: 0; rfs_event: 1; rfs_time (years): 3.34; rfs_event_censored: 1; rfs_time_censored (years): 3.34; relapse_5years: 1; os_event: 0; os_time (years): 7.37; ', 'tissue: breast tumor; cohort id: BC35; geo_accn_gse20713_27k: GSM519870; geo_accn_gse20713_expr: GSM519746; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 90; str-ly: 10; grade: 3; size_bin: 1; size_cm: 2.5; nodal_status: 1; er_ihc_status: 0; her2_status: 0; age_diagnosis: 54.16; age_bin: 1; rfs_event: 1; rfs_time (years): 0; rfs_event_censored: 1; rfs_time_censored (years): 0; relapse_5years: 1; os_event: 0; os_time (years): 7.81; ', 'tissue: breast tumor; cohort id: BC36; geo_accn_gse20713_27k: GSM519871; geo_accn_gse20713_expr: null; subtype_ihc: LumB; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 3.5; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 41.92; age_bin: 0; rfs_event: 0; rfs_time (years): 1.44; rfs_event_censored: 0; rfs_time_censored (years): 1.44; relapse_5years: 0; os_event: 1; os_time (years): 1.5; ', 'tissue: breast tumor; cohort id: BC37; geo_accn_gse20713_27k: GSM519872; geo_accn_gse20713_expr: GSM519747; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 70; str-ly: 0; grade: 3; size_bin: 1; size_cm: 2.8; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 51.95; age_bin: 1; rfs_event: 0; rfs_time (years): 7.84; rfs_event_censored: 0; rfs_time_censored (years): 7.84; relapse_5years: 0; os_event: 0; os_time (years): 7.84; ', 'tissue: breast tumor; cohort id: BC38; geo_accn_gse20713_27k: GSM519873; geo_accn_gse20713_expr: GSM519748; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: null; str-ly: null; grade: 3; size_bin: 1; size_cm: 2.5; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 77.17; age_bin: 1; rfs_event: 1; rfs_time (years): 2.05; rfs_event_censored: 1; rfs_time_censored (years): 2.05; relapse_5years: 1; os_event: 1; os_time (years): 3.77; ', 'tissue: breast tumor; cohort id: BC39; geo_accn_gse20713_27k: GSM519874; geo_accn_gse20713_expr: GSM519749; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 20; str-ly: 10; grade: 3; size_bin: 1; size_cm: 10; nodal_status: 1; er_ihc_status: 1; her2_status: 1; age_diagnosis: 65.32; age_bin: 1; rfs_event: 1; rfs_time (years): 3.38; rfs_event_censored: 1; rfs_time_censored (years): 3.38; relapse_5years: 1; os_event: 1; os_time (years): 5.28; ', 'tissue: breast tumor; cohort id: BC40; geo_accn_gse20713_27k: GSM519876; geo_accn_gse20713_expr: GSM519750; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 2.65; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 51.96; age_bin: 1; rfs_event: 0; rfs_time (years): 8.39; rfs_event_censored: 0; rfs_time_censored (years): 8.39; relapse_5years: 0; os_event: 0; os_time (years): 8.39; ', 'tissue: breast tumor; cohort id: BC41; geo_accn_gse20713_27k: GSM519877; geo_accn_gse20713_expr: null; subtype_ihc: Basal; subtype_pam50: null; itu-ly: 5; str-ly: 0; grade: 3; size_bin: 1; size_cm: 3; nodal_status: 1; er_ihc_status: 0; her2_status: 0; age_diagnosis: 59.38; age_bin: 1; rfs_event: 0; rfs_time (years): 6.07; rfs_event_censored: 0; rfs_time_censored (years): 6.07; relapse_5years: 0; os_event: 0; os_time (years): 6.07; ', 'tissue: breast tumor; cohort id: BC42; geo_accn_gse20713_27k: GSM519878; geo_accn_gse20713_expr: GSM519751; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 3.5; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 47.75; age_bin: 0; rfs_event: 1; rfs_time (years): 0; rfs_event_censored: 1; rfs_time_censored (years): 0; relapse_5years: 1; os_event: 0; os_time (years): 7.63; ', 'tissue: breast tumor; cohort id: BC43; geo_accn_gse20713_27k: GSM519879; geo_accn_gse20713_expr: GSM519752; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 5.5; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 82.13; age_bin: 1; rfs_event: 0; rfs_time (years): 1.4; rfs_event_censored: 0; rfs_time_censored (years): 1.4; relapse_5years: 0; os_event: 1; os_time (years): 1.52; ', 'tissue: breast tumor; cohort id: BC44; geo_accn_gse20713_27k: GSM519880; geo_accn_gse20713_expr: null; subtype_ihc: LumA; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 1; size_cm: 2.3; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 71.51; age_bin: 1; rfs_event: 0; rfs_time (years): 6.82; rfs_event_censored: 0; rfs_time_censored (years): 6.82; relapse_5years: 0; os_event: 0; os_time (years): 6.82; ', 'tissue: breast tumor; cohort id: BC45; geo_accn_gse20713_27k: GSM519881; geo_accn_gse20713_expr: GSM519753; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 10; str-ly: 20; grade: 3; size_bin: 0; size_cm: 0.9; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 54.86; age_bin: 1; rfs_event: 0; rfs_time (years): 7.16; rfs_event_censored: 0; rfs_time_censored (years): 7.16; relapse_5years: 0; os_event: 0; os_time (years): 7.16; ', 'tissue: breast tumor; cohort id: BC46; geo_accn_gse20713_27k: GSM519882; geo_accn_gse20713_expr: null; subtype_ihc: LumB; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 2.1; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 39.36; age_bin: 0; rfs_event: 0; rfs_time (years): 7.32; rfs_event_censored: 0; rfs_time_censored (years): 7.32; relapse_5years: 0; os_event: 0; os_time (years): 7.32; ', 'tissue: breast tumor; cohort id: BC47; geo_accn_gse20713_27k: GSM519883; geo_accn_gse20713_expr: null; subtype_ihc: LumA; subtype_pam50: null; itu-ly: null; str-ly: null; grade: 1; size_bin: 1; size_cm: 2.3; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 62.23; age_bin: 1; rfs_event: 0; rfs_time (years): 7.11; rfs_event_censored: 0; rfs_time_censored (years): 7.11; relapse_5years: 0; os_event: 0; os_time (years): 7.11; ', 'tissue: breast tumor; cohort id: BC48; geo_accn_gse20713_27k: GSM519884; geo_accn_gse20713_expr: GSM519754; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 20; str-ly: 60; grade: 3; size_bin: 1; size_cm: 9.5; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 45.42; age_bin: 0; rfs_event: 1; rfs_time (years): 3.9; rfs_event_censored: 1; rfs_time_censored (years): 3.9; relapse_5years: 1; os_event: 0; os_time (years): 7.23; ', 'tissue: breast tumor; cohort id: BC49; geo_accn_gse20713_27k: GSM519885; geo_accn_gse20713_expr: GSM519755; subtype_ihc: LumB; subtype_pam50: Basal; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 0; size_cm: 1.6; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 60.46; age_bin: 1; rfs_event: 0; rfs_time (years): 6.71; rfs_event_censored: 0; rfs_time_censored (years): 6.71; relapse_5years: 0; os_event: 0; os_time (years): 6.71; ', 'tissue: breast tumor; cohort id: BC50; geo_accn_gse20713_27k: GSM519887; geo_accn_gse20713_expr: GSM519756; subtype_ihc: HER2; subtype_pam50: LumB; itu-ly: null; str-ly: null; grade: 3; size_bin: 1; size_cm: 2.5; nodal_status: 0; er_ihc_status: 1; her2_status: 1; age_diagnosis: 70.34; age_bin: 1; rfs_event: 0; rfs_time (years): 6.36; rfs_event_censored: 0; rfs_time_censored (years): 6.36; relapse_5years: 0; os_event: 0; os_time (years): 6.36; ', 'tissue: breast tumor; cohort id: BC51; geo_accn_gse20713_27k: GSM519888; geo_accn_gse20713_expr: GSM519757; subtype_ihc: Basal; subtype_pam50: Her2; itu-ly: 30; str-ly: 10; grade: 3; size_bin: 0; size_cm: 2; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 73.69; age_bin: 1; rfs_event: 1; rfs_time (years): 5.01; rfs_event_censored: 1; rfs_time_censored (years): 5.01; relapse_5years: 0; os_event: 0; os_time (years): 6.55; ', 'tissue: breast tumor; cohort id: BC52; geo_accn_gse20713_27k: GSM519889; geo_accn_gse20713_expr: null; subtype_ihc: LumA; subtype_pam50: null; itu-ly: 0; str-ly: 20; grade: 1; size_bin: 0; size_cm: 1.8; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 51.82; age_bin: 1; rfs_event: 0; rfs_time (years): 6.78; rfs_event_censored: 0; rfs_time_censored (years): 6.78; relapse_5years: 0; os_event: 0; os_time (years): 6.78; ', 'tissue: breast tumor; cohort id: BC55; geo_accn_gse20713_27k: GSM519890; geo_accn_gse20713_expr: GSM519758; subtype_ihc: HER2; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 3; nodal_status: 0; er_ihc_status: 0; her2_status: 1; age_diagnosis: 34.14; age_bin: 0; rfs_event: 1; rfs_time (years): 3.37; rfs_event_censored: 1; rfs_time_censored (years): 3.37; relapse_5years: 1; os_event: 1; os_time (years): 4.98; ', 'tissue: breast tumor; cohort id: BC56; geo_accn_gse20713_27k: GSM519891; geo_accn_gse20713_expr: GSM519759; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 5; str-ly: 50; grade: 3; size_bin: 1; size_cm: 3.9; nodal_status: 1; er_ihc_status: 0; her2_status: 0; age_diagnosis: 36.17; age_bin: 0; rfs_event: 0; rfs_time (years): 6.2; rfs_event_censored: 0; rfs_time_censored (years): 6.2; relapse_5years: 0; os_event: 0; os_time (years): 6.2; ', 'tissue: breast tumor; cohort id: BC57; geo_accn_gse20713_27k: GSM519892; geo_accn_gse20713_expr: GSM519760; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 0; size_cm: 1.8; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 48.7; age_bin: 0; rfs_event: 0; rfs_time (years): 6.21; rfs_event_censored: 0; rfs_time_censored (years): 6.21; relapse_5years: 0; os_event: 0; os_time (years): 6.21; ', 'tissue: breast tumor; cohort id: BC58; geo_accn_gse20713_27k: GSM519893; geo_accn_gse20713_expr: GSM519761; subtype_ihc: Basal; subtype_pam50: LumB; itu-ly: 5; str-ly: 20; grade: 3; size_bin: 1; size_cm: 3.5; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 68.48; age_bin: 1; rfs_event: 1; rfs_time (years): 1.47; rfs_event_censored: 1; rfs_time_censored (years): 1.47; relapse_5years: 1; os_event: 1; os_time (years): 5.56; ', 'tissue: breast tumor; cohort id: BC59; geo_accn_gse20713_27k: GSM519894; geo_accn_gse20713_expr: null; subtype_ihc: LumB; subtype_pam50: null; itu-ly: 10; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.5; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 35.85; age_bin: 0; rfs_event: 1; rfs_time (years): 1.31; rfs_event_censored: 1; rfs_time_censored (years): 1.31; relapse_5years: 1; os_event: 0; os_time (years): 6.58; ', 'tissue: breast tumor; cohort id: BC60; geo_accn_gse20713_27k: GSM519896; geo_accn_gse20713_expr: GSM519762; subtype_ihc: LumA; subtype_pam50: LumA; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 0; size_cm: 1.7; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 48.64; age_bin: 0; rfs_event: 0; rfs_time (years): 6.83; rfs_event_censored: 0; rfs_time_censored (years): 6.83; relapse_5years: 0; os_event: 0; os_time (years): 6.83; ', 'tissue: breast tumor; cohort id: BC61; geo_accn_gse20713_27k: GSM519897; geo_accn_gse20713_expr: GSM519763; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 2.5; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 61.7; age_bin: 1; rfs_event: 1; rfs_time (years): 4.58; rfs_event_censored: 1; rfs_time_censored (years): 4.58; relapse_5years: 1; os_event: 0; os_time (years): 7.08; ', 'tissue: breast tumor; cohort id: BC62; geo_accn_gse20713_27k: GSM519898; geo_accn_gse20713_expr: GSM519764; subtype_ihc: HER2; subtype_pam50: Basal; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 2.7; nodal_status: 0; er_ihc_status: 1; her2_status: 1; age_diagnosis: 33.44; age_bin: 0; rfs_event: 1; rfs_time (years): 2.63; rfs_event_censored: 1; rfs_time_censored (years): 2.63; relapse_5years: 1; os_event: 1; os_time (years): 6.45; ', 'tissue: breast tumor; cohort id: BC63; geo_accn_gse20713_27k: GSM519899; geo_accn_gse20713_expr: null; subtype_ihc: LumA; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 0; size_cm: 1; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 60.2; age_bin: 1; rfs_event: 0; rfs_time (years): 5.99; rfs_event_censored: 0; rfs_time_censored (years): 5.99; relapse_5years: 0; os_event: 0; os_time (years): 5.99; ', 'tissue: breast tumor; cohort id: BC64; geo_accn_gse20713_27k: GSM519900; geo_accn_gse20713_expr: null; subtype_ihc: HER2; subtype_pam50: null; itu-ly: 0; str-ly: 10; grade: 2; size_bin: 0; size_cm: 1.1; nodal_status: 0; er_ihc_status: 1; her2_status: 1; age_diagnosis: 44.34; age_bin: 0; rfs_event: 0; rfs_time (years): 6.09; rfs_event_censored: 0; rfs_time_censored (years): 6.09; relapse_5years: 0; os_event: 0; os_time (years): 6.09; ', 'tissue: breast tumor; cohort id: BC65; geo_accn_gse20713_27k: GSM519901; geo_accn_gse20713_expr: GSM519765; subtype_ihc: Basal; subtype_pam50: LumA; itu-ly: null; str-ly: null; grade: 3; size_bin: 0; size_cm: 1.2-1.3; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 54.01; age_bin: 1; rfs_event: 0; rfs_time (years): 6.22; rfs_event_censored: 0; rfs_time_censored (years): 6.22; relapse_5years: 0; os_event: 0; os_time (years): 6.22; ', 'tissue: breast tumor; cohort id: BC66; geo_accn_gse20713_27k: GSM519902; geo_accn_gse20713_expr: GSM519767; subtype_ihc: HER2; subtype_pam50: LumA; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 2.1; nodal_status: 1; er_ihc_status: 1; her2_status: 1; age_diagnosis: 49.18; age_bin: 0; rfs_event: 0; rfs_time (years): 0.56; rfs_event_censored: 0; rfs_time_censored (years): 0.56; relapse_5years: 0; os_event: 1; os_time (years): 1.97; ', 'tissue: breast tumor; cohort id: BC67; geo_accn_gse20713_27k: GSM519903; geo_accn_gse20713_expr: GSM519768; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 50; str-ly: 80; grade: 2; size_bin: 0; size_cm: 1.4; nodal_status: 1; er_ihc_status: 0; her2_status: 0; age_diagnosis: 32.16; age_bin: 0; rfs_event: 0; rfs_time (years): 14.08; rfs_event_censored: 0; rfs_time_censored (years): 10; relapse_5years: 0; os_event: 0; os_time (years): 14.08; ', 'tissue: breast tumor; cohort id: BC68; geo_accn_gse20713_27k: GSM519904; geo_accn_gse20713_expr: GSM519769; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: null; str-ly: null; grade: 3; size_bin: 0; size_cm: 1.6; nodal_status: 0; er_ihc_status: 1; her2_status: 1; age_diagnosis: 66.72; age_bin: 1; rfs_event: 0; rfs_time (years): 6.17; rfs_event_censored: 0; rfs_time_censored (years): 6.17; relapse_5years: 0; os_event: 0; os_time (years): 6.17; ', 'tissue: breast tumor; cohort id: BC69; geo_accn_gse20713_27k: GSM519905; geo_accn_gse20713_expr: GSM519770; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 1; size_cm: 5.5; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 78.29; age_bin: 1; rfs_event: 1; rfs_time (years): 0.08; rfs_event_censored: 1; rfs_time_censored (years): 0.08; relapse_5years: 1; os_event: 1; os_time (years): 2.97; ', 'tissue: breast tumor; cohort id: BC70; geo_accn_gse20713_27k: GSM519907; geo_accn_gse20713_expr: GSM519771; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 2.2; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 39.78; age_bin: 0; rfs_event: 1; rfs_time (years): 7.46; rfs_event_censored: 1; rfs_time_censored (years): 7.46; relapse_5years: 0; os_event: 0; os_time (years): 12.8; ', 'tissue: breast tumor; cohort id: BC71; geo_accn_gse20713_27k: GSM519908; geo_accn_gse20713_expr: GSM519772; subtype_ihc: LumA; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 0; size_cm: 1.6; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 42.07; age_bin: 0; rfs_event: 0; rfs_time (years): 5.95; rfs_event_censored: 0; rfs_time_censored (years): 5.95; relapse_5years: 0; os_event: 0; os_time (years): 5.95; ', 'tissue: breast tumor; cohort id: BC72; geo_accn_gse20713_27k: GSM519909; geo_accn_gse20713_expr: GSM519773; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 1; size_cm: 2.1; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 53.82; age_bin: 1; rfs_event: 1; rfs_time (years): 1.69; rfs_event_censored: 1; rfs_time_censored (years): 1.69; relapse_5years: 1; os_event: 1; os_time (years): 4.58; ', 'tissue: breast tumor; cohort id: BC73; geo_accn_gse20713_27k: GSM519910; geo_accn_gse20713_expr: GSM519774; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 10; str-ly: 30; grade: 3; size_bin: 0; size_cm: 1.7; nodal_status: 1; er_ihc_status: 0; her2_status: 0; age_diagnosis: 75.13; age_bin: 1; rfs_event: 0; rfs_time (years): 5.74; rfs_event_censored: 0; rfs_time_censored (years): 5.74; relapse_5years: 0; os_event: 0; os_time (years): 5.74; ', 'tissue: breast tumor; cohort id: BC74; geo_accn_gse20713_27k: GSM519911; geo_accn_gse20713_expr: GSM519775; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: null; str-ly: null; grade: 3; size_bin: 1; size_cm: 2.3; nodal_status: 1; er_ihc_status: 0; her2_status: 0; age_diagnosis: 79.86; age_bin: 1; rfs_event: 1; rfs_time (years): 4.43; rfs_event_censored: 1; rfs_time_censored (years): 4.43; relapse_5years: 1; os_event: 0; os_time (years): 4.52; ', 'tissue: breast tumor; cohort id: BC75; geo_accn_gse20713_27k: GSM519912; geo_accn_gse20713_expr: GSM519776; subtype_ihc: HER2; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 5.5; nodal_status: 1; er_ihc_status: 1; her2_status: 1; age_diagnosis: 48.34; age_bin: 0; rfs_event: 0; rfs_time (years): 6.12; rfs_event_censored: 0; rfs_time_censored (years): 6.12; relapse_5years: 0; os_event: 0; os_time (years): 6.12; ', 'tissue: breast tumor; cohort id: BC77; geo_accn_gse20713_27k: GSM519913; geo_accn_gse20713_expr: null; subtype_ihc: LumA; subtype_pam50: null; itu-ly: null; str-ly: null; grade: 1; size_bin: 0; size_cm: 1.3; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 61.52; age_bin: 1; rfs_event: 0; rfs_time (years): 5.84; rfs_event_censored: 0; rfs_time_censored (years): 5.84; relapse_5years: 0; os_event: 0; os_time (years): 5.84; ', 'tissue: breast tumor; cohort id: BC78; geo_accn_gse20713_27k: GSM519914; geo_accn_gse20713_expr: GSM519777; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 50; str-ly: 30; grade: 3; size_bin: 0; size_cm: 1.6; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 50.29; age_bin: 1; rfs_event: 1; rfs_time (years): 1.08; rfs_event_censored: 1; rfs_time_censored (years): 1.08; relapse_5years: 1; os_event: 1; os_time (years): 1.58; ', 'tissue: breast tumor; cohort id: BC79; geo_accn_gse20713_27k: GSM519915; geo_accn_gse20713_expr: GSM519778; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 10; str-ly: 90; grade: 3; size_bin: 1; size_cm: 2.2; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 45.98; age_bin: 0; rfs_event: 0; rfs_time (years): 5.43; rfs_event_censored: 0; rfs_time_censored (years): 5.43; relapse_5years: 0; os_event: 0; os_time (years): 5.43; ', 'tissue: breast tumor; cohort id: BC80; geo_accn_gse20713_27k: GSM519917; geo_accn_gse20713_expr: GSM519779; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 30; str-ly: 90; grade: 3; size_bin: 0; size_cm: 1.1; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 53.98; age_bin: 1; rfs_event: 1; rfs_time (years): 2.05; rfs_event_censored: 1; rfs_time_censored (years): 2.05; relapse_5years: 1; os_event: 1; os_time (years): 5.33; ', 'tissue: breast tumor; cohort id: BC81; geo_accn_gse20713_27k: GSM519918; geo_accn_gse20713_expr: null; subtype_ihc: HER2; subtype_pam50: null; itu-ly: 10; str-ly: 20; grade: 3; size_bin: 0; size_cm: 1.1; nodal_status: 0; er_ihc_status: 0; her2_status: 1; age_diagnosis: 61; age_bin: 1; rfs_event: 0; rfs_time (years): 4.95; rfs_event_censored: 0; rfs_time_censored (years): 4.95; relapse_5years: 0; os_event: 0; os_time (years): 4.95; ', 'tissue: breast tumor; cohort id: BC83; geo_accn_gse20713_27k: GSM519919; geo_accn_gse20713_expr: null; subtype_ihc: HER2; subtype_pam50: null; itu-ly: null; str-ly: null; grade: 2; size_bin: 0; size_cm: 1.1; nodal_status: 0; er_ihc_status: 0; her2_status: 1; age_diagnosis: 61.86; age_bin: 1; rfs_event: 0; rfs_time (years): 6.06; rfs_event_censored: 0; rfs_time_censored (years): 6.06; relapse_5years: 0; os_event: 0; os_time (years): 6.06; ', 'tissue: breast tumor; cohort id: BC84; geo_accn_gse20713_27k: GSM519920; geo_accn_gse20713_expr: GSM519780; subtype_ihc: Basal; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 2; size_bin: 0; size_cm: 1.3; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 36.3; age_bin: 0; rfs_event: 1; rfs_time (years): 2.42; rfs_event_censored: 1; rfs_time_censored (years): 2.42; relapse_5years: 1; os_event: 0; os_time (years): 7.08; ', 'tissue: breast tumor; cohort id: BC85; geo_accn_gse20713_27k: GSM519921; geo_accn_gse20713_expr: GSM519781; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 50; str-ly: 80; grade: 2; size_bin: 1; size_cm: 2.5; nodal_status: 1; er_ihc_status: null; her2_status: 1; age_diagnosis: 63.61; age_bin: 1; rfs_event: 0; rfs_time (years): 13.96; rfs_event_censored: 0; rfs_time_censored (years): 10; relapse_5years: 0; os_event: 0; os_time (years): 13.96; ', 'tissue: breast tumor; cohort id: BC86; geo_accn_gse20713_27k: GSM519922; geo_accn_gse20713_expr: GSM519782; subtype_ihc: HER2; subtype_pam50: LumB; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 1; size_cm: 3; nodal_status: 0; er_ihc_status: 0; her2_status: 1; age_diagnosis: 46.95; age_bin: 0; rfs_event: 0; rfs_time (years): 13.39; rfs_event_censored: 0; rfs_time_censored (years): 10; relapse_5years: 0; os_event: 0; os_time (years): 13.39; ', 'tissue: breast tumor; cohort id: BC87; geo_accn_gse20713_27k: GSM519923; geo_accn_gse20713_expr: null; subtype_ihc: Basal; subtype_pam50: null; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.4; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 58.03; age_bin: 1; rfs_event: 1; rfs_time (years): 0.67; rfs_event_censored: 1; rfs_time_censored (years): 0.67; relapse_5years: 1; os_event: 1; os_time (years): 1.58; ', 'tissue: breast tumor; cohort id: BC88; geo_accn_gse20713_27k: GSM519924; geo_accn_gse20713_expr: GSM519783; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 3; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 64.86; age_bin: 1; rfs_event: 1; rfs_time (years): 5.92; rfs_event_censored: 1; rfs_time_censored (years): 5.92; relapse_5years: 0; os_event: 0; os_time (years): 7.93; ', 'tissue: breast tumor; cohort id: BC89; geo_accn_gse20713_27k: GSM519925; geo_accn_gse20713_expr: null; subtype_ihc: LumA; subtype_pam50: null; itu-ly: 0; str-ly: 5; grade: 1; size_bin: 0; size_cm: 2; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 48.48; age_bin: 0; rfs_event: 1; rfs_time (years): 9.01; rfs_event_censored: 1; rfs_time_censored (years): 9.01; relapse_5years: 0; os_event: 0; os_time (years): 12.83; ', 'tissue: breast tumor; cohort id: BC90; geo_accn_gse20713_27k: GSM519927; geo_accn_gse20713_expr: GSM519784; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 2.4; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 54.19; age_bin: 1; rfs_event: 0; rfs_time (years): 3.82; rfs_event_censored: 0; rfs_time_censored (years): 3.82; relapse_5years: 0; os_event: 1; os_time (years): 7.42; ', 'tissue: breast tumor; cohort id: BC91; geo_accn_gse20713_27k: GSM519928; geo_accn_gse20713_expr: null; subtype_ihc: LumA; subtype_pam50: null; itu-ly: 0; str-ly: 10; grade: 1; size_bin: 0; size_cm: 1.8; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 49.26; age_bin: 0; rfs_event: 1; rfs_time (years): 10.16; rfs_event_censored: 0; rfs_time_censored (years): 10; relapse_5years: 0; os_event: 0; os_time (years): 13.33; ', 'tissue: breast tumor; cohort id: BC92; geo_accn_gse20713_27k: GSM519929; geo_accn_gse20713_expr: GSM519785; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 0; str-ly: 0; grade: 2; size_bin: 1; size_cm: 3; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 76.43; age_bin: 1; rfs_event: 1; rfs_time (years): 2.09; rfs_event_censored: 1; rfs_time_censored (years): 2.09; relapse_5years: 1; os_event: 1; os_time (years): 5.89; ', 'tissue: breast tumor; cohort id: BC93; geo_accn_gse20713_27k: GSM519930; geo_accn_gse20713_expr: null; subtype_ihc: LumB; subtype_pam50: null; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 1; size_cm: 2.1; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 65.53; age_bin: 1; rfs_event: 1; rfs_time (years): 4.18; rfs_event_censored: 1; rfs_time_censored (years): 4.18; relapse_5years: 1; os_event: 1; os_time (years): 4.19; ', 'tissue: breast tumor; cohort id: BC94; geo_accn_gse20713_27k: GSM519931; geo_accn_gse20713_expr: GSM519786; subtype_ihc: HER2; subtype_pam50: LumB; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 1; size_cm: 3.5; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 43.96; age_bin: 0; rfs_event: 1; rfs_time (years): 8.67; rfs_event_censored: 1; rfs_time_censored (years): 8.67; relapse_5years: 0; os_event: 1; os_time (years): 11.32; ', 'tissue: breast tumor; cohort id: BC95; geo_accn_gse20713_27k: GSM519932; geo_accn_gse20713_expr: GSM519787; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 50; str-ly: 80; grade: 3; size_bin: 1; size_cm: 2.5; nodal_status: 1; er_ihc_status: 0; her2_status: 0; age_diagnosis: 56.55; age_bin: 1; rfs_event: 1; rfs_time (years): 1.48; rfs_event_censored: 1; rfs_time_censored (years): 1.48; relapse_5years: 1; os_event: 1; os_time (years): 1.92; ', 'tissue: breast tumor; cohort id: BC96; geo_accn_gse20713_27k: GSM519933; geo_accn_gse20713_expr: GSM519788; subtype_ihc: LumA; subtype_pam50: LumA; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 0; size_cm: 1.5; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 47.88; age_bin: 0; rfs_event: 0; rfs_time (years): 6.38; rfs_event_censored: 0; rfs_time_censored (years): 6.38; relapse_5years: 0; os_event: 0; os_time (years): 6.38; ', 'tissue: breast tumor; cohort id: BC97; geo_accn_gse20713_27k: GSM519934; geo_accn_gse20713_expr: GSM519789; subtype_ihc: LumA; subtype_pam50: LumA; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 0; size_cm: 1.6; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 52.56; age_bin: 1; rfs_event: 0; rfs_time (years): 5.96; rfs_event_censored: 0; rfs_time_censored (years): 5.96; relapse_5years: 0; os_event: 0; os_time (years): 5.96; ', 'tissue: breast tumor; cohort id: BC99; geo_accn_gse20713_27k: GSM519935; geo_accn_gse20713_expr: GSM519790; subtype_ihc: LumA; subtype_pam50: LumA; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 0; size_cm: 1.5; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 59.36; age_bin: 1; rfs_event: 0; rfs_time (years): 13.45; rfs_event_censored: 0; rfs_time_censored (years): 10; relapse_5years: 0; os_event: 0; os_time (years): 13.45; ', 'tissue: breast tumor; cohort id: BC101; geo_accn_gse20713_27k: GSM519819; geo_accn_gse20713_expr: GSM519791; subtype_ihc: LumA; subtype_pam50: LumA; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 0; size_cm: 1.5; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 67.57; age_bin: 1; rfs_event: 0; rfs_time (years): 7.9; rfs_event_censored: 0; rfs_time_censored (years): 7.9; relapse_5years: 0; os_event: 0; os_time (years): 7.9; ', 'tissue: breast tumor; cohort id: BC102; geo_accn_gse20713_27k: GSM519820; geo_accn_gse20713_expr: GSM519792; subtype_ihc: HER2; subtype_pam50: Basal; itu-ly: 5; str-ly: 10; grade: 3; size_bin: 1; size_cm: 5; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 52.94; age_bin: 1; rfs_event: 0; rfs_time (years): 13.42; rfs_event_censored: 0; rfs_time_censored (years): 10; relapse_5years: 0; os_event: 0; os_time (years): 13.42; ', 'tissue: breast tumor; cohort id: BC103; geo_accn_gse20713_27k: GSM519821; geo_accn_gse20713_expr: GSM519793; subtype_ihc: Basal; subtype_pam50: LumB; itu-ly: 0; str-ly: 5; grade: 2; size_bin: 1; size_cm: 3; nodal_status: 1; er_ihc_status: 0; her2_status: 0; age_diagnosis: 46.83; age_bin: 0; rfs_event: 0; rfs_time (years): 13.27; rfs_event_censored: 0; rfs_time_censored (years): 10; relapse_5years: 0; os_event: 0; os_time (years): 13.27; ', 'tissue: breast tumor; cohort id: BC104; geo_accn_gse20713_27k: GSM519822; geo_accn_gse20713_expr: null; subtype_ihc: LumA; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 1; size_cm: 2.7; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 66.18; age_bin: 1; rfs_event: 0; rfs_time (years): 7.98; rfs_event_censored: 0; rfs_time_censored (years): 7.98; relapse_5years: 0; os_event: 0; os_time (years): 7.98; ', 'tissue: breast tumor; cohort id: BC105; geo_accn_gse20713_27k: GSM519823; geo_accn_gse20713_expr: GSM519794; subtype_ihc: Basal; subtype_pam50: LumB; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.3; nodal_status: 1; er_ihc_status: 0; her2_status: 0; age_diagnosis: 41.54; age_bin: 0; rfs_event: 0; rfs_time (years): 8.74; rfs_event_censored: 0; rfs_time_censored (years): 8.74; relapse_5years: 0; os_event: 0; os_time (years): 8.74; ', 'tissue: breast tumor; cohort id: BC106; geo_accn_gse20713_27k: GSM519824; geo_accn_gse20713_expr: GSM519795; subtype_ihc: LumA; subtype_pam50: LumA; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 1; size_cm: 2.4; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 51.81; age_bin: 1; rfs_event: 0; rfs_time (years): 5.36; rfs_event_censored: 0; rfs_time_censored (years): 5.36; relapse_5years: 0; os_event: 0; os_time (years): 5.36; ', 'tissue: breast tumor; cohort id: BC107; geo_accn_gse20713_27k: GSM519825; geo_accn_gse20713_expr: GSM519796; subtype_ihc: LumB; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: >2; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 53.8; age_bin: 1; rfs_event: 1; rfs_time (years): 9.19; rfs_event_censored: 1; rfs_time_censored (years): 9.19; relapse_5years: 0; os_event: 0; os_time (years): 12.41; ', 'tissue: breast tumor; cohort id: BC108; geo_accn_gse20713_27k: GSM519826; geo_accn_gse20713_expr: GSM519797; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 0; str-ly: 30; grade: 3; size_bin: 1; size_cm: 2.6; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 55.22; age_bin: 1; rfs_event: 1; rfs_time (years): 0.74; rfs_event_censored: 1; rfs_time_censored (years): 0.74; relapse_5years: 1; os_event: 1; os_time (years): 0.87; ', 'tissue: breast tumor; cohort id: BC109; geo_accn_gse20713_27k: GSM519827; geo_accn_gse20713_expr: GSM519798; subtype_ihc: LumA; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 1; size_cm: 3; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 67.77; age_bin: 1; rfs_event: 1; rfs_time (years): 6.48; rfs_event_censored: 1; rfs_time_censored (years): 6.48; relapse_5years: 0; os_event: 1; os_time (years): 7.92; ', 'tissue: breast tumor; cohort id: BC110; geo_accn_gse20713_27k: GSM519829; geo_accn_gse20713_expr: null; subtype_ihc: LumB; subtype_pam50: null; itu-ly: null; str-ly: null; grade: 2; size_bin: 1; size_cm: 1.1+2.1; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 39.69; age_bin: 0; rfs_event: 0; rfs_time (years): 5.19; rfs_event_censored: 0; rfs_time_censored (years): 5.19; relapse_5years: 0; os_event: 0; os_time (years): 5.19; ', 'tissue: breast tumor; cohort id: BC112; geo_accn_gse20713_27k: GSM519830; geo_accn_gse20713_expr: GSM519799; subtype_ihc: HER2; subtype_pam50: Basal; itu-ly: null; str-ly: null; grade: 3; size_bin: 1; size_cm: 6; nodal_status: 0; er_ihc_status: 0; her2_status: 1; age_diagnosis: 47.82; age_bin: 0; rfs_event: 1; rfs_time (years): 10.22; rfs_event_censored: 0; rfs_time_censored (years): 10; relapse_5years: 0; os_event: 0; os_time (years): 10.82; ', 'tissue: breast tumor; cohort id: BC113; geo_accn_gse20713_27k: GSM519831; geo_accn_gse20713_expr: GSM519800; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 1; size_cm: 3; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 64.83; age_bin: 1; rfs_event: 1; rfs_time (years): 3.94; rfs_event_censored: 1; rfs_time_censored (years): 3.94; relapse_5years: 1; os_event: 0; os_time (years): 1.21; ', 'tissue: breast tumor; cohort id: BC115; geo_accn_gse20713_27k: GSM519832; geo_accn_gse20713_expr: GSM519801; subtype_ihc: Basal; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 2.5; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 59.08; age_bin: 1; rfs_event: 1; rfs_time (years): 2.56; rfs_event_censored: 1; rfs_time_censored (years): 2.56; relapse_5years: 1; os_event: 1; os_time (years): 4.89; ', 'tissue: breast tumor; cohort id: BC116; geo_accn_gse20713_27k: GSM519833; geo_accn_gse20713_expr: GSM519802; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 3.7; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 57.32; age_bin: 1; rfs_event: 0; rfs_time (years): 9.78; rfs_event_censored: 0; rfs_time_censored (years): 9.78; relapse_5years: 0; os_event: 0; os_time (years): 9.78; ', 'tissue: breast tumor; cohort id: BC117; geo_accn_gse20713_27k: GSM519834; geo_accn_gse20713_expr: null; subtype_ihc: Basal; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 3.2; nodal_status: 1; er_ihc_status: 0; her2_status: 0; age_diagnosis: 41.86; age_bin: 0; rfs_event: 1; rfs_time (years): 1.89; rfs_event_censored: 1; rfs_time_censored (years): 1.89; relapse_5years: 1; os_event: 1; os_time (years): 3.26; ', 'tissue: breast tumor; cohort id: BC118; geo_accn_gse20713_27k: GSM519835; geo_accn_gse20713_expr: null; subtype_ihc: HER2; subtype_pam50: null; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 2.8; nodal_status: 1; er_ihc_status: 0; her2_status: 1; age_diagnosis: 66.04; age_bin: 1; rfs_event: 1; rfs_time (years): 1.17; rfs_event_censored: 1; rfs_time_censored (years): 1.17; relapse_5years: 1; os_event: 1; os_time (years): 2.77; ', 'tissue: breast tumor; cohort id: BC119; geo_accn_gse20713_27k: GSM519836; geo_accn_gse20713_expr: GSM519803; subtype_ihc: Basal; subtype_pam50: LumB; itu-ly: 0; str-ly: 0; grade: 3; size_bin: 1; size_cm: 3.5; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 62.62; age_bin: 1; rfs_event: 1; rfs_time (years): 4.25; rfs_event_censored: 1; rfs_time_censored (years): 4.25; relapse_5years: 1; os_event: 1; os_time (years): 4.69; ', 'tissue: breast tumor; cohort id: BC120; geo_accn_gse20713_27k: GSM519838; geo_accn_gse20713_expr: GSM519804; subtype_ihc: LumA; subtype_pam50: LumA; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 1; size_cm: 3; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 57.7; age_bin: 1; rfs_event: 0; rfs_time (years): 9.99; rfs_event_censored: 0; rfs_time_censored (years): 9.99; relapse_5years: 0; os_event: 0; os_time (years): 9.99; ', 'tissue: breast tumor; cohort id: BC121; geo_accn_gse20713_27k: GSM519839; geo_accn_gse20713_expr: GSM519805; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 1; size_cm: >4.5; nodal_status: 1; er_ihc_status: 1; her2_status: 1; age_diagnosis: 52.35; age_bin: 1; rfs_event: 1; rfs_time (years): 2.65; rfs_event_censored: 1; rfs_time_censored (years): 2.65; relapse_5years: 1; os_event: 0; os_time (years): 5.58; ', 'tissue: breast tumor; cohort id: BC122; geo_accn_gse20713_27k: GSM519840; geo_accn_gse20713_expr: GSM519806; subtype_ihc: HER2; subtype_pam50: Her2; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 1; size_cm: 3; nodal_status: 0; er_ihc_status: 0; her2_status: 1; age_diagnosis: 69.25; age_bin: 1; rfs_event: 1; rfs_time (years): 0.64; rfs_event_censored: 1; rfs_time_censored (years): 0.64; relapse_5years: 1; os_event: 1; os_time (years): 3.55; ', 'tissue: breast tumor; cohort id: BC123; geo_accn_gse20713_27k: GSM519841; geo_accn_gse20713_expr: GSM519807; subtype_ihc: LumA; subtype_pam50: LumA; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 0; size_cm: 1.3; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 66.14; age_bin: 1; rfs_event: 1; rfs_time (years): 3.75; rfs_event_censored: 1; rfs_time_censored (years): 3.75; relapse_5years: 1; os_event: 1; os_time (years): 5.18; ', 'tissue: breast tumor; cohort id: BC124; geo_accn_gse20713_27k: GSM519842; geo_accn_gse20713_expr: GSM519808; subtype_ihc: Basal; subtype_pam50: Basal; itu-ly: 10; str-ly: 40; grade: 3; size_bin: 0; size_cm: 1.7; nodal_status: 0; er_ihc_status: 0; her2_status: 0; age_diagnosis: 53.7; age_bin: 1; rfs_event: 0; rfs_time (years): 6.19; rfs_event_censored: 0; rfs_time_censored (years): 6.19; relapse_5years: 0; os_event: 0; os_time (years): 6.19; ', 'tissue: breast tumor; cohort id: BC125; geo_accn_gse20713_27k: GSM519843; geo_accn_gse20713_expr: GSM519809; subtype_ihc: LumA; subtype_pam50: LumA; itu-ly: 0; str-ly: 0; grade: 1; size_bin: 1; size_cm: 2.3; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 67.41; age_bin: 1; rfs_event: 0; rfs_time (years): 6.11; rfs_event_censored: 0; rfs_time_censored (years): 6.11; relapse_5years: 0; os_event: 0; os_time (years): 6.11; ', 'tissue: breast tumor; cohort id: BC126; geo_accn_gse20713_27k: GSM519844; geo_accn_gse20713_expr: GSM519810; subtype_ihc: LumA; subtype_pam50: LumA; itu-ly: 0; str-ly: 20; grade: 1; size_bin: 1; size_cm: 3.2; nodal_status: 1; er_ihc_status: 1; her2_status: 0; age_diagnosis: 71.68; age_bin: 1; rfs_event: 1; rfs_time (years): 0.01; rfs_event_censored: 1; rfs_time_censored (years): 0.01; relapse_5years: 1; os_event: 0; os_time (years): 6.1; ', 'tissue: breast tumor; cohort id: BC129; geo_accn_gse20713_27k: GSM519845; geo_accn_gse20713_expr: null; subtype_ihc: LumB; subtype_pam50: null; itu-ly: null; str-ly: null; grade: 3; size_bin: 0; size_cm: 1.9; nodal_status: 0; er_ihc_status: 1; her2_status: 0; age_diagnosis: 58.49; age_bin: 1; rfs_event: 1; rfs_time (years): 5.06; rfs_event_censored: 1; rfs_time_censored (years): 5.06; relapse_5years: 0; os_event: 0; os_time (years): 11.44; ', 'tissue: breast tumor; cohort id: 2-1; geo_accn_gse20713_27k: GSM553826; subtype_ihc: LumA; itu-ly: 0; str-ly: 1; grade: 1; size_bin: 0; size_cm: 1.3; nodes_pos: 0; nodes_extracted: 2; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 74.22; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 3.44; ddfs_event: 0; ddfs_time (years): 3.44; os_event: 0; os_time (years): 3.44; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-2; geo_accn_gse20713_27k: GSM553827; subtype_ihc: LumA; itu-ly: null; str-ly: null; grade: 1; size_bin: 0; size_cm: 1.4; nodes_pos: 0; nodes_extracted: 2; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 42.22; age_bin: 0; ki67: 10; idfs_event: 0; idfs_time (years): 4.13; ddfs_event: 0; ddfs_time (years): 4.13; os_event: 0; os_time (years): 4.13; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-3; geo_accn_gse20713_27k: GSM553828; subtype_ihc: LumA; itu-ly: null; str-ly: null; grade: 1; size_bin: 0; size_cm: 1.4; nodes_pos: 0; nodes_extracted: 2; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 61.28; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 4.4; ddfs_event: 0; ddfs_time (years): 4.4; os_event: 0; os_time (years): 4.4; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-4; geo_accn_gse20713_27k: GSM553829; subtype_ihc: LumA; itu-ly: 0; str-ly: 1; grade: 1; size_bin: 0; size_cm: 1.8; nodes_pos: 0; nodes_extracted: NK; nodal_status: 0; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 50.59; age_bin: 1; ki67: 20; idfs_event: 0; idfs_time (years): 4.42; ddfs_event: 0; ddfs_time (years): 4.42; os_event: 0; os_time (years): 4.42; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-5; geo_accn_gse20713_27k: GSM553830; subtype_ihc: LumA; itu-ly: 0; str-ly: 1; grade: 1; size_bin: 0; size_cm: 1.3; nodes_pos: 2; nodes_extracted: 16; nodal_status: 1; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 6; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 49.51; age_bin: 0; ki67: 5; idfs_event: 0; idfs_time (years): 5.01; ddfs_event: 0; ddfs_time (years): 5.01; os_event: 0; os_time (years): 5.01; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-6; geo_accn_gse20713_27k: GSM553831; subtype_ihc: LumA; itu-ly: 1; str-ly: 30; grade: 1; size_bin: 0; size_cm: 1.6; nodes_pos: 1; nodes_extracted: 17; nodal_status: 1; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 51.97; age_bin: 1; ki67: 15; idfs_event: 1; idfs_time (years): 4.93; ddfs_event: 0; ddfs_time (years): 5.62; os_event: 0; os_time (years): 5.62; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-7; geo_accn_gse20713_27k: GSM553832; subtype_ihc: LumA; itu-ly: 0; str-ly: 1; grade: 1; size_bin: 0; size_cm: 1.1; nodes_pos: 0; nodes_extracted: 1; nodal_status: 0; er_score: 5; er_score_max: 8; er_ihc_status: 1; pgr_score: 7; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 47.78; age_bin: 0; ki67: 5; idfs_event: 0; idfs_time (years): 4.78; ddfs_event: 0; ddfs_time (years): 4.78; os_event: 0; os_time (years): 4.78; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-8; geo_accn_gse20713_27k: GSM553833; subtype_ihc: LumA; itu-ly: null; str-ly: null; grade: 1; size_bin: 0; size_cm: 1.4; nodes_pos: 0; nodes_extracted: 13; nodal_status: 0; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 42.04; age_bin: 0; ki67: 10; idfs_event: 0; idfs_time (years): 5.12; ddfs_event: 0; ddfs_time (years): 5.12; os_event: 0; os_time (years): 5.12; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-9; geo_accn_gse20713_27k: GSM553834; subtype_ihc: LumA; itu-ly: 0; str-ly: 5; grade: 1; size_bin: 0; size_cm: 1.3; nodes_pos: 0; nodes_extracted: 3; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 4; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 68.3; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 0.95; ddfs_event: 0; ddfs_time (years): 0.95; os_event: 0; os_time (years): 0.95; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-10; geo_accn_gse20713_27k: GSM553823; subtype_ihc: LumA; itu-ly: 0; str-ly: 5; grade: 1; size_bin: 0; size_cm: 1.3; nodes_pos: 0; nodes_extracted: 3; nodal_status: 0; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 47.36; age_bin: 0; ki67: 10; idfs_event: 0; idfs_time (years): 4.82; ddfs_event: 0; ddfs_time (years): 4.82; os_event: 0; os_time (years): 4.82; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-11; geo_accn_gse20713_27k: GSM553824; subtype_ihc: LumA; itu-ly: 0; str-ly: 5; grade: 1; size_bin: 0; size_cm: 0.9; nodes_pos: 0; nodes_extracted: 6; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 49.95; age_bin: 0; ki67: 10; idfs_event: 0; idfs_time (years): 5.06; ddfs_event: 0; ddfs_time (years): 5.06; os_event: 0; os_time (years): 5.06; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-12; geo_accn_gse20713_27k: GSM553825; subtype_ihc: LumA; itu-ly: 1; str-ly: 5; grade: 1; size_bin: 0; size_cm: 1.1; nodes_pos: 0; nodes_extracted: 1; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 7; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 72.08; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 7.06; ddfs_event: 0; ddfs_time (years): 7.06; os_event: 0; os_time (years): 7.06; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-13; geo_accn_gse20713_27k: GSM553813; subtype_ihc: LumA; itu-ly: 2; str-ly: 10; grade: 1; size_bin: 0; size_cm: 1.6; nodes_pos: null; nodes_extracted: null; nodal_status: null; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 6; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 91.43; age_bin: 1; ki67: 13; idfs_event: 0; idfs_time (years): 1.34; ddfs_event: 0; ddfs_time (years): 1.34; os_event: 1; os_time (years): 1.34; date_death: 11 September 2005; cause_death: NK; ', 'tissue: breast tumor; cohort id: 2-14; geo_accn_gse20713_27k: GSM553814; subtype_ihc: LumA; itu-ly: 2; str-ly: 5; grade: 1; size_bin: 0; size_cm: 1.1; nodes_pos: 0; nodes_extracted: 2; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 76.1; age_bin: 1; ki67: 5; idfs_event: 0; idfs_time (years): 7.88; ddfs_event: 0; ddfs_time (years): 7.88; os_event: 0; os_time (years): 7.88; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-15; geo_accn_gse20713_27k: GSM553815; subtype_ihc: LumA; itu-ly: 10; str-ly: 25; grade: 1; size_bin: 0; size_cm: 0.7; nodes_pos: 0; nodes_extracted: 1; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 3; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 47.8; age_bin: 0; ki67: 5; idfs_event: 0; idfs_time (years): 0.03; ddfs_event: 0; ddfs_time (years): 0.03; os_event: 0; os_time (years): 0.03; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-16; geo_accn_gse20713_27k: GSM553810; subtype_ihc: LumA; itu-ly: 0; str-ly: 1; grade: 1; size_bin: 0; size_cm: 1.1; nodes_pos: 0; nodes_extracted: 2; nodal_status: 0; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 62.25; age_bin: 1; ki67: 5; idfs_event: 1; idfs_time (years): 4.17; ddfs_event: 1; ddfs_time (years): 4.17; os_event: 0; os_time (years): 7.76; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-17; geo_accn_gse20713_27k: GSM553811; subtype_ihc: LumA; itu-ly: 0; str-ly: 5; grade: 1; size_bin: 1; size_cm: 9; nodes_pos: 0; nodes_extracted: 20; nodal_status: 0; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 67.06; age_bin: 1; ki67: 5; idfs_event: 1; idfs_time (years): 3.28; ddfs_event: 0; ddfs_time (years): 3.4; os_event: 0; os_time (years): 3.4; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-18; geo_accn_gse20713_27k: GSM553812; subtype_ihc: LumA; itu-ly: 1; str-ly: null; grade: 1; size_bin: 0; size_cm: 1.4; nodes_pos: 0; nodes_extracted: 9; nodal_status: 0; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 50.92; age_bin: 1; ki67: 5; idfs_event: 1; idfs_time (years): 1.91; ddfs_event: 0; ddfs_time (years): 5.73; os_event: 0; os_time (years): 5.73; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-19; geo_accn_gse20713_27k: GSM553808; subtype_ihc: LumA; itu-ly: null; str-ly: null; grade: 1; size_bin: 1; size_cm: 2.3; nodes_pos: NK; nodes_extracted: NK; nodal_status: null; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 83.44; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 5.39; ddfs_event: 0; ddfs_time (years): 5.39; os_event: 0; os_time (years): 5.39; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-20; geo_accn_gse20713_27k: GSM553809; subtype_ihc: LumA; itu-ly: 0; str-ly: 5; grade: 1; size_bin: 0; size_cm: 1.7; nodes_pos: 0; nodes_extracted: 6; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 84.33; age_bin: 1; ki67: 15; idfs_event: 0; idfs_time (years): 3.17; ddfs_event: 0; ddfs_time (years): 3.17; os_event: 0; os_time (years): 3.17; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-21; geo_accn_gse20713_27k: GSM553816; subtype_ihc: LumA; itu-ly: 0; str-ly: 5; grade: 1; size_bin: 0; size_cm: 1.9; nodes_pos: 1; nodes_extracted: 18; nodal_status: 1; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 43.68; age_bin: 0; ki67: 5; idfs_event: 0; idfs_time (years): 6.41; ddfs_event: 0; ddfs_time (years): 6.41; os_event: 0; os_time (years): 6.41; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-22; geo_accn_gse20713_27k: GSM553817; subtype_ihc: LumA; itu-ly: 0; str-ly: 1; grade: 1; size_bin: 0; size_cm: 1; nodes_pos: 0; nodes_extracted: 6; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 64.61; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 6.98; ddfs_event: 0; ddfs_time (years): 6.98; os_event: 0; os_time (years): 6.98; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-23; geo_accn_gse20713_27k: GSM553822; subtype_ihc: LumA; itu-ly: 0; str-ly: 5; grade: 1; size_bin: 0; size_cm: 1.9; nodes_pos: 0; nodes_extracted: 22; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 6; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 62.32; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 7.2; ddfs_event: 0; ddfs_time (years): 7.2; os_event: 0; os_time (years): 7.2; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-24; geo_accn_gse20713_27k: null; subtype_ihc: null; itu-ly: 0; str-ly: 5; grade: 1; size_bin: 0; size_cm: 1.5; nodes_pos: 0; nodes_extracted: 4; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 7; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 58.56; age_bin: 1; ki67: 10; idfs_event: 1; idfs_time (years): 4.43; ddfs_event: 0; ddfs_time (years): 6.55; os_event: 0; os_time (years): 6.55; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-25; geo_accn_gse20713_27k: GSM553820; subtype_ihc: LumA; itu-ly: 0; str-ly: 5; grade: 1; size_bin: 0; size_cm: 1.6; nodes_pos: 0; nodes_extracted: 16; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 7; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 47.25; age_bin: 0; ki67: 10; idfs_event: 0; idfs_time (years): 7.33; ddfs_event: 0; ddfs_time (years): 7.33; os_event: 0; os_time (years): 7.33; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-26; geo_accn_gse20713_27k: GSM553821; subtype_ihc: LumA; itu-ly: 0; str-ly: 5; grade: 1; size_bin: 0; size_cm: 1.3; nodes_pos: 0; nodes_extracted: 5; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 7; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 56.18; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 4.85; ddfs_event: 0; ddfs_time (years): 4.85; os_event: 0; os_time (years): 4.85; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-27; geo_accn_gse20713_27k: GSM553818; subtype_ihc: LumA; itu-ly: 0; str-ly: 1; grade: 1; size_bin: 0; size_cm: 1.8; nodes_pos: 0; nodes_extracted: 12; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 7; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 48.68; age_bin: 0; ki67: 5; idfs_event: 0; idfs_time (years): 2.4; ddfs_event: 0; ddfs_time (years): 2.4; os_event: 0; os_time (years): 2.4; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-28; geo_accn_gse20713_27k: GSM553819; subtype_ihc: LumA; itu-ly: 5; str-ly: 20; grade: 1; size_bin: 0; size_cm: 1.7; nodes_pos: 0; nodes_extracted: 11; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 58.54; age_bin: 1; ki67: 5; idfs_event: 0; idfs_time (years): 2.48; ddfs_event: 0; ddfs_time (years): 2.48; os_event: 0; os_time (years): 2.48; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-29; geo_accn_gse20713_27k: GSM553857; subtype_ihc: LumB; itu-ly: null; str-ly: null; grade: 3; size_bin: 0; size_cm: 2; nodes_pos: 1; nodes_extracted: 12; nodal_status: 1; er_score: 3; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 31.95; age_bin: 0; ki67: 70; idfs_event: 0; idfs_time (years): 12.73; ddfs_event: 0; ddfs_time (years): 12.73; os_event: 0; os_time (years): 12.73; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-30; geo_accn_gse20713_27k: GSM553858; subtype_ihc: LumB; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 1; size_cm: 3; nodes_pos: null; nodes_extracted: null; nodal_status: null; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 47.5; age_bin: 0; ki67: 10; idfs_event: 1; idfs_time (years): 10.59; ddfs_event: 1; ddfs_time (years): 10.59; os_event: 0; os_time (years): 13.48; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-31; geo_accn_gse20713_27k: GSM553860; subtype_ihc: LumB; itu-ly: null; str-ly: null; grade: 3; size_bin: 0; size_cm: 2; nodes_pos: 0; nodes_extracted: 20; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 30.19; age_bin: 0; ki67: 50; idfs_event: 0; idfs_time (years): 2.96; ddfs_event: 0; ddfs_time (years): 2.96; os_event: 0; os_time (years): 2.96; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-32; geo_accn_gse20713_27k: GSM553862; subtype_ihc: LumB; itu-ly: 2; str-ly: 15; grade: 3; size_bin: 0; size_cm: 1.9; nodes_pos: 0; nodes_extracted: 8; nodal_status: 0; er_score: 2; er_score_max: 8; er_ihc_status: 1; pgr_score: 4; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 49.26; age_bin: 0; ki67: 12.5; idfs_event: 0; idfs_time (years): 1.28; ddfs_event: 0; ddfs_time (years): 1.28; os_event: 0; os_time (years): 1.28; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-33; geo_accn_gse20713_27k: GSM553863; subtype_ihc: LumB; itu-ly: 0; str-ly: 1; grade: 3; size_bin: 0; size_cm: 0.8; nodes_pos: 0; nodes_extracted: 3; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 80.58; age_bin: 1; ki67: 30; idfs_event: 0; idfs_time (years): 2.1; ddfs_event: 0; ddfs_time (years): 2.1; os_event: 0; os_time (years): 2.1; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-34; geo_accn_gse20713_27k: GSM553864; subtype_ihc: LumB; itu-ly: null; str-ly: null; grade: 3; size_bin: 1; size_cm: 2.3; nodes_pos: 0; nodes_extracted: 5; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 56.7; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 3.61; ddfs_event: 0; ddfs_time (years): 3.61; os_event: 0; os_time (years): 3.61; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-35; geo_accn_gse20713_27k: GSM553854; subtype_ihc: LumB; itu-ly: null; str-ly: null; grade: 3; size_bin: 0; size_cm: 2; nodes_pos: 0; nodes_extracted: 25; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 61.53; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 3.32; ddfs_event: 0; ddfs_time (years): 3.32; os_event: 0; os_time (years): 3.32; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-36; geo_accn_gse20713_27k: GSM553855; subtype_ihc: LumB; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.9; nodes_pos: 3; nodes_extracted: 15; nodal_status: 1; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 70.62; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 3.06; ddfs_event: 0; ddfs_time (years): 3.06; os_event: 0; os_time (years): 3.06; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-37; geo_accn_gse20713_27k: GSM553856; subtype_ihc: LumB; itu-ly: null; str-ly: null; grade: 3; size_bin: 1; size_cm: 4; nodes_pos: 0; nodes_extracted: 20; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: 1.77; her2_fish_bin: 0; age_diagnosis: 75.32; age_bin: 1; ki67: 15; idfs_event: 1; idfs_time (years): 0.47; ddfs_event: 1; ddfs_time (years): 0.47; os_event: 0; os_time (years): 0.62; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-38; geo_accn_gse20713_27k: GSM553840; subtype_ihc: LumB; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 1; size_cm: 2.7; nodes_pos: 14; nodes_extracted: 17; nodal_status: 1; er_score: 6; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 56.33; age_bin: 1; ki67: 10; idfs_event: 1; idfs_time (years): 0.38; ddfs_event: 1; ddfs_time (years): 0.38; os_event: 1; os_time (years): 1.4; date_death: 05 March 2009; cause_death: cancer+general conditions (alcoholist); ', 'tissue: breast tumor; cohort id: 2-39; geo_accn_gse20713_27k: GSM553861; subtype_ihc: LumB; itu-ly: 2; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.7; nodes_pos: 0; nodes_extracted: 6; nodal_status: 0; er_score: 5; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 72.34; age_bin: 1; ki67: 50; idfs_event: 0; idfs_time (years): 0.36; ddfs_event: 0; ddfs_time (years): 0.36; os_event: 0; os_time (years): 0.36; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-40; geo_accn_gse20713_27k: GSM553841; subtype_ihc: LumB; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 0; size_cm: 1.7; nodes_pos: 9; nodes_extracted: 21; nodal_status: 1; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 6; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 47.3; age_bin: 0; ki67: 15; idfs_event: 0; idfs_time (years): 5.83; ddfs_event: 0; ddfs_time (years): 5.83; os_event: 0; os_time (years): 5.83; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-41; geo_accn_gse20713_27k: GSM553838; subtype_ihc: LumB; itu-ly: 2; str-ly: 15; grade: 3; size_bin: 0; size_cm: 1.8; nodes_pos: 6; nodes_extracted: 21; nodal_status: 1; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 3; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 58.44; age_bin: 1; ki67: 20; idfs_event: 0; idfs_time (years): 5.74; ddfs_event: 0; ddfs_time (years): 5.74; os_event: 0; os_time (years): 5.74; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-42; geo_accn_gse20713_27k: GSM553839; subtype_ihc: LumB; itu-ly: 1; str-ly: 10; grade: 3; size_bin: 0; size_cm: 2; nodes_pos: 0; nodes_extracted: 13; nodal_status: 0; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 7; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 31.25; age_bin: 0; ki67: 30; idfs_event: 0; idfs_time (years): 5.63; ddfs_event: 0; ddfs_time (years): 5.63; os_event: 0; os_time (years): 5.63; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-43; geo_accn_gse20713_27k: GSM553859; subtype_ihc: LumB; itu-ly: 5; str-ly: 35; grade: 3; size_bin: 1; size_cm: 21; nodes_pos: 1; nodes_extracted: 13; nodal_status: 1; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 64.83; age_bin: 1; ki67: 80; idfs_event: 0; idfs_time (years): 5.87; ddfs_event: 0; ddfs_time (years): 5.87; os_event: 0; os_time (years): 5.87; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-44; geo_accn_gse20713_27k: GSM553835; subtype_ihc: LumB; itu-ly: 1; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.6; nodes_pos: 0; nodes_extracted: 1; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 74.93; age_bin: 1; ki67: 7.5; idfs_event: 0; idfs_time (years): 5.08; ddfs_event: 0; ddfs_time (years): 5.08; os_event: 0; os_time (years): 5.08; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-45; geo_accn_gse20713_27k: GSM553836; subtype_ihc: LumB; itu-ly: 2; str-ly: 15; grade: 3; size_bin: 0; size_cm: 1.6; nodes_pos: 0; nodes_extracted: 11; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 7; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 64.96; age_bin: 1; ki67: 20; idfs_event: 0; idfs_time (years): 4.2; ddfs_event: 0; ddfs_time (years): 4.2; os_event: 0; os_time (years): 4.2; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-46; geo_accn_gse20713_27k: GSM553837; subtype_ihc: LumB; itu-ly: 0; str-ly: 1; grade: 3; size_bin: 1; size_cm: 2.5; nodes_pos: 0; nodes_extracted: 25; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 58.18; age_bin: 1; ki67: 5; idfs_event: 0; idfs_time (years): 5.33; ddfs_event: 0; ddfs_time (years): 5.33; os_event: 0; os_time (years): 5.33; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-47; geo_accn_gse20713_27k: GSM553851; subtype_ihc: LumB; itu-ly: 0; str-ly: 2; grade: 3; size_bin: 0; size_cm: 1.3; nodes_pos: 0; nodes_extracted: 1; nodal_status: 0; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 59.75; age_bin: 1; ki67: 15; idfs_event: 0; idfs_time (years): 4.93; ddfs_event: 0; ddfs_time (years): 4.93; os_event: 0; os_time (years): 4.93; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-48; geo_accn_gse20713_27k: GSM553842; subtype_ihc: LumB; itu-ly: 5; str-ly: 30; grade: 3; size_bin: 0; size_cm: 1.5; nodes_pos: 2; nodes_extracted: 15; nodal_status: 1; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 61.9; age_bin: 1; ki67: 30; idfs_event: 0; idfs_time (years): 5.16; ddfs_event: 0; ddfs_time (years): 5.16; os_event: 0; os_time (years): 5.16; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-49; geo_accn_gse20713_27k: GSM553844; subtype_ihc: LumB; itu-ly: 2; str-ly: 15; grade: 3; size_bin: 1; size_cm: 3.8; nodes_pos: 6; nodes_extracted: 16; nodal_status: 1; er_score: 6; er_score_max: 8; er_ihc_status: 1; pgr_score: 4; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 71.43; age_bin: 1; ki67: 25; idfs_event: 0; idfs_time (years): 5.5; ddfs_event: 0; ddfs_time (years): 5.5; os_event: 0; os_time (years): 5.5; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-50; geo_accn_gse20713_27k: GSM553853; subtype_ihc: LumB; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 1; size_cm: 2.3; nodes_pos: 1; nodes_extracted: 14; nodal_status: 1; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 7; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 82.52; age_bin: 1; ki67: 25; idfs_event: 0; idfs_time (years): 4.22; ddfs_event: 0; ddfs_time (years): 4.22; os_event: 0; os_time (years): 4.22; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-51; geo_accn_gse20713_27k: GSM553852; subtype_ihc: LumB; itu-ly: 0; str-ly: 5; grade: null; size_bin: null; size_cm: null; nodal_status: 1; er_score: null; er_score_max: 8; er_ihc_status: 1; pgr_score: null; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 44.47; age_bin: 0; ki67: null; idfs_event: 0; idfs_time (years): 1.04; ddfs_event: 0; ddfs_time (years): 1.04; os_event: 0; os_time (years): 1.04; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-52; geo_accn_gse20713_27k: GSM553843; subtype_ihc: LumB; itu-ly: null; str-ly: null; grade: 3; size_bin: 1; size_cm: 3; nodes_pos: 1; nodes_extracted: 5; nodal_status: 1; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 6; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 35.81; age_bin: 0; ki67: 17.5; idfs_event: 0; idfs_time (years): 2.82; ddfs_event: 0; ddfs_time (years): 2.82; os_event: 0; os_time (years): 2.82; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-53; geo_accn_gse20713_27k: GSM553848; subtype_ihc: LumB; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 1; size_cm: 2.1; nodes_pos: 11; nodes_extracted: 23; nodal_status: 1; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 5; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 67.95; age_bin: 1; ki67: 15; idfs_event: 0; idfs_time (years): 1.13; ddfs_event: 0; ddfs_time (years): 1.13; os_event: 0; os_time (years): 1.13; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-54; geo_accn_gse20713_27k: GSM553849; subtype_ihc: LumB; itu-ly: 5; str-ly: 35; grade: 3; size_bin: 0; size_cm: 1.9; nodes_pos: 0; nodes_extracted: 20; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 76.12; age_bin: 1; ki67: 35; idfs_event: 0; idfs_time (years): 7.24; ddfs_event: 0; ddfs_time (years): 7.24; os_event: 0; os_time (years): 7.24; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-55; geo_accn_gse20713_27k: GSM553850; subtype_ihc: LumB; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 0; size_cm: 1.5; nodes_pos: 1; nodes_extracted: 14; nodal_status: 1; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 7; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 51.38; age_bin: 1; ki67: 30; idfs_event: 0; idfs_time (years): 6.64; ddfs_event: 0; ddfs_time (years): 6.64; os_event: 0; os_time (years): 6.64; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-56; geo_accn_gse20713_27k: GSM553845; subtype_ihc: LumB; itu-ly: 5; str-ly: 15; grade: 3; size_bin: 0; size_cm: 1.5; nodes_pos: 0; nodes_extracted: 4; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 48.23; age_bin: 0; ki67: 20; idfs_event: 0; idfs_time (years): 7.55; ddfs_event: 0; ddfs_time (years): 7.55; os_event: 0; os_time (years): 7.55; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-57; geo_accn_gse20713_27k: GSM553846; subtype_ihc: LumB; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 1; size_cm: 2.9; nodes_pos: 0; nodes_extracted: 25; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 7; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 74.48; age_bin: 1; ki67: 17.5; idfs_event: 1; idfs_time (years): 3.38; ddfs_event: 1; ddfs_time (years): 3.38; os_event: 1; os_time (years): 7.39; date_death: 14 December 2011; cause_death: general conditions; ', 'tissue: breast tumor; cohort id: 2-58; geo_accn_gse20713_27k: GSM553847; subtype_ihc: LumB; itu-ly: 0; str-ly: 2; grade: 3; size_bin: 0; size_cm: 1.6; nodes_pos: 1; nodes_extracted: 14; nodal_status: 1; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 6; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: 1.26; her2_fish_bin: 0; age_diagnosis: 70.49; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 8.05; ddfs_event: 0; ddfs_time (years): 8.05; os_event: 0; os_time (years): 8.05; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-59; geo_accn_gse20713_27k: GSM553801; subtype_ihc: HER2; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 1; size_cm: 3.5; nodes_pos: 1; nodes_extracted: 18; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 4.33; her2_fish_bin: 1; age_diagnosis: 73.53; age_bin: 1; ki67: 25; idfs_event: 0; idfs_time (years): 4.48; ddfs_event: 0; ddfs_time (years): 4.48; os_event: 0; os_time (years): 4.48; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-60; geo_accn_gse20713_27k: GSM553802; subtype_ihc: HER2; itu-ly: 5; str-ly: 20; grade: 3; size_bin: 0; size_cm: 1.8; nodes_pos: 0; nodes_extracted: 26; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 3.82; her2_fish_bin: 1; age_diagnosis: 58.77; age_bin: 1; ki67: 30; idfs_event: 0; idfs_time (years): 4.09; ddfs_event: 0; ddfs_time (years): 4.09; os_event: 0; os_time (years): 4.09; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-61; geo_accn_gse20713_27k: GSM553803; subtype_ihc: HER2; itu-ly: 5; str-ly: 40; grade: 3; size_bin: 1; size_cm: 2.1; nodes_pos: 7; nodes_extracted: 12; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 8.1; her2_fish_bin: 1; age_diagnosis: 31.44; age_bin: 0; ki67: 70; idfs_event: 0; idfs_time (years): 4.58; ddfs_event: 0; ddfs_time (years): 4.58; os_event: 0; os_time (years): 4.58; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-62; geo_accn_gse20713_27k: GSM553804; subtype_ihc: HER2; itu-ly: 2; str-ly: 20; grade: 3; size_bin: 1; size_cm: 3.3; nodes_pos: 2; nodes_extracted: 16; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 12.5; her2_fish_bin: 1; age_diagnosis: 76.64; age_bin: 1; ki67: 12.5; idfs_event: 1; idfs_time (years): 1.17; ddfs_event: 0; ddfs_time (years): 4.62; os_event: 0; os_time (years): 4.62; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-63; geo_accn_gse20713_27k: GSM553805; subtype_ihc: HER2; itu-ly: 2; str-ly: 60; grade: 3; size_bin: 1; size_cm: 2.1; nodes_pos: 1; nodes_extracted: 23; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 10.3; her2_fish_bin: 1; age_diagnosis: 60.48; age_bin: 1; ki67: 20; idfs_event: 0; idfs_time (years): 4.16; ddfs_event: 0; ddfs_time (years): 4.16; os_event: 0; os_time (years): 4.16; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-64; geo_accn_gse20713_27k: GSM553806; subtype_ihc: HER2; itu-ly: 0; str-ly: 2; grade: 3; size_bin: 1; size_cm: 6; nodes_pos: 0; nodes_extracted: 16; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 6.2; her2_fish_bin: 1; age_diagnosis: 40.94; age_bin: 0; ki67: 90; idfs_event: 0; idfs_time (years): 4.69; ddfs_event: 0; ddfs_time (years): 4.69; os_event: 0; os_time (years): 4.69; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-65; geo_accn_gse20713_27k: GSM553799; subtype_ihc: HER2; itu-ly: 2; str-ly: 15; grade: 2; size_bin: 1; size_cm: 3; nodes_pos: 10; nodes_extracted: 28; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 8; her2_fish_bin: 1; age_diagnosis: 46.85; age_bin: 0; ki67: 50; idfs_event: 1; idfs_time (years): 3.14; ddfs_event: 1; ddfs_time (years): 3.35; os_event: 1; os_time (years): 4.12; date_death: 01 April 2011; cause_death: cancer; ', 'tissue: breast tumor; cohort id: 2-66; geo_accn_gse20713_27k: GSM553800; subtype_ihc: HER2; itu-ly: 50; str-ly: 5; grade: 3; size_bin: 1; size_cm: 5.5; nodes_pos: 3; nodes_extracted: 19; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 3.9; her2_fish_bin: 1; age_diagnosis: 57.32; age_bin: 1; ki67: 40; idfs_event: 0; idfs_time (years): 5.2; ddfs_event: 0; ddfs_time (years): 5.2; os_event: 0; os_time (years): 5.2; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-67; geo_accn_gse20713_27k: GSM553807; subtype_ihc: HER2; itu-ly: null; str-ly: null; grade: 3; size_bin: 1; size_cm: 2.2; nodes_pos: 2; nodes_extracted: 12; nodal_status: 1; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 3.32; her2_fish_bin: 1; age_diagnosis: 66.5; age_bin: 1; ki67: 40; idfs_event: 0; idfs_time (years): 3.68; ddfs_event: 0; ddfs_time (years): 3.68; os_event: 0; os_time (years): 3.68; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-68; geo_accn_gse20713_27k: GSM553788; subtype_ihc: HER2; itu-ly: 2; str-ly: 20; grade: 3; size_bin: 1; size_cm: 4; nodes_pos: 2; nodes_extracted: 10; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 3; pgr_score_max: 8; pgr_status: 1; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 11.3; her2_fish_bin: 1; age_diagnosis: 40.67; age_bin: 0; ki67: 30; idfs_event: 0; idfs_time (years): 2.99; ddfs_event: 0; ddfs_time (years): 2.99; os_event: 0; os_time (years): 2.99; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-69; geo_accn_gse20713_27k: GSM553789; subtype_ihc: HER2; itu-ly: 5; str-ly: 50; grade: 3; size_bin: 0; size_cm: 1.7; nodes_pos: 6; nodes_extracted: 17; nodal_status: 1; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 5; pgr_score_max: 8; pgr_status: 1; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 4.56; her2_fish_bin: 1; age_diagnosis: 39.36; age_bin: 0; ki67: 25; idfs_event: 0; idfs_time (years): 2.18; ddfs_event: 0; ddfs_time (years): 2.18; os_event: 0; os_time (years): 2.18; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-70; geo_accn_gse20713_27k: GSM553790; subtype_ihc: HER2; itu-ly: 5; str-ly: 5; grade: 3; size_bin: 0; size_cm: 1.4; nodes_pos: 0; nodes_extracted: 7; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 1; her2_ihc: NK; her2_ihc_max: 3; her2_fish: NK; her2_fish_bin: 1; age_diagnosis: 60.75; age_bin: 1; ki67: 25; idfs_event: 0; idfs_time (years): 0.51; ddfs_event: 0; ddfs_time (years): 0.51; os_event: 0; os_time (years): 0.51; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-71; geo_accn_gse20713_27k: GSM553785; subtype_ihc: HER2; itu-ly: 5; str-ly: 35; grade: 3; size_bin: 1; size_cm: 3.5; nodes_pos: 1; nodes_extracted: 16; nodal_status: 1; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 11.05; her2_fish_bin: 1; age_diagnosis: 62.77; age_bin: 1; ki67: 30; idfs_event: 0; idfs_time (years): 5.27; ddfs_event: 0; ddfs_time (years): 5.27; os_event: 0; os_time (years): 5.27; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-72; geo_accn_gse20713_27k: GSM553786; subtype_ihc: HER2; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 0; size_cm: 1.7; nodes_pos: 1; nodes_extracted: 14; nodal_status: 1; er_score: 7; er_score_max: 8; er_ihc_status: 1; pgr_score: 3; pgr_score_max: 8; pgr_status: 1; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 15.2; her2_fish_bin: 1; age_diagnosis: 48.72; age_bin: 0; ki67: 70; idfs_event: 0; idfs_time (years): 2.84; ddfs_event: 0; ddfs_time (years): 2.84; os_event: 0; os_time (years): 2.84; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-73; geo_accn_gse20713_27k: GSM553787; subtype_ihc: HER2; itu-ly: 0; str-ly: 2; grade: 3; size_bin: 1; size_cm: 11; nodes_pos: 16; nodes_extracted: 16; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 16.1; her2_fish_bin: 1; age_diagnosis: 35.05; age_bin: 0; ki67: 50; idfs_event: 1; idfs_time (years): 1.25; ddfs_event: 1; ddfs_time (years): 2.59; os_event: 1; os_time (years): 4.38; date_death: 18 June 2007; cause_death: cancer; ', 'tissue: breast tumor; cohort id: 2-74; geo_accn_gse20713_27k: GSM553783; subtype_ihc: HER2; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.2; nodes_pos: 0; nodes_extracted: 1; nodal_status: 0; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 11.5; her2_fish_bin: 1; age_diagnosis: 77.95; age_bin: 1; ki67: 25; idfs_event: 0; idfs_time (years): 5; ddfs_event: 0; ddfs_time (years): 5; os_event: 0; os_time (years): 5; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-75; geo_accn_gse20713_27k: GSM553784; subtype_ihc: HER2; itu-ly: 0; str-ly: 15; grade: 3; size_bin: 0; size_cm: 1.1; nodes_pos: 3; nodes_extracted: 16; nodal_status: 1; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 5; pgr_score_max: 8; pgr_status: 1; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 12.78; her2_fish_bin: 1; age_diagnosis: 62.16; age_bin: 1; ki67: 30; idfs_event: 0; idfs_time (years): 3.47; ddfs_event: 0; ddfs_time (years): 3.47; os_event: 0; os_time (years): 3.47; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-76; geo_accn_gse20713_27k: GSM553791; subtype_ihc: HER2; itu-ly: 0; str-ly: 5; grade: 2; size_bin: 0; size_cm: 1.3; nodes_pos: 0; nodes_extracted: 2; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 7.83; her2_fish_bin: 1; age_diagnosis: 59.42; age_bin: 1; ki67: 20; idfs_event: 0; idfs_time (years): 3.4; ddfs_event: 0; ddfs_time (years): 3.4; os_event: 0; os_time (years): 3.4; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-77; geo_accn_gse20713_27k: GSM553792; subtype_ihc: HER2; itu-ly: 0; str-ly: 2; grade: 2; size_bin: 0; size_cm: 2; nodes_pos: 0; nodes_extracted: 1; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 6.08; her2_fish_bin: 1; age_diagnosis: 55.42; age_bin: 1; ki67: 15; idfs_event: 1; idfs_time (years): 21.18; ddfs_event: 1; ddfs_time (years): 21.18; os_event: 1; os_time (years): 27.33; date_death: 24 March 2011; cause_death: cancer; ', 'tissue: breast tumor; cohort id: 2-79; geo_accn_gse20713_27k: GSM553798; subtype_ihc: HER2; itu-ly: 15; str-ly: 10; grade: 3; size_bin: 1; size_cm: 4; nodes_pos: 0; nodes_extracted: 14; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 7.5; her2_fish_bin: 1; age_diagnosis: 71.38; age_bin: 1; ki67: 75; idfs_event: 0; idfs_time (years): 3.8; ddfs_event: 0; ddfs_time (years): 3.8; os_event: 0; os_time (years): 3.8; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-80; geo_accn_gse20713_27k: GSM553795; subtype_ihc: HER2; itu-ly: 2; str-ly: 30; grade: 3; size_bin: 0; size_cm: 1.9; nodes_pos: 0; nodes_extracted: 16; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 12.45; her2_fish_bin: 1; age_diagnosis: 48.91; age_bin: 0; ki67: 40; idfs_event: 0; idfs_time (years): 4.12; ddfs_event: 0; ddfs_time (years): 4.12; os_event: 0; os_time (years): 4.12; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-81; geo_accn_gse20713_27k: GSM553796; subtype_ihc: HER2; itu-ly: null; str-ly: null; grade: 2; size_bin: 0; size_cm: 1.7; nodes_pos: 2; nodes_extracted: 12; nodal_status: 1; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 5.77; her2_fish_bin: 1; age_diagnosis: 60.19; age_bin: 1; ki67: 35; idfs_event: 1; idfs_time (years): 1.95; ddfs_event: 1; ddfs_time (years): 1.95; os_event: 0; os_time (years): 3.31; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-82; geo_accn_gse20713_27k: GSM553794; subtype_ihc: HER2; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 0; size_cm: 1.5; nodes_pos: 1; nodes_extracted: 24; nodal_status: 1; er_score: 8; er_score_max: 8; er_ihc_status: 1; pgr_score: 8; pgr_score_max: 8; pgr_status: 1; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 2; her2_fish_bin: 1; age_diagnosis: 79.85; age_bin: 1; ki67: 20; idfs_event: 0; idfs_time (years): 0.94; ddfs_event: 0; ddfs_time (years): 0.94; os_event: 0; os_time (years): 0 .94; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-83; geo_accn_gse20713_27k: GSM553793; subtype_ihc: HER2; itu-ly: null; str-ly: null; grade: 3; size_bin: 1; size_cm: 14; nodes_pos: 5; nodes_extracted: 15; nodal_status: 1; er_score: 4; er_score_max: 8; er_ihc_status: 1; pgr_score: 2; pgr_score_max: 8; pgr_status: 0*; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 12; her2_fish_bin: 1; age_diagnosis: 37.99; age_bin: 0; ki67: 15; idfs_event: 1; idfs_time (years): 13.62; ddfs_event: 1; ddfs_time (years): 13.62; os_event: 0; os_time (years): 20.25; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-84; geo_accn_gse20713_27k: GSM553797; subtype_ihc: HER2; itu-ly: null; str-ly: null; grade: 3; size_bin: 1; size_cm: 3.4; nodes_pos: 1; nodes_extracted: 18; nodal_status: 1; er_score: 6; er_score_max: 8; er_ihc_status: 1; pgr_score: 3; pgr_score_max: 8; pgr_status: 1; her2_status: 1; her2_ihc: 3; her2_ihc_max: 3; her2_fish: 8.67; her2_fish_bin: 1; age_diagnosis: 82.83; age_bin: 1; ki67: 40; idfs_event: 0; idfs_time (years): 3.71; ddfs_event: 0; ddfs_time (years): 3.71; os_event: 0; os_time (years): 3.71; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-85; geo_accn_gse20713_27k: GSM553774; subtype_ihc: Basal; itu-ly: 5; str-ly: 40; grade: 3; size_bin: 0; size_cm: 1.6; nodes_pos: 0; nodes_extracted: 1; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 59.77; age_bin: 1; ki67: 60; idfs_event: 0; idfs_time (years): 7.31; ddfs_event: 0; ddfs_time (years): 7.31; os_event: 0; os_time (years): 7.31; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-86; geo_accn_gse20713_27k: GSM553775; subtype_ihc: Basal; itu-ly: 5; str-ly: 70; grade: 3; size_bin: 1; size_cm: 4.3; nodes_pos: 0; nodes_extracted: 8; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 78.39; age_bin: 1; ki67: 55; idfs_event: 1; idfs_time (years): 2.73; ddfs_event: 0; ddfs_time (years): 3.75; os_event: 0; os_time (years): 3.75; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-87; geo_accn_gse20713_27k: GSM553753; subtype_ihc: Basal; itu-ly: 5; str-ly: 100; grade: 3; size_bin: 0; size_cm: 1.6; nodes_pos: 1; nodes_extracted: 7; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 57.6; age_bin: 1; ki67: 50; idfs_event: 0; idfs_time (years): 7.2; ddfs_event: 0; ddfs_time (years): 7.2; os_event: 0; os_time (years): 7.2; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-88; geo_accn_gse20713_27k: GSM553776; subtype_ihc: Basal; itu-ly: 0; str-ly: 15; grade: 3; size_bin: 1; size_cm: 2.8; nodes_pos: 0; nodes_extracted: 12; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 35.27; age_bin: 0; ki67: 80; idfs_event: 0; idfs_time (years): 5; ddfs_event: 0; ddfs_time (years): 5; os_event: 0; os_time (years): 5; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-89; geo_accn_gse20713_27k: GSM553777; subtype_ihc: Basal; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.8; nodes_pos: 0; nodes_extracted: 18; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 53.92; age_bin: 1; ki67: 70; idfs_event: 0; idfs_time (years): 5.7; ddfs_event: 0; ddfs_time (years): 5.7; os_event: 0; os_time (years): 5.7; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-90; geo_accn_gse20713_27k: GSM553754; subtype_ihc: Basal; itu-ly: 30; str-ly: 20; grade: 3; size_bin: 1; size_cm: 3; nodes_pos: 0; nodes_extracted: 8; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 66.91; age_bin: 1; ki67: 100; idfs_event: 0; idfs_time (years): 3.07; ddfs_event: 0; ddfs_time (years): 3.07; os_event: 0; os_time (years): 3.07; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-91; geo_accn_gse20713_27k: GSM553778; subtype_ihc: Basal; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 1; size_cm: 3; nodes_pos: 9; nodes_extracted: 18; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 33.14; age_bin: 0; ki67: 60; idfs_event: 0; idfs_time (years): 2.34; ddfs_event: 0; ddfs_time (years): 2.34; os_event: 1; os_time (years): 2.34; date_death: 01 October 2005; cause_death: cancer; ', 'tissue: breast tumor; cohort id: 2-92; geo_accn_gse20713_27k: GSM553779; subtype_ihc: Basal; itu-ly: 0; str-ly: 15; grade: 3; size_bin: 1; size_cm: 3; nodes_pos: 4; nodes_extracted: 18; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 67.61; age_bin: 1; ki67: 20; idfs_event: 0; idfs_time (years): 2.38; ddfs_event: 0; ddfs_time (years): 2.38; os_event: 1; os_time (years): 2.38; date_death: 14 June 2006; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-93; geo_accn_gse20713_27k: GSM553780; subtype_ihc: Basal; itu-ly: 2; str-ly: 35; grade: 3; size_bin: 0; size_cm: 1.9; nodes_pos: 1; nodes_extracted: 13; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 63.8; age_bin: 1; ki67: 75; idfs_event: 0; idfs_time (years): 7.65; ddfs_event: 0; ddfs_time (years): 7.65; os_event: 0; os_time (years): 7.65; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-94; geo_accn_gse20713_27k: GSM553781; subtype_ihc: Basal; itu-ly: 50; str-ly: 20; grade: 3; size_bin: 0; size_cm: 0.9; nodes_pos: 0; nodes_extracted: 1; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 80.7; age_bin: 1; ki67: 50; idfs_event: 0; idfs_time (years): 2.42; ddfs_event: 0; ddfs_time (years): 2.42; os_event: 0; os_time (years): 2.42; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-95; geo_accn_gse20713_27k: GSM553773; subtype_ihc: Basal; itu-ly: 0; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.8; nodes_pos: 1; nodes_extracted: 9; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 41.93; age_bin: 0; ki67: 80; idfs_event: 0; idfs_time (years): 7.22; ddfs_event: 0; ddfs_time (years): 7.22; os_event: 0; os_time (years): 7.22; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-96; geo_accn_gse20713_27k: GSM553782; subtype_ihc: Basal; itu-ly: 0; str-ly: 1; grade: 3; size_bin: 1; size_cm: 5.5; nodes_pos: 12; nodes_extracted: 16; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 82.12; age_bin: 1; ki67: 15; idfs_event: 1; idfs_time (years): 1.13; ddfs_event: 1; ddfs_time (years): 1.94; os_event: 1; os_time (years): 3.5; date_death: 09 June 2007; cause_death: cancer; ', 'tissue: breast tumor; cohort id: 2-97; geo_accn_gse20713_27k: GSM553771; subtype_ihc: Basal; itu-ly: 15; str-ly: 35; grade: 3; size_bin: 0; size_cm: 1.6; nodes_pos: 0; nodes_extracted: 13; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 39.32; age_bin: 0; ki67: 80; idfs_event: 1; idfs_time (years): 1.44; ddfs_event: 1; ddfs_time (years): 1.44; os_event: 0; os_time (years): 1.7; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-98; geo_accn_gse20713_27k: GSM553772; subtype_ihc: Basal; itu-ly: 10; str-ly: 25; grade: 3; size_bin: 0; size_cm: 1.1; nodes_pos: 0; nodes_extracted: 2; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 50.56; age_bin: 1; ki67: 80; idfs_event: 0; idfs_time (years): 0.02; ddfs_event: 0; ddfs_time (years): 0.02; os_event: 0; os_time (years): 0.02; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-99; geo_accn_gse20713_27k: GSM553755; subtype_ihc: Basal; itu-ly: 5; str-ly: 30; grade: 2; size_bin: 0; size_cm: 0.7; nodes_pos: 3; nodes_extracted: 7; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 56.84; age_bin: 1; ki67: 90; idfs_event: 1; idfs_time (years): 0.53; ddfs_event: 1; ddfs_time (years): 0.73; os_event: 1; os_time (years): 1.25; date_death: 14 February 2007; cause_death: cancer; ', 'tissue: breast tumor; cohort id: 2-100; geo_accn_gse20713_27k: null; subtype_ihc: null; itu-ly: 5; str-ly: 30; grade: 3; size_bin: 0; size_cm: 1.8; nodes_pos: 0; nodes_extracted: 13; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 1; her2_ihc_max: 3; her2_fish: 1.31; her2_fish_bin: 0; age_diagnosis: 47.72; age_bin: 0; ki67: 60; idfs_event: 0; idfs_time (years): 6.03; ddfs_event: 0; ddfs_time (years): 6.03; os_event: 0; os_time (years): 6.03; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-101; geo_accn_gse20713_27k: GSM553751; subtype_ihc: Basal; itu-ly: 2; str-ly: 15; grade: 3; size_bin: 1; size_cm: 4; nodes_pos: 0; nodes_extracted: 25; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 68.97; age_bin: 1; ki67: 20; idfs_event: 0; idfs_time (years): 0.96; ddfs_event: 0; ddfs_time (years): 0.96; os_event: 0; os_time (years): 0.96; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-102; geo_accn_gse20713_27k: GSM553752; subtype_ihc: Basal; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 0; size_cm: 0.4; nodes_pos: 0; nodes_extracted: 14; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 72.99; age_bin: 1; ki67: 60; idfs_event: 0; idfs_time (years): 4.89; ddfs_event: 0; ddfs_time (years): 4.89; os_event: 0; os_time (years): 4.89; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-103; geo_accn_gse20713_27k: GSM553749; subtype_ihc: Basal; itu-ly: 5; str-ly: 20; grade: 3; size_bin: 1; size_cm: 5.5; nodes_pos: 1; nodes_extracted: 16; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 56.54; age_bin: 1; ki67: 30; idfs_event: 0; idfs_time (years): 5.14; ddfs_event: 0; ddfs_time (years): 5.14; os_event: 0; os_time (years): 5.14; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-104; geo_accn_gse20713_27k: GSM553748; subtype_ihc: Basal; itu-ly: 60; str-ly: 40; grade: 3; size_bin: 1; size_cm: 3; nodes_pos: 0; nodes_extracted: 20; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 65.38; age_bin: 1; ki67: 90; idfs_event: 0; idfs_time (years): 4.65; ddfs_event: 0; ddfs_time (years): 4.65; os_event: 0; os_time (years): 4.65; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-105; geo_accn_gse20713_27k: GSM553750; subtype_ihc: Basal; itu-ly: 1; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.4; nodes_pos: 0; nodes_extracted: 3; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 55.48; age_bin: 1; ki67: 30; idfs_event: 1; idfs_time (years): 1.09; ddfs_event: 1; ddfs_time (years): 1.09; os_event: 0; os_time (years): 4.75; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-106; geo_accn_gse20713_27k: GSM553757; subtype_ihc: Basal; itu-ly: 5; str-ly: 45; grade: 3; size_bin: 0; size_cm: 0.8; nodes_pos: 0; nodes_extracted: 2; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 60.21; age_bin: 1; ki67: 70; idfs_event: 0; idfs_time (years): 3.81; ddfs_event: 0; ddfs_time (years): 3.81; os_event: 0; os_time (years): 3.81; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-107; geo_accn_gse20713_27k: GSM553758; subtype_ihc: Basal; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 0; size_cm: 1.6; nodes_pos: 0; nodes_extracted: 21; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 36.96; age_bin: 0; ki67: 80; idfs_event: 0; idfs_time (years): 4.44; ddfs_event: 0; ddfs_time (years): 4.44; os_event: 0; os_time (years): 4.44; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-108; geo_accn_gse20713_27k: GSM553769; subtype_ihc: Basal; itu-ly: 5; str-ly: 60; grade: 3; size_bin: 1; size_cm: 2.9; nodes_pos: 0; nodes_extracted: 11; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 72.29; age_bin: 1; ki67: 50; idfs_event: 1; idfs_time (years): 0.82; ddfs_event: 1; ddfs_time (years): 0.82; os_event: 1; os_time (years): 1.01; date_death: 25 June 2008; cause_death: cancer; ', 'tissue: breast tumor; cohort id: 2-109; geo_accn_gse20713_27k: GSM553756; subtype_ihc: Basal; itu-ly: 1; str-ly: 25; grade: 3; size_bin: 1; size_cm: 2.2; nodes_pos: 3; nodes_extracted: 22; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 46.73; age_bin: 0; ki67: 90; idfs_event: 0; idfs_time (years): 1.96; ddfs_event: 0; ddfs_time (years): 1.96; os_event: 0; os_time (years): 1.96; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-110; geo_accn_gse20713_27k: GSM553767; subtype_ihc: LumB; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 0; size_cm: 1.5; nodes_pos: 2; nodes_extracted: 18; nodal_status: 1; er_score: 6; er_score_max: 8; er_ihc_status: 1; pgr_score: 7; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 41.4; age_bin: 0; ki67: 15; idfs_event: 0; idfs_time (years): 4.32; ddfs_event: 0; ddfs_time (years): 4.32; os_event: 0; os_time (years): 4.32; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-111; geo_accn_gse20713_27k: GSM553768; subtype_ihc: Basal; itu-ly: 0; str-ly: 15; grade: 3; size_bin: 0; size_cm: 1.8; nodes_pos: 2; nodes_extracted: 16; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 65.58; age_bin: 1; ki67: 90; idfs_event: 0; idfs_time (years): 3.42; ddfs_event: 0; ddfs_time (years): 3.42; os_event: 0; os_time (years): 3.42; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-112; geo_accn_gse20713_27k: GSM553770; subtype_ihc: Basal; itu-ly: 2; str-ly: 10; grade: 3; size_bin: 0; size_cm: 1.8; nodes_pos: 1; nodes_extracted: 33; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 35.15; age_bin: 0; ki67: 80; idfs_event: 1; idfs_time (years): 1.9; ddfs_event: 1; ddfs_time (years): 1.9; os_event: 1; os_time (years): 3.01; date_death: 25 September 2009; cause_death: cancer; ', 'tissue: breast tumor; cohort id: 2-113; geo_accn_gse20713_27k: GSM553763; subtype_ihc: Basal; itu-ly: 0; str-ly: 5; grade: 3; size_bin: 0; size_cm: 1.7; nodes_pos: 1; nodes_extracted: 13; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 60.16; age_bin: 1; ki67: 30; idfs_event: 0; idfs_time (years): 4.99; ddfs_event: 0; ddfs_time (years): 4.99; os_event: 0; os_time (years): 4.99; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-114; geo_accn_gse20713_27k: GSM553764; subtype_ihc: Basal; itu-ly: 1; str-ly: 30; grade: 3; size_bin: 0; size_cm: 1.1; nodes_pos: 0; nodes_extracted: 2; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 60.96; age_bin: 1; ki67: 10; idfs_event: 0; idfs_time (years): 3.06; ddfs_event: 0; ddfs_time (years): 3.06; os_event: 0; os_time (years): 3.06; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-115; geo_accn_gse20713_27k: GSM553765; subtype_ihc: Basal; itu-ly: 15; str-ly: 60; grade: 3; size_bin: 1; size_cm: 2.2; nodes_pos: 0; nodes_extracted: 12; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 55.99; age_bin: 1; ki67: 70; idfs_event: 0; idfs_time (years): 3.61; ddfs_event: 0; ddfs_time (years): 3.61; os_event: 0; os_time (years): 3.61; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-116; geo_accn_gse20713_27k: GSM553766; subtype_ihc: Basal; itu-ly: 1; str-ly: 20; grade: 3; size_bin: 0; size_cm: 1.4; nodes_pos: 0; nodes_extracted: 2; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 3; pgr_score_max: 8; pgr_status: 1; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 23.38; age_bin: 0; ki67: 80; idfs_event: 0; idfs_time (years): 3.18; ddfs_event: 0; ddfs_time (years): 3.18; os_event: 0; os_time (years): 3.18; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-117; geo_accn_gse20713_27k: GSM553760; subtype_ihc: Basal; itu-ly: null; str-ly: null; grade: 3; size_bin: 1; size_cm: 4.2; nodes_pos: 0; nodes_extracted: 16; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 38.92; age_bin: 0; ki67: 90; idfs_event: 0; idfs_time (years): 3.53; ddfs_event: 0; ddfs_time (years): 3.53; os_event: 0; os_time (years): 3.53; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-118; geo_accn_gse20713_27k: GSM553761; subtype_ihc: Basal; itu-ly: 5; str-ly: 40; grade: 3; size_bin: 1; size_cm: 2.2; nodes_pos: 37; nodes_extracted: 51; nodal_status: 1; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 48.9; age_bin: 0; ki67: 95; idfs_event: 0; idfs_time (years): 2.07; ddfs_event: 0; ddfs_time (years): 2.07; os_event: 0; os_time (years): 2.07; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-119; geo_accn_gse20713_27k: GSM553762; subtype_ihc: Basal; itu-ly: null; str-ly: null; grade: 3; size_bin: 0; size_cm: 1.9; nodes_pos: 0; nodes_extracted: 13; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 50.99; age_bin: 1; ki67: 80; idfs_event: 0; idfs_time (years): 2.06; ddfs_event: 0; ddfs_time (years): 2.06; os_event: 0; os_time (years): 2.06; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 2-120; geo_accn_gse20713_27k: GSM553759; subtype_ihc: Basal; itu-ly: 5; str-ly: 30; grade: 3; size_bin: 1; size_cm: 2.1; nodes_pos: 0; nodes_extracted: 20; nodal_status: 0; er_score: 0; er_score_max: 8; er_ihc_status: 0; pgr_score: 0; pgr_score_max: 8; pgr_status: 0; her2_status: 0; her2_ihc: 0; her2_ihc_max: 3; her2_fish: null; her2_fish_bin: null; age_diagnosis: 41.24; age_bin: 0; ki67: 80; idfs_event: 0; idfs_time (years): 2.18; ddfs_event: 0; ddfs_time (years): 2.18; os_event: 0; os_time (years): 2.18; date_death: null; cause_death: null; ', 'tissue: breast tumor; cohort id: 1109; geo_accn_gse16446: GSM411332; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.13; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 693; dmfs_event: 0; dmfs_time (days): 693; pcr: 0; ', 'tissue: breast tumor; cohort id: 123; geo_accn_gse16446: GSM411364; grade: 3; t: T1; n: N0; esr1bimod: 0; her2_fish: 2.34; her2_fish_bin: 1; erbb2bimod: 0; age_bin: 1; os_event: null; os_time (days): null; dmfs_event: null; dmfs_time (days): null; pcr: 0; ', 'tissue: breast tumor; cohort id: 1312; geo_accn_gse16446: GSM411363; grade: 3; t: T1; n: N0; esr1bimod: 0; her2_fish: 6.37; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 860; dmfs_event: 0; dmfs_time (days): 860; pcr: 0; ', 'tissue: breast tumor; cohort id: 1366; geo_accn_gse16446: GSM411346; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.18; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 1404; dmfs_event: 0; dmfs_time (days): 1404; pcr: 0; ', 'tissue: breast tumor; cohort id: 1391; geo_accn_gse16446: GSM411300; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 6.96; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 1; os_event: 0; os_time (days): 1082; dmfs_event: 0; dmfs_time (days): 1082; pcr: 0; ', 'tissue: breast tumor; cohort id: 1536; geo_accn_gse16446: GSM411407; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 11.56; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 620; dmfs_event: 0; dmfs_time (days): 620; pcr: 1; ', 'tissue: breast tumor; cohort id: 1674; geo_accn_gse16446: GSM411371; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 1852; dmfs_event: 0; dmfs_time (days): 1852; pcr: 0; ', 'tissue: breast tumor; cohort id: 1767; geo_accn_gse16446: GSM411402; grade: 2; t: T2; n: N0; esr1bimod: 0; her2_fish: 2.25; her2_fish_bin: 1; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 2011; dmfs_event: 0; dmfs_time (days): 2011; pcr: 1; ', 'tissue: breast tumor; cohort id: 2090; geo_accn_gse16446: GSM411360; grade: 3; t: T4; n: N1; esr1bimod: 0; her2_fish: 1.76; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 1; os_time (days): null; dmfs_event: 1; dmfs_time (days): null; pcr: 0; ', 'tissue: breast tumor; cohort id: 2165; geo_accn_gse16446: GSM411366; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 4.55; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 991; dmfs_event: 0; dmfs_time (days): 991; pcr: 0; ', 'tissue: breast tumor; cohort id: 220; geo_accn_gse16446: GSM411324; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.05; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1358; dmfs_event: 0; dmfs_time (days): 1358; pcr: 0; ', 'tissue: breast tumor; cohort id: 2325; geo_accn_gse16446: GSM411293; grade: 3; t: T4; n: N1; esr1bimod: 0; her2_fish: 4.29; her2_fish_bin: 1; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 675; dmfs_event: 0; dmfs_time (days): 675; pcr: 0; ', 'tissue: breast tumor; cohort id: 2337; geo_accn_gse16446: GSM411326; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.06; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 710; dmfs_event: 0; dmfs_time (days): 710; pcr: 0; ', 'tissue: breast tumor; cohort id: 2744; geo_accn_gse16446: GSM411369; grade: 3; t: T1; n: N3; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 2069; dmfs_event: 0; dmfs_time (days): 2069; pcr: 0; ', 'tissue: breast tumor; cohort id: 3276; geo_accn_gse16446: GSM411333; grade: 3; t: T1; n: N0; esr1bimod: 0; her2_fish: 1.07; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1041; dmfs_event: 0; dmfs_time (days): 1041; pcr: 0; ', 'tissue: breast tumor; cohort id: 3414; geo_accn_gse16446: GSM411351; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 7.5; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 1; os_event: 0; os_time (days): 2187; dmfs_event: 1; dmfs_time (days): 254; pcr: 0; ', 'tissue: breast tumor; cohort id: 3731; geo_accn_gse16446: GSM411294; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 4.67; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 845; dmfs_event: 0; dmfs_time (days): 845; pcr: 0; ', 'tissue: breast tumor; cohort id: 4082; geo_accn_gse16446: GSM411354; grade: 3; t: T4; n: N1; esr1bimod: 0; her2_fish: 1.34; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 1; os_time (days): 314; dmfs_event: 1; dmfs_time (days): 314; pcr: 0; ', 'tissue: breast tumor; cohort id: 4270; geo_accn_gse16446: GSM411387; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 0; age_bin: 1; os_event: 1; os_time (days): 359; dmfs_event: 1; dmfs_time (days): 63; pcr: 0; ', 'tissue: breast tumor; cohort id: 4291; geo_accn_gse16446: GSM411337; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.09; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 1; os_time (days): 1932; dmfs_event: 1; dmfs_time (days): 1414; pcr: 0; ', 'tissue: breast tumor; cohort id: 4511; geo_accn_gse16446: GSM411353; grade: 3; t: T3; n: N0; esr1bimod: 0; her2_fish: 1.34; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1839; dmfs_event: 0; dmfs_time (days): 1839; pcr: 0; ', 'tissue: breast tumor; cohort id: 4864; geo_accn_gse16446: GSM411331; grade: 3; t: T1; n: N0; esr1bimod: 0; her2_fish: 1.07; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1211; dmfs_event: 1; dmfs_time (days): 627; pcr: 0; ', 'tissue: breast tumor; cohort id: 4917; geo_accn_gse16446: GSM411312; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.15; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 771; dmfs_event: 0; dmfs_time (days): 771; pcr: 0; ', 'tissue: breast tumor; cohort id: 4938; geo_accn_gse16446: GSM411379; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 449; dmfs_event: 0; dmfs_time (days): 449; pcr: 0; ', 'tissue: breast tumor; cohort id: 4984; geo_accn_gse16446: GSM411295; grade: 3; t: T2; n: N3; esr1bimod: 0; her2_fish: 3.96; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 1856; dmfs_event: 0; dmfs_time (days): 1856; pcr: 0; ', 'tissue: breast tumor; cohort id: 5180; geo_accn_gse16446: GSM411347; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.22; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 1; os_time (days): 431; dmfs_event: 1; dmfs_time (days): 223; pcr: 0; ', 'tissue: breast tumor; cohort id: 5328; geo_accn_gse16446: GSM411398; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.05; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1132; dmfs_event: 0; dmfs_time (days): 1132; pcr: 1; ', 'tissue: breast tumor; cohort id: 5437; geo_accn_gse16446: GSM411352; grade: 3; t: T1; n: N0; esr1bimod: 0; her2_fish: 1.33; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 669; dmfs_event: 0; dmfs_time (days): 669; pcr: 0; ', 'tissue: breast tumor; cohort id: 5622; geo_accn_gse16446: GSM411305; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 7.23; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 794; dmfs_event: 0; dmfs_time (days): 794; pcr: 0; ', 'tissue: breast tumor; cohort id: 5706; geo_accn_gse16446: GSM411362; grade: 2; t: T2; n: N0; esr1bimod: 0; her2_fish: 2.3; her2_fish_bin: 1; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1524; dmfs_event: 1; dmfs_time (days): 1072; pcr: 0; ', 'tissue: breast tumor; cohort id: 5751; geo_accn_gse16446: GSM411376; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 919; dmfs_event: 0; dmfs_time (days): 919; pcr: 0; ', 'tissue: breast tumor; cohort id: 5783; geo_accn_gse16446: GSM411399; grade: 3; t: T2; n: N0; esr1bimod: 1; her2_fish: 1.1; her2_fish_bin: 0; erbb2bimod: null; age_bin: 1; os_event: null; os_time (days): null; dmfs_event: null; dmfs_time (days): null; pcr: 1; ', 'tissue: breast tumor; cohort id: 5920; geo_accn_gse16446: GSM411340; grade: 3; t: T2; n: N2; esr1bimod: 0; her2_fish: 1.13; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): null; dmfs_event: 0; dmfs_time (days): null; pcr: 0; ', 'tissue: breast tumor; cohort id: 6181; geo_accn_gse16446: GSM411322; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.03; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 777; dmfs_event: 0; dmfs_time (days): 777; pcr: 0; ', 'tissue: breast tumor; cohort id: 6198; geo_accn_gse16446: GSM411314; grade: 2; t: T2; n: N1; esr1bimod: 0; her2_fish: 1; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1259; dmfs_event: 0; dmfs_time (days): 1259; pcr: 0; ', 'tissue: breast tumor; cohort id: 6276; geo_accn_gse16446: GSM411318; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.09; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 748; dmfs_event: 0; dmfs_time (days): 748; pcr: 0; ', 'tissue: breast tumor; cohort id: 6754; geo_accn_gse16446: GSM411320; grade: 2; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.06; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1376; dmfs_event: 0; dmfs_time (days): 1376; pcr: 0; ', 'tissue: breast tumor; cohort id: 6767; geo_accn_gse16446: GSM411317; grade: 3; t: T4; n: N1; esr1bimod: 0; her2_fish: 0.98; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 1; os_time (days): 464; dmfs_event: 1; dmfs_time (days): 464; pcr: 0; ', 'tissue: breast tumor; cohort id: 682; geo_accn_gse16446: GSM411339; grade: 2; t: T4; n: N2; esr1bimod: 0; her2_fish: 1.12; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 1; os_time (days): 732; dmfs_event: 1; dmfs_time (days): 732; pcr: 0; ', 'tissue: breast tumor; cohort id: 6839; geo_accn_gse16446: GSM411359; grade: 3; t: T1; n: N1; esr1bimod: 0; her2_fish: 1.7; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1390; dmfs_event: 0; dmfs_time (days): 1390; pcr: 0; ', 'tissue: breast tumor; cohort id: 6951; geo_accn_gse16446: GSM411325; grade: 2; t: T4; n: N1; esr1bimod: 0; her2_fish: 1.03; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 725; dmfs_event: 0; dmfs_time (days): 725; pcr: 0; ', 'tissue: breast tumor; cohort id: 7173; geo_accn_gse16446: GSM411406; grade: 3; t: T2; n: N2; esr1bimod: 0; her2_fish: 7.18; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 1; os_event: 0; os_time (days): 1130; dmfs_event: 0; dmfs_time (days): 1130; pcr: 1; ', 'tissue: breast tumor; cohort id: 7182; geo_accn_gse16446: null; grade: null; t: null; n: null; esr1bimod: null; her2_fish: null; her2_fish_bin: null; erbb2bimod: null; age_bin: null; os_event: null; os_time (days): null; dmfs_event: null; dmfs_time (days): null; pcr: 0; ', 'tissue: breast tumor; cohort id: 7469; geo_accn_gse16446: GSM411309; grade: 3; t: T3; n: N1; esr1bimod: 0; her2_fish: 1.08; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 1; os_time (days): 858; dmfs_event: 1; dmfs_time (days): 291; pcr: 0; ', 'tissue: breast tumor; cohort id: 7500; geo_accn_gse16446: GSM411377; grade: 3; t: T3; n: N1; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 726; dmfs_event: 1; dmfs_time (days): 558; pcr: 0; ', 'tissue: breast tumor; cohort id: 7634; geo_accn_gse16446: GSM411396; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 1208; dmfs_event: 0; dmfs_time (days): 1208; pcr: 1; ', 'tissue: breast tumor; cohort id: 8319; geo_accn_gse16446: GSM411323; grade: 2; t: T4; n: N1; esr1bimod: 0; her2_fish: 1018; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 1772; dmfs_event: 0; dmfs_time (days): 1772; pcr: 0; ', 'tissue: breast tumor; cohort id: 845; geo_accn_gse16446: GSM411365; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 4.4; her2_fish_bin: 1; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 1647; dmfs_event: 0; dmfs_time (days): 1647; pcr: 0; ', 'tissue: breast tumor; cohort id: 8660; geo_accn_gse16446: GSM411297; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 1; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): null; dmfs_event: 0; dmfs_time (days): null; pcr: 0; ', 'tissue: breast tumor; cohort id: 8739; geo_accn_gse16446: GSM411296; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 0.71; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 1; os_event: null; os_time (days): null; dmfs_event: null; dmfs_time (days): null; pcr: 0; ', 'tissue: breast tumor; cohort id: 8999; geo_accn_gse16446: GSM411373; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 0; age_bin: 0; os_event: 1; os_time (days): 547; dmfs_event: 1; dmfs_time (days): 249; pcr: 0; ', 'tissue: breast tumor; cohort id: 9049; geo_accn_gse16446: GSM411345; grade: 1; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.2; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 599; dmfs_event: 0; dmfs_time (days): 599; pcr: 0; ', 'tissue: breast tumor; cohort id: 9064; geo_accn_gse16446: GSM411348; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 1.22; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 1408; dmfs_event: 0; dmfs_time (days): 1408; pcr: 0; ', 'tissue: breast tumor; cohort id: 9171; geo_accn_gse16446: GSM411299; grade: 3; t: T2; n: N1; esr1bimod: 0; her2_fish: 4.81; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 1719; dmfs_event: 0; dmfs_time (days): 1719; pcr: 0; ', 'tissue: breast tumor; cohort id: 9386; geo_accn_gse16446: GSM411343; grade: 2; t: T2; n: N0; esr1bimod: 0; her2_fish: 1.16; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 956; dmfs_event: 0; dmfs_time (days): 956; pcr: 0; ', 'tissue: breast tumor; cohort id: 9434; geo_accn_gse16446: GSM411374; grade: 3; t: T4; n: N1; esr1bimod: 0; her2_fish: null; her2_fish_bin: null; erbb2bimod: 0; age_bin: 1; os_event: 0; os_time (days): 737; dmfs_event: 1; dmfs_time (days): 160; pcr: 0; ', 'tissue: breast tumor; cohort id: 9576; geo_accn_gse16446: GSM411400; grade: 3; t: T4; n: N1; esr1bimod: 0; her2_fish: 1.11; her2_fish_bin: 0; erbb2bimod: 0; age_bin: 0; os_event: 0; os_time (days): 1748; dmfs_event: 0; dmfs_time (days): 1748; pcr: 1; ', 'tissue: breast tumor; cohort id: 9665; geo_accn_gse16446: GSM411338; grade: 3; t: T2; n: N0; esr1bimod: 0; her2_fish: 6.67; her2_fish_bin: 1; erbb2bimod: 1; age_bin: 0; os_event: 0; os_time (days): 1008; dmfs_event: 0; dmfs_time (days): 1008; pcr: 0; ' GSE128617 Homo sapiens 6 Expression profiling by array GPL21185 Late recurrence-associated long non-coding RNA NR2F1 antisense 1 (NR2F1-AS1) II 2019-03-20 Long non-coding RNA NR2F1 antisense RNA1 (lncRNA NR2F1-AS1) was identified as the main candidate associated to late recurrence in ER-positive breast cancer clinical samples. Gain-of-function of NR2F1-AS1 induced the expression of dormancy-inducers BMP4 and DEC2, and upregulated pluripotency markers NANOG and OCT4. Representative pathways entailed to metastatic events such as HER2/Neu, hypoxia, EMT and inflammatory-response were also found enriched. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE128617 Long non-coding NR2F1-AS1 is associated with tumor recurrence in estrogen receptor-positive breast cancers. Molecular oncology 5.962 https://doi.org/10.1002/1878-0261.12704 {Molecular oncology (5.962): 10.1002/1878-0261.12704} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA528288 https://www.ebi.ac.uk/ena/browser/view/PRJNA528288 None [Overal design]We identified the lncRNA NR2F1 antisense RNA1 (NR2F1-AS1) as the main candidate associated to late recurrence in ER-positive breast cancer. We conducted in vitro gain-of-function of NR2F1-AS1 variant1 and variant 4 in breast cancer BT474 cell line and applied microarray-based analysis.; [Treatment]'BT474 cell lines transfected with emtpy pcDNA3.1 were named as MOCK , BT474 transfected with pcDNA3.1-NR2F1-AS1variant1 were named as BT474-Var1, BT474 transfected with pcDNA3.1-NR2F1-AS1variant4 were named as BT474-Var4. All cell types were maintained in RPMI-1640 (Nissui Pharmaceutical, Tokyo, Japan) supplemented with 10% heat-inactivated FBS at 37 °C in 5% CO2.'; [Growth]'BT474 cell lines were cultured in RPMI-1640 (Nissui Pharmaceutical, Tokyo, Japan) supplemented with 10% heat-inactivated FBS at 37 °C in 5% CO2.'; [Extraction]'Total RNA was extracted using QIAzol and the RNeasy Mini Kit (Qiagen, Hilden, Germany) according to manufacturer’s protocols. RNA was quantified using a NanoDrop-1000 spectrophotometer and a Agilent 2100 bioanalyzer (Agilent Technologies, Palo Alto, Calif.).'; [Cell type]'Source: ''cell line: BT474; transfection: emtpy pcDNA3.1; ', 'cell line: BT474; transfection: pcDNA3.1-NR2F1-AS1variant4; ', 'cell line: BT474; transfection: pcDNA3.1-NR2F1-AS1variant1; ' GSE61724 Homo sapiens 68 Expression profiling by array GPL6244 Novel transcripts associated with lymph node metastasis in triple negative breast cancer [validation cohort] 2014-09-24 Triple negative breast cancer (TNBC) is the most aggressive breast cancer subtype with the worst prognosis. It is characterised by the absence of hormone receptors for estrogen, progesterone, and human epidermal growth factor 2, and as a consequence there are no targeted endocrine treatments available. TNBC patients are more likely to develop metastases and disease relapse than patients with other breast cancer subtypes. The identification of biomarkers that can be used to predict which patient is likely to develop metastatic disease remains a priority since this is the major cause of cancer-related death in these women. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE61724 Novel genes associated with lymph node metastasis in triple negative breast cancer. Scientific reports 4.011 https://doi.org/10.1038/srep15832 {Scientific reports (4.011): 10.1038/srep15832} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA261958 https://www.ebi.ac.uk/ena/browser/view/PRJNA261958 None [Overal design]To validate results of the gene expression arrays, we used an independent cohort with 16 TNBC primary tumours and 4 normal adjacent tissues, and 48 IDCs from patients with breast cancer other than TNBC.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted from fresh frozen tissue samples, using Rneasy kit (Qiagen, Doncaster, VIC, Australia).'; [Cell type]'Source: ''tnbc type: No; tissue type: invasive ductal carcinomas (IDC); ', 'tnbc type: Normal; tissue type: matched normal adjacent tissues from the tumour specimen (NAT); ', 'tnbc type: Yes; tissue type: invasive ductal carcinomas (IDC); ' GSE37243 Homo sapiens 4 Expression profiling by array GPL570 Expression data by ACLY knockdown 2012-04-13 De novo lipogenesis is activated in most cancers. Several lipogenic enzymes are implicated in oncogenesis and represent potential cancer therapeutic targets. RNA interference-mediated depletion of ATP citrate lyase (ACLY), the enzyme that catalyzes the first step of de novo lipogenesis, leads to growth suppression in a subset of human cancer cells. Here we demonstrate the molecular basis and potential biomarkers for ACLY-targeting therapy. First, suppression of cancer cell growth by ACLY depletion involves down-regulation of fatty acid elongase ELOVL6 at the transcriptional level. Lipid profiling revealed that ACLY depletion alters fatty acid composition in triglyceride; increased palmitate and decreased longer fatty acids, in accordance with ELOVL6 down-regulation. Second, ACLY depletion increases reactive oxygen species (ROS), whereas addition of antioxidant reduces ROS and attenuates the growth suppression. Third, ACLY depletion or ROS stimulation induce phosphorylation of AMP-activated protein kinase (AMPK), a sensor of energy and lipid metabolism. Analysis of various cancer cell lines revealed that the levels of AMPK phosphorylation (p-AMPK) correlate with the basal ROS levels, and that cancer cells with low basal p-AMPK (i.e., low basal ROS) levels are highly susceptible to ACLY depletion-mediated growth suppression. Finally, in clinical colon cancer tissues, p-AMPK levels are significantly decreased in aggressive tumors and correlate with the levels of 8-hydroxydeoxyguanosine, a hallmark of ROS stimulation. Together, these data suggest that ACLY inhibition suppresses cancer growth via palmitate-mediated lipotoxicity, and p-AMPK could be a predictive biomarker for its therapeutic outcome. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE37243 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA159187 https://www.ebi.ac.uk/ena/browser/view/PRJNA159187 None [Overal design]Two cell lines are treated with ACLY siRNA. The samples include controls of each cell line.; [Treatment]'None'; [Growth]'The cell line was cultured in vitro in 10cm dishes until 80-90% confluency and then total RNA was isolated.'; [Extraction]"RNeasy extraction of total RNA was performed according to the manufacturer's instructions (Qiagen)."; [Cell type]'Human breast cancer', 'Human prostate cancer''cell line: HBC5; cell type: Human breast cancer; treated with: ACLY siRNA; ', 'cell line: HBC5; cell type: Human breast cancer; ', 'cell line: LNCaP; cell type: Human prostate cancer; treated with: ACLY siRNA; ', 'cell line: LNCaP; cell type: Human prostate cancer; ' GSE43566 Mus musculus 38 Expression profiling by array GPL7202 Biomarkers of residual disease, disseminated tumor cells, and metastases in the MMTV-PyMT breast cancer model 2013-01-17 Gene expression profiling of disseminated tumor cells in lung, lung metastatses and residual tumor cells in the MMTV-PyMT breast cancer model. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43566 Biomarkers of residual disease, disseminated tumor cells, and metastases in the MMTV-PyMT breast cancer model. PloS one 2.776 https://doi.org/10.1371/journal.pone.0058183 {PloS one (2.776): 10.1371/journal.pone.0058183} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA186723 https://www.ebi.ac.uk/ena/browser/view/PRJNA186723 None [Overal design]Profiling gene expression change between disseminated tumor cells, lung metastases and residual tumor cells from the MMTV-PyMT breast cancer model.; [Treatment]'We treated early carcinomas (2 months post-transplant) with docetaxel + doxorubicin + cyclophosphamide, and the resulting tumors undergo 90% tumor shrinkage.'; [Growth]'None'; [Extraction]"Qiagen AllPrep extraction kit was used according to the manufacturer's instructions"; [Cell type]'Source: ''sampleID: SAM607559; tissue: Control_breast cancer; treatment: control; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'reference: pooled mouse reference RNA; ', 'sampleID: SAM607560; tissue: Regressed tumor; treatment: chemo; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM608282; tissue: Regressed tumor; treatment: chemo; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM611866; tissue: Control_breast cancer; treatment: control; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM611867; tissue: Control_breast cancer; treatment: control; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM611868; tissue: Control_breast cancer; treatment: control; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM612279; tissue: Control_breast cancer; treatment: control; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM612280; tissue: Control_breast cancer; treatment: control; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM620542; tissue: Regressed tumor; treatment: chemo; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM620543; tissue: Regressed tumor; treatment: chemo; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM620544; tissue: Regressed tumor; treatment: chemo; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM620545; tissue: Regressed tumor; treatment: chemo; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM620546; tissue: Resistant tumor; treatment: chemo; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM620548; tissue: Resistant tumor; treatment: chemo; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM620550; tissue: Resistant tumor; treatment: chemo; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM620551; tissue: Resistant tumor; treatment: chemo; strain/background: FVB/n; experimentid: Spr784; diagnosis: breast cancer; ', 'sampleID: SAM611223; tissue: Adenoma; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM611224; tissue: Carcinoma; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM611225; tissue: Carcinoma; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM611226; tissue: Carcinoma; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM611227; tissue: Disseminated cells; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM611228; tissue: Disseminated cells; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM611229; tissue: Disseminated cells; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM611230; tissue: Disseminated cells; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM611231; tissue: Metastases; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM611232; tissue: Metastases; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM611233; tissue: Metastases; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM611234; tissue: Metastases; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM611251; tissue: Disseminated cells; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM620835; tissue: Adenoma; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM620836; tissue: Adenoma; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM620837; tissue: Adenoma; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM620838; tissue: Adenoma; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM620958; tissue: Carcinoma; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM620959; tissue: Carcinoma; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM620960; tissue: Carcinoma; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM620961; tissue: Disseminated cells; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ', 'sampleID: SAM620962; tissue: Metastases; strain/background: FVB/n; experimentid: Spr799; diagnosis: breast cancer; ' GSE25428 Homo sapiens 95 Expression profiling by array GPL3921 Gene expression profiles of ovarian cancer cell lines in the presence and absence of a DNA methyltransferase inhibitor 2010-11-16 Epithelial ovarian cancer is the leading cause of death among gynecologic malignancies. Diagnosis usually occurs after metastatic spread, largely reflecting vague symptoms of early disease combined with lack of an effective screening strategy. Epigenetic mechanisms of gene regulation, including DNA methylation, are fundamental to normal cellular function and also play a major role in carcinogenesis. To elucidate the biological and clinical relevance of DNA methylation in ovarian cancer, we conducted expression microarray analysis of 39 cell lines and 17 primary culture specimens grown in the presence or absence of DNA methyltransferase (DNMT) inhibitors. Two parameters, induction of expression and standard deviation among untreated samples, identified 378 candidate methylated genes, many relevant to TGF-beta signaling. We analyzed 43 of these genes and they all exhibited methylation. Treatment with DNMT inhibitors increased TGF-beta pathway activity. Hierarchical clustering of ovarian cancers using the 378 genes reproducibly generated a distinct gene cluster strongly correlated with TGF-beta pathway activity that discriminates patients based on age. These data suggest that accumulation of age-related epigenetic modifications leads to suppression of TGF-beta signaling and contributes to ovarian carcinogenesis. The cancer stem cell hypothesis posits that malignant growth arises from a rare population of progenitor cells within a tumor that provide it with unlimited regenerative capacity. Such cells also possess increased resistance to chemotherapeutic agents. Resurgence of chemoresistant disease following primary therapy typifies epithelial ovarian cancer and may be attributable to residual cancer stem cells, or cancer initiating cells, that survive initial treatment. As the cell surface marker CD133 identifies cancer initiating cells in a number of other malignancies, we sought to determine the potential role of CD133+ cells in epithelial ovarian cancer. We detected CD133 on ovarian cancer cell lines, in primary cancers, and on purified epithelial cells from ascitic fluid of ovarian cancer patients. We found CD133+ ovarian cancer cells generate both CD133+ and CD133- daughter cells, whereas CD133- cells divide symmetrically. CD133+ cells exhibit enhanced resistance to platinum-based therapy, drugs commonly used as first line agents for treatment of ovarian cancer. Sorted CD133+ ovarian cancer cells also form more aggressive tumor xenografts at a lower inoculum than their CD133- progeny. Epigenetic changes may be integral to the behavior of cancer progenitor cells and their progeny. In this regard, we found that CD133 transcription is controlled by both histone modifications and promoter methylation. Sorted CD133- ovarian cancer cells treated with DNA methyltransferase and histone deacetylase inhibitors show a synergistic increase in cell surface CD133 expression. Moreover, DNA methylation at the ovarian tissue active P2 promoter is inversely correlated with CD133 transcription. We also found that promoter methylation increases in CD133- progeny of CD133+ cells, with CD133+ cells retaining a less methylated or unmethylated state. Taken together, our results show that CD133 expression in ovarian cancer is directly regulated by epigenetic modifications and support the idea that CD133 demarcates an ovarian cancer initiating cell population. The activity of these cells may be epigenetically detected and such cells might serve as pertinent chemotherapeutic targets for reducing disease recurrence. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE25428 Epigenetic suppression of the TGF-beta pathway revealed by transcriptome profiling in ovarian cancer. Genome research 9.944 https://doi.org/10.1101/gr.108803.110 {Genome research (9.944) doi:10.1101/gr.108803.110}; {Oncogene (6.634) doi:10.1038/onc.2008.374}; {Frontiers in oncology (4.137) doi:10.3389/fonc.2013.00269}; {Frontiers in oncology (4.137) doi:10.3389/fonc.2013.00131}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA142615 https://www.ebi.ac.uk/ena/browser/view/PRJNA142615 None [Overal design]The objective of the study was to identify genes that are subject to DNA methylation through pharmacological inhibition of DNA methyltransferase activity in a panel of cancer cell lines. Cells were mock treated with culture media (mock treated) or treated with 5 µM decitabine for 72 hours. Resulting expression profiles were compared to identify genes with altered expression following decitabine treatment. These data represent two experiments: In the first, 43 established cell lines were mock treated or treated with decitabine to enable identification of genes differentially expressed as a result of inhibition of DNA methyltransferase activity. HEYA8-decitabine treated cells were run in replicate. In the second experiment, A2780 and PEO1 cells underwent flow activated cell sorting to separate CD133(+) from CD133(-) cells in each cell line; the sorted cell populations were cultured in the same manner as the first experiment and similarly mock treated or treated with decitabine. All specimens were arrayed in parallel and used for RMA normalization.; [Treatment]"At ~70% confluence, cells were either mock treated with tissue culture media (Mock) or with 5 µM 5-aza-2'-deoxxycytidine (Decitabine) for 72 hours."; [Growth]'All cells, including sorted CD133+ and CD133- A2780 and PEO1 cells, were grown in RPMI1640 media with 10% FBS in a humidifed incubator maintained at 37 degrees Celsius with 5% CO2 until ~70% confluent.'; [Extraction]'RNA Stat-60.'; [Cell type]'ovarian cancer cells', 'breast cancer cells', 'cervical cancer cells''cell line: 41M-cisR; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: HEY; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: HEYA8; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: HEYC2; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: PEO1; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: PEO4; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: MCF7; cell type: breast cancer cells; gender: female; treatment: mock; ', 'cell line: OVCAR-2; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCAR-3; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCAR-5; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCAR-8; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCAR-10; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: SKOV-3; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: SKOV-4; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: SKOV-6; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: SKOV-8; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCA420; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCA429; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCA432; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVCA433; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OVARY1847; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: PA-1; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: DOV13A; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: DOV13B; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: DOV13; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: CAOV-2; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: CAOV-3; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: CH1; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: CH1-cisR; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: TOV-112D; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: Tyk-nu; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: Tyk-nu-cisR; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: A2780; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: A2780-cisR; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: FUOV1; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: OV90; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: ME-180; cell type: cervical cancer cells; gender: female; treatment: mock; ', 'cell line: IGROV1; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: ME-180A; cell type: cervical cancer cells; gender: female; treatment: mock; ', 'cell line: 41M; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: TOV-21G; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: ME-180C; cell type: cervical cancer cells; gender: female; treatment: mock; ', 'cell line: MCAS; cell type: ovarian cancer cells; gender: female; treatment: mock; ', 'cell line: 41M-cisR; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: HEY; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: HEYA8; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: HEYC2; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: PEO1; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: PEO4; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: MCF7; cell type: breast cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCAR-2; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCAR-3; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCAR-5; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCAR-8; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCAR-10; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: SKOV-3; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: SKOV-4; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: SKOV-6; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: SKOV-8; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCA420; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCA429; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCA432; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVCA433; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OVARY1847; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: PA-1; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: DOV13A; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: DOV13B; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: DOV13; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: CAOV-2; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: CAOV-3; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: CH1; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: CH1-cisR; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: TOV-112D; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: Tyk-nu; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: Tyk-nu-cisR; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: A2780; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: A2780-cisR; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: FUOV1; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: OV90; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: ME-180; cell type: cervical cancer cells; gender: female; treatment: decitabine; ', 'cell line: IGROV1; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: ME-180A; cell type: cervical cancer cells; gender: female; treatment: decitabine; ', 'cell line: 41M; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: TOV-21G; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: ME-180C; cell type: cervical cancer cells; gender: female; treatment: decitabine; ', 'cell line: MCAS; cell type: ovarian cancer cells; gender: female; treatment: decitabine; ', 'cell line: A2780; cell type: ovarian cancer cells; cell population: CD133+; gender: female; treatment: mock; ', 'cell line: A2780; cell type: ovarian cancer cells; cell population: CD133+; gender: female; treatment: decitabine; ', 'cell line: A2780; cell type: ovarian cancer cells; cell population: CD133-; gender: female; treatment: mock; ', 'cell line: A2780; cell type: ovarian cancer cells; cell population: CD133-; gender: female; treatment: decitabine; ', 'cell line: PEO1; cell type: ovarian cancer cells; cell population: CD133+; gender: female; treatment: mock; ', 'cell line: PEO1; cell type: ovarian cancer cells; cell population: CD133+; gender: female; treatment: decitabine; ', 'cell line: PEO1; cell type: ovarian cancer cells; cell population: CD133-; gender: female; treatment: mock; ', 'cell line: PEO1; cell type: ovarian cancer cells; cell population: CD133-; gender: female; treatment: decitabine; ' GSE165854 Homo sapiens 9 Expression profiling by array GPL17586 Effect of the expression of ELOVL5 and IGFBP6 genes on the metastatic potential of breast cancer cells 2021-01-31 Previously, it was shown that expression of ELOVL5 and IGFBP6 genes is associated with the risk of the formation of distant metastases in breast cancer. In this work, we studied the change in phenotypical traits, as well as in the transcriptomic and proteomic profiles of breast cancer cells as a result of knockdown of ELOVL5 and IGFBP6 genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE165854 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA698352 https://www.ebi.ac.uk/ena/browser/view/PRJNA698352 None [Overal design]Total RNA was prepared from MDA-MB-231 cells with shRNA mediated knockdown of ELOVL5 and IGFBP6 genes as well as from control MDA-MB-231(LUC) cells.; [Treatment]'not applicable'; [Growth]'MDA-MB-231 breast cancer cell line was cultured in complete cell culture medium consisting of DMEM high glucose (Gibco) supplemented with 10% vol. fetal bovine serum (Gibco), 2 mM L-glutamine (PanEco), 1% vol. pencillin-streptomycin solution (Gibco). The cells were incubated in cell culture incubator (37 °C, 5% CO2).'; [Extraction]'RNA was extracted from frozen tumor samples using the miRNeasy Micro Kit (Qiagen) as recommended by the manufacturer.'; [Cell type]'Source: ''origin: Cell line; knockdown elovl5: yes; knockdown igfbp6: no; cell line: MDA-MB-231; ', 'origin: Cell line; knockdown elovl5: no; knockdown igfbp6: yes; cell line: MDA-MB-231; ', 'origin: Cell line; knockdown elovl5: no; knockdown igfbp6: no; cell line: MDA-MB-231; ' GSE62259 Homo sapiens 8 Expression profiling by array GPL6244 MicroRNA profiling of the developing mammary gland identifies miR-184 as a candidate breast tumour suppressor gene (Affymetrix) 2014-10-10 The study of mammalian development has offered many insights into the molecular aetiology of cancer. We previously used analysis of mammary morphogenesis to discover a critical role for GATA-3 in mammary developmental and carcinogenesis. In recent years an important role for MicroRNAs (miRNAs) in a myriad of cellular processes in development and in oncogenesis has emerged. In this study, microRNA profiling of stromal and epithelial cellular subsets microdissected from the developing mouse mammary gland revealed many microRNAs with expression restricted to various cellular subsets. MicroRNA-184 (miR-184) was exclusively expressed in epithelial cells and markedly upregulated during differentiation of the proliferative, invasive cells of the pubertal terminal end bud (TEB) into ductal epithelial cells in vivo and in FACS-sorted mammary stem cells (MaSCs) versus luminal epithelial cells. miR-184 expression was silenced in mouse tumour models compared to non-transformed epithelium and in a majority of breast cancer cell line models. Ectopic reactivation of miR-184 inhibited the proliferation and self-renewal of metastatic triple negative breast cancer (TNBC) cell lines in vitro and delayed tumour formation and reduced metastasis in vivo. Gene expression studies uncovered multi-factorial direct regulation of genes in the AKT/mTORC1 pathway by miR-184. In clinical breast cancer tissues, expression of miR-184 is lost in primary TNBCs while the miR-184 promoter is methylated in a subset of lymph node metastases from TNBC patients. These studies elucidated a new layer of regulation in the PI3K/AKT/mTOR pathway with relevance to mammary development and tumour proliferation and metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE62259 MicroRNA profiling of the pubertal mouse mammary gland identifies miR-184 as a candidate breast tumour suppressor gene. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-015-0593-0 {Breast cancer research : BCR (5.676): 10.1186/s13058-015-0593-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA263603 https://www.ebi.ac.uk/ena/browser/view/PRJNA263603 None [Overal design]Gene expression analysis of MDA-MB-231 cells 48 hours after transfection with mir-184 mimics with negative control comparisons; [Treatment]'MDA-MB-231 cells were seeded in 6 well plates at a cell density of 1.8 x 105 cells/ well. The next day, miRIDIAN miRNA mimics (Dharmacon) were transfected into cells using Lipofectamine 2000 (Invitrogen) according to the manufacturers protocol for transfecting siRNA. Mimics (Final concentration of 50nm) was mixed with 1% lipofectamine 2000 (v/v) diluted in Opti-MEM transfection medium (Invitrogen) and incubated for 20 minutes. The mimics were added dropwise onto cells in growth medium at a final concentration of 50nm. Fresh medium was replaced 24hours post transfection.'; [Growth]'MDA-MB-231 cells were cultured in RPMI 1640 media supplemented with 10% FCS at 37°C, 5% CO2. Cells were subcultured every 3 to 4 days.'; [Extraction]'RNA was extracted using Trizol reagent (Invitrogen) using the manufacturers protocol and further ethanol precipitated to remove salt contaminants. The RNA was quantified using the Nanodrop 1000 spectrophotometre and the integrity of the RNA was determined using the Agilent 2100 bioanalyser. (Agilent Technologies, Santa Clara, CA)'; [Cell type]'Source: ''cell line: MDA-MB-231; gender: female; tissue: breast; transfection: mir-184 mimic negative control, 48 hours; ', 'cell line: MDA-MB-231; gender: female; tissue: breast; transfection: mir-184 mimic, 48 hours; ' GSE95222 Homo sapiens 3 Genome binding/occupancy profiling by high throughput sequencing GPL9052 Identification of enhancer landscape in MDA-MB-231 cells 2017-02-22 To identify typical enhancers and super-enhancers in the MDA-MB-231 triple-negative breast cancer cell line, we performed ChIP-seq using DNA isolated from untreated MDA-MB-231 cells using an H3K27ac antibody. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95222 Mitotic Vulnerability in Triple-Negative Breast Cancer Associated with LIN9 Is Targetable with BET Inhibitors. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-17-1571 {Cancer research (8.378): 10.1158/0008-5472.CAN-17-1571} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA376433 https://www.ebi.ac.uk/ena/browser/view/PRJNA376433 https://www.ncbi.nlm.nih.gov/sra?term=SRP100561 [Overal design]Examination of H3K27ac binding profiles in MDA-MB-231 cells; [Treatment]'None'; [Growth]'None'; [Extraction]"Lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with H3K27ac antibody.\nLibraries were prepared using the ThruPlex DNA-seq kit from Rubicon Genomics using 20ng of ChIP DNA. Two unique tags were used. Two final pools were made. Each library was QC'ed using Qbit HS dsDNA kit for concentration and Agilent Bioanalyzer DNA HS chip for quality and fragment size. DNA was pooled based on qubit concentration, and qPCR was performed using Kappa Biosystems Illumina LIbrary Quant kit on the pool for nM concentration. DNA was then loaded onto an Illumina HiSeq 2500 50bp rapid run v2 flowcell."; [Cell type]'Source: ''chip antibody: H3K27ac (Abcam, ab5079); ', 'chip antibody: none; ' GSE148991 Homo sapiens 11 Expression profiling by high throughput sequencing GPL16791 Efficient Propagation of Circulating Tumor Cells: A First Step for Probing Tumor Metastasis. 2020-04-20 Circulating Tumor Cells (CTCs) from metastatic breast cancer patients were harvested and grown in vitro for 30+ days in a novel short-term culture method. Additionally, RNA from the buffy coat of 5 healthy donors were sequenced and subjected to culture conditions; 0/5 cultures successfully grew. This new culture method is highly efficient and allows for the molecular characterization of CTCs and identification of potential targets for therapy against tumor metastasis. Using this method, we established 12/12 cultures of CTCs. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148991 Efficient Propagation of Circulating Tumor Cells: A First Step for Probing Tumor Metastasis. Cancers 6.162 https://doi.org/10.3390/cancers12102784 {Cancers (6.162): 10.3390/cancers12102784} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA626675 https://www.ebi.ac.uk/ena/browser/view/PRJNA626675 https://www.ncbi.nlm.nih.gov/sra?term=SRP257712 [Overal design]One sample each from six MBC patients of various receptor subtype (HER2+ n=2; ER/PR+ n=3, TNBC n=1) were sequenced alongside RNA from 5 healthy donors.; [Treatment]'None'; [Growth]'CTC samples were extracted from patient samples using a Ficoll-based gradient selection. Cells were grown in hypoxia on ultra-low attachment plates using a modified conditional-reprogramming (CR)-based medium.'; [Extraction]'RNA was extracted using Invitrogen RNAqueous Micro-RNA kit following manufacturer protocol.\nClonetech SMARTer kit was used for conversion to cDNA from ulta-low input RNA. NEBNextUltra DNA library prep kit was then used to finish the library construction. Library contstructions were done through a third-party company, Genewiz. Libraries were read using an Illumina HiSeq 2x150 PE HO configuration.\nGenewiz was consulted for the construction and preparation of all libraries.'; [Cell type]'cultured circulating tumor cell', 'plasma + buffy coat''cell type: cultured circulating tumor cell; gender: Female; disease state: Metastatic Breast Cancer; ', 'cell type: plasma + buffy coat; gender: Female; disease state: Healthy Individual; ', 'cell type: plasma + buffy coat; gender: Male; disease state: Healthy Individual; ' GSE99116 Homo sapiens 120 Expression profiling by high throughput sequencing GPL18573 Multiomics Profiling Establishes the Polypharmacology of FDA-Approved CDK4/6 Inhibitors and the Potential for Differential Clinical Activity. 2017-05-19 We compared three CDK4/6 inhibitors that have recently emerged as highly promising agents for advanced breast cancers by performing transcriptional profiling (mRNA-Seq) on a panel of seven breast cancer cell lines following 6 or 24 hours of drug exposure at concentrations ranging from 0.3 to 3.0 uM. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99116 Multiomics Profiling Establishes the Polypharmacology of FDA-Approved CDK4/6 Inhibitors and the Potential for Differential Clinical Activity. Cell chemical biology 6.762 https://doi.org/10.1016/j.chembiol.2019.05.005 {Cell chemical biology (6.762): 10.1016/j.chembiol.2019.05.005} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA387311 https://www.ebi.ac.uk/ena/browser/view/PRJNA387311 https://www.ncbi.nlm.nih.gov/sra?term=SRP107565 [Overal design]mRNA levels for 7 breast cancer cell lines treated with one of three CDK4/6 inhibitors (abemaciclib, palbociclib, or ribociclib) at either 0.3 uM, 1.0 uM (only for MCF7), or 3.0 uM for either 6 or 24 hours.; [Treatment]'24 hours after seeding cells CDK4/6 inhibitors were added. Cells were lysed in the plates after 6 or 24 hours.'; [Growth]'Cells were seeded in 12 well plates, and allowed to adhere for 24 hours'; [Extraction]'RNA was extracted using Applied Biosystems MagMax 96 total RNA isolation kit (AM1830) with DNAse digestion according to the manufacturer’s protocol.\nLibraries were prepared using Illumina TruSeq Stranded mRNA sample preparation kit (RS-122-2103) from 500 ng of purified total RNA according to the manufacturer’s protocol in a reduced reaction volume.'; [Cell type]'Source: ''cell line: BT20; agent: Control; dose: 0 uM; time: 24 hr; ', 'cell line: BT20; agent: Abemaciclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: BT20; agent: Abemaciclib; dose: 3 uM; time: 24 hr; ', 'cell line: BT20; agent: Palbociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: BT20; agent: Palbociclib; dose: 3 uM; time: 24 hr; ', 'cell line: BT20; agent: Ribociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: BT20; agent: Ribociclib; dose: 3 uM; time: 24 hr; ', 'cell line: BT549; agent: Control; dose: 0 uM; time: 24 hr; ', 'cell line: BT549; agent: Abemaciclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: BT549; agent: Abemaciclib; dose: 3 uM; time: 24 hr; ', 'cell line: BT549; agent: Palbociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: BT549; agent: Palbociclib; dose: 3 uM; time: 24 hr; ', 'cell line: BT549; agent: Ribociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: BT549; agent: Ribociclib; dose: 3 uM; time: 24 hr; ', 'cell line: HCC1419; agent: Control; dose: 0 uM; time: 24 hr; ', 'cell line: HCC1419; agent: Abemaciclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: HCC1419; agent: Abemaciclib; dose: 3 uM; time: 24 hr; ', 'cell line: HCC1419; agent: Palbociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: HCC1419; agent: Palbociclib; dose: 3 uM; time: 24 hr; ', 'cell line: HCC1419; agent: Ribociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: HCC1419; agent: Ribociclib; dose: 3 uM; time: 24 hr; ', 'cell line: HCC1806; agent: Control; dose: 0 uM; time: 24 hr; ', 'cell line: HCC1806; agent: Abemaciclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: HCC1806; agent: Abemaciclib; dose: 3 uM; time: 24 hr; ', 'cell line: HCC1806; agent: Palbociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: HCC1806; agent: Palbociclib; dose: 3 uM; time: 24 hr; ', 'cell line: HCC1806; agent: Ribociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: HCC1806; agent: Ribociclib; dose: 3 uM; time: 24 hr; ', 'cell line: HS578T; agent: Control; dose: 0 uM; time: 24 hr; ', 'cell line: HS578T; agent: Abemaciclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: HS578T; agent: Abemaciclib; dose: 3 uM; time: 24 hr; ', 'cell line: HS578T; agent: Palbociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: HS578T; agent: Palbociclib; dose: 3 uM; time: 24 hr; ', 'cell line: HS578T; agent: Ribociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: HS578T; agent: Ribociclib; dose: 3 uM; time: 24 hr; ', 'cell line: T47D; agent: Control; dose: 0 uM; time: 24 hr; ', 'cell line: T47D; agent: Abemaciclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: T47D; agent: Abemaciclib; dose: 3 uM; time: 24 hr; ', 'cell line: T47D; agent: Palbociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: T47D; agent: Palbociclib; dose: 3 uM; time: 24 hr; ', 'cell line: T47D; agent: Ribociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: T47D; agent: Ribociclib; dose: 3 uM; time: 24 hr; ', 'cell line: BT20; agent: Control; dose: 0 uM; time: 6 hr; ', 'cell line: BT20; agent: Abemaciclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: BT20; agent: Abemaciclib; dose: 3 uM; time: 6 hr; ', 'cell line: BT20; agent: Palbociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: BT20; agent: Palbociclib; dose: 3 uM; time: 6 hr; ', 'cell line: BT20; agent: Ribociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: BT20; agent: Ribociclib; dose: 3 uM; time: 6 hr; ', 'cell line: BT549; agent: Control; dose: 0 uM; time: 6 hr; ', 'cell line: BT549; agent: Abemaciclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: BT549; agent: Abemaciclib; dose: 3 uM; time: 6 hr; ', 'cell line: BT549; agent: Palbociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: BT549; agent: Palbociclib; dose: 3 uM; time: 6 hr; ', 'cell line: BT549; agent: Ribociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: BT549; agent: Ribociclib; dose: 3 uM; time: 6 hr; ', 'cell line: HCC1419; agent: Control; dose: 0 uM; time: 6 hr; ', 'cell line: HCC1419; agent: Abemaciclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: HCC1419; agent: Abemaciclib; dose: 3 uM; time: 6 hr; ', 'cell line: HCC1419; agent: Palbociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: HCC1419; agent: Palbociclib; dose: 3 uM; time: 6 hr; ', 'cell line: HCC1419; agent: Ribociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: HCC1419; agent: Ribociclib; dose: 3 uM; time: 6 hr; ', 'cell line: HCC1806; agent: Control; dose: 0 uM; time: 6 hr; ', 'cell line: HCC1806; agent: Abemaciclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: HCC1806; agent: Abemaciclib; dose: 3 uM; time: 6 hr; ', 'cell line: HCC1806; agent: Palbociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: HCC1806; agent: Palbociclib; dose: 3 uM; time: 6 hr; ', 'cell line: HCC1806; agent: Ribociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: HCC1806; agent: Ribociclib; dose: 3 uM; time: 6 hr; ', 'cell line: HS578T; agent: Control; dose: 0 uM; time: 6 hr; ', 'cell line: HS578T; agent: Abemaciclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: HS578T; agent: Abemaciclib; dose: 3 uM; time: 6 hr; ', 'cell line: HS578T; agent: Palbociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: HS578T; agent: Palbociclib; dose: 3 uM; time: 6 hr; ', 'cell line: HS578T; agent: Ribociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: HS578T; agent: Ribociclib; dose: 3 uM; time: 6 hr; ', 'cell line: T47D; agent: Control; dose: 0 uM; time: 6 hr; ', 'cell line: T47D; agent: Abemaciclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: T47D; agent: Abemaciclib; dose: 3 uM; time: 6 hr; ', 'cell line: T47D; agent: Palbociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: T47D; agent: Palbociclib; dose: 3 uM; time: 6 hr; ', 'cell line: T47D; agent: Ribociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: T47D; agent: Ribociclib; dose: 3 uM; time: 6 hr; ', 'cell line: MCF7; agent: Control; dose: 0 uM; time: 6 hr; ', 'cell line: MCF7; agent: Abemaciclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: MCF7; agent: Abemaciclib; dose: 1 uM; time: 6 hr; ', 'cell line: MCF7; agent: Abemaciclib; dose: 3 uM; time: 6 hr; ', 'cell line: MCF7; agent: Palbociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: MCF7; agent: Palbociclib; dose: 3 uM; time: 6 hr; ', 'cell line: MCF7; agent: Ribociclib; dose: 0.3 uM; time: 6 hr; ', 'cell line: MCF7; agent: Ribociclib; dose: 3 uM; time: 6 hr; ', 'cell line: MCF7; agent: Control; dose: 0 uM; time: 24 hr; ', 'cell line: MCF7; agent: Abemaciclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: MCF7; agent: Abemaciclib; dose: 1 uM; time: 24 hr; ', 'cell line: MCF7; agent: Abemaciclib; dose: 3 uM; time: 24 hr; ', 'cell line: MCF7; agent: Palbociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: MCF7; agent: Palbociclib; dose: 3 uM; time: 24 hr; ', 'cell line: MCF7; agent: Ribociclib; dose: 0.3 uM; time: 24 hr; ', 'cell line: MCF7; agent: Ribociclib; dose: 3 uM; time: 24 hr; ' GSE148843 Mus musculus 56 Expression profiling by high throughput sequencing GPL19057 β-catenin is a node at orchestrating distinct aspects of epithelial-mesenchymal transition (EMT) and malignant mammary tumor progression 2020-04-17 Canonical Wnt signaling plays crucial roles in the progression of many cancer types. In canonical Wnt signaling, β-catenin acts as a controller determining the transcriptional output: via its N-terminus it recruits the signaling coactivators Bcl9 and Bcl9/9l and via the C-terminus it interacts with the general transcriptional machinery. In the intestine, the C terminal output is essential, while the N-terminus controls only a subset of target genes. In breast cancer, the relative contribution of b-catenin’s different output is not known. Also not known is the functional contribution of β-catenin’s a role in cadherin-mediated cell adhesion, a function which confounds the analysis of conventional loss of function models. To address these unknowns, we combined the MMTV-PyMT mouse model of metastatic breast cancer with mouse lines carrying mutations in β-catenin that abolish its function completely or specifically target the N or C-terminal transcriptional outputs. Notably, the complete lack of β-catenin resulted in apoptosis of mammary tumor cells in vivo and in vitro. In contrast, the loss of β-catenin’s transcriptional functions did not provoke apoptosis but did diminish cell proliferation, epithelial-mesenchymal transition (EMT) and cell migration in vitro. This was also reflected in a reduction in primary tumor growth, tumor invasion, and metastasis formation in vivo. Whole transcriptome analysis identified subsets of genes, which were specifically regulated either by β-catenin’s N or C-terminal activities. Intriguingly, the N-terminal output was critical for TGFb-induced EMT and metastasis formation. The observations from the mouse models correlated with expression studies in human breast cancers. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148843 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA625946 https://www.ebi.ac.uk/ena/browser/view/PRJNA625946 https://www.ncbi.nlm.nih.gov/sra?term=SRP256918 [Overal design]RNA-Seq of β-cateninfl/fl ( WT) and β-cateninD164A/-,β-cateninΔC/- and β-catenindm/- mutant cell lines on treatment with TGFb or Wnt3a was performed in biological duplicates; [Treatment]'For Wnt3a treatment, Pygo2 WT (+/+) and mutant (AE/AE) cell lines were treated with 100 ng/ml Wnt3a for 3 days. Medium was changed and fresh Wnt3a was added daily. Untreated cells served as control. For TGFb treatment, Pygo2 WT (+/+) and mutant (AE/AE) cell lines were treated with 2 ng/ml TGFb for 4 days. Medium was changed every second day with fresh addition of TGFb. Untreated cells served as control.'; [Growth]'WT and mutant cell lines were cultured in Dulbecco’s modified Eagle’s medium (DMEM) (Sigma-Aldrich, D5671) supplemented with 10% Fetal Bovine Serum (FBS, 10%; Sigma-Aldrich), 2 mM glutamine (Sigma-Aldrich, G7513), 100 U penicillin (Sigma-Aldrich) and 0.1 mg/ml streptomycin (Sigma-Aldrich). All cell lines were grown at 37°C, 5% CO2, 95% humidity.'; [Extraction]'Total RNA was isolated from the samples above using the miRNeasy Mini Kit (Qiagen, 217004) with on-column DNAse digestion according to the manufacturer’s instructions.\nRNA-sequencing libraries were prepared from total RNA using poly(A) enrichment with the TruSeq stranded mRNA Sample prep from Illumina using 200 ng input RNA. QC was performed with a fragment analyzer using DNF-473-33-SS NGS Fragment 1-6000bp kit. The RNA-sequence libraries were sequenced on a NextSeq 500 using 75 cycles kit High Output (Illumina).'; [Cell type]'Breast cancer cells''cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-cateninfl/fl; treatment: UT (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-cateninfl/fl; treatment: Wnt3a treated (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-cateninD164A/fl; treatment: UT (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-cateninD164A/fl; treatment: Wnt3a treated (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-cateninD164A/-; treatment: UT (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-cateninD164A/-; treatment: Wnt3a treated (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenin{delta}C/fl; treatment: UT (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenin{delta}C/fl; treatment: Wnt3a treated (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenin{delta}C/-; treatment: UT (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenin{delta}C/-; treatment: Wnt3a treated (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenindm/fl; treatment: UT (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenindm/fl; treatment: Wnt3a treated (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenindm/-; treatment: UT (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenindm/-; treatment: Wnt3a treated (3 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-cateninfl/fl; treatment: UT (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-cateninfl/fl; treatment: TGFb treated (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-cateninD164A/fl; treatment: UT (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-cateninD164A/fl; treatment: TGFb treated (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-cateninD164A/-; treatment: UT (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-cateninD164A/-; treatment: TGFb treated (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenin{delta}C/fl; treatment: UT (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenin{delta}C/fl; treatment: TGFb treated (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenin{delta}C/-; treatment: UT (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenin{delta}C/-; treatment: TGFb treated (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenindm/fl; treatment: UT (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenindm/fl; treatment: TGFb treated (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenindm/-; treatment: UT (4 days); ', 'cell type: Breast cancer cells; strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; mutation: beta-catenindm/-; treatment: TGFb treated (4 days); ' GSE56245 Homo sapiens 8 Expression profiling by array GPL13252 Effect of Epigallocatechin gallate (EGCG), a green tea ployphenol, on estrogen regulated genes in breast cancer cell line MCF7. 2014-03-26 Epigallocatechin gallate (EGCG), the major green tea polyphenol, has been a subject of global interest as a potential chemopreventive or chemotherapeutic supplement for breast cancer. While on one hand epidemiological studies suggest inverse correlation between green tea consumption and breast cancer risk, investigations using cell culture and animal models of breast carcinogenesis on the other hand have demonstrated antiproliferative, antitumor, anti-invasive and anti-metastatic properties of EGCG. Mechanism of how EGCG affects cell proliferation, apoptosis, migration and cell cycle by affecting the function of a wide range of molecular targets have also been studied. However, the question as to how EGCG impacts on estrogen responsive genes has not been addressed. This issue is of relevance to our notion of EGCG as a potential chemopreventive or chemotherapeutic agent against breast cancer, which is estrogen dependent in majority of the newly diagnosed cases. Here, using the estrogen receptor α (ERα) positive MCF-7 breast cancer cells as a model, we have examined the effect of EGCG on the estrogen regulated genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE56245 Expression profiling of genes modulated by estrogen, EGCG or both in MCF-7 breast cancer cells. Genomics data 0.527 https://doi.org/10.1016/j.gdata.2015.05.040 {Genomics data (0.527): 10.1016/j.gdata.2015.05.040} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA242734 https://www.ebi.ac.uk/ena/browser/view/PRJNA242734 None [Overal design]MCF7 cells were treated with vehicle (Ethanol) or EGCG in the presence or absence of estrogen for 24hrs. Total RNA was extracted; Cy3 labeled cRNA was hybridized to Genotypic Technology designed Custom Human Whole Genome 8x60k Microarray (Agilent-027114). Median signal intensities were used for the analysis. After background subtraction (normexp) and normalization (quantile) differentially expressed genes were identified using linear models.; [Treatment]'Cells were incubated in phenol red free medium for 4hr (to ensure complete removal of phenol red) and treatment was started, after a DPBS wash, by adding fresh phenol red free medium along with appropriate drug or vehicle.'; [Growth]'MCF7 cells were maintained in phenol red containing DMEM-F12 supplemented with 10%FBS. For experiments cells were seeded in 6 well plates at a density of 2*10^5 cells/well in phenol red containing medium. After 48hr spent medium was removed, cells were washed with DPBS and phenol red free DMEM-F12, supplemented with 10% charcoal stripped dextran treated FCS, was added.'; [Extraction]'After the After 24hr of treatment the spent medium was removed and cells were lysed in RLT lysis buffer and total RNA was isolated by Qiagen’s RNeasy minikit.'; [Cell type]'epithelial''cell line: MCF7; tissue: mammary gland/breast; cell type: epithelial; treated with: vehicle (EtOH) for 24hrs; ', 'cell line: MCF7; tissue: mammary gland/breast; cell type: epithelial; treated with: vehicle (EtOH) + estrogen for 24hrs; ', 'cell line: MCF7; tissue: mammary gland/breast; cell type: epithelial; treated with: EGCG for 24hrs; ', 'cell line: MCF7; tissue: mammary gland/breast; cell type: epithelial; treated with: EGCG + estrogen for 24hrs; ' GSE150580 Mus musculus 7 Expression profiling by high throughput sequencing GPL21273 Aging-associated alterations in mammary epithelia and stroma revealed by single-cell RNA sequencing 2020-05-14 Aging of the mammary gland is closely associated with increased susceptibility to breast cancer, yet there have been limited systematic studies of aging-induced alterations within this organ. Here we leveraged the power of high-throughput single-cell RNA-sequencing (scRNA-seq) to generate a detailed transcriptomic atlas of young and aged murine mammary tissues, including both epithelial and stromal cell types. This analysis identified altered proportions and distinct gene expression patterns in multiple cell populations as a consequence of aging, independent of history of pregnancy and hormone cycle. In addition, we detected a rare luminal cell type that expresses both hormone-sensing and alveolar lineage markers as well as a unique gene expression signature. In addition, these cells exhibit a significant decrease in relative abundance with age. Overall, this high-resolution transcriptomic landscape reveals the effects of aging on normal mammary gland physiology and can serve as a valuable resource for understanding aging-associated susceptibility to breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE150580 Aging-Associated Alterations in Mammary Epithelia and Stroma Revealed by Single-Cell RNA Sequencing. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2020.108566 {Cell reports (7.815): 10.1016/j.celrep.2020.108566} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA632852 https://www.ebi.ac.uk/ena/browser/view/PRJNA632852 https://www.ncbi.nlm.nih.gov/sra?term=SRP261618 [Overal design]Single-cell RNA-seq (scRNA-seq) analysis of mammary tissues of 3 young mice (3-4 months of age) and 4 aged mice (13-14 months of age) using the 10X Chromium v2 platform.; [Treatment]'None'; [Growth]'None'; [Extraction]'Abdominal #4 mammary glands, with lymph nodes removed, were finely minced and then incubated in a digestion solution containing DMEM/F12 (Gibco 11330), 10% heat-inactivated fetal bovine serum, 2 mg/ml collagenase XI (Sigma C9407), and 0.1 mg/ml hyaluronidase (Sigma H3506) for 1.5 hours at 37°C with constant shaking at 150 rpm. The dissociated cells were then subjected to red blood cell lysis (Biolegend 420301), a 5-minute treatment with 1 U/ml dispase (Stem Cell Technologies 07913) and 0.1 mg/ml DNase (Stem Cell Technologies 7470), a 5-minute treatment with TrypLE (Gibco 12605010), and filtered through a 40 µm cell strainer. Cells were resuspended in PBS containing 0.04% BSA, counted manually under the microscope, and adjusted for loading 7,000 viable cells for single-cell RNA sequencing.\nSingle cell capturing and cDNA library generation were performed using the 10X Chromium 3’ library construction kit v2 following the manufacturer’s instruction.'; [Cell type]'Source: ''tissue type: Mammary glands (#4, abdominal glands); Sex: Female; age group: Young (3-4 months); ', 'tissue type: Mammary glands (#4, abdominal glands); Sex: Female; age group: Aged (13-14 months); ' GSE72111 Homo sapiens 8 Expression profiling by high throughput sequencing GPL16791 Genome-wide RNA-seq from GALNT14-depleted and GALNT14 overexpressing MDA-MB-231 LM2 and Par cells 2015-08-17 Purpose: To identify downstream signaling pathways that mediate functions of GALNT14 Methods: RNAs isolated from MDA231-LM2 cells expressing shCntr or shGALNT14 and MDA231-Par cells expressing pBabe-Hygro control vector or GALNT14 expression vector were analyzed by using an Illumina HiSeq 2500 Conclusions: Our study represents the first transcriptome profile of GALNT14-depleted MDA231-LM2 and GALNT14-overexpressing Par cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72111 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA293035 https://www.ebi.ac.uk/ena/browser/view/PRJNA293035 https://www.ncbi.nlm.nih.gov/sra?term=SRP062469 [Overal design]mRNAs prepared from GALNT14 knockdown or GALNT14 over-expressing MDA-MB-231 cells were analyzed in duplicaters by Illumina HiSeq 2500. RNA-Seq reads were aligned to the human reference genome (NCBI 37, hg19) using the spliced read aligner TopHat version 1.4.0.; [Treatment]'NA'; [Growth]'MDA-MB-231 cells were cultured in DMEM (Welgene, Republic of Korea) supplemented with 10% fetal bovine serum (FBS; JR Scientific, Woodland, CA) for 2 days.'; [Extraction]'Total RNAs were isolated using Qiazol (Qiagen, Valencia, CA) followed by chloroform extraction.\nTotal RNAs were subjected to enrichment of polyA+ RNA using Dynabeads Oligo (dT)25 (Invitrogen, Carlsbad, CA). Strand-specific RNA-seq libraries were prepared from the polyA+ RNA. The RNA-seq libraries were sequenced using single-end methodology with a length of 50 nt (SE50) (two replicates each) using an Illumina HiSeq 2500.'; [Cell type]'Lung metastatic derivative of MDA-MB-231', 'MDA-MB-231 parental''cell type: Lung metastatic derivative of MDA-MB-231; passage: 5-10; genotype: nontargeting shRNA; ', 'cell type: Lung metastatic derivative of MDA-MB-231; passage: 5-10; genotype: GALNT14 knockdown; ', 'cell type: MDA-MB-231 parental; passage: 5-10; genotype: vector control; ', 'cell type: MDA-MB-231 parental; passage: 5-10; genotype: GALNT14 over-expression; ' GSE6548 Homo sapiens 8 Expression profiling by array GPL570 An estrogen-dependent model of breast cancer created by transformation of normal human mammary epithelial cells 2006-12-16 This study was performed to check that ESR1 and BMI1 are biologically active after lentiviral transduction of primary human mammary epithelial cells (HMECs) with lentiviral vectors expressing ESR1 and BMI1 from the human PGK promoter. ESR1 targets like PGR, PRLR and GREB1, but not TFF1 and XBP1, were induced by estradiol in the ESR1-expressing cells. BMI1 targets like BMI1, NEFL and CCND2 were repressed in the BMI1-expressing cells. BMI1 suppressed genes associated with squamous and neural differentiation in the ESR1 plus BMI1-expressing cells. Keywords: Drug response https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE6548 An oestrogen-dependent model of breast cancer created by transformation of normal human mammary epithelial cells. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr1734 {Breast cancer research : BCR (5.676): 10.1186/bcr1734} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA98591 https://www.ebi.ac.uk/ena/browser/view/PRJNA98591 None [Overal design]Infect with lentiviruses 24 hours after reduction mammmoplasty. Grow cells in human mammosphere medium: Hepes-buffered DMEM/F12 supplemented with 20 ng/ml EGF, 1x B-27 (GIBCO) plus 1 nM 17-β-estradiol or 1 uM fulvestrant (ICI 182,780). Lentiviral vectors: pSD-82, ESR1; pSD-84, BMI1; pSD-86, gusA.; [Treatment]'Estradiol', 'Fulvestrant'; [Growth]'Mammosphere medium'; [Extraction]'RNeasy'; [Cell type]'Source: ''' GSE99596 Homo sapiens 6 Expression profiling by high throughput sequencing GPL11154 SIRT7 Antagonizes TGF-β Signaling and Inhibits Breast Cancer Metastasis 2017-06-02 Protein deacetylase SIRT7 is significantly downregulated in lung metastases of human patient and mouse tissues, and predicted metastasis-free survival. To explore the roles of SIRT7 in breast cancer, we analysed the gene expressions in breast cancer BT549 cells with SIRT7 knockdown or not. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99596 SIRT7 antagonizes TGF-β signaling and inhibits breast cancer metastasis. Nature communications 11.878 https://doi.org/10.1038/s41467-017-00396-9 {Nature communications (11.878): 10.1038/s41467-017-00396-9} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA388881 https://www.ebi.ac.uk/ena/browser/view/PRJNA388881 https://www.ncbi.nlm.nih.gov/sra?term=SRP108472 [Overal design]The mRNA profiles of breast cancer BT549 cells with SIRT7 knockdown or not were generated by deep sequencing using Illumina HiSeq-2000; [Treatment]'BT549 cells were transfected with control siRNAs or SIRT7-targeted siRNAs by using Lipofectamine®3000 (Thermo).'; [Growth]'BT549 cells were cultured in RPMI-1640 (Gibco®) with 10% FBS.'; [Extraction]'Total RNA extracts are first treated with DNase I to degrade DNA contamination. Next, by using the oligo (dT) magnetic beads the mRNA is enriched . Mixed with the fragmentation buffer, the mRNA is fragmented into short fragments. The first strand of cDNA is synthesized by using random hexamer-primer. Buffer, dNTPs, RNase H and DNA polymerase I are added to synthesize the second strand. The double strand cDNA is purified with AMPure XP beads. End reparation and 3’-end single nucleotide A (adenine) addition is then performed. Finally, sequencing adaptors are ligated to the fragments. The fragments are enriched by PCR amplification.\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'breast cancer cells''cell line: BT549; cell type: breast cancer cells; transfected with: control siRNAs; ', 'cell line: BT549; cell type: breast cancer cells; transfected with: SIRT7-targeted siRNAs; ' GSE26539 Homo sapiens 13 Expression profiling by array GPL7504 Generation of tumor initiating cells by exogenous delivery of OCT4 transcription factor 2011-01-10 Introduction: Tumor initiating cells (TICs) are being extensively studied for their role in tumor etiology, maintenance and resistance to treatment. The isolation of TICs has been limited by the scarcity of this population in the tissue of origin and because the molecular signatures that characterize these cells are not well understood. Herein, we describe the generation of TIC-like cell lines by ectopic expression of the OCT4 transcription factor (TF) in primary breast cell preparations. Methods: OCT4 cDNA was over-expressed in four different primary human mammary epithelial (HMEC) breast cell preparations from reduction mammoplasty donors. OCT4-transduced breast cells (OTBCs) generated colonies (frequency ~0.01%) in self-renewal conditions (feeder cultures in human embryonic stem cell media). Differentiation assays, immunofluorescence, immunohistochemistry, and flow cytometry were performed to investigate the cell of origin of OTBCs. Serial dilutions of OTBCs were injected in nude mice to address their tumorigenic capabilities. Gene expression microarrays were performed in OTBCs, and the role of downstream targets of OCT4 in maintaining self-renewal was investigated by knock-down experiments. Results: OTBCs overcame senescence, overexpressed telomerase, and down-regulated p16INK4A. In differentiation conditions, OTBCs generated populations of both myoepithelial and luminal cells at low frequency, suggesting that the cell of origin of some OTBCs was a bi-potent stem cell. Injection of OTBCs in nude mice generated poorly differentiated breast carcinomas with colonization capabilities. Gene expression microarrays of OTBC lines revealed a gene signature that was over-represented in the claudin-low molecular subtype of breast cancer. Lastly, siRNA-mediated knockdown of OCT4 or downstream embryonic targets of OCT4, such as NANOG and ZIC1, suppressed the ability of OTBCs to self-renew. Conclusions: Transduction of OCT4 in normal breast preparations lead to the generation of cell lines possessing tumor initiating and colonization capabilities. These cells developed high-grade, poorly differentiated breast carcinomas in nude mice. Genome-wide analysis of OTBCs outlined an embryonic TF circuitry that could be operative in TICs, resulting in up-regulation of oncogenes and loss of tumor suppressive functions. These OTBCs represent a patient-specific model system for the discovery of novel oncogenic targets in claudin-low tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26539 Generation of tumor-initiating cells by exogenous delivery of OCT4 transcription factor. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr3019 {Breast cancer research : BCR (5.676): 10.1186/bcr3019} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA136665 https://www.ebi.ac.uk/ena/browser/view/PRJNA136665 None [Overal design]12 cell lines; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA isolated by Stratagene', 'Qiagen Rneasy Kit'; [Cell type]'Source: ''reference: Human Reference B; ', 'cell line: p48 human mammary epithelial cell preparation; ', 'cell line: p52 human mammary epithelial cell preparation; ', 'cell line: p78 human mammary epithelial cell preparation; ', 'cell line: p86 human mammary epithelial cell preparation; ', 'cell line: OTBCs52-L1 OCT4 transduced breast cells; ', 'cell line: OTBCs78-L1 OCT4 transduced breast cells; ', 'cell line: OTBCs86-L1 OCT4 transduced breast cells; ', 'cell line: OTBCs48-L1 OCT4 transduced breast cells; ', 'cell line: OTBCs86-L4 OCT4 transduced breast cells; ', 'cell line: OTBCs86-L6 OCT4 transduced breast cells; ', 'cell line: OTBCs81-L1 OCT4 transduced breast cells transfected with an OCT4 siRNA; ', 'cell line: OTBCs81-L1 OCT4 transduced breast cells transfected with an OCT4 siRNA replicate; ', 'tumor: from OTBCs86-L1; ' GSE25055 Homo sapiens 310 Expression profiling by array GPL96 Discovery cohort for genomic predictor of response and survival following neoadjuvant taxane-anthracycline chemotherapy in breast cancer 2010-11-01 PURPOSE: To develop a predictive test for response and survival following neoadjuvant taxane-anthracycline chemotherapy for HER2-negative invasive breast cancer. METHODS: We developed a microarray-based gene expression test from pre-treatment tumor biopsies (310 patients) to predict favorable outcome based on estrogen receptor (ER) status,pathologic response to chemotherapy, 3-year disease outcomes, and sensitivity to endocrine therapy. Tumors were classified as treatment-sensitive if predicted to have pathologic response (and not resistance) to chemotherapy, or sensitive to endocrine therapy. We tested predictive accuracy, with 95% confidence interval (CI), for pathologic response (PPV, positive predictive value), distant relapse-free survival (DRFS), and absolute risk reduction at median follow-up in 198 other patients. Independence from clinical-pathologic factors was assessed in a multivariate Cox regression analysis based on the likelihood ratio test. Other evaluable, published response predictors (genomic grade index (GGI), intrinsic subtype (PAM50), pCR predictor (DLDA30)) were compared. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE25055 A genomic predictor of response and survival following taxane-anthracycline chemotherapy for invasive breast cancer. JAMA 51.273 https://doi.org/10.1001/jama.2011.593 {JAMA (51.273): 10.1001/jama.2011.593} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA142759 https://www.ebi.ac.uk/ena/browser/view/PRJNA142759 None [Overal design]Neoadjuvant study of 310 HER2-negative breast cancer cases treated with taxane-anthracycline chemotherapy pre-operatively and endocrine therapy if ER-positive. Response was assessed at the end of neoadjuvant treatment and distant-relapse-free survival was followed for at least 3 years post-surgery.; [Treatment]'Patients prospectively consented to a research biopsy by fine needle aspiration (FNA) or core biopsy (CBX) prior to any systemic therapy, and to the future assessment of pathologic response and/or survival endpoints'; [Growth]'None'; [Extraction]'Total RNA was extracted from tissue using Qiagen Rneasy columns'; [Cell type]'Source: ''sample id: 1002; source: ISPY; age_years: 37.8; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.346; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1005; source: ISPY; age_years: 45.8; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: NA; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.552; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1009; source: ISPY; age_years: 40.7; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.503; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1011; source: ISPY; age_years: 40.8; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 4=Indeterminate; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.424; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1016; source: ISPY; age_years: 35.5; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.580; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1019; source: ISPY; age_years: 52.2; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N0; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.205; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1027; source: ISPY; age_years: 38.2; er_status_ihc: N; pr_status_ihc: N; her2_status: I; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.732; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1031; source: ISPY; age_years: 54.2; er_status_ihc: I; pr_status_ihc: I; her2_status: NA; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: NA; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: NA; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.300; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1034; source: ISPY; age_years: 46.6; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.783; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1035; source: ISPY; age_years: 40.8; er_status_ihc: P; pr_status_ihc: P; her2_status: P; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 2; pathologic_response_pcr_rd: NA; pathologic_response_rcb_class: NA; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.000; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1037; source: ISPY; age_years: 51.1; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.156; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1038; source: ISPY; age_years: 37.8; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.370; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1041; source: ISPY; age_years: 46.6; er_status_ihc: P; pr_status_ihc: P; her2_status: P; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.597; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1044; source: ISPY; age_years: 58.8; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.248; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1045; source: ISPY; age_years: 49.6; er_status_ihc: I; pr_status_ihc: I; her2_status: NA; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.953; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1049; source: ISPY; age_years: 50.4; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: Inflammatory; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.988; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1050; source: ISPY; age_years: 63.2; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.832; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1054; source: ISPY; age_years: 42.8; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.307; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1055; source: ISPY; age_years: 52.8; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.104; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1057; source: ISPY; age_years: 44.2; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: Inflammatory; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.151; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1061; source: ISPY; age_years: 54.2; er_status_ihc: N; pr_status_ihc: N; her2_status: P; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.964; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1062; source: ISPY; age_years: 34.6; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.115; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1064; source: ISPY; age_years: 60.1; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: NA; pathologic_response_rcb_class: NA; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.415; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1067; source: ISPY; age_years: 58.4; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: NA; pathologic_response_rcb_class: NA; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.872; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Basal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1068; source: ISPY; age_years: 53.2; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.706; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1074; source: ISPY; age_years: 36.5; er_status_ihc: P; pr_status_ihc: N; her2_status: NA; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.222; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1078; source: ISPY; age_years: 31.3; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.822; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1088; source: ISPY; age_years: 53.1; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.304; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1089; source: ISPY; age_years: 61.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.162; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1092; source: ISPY; age_years: 44.1; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.074; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1095; source: ISPY; age_years: 43.6; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N0; clinical_ajcc_stage: Inflammatory; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.800; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1100; source: ISPY; age_years: 63.3; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.126; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1106; source: ISPY; age_years: 50.4; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: NA; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.344; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1113; source: ISPY; age_years: 53.5; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.954; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1114; source: ISPY; age_years: 44.8; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.019; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Her2; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1123; source: ISPY; age_years: 61.9; er_status_ihc: P; pr_status_ihc: P; her2_status: I; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.883; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1127; source: ISPY; age_years: 47.6; er_status_ihc: P; pr_status_ihc: P; her2_status: I; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.574; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1132; source: ISPY; age_years: 51.4; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.617; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1134; source: ISPY; age_years: 43.1; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.696; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1135; source: ISPY; age_years: 58.9; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.841; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1136; source: ISPY; age_years: 60.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.545; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1138; source: ISPY; age_years: 35.1; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 4=Indeterminate; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.464; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1140; source: ISPY; age_years: 35.1; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.904; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1144; source: ISPY; age_years: 56.3; er_status_ihc: N; pr_status_ihc: N; her2_status: NA; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.360; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1145; source: ISPY; age_years: 39.4; er_status_ihc: N; pr_status_ihc: N; her2_status: P; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.032; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1149; source: ISPY; age_years: 59.2; er_status_ihc: NA; pr_status_ihc: NA; her2_status: NA; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: Inflammatory; grade: NA; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.239; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1150; source: ISPY; age_years: 51.5; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.946; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1155; source: ISPY; age_years: 42.7; er_status_ihc: N; pr_status_ihc: P; her2_status: NA; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.902; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1158; source: ISPY; age_years: 61.8; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.261; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1160; source: ISPY; age_years: 55.7; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: NA; drfs_1_event_0_censored: 0; drfs_even_time_years: 0.898; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1163; source: ISPY; age_years: 38.9; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.533; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1164; source: ISPY; age_years: 60.1; er_status_ihc: P; pr_status_ihc: P; her2_status: I; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: NA; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.872; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1165; source: ISPY; age_years: 39.7; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.669; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1169; source: ISPY; age_years: 44.2; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.715; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1170; source: ISPY; age_years: 44.4; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.174; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1172; source: ISPY; age_years: 44.6; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 0.914; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1173; source: ISPY; age_years: 44.0; er_status_ihc: I; pr_status_ihc: I; her2_status: NA; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.798; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1175; source: ISPY; age_years: 64.3; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.672; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1177; source: ISPY; age_years: 40.8; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.530; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1180; source: ISPY; age_years: 31.5; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.192; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1188; source: ISPY; age_years: 38.3; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.026; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1191; source: ISPY; age_years: 45.9; er_status_ihc: P; pr_status_ihc: I; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.045; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1193; source: ISPY; age_years: 59.6; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.275; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1197; source: ISPY; age_years: 44.7; er_status_ihc: N; pr_status_ihc: P; her2_status: NA; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.692; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1199; source: ISPY; age_years: 37.7; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.383; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1200; source: ISPY; age_years: 43.8; er_status_ihc: I; pr_status_ihc: I; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.401; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1203; source: ISPY; age_years: 42.3; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: NA; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.508; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1205; source: ISPY; age_years: 42.6; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: NA; pathologic_response_pcr_rd: NA; pathologic_response_rcb_class: NA; drfs_1_event_0_censored: 0; drfs_even_time_years: 0.523; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1208; source: ISPY; age_years: 42.1; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.432; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1209; source: ISPY; age_years: 43.4; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.640; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1210; source: ISPY; age_years: 40.6; er_status_ihc: P; pr_status_ihc: P; her2_status: NA; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.119; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1216; source: ISPY; age_years: 34.4; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.133; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1217; source: ISPY; age_years: 50.1; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 4=Indeterminate; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: NA; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.361; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1218; source: ISPY; age_years: 47.8; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.264; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1219; source: ISPY; age_years: 46.0; er_status_ihc: P; pr_status_ihc: P; her2_status: NA; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.198; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1220; source: ISPY; age_years: 43.1; er_status_ihc: N; pr_status_ihc: N; her2_status: NA; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: NA; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.390; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1223; source: ISPY; age_years: 59.8; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.587; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1225; source: ISPY; age_years: 47.8; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T1; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: NA; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.086; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1226; source: ISPY; age_years: 42.1; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.478; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1227; source: ISPY; age_years: 42.5; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.527; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: 1231; source: ISPY; age_years: 45.5; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.453; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1232; source: ISPY; age_years: 50.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: NA; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.744; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: 1236; source: ISPY; age_years: 38.6; er_status_ihc: N; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.936; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: M106; source: MDACC; age_years: 56.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 7.083; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: M107; source: MDACC; age_years: 47.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.758; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; tissue: breast cancer tumor; ', 'sample id: M111; source: MDACC; age_years: 49.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_s tatus_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 7.395; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; tissue: breast cancer tumor; ', 'sample id: M113; source: MDACC; age_years: 75.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 7.439; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M117; source: MDACC; age_years: 34.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.710; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M120; source: MDACC; age_years: 51.0; er_status_ihc: N; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 7.302; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M121; source: MDACC; age_years: 65.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T1; clinical_nodal_status: N0; clinical_ajcc_stage: I; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 1; drfs_even_time_years: 5.591; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M123; source: MDACC; age_years: 51.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 1; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.661; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M128; source: MDACC; age_years: 66.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.834; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M129; source: MDACC; age_years: 61.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.717; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M130; source: MDACC; age_years: 65.0; er_status_ihc: N; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.144; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M133; source: MDACC; age_years: 37.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 7.127; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M136; source: MDACC; age_years: 37.0; er_status_ihc: N; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T1; clinical_nodal_status: N0; clinical_ajcc_stage: I; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.341; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M139; source: MDACC; age_years: 51.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 7.326; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M146; source: MDACC; age_years: 40.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T1; clinical_nodal_status: N0; clinical_ajcc_stage: I; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.439; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M153; source: MDACC; age_years: 61.0; er_status_ihc: N; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T1; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.519; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M154; source: MDACC; age_years: 29.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.764; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M155; source: MDACC; age_years: 61.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.467; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M156; source: MDACC; age_years: 67.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.612; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M157; source: MDACC; age_years: 57.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.593; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M158; source: MDACC; age_years: 38.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.535; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M165; source: MDACC; age_years: 49.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 3.452; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M177; source: MDACC; age_years: 41.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.111; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M180; source: MDACC; age_years: 42.0; er_status_ihc: N; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.453; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M181; source: MDACC; age_years: 73.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.505; esr1_status: P; erbb2_status: P; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M182; source: MDACC; age_years: 46.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T1; clinical_nodal_status: N0; clinical_ajcc_stage: I; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.311; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M188; source: MDACC; age_years: 68.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 6.059; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M189; source: MDACC; age_years: 47.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.829; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M195; source: MDACC; age_years: 42.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.793; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M196; source: MDACC; age_years: 69.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.870; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M199; source: MDACC; age_years: 56.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.133; esr1_status: N; erbb2_status: P; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M201; source: MDACC; age_years: 75.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.892; esr1_status: P; erbb2_status: P; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M205; source: MDACC; age_years: 35.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.142; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M206; source: MDACC; age_years: 48.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.684; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M211; source: MDACC; age_years: 53.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.624; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M214; source: MDACC; age_years: 54.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.536; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M215; source: MDACC; age_years: 44.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.251; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M216; source: MDACC; age_years: 58.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.669; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M217; source: MDACC; age_years: 52.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.645; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M219; source: MDACC; age_years: 56.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.575; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M220; source: MDACC; age_years: 38.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 0.482; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M226; source: MDACC; age_years: 31.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.966; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M227; source: MDACC; age_years: 38.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 3.362; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M228; source: MDACC; age_years: 48.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.536; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M229; source: MDACC; age_years: 57.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.624; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M231; source: MDACC; age_years: 52.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.597; esr1_status: P; erbb2_status: P; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M233; source: MDACC; age_years: 60.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.329; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M234; source: MDACC; age_years: 58.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.378; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M236; source: MDACC; age_years: 52.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 5.183; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M246; source: MDACC; age_years: 42.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T1; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.580; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M255; source: MDACC; age_years: 48.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.890; esr1_status: N; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M259; source: MDACC; age_years: 39.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.008; esr1_status: P; erbb2_status: P; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M260; source: MDACC; age_years: 49.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.528; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M261; source: MDACC; age_years: 56.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.888; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M263; source: MDACC; age_years: 72.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.791; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M266; source: MDACC; age_years: 45.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.348; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M270; source: MDACC; age_years: 67.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N0; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.887; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M280; source: MDACC; age_years: 71.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.877; esr1_status: P; erbb2_status: P; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M281; source: MDACC; age_years: 45.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.575; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M282; source: MDACC; age_years: 44.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.233; esr1_status: P; erbb2_status: P; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M283; source: MDACC; age_years: 46.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.110; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M295; source: MDACC; age_years: 48.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.803; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M297; source: MDACC; age_years: 63.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.052; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M301; source: MDACC; age_years: 46.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.485; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M304; source: MDACC; age_years: 46.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.298; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M310; source: MDACC; age_years: 51.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T1; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.063; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M315; source: MDACC; age_years: 36.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.256; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M319; source: MDACC; age_years: 26.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.542; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M323; source: MDACC; age_years: 40.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T1; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.027; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M332; source: MDACC; age_years: 42.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.214; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M333; source: MDACC; age_years: 67.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 3.756; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M334; source: MDACC; age_years: 63.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T1; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.745; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M339; source: MDACC; age_years: 44.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.754; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M340; source: MDACC; age_years: 54.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.194; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M341; source: MDACC; age_years: 41.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.057; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M343; source: MDACC; age_years: 49.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.153; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M345; source: MDACC; age_years: 39.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.854; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M353; source: MDACC; age_years: 51.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.647; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M355; source: MDACC; age_years: 59.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.540; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M356; source: MDACC; age_years: 55.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.469; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M357; source: MDACC; age_years: 62.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.775; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M360; source: MDACC; age_years: 56.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T0; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.752; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M363; source: MDACC; age_years: 58.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.973; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M365; source: MDACC; age_years: 42.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 4.783; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M367; source: MDACC; age_years: 61.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.992; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M373; source: MDACC; age_years: 45.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.732; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M375; source: MDACC; age_years: 63.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.685; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M384; source: MDACC; age_years: 60.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.518; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M386; source: MDACC; age_years: 42.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 3.277; esr1_status: P; erbb2_status: P; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M396; source: MDACC; age_years: 35.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.504; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M399; source: MDACC; age_years: 40.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.283; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M402; source: MDACC; age_years: 38.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.715; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M411; source: MDACC; age_years: 44.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.881; esr1_status: N; erbb2_status: P; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M417; source: MDACC; age_years: 63.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_ce nsored: 0; drfs_even_time_years: 3.775; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumB; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M421; source: MDACC; age_years: 48.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.281; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M423; source: MDACC; age_years: 68.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T0; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.794; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M425; source: MDACC; age_years: 60.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.396; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M430; source: MDACC; age_years: 52.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.272; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M431; source: MDACC; age_years: 50.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.587; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M433; source: MDACC; age_years: 47.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.250; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M434; source: MDACC; age_years: 50.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.188; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M442; source: MDACC; age_years: 41.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.447; esr1_status: P; erbb2_status: P; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M447; source: MDACC; age_years: 44.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.489; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M463; source: MDACC; age_years: 60.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.009; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M469; source: MDACC; age_years: 57.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.187; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M485; source: MDACC; age_years: 50.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.842; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M486; source: MDACC; age_years: 44.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.368; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M497; source: MDACC; age_years: 62.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.159; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M502; source: MDACC; age_years: 50.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.717; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M503; source: MDACC; age_years: 38.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T1; clinical_nodal_status: N0; clinical_ajcc_stage: I; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.604; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M506; source: MDACC; age_years: 46.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.028; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M507; source: MDACC; age_years: 66.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.151; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M513; source: MDACC; age_years: 59.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.709; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M523; source: MDACC; age_years: 47.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.371; esr1_status: P; erbb2_status: N; set_class: SET-High; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M524; source: MDACC; age_years: 31.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.372; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M525; source: MDACC; age_years: 45.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 3.047; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M531; source: MDACC; age_years: 53.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.856; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M534; source: MDACC; age_years: 46.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.105; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M545; source: MDACC; age_years: 58.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.341; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M549; source: MDACC; age_years: 40.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.990; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M556; source: MDACC; age_years: 47.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T1; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.667; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M557; source: MDACC; age_years: 57.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.884; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M558; source: MDACC; age_years: 62.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.552; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M559; source: MDACC; age_years: 55.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.851; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M564; source: MDACC; age_years: 68.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.344; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M565; source: MDACC; age_years: 57.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T1; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.916; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M566; source: MDACC; age_years: 39.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.648; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M569; source: MDACC; age_years: 58.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.818; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M571; source: MDACC; age_years: 32.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.817; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M577; source: MDACC; age_years: 51.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.754; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M578; source: MDACC; age_years: 45.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.845; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M580; source: MDACC; age_years: 64.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.338; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M581; source: MDACC; age_years: 34.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.694; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M583; source: MDACC; age_years: 51.0; er_status_ihc: N; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.706; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Basal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M599; source: MDACC; age_years: 50.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T1; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.617; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M601; source: MDACC; age_years: 71.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.264; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M603; source: MDACC; age_years: 32.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.890; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M607; source: MDACC; age_years: 67.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T1; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.884; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M608; source: MDACC; age_years: 47.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.700; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M610; source: MDACC; age_years: 47.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.371; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M611; source: MDACC; age_years: 63.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.278; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M612; source: MDACC; age_years: 40.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.350; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M617; source: MDACC; age_years: 50.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.516; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M619; source: MDACC; age_years: 52.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.799; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M624; source: MDACC; age_years: 32.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.881; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M625; source: MDACC; age_years: 49.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T1; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.456; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M635; source: MDACC; age_years: 43.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T1; clinical_nodal_status: N3; clinical_ajcc_stage: IIIC; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.146; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M636; source: MDACC; age_years: 57.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.480; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M639; source: MDACC; age_years: 65.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.533; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M642; source: MDACC; age_years: 45.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.357; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M643; source: MDACC; age_years: 41.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.059; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M647; source: MDACC; age_years: 65.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.797; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M651; source: MDACC; age_years: 61.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.188; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M652; source: MDACC; age_years: 66.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.437; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M657; source: MDACC; age_years: 48.0; er_status_ihc: N; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T1; clinical_nodal_status: N0; clinical_ajcc_stage: I; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.234; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M658; source: MDACC; age_years: 61.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.198; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M659; source: MDACC; age_years: 51.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.923; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M661; source: MDACC; age_years: 49.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.261; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M662; source: MDACC; age_years: 46.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.182; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M665; source: MDACC; age_years: 57.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.064; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M666; source: MDACC; age_years: 58.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.171; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M668; source: MDACC; age_years: 50.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.094; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M669; source: MDACC; age_years: 47.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.223; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M670; source: MDACC; age_years: 43.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.958; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M671; source: MDACC; age_years: 30.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T1; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.845; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M673; source: MDACC; age_years: 58.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.377; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M675; source: MDACC; age_years: 64.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.059; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M677; source: MDACC; age_years: 42.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.306; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M679; source: MDACC; age_years: 72.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 2.253; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M681; source: MDACC; age_years: 33.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.303; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M682; source: MDACC; age_years: 50.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.333; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M683; source: MDACC; age_years: 59.0; er_status_ihc: N; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.281; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M685; source: MDACC; age_years: 53.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.393; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M690; source: MDACC; age_years: 73.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.160; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M691; source: MDACC; age_years: 46.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T1; clinical_nodal_status: N1; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.670; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M692; source: MDACC; age_years: 46.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.415; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M693; source: MDACC; age_years: 47.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.010; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M695; source: MDACC; age_years: 43.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.161; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M696; source: MDACC; age_years: 53.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.744; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M706; source: MDACC; age_years: 69.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N0; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.076; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M709; source: MDACC; age_years: 51.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.728; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M710; source: MDACC; age_years: 53.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.979; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M714; source: MDACC; age_years: 64.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.892; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Normal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M717; source: MDACC; age_years: 52.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.963; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M718; source: MDACC; age_years: 36.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.613; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insens itive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M722; source: MDACC; age_years: 34.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.541; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M723; source: MDACC; age_years: 63.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.927; esr1_status: P; erbb2_status: P; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M725; source: MDACC; age_years: 46.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.878; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M728; source: MDACC; age_years: 49.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.517; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M729; source: MDACC; age_years: 28.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.728; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M732; source: MDACC; age_years: 50.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.900; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M734; source: MDACC; age_years: 36.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.336; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M735; source: MDACC; age_years: 67.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.711; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M739; source: MDACC; age_years: 39.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.695; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M744; source: MDACC; age_years: 44.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.029; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M746; source: MDACC; age_years: 56.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.665; esr1_status: P; erbb2_status: P; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M750; source: MDACC; age_years: 75.0; er_status_ihc: N; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.240; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M751; source: MDACC; age_years: 51.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.133; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M753; source: MDACC; age_years: 49.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N0; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.719; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M757; source: MDACC; age_years: 41.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.120; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M758; source: MDACC; age_years: 62.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.144; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M763; source: MDACC; age_years: 40.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.170; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M765; source: MDACC; age_years: 62.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.008; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M766; source: MDACC; age_years: 59.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.142; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M767; source: MDACC; age_years: 51.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.243; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M768; source: MDACC; age_years: 57.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.284; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M771; source: MDACC; age_years: 37.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.128; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M774; source: MDACC; age_years: 49.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 0.879; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M779; source: MDACC; age_years: 38.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.391; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M781; source: MDACC; age_years: 40.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N0; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 0.778; esr1_status: P; erbb2_status: N; set_class: SET-Int; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M782; source: MDACC; age_years: 53.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N3; clinical_ajcc_stage: IIIB; grade: 1; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.147; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M783; source: MDACC; age_years: 46.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.487; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M784; source: MDACC; age_years: 58.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N0; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.188; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M791; source: MDACC; age_years: 65.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.085; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M792; source: MDACC; age_years: 43.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.265; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M794; source: MDACC; age_years: 62.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.194; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M795; source: MDACC; age_years: 64.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N0; clinical_ajcc_stage: IIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.062; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M802; source: MDACC; age_years: 32.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T3; clinical_nodal_status: N1; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 0.824; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M805; source: MDACC; age_years: 57.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T2; clinical_nodal_status: N1; clinical_ajcc_stage: IIB; grade: 2; pathologic_response_pcr_rd: pCR; pathologic_response_rcb_class: RCB-0/I; drfs_1_event_0_censored: 0; drfs_even_time_years: 0.931; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Sensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-0/I; ', 'sample id: M806; source: MDACC; age_years: 49.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.192; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: M810; source: MDACC; age_years: 51.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T3; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 1.051; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: PERU01; source: MDACC; age_years: 73.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.746; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: Low; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-0/I; ', 'sample id: PERU07; source: MDACC; age_years: 71.0; er_status_ihc: P; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.511; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: PERU09; source: MDACC; age_years: 47.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.363; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumA; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: PERU11; source: MDACC; age_years: 50.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N1; clinical_ajcc_stage: IIIB; grade: 2; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-II; drfs_1_event_0_censored: 1; drfs_even_time_years: 1.265; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Basal; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ', 'sample id: PERU12_14; source: MDACC; age_years: 65.0; er_status_ihc: P; pr_status_ihc: P; her2_status: N; er_status_ihc_esr1_for indeterminate: P; clinical_t_stage: T2; clinical_nodal_status: N2; clinical_ajcc_stage: IIIA; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 0; drfs_even_time_years: 2.198; esr1_status: P; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: LumB; dlda30_prediction: RD; rcb_0_i_prediction: RCB-II/III; ', 'sample id: PERU14_16; source: MDACC; age_years: 58.0; er_status_ihc: N; pr_status_ihc: N; her2_status: N; er_status_ihc_esr1_for indeterminate: N; clinical_t_stage: T4; clinical_nodal_status: N2; clinical_ajcc_stage: IIIB; grade: 3; pathologic_response_pcr_rd: RD; pathologic_response_rcb_class: RCB-III; drfs_1_event_0_censored: 1; drfs_even_time_years: 0.517; esr1_status: N; erbb2_status: N; set_class: SET-Low; chemosensitivity_prediction: Rx Insensitive; ggi_class: High; pam50_class: Her2; dlda30_prediction: pCR; rcb_0_i_prediction: RCB-II/III; ' GSE26214 Homo sapiens 49 Genome variation profiling by genome tiling array GPL14645 Genomic profiles vary with race and subtype in young African American and European American breast cancer (aCGH) 2010-12-20 In the United States, African-American (AA) women are more likely to develop early-onset breast cancer and have historically poorer outcomes due to this disease compared to European-American (EA) women. Here, we analyzed genomic profiles of breast tumors from young women (<50 years old), matched by tumor subtype, histological grade, and ethnicity (African-American, AA, compared to European-American, EA). DNA copy number alterations (CNAs) were analyzed using a 32K BAC tiling path array. The study provides insight into the genetic component of ethnicity-related breast cancer health disparities. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26214 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA142329 https://www.ebi.ac.uk/ena/browser/view/PRJNA142329 None [Overal design]Breast tumor samples from young women (< 50 years old) were matched as follows: a matched pair consists of one AA and one EA sample, matched for tumor grade and tumor subtype (based on immunohistochemical analysis of ER, PR, and HER2 status). 44 experiments; each experiment is tumor DNA versus reference control DNA (AF) isolated from the blood of a 25-year-old African-American female with no familial or personal history of breast cancer. Additional control experiments included the AF reference versus the well-characterized F1 reference, and 3 self-self hybridization controls (AF versus AF).; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was isolated with phenol extraction according to the standard protocol (Sambrook, J., Fritsch, E. F. & Maniatis, T. Molecular cloning; a laboratory manual. Cold Spring Harbor Laboratory Press, Cold Spring Harbor, New York, 1989).'; [Cell type]'Source: ''gender: female; age: 22; tissue: breast (tumor); tumor grade: 2; race: European-American; diagnosis: invasive ductal carcinoma & associated ductal carcinoma in situ; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 25; tissue: blood; race: African-American; sample type: reference; ', 'gender: female; age: 39; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: invasive lobular carcinoma; subtype: luminal A; estrogen receptor: positive; progesterone receptor: positive; her2: equivocal; ', 'gender: female; age: 47; tissue: breast (tumor); tumor grade: 2; race: African-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 43; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: invasive ductal carcinoma with focal mucinous features; subtype: luminal B; estrogen receptor: positive; progesterone receptor: negative; her2: positive; ', 'gender: female; age: 50; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: 30% ductal carcinoma in situ/20% Invasive ductal carcinoma/20% fibrocystic; subtype: luminal A; estrogen receptor: positive; progesterone receptor: positive; her2: equivocal; ', 'gender: female; age: 47; tissue: breast (tumor); tumor grade: 2; race: European-American; diagnosis: invasive mammary carcinoma with ductal features; subtype: luminal A; estrogen receptor: positive; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 47; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: mucinous carcinoma; subtype: luminal A; estrogen receptor: positive; progesterone receptor: negative; her2: equivocal; ', 'gender: female; age: 47; tissue: breast (tumor); tumor grade: 2; race: European-American; diagnosis: lobular carcinoma; subtype: luminal A; estrogen receptor: positive; progesterone receptor: positive; her2: negative; ', 'gender: female; age: 50; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: metastatic ductal carcinoma to the lymph nodes; subtype: luminal B; estrogen receptor: positive; progesterone receptor: negative; her2: positive; ', 'gender: female; age: 44; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: metastatic ductal carcinoma to the lymph nodes; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 42; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: metastatic ductal carcinoma to the lymph nodes; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: equivocal; ', 'gender: female; age: 48; tissue: breast (tumor); tumor grade: 2; race: European-American; diagnosis: invasive ductal carcinoma, ductal carcinoma in situ (2%); subtype: luminal B; estrogen receptor: positive; progesterone receptor: positive; her2: positive; ', 'gender: female; age: 49; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 49; tissue: breast (tumor); tumor grade: 2; race: European-American; diagnosis: metastatic ductal carcinoma to the lymph nodes; subtype: luminal A; estrogen receptor: positive; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 42; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 40; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 34; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma, ductal carcinoma in situ 20/10; subtype: Her2+/ER-; estrogen receptor: negative; progesterone receptor: negative; her2: positive; ', 'gender: female; age: 43; tissue: breast (tumor); tumor grade: 2; race: European-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 50; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 43; tissue: breast (tumor); tumor grade: 2; race: African-American; diagnosis: invasive lobular carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 47; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma; subtype: luminal B; estrogen receptor: negative; progesterone receptor: positive; her2: positive; ', 'gender: female; age: 46; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 50; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: equivocal; ', 'gender: female; age: 47; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma; subtype: luminal B; estrogen receptor: positive; progesterone receptor: negative; her2: positive; ', 'gender: female; age: 40; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma (ductal carcinoma in situ <10/0); subtype: luminal B; estrogen receptor: positive; progesterone receptor: positive; her2: positive; ', 'gender: female; age: 47; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 50; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: invasive ductal carcinoma; subtype: Her2+/ER-; estrogen receptor: negative; progesterone receptor: negative; her2: positive; ', 'gender: female; age: 45; tissue: breast (tumor); tumor grade: 2; race: African-American; diagnosis: metastatic adenocarcinoma; subtype: luminal A; estrogen receptor: positive; progesterone receptor: positive; her2: negative; ', 'gender: female; age: 48; tissue: breast (tumor); tumor grade: 2; race: African-American; diagnosis: metastatic lobular carcinoma; subtype: luminal A; estrogen receptor: positive; progesterone receptor: positive; her2: equivocal; ', 'gender: female; age: 38; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: invasive ductal carcinoma; subtype: luminal A; estrogen receptor: positive; progesterone receptor: negative; her2: equivocal; ', 'gender: female; age: 44; tissue: breast (tumor); tumor grade: 2; race: African-American; diagnosis: invasive ductal carcinoma; subtype: luminal A; estrogen receptor: positive; progesterone receptor: positive; her2: negative; ', 'gender: female; age: 50; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: invasive ductal carcinoma; subtype: luminal B; estrogen receptor: positive; progesterone receptor: negative; her2: positive; ', 'gender: female; age: 43; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: invasive mammary carcinoma with ductal and lobular features; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 23; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: invasive ductal carcinoma; subtype: luminal A; estrogen receptor: positive; progesterone receptor: positive; her2: equivocal; ', 'gender: female; age: 35; tissue: breast (tumor); tumor grade: 3; race: African-American; diagnosis: invasive ductal carcinoma; subtype: luminal B; estrogen receptor: positive; progesterone receptor: positive; her2: positive; ', 'gender: female; age: 45; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma; subtype: luminal A; estrogen receptor: positive; progesterone receptor: positive; her2: equivocal; ', 'gender: female; age: 49; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 47; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 40; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: metastatic ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: negative; ', 'gender: female; age: 37; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma; subtype: luminal A; estrogen receptor: positive; progesterone receptor: positive; her2: negative; ', 'gender: female; age: 43; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: equivocal; ', 'gender: female; age: 38; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: equivocal; ', 'gender: female; age: 34; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma; subtype: luminal A; estrogen receptor: positive; progesterone receptor: positive; her2: equivocal; ', 'gender: female; age: 50; tissue: breast (tumor); tumor grade: 3; race: European-American; diagnosis: invasive ductal carcinoma; subtype: basal; estrogen receptor: negative; progesterone receptor: negative; her2: equivocal; ', 'gender: female; age: 25; tissue: blood; race: African-American; ', 'gender: female; age: unknown; tissue: blood; race: Caucasian; ' GSE44272 Homo sapiens 53 Expression profiling by array GPL13667 The Long-HER Study 2013-02-12 Trastuzumab improves survival outcomes in patients with HER2+ metastatic breast cancer. Some of these patients may become long-term survivors. The Long-Her study was designed to identify clinical and molecular markers that could differentiate long-term survivors from patients having early progression to trastuzumab. 103 patients were registered in the Long-HER study, of whom 71 had obtained a durable complete response. Median age was 58 years. Metastatic disease was diagnosed after a median of 24.7 months since primary diagnosis. Sixty-five per cent of tumours were poorly differentiated ductal carcinomas and hormonal receptors were present in 47%. Metastases were present in the liver (25%), lungs (25%), bones (23%) and soft tissues (23%), with 20% of patients having multiple locations of metastases. Median progression-free survival was 10.6 years after the diagnosis of metastatic disease. Absence of trastuzumab as part of adjuvant therapy was the only clinical factor associated with long-term survival . Gene ontology analysis demonstrated that genes involved in HIF activation, EGF receptor signalling pathway, PI3 kinase pathway, apoptosis signalling pathway and p53 pathway significantly correlated with response. The PI3K pathway was the most strongly associated with poor response to trastuzumab-based therapy: tumours in the control group usually had four or five alterations in this pathway, whereas tumours in the Long-HER group had two alterations at most. These findings support that trastuzumab may provide a substantial long-term survival benefit in a selected group of patients. Whole genome expression analysis comparing long-term survivors vs. a control group predicted early progression to trastuzumab-based therapy. Multiple alterations in genes related to the PI3K-mTOR pathway seem to be required to confer resistance to this therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE44272 The Long-HER study: clinical and molecular analysis of patients with HER2+ advanced breast cancer who become long-term survivors with trastuzumab-based therapy. PloS one 2.776 https://doi.org/10.1371/journal.pone.0109611 {PloS one (2.776): 10.1371/journal.pone.0109611} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA189275 https://www.ebi.ac.uk/ena/browser/view/PRJNA189275 None [Overal design]53 FFPE samples, which passed the RNA quality control criteria, were analyzed (45 primary tumours and 8 metastases). Among these 53 samples, 35 samples corresponded to long-term responders and 18 to the control group.; [Treatment]'Participants had to fulfill all the following criteria: a confirmed diagnosis of metastatic breast cancer; HER2 positive disease, as determined by 3+ immunohistochemistry or positive FISH; treatment with chemotherapy plus trastuzumab; stable disease or a complete response lasting at least 3 years. A control group was also created with patients who had had a progression within the first 12 months of first-line trastuzumab-based therapy.'; [Growth]'None'; [Extraction]'Selected FFPE tumour specimens were cut into serial sections with a thickness of 10 µm. RNA was then extracted with the RecoverAll Total Nucleic Acid Isolation Kit (Life Technologies).'; [Cell type]'Source: ''age (years): 47; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T4; lymph node status (n): N2; tumor grade (g): G3; er status: -; pgr status: ND; ', 'age (years): 64; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T1; lymph node status (n): N0; tumor grade (g): ND; er status: -; pgr status: -; ', 'age (years): 62; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T3; lymph node status (n): N1; tumor grade (g): G2; er status: -; pgr status: -; ', 'age (years): 57; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T1; lymph node status (n): N2; tumor grade (g): G2; er status: -; pgr status: -; ', 'age (years): 78; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N1; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 54; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T3; lymph node status (n): N1; tumor grade (g): ND; er status: -; pgr status: -; ', 'age (years): 68; sample type: primary tumor; sample group: Control; tumor size (t): T2; lymph node status (n): N0; tumor grade (g): G2; er status: -; pgr status: +; ', 'age (years): 79; sample type: metastasis; sample group: Long-HER (long-term responder); tumor size (t): T4; lymph node status (n): Nx; tumor grade (g): ND; er status: +; pgr status: -; ', 'age (years): 69; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T3; lymph node status (n): N2; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 56; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N1; tumor grade (g): ND; er status: +; pgr status: +; ', 'age (years): 48; sample type: metastasis; sample group: Long-HER (long-term responder); tumor size (t): T1; lymph node status (n): N0; tumor grade (g): G3; er status: +; pgr status: +; ', 'age (years): 66; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T4; lymph node status (n): N2; tumor grade (g): G2; er status: -; pgr status: -; ', 'age (years): 40; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T1; lymph node status (n): N1; tumor grade (g): G2; er status: +; pgr status: +; ', 'age (years): 54; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): Nx; tumor grade (g): ND; er status: +; pgr status: +; ', 'age (years): 78; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T1; lymph node status (n): Nx; tumor grade (g): ND; er status: +; pgr status: -; ', 'age (years): 80; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N1; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 87; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T4; lymph node status (n): N1; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 52; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N3; tumor grade (g): G2; er status: +; pgr status: +; ', 'age (years): 54; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T3; lymph node status (n): N2; tumor grade (g): G2; er status: -; pgr status: -; ', 'age (years): 57; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T1; lymph node status (n): N0; tumor grade (g): G3; er status: +; pgr status: +; ', 'age (years): 60; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N1; tumor grade (g): G3; er status: +; pgr status: +; ', 'age (years): 65; sample type: metastasis; sample group: Long-HER (long-term responder); tumor size (t): T1; lymph node status (n): N1; tumor grade (g): G2; er status: -; pgr status: -; ', 'age (years): 47; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): Tx; lymph node status (n): Nx; tumor grade (g): G2; er status: -; pgr status: +; ', 'age (years): 82; sample type: metastasis; sample group: Long-HER (long-term responder); tumor size (t): T1; lymph node status (n): N0; tumor grade (g): ND; er status: ND; pgr status: ND; ', 'age (years): 49; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N0; tumor grade (g): G3; er status: -; pgr status: +; ', 'age (years): 79; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N0; tumor grade (g): ND; er status: -; pgr status: -; ', 'age (years): 54; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N1; tumor grade (g): G3; er status: +; pgr status: -; ', 'age (years): 58; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T4; lymph node status (n): Nx; tumor grade (g): ND; er status: -; pgr status: -; ', 'age (years): 56; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N2; tumor grade (g): G3; er status: +; pgr status: +; ', 'age (years): 56; sample type: metastasis; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N0; tumor grade (g): G3; er status: +; pgr status: +; ', 'age (years): 59; sample type: metastasis; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): Nx; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 64; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N1; tumor grade (g): G3; er status: +; pgr status: +; ', 'age (years): 76; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N1; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 52; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N1; tumor grade (g): G3; er status: +; pgr status: +; ', 'age (years): 66; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T2; lymph node status (n): N0; tumor grade (g): G3; er status: -; pgr status: +; ', 'age (years): 76; sample type: primary tumor; sample group: Long-HER (long-term responder); tumor size (t): T3; lymph node status (n): Nx; tumor grade (g): G1; er status: +; pgr status: +; ', 'age (years): 63; sample type: primary tumor; sample group: Control; tumor size (t): T2; lymph node status (n): N0; tumor grade (g): G3; er status: +; pgr status: +; ', 'age (years): 49; sample type: primary tumor; sample group: Control; tumor size (t): T2; lymph node status (n): N1; tumor grade (g): G3; er status: +; pgr status: +; ', 'age (years): 55; sample type: primary tumor; sample group: Control; tumor size (t): T2; lymph node status (n): N1; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 59; sample type: metastasis; sample group: Control; tumor size (t): T2; lymph node status (n): N0; tumor grade (g): G3; er status: +; pgr status: -; ', 'age (years): 46; sample type: primary tumor; sample group: Control; tumor size (t): T2; lymph node status (n): N1; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 74; sample type: primary tumor; sample group: Control; tumor size (t): T4; lymph node status (n): N2; tumor grade (g): G3; er status: +; pgr status: +; ', 'age (years): 41; sample type: primary tumor; sample group: Control; tumor size (t): T2; lymph node status (n): N1; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 53; sample type: primary tumor; sample group: Control; tumor size (t): T1; lymph node status (n): N2; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 66; sample type: primary tumor; sample group: Control; tumor size (t): T4; lymph node status (n): N2; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 73; sample type: primary tumor; sample group: Control; tumor size (t): T1; lymph node status (n): N1; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 81; sample type: primary tumor; sample group: Control; tumor size (t): T2; lymph node status (n): N0; tumor grade (g): G3; er status: +; pgr status: +; ', 'age (years): 61; sample type: primary tumor; sample group: Control; tumor size (t): T2; lymph node status (n): N0; tumor grade (g): G3; er status: -; pgr status: -; ', 'age (years): 41; sample type: metastasis; sample group: Control; tumor size (t): Tx; lymph node status (n): Nx; tumor grade (g): G3; er status: +; pgr status: -; ', 'age (years): 53; sample type: primary tumor; sample group: Control; tumor size (t): T2; lymph node status (n): N2; tumor grade (g): G2; er status: -; pgr status: +; ', 'age (years): 48; sample type: primary tumor; sample group: Control; tumor size (t): T2; lymph node status (n): N1; tumor grade (g): G3; er status: +; pgr status: -; ', 'age (years): 83; sample type: primary tumor; sample group: Control; tumor size (t): Tx; lymph node status (n): N2; tumor grade (g): G1; er status: ND; pgr status: ND; ', 'age (years): 54; sample type: primary tumor; sample group: Control; tumor size (t): T1; lymph node status (n): N1; tumor grade (g): G3; er status: +; pgr status: +; ' GSE93332 Homo sapiens 8 Expression profiling by array GPL570 Fresh-Frozen samples profiled on HG-U133plus2 array with Affymetrix's GeneChip® 3' IVT Express kit 2017-01-09 The reliability of differential expression analysis on FFPE expression profiles from Affymetrix arrays is questionable, due to the wide range of percent-present values reported in studies which profiled FFPE samples on Affymetrix arrays. Moreover the validity of externally defined gene-modules in FFPE microarray expression profiles is unknown. Using eight breast cancer tumors with available frozen and FFPE samples, five sample-matched data sets were generated from different combination of Affymetrix arrays, amplification-and-labeling kit and sample preservation method. The reliability of differential expression analysis was investigated by developing de novo ER/HER2 pathway gene-modules from matched data sets and validating it on external data set using ROC analysis. Spearman's rank correlation coefficient of module scores between matched FFPE-frozen expression profiles was used to measure reliability of externally defined gene-modules in FFPE expression profiles. Independent of array/amplification-kit/sample preservation method used, de novo ER/HER2 gene-modules derived from all matching data sets showed similar prediction performance during independent validation (AUC range; ER: 0.92-0.95, HER2: 0.88-0.91), except for de novo HER2 gene-module derived from FFPE data set with 3'IVT kit (AUC: 0.67-0.72). Further not all gene-module based biological signals present in frozen expression profiles can be recovered from matching FFPE microarray expression profiles using the currently available FFPE specific sample preparation kits. The gene-module based biological signal extracted from FFPE RNA, using microarrays, may not be as reliable as that from their frozen counterpart, if the sample preparation protocol used with FFPE RNA failed to recover relevant genes involved in the biological signal. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93332 Feasibility of developing reliable gene expression modules from FFPE derived RNA profiled on Affymetrix arrays. PloS one 2.776 https://doi.org/10.1371/journal.pone.0203346 {PloS one (2.776): 10.1371/journal.pone.0203346} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA360635 https://www.ebi.ac.uk/ena/browser/view/PRJNA360635 None [Overal design]RNAs were extracted from eight Fresh-Frozen preserved breast cancers. RNAs were amplified and labeled using Affymetrix's GeneChip® 3' IVT Express kit, and profiled on Affymetrix's GeneChip® HG-U133 Plus2.0 Array according to Affymetrix's standard procedure.; [Treatment]'NA'; [Growth]'NA'; [Extraction]"Total RNA from frozen samples was extracted using TRIzol® Reagent according to Thermo Fisher Scientific's (Invitrogen) recommendations."; [Cell type]'Source: ''tissue: breast tumor; er status: negative; her2 status: negative; tissue preservation method: Fresh-Frozen; ', 'tissue: breast tumor; er status: positive; her2 status: negative; tissue preservation method: Fresh-Frozen; ', 'tissue: breast tumor; er status: negative; her2 status: positive; tissue preservation method: Fresh-Frozen; ', 'tissue: breast tumor; er status: positive; her2 status: positive; tissue preservation method: Fresh-Frozen; ' GSE160295 Homo sapiens 6 Non-coding RNA profiling by high throughput sequencing GPL16791 miRNA expression profiles of MDA-MB-231 TNBC cells with defected RARalpha serine-77 phosphorylation 2020-10-28 microRNAs have been shown to be involved in the pathogenesis of TNBC as important regulators of cell proliferation and apoptosis. However, whether the activation of retinoic acid receptor alpha (RARα), a transcription factor, is involved in mediating transcriptional regulation of microRNAs remains elusive. Here, we investigated the differentially expressed miRNAs in triple negative breast cancer cell line MDA-MB-231 overexpressing a phosphorylation-defective mutant RARαS77A, which mimicked activated RARα, in comparison to non-transfected control cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE160295 Inhibition of retinoic acid receptor α phosphorylation represses the progression of triple-negative breast cancer via transactivating miR-3074-5p to target DHRS3. Journal of experimental & clinical cancer research : CR 5.646 https://doi.org/10.1186/s13046-021-01941-7 {Journal of experimental & clinical cancer research : CR (5.646): 10.1186/s13046-021-01941-7} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA672909 https://www.ebi.ac.uk/ena/browser/view/PRJNA672909 https://www.ncbi.nlm.nih.gov/sra?term=SRP289456 [Overal design]MDA-MB-231 cells were transfected with lentiviral RARαS77A, a total amount of 3 μg total RNA per sample was used as input material for the small RNA library. Sequencing libraries were generated using NEBNext® Multiplex Small RNA Library Prep Set for Illumina® (NEB, USA.) following the manufacturer’s recommendations and index codes were added to attribute sequences to each sample. Non-transfected cells were used as controls, experiments were performed in triplicates.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with Trizol reagent. RNA degradation and contamination was monitored on 1% agarose gels. RNA purity was checked using the NanoPhotometer® spectrophotometer (IMPLEN, CA, USA). RNA concentration was measured using Qubit® RNA Assay Kit in Qubit® 2.0 Flurometer (Life Technologies, CA, USA). RNA integrity was assessed using the RNA Nano 6000 Assay Kit of the Agilent Bioanalyzer 2100 system (Agilent Technologies, CA, USA).\nA total amount of 3 μg total RNA per sample was used as input material for the small RNA library. Sequencing libraries were generated using NEBNext® Multiplex Small RNA Library Prep Set for Illumina® (NEB, USA.) following manufacturer’s recommendations and index codes were added to attribute sequences to each sample.'; [Cell type]'triple negative breast cancer cell''cell line: MDA-MB-231; cell type: triple negative breast cancer cell; genotype/variation: non-transfected; ', 'cell line: MDA-MB-231; cell type: triple negative breast cancer cell; genotype/variation: transfected with RARalphaS77A; ' GSE85208 Homo sapiens 203 Expression profiling by RT-PCR GPL19921 Expression of oxysterol pathway genes in estrogen positive breast carcinomas 2016-08-04 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE85208 Expression of oxysterol pathway genes in oestrogen-positive breast carcinomas. Clinical endocrinology 2.897 https://doi.org/10.1111/cen.13337 {Clinical endocrinology (2.897): 10.1111/cen.13337} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA336551 https://www.ebi.ac.uk/ena/browser/view/PRJNA336551 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was isolated from frozen tissues using Trizol reagent according to manufacturers protocol (Invitrogen, Carlsbad, CA, USA)'; [Cell type]'Source: ''age (years): 59; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 5; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 45; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 20; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 65; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 15; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 43; menopause: unknown; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 3; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 37; menopause: pre; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 50; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 56; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 5; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 53; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 7; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 69; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIIA; pt: 1; pn: 2; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): 20; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 55; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 20; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 70; menopause: post; histology (1=idc, 0=other): 0; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 5; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 67; menopause: post; histology (1=idc, 0=other): 0; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 8; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 81; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 15; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 59; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 25; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 51; menopause: unknown; histology (1=idc, 0=other): 0; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 8; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 79; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 2; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 83; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 3; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 67; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 10; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 66; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 20; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 77; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 7; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 73; menopause: post; histology (1=idc, 0=other): unknown; grade: 1; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 3; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 68; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 35; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 67; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 15; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 45; menopause: pre; histology (1=idc, 0=other): 0; grade: 1; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 10; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 72; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 15; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 66; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 10; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 56; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 15; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 79; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): 7; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 68; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 5; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 63; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 5; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 70; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): 8; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 63; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 3; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 65; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): 3; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 73; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 5; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 59; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 25; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 64; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 8; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 58; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 10; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 54; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 3; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 60; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 5; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 58; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 8; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 66; menopause: post; histology (1=idc, 0=other): 0; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): 2; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 79; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 2; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 86; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 5; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 50; menopause: post; histology (1=idc, 0=other): unknown; grade: unknown; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 10; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 52; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): 20; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 54; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 3; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 54; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 7; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 75; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 5; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 71; menopause: post; histology (1=idc, 0=other): 0; grade: 3; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 8; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 50; menopause: pre; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): 5; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 70; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 6; tissue type: Tumor; ', 'age (years): 66; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 104; tissue type: Tumor; ', 'age (years): 58; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 99; tissue type: Tumor; ', 'age (years): 53; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 103; tissue type: Tumor; ', 'age (years): 60; menopause: post; histology (1=idc, 0=other): 0; grade: 2; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 104; tissue type: Tumor; ', 'age (years): 62; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 97; tissue type: Tumor; ', 'age (years): 63; menopause: post; histology (1=idc, 0=other): 0; grade: unknown; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 101; tissue type: Tumor; ', 'age (years): 57; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 96; tissue type: Tumor; ', 'age (years): 82; menopause: post; histology (1=idc, 0=other): 0; grade: unknown; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 76; tissue type: Tumor; ', 'age (years): 51; menopause: post; histology (1=idc, 0=other): 0; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 99; tissue type: Tumor; ', 'age (years): 58; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 102; tissue type: Tumor; ', 'age (years): 62; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 1; dfs (months): 16; tissue type: Tumor; ', 'age (years): 81; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 80; tissue type: Tumor; ', 'age (years): 59; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 1; dfs (months): 36; tissue type: Tumor; ', 'age (years): 83; menopause: post; histology (1=idc, 0=other): 1; grade: 3; pt: 2; pn: unknown; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 16; tissue type: Tumor; ', 'age (years): 56; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 80; tissue type: Tumor; ', 'age (years): 62; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 142; tissue type: Tumor; ', 'age (years): 65; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 49; tissue type: Tumor; ', 'age (years): 55; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 71; tissue type: Tumor; ', 'age (years): 53; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 77; tissue type: Tumor; ', 'age (years): 56; menopause: pre; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 1; dfs (months): 65; tissue type: Tumor; ', 'age (years): 43; menopause: pre; histology (1=idc, 0=other): 1; grade: 2; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 71; tissue type: Tumor; ', 'age (years): 79; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 75; tissue type: Tumor; ', 'age (years): 62; menopause: post; histology (1=idc, 0=other): 0; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 84; tissue type: Tumor; ', 'age (years): 57; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: IIIA; pt: 2; pn: 2; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 72; tissue type: Tumor; ', 'age (years): 81; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 47; tissue type: Tumor; ', 'age (years): 71; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 13; tissue type: Tumor; ', 'age (years): 61; menopause: post; histology (1=idc, 0=other): 0; grade: 2; Stage: IIIA; pt: 3; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 119; tissue type: Tumor; ', 'age (years): 60; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 53; tissue type: Tumor; ', 'age (years): 55; menopause: pre; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 71; tissue type: Tumor; ', 'age (years): 49; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIIA; pt: 1; pn: 2; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 63; tissue type: Tumor; ', 'age (years): 44; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 77; tissue type: Tumor; ', 'age (years): 64; menopause: post; histology (1=idc, 0=other): 0; grade: 3; Stage: 0; pt: 0; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 66; tissue type: Tumor; ', 'age (years): 62; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 90; tissue type: Tumor; ', 'age (years): 59; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 66; tissue type: Tumor; ', 'age (years): 78; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 62; tissue type: Tumor; ', 'age (years): 74; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 64; tissue type: Tumor; ', 'age (years): 59; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 63; tissue type: Tumor; ', 'age (years): 55; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 61; tissue type: Tumor; ', 'age (years): 80; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIIB; pt: 1; pn: 3; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 33; tissue type: Tumor; ', 'age (years): 58; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 63; tissue type: Tumor; ', 'age (years): 78; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 65; tissue type: Tumor; ', 'age (years): 62; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIIB; pt: 3; pn: 3; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 51; tissue type: Tumor; ', 'age (years): 73; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 108; tissue type: Tumor; ', 'age (years): 76; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 63; tissue type: Tumor; ', 'age (years): 67; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 99; tissue type: Tumor; ', 'age (years): 80; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIIB; pt: 4; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 24; tissue type: Tumor; ', 'age (years): 63; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 90; tissue type: Tumor; ', 'age (years): 50; menopause: pre; histology (1=idc, 0=other): 1; grade: 1; Stage: 0; pt: 0; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 99; tissue type: Tumor; ', 'age (years): 78; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 53; menopause: pre; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 97; tissue type: Tumor; ', 'age (years): 75; menopause: post; histology (1=idc, 0=other): 0; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 56; tissue type: Tumor; ', 'age (years): 59; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 95; tissue type: Tumor; ', 'age (years): 76; menopause: post; histology (1=idc, 0=other): 0; grade: unknown; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 1; dfs (months): 5; tissue type: Tumor; ', 'age (years): 60; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIIB; pt: 1; pn: 3; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 69; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 97; tissue type: Tumor; ', 'age (years): 71; menopause: post; histology (1=idc, 0=other): 0; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 49; tissue type: Tumor; ', 'age (years): 62; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 93; tissue type: Tumor; ', 'age (years): 54; menopause: post; histology (1=idc, 0=other): 0; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 92; tissue type: Tumor; ', 'age (years): 81; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIIA; pt: 1; pn: 2; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 95; tissue type: Tumor; ', 'age (years): 76; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIIA; pt: 2; pn: 2; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 85; tissue type: Tumor; ', 'age (years): 66; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 21; tissue type: Tumor; ', 'age (years): 62; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 88; tissue type: Tumor; ', 'age (years): 60; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIIA; pt: 2; pn: 2; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 89; tissue type: Tumor; ', 'age (years): 56; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 85; tissue type: Tumor; ', 'age (years): 54; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIIA; pt: 1; pn: 2; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 23; tissue type: Tumor; ', 'age (years): 60; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 81; tissue type: Tumor; ', 'age (years): 55; menopause: pre; histology (1=idc, 0=other): unknown; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 87; tissue type: Tumor; ', 'age (years): 52; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 83; tissue type: Tumor; ', 'age (years): 64; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 24; tissue type: Tumor; ', 'age (years): 61; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 84; tissue type: Tumor; ', 'age (years): 54; menopause: post; histology (1=idc, 0=other): 0; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 85; tissue type: Tumor; ', 'age (years): 66; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 84; tissue type: Tumor; ', 'age (years): 60; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 85; tissue type: Tumor; ', 'age (years): 64; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 83; tissue type: Tumor; ', 'age (years): 68; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 81; tissue type: Tumor; ', 'age (years): 77; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIIA; pt: 2; pn: 2; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 77; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 54; tissue type: Tumor; ', 'age (years): 34; menopause: pre; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 81; tissue type: Tumor; ', 'age (years): 71; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 72; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 79; tissue type: Tumor; ', 'age (years): 63; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIIA; pt: 2; pn: 2; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 54; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 82; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 25; tissue type: Tumor; ', 'age (years): 67; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 75; tissue type: Tumor; ', 'age (years): 47; menopause: pre; histology (1=idc, 0=other): 1; grade: 1; Stage: unknown; pt: 1; pn: unknown; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 60; tissue type: Tumor; ', 'age (years): 82; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 59; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 75; tissue type: Tumor; ', 'age (years): 55; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 1; dfs (months): 52; tissue type: Tumor; ', 'age (years): 51; menopause: pre; histology (1=idc, 0=other): 1; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 75; tissue type: Tumor; ', 'age (years): 41; menopause: post; histology (1=idc, 0=other): 0; grade: 2; Stage: IIA; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 77; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIIA; pt: 1; pn: 2; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 72; tissue type: Tumor; ', 'age (years): 51; menopause: pre; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 73; tissue type: Tumor; ', 'age (years): 56; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 70; tissue type: Tumor; ', 'age (years): 76; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 64; tissue type: Tumor; ', 'age (years): 78; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 63; menopause: pre; histology (1=idc, 0=other): 0; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 66; tissue type: Tumor; ', 'age (years): 72; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: IIIA; pt: 2; pn: 2; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 42; tissue type: Tumor; ', 'age (years): 78; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: IIA; pt: 1; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 64; tissue type: Tumor; ', 'age (years): 81; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 68; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 62; tissue type: Tumor; ', 'age (years): 46; menopause: pre; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 1; dfs (months): 41; tissue type: Tumor; ', 'age (years): 66; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 62; tissue type: Tumor; ', 'age (years): 80; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 0; dfs (months): 61; tissue type: Tumor; ', 'age (years): 65; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: IIB; pt: 2; pn: 1; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 59; tissue type: Tumor; ', 'age (years): 55; menopause: post; histology (1=idc, 0=other): 0; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 61; menopause: post; histology (1=idc, 0=other): 0; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 1; relapse (0=no, 1=yes): 1; dfs (months): 35; tissue type: Tumor; ', 'age (years): 45; menopause: pre; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 55; tissue type: Tumor; ', 'age (years): 63; menopause: post; histology (1=idc, 0=other): 1; grade: unknown; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 48; menopause: pre; histology (1=idc, 0=other): 0; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 48; tissue type: Tumor; ', 'age (years): 77; menopause: post; histology (1=idc, 0=other): 1; grade: 1; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'age (years): 61; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 51; tissue type: Tumor; ', 'age (years): 53; menopause: post; histology (1=idc, 0=other): 1; grade: 2; Stage: I; pt: 1; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): 0; dfs (months): 51; tissue type: Tumor; ', 'age (years): 62; menopause: post; histology (1=idc, 0=other): 1; grade: 3; Stage: I; pt: 2; pn: 0; er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; ki67 (%): unknown; her2 (0=negative, 1= positive): 0; relapse (0=no, 1=yes): unknown; dfs (months): unknown; tissue type: Tumor; ', 'er (0=negative, 1= positive): NA; pr (0=negative, 1= positive): NA; her2 (0=negative, 1= positive): NA; tissue type: Non-tumor; ', 'er (0=negative, 1= positive): 0; pr (0=negative, 1= positive): 0; her2 (0=negative, 1= positive): 0; tissue type: Tumor; ', 'er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 1; her2 (0=negative, 1= positive): 0; tissue type: Tumor; ', 'er (0=negative, 1= positive): 1; pr (0=negative, 1= positive): 0; her2 (0=negative, 1= positive): 0; tissue type: Tumor; ' GSE155437 Homo sapiens 9 Expression profiling by high throughput sequencing GPL20301 Transcriptome profile of ZIP7 knockdown cells 2020-07-30 We analysed the transcriptome profile by RNA-seq when knockdown ZIP7 by two individual siRNAs in MDAMB231 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE155437 Zinc transporter ZIP7 is a novel determinant of ferroptosis. Cell death & disease 5.959 https://doi.org/10.1038/s41419-021-03482-5 {Cell death & disease (5.959): 10.1038/s41419-021-03482-5} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA649762 https://www.ebi.ac.uk/ena/browser/view/PRJNA649762 https://www.ncbi.nlm.nih.gov/sra?term=SRP274341 [Overal design]Compare the transcriptome profile between NC (nontargeting control) and two individual ZIP7 siRNA in MDAMB231 cells; [Treatment]'siRNA for 96 h by reverse transfection'; [Growth]"Cells were cultured at 37'C with 5%CO2 in DMEM (with FBS and penicillin/streptomycin)"; [Extraction]'RNeasy mini kit and DNase I treatment\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'triple negative breast cancer''tissue: breast; cell type: triple negative breast cancer; cell line: MDAMB231; treatment: nontargeting control siRNA; ', 'tissue: breast; cell type: triple negative breast cancer; cell line: MDAMB231; treatment: ZIP7 siRNA_1; ', 'tissue: breast; cell type: triple negative breast cancer; cell line: MDAMB231; treatment: ZIP7 siRNA_2; ' GSE77566 Homo sapiens 2 Expression profiling by array GPL17586 Analysis of differentially expressed genes in MDA-MB-453 after treatment with the compound sulforaphene 2016-02-04 This study aimed to identify differential expressed genes before and after treatment with the compound sulforaphene, using the MDA-MB-453 breast cancer cell line as a model. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE77566 Sulforaphene inhibits triple negative breast cancer through activating tumor suppressor Egr1. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-016-3888-7 {Breast cancer research and treatment (3.471): 10.1007/s10549-016-3888-7} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA310831 https://www.ebi.ac.uk/ena/browser/view/PRJNA310831 None [Overal design]There were a total of 2 samples examined.; [Treatment]'15µM sulforaphene was used for treatment in L15 medium. Total RNA were prepared after treatment 48h.'; [Growth]'Volumes used in this protocol are for 25 cm2 flask; proportionally reduce or increase amount of dissociation medium for culture vessels of other sizes. Remove and discard culture medium. Briefly rinse the cell layer with 0.25% (w/v) Trypsin- 0.53 mM EDTA solution to remove all traces of serum that contains trypsin inhibitor. Add 1.0 mL of Trypsin-EDTA solution to flask and observe cells under an inverted microscope until cell layer is dispersed (usually within 1 minutes). Note: To avoid clumping do not agitate the cells by hitting or shaking the flask while waiting for the cells to detach. Cells that are difficult to detach may be placed at 37°C to facilitate dispersal. Add 3.0 to 4.0 mL of complete growth medium and aspirate cells by gently pipetting. Add appropriate aliquots of the cell suspension to new culture vessels. Cultures can be established between 2 x 103 and 1 x 104 viable cells/cm2. Do not exceed 7 x 104 cels/cm2. Incubate cultures at 37°C. Interval: Maintain cultures at a cell concentration between 6 X 103 and 6 X 104 cell/cm2. Subcultivation Ratio: A subcultivation ratio of 1:3 to 1:8 is recommended Medium Renewal: 2 to 3 times per week'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'breast carcinoma''cell line: MDA-MB-453; gender: female; cell type: breast carcinoma; age: 48 years adult; ethnicity: Caucasian; ' GSE144848 Homo sapiens 16 Expression profiling by high throughput sequencing GPL20301 Leptomeningeal metastatic cells outcompete macrophages for iron through Lipocalin-2 2020-02-06 The tumor microenvironment plays a critical regulatory role in cancer progression, especially in metastases to the central nervous system. Cancer cells inhabiting the cerebrospinal spinal fluid (CSF)-filled leptomeningeal space face substantial microenvironmental challenges including inflammation and sparse extracellular iron. Unlike CSF leukocytes, we find that cancer cells within the CSF express the iron-binding protein LCN2 and its receptor SCL22A17. Employing mouse models of LM, we find that the LCN2/SLC22A17 system is necessary to support leptomeningeal cancer cell growth. We find that infiltrating CSF macrophages generate inflammatory cytokines that induce cancer cell LCN2 expression. This LCN2/SLC22A17 system provides cancer cells superior access to limiting extracellular iron, allowing LCN2-expressing cancer cells to outcompete CSF macrophages for this resource. Finally, pharmacologic interruption of these interactions prevents cancer cell growth within the leptomeninges. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144848 Cancer cells deploy lipocalin-2 to collect limiting iron in leptomeningeal metastasis. Science (New York, N.Y.) 41.037 https://doi.org/10.1126/science.aaz2193 {Science (New York, N.Y.) (41.037): 10.1126/science.aaz2193} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA605149 https://www.ebi.ac.uk/ena/browser/view/PRJNA605149 https://www.ncbi.nlm.nih.gov/sra?term=SRP247504 [Overal design]Leptomeningeal metastatic cells were depleted for Lipocalin-2 with two lentiviral shRNAs or control shRNA and along with Parental cells subjected for transcriptomic analysis; [Treatment]'Lipocalin-2 (LCN2) knock-down cell were generated by transduction of LeptoM cells with two independed lentiviral hairpins (shLCN2_1 and shLCN2_2), and compared to control hairpin (shCTL)'; [Growth]'Parental cancer cell lines (Par) and their metastatic leptomenigeal derivatives (LeptoM, and their genetically manipulated counterparts) were cultured as described previously (Boire 2017). Approximately 1x10*6 cells were seeded into 100 mm dish. Two days later, cells were lysed in RNA lysis buffer (RLT).'; [Extraction]'RNA was extracted from lysates using Rneasy Mini columns (Qiagen).\nAfter RiboGreen quantification and quality control by Agilent BioAnalyzer, 500ng of total RNA underwent polyA selection and TruSeq library preparation according to instructions provided by Illumina (TruSeq Stranded mRNA LT Kit, #RS-122-2102), with 8 cycles of PCR.'; [Cell type]'leptomeningeal metastatic cells', 'Parental cells''derivative: LeptoM; hairpin: shLCN2_1; cell line: PC9; primary tumor type: lung cancer; cell type: leptomeningeal metastatic cells; ', 'derivative: LeptoM; hairpin: shLCN2_2; cell line: PC9; primary tumor type: lung cancer; cell type: leptomeningeal metastatic cells; ', 'derivative: LeptoM; hairpin: shCTL; cell line: PC9; primary tumor type: lung cancer; cell type: leptomeningeal metastatic cells; ', 'derivative: Parental; hairpin: n/a; cell line: PC9; primary tumor type: lung cancer; cell type: Parental cells; ', 'derivative: LeptoM; hairpin: shLCN2_1; cell line: MDA231; primary tumor type: breast cancer; cell type: leptomeningeal metastatic cells; ', 'derivative: LeptoM; hairpin: shLCN2_2; cell line: MDA231; primary tumor type: breast cancer; cell type: leptomeningeal metastatic cells; ', 'derivative: LeptoM; hairpin: shCTL; cell line: MDA231; primary tumor type: breast cancer; cell type: leptomeningeal metastatic cells; ', 'derivative: Parental; hairpin: n/a; cell line: MDA231; primary tumor type: breast cancer; cell type: Parental cells; ' GSE160582 Homo sapiens 8 Genome binding/occupancy profiling by high throughput sequencing GPL20301 Impact of the bone microenvironment on phenotypic plasticity of ER+ breast cancer cells [ATAC-Seq] 2020-11-01 ATAC sequencing was performed to evaluate epigenetic changes induced by the bone microenvironment. We found a global epigenetic reprogramming of ER+ cancer cells deriving from bone which drives stemness and endocrine resistance https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE160582 The bone microenvironment increases phenotypic plasticity of ER+ breast cancer cells. Developmental cell 9.190 https://doi.org/10.1016/j.devcel.2021.03.008 {Developmental cell (9.190): 10.1016/j.devcel.2021.03.008} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA673696 https://www.ebi.ac.uk/ena/browser/view/PRJNA673696 https://www.ncbi.nlm.nih.gov/sra?term=SRP290685 [Overal design]SCP2 (Single Cell-derived population #2) cells that derived from MCF7 cells were injected to bone via Intra-iliac artery injection (IIA). SCP2-Bo cell line was generated from bone lesions and passaged in parallele with the control SCP2 cells in vitro. ATACseq was performed over multiple passages (2 to 12) on both samples.; [Treatment]'None'; [Growth]'SCP2 cells were maintained in DMEM 10% FBS'; [Extraction]'Samples were processed as previously (https://doi.org/10.1038/nmeth.2688)\nLibrary was prepared using customized primers as previously described (https://doi.org/10.1038/nmeth.2688)'; [Cell type]'SCP2 (MCF7_clone-derived)''cell type: SCP2 (MCF7_clone-derived); collection process: un-entrained; passage: 2; ', 'cell type: SCP2 (MCF7_clone-derived); collection process: Bone-entrained; passage: 2; ', 'cell type: SCP2 (MCF7_clone-derived); collection process: un-entrained; passage: 4; ', 'cell type: SCP2 (MCF7_clone-derived); collection process: Bone-entrained; passage: 4; ', 'cell type: SCP2 (MCF7_clone-derived); collection process: un-entrained; passage: 6; ', 'cell type: SCP2 (MCF7_clone-derived); collection process: Bone-entrained; passage: 6; ', 'cell type: SCP2 (MCF7_clone-derived); collection process: un-entrained; passage: 12; ', 'cell type: SCP2 (MCF7_clone-derived); collection process: Bone-entrained; passage: 12; ' GSE142010 Homo sapiens 21 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Transcriptional regulation in MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [rna_polii_chIP-seq] 2019-12-13 We report whole genome chromatin immunoprecipitation followed by sequencing (ChIP-seq) of 3 different RNA Pol II CTD modifications in MCF-7 breast cancer cells treated with vehicle (UNTR) or the proteasome inhibitor MG132 for 4 (MG4H) or 24 (MG24H) hours. We find the non-phosphorylated form of RNA Pol II CTD accumulates at TSS of all expressed genes in proteasome inhibited cells, particularly after 24H of MG132 treatment. Proteasome inhibition enhances Ser5-P and Ser2-P binding at TSS of genes induced by MG132. We note that proteasome inhibition establishes unique Ser2-P 5’ to 3’ gene profiles at induced compared to repressed genes. Overall proteasome inhibition enhances RNA Pol II processivity and expression of gene networks relevant to breast cancer. The study provides a comprehensive resource of RNA Pol II binding in proteasome inhibited cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE142010 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA595566 https://www.ebi.ac.uk/ena/browser/view/PRJNA595566 https://www.ncbi.nlm.nih.gov/sra?term=SRP237532 [Overal design]Examining whole genome RNA Pol II binding in proteasome inhibited MCF-7 breast cancer cells; [Treatment]'None'; [Growth]'MCF-7 cells were grown in a humidified incubator at 37°C with 5% CO2 in MEM, supplemented with 10% fetal bovine serum 100 μg/mL penicillin/streptomycin, 2 mM glutamine and 10 mM HEPES. For MG132 treatment, cells were seeded overnight in phenol red-free MEM supplemented with 5% charcoal-stripped calf serum and 2 mM glutamate. Next day, cells were treated with, vehicle (DMSO) or 1uM MG132 for 4 or 24 hours.'; [Extraction]'ChIP DNA was collected from MCF7 cells cultured in phenol red free MEM, supplemented with charcoal stripped serum and containing 0.1% DMSO or 1 uM MG132 for 4 or 24H. Cells were incubated for 4 or 24 hours at 37 ºC in a humidified incubator with 5% CO2.\nNEXTFlex Rapid DNA-Seq Kit BIOO Scientific Cat#5144-02'; [Cell type]'breast cancer cells''cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: PolIISer2; chip antibody info.: Abcam Ab5095; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: PolIISer5; chip antibody info.: Abcam Ab5131; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: PolII8WG16; chip antibody info.: Santa Cruz Biotechnology Sc-56767; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: Vehicle; chip antibody: none (input); ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: PolIISer2; chip antibody info.: Abcam Ab5095; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: PolIISer5; chip antibody info.: Abcam Ab5131; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: PolII8WG16; chip antibody info.: Santa Cruz Biotechnology Sc-56767; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (4H); chip antibody: none (input); ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: PolIISer2; chip antibody info.: Abcam Ab5095; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: PolIISer5; chip antibody info.: Abcam Ab5131; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: PolII8WG16; chip antibody info.: Santa Cruz Biotechnology Sc-56767; ', 'cell line: MCF-7; cell type: breast cancer cells; treatment: MG132 (24H); chip antibody: none (input); ' GSE80722 Homo sapiens 10 Expression profiling by high throughput sequencing GPL17303 Transcriptome analysis of patient-derived xenograft models of HER2+ breast cancer brain metastases 2016-04-27 To gain insights into tumor heterogeneity in anti-cancer drug responses of patient-derived xenograft models of HER2+ breast cancer brain metastases, we performed transcriptome gene expression profiling by Ion AmpliSeq™ Transcriptome sequencing that targets more than 20,000 human genes. Our data found that all anti-cancer drugs responders have significantly higher expression levels of AKT-mTOR-dependent signature genes as compared to the non-responders, suggesting that most HER2+ breast cancer brain metastases are depend on the AKT-mTOR pathway https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80722 Combination inhibition of PI3K and mTORC1 yields durable remissions in mice bearing orthotopic patient-derived xenografts of HER2-positive breast cancer brain metastases. Nature medicine 30.641 https://doi.org/10.1038/nm.4120 {Nature medicine (30.641): 10.1038/nm.4120} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA319811 https://www.ebi.ac.uk/ena/browser/view/PRJNA319811 https://www.ncbi.nlm.nih.gov/sra?term=SRP074069 [Overal design]Gene expression profiles of five PDX samples were generated by Ion AmpliSeq Transcriptome sequencing, in duplcate, using Ion torrent Proton machine.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was isolated using Trizol (Invitrogen) and the RNeasy Mini Kit (Qiagen).\ncDNA libraries were constructed using\xa0the Ion AmpliSeq Transcriptome Human Gene Expression Kit (Thermo Fisher). Samples were barcoded using the Ion Xpress™ Barcode Adapter kits (Thermo Fisher)'; [Cell type]'Source: ''sample type: breast cancer brain metastases; tissue: patient-derived xenograft; tumor type: HER2+; ' GSE78100 Homo sapiens 8 Other GPL16791; GPL20301 Capture-C reveals preformed chromatin interactions between HIF-binding sites and distant promoters 2016-02-19 Hypoxia inducible factor (HIF) directs an extensive transcriptional cascade that transduces numerous adaptive responses to hypoxia. Pan-genomic analyses, using chromatin immunoprecipitation and transcript profiling, have revealed large numbers of HIF-binding sites that are generally associated with hypoxia-inducible transcripts, even over long chromosomal distances. However, these studies do not define the specific targets of HIF-binding sites and do not reveal how induction of HIF affects chromatin conformation over distantly connected functional elements. To address these questions we deployed a recently developed chromosome conformation assay that enables simultaneous high-resolution analyses from multiple viewpoints. These assays defined specific long-range interactions between intergenic HIF-binding regions and one or more promoters of hypoxia-inducible genes, revealing the existence of multiple enhancer-promoter, promoter-enhancer and enhancer-enhancer interactions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE78100 Capture-C reveals preformed chromatin interactions between HIF-binding sites and distant promoters. EMBO reports 8.383 https://doi.org/10.15252/embr.201642198 {EMBO reports (8.383): 10.15252/embr.201642198} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA312614 https://www.ebi.ac.uk/ena/browser/view/PRJNA312614 https://www.ncbi.nlm.nih.gov/sra?term=SRP070559 [Overal design]We utilised Capture-C to study chromatin looping from distal HIF binding sites (enhancers) and the promoters of HIF regulated genes. Studying the dynamics in normoxia and hypoxia and across different cell types.; [Treatment]'For hypoxia treatment cells, were incubated for 16 hr in an In Vivo2 Hypoxia Work station (Ruskinn Technology) at 0.5% oxygen.'; [Growth]'Dulbecco Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum, 2 mM L-glutamine, 100U/ml penicillin and 100 μg/ml streptomycin.'; [Extraction]'Capture-C libraries were prepared as previously described (Davies et al. 2016 Nature Methods). Cells were fixed with 2% (vol/vol) formaldehyde for 10 min, quenched with 125 mM glycine in PBS and then lysed in cold lysis buffer (10 mM Tris-HCl, pH 8, 10 mM NaCl, 0.2% Igepal, 1× cOmplete Protease Inhibitor Cocktail (Roche). Chromatin was digested with Dpn2 (New England Biolabs) at 37oC overnight. Fragments were then diluted and ligated with T4 DNA ligase (Thermo Scientific) at 16oC overnight. Crosslinking was reversed by overnight incubation at 60oC with proteinase K (Bioline). The 3C libraries were then purified by phenol-chloroform and chloroform extraction followed by precipitation in ethanol at -80oC overnight. Digestion efficiency was determined by qPCR and gel electrophoresis. Sequencing libraries were prepared from 5 μg of each 3C library by sonication using a S220 focused-ultrasonicator (Covaris) to a average size of 200bp and indexed using NEBnext reagents (New England Bioloabs) according to protocol. Enrichment of 1-2 μg of indexed library incubated with 13 pmol of a pool of biotinylated oligonucleotides (Intergrated DNA technologies or Sigma) was performed using the SeqCap EZ system (#06953212001, Roche/Nimblegen) following the manufacturer’s instructions. Two rounds of capture employing 48-72 hr and 24 hr hybridizations respectively were used. Capture enrichment was determined by qPCR. Correct library size was confirmed using a Bioanalyzer DNA 1000 or Tapestation D1000 kit (Agilent), and DNA concentrations were determined using a Qubit 2.0 Fluorometer (ThermoFisher Scientific).'; [Cell type]'Source: ''cell line: 786-O; treatment: Normoxia; cell line modification: none; ', 'cell line: MCF-7; treatment: Normoxia; cell line modification: none; ', 'cell line: MCF-7; treatment: Hypoxia; cell line modification: none; ', 'cell line: 786-O+VHL; treatment: Normoxia; cell line modification: stable WT VHL expression; ', 'cell line: 786-O+VHL; treatment: Hypoxia; cell line modification: stable WT VHL expression; ' GSE97985 Homo sapiens 17 Expression profiling by array GPL570 Cooperative Targets of Combined mTOR/HDAC Inhibition Promote MYC Degradation 2017-04-19 Cancer treatments often require combinations of molecularly targeted agents to be effective. mTORi (rapamycin) and HDACi (MS-275/entinostat) inhibitors have been shown to be effective in limiting tumor growth, and here we define part of the cooperative action of this drug combination. More than 60 human cancer cell lines responded synergistically (CI<1) when treated with this drug combination compared to single agents. In addition, a breast cancer patient-derived xenograft, and a BCL-XL plasmacytoma mouse model both showed enhanced responses to the combination compared to single agents. Mice, bearing plasma cell tumors lived an average of 70 days longer on combination treatment compared to single agents. A set of 37 genes cooperatively affected (34 down-regulated; 3 up-regulated) by the combination responded pharmacodynamically in human myeloma cell lines, xenografts, and a P493 model, and were both enriched in tumors, and correlated with prognostic markers in myeloma patient datasets. Genes down-regulated by the combination were overexpressed in several untreated cancers (breast, lung, colon, sarcoma, head and neck, myeloma) compared to normal tissues. The MYC/E2F axis, identified by upstream regulator analyses and validated by immunoblots, was significantly inhibited by the drug combination in several myeloma cell lines. Furthermore, 88% of the 34 genes downregulated have MYC binding sites in their promoters, and the drug combination cooperatively reduced MYC half-life by 55% and increased degradation. Thus, integrative approaches to understand drug synergy identified a clinically actionable strategy to inhibit MYC/E2F activity and tumor cell growth in vivo. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE97985 Cooperative Targets of Combined mTOR/HDAC Inhibition Promote MYC Degradation. Molecular cancer therapeutics 4.856 https://doi.org/10.1158/1535-7163.MCT-17-0171 {Molecular cancer therapeutics (4.856): 10.1158/1535-7163.MCT-17-0171} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA383575 https://www.ebi.ac.uk/ena/browser/view/PRJNA383575 None [Overal design]Gene expression was profiled from L363 cells treated with either 1nM or 10nM rapamycin, 0.5uM MS-275 or the combination for 48 hours. Three replicates per control and treatment groups were done; one array was disqualifed with QC.; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was extracted with TRIzol® (Invitrogen) according to the manufacturer's instructions."; [Cell type]'Source: ''cancer type: Multiple Myeloma; ' GSE99495 Mus musculus 10 Genome variation profiling by array GPL10448 microRNA-143/145 loss induces Ras-signaling and cooperates with Pten-deficiency to promote basal-like breast cancer [CGH] 2017-05-31 The tumor suppressor PTEN is frequently inactivated in breast and other cancers; yet, germ-line mutations in this gene induce non-malignant hamartomas, indicating dependency on additional cooperating events. Here we show that most tumors derived from conditional deletion of mouse Pten in mammary epithelium are highly differentiated and lack transplantable tumor initiating cells (TICs) capable of seeding new tumors following orthotopic injection of FACS-sorted or tumorsphere cells. A rare group of poorly differentiated tumors did harbour transplantable TICs. These transplantable tumors exhibited distinct molecular classification, signaling pathways, chromosomal aberrations and mutational landscape, as well as reduced expression of microRNA-143/145. Stable knockdown of miR-143/145 conferred tumorigenic potential upon poorly transplantable Pten-deficient tumor cells through a mechanism involving induction of RAS signaling, leading to increased sensitivity to MEK inhibition. In humans, miR145-deficiency significantly correlated with elevated RAS pathway activity in basal-like breast cancer, and patients with combined PTEN/miR-145 loss or PTEN-loss/RAS pathway activation exhibited poor clinical outcome. These results underscore a selective pressure for combined PTEN loss together with miR-145 loss or high RAS-pathway activity in aggressive forms of breast cancer, and a need to identify and prioritize these tumors for aggressive therapy. Array CGH data comparing 2 types of Pten-deficient tumors (well and poorly differentiated) with other modles of mouse mammary tumors https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99495 microRNA-143/145 loss induces Ras signaling to promote aggressive Pten-deficient basal-like breast cancer. JCI insight 6.014 https://doi.org/10.1172/jci.insight.93313 {JCI insight (6.014): 10.1172/jci.insight.93313} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA399096 https://www.ebi.ac.uk/ena/browser/view/PRJNA399096 None [Overal design]2 histological types of Wap-Cre:Ptenfl/fl were compared Raw data files for GSM2644828, GSM2644834, GSM2644836 and GSM2644837 are incomplete and contain duplicated data rows and have missing data. Please see sample records for description of file errors.; [Treatment]'Total DNA obtained from primary tumors were used for arrayCGH analysis to determine changes in copy number'; [Growth]'Samples from independent primary mammary tumors were frozen and kept in -80 degree.'; [Extraction]'Total DNA was extracted using QIAGEN DNeasy Blood & Tissue Kits'; [Cell type]'Source: ''tissue: mammary tumor; histology: Poorly differentiated; sample dimension: Mammary Tumor less than 1.0 cm diameter; ', 'sample type: pooled mouse DNA; ', 'tissue: mammary tumor; histology: Well differentiated; sample dimension: Mammary Tumor less than 1.0 cm diameter; ' GSE14491 Homo sapiens 16 Expression profiling by array GPL570 TGFβ/mutant-p53 jointly controlled genes 2009-01-21 TGFβ ligands act as tumor suppressors in early stage tumors but are paradoxically diverted into potent prometastatic factors in advanced cancers. The molecular nature of this switch remains enigmatic. We now show that TGFβ-dependent cell migration, invasion and metastasis are empowered by mutant-p53. To investigate the specific gene expression program by which mutant-p53 and TGFβ control invasion and metastasis in breast cancer cells, we compared the TGFβ transcriptomic profile of control and mutant-p53 depleted MDA-MB-231 cells. Keywords: expression profiling by array https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE14491 A Mutant-p53/Smad complex opposes p63 to empower TGFbeta-induced metastasis. Cell 36.216 https://doi.org/10.1016/j.cell.2009.01.039 {Cell (36.216): 10.1016/j.cell.2009.01.039} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA111547 https://www.ebi.ac.uk/ena/browser/view/PRJNA111547 None [Overal design]MDA-MB-231 cells, stably expressing either control (shGFP) or anti-p53 (shp53) short-hairpin RNAs, were left untreated or treated with TGFbeta. Samples were then processed for total RNA extraction and hybridization on Affymetrix microarrays. Four biological replicas (A, B, C, D) were used for each of the 4 conditions (1: untreated control; 2: TGFbeta treated control; 3: untreated p53-depleted cells; 4: TGFbeta treated mutant-p53-depleted cells), for a total of 16 samples.; [Treatment]'Cells were serum starved for 24 hours and then treated in DMEM/F12 without serum'; [Growth]'MDA-MB-231 were maintained in a 1:1 mixture of DMEM and F12 (DMEM/F12) supplemented with 10% serum and 2 mM glutamine.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''' GSE7578 Homo sapiens 15 Expression profiling by array GPL570 shRNA-mediated knock down of Bmi-1 and Mel-18 in medulloblastoma cells 2007-04-23 Bmi-1 and Mel-18 are close structural homologues that belong to the polycomb group (PcG) of transcriptional regulators of homeotic gene expression in development. They are believed to stably maintain repression of gene expression by altering the state of chromatin at specific promoters. A number of clinical and experimental observations have also implicated Bmi-1 in tumorigenesis and stem cell maintenance. Bmi-1 overexpression or amplification has been observed in a number of human malignancies, particularly in B-cell lymphomas, medulloblastomas and breast cancer. We report here that shRNA-mediated knock-down of either Bmi-1 or Mel-18 in human medulloblastoma DAOY cells results in the inhibition of proliferation, loss of clonogenic survival and anchorage-independent growth, and suppression of xenograft tumor formation in nude mice. Furthermore, overexpression of both Bmi-1 and Mel-18 significantly increased clonogenic survival of Rat1 fibroblasts. In contrast, stable downregulation of Bmi-1 or Mel-18 alone did not affect the growth of SK-OV-3 or U2OS cancer cell lines or normal human WI38 fibroblasts. Gene expression analysis of shRNA-expressing DAOY cells has demonstrated a significant overlap in the Bmi-1- and Mel-18-regulated genes and revealed novel gene targets under their control. Taken together, these results suggest that Bmi-1 and Mel-18 might have overlapping functions in human tumorigenesis. Keywords: shRNA knock-down https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7578 Contribution of polycomb homologues Bmi-1 and Mel-18 to medulloblastoma pathogenesis. Molecular and cellular biology 3.735 https://doi.org/10.1128/MCB.02244-06 {Molecular and cellular biology (3.735): 10.1128/MCB.02244-06} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA100319 https://www.ebi.ac.uk/ena/browser/view/PRJNA100319 None [Overal design]DAOY cells were transduced with the indicated lentiviral shRNA and stable cell lines were generated by selection in puromycin (1 µg/ml). 2 x 105 cells of each stable cell line were plated onto 60 mm dishes in triplicates and harvested 4 days later. Triplicate total RNA samples from shRNA-expressing and mock-transduced DAOY cells were isolated using affinity resin (Qiagen RNeasy Mini Kit, Qiagen AG). RNA Integrity and purity were assessed with the RNA 6000 Nano LabChip system on Bioanalyzer 2100 (Agilent Technologies). Gene array analysis was conducted at the Genomics Factory at Novartis PHARMA AG, Basel, Switzerland using Gene Chip Human Genome 133 2.0 Plus Expression Array (Affymetrix Inc.).; [Treatment]'DAOY cells were transduced with the indicated lentiviral shRNA and stable cell lines were generated by selection in puromycin (1 µg/ml). 2 x 105 cells of each stable cell line were plated onto 60 mm dishes in triplicates and harvested 4 days later.', 'Cells were mock transduced and 2 x 105 cells were plated onto 60 mm dishes in triplicates and harvested 4 days later.'; [Growth]'Cells were grown in DMEM/10% fetal bovine serum in the presence of antibiotics and 1 µg/ml puromycin.', 'Cells were grown in DMEM/10% fetal bovine serum in the presence of antibiotics.'; [Extraction]'Total RNA was isolated using affinity resin (Qiagen RNEasy Mini Kit, Qiagen AG). RNA integrity and purity were assessed wit the RNA 6000 Nano LabCHip system on the Bionalyzer 2100 (Agilent Technologies)'; [Cell type]'Source: ''' GSE108632 Homo sapiens 8 Expression profiling by high throughput sequencing GPL20301 Paclitaxel plus Cirmtuzumab Achieves Greater Clearance of Patient-derived Xenografts By Targeting ROR1+ Breast Cancer Stem Cells 2017-12-29 We applied high-throughput sequence to identify signaling pathways, stem cell gene signature or target genes of BMI1 that were affected by our newly development humainzed anti-ROR1 antibody (cirmtuzumab) in breast cancer patient-derived xenograft (PDX) mice model https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE108632 Inhibition of chemotherapy resistant breast cancer stem cells by a ROR1 specific antibody. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1816262116 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1816262116} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA427913 https://www.ebi.ac.uk/ena/browser/view/PRJNA427913 https://www.ncbi.nlm.nih.gov/sra?term=SRP127731 [Overal design]Examination of 8 PDX samples isolated from control-treated mice (N=4) versus cirmtuzumab-treated mice (N=4); [Treatment]'Mice bearing PDX tumors were treated with eithor control antibody or cirmtuzuma at 10mg/Kg biweekly'; [Growth]'Equal number of single cell suspension isolated from PDX4 tumors were implanted in Rag2-/-γc-/- mice.'; [Extraction]'Total RNA was prepared from tumor tissues excised from mice received either hIgG or Cirmtuzumab treatment using Trizol RNA extracting protocol, followed with RNeasy column (Qiagen kit) purification.\nRNA libraries were generated from 1 µg of RNA using Illumina’s TruSeq Stranded mRNA Sample Prep Kit following manufacturer’s instructions, modifying the shear time to 5 minutes'; [Cell type]'Source: ''tissue: breast cancer patient-derived xenograft; ' GSE152600 Homo sapiens 8 Expression profiling by high throughput sequencing GPL16791 PTEN-dependent regulation of genome-wide transcription during metabolic stress [RNA-Seq] 2020-06-16 PTEN is implicated in a wide variety of pathophysiological conditions and traditionally studied in the context of the PIK3-AKT-mTOR axis. Recent studies from our group and others have reported a novel role of PTEN in the regulation of transcription at the genome-wide scale. This emerging role of PTEN on global transcriptional regulation is providing a better understanding of various diseases, including cancer. Since cancer progression is an energy-demanding process and PTEN is known to regulate metabolic processes, we sought to understand the role of PTEN in transcriptional regulation under metabolic stress, a condition often developing in the tumor microenvironment. In the present study, we demonstrate that PTEN modulates genome-wide RNA Polymerase II (Pol II) occupancy in cells undergoing glucose deprivation. The glucose-deprived PTEN null cells were found to continue global gene transcription, which may activate a survival mode. However, cells with constitutive PTEN expression slow transcription, an evolutionary mechanism that may save cellular energy and activate programmed cell death pathways, in the absence of glucose. Interestingly, alternative exon usage by PTEN null cells is increased under metabolic stress compared to PTEN expressing cells. Overall, our study comprehensively demonstrates distinct mechanisms involved in PTEN-dependent genome-wide transcriptional control under metabolic stress. Our findings provide a new insight in understanding the tumor microenvironment and how PTEN loss of function, whether by genetic or non-genetic mechanisms, can contribute to a favorable transcriptional program employed by tumor cells to escape apoptosis, hence developing more aggressive and metastatic phenotypes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE152600 Metabolic stress regulates genome-wide transcription in a PTEN-dependent manner. Human molecular genetics 4.544 https://doi.org/10.1093/hmg/ddaa168 {Human molecular genetics (4.544): 10.1093/hmg/ddaa168} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA639816 https://www.ebi.ac.uk/ena/browser/view/PRJNA639816 https://www.ncbi.nlm.nih.gov/sra?term=SRP267542 [Overal design]RNA-seq was performed on BT-549 control and PTEN over-expressing BT-549_PTEN cell.; [Treatment]'Three hours of glucose deprivation'; [Growth]'Cells were cultured in DMEM/F-12 medium (Life Technologies, Grand Island, NY) supplemented with 10% FBS (Thermo Scientific Gibco, Waltham, MA) at 37°C with 5% CO2.'; [Extraction]'Total RNA was extracted from cells using the RNeasy kit (Qiagen, Germantown, MD). On-column DNase treatment was given following the procedure provided by the manufacturer.\nStrand-specific library was prepared using Illumina TruSeq stranded RNA library prep kit (Illumina, San Diego, CA) according to manufacturer’s protocols.'; [Cell type]'Source: ''cell line: BT-549; genotype: WT; treatment: 3 hrs Glucose deprivation; ', 'cell line: BT-549; genotype: PTEN over-expressed; treatment: 3 hrs Glucose deprivation; ', 'cell line: BT-549; genotype: WT; treatment: control; ', 'cell line: BT-549; genotype: PTEN over-expressed; treatment: control; ' GSE81254 Homo sapiens 21 Non-coding RNA profiling by high throughput sequencing GPL15520 miRNA Profile in Three Different Normal Human Ocular Tissues by miRNA-Seq 2016-05-09 Since microRNAs (miRNAs) have been associated with eye diseases, our study aims to profile ocular miRNA expression in normal human eye tissue using miRNA-Seq in order to provide a foundation for future disease research. Total RNAs were extracted from normal human ciliary body (CB) (n=7), cornea (n=7), and trabecular meshwork (TM) (n=7) samples using mirVana total RNA isolation kit. The sequencing library was prepared using the Illumina TruSeq Small RNA Sample Prep kit and was sequenced using Illumina MiSeq. Generated sequence reads were trimmed and aligned against human reference database using the Bowtie software, and only exact matches to mature miRNAs from miRBase were included. miRTarBase database was used to analyze the gene targets of the miRNAs in our tissues, and expression of a few selected miRNAs were validated using droplet digital PCR (ddPCR). We found 378 miRNAs expressed collectively in our samples, of which miR-143-3p, miR-184, miR-26a-5p, and miR-204-5p were most abundantly expressed. With the expression patterns and gene targets, we identified several uniquely expressed miRNAs and created a profile of miRNAs known to target genes associated with keratoconus and glaucoma. Using ddPCR, we were able to validate the expression profile created using miRNA-Seq. For the first time, we profiled miRNA expression in three human ocular tissues using miRNA-Seq, identifying many miRNAs that had not been previously reported in ocular tissue. Knowing the expression of miRNAs in non-diseased eye tissues could help elucidate miRNA changes that accompany diseases such as glaucoma and keratoconus. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE81254 miRNA Profile in Three Different Normal Human Ocular Tissues by miRNA-Seq. Investigative ophthalmology & visual science 3.812 https://doi.org/10.1167/iovs.16-19155 {Investigative ophthalmology & visual science (3.812): 10.1167/iovs.16-19155} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA321066 https://www.ebi.ac.uk/ena/browser/view/PRJNA321066 https://www.ncbi.nlm.nih.gov/sra?term=SRP074625 [Overal design]This study profiled the expression of miRNAs in normal human ciliary body (n=7), cornea (n=7), and trabecualr meshwork (n=7) tissue; [Treatment]'The ocular tissues were dissected out by the surgeon (RRA) and immersed in RNALater (Ambion, Inc.), to preserve the RNA at 4˚C overnight, and then stored at -80˚C until RNA extraction.'; [Growth]'None'; [Extraction]'Total RNA was extracted using the mirVana miRNA Isolation Kit from ThermoFisher Scientific Inc. (Waltham, MA, USA) according to the recommended procedure. The quantity of RNA yield was determined with NanoDrop from ThermoFisher Scientific Inc. (Waltham, MA, USA), and the quality was assessed using the RNA 6000 Nano Kit with Bioanalyzer 2100 from Agilent Technologies (Santa Clara, CA, USA).\nThe TruSeq Small RNA Sample Prep kit from Illumina (San Diego, CA, USA) was used to generate the small RNA sequencing library. Briefly, 1 µg of total RNA was ligated using the manufacturer supplied RNA 3’ and RNA 5’ adapters. To produce cDNA constructs, the ligated small RNA was subjected to RT-PCR with a sample specific index sequence followed by gel purification. Amplified miRNAs were enriched and validated with the Agilent Bioanalyzer 2100 using High Sensitivity DNA chips. Using a MiSeq Reagent Kit v2 with 50 cycles, the validated small RNA sequencing libraries were normalized, denatured, and loaded to the Illumina MiSeq sequencer.'; [Cell type]'Source: ''age (years): 67; race: Caucasian; Sex: Male; postmortem delay (hr): 5:25; primary cause of death: Lung Cancer; tissue: ciliary body; ', 'age (years): 72; race: Caucasian; Sex: Female; postmortem delay (hr): 4:53; primary cause of death: Pancreatic Cancer; tissue: ciliary body; ', 'age (years): 53; race: African; Sex: Female; postmortem delay (hr): 4:00; primary cause of death: Breast Cancer; tissue: ciliary body; ', 'age (years): 55; race: African; Sex: Female; postmortem delay (hr): 2:25; primary cause of death: Breast Cancer; tissue: ciliary body; ', 'age (years): 66; race: Caucasian; Sex: Male; postmortem delay (hr): 3:56; primary cause of death: N/A; tissue: ciliary body; ', 'age (years): 76; race: Caucasian; Sex: Female; postmortem delay (hr): 4:14; primary cause of death: MI; tissue: ciliary body; ', 'age (years): 66; race: Caucasian; Sex: Female; postmortem delay (hr): 4:00; primary cause of death: Sepsis; tissue: ciliary body; ', 'age (years): 53; race: African; Sex: Female; postmortem delay (hr): 4:00; primary cause of death: Breast Cancer; tissue: cornea; ', 'age (years): 49; race: African-American; Sex: Male; postmortem delay (hr): 4:07; primary cause of death: Renal Cancer; tissue: cornea; ', 'age (years): 66; race: Caucasian; Sex: Female; postmortem delay (hr): 4:00; primary cause of death: Sepsis; tissue: cornea; ', 'age (years): 73; race: Caucasian; Sex: Male; postmortem delay (hr): 6:46; primary cause of death: Sepsis; tissue: cornea; ', 'age (years): 67; race: Caucasian; Sex: Male; postmortem delay (hr): 5:25; primary cause of death: Lung Cancer; tissue: cornea; ', 'age (years): 76; race: Caucasian; Sex: Female; postmortem delay (hr): 4:14; primary cause of death: MI; tissue: cornea; ', 'age (years): 61; race: African; Sex: Female; postmortem delay (hr): 6:24; primary cause of death: CVA; tissue: cornea; ', 'age (years): 77; race: Caucasian; Sex: Male; postmortem delay (hr): 3:33; primary cause of death: IC Bleed; tissue: trabecular meshwork; ', 'age (years): 67; race: Caucasian; Sex: Female; postmortem delay (hr): 5:05; primary cause of death: Lymphoma; tissue: trabecular meshwork; ', 'age (years): 59; race: African-American; Sex: Female; postmortem delay (hr): 4:01; primary cause of death: ARDS; tissue: trabecular meshwork; ', 'age (years): 61; race: African; Sex: Female; postmortem delay (hr): 6:24; primary cause of death: CVA; tissue: trabecular meshwork; ', 'age (years): 73; race: Caucasian; Sex: Male; postmortem delay (hr): 3:41; primary cause of death: MI; tissue: trabecular meshwork; ', 'age (years): 73; race: Caucasian; Sex: Male; postmortem delay (hr): 6:46; primary cause of death: Sepsis; tissue: trabecular meshwork; ', 'age (years): 49; race: African-American; Sex: Male; postmortem delay (hr): 4:07; primary cause of death: Renal Cancer; tissue: trabecular meshwork; ' GSE139274 Homo sapiens 8 Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing GPL20795 Identification of differentially expressed lncRNAs and mRNAs in luminal-B breast cancer by RNA-sequencing 2019-10-23 Background: Luminal B cancers show much worse outcomes compared to luminal A. This present study aims to screen key lncRNAs and mRNAs correlated with luminal-B breast cancer. Methods: Luminal-B breast cancer tissue samples and adjacent tissue samples were obtained from 4 patients with luminal-B breast cancer. To obtain differentially expressed mRNAs (DEmRNAs) and lncRNAs (DElncRNAs) between luminal-B breast cancer tumor tissues and adjacent tissues, RNA-sequencing and bioinformatics analysis were performed. Functional annotation of DEmRNAs and protein-protein interaction networks (PPI) construction were performed. DEmRNAs transcribed within a 100kb window up- or down-stream of DElncRNAs were searched, which were defined as cis nearby-targeted DEmRNAs of DElncRNAs. DElncRNA-DEmRNA co-expression networks were performed. Results: A total of 1178 DEmRNAs and 273 DElncRNAs between luminal-B breast cancer tumor tissues and adjacent tissues were obtained. Hematopoietic cell lineage, Cytokine-cytokine receptor interaction, Cell adhesion molecules (CAMs) and Primary immunodeficiency were significantly enriched KEGG pathways in luminal-B breast cancer. FN1, EGFR, JAK3, TUBB3 and PTPRC were five hub proteins of the PPI networks. A total of 99 DElncRNAs-nearby-targeted DEmRNA pairs and 1878 DElncRNA-DEmRNA co-expression pairs were obtained. Conclusion: This study determined key genes and lncRNAs involved in luminal-B breast cancer, which expected to present a new avenue for the diagnosis and treatment of luminal-B breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE139274 Identification of differentially expressed lncRNAs and mRNAs in luminal-B breast cancer by RNA-sequencing. BMC cancer 2.933 https://doi.org/10.1186/s12885-019-6395-5 {BMC cancer (2.933): 10.1186/s12885-019-6395-5} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA579053 https://www.ebi.ac.uk/ena/browser/view/PRJNA579053 https://www.ncbi.nlm.nih.gov/sra?term=SRP226692 [Overal design]mRNA and lncRNA profiles of cancer tissue and adjacent tissues from 4 patients with luminal-B breast cancer were obtained based on the Illumina Hiseq X-ten platform with PE150 bp sequencing mode.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA isolation was conducted on the manufacturer’s protocol with PAXgene blood RNA kit (PreAnalytiX GmbH, Hombrechtikon, CH, Switzerland).\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'Source: ''tissue: Luminal-B breast cancer tissue samples; ', 'tissue: Luminal-B breast cancer adjacent tissue samples; ' GSE27018 Homo sapiens 17 Expression profiling by array GPL570 Fibroblast triggered gene expression in tumor 2011-02-02 Personalized biological insights into heterogeneous tumors, such as breast cancer could improve clinical management. While genomic analysis has contributed significantly towards dissecting breast cancer heterogeneity, limitations in clinical application are partly rooted in the inter-tumor variability arising from a largely uncharacterized interactive exchange between diverse cell types in the tumor microenvironment. Here we first identified a common response signature to stromal coculture across breast cancer of varying clinicopathologic phenotypes. Proximity to fibroblasts resulted in gene transcript alterations of >2-fold for 107 probe sets, collectively designated as Fibroblast Triggered Gene Expression in Tumor (FTExT). Prominent features of tumor cell response included transcript repression related to biofunctions encompassing inflammatory signaling, cell movement, cell death, and cell growth and proliferation. In an evaluation of intertumor heterogeneity, the FTExT classifier stratified moderate and high histopathologic grade breast cancer according to clinical outcome (dataset 1, n=401, p=0.031; dataset 2, n=200, p=0.013), delineating a novel phenotype of stromal crosstalk underlying the prognostic potential of tumor grade. Extending correlative data through functional analysis of stromal-epithelial cocultures of both malignant and nonmalignant derivation, significant differences in cell cycle regulation, rate of proliferation, resistance to therapy-induced apoptosis, and growth arrest were observed in FTExT-based subgroups. Instead of a stromal impact that is uniformly cancer promoting, our data demonstrate striking variability in tumor cell response that directly contributes to contrasting functional aggressiveness of malignant breast tissue. Our findings uniquely reveal dynamically interacting paracrine components underlying the molecular and functional heterogeneity of breast cancer, thus presenting novel opportunities for tumor targeting. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE27018 Distinctive responsiveness to stromal signaling accompanies histologic grade programming of cancer cells. PloS one 2.776 https://doi.org/10.1371/journal.pone.0020016 {PloS one (2.776): 10.1371/journal.pone.0020016} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA137697 https://www.ebi.ac.uk/ena/browser/view/PRJNA137697 None [Overal design]10 tumor samples cocultured with fibroblast were profiled in their gene expression with microarrays, and compared with 7 tumor samples cultured without fibroblast. Immortalized tumor cell lines of varying histologic grade were developed and maintained in a growth median as described in Dairkee, et al., Oncogene, 2007. In the coculture set up, epithelial cells were seeded in 6-well plates, and fibroblasts in 0.4 μm inserts with hanging geometry (BD Biosciences, Franklin Lakes, NJ) at a 3:1 ratio in a common pool of growth medium for 3-day harvests. Controls were comprised of each epithelial sample maintained in the absence of fibroblast-seeded inserts under the same culture conditions.; [Treatment]'None'; [Growth]'None'; [Extraction]'total epithelial cell RNA was directly extracted from duplicate wells of each treatment using the Rneasy kit (Qiagen)'; [Cell type]'Source: ''sample name: C25_04-18-06; tumor sample id: CCdl1797TT; tumor sample histological grade: low, T1; fibroblast sample id: none; treatment class: none; time: 3d; tissue: breat cancer tumor; treatment: tumor not co-cultured with fibroblast; ', 'sample name: D25_04-18-06; tumor sample id: CCdl22TT; tumor sample histological grade: low, T1; fibroblast sample id: none; treatment class: none; time: 3d; tissue: breat cancer tumor; treatment: tumor not co-cultured with fibroblast; ', 'sample name: C23_04-15-06; tumor sample id: CCdl66TT; tumor sample histological grade: low, T1; fibroblast sample id: none; treatment class: none; time: 3d; tissue: breat cancer tumor; treatment: tumor not co-cultured with fibroblast; ', 'sample name: D23_04-18-06; tumor sample id: CCdl68TT; tumor sample histological grade: low, T1; fibroblast sample id: none; treatment class: none; time: 3d; tissue: breat cancer tumor; treatment: tumor not co-cultured with fibroblast; ', 'sample name: C15_04-07-06; tumor sample id: CCdl1797TT; tumor sample histological grade: low, T1; fibroblast sample id: CCdl67TF; fibroblast sample histological grade: low, TF1; time: 3d; tissue: breat cancer tumor; treatment: tumor co-cultured with fibroblast; ', 'sample name: C13_04-07-06; tumor sample id: CCdl67TT; tumor sample histological grade: low, T1; fibroblast sample id: CCdl67TF; fibroblast sample histological grade: low, TF1; time: 3d; tissue: breat cancer tumor; treatment: tumor co-cultured with fibroblast; ', 'sample name: D15_04-12-06; tumor sample id: CCdl1797TT; tumor sample histological grade: low, T1; fibroblast sample id: CCdl257TF; fibroblast sample histological grade: high, TF2; time: 3d; tissue: breat cancer tumor; treatment: tumor co-cultured with fibroblast; ', 'sample name: D19_04-12-06; tumor sample id: CCdl22TT; tumor sample histological grade: low, T1; fibroblast sample id: CCdl257TF; fibroblast sample histological grade: high, TF2; time: 3d; tissue: breat cancer tumor; treatment: tumor co-cultured with fibroblast; ', 'sample name: D21_04-18-06; tumor sample id: CCdl67TT; tumor sample histological grade: low, T1; fibroblast sample id: CCdl257TF; fibroblast sample histological grade: high, TF2; time: 3d; tissue: breat cancer tumor; treatment: tumor co-cultured with fibroblast; ', 'sample name: D17_04-12-06; tumor sample id: CCdl68TT; tumor sample histological grade: low, T1; fibroblast sample id: CCdl257TF; fibroblast sample histological grade: high, TF2; time: 3d; tissue: breat cancer tumor; treatment: tumor co-cultured with fibroblast; ', 'sample name: C31_04-18-06; tumor sample id: CCdl257T; tumor sample histological grade: high, T2; fibroblast sample id: none; treatment class: none; time: 3d; tissue: breat cancer tumor; treatment: tumor not co-cultured with fibroblast; ', 'sample name: C29_04-15-06; tumor sample id: CCdl54TT; tumor sample histological grade: high, T2; fibroblast sample id: none; treatment class: none; time: 3d; tissue: breat cancer tumor; treatment: tumor not co-cultured with fibroblast; ', 'sample name: C27_04-15-06; tumor sample id: CCdl672TT; tumor sample histological grade: high, T2; fibroblast sample id: none; treatment class: none; time: 3d; tissue: breat cancer tumor; treatment: tumor not co-cultured with fibroblast; ', 'sample name: C21_04-15-06; tumor sample id: CCdl257T; tumor sample histological grade: high, T2; fibroblast sample id: CCdl67TF; fibroblast sample histological grade: low, TF1; time: 3d; tissue: breat cancer tumor; treatment: tumor co-cultured with fibroblast; ', 'sample name: C19_04-07-06; tumor sample id: CCdl54TT; tumor sample histological grade: high, T2; fibroblast sample id: CCdl67TF; fibroblast sample histological grade: low, TF1; time: 3d; tissue: breat cancer tumor; treatment: tumor co-cultured with fibroblast; ', 'sample name: C17_04-07-06; tumor sample id: CCdl672TT; tumor sample histological grade: high, T2; fibroblast sample id: CCdl67TF; fibroblast sample histological grade: low, TF1; time: 3d; tissue: breat cancer tumor; treatment: tumor co-cultured with fibroblast; ', 'sample name: D13_04-12-06; tumor sample id: CCdl257T; tumor sample histological grade: high, T2; fibroblast sample id: CCdl257TF; fibroblast sample histological grade: high, TF2; time: 3d; tissue: breat cancer tumor; treatment: tumor co-cultured with fibroblast; ' GSE73736 Homo sapiens 20 Non-coding RNA profiling by array GPL20986 MicroRNA microarray identifies a miRNA signature to predict chemotherapy response in breast cancers 2015-10-05 To identify miRNAs involved in drug resistance of human breast cancer, a miRNA microarray was performed on 10 cases of drug resistant tissues and 10 cases of drug sensitive tissues. There were 29 differentially expressed miRNAs between drug resistant and drug sensitive tissues, including 22 significantly up-regulated and 7 down-regulated RNAs in drug resistant tissues compared to drug sensitive tissues. A signature of five miRNAs, including miR-23a-3p, miR-200c-3p, miR-214-3p, miR-638, and miR-451a was established. A risk score from the miRNA signature was calculated and patients were classified into high-risk and low-risk groups. Compared with the patients with low-risk scores, the patients with high risk scores showed resistant response to chemotherapy in the training, internal testing and independent sets. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE73736 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA297792 https://www.ebi.ac.uk/ena/browser/view/PRJNA297792 None [Overal design]Group 1: Examination of miRNAs in drug resistant tissues (10 cases), including C22, C28, C29, C100, C142, C149, C151, C153, C173, and C178. Group 2: Examination of miRNAs in drug sensitive tissues (10 cases), including H8, H15, H19, H20, H31, H32, H80, H131, H135 and H170.; [Treatment]'None'; [Growth]'None'; [Extraction]"MiRNAs were isolated from breast cancer tissues using a miRNeasy FFPE Kit (Bioteke, Beijing, China) according to the manufacturer's instructions."; [Cell type]'Source: ''tissue: human breast cancer tissue; phenotype: drug resistant; ', 'tissue: human breast cancer tissue; phenotype: drug sensitive; ' GSE59535 Homo sapiens 6 Expression profiling by high throughput sequencing GPL9115 c-Src Modulates Estrogen-Induced Stress and Apoptosis in Estrogen-Deprived Breast Cancer Cells [MCF-7:5C] 2014-07-17 The emergence of anti-estrogen resistance in breast cancer is an important clinical phenomenon affecting long-term survival in this disease. Identifying factors that convey cell survival in this setting may guide improvements in treatment. Estrogen (E2) can induce apoptosis in breast cancer cells that have been selected for survival after E2 deprivation for long periods (MCF-7:5C cells), but the mechanisms underlying E2-induced stress in this setting have not been elucidated. Here, we report that the c-Src kinase functions as a key adapter protein for the estrogen receptor (ER, ESR1) in its activation of stress responses induced by E2 in MCF-7:5C cells. E2 elevated phosphorylation of c-Src, which was blocked by 4-hydroxytamoxifen (4-OHT), suggesting that E2 activated c-Src through the ER. We found that E2 activated the sensors of the unfolded protein response (UPR), IRE1α (ERN1) and PERK kinase (EIF2AK3), the latter of which phosphorylates eukaryotic translation initiation factor-2α (eIF2α). E2 also dramatically increased reactive oxygen species production and upregulated expression of heme oxygenase HO-1 (HMOX1), an indicator of oxidative stress, along with the central energy sensor kinase AMPK (PRKAA2). Pharmacologic or RNA interference-mediated inhibition of c-Src abolished the phosphorylation of eIF2α and AMPK, blocked E2-induced ROS production, and inhibited E2-induced apoptosis. Together, our results establish that c-Src kinase mediates stresses generated by E2 in long-term E2-deprived cells that trigger apoptosis. This work offers a mechanistic rationale for a new approach in the treatment of endocrine-resistant breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59535 c-Src modulates estrogen-induced stress and apoptosis in estrogen-deprived breast cancer cells. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-12-4152 {Cancer research (8.378): 10.1158/0008-5472.CAN-12-4152} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA255515 https://www.ebi.ac.uk/ena/browser/view/PRJNA255515 https://www.ncbi.nlm.nih.gov/sra?term=SRP044610 [Overal design]MCF-7:5C cells were treated with vehicle (0.1% EtOH) as control, E2 (10-9mol/L), 4-OHT (10-6mol/L), E2 (10-9mol/L) plus 4-OHT (10-6mol/L), PP2 (5x10-6mol/L), and E2 (10-9mol/L) plus PP2 (5x10-6mol/L) respectively for 72 hours.; [Treatment]'The next day, cells were treated with vehicle (0.1% EtOH) as control, E2 (10-9mol/L), 4-OHT (10-6mol/L), E2 (10-9mol/L) plus 4-OHT (10-6mol/L), PP2 (5x10-6mol/L), and E2 (10-9mol/L) plus PP2 (5x10-6mol/L) respectively for 72 hours.'; [Growth]'MCF-7:5C cells were seeded in 10cm dishes.'; [Extraction]'Cells were harvested in TRIzol. Total RNA was isolated with an RNeasy Micro kit.\nThese long RNA samples were first converted into a library of cDNA fragments. Sequencing adaptors were subsequently added to each cDNA fragment and a 2x100 bp paired-end sequence was obtained from each cDNA using high-throughput sequencing technology (Illumina GAII).'; [Cell type]'breast cancer cell line''cell line: MCF-7:5C; cell type: breast cancer cell line; treated with: vehicle (0.1% EtOH) as control for 72hrs; ', 'cell line: MCF-7:5C; cell type: breast cancer cell line; treated with: E2 (10-9mol/L)for 72 hrs; ', 'cell line: MCF-7:5C; cell type: breast cancer cell line; treated with: 4-OHT (10-6mol/L) for 72 hrs; ', 'cell line: MCF-7:5C; cell type: breast cancer cell line; treated with: E2 (10-9mol/L) plus 4-OHT (10-6mol/L) for 72 hrs; ', 'cell line: MCF-7:5C; cell type: breast cancer cell line; treated with: PP2 (5x10-6mol/L) for 72 hrs; ', 'cell line: MCF-7:5C; cell type: breast cancer cell line; treated with: E2 (10-9mol/L) plus PP2 (5x10-6mol/L) for 72 hrs; ' GSE72906 Homo sapiens 108 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL6984; GPL13135; GPL18224; GPL18636 Signatures of post-zygotic structural genetic aberrations in the cells of histologically normal breast tissue that can predispose to sporadic breast cancer [SET 14] 2015-09-10 Sporadic breast cancer (SBC) is a common and heterogeneous disease. There is no reliable way of early prediction of risk for SBC in the general population. We studied 282 females with SBC concentrating on copy number aberrations in tumor-free breast tissue (uninvolved margin, UM) outside the area of primary tumor (PT). Totally 1162 UMs (1-14 per breast) were studied. PT and blood/skin as control was also analyzed. Comparative analysis between genetic profiles for UM(s), PT(s) and blood/skin from the same patient is the core of study design. We identified 108 patients with at least one aberrant UM specimen, representing 38.3% of all cases. Gains were the dominating mutations in microscopically normal breast cells and gain of ERBB2, with overexpression of HER2 protein, was the most common aberration in normal cells. Five additional receptor genes (EGFR, FGFR1, IGF1R, LIFR and NGFR) also showed gains, and these were occasionally present in combination with the gain of ERBB2. Up to 67.6% of patients showed gain of one or more of these genes in normal cells. The aberrations found in normal cells from UMs were previously described in cancer literature, which suggest their causative, driving role in this disease. We demonstrate that analysis of normal cells from cancer-bearing patients leads to identification of genetic signatures that may predispose to SBC. Early detection of signals suggesting a predisposition towards development of SBC, long before detectable tumors are formed, is a key to the anticipated shift into a preventive paradigm of personalized medicine of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72906 Signatures of post-zygotic structural genetic aberrations in the cells of histologically normal breast tissue that can predispose to sporadic breast cancer. Genome research 9.944 https://doi.org/10.1101/gr.187823.114 {Genome research (9.944): 10.1101/gr.187823.114} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA295305 https://www.ebi.ac.uk/ena/browser/view/PRJNA295305 None [Overal design]We studied 282 female breast cancer patients that were assessed as affected by sporadic disease at the time of diagnosis and all underwent mastectomy. In total, 1162 UMs (uninvolved margin tissues), ranging from 1 to 14 UMs per patient, taken outside the location of clinically characterized index primary tumor, were analyzed on Illumina arrays. For each subject, DNA from at least one control tissue was also analyzed, which was predominantly blood DNA, alternatively skin-derived DNA. We also studied primary tumor (PT), or up to 3 primary tumor foci from patients with diagnosis of multifocal disease. This GEO project contains the genotyping profiles (processed and normalized data including Log R Ratio and B allele frequency) for these 1162 UMs used in the study. Information on phenotypes (age at diagnosis, tumor focality, tumor grade, tumor molecular phenotype) is also provided, whenever available. This subSeries represents 108 controls (genotype data from whool blood/skin ) from subject showing at least one UM sample with aberration. [23_controls_GPL6984.txt] 23 control experiments (blood/skin tissue) run on the platform GPL6984 (Human1M-Duov3_B) [2_controls_GPL13135.txt] 2 control experiments (blood/skin tissue) run on the platform GPL13135 (HumanOmniExpress BeadChip). [5_controls_GPL18636.txt] 5 control experiments (blood/skin tissue) run on the platform GPL18636 (Illumina Human660W-Quad v1.0). Please note that GPL18636 on GEO has chromosome coordinates in genome buid 36. In the matrix table I'm maintaining the same IDs as on GEO, but the chromosomal positions (“Position_hg19”) is reported in chromosomal build 37. I did this to provide with experiments which can be directly compared with all the others, which are run on platforms that already support chromosome build 37. [78_controls_GPL18224.txt] 78 control experiments (blood/skin tissue) run on the platform GPL18224 (Infinium HumanOmniExpressExome).; [Treatment]'None'; [Growth]'None'; [Extraction]'The tissues were stored at -70 degrees C prior to DNA extraction. The solid tissues were homogenized with a Tissuerupter (Qiagen). Proteinase K and Sarcosine was then added and the sample was incubated at 50oC over-night. The samples were transferred to PhaseLock Gel tubes and the DNA was purified with phenol/chloroform extraction. Due to very rich content of fat in UMs, phenol/chloroform extraction was repeated 6 times for all UMs, and 3 times for PTs and control samples from skin. The purified DNA was precipitated with sodium acetate, pH 5.4 and 95% ethanol. The DNA precipitate was dried before dissolving in water. Control samples of blood were extracted with QIAmp DNA Blood Maxi Kit (Qiagen).'; [Cell type]'Source: ''subject_code: BK9; gender: female; age at cancer diagnosis: -; tumor grade: -; molecular_phenotype: -; tumor focality: -; tissue: whole blood; ', 'subject_code: JD67; gender: female; age at cancer diagnosis: 40; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: ML36; gender: female; age at cancer diagnosis: 60; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: NM48; gender: female; age at cancer diagnosis: 66; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: OH113; gender: female; age at cancer diagnosis: 47; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 023GC; gender: female; age at cancer diagnosis: 56; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: mulifocal; tissue: skin biopsy; ', 'subject_code: KS141; gender: female; age at cancer diagnosis: 33; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 006MK; gender: female; age at cancer diagnosis: 51; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: 011BM; gender: female; age at cancer diagnosis: 53; tumor grade: 2; molecular_phenotype: HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 012MC; gender: female; age at cancer diagnosis: 84; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 013WS; gender: female; age at cancer diagnosis: 65; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: 016JS; gender: female; age at cancer diagnosis: 72; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 017KM; gender: female; age at cancer diagnosis: 82; tumor grade: 2; molecular_phenotype: HER2+; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: 021MB; gender: female; age at cancer diagnosis: 64; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 024MZ; gender: female; age at cancer diagnosis: 35; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 025JT; gender: female; age at cancer diagnosis: 56; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 026MS; gender: female; age at cancer diagnosis: 48; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 037MC; gender: female; age at cancer diagnosis: 58; molecular_phenotype: Luminal A; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 043WB; gender: female; age at cancer diagnosis: 79; molecular_phenotype: Luminal A; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 044JD; gender: female; age at cancer diagnosis: 74; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 049ASZ; gender: female; age at cancer diagnosis: 61; molecular_phenotype: Luminal A; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 053KS; gender: female; age at cancer diagnosis: 57; tumor grade: DCIS HG; molecular_phenotype: -; tumor focality: DCIS multifocal; tissue: whole blood; ', 'subject_code: 054MJ; gender: female; age at cancer diagnosis: 55; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 061AS; gender: female; age at cancer diagnosis: 75; molecular_phenotype: HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 062BI; gender: female; age at cancer diagnosis: 55; tumor grade: 3; molecular_phenotype: Luminal A; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 063JB; gender: female; age at cancer diagnosis: 67; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: 065AS; gender: female; age at cancer diagnosis: 82; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 070ZNK; gender: female; age at cancer diagnosis: 53; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 071ZB; gender: female; age at cancer diagnosis: 66; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 075JS; gender: female; age at cancer diagnosis: 65; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: 077EP; gender: female; age at cancer diagnosis: 61; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 078AW; gender: female; age at cancer diagnosis: 63; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 081BS; gender: female; age at cancer diagnosis: 48; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 085AS; gender: female; age at cancer diagnosis: 74; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 086AFT; gender: female; age at cancer diagnosis: 71; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 089SD; gender: female; age at cancer diagnosis: 60; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 095ESZ; gender: female; age at cancer diagnosis: 49; molecular_phenotype: HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 098WC; gender: female; age at cancer diagnosis: 69; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: 099OLZ; gender: female; age at cancer diagnosis: 63; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: 100AW; gender: female; age at cancer diagnosis: 60; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: 129EB; gender: female; age at cancer diagnosis: 69; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: 130JT; gender: female; age at cancer diagnosis: 50; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: 131SD; gender: female; age at cancer diagnosis: 82; molecular_phenotype: Luminal A; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: 133ML; gender: female; age at cancer diagnosis: 34; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: 138BM; gender: female; age at cancer diagnosis: 35; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: 139MD; gender: female; age at cancer diagnosis: 48; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: 141BB; gender: female; age at cancer diagnosis: 58; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: 142AK; gender: female; age at cancer diagnosis: 54; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: 143DMG; gender: female; age at cancer diagnosis: 46; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: ACV037; gender: female; age at cancer diagnosis: 64; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: AE031; gender: female; age at cancer diagnosis: 49; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: AH028; gender: female; age at cancer diagnosis: 70; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: AW020; gender: female; age at cancer diagnosis: 36; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: BD038; gender: female; age at cancer diagnosis: 53; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: BK008; gender: female; age at cancer diagnosis: 48; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: EG163; gender: female; age at cancer diagnosis: 45; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: multifocal???; tissue: whole blood; ', 'subject_code: EJ001; gender: female; age at cancer diagnosis: 80; tumor grade: 2; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: EW155; gender: female; age at cancer diagnosis: 67; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: GC147; gender: female; age at cancer diagnosis: 70; tumor grade: 3; molecular_phenotype: Luminal A; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: GGB040; gender: female; age at cancer diagnosis: 63; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: GS011; gender: female; age at cancer diagnosis: 74; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: skin biopsy; ', 'subject_code: GS166; gender: female; age at cancer diagnosis: 56; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: HZK162; gender: female; age at cancer diagnosis: 75; tumor grade: 1; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: IP008; gender: female; age at cancer diagnosis: 41; tumor grade: 3; molecular_phenotype: Luminal A; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: JP149; gender: female; age at cancer diagnosis: 44; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: KK151; gender: female; age at cancer diagnosis: 54; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: KM159; gender: female; age at cancer diagnosis: 84; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: KS150; gender: female; age at cancer diagnosis: 35; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: LF042; gender: female; age at cancer diagnosis: 50; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: LH045; gender: female; age at cancer diagnosis: 85; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: MA018; gender: female; age at cancer diagnosis: 84; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: MB032; gender: female; age at cancer diagnosis: 56; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: MD006; gender: female; age at cancer diagnosis: 49; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: MD052; gender: female; age at cancer diagnosis: 63; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: ME029; gender: female; age at cancer diagnosis: 58; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: MH047; gender: female; age at cancer diagnosis: 44; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: ML012; gender: female; age at cancer diagnosis: 49; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: MN036; gender: female; age at cancer diagnosis: 50; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: MS168; gender: female; age at cancer diagnosis: 71; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: MW158; gender: female; age at cancer diagnosis: 39; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: SD164; gender: female; age at cancer diagnosis: 47; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: SK056; gender: female; age at cancer diagnosis: 49; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: TP169; gender: female; age at cancer diagnosis: 62; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: UV023; gender: female; age at cancer diagnosis: 49; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: ZL152; gender: female; age at cancer diagnosis: 57; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: AL002; gender: female; age at cancer diagnosis: 49; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: BK152; gender: female; age at cancer diagnosis: 55; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: BMF005; gender: female; age at cancer diagnosis: 55; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: BMK015; gender: female; age at cancer diagnosis: 53; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: BU97; gender: female; age at cancer diagnosis: 46; tumor grade: 2; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: CG010; gender: female; age at cancer diagnosis: 38; tumor grade: 3; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: CJ112; gender: female; age at cancer diagnosis: 55; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: DH74; gender: female; age at cancer diagnosis: 40; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: DM138; gender: female; age at cancer diagnosis: 46; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: IMH013; gender: female; age at cancer diagnosis: 73; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: JU32; gender: female; age at cancer diagnosis: 62; tumor grade: 2; molecular_phenotype: HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: KB132; gender: female; age at cancer diagnosis: 64; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; tissue: whole blood; ', 'subject_code: KK123; gender: female; age at cancer diagnosis: 62; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: KZ54; gender: female; age at cancer diagnosis: 52; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: LK003; gender: female; age at cancer diagnosis: 64; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: ME114; gender: female; age at cancer diagnosis: 56; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: MH016; gender: female; age at cancer diagnosis: 53; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: multifocal; tissue: skin biopsy; ', 'subject_code: MK120; gender: female; age at cancer diagnosis: 57; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: PI33; gender: female; age at cancer diagnosis: 79; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: PM102; gender: female; age at cancer diagnosis: 65; tumor grade: 2; molecular_phenotype: Triple negative; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: RH117; gender: female; age at cancer diagnosis: 64; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ', 'subject_code: SE135; gender: female; age at cancer diagnosis: 62; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; tissue: whole blood; ' GSE52066 Homo sapiens 12 Expression profiling by array GPL10904 14-3-3ζ promotes TGF-β-induced bone metastasis program in 231 cells 2013-11-04 To explore the regulatory role of 14-3-3ζ in TGF-β induced bone metastasis program in 231 cells, we generated MDA-MB-231 human breast cancer cell sublines with 14-3-3ζ shRNA knockdown (231.ZKD-4 and 231.ZKD-5) and scrambled shRNA (231.Scr) We performed cDNA microarray analysis on these cells treated with vehicle or TGF-β (5ng/ml, 2 hours) respectively in vitro https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE52066 14-3-3ζ turns TGF-β's function from tumor suppressor to metastasis promoter in breast cancer by contextual changes of Smad partners from p53 to Gli2. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2014.11.025 {Cancer cell (23.916): 10.1016/j.ccell.2014.11.025} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA226611 https://www.ebi.ac.uk/ena/browser/view/PRJNA226611 None [Overal design]Total RNA were extracted from 231.scr, 231.ZKD-4, 231.ZKD-5 cells treated with vehicle or TGF-β, and subjected to illumina Human HT-12 v4 arrays analysis; [Treatment]'cells were treated with TGF-β (5ng/ml) for 2 hours'; [Growth]'cells were cultured and maintained in 231 culture medium'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'breast cancer''cell line: MDA-MB-231; cell type: breast cancer; cell subline: 231.Scr; ', 'cell line: MDA-MB-231; cell type: breast cancer; cell subline: 231.ZKD4; ', 'cell line: MDA-MB-231; cell type: breast cancer; cell subline: 231.ZKD5; ' GSE158960 Mus musculus 16 Expression profiling by high throughput sequencing GPL21103 Hypothalamic estrogen receptor alpha mediates key side effects of tamoxifen therapy in mice 2020-10-02 Adjuvant tamoxifen therapy for invasive breast cancer improves patient survival but comes with side effects that impact health and quality of life. Partly due to a lack of proven animal models, the tissues and cells that mediate these negative side effects are largely unknown. Here we show that mice undergoing a 28-day course of tamoxifen treatment experience dysregulation of core and skin temperature, changes in bone density, and decreased physical activity, recapitulating several aspects of the human response. Single cell RNA sequencing reveals that tamoxifen induces widespread gene expression changes in the hypothalamus, particularly in neurons and ependymal cells. These effects are largely dependent on estrogen receptor alpha (ERα), as conditional ERα knockout ablated or reversed tamoxifen-induced changes in gene expression, thermoregulation, bone, and movement. These findings provide mechanistic insights into the effects of tamoxifen on the hypothalamus and suggest that hypothalamic ERα mediates several side effects of tamoxifen therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE158960 Estrogen receptor alpha in the brain mediates tamoxifen-induced changes in physiology in mice. eLife 7.551 https://doi.org/10.7554/eLife.63333 {eLife (7.551): 10.7554/eLife.63333} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA667095 https://www.ebi.ac.uk/ena/browser/view/PRJNA667095 https://www.ncbi.nlm.nih.gov/sra?term=SRP286217 [Overal design]A total of sixteen hypothalami were analyzed. Group sizes are as follows: Wild-type, control injections n = 3; Wild-type, tamoxifen injections n = 5; Esr1cKO, control injections n = 4, Esr1cKO tamoxifen injections n = 4; [Treatment]'None'; [Growth]'None'; [Extraction]'prepared single cell suspensions, EvaGreen droplet generation oil (BIO-RAD, Hercules, CA, USA), and ChemGenes barcoded microparticles (ChemGenes, Wilmington, MA, USA) containing unique molecular identifiers (UMIs) and cell barcodes were co-flowed through a FlowJEM aquapel-treated Drop-seq microfluidic device (FlowJEM, Toronto, Canada) at recommended flow speeds (oil: 15,000 μl/h, cells: 4000 μl/h, and beads 4000 μl/h). After breakage of the droplets, the beads were washed and suspended in reverse transcriptase solution.\nNextera DNA Library Preparation kit'; [Cell type]'Source: ''strain: CD-1;129P2 mixed (wild-type); injection: Oil; Sex: Female; tissue: Hypothalamus; ', 'strain: CD-1;129P2 Esr1cKO; injection: Tamoxifen; Sex: Female; tissue: Hypothalamus; ', 'strain: CD-1;129P2 mixed (wild-type); injection: Tamoxifen; Sex: Female; tissue: Hypothalamus; ', 'strain: CD-1;129P2 Esr1cKO; injection: Oil; Sex: Female; tissue: Hypothalamus; ' GSE96860 Homo sapiens 52 Expression profiling by high throughput sequencing GPL11154 Enhancer Transcription Reveals Subtype-Specific Transcription Programs Controlling Breast Cancer Pathogenesis [RNA-Seq] 2017-03-21 Noncoding transcription is a defining feature of active enhancers, linking transcription factor (TF) binding to the molecular mechanisms controlling gene expression. To determine the relationship between enhancer activity and biological outcomes in breast cancers, we profiled the transcriptomes (using GRO-seq and RNA-seq) and epigenomes (using ChIP-seq) of 13 different breast cancer cell lines representing the five major molecular subtypes of breast cancer. In addition, we developed a robust and unbiased computational pipeline that simultaneously identifies putative subtype-specific enhancers and their cognate TFs by integrating the magnitude of enhancer transcription, TF mRNA expression levels, TF motif p-values, and enrichment of H3K4me1 and H3KK27. When applied across the 13 different breast cancer cell lines, the Total Functional Score of Enhancer Elements (TFSEE) identified key breast cancer subtype specific transcription factors that act at transcribed enhancers to dictate gene expression patterns determining growth outcomes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE96860 Enhancer transcription reveals subtype-specific gene expression programs controlling breast cancer pathogenesis. Genome research 9.944 https://doi.org/10.1101/gr.226019.117 {Genome research (9.944) doi:10.1101/gr.226019.117}; {BMC genomics (3.501) doi:10.1186/s12864-018-4533-0}; 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA379957 https://www.ebi.ac.uk/ena/browser/view/PRJNA379957 https://www.ncbi.nlm.nih.gov/sra?term=SRP102239 [Overal design]To determine the relationship between enhancer activity and biological outcomes in breast cancers, we profiled the transcriptomes (using GRO-seq and RNA-seq) and epigenomes (using ChIP-seq) of 13 different breast cancer cell lines representing the five major molecular subtypes of breast cancer.; [Treatment]'Basal Growth Conditions'; [Growth]'All cell lines were purchased from the American Type Culture Collection (ATCC) and were maintained, propagated, and plated for experiments in the laboratory of Dr. Khandan Keyomarsi at the MD Anderson Cancer Center. The use of a centralized cell culture core facility facilitated consistency and reproducibility among all of the labs in the LONESTAR consortium conducting assays for this work. All collections of RNA, protein, chromatin, and nuclei were performed in the cell culture core facility and distributed to the different labs for use in the various assays described herein. The two immortalized breast epithelial cell lines, MCF-10A and 76N-F2V, were grown in D medium (described below). All other cell lines were grown in Alpha-MEM medium (Sigma, M8042). All cells were grown as adherent cultures at 37oC with 6.5% CO2. The D medium comprised a 1:1 mixture of Alpha-MEM medium (Sigma, M8042) and Ham’s F12 base medium (Fisher, MT10080CV) containing the following additives: 0.1 M HEPES, 2 mM L-glutamine, 1% fetal bovine serum (Sigma, F4135), 0.035 mg/ml of bovine pituitary extract (Hammond Cell Tech, 1078NZ), 0.01 mM ascorbic acid, 2 nM β-estradiol, 2.5 ng/mL sodium selenite, 10 nM triiodothryonine, ethanolamine, 1 μg/mL insulin, 1 ng/mL hydrocortisone, 0.1 mM phosphoethanolamine, 0.01 mg/mL transferrin, 12.5 ng/mL epidermal growth factor, and 1% Penicillin/Streptomycin. The Alpha-MEM contained the following additives: 0.1 M HEPES, 10% fetal bovine serum (Sigma, F4135), 1% non-essential amino acids, 2 mM L-glutamine, 1% sodium pyruvate, 1 μg/mL insulin, 1 ng/mL hydrocortisone, 12.5 ng/mL epidermal growth factor, and 1% Penicillin/Streptomycin.'; [Extraction]'The cells were collected at ~70-80% confluence. RNA isolation for RT-qPCR and RNA-seq was performed using the RNeasy Mini Kit (Qiagen).\nTotal RNA was isolated as described above. The integrity of the RNA was assessed and verified using an Experion Automated Electrophoresis System (Bio-Rad) before mRNA-seq libraries were prepared using methods described previously (Zhong et al., 2011). Briefly, polyA+ RNA was enriched using Dynabeads oligo(dT)25 (Invitrogen), heat fragmented, and reverse transcribed using random hexamers in the presence of dNTPs. Second strand cDNA synthesis was performed with dNTPs, but replacing dTTP with dUTP. After end-repair, dA-tailing, ligation to adaptors containing barcode sequences, and size selection using AMPure beads (Agencourt), the synthesized second-strand was digested using uracil DNA glycosylase (Enzymatics). A final PCR reaction was performed using Phusion high-fidelity DNA polymerase (NEB). After library quality control assessment using a Bioanalyzer (Agilent), the samples were subjected to 50 bp single-end sequencing using an Illumina HiSeq 2000 Sequencing System. At least two biological replicates for each cell line were sequenced'; [Cell type]'Mammary Brest Epithelium', 'Mammary Gland Fibrocystic', 'Luminal A Breast Cancer Cell line', 'Luminal B Breast Cancer Cell line', 'HER2+ Breast Cancer Cell Line', 'TNBC Basal Breast Cancer Cell Line', 'TNBC Claudin Low Breast Cancer Cell Line''cell type: Mammary Brest Epithelium; cell line: 76NF2V; ', 'cell type: Mammary Gland Fibrocystic; cell line: MCF10A; ', 'cell type: Luminal A Breast Cancer Cell line; cell line: MCF-7; ', 'cell type: Luminal A Breast Cancer Cell line; cell line: ZR751; ', 'cell type: Luminal B Breast Cancer Cell line; cell line: MDA MB-361; ', 'cell type: Luminal B Breast Cancer Cell line; cell line: UACC812; ', 'cell type: HER2+ Breast Cancer Cell Line; cell line: SKBR3; ', 'cell type: HER2+ Breast Cancer Cell Line; cell line: AU565; ', 'cell type: HER2+ Breast Cancer Cell Line; cell line: HCC1954; ', 'cell type: TNBC Basal Breast Cancer Cell Line; cell line: MB468; ', 'cell type: TNBC Basal Breast Cancer Cell Line; cell line: HCC1937; ', 'cell type: TNBC Claudin Low Breast Cancer Cell Line; cell line: MDA MB-231; ', 'cell type: TNBC Claudin Low Breast Cancer Cell Line; cell line: MDA MB-436; ' GSE69774 Homo sapiens 37 Expression profiling by array GPL20311 T47D cell line transfected with various ESR1 fusion genes (or with estrogen treatment), vs. YFP transfection alone 2015-06-11 Gene expression profiling of the downstream transcriptional changes induced by ESR1 fusion genes observed in human breast tumors resistant to hormone therapy https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE69774 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA286743 https://www.ebi.ac.uk/ena/browser/view/PRJNA286743 None [Overal design]Experimental T47D cells stably expressing ESR1 fusion genes (or T47D cells treated with estradiol) vs. T47D cells expressing YFP; [Treatment]'see above for estradiol-treated cells'; [Growth]'T47D stable cells expressing various transgenes were cultured in hormone-deprived media containing charcoal-stripped serum for seven days. YFP-expressing control cells were stimulated or not with 1nM beta-estradiol at day 6 for 24 hours.'; [Extraction]'Qiagen Rneasy Kit'; [Cell type]'Source: ''cell line: T47D; treatment: YFP cRNA 0.85ug; ', 'cell line: T47D; treatment: ESR1-NOP2 cRNA 0.85ug; ', 'cell line: T47D; treatment: ESR1-POLH cRNA 0.85ug; ', 'cell line: T47D; treatment: ESR1-YAP1 cRNA 0.85ug; ', 'cell line: T47D; treatment: ESR1-CCDC170 cRNA 0.85ug; ', 'cell line: T47D; treatment: ESR1(365) cRNA 0.85ug; ', 'cell line: T47D; treatment: ESR1(412) cRNA 0.85ug; ', 'cell line: T47D; treatment: ESR1-PCDH11X cRNA 0.85ug; ', 'cell line: T47D; treatment: POLH cRNA 0.85ug; ', 'cell line: T47D; treatment: ESR1 Y537S cRNA 0.85ug; ', 'cell line: T47D; treatment: YFP+E2 cRNA 0.85ug; ' GSE45240 Mus musculus; Homo sapiens 23 Methylation profiling by genome tiling array GPL5082; GPL5811 Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer [Methylation profiling by array] 2013-03-18 Genetic and epigenetic alterations are essential for the initiation and progression of human cancer. We previously reported that primary human medulloblastomas showed extensive cancer-specific CpG island DNA hypermethylation in critical developmental pathways. To determine whether genetically engineered mouse models (GEMMs) of medulloblastoma have comparable epigenetic changes, we assessed genome-wide DNA methylation in three mouse models of medulloblastoma. In contrast to human samples, very few loci with cancer-specific DNA hypermethylation were detected, and in almost all cases the degree of methylation was relatively modest compared to the dense hypermethylation in the human cancers. To determine if this finding was common to other GEMMs, we examined a Burkitt lymphoma and breast cancer model and did not detect promoter CpG island DNA hypermethylation, suggesting that human cancers and at least some GEMMs are fundamentally different with respect to this epigenetic modification. These findings provide an opportunity to both better understand the mechanism of aberrant DNA methylation in human cancer and construct better GEMMs to serve as preclinical platforms for therapy development. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE45240 Fundamental differences in promoter CpG island DNA hypermethylation between human cancer and genetically engineered mouse models of cancer. Epigenetics 4.173 https://doi.org/10.4161/epi.26486 {Epigenetics (4.173): 10.4161/epi.26486} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA193489 https://www.ebi.ac.uk/ena/browser/view/PRJNA193489 None [Overal design]Genome-wide DNA methylation profiles generated using the Denaturation Analysis of Methylation Differences (DAMD) assay of cancer versus normal samples.; [Treatment]'None'; [Growth]'None'; [Extraction]"Genomic DNA was extracted from cell lines, primary human medulloblastoma, normal cerebellum, and mouse tumors using a QIAGEN Blood & Cell Culture DNA kit per manufacturer's instructions. The DAMD assay was performed as described (Mahoney SE, Yao Z, Keyes CC, Tapscott SJ, & Diede SJ (2012). Genome-wide DNA methylation studies suggest distinct DNA methylation patterns in pediatric embryonal and alveolar rhabdomyosarcomas. Epigenetics 7(4))."; [Cell type]'Burkitt lymphoma cancer cell', 'peripheral white blood cells', 'Source: ', 'fibroblast cell', 'primary fibroblasts''cell line: Daudi; cell type: Burkitt lymphoma cancer cell; ', 'cell type: peripheral white blood cells; ', 'cell line: Raji; cell type: Burkitt lymphoma cancer cell; ', 'background strain: C57BL/6; tissue: Eµ-MYC Burkitt lymphoma tumor; ', 'background strain: C57BL/6; tissue: normal mesenteric lymph node; ', 'background strain: C57BL/6; tissue: normal spleen; ', 'background strain: C57BL/6; tissue: Chodish breast carcinoma tumor; ', 'background strain: C57BL/6; cell type: peripheral white blood cells; ', 'background strain: C57BL/6; tissue: SmoA1 medulloblastoma tumor; ', 'background strain: C57BL/6; tissue: normal cerebellum; ', 'background strain: C57BL/6; tissue: SmoA2 medulloblastoma tumor; ', 'background strain: C57BL/6; cell line: 3T3; cell type: fibroblast cell; ', 'background strain: C57BL/6; cell type: primary fibroblasts; ', 'background strain: C57BL/6; cell line: 10T; cell type: fibroblast cell; ', 'background strain: C57BL/6; cell line: iMF1; cell type: fibroblast cell; ', 'background strain: C57BL/6; cell line: iMF2; cell type: fibroblast cell; ' GSE132426 Homo sapiens 22 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer [ChIP-seq] 2019-06-10 Estrogen receptor alpha (ESR1) mutations have been identified in hormone therapy resistant breast cancer and primary endometrial cancer. Analyses in breast cancer suggests that mutant ESR1 exhibits estrogen independent activity. In endometrial cancer, ESR1 mutations are associated with worse outcomes and less obesity, however experimental investigation of these mutations has not been performed. Using a unique CRISPR/Cas9 strategy, we introduced the D538G mutation, a common endometrial cancer mutation that alters the ligand binding domain of ESR1, while epitope tagging the endogenous locus. We discovered estrogen-independent mutant ESR1 genomic binding that is significantly altered from wildtype ESR1. The D538G mutation impacted expression, including a large set of non-estrogen regulated genes, and chromatin accessibility, with most affected loci bound by mutant ESR1. Mutant ESR1 is unique from constitutive ESR1 activity as mutant-specific changes are not recapitulated with prolonged estrogen exposure. Overall, D538G mutant ESR1 confers estrogen-independent activity while causing additional regulatory changes in endometrial cancer cells that are distinct from breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132426 Estrogen-independent molecular actions of mutant estrogen receptor 1 in endometrial cancer. Genome research 9.944 https://doi.org/10.1101/gr.244780.118 {Genome research (9.944): 10.1101/gr.244780.118} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA548067 https://www.ebi.ac.uk/ena/browser/view/PRJNA548067 https://www.ncbi.nlm.nih.gov/sra?term=SRP200954 [Overal design]ChIP-seq was used to study the effects of the D538G ESR1 mutation on genomic binding; [Treatment]'Media was changed 1 day prior to inductions and Ishikawa ESR1 mutant and wildtype clonal cell lines were induced with DMSO or 10 nM E2 for one hour.'; [Growth]'Ishikawa ESR1 LBD mutant and wildtype cells were cultured in full media: RPMI-1640 with 10% fetal bovine serum and 1% penicillin-streptomycin. Cells were incubated at 37°C with 5% CO2 for the duration of all experiments. At least 5 days prior to inductions, cells were placed in hormone deprived media: phenol-red free RPMI-1640 media (Thermo Fisher Scientific), since phenol-red is estrogenic, with 10% charcoal-dextran stripped fetal bovine serum (Thermo Fisher Scientific) and 1% penicillin-streptomycin.'; [Extraction]'Fixation was performed by treating cells with 1% formaldehyde for 10 minutes at room temperature. The cross-linking reaction was stopped with the addition of glycine to a final concentration of 125 mM. Cells were then washed with cold PBS and harvested via cell scraping in Farnham lysis buffer supplemented with protease inhibitors.\nChromatin immunoprecipitation was performed as previously described (Reddy et al. Genome Research 2009) with an Anti-FLAG (Sigma-Aldrich M2) antibody that recognizes a FLAG tag on ESR1.'; [Cell type]'Source: ''cell line: Ishikawa WT ESR1 clone 1; genotype: WT ESR1; treatment: 10nM E2; time: 1 hr; chip antibody: Anti-FLAG (Sigma-Aldrich M2, lot# SLBX2256) antibody that recognizes FLAG tag on ESR1; ', 'cell line: Ishikawa WT ESR1 clone 1; genotype: WT ESR1; treatment: 0.1% DMSO; time: 1 hr; chip antibody: Anti-FLAG (Sigma-Aldrich M2, lot# SLBX2256) antibody that recognizes FLAG tag on ESR1; ', 'cell line: Ishikawa WT ESR1 clone 2; genotype: WT ESR1; treatment: 10nM E2; time: 1 hr; chip antibody: Anti-FLAG (Sigma-Aldrich M2, lot# SLBX2256) antibody that recognizes FLAG tag on ESR1; ', 'cell line: Ishikawa WT ESR1 clone 2; genotype: WT ESR1; treatment: 0.1% DMSO; time: 1 hr; chip antibody: Anti-FLAG (Sigma-Aldrich M2, lot# SLBX2256) antibody that recognizes FLAG tag on ESR1; ', 'cell line: Ishikawa D538G ESR1 clone 1; genotype: D538G ESR1; treatment: 10nM E2; time: 1 hr; chip antibody: Anti-FLAG (Sigma-Aldrich M2, lot# SLBX2256) antibody that recognizes FLAG tag on ESR1; ', 'cell line: Ishikawa D538G ESR1 clone 1; genotype: D538G ESR1; treatment: 0.1% DMSO; time: 1 hr; chip antibody: Anti-FLAG (Sigma-Aldrich M2, lot# SLBX2256) antibody that recognizes FLAG tag on ESR1; ', 'cell line: Ishikawa D538G ESR1 clone 2; genotype: D538G ESR1; treatment: 10nM E2; time: 1 hr; chip antibody: Anti-FLAG (Sigma-Aldrich M2, lot# SLBX2256) antibody that recognizes FLAG tag on ESR1; ', 'cell line: Ishikawa D538G ESR1 clone 2; genotype: D538G ESR1; treatment: 0.1% DMSO; time: 1 hr; chip antibody: Anti-FLAG (Sigma-Aldrich M2, lot# SLBX2256) antibody that recognizes FLAG tag on ESR1; ', 'cell line: Ishikawa D538G ESR1 clone 3; genotype: D538G ESR1; treatment: 10nM E2; time: 1 hr; chip antibody: Anti-FLAG (Sigma-Aldrich M2, lot# SLBX2256) antibody that recognizes FLAG tag on ESR1; ', 'cell line: Ishikawa D538G ESR1 clone 3; genotype: D538G ESR1; treatment: 0.1% DMSO; time: 1 hr; chip antibody: Anti-FLAG (Sigma-Aldrich M2, lot# SLBX2256) antibody that recognizes FLAG tag on ESR1; ', 'cell line: Ishikawa WT ESR1; genotype: WT ESR1; chip antibody: none; ', 'cell line: Ishikawa D538G ESR1; genotype: D538G ESR1; chip antibody: none; ' GSE59247 Homo sapiens 48 Non-coding RNA profiling by array GPL15019 Molecular features of subtype-specific progression from ductal carcinoma in situ to invasive breast cancer [miRNA data] 2014-07-09 Breast cancer consists of at least five main molecular “intrinsic” subtypes, which are reflected in both pre-invasive and invasive disease. Although previous studies have suggested that many of the molecular features of invasive breast cancer are established early, it is unclear what mechanisms drive progression, and whether the mechanisms of progression are dependent or independent of subtype. We have generated mRNA, miRNA and DNA copy number profiles from a total of 59 in situ lesions and 85 invasive tumors, in order to comprehensively identify those genes, signaling pathways, processes, and cell types that are involved in breast cancer progression. Our work provides evidence that there are molecular features associated with disease progression that are unique to the intrinsic subtypes. We additionally establish subtype-specific signatures that are able to identify a small proportion of pre-invasive tumors with expression profiles that resemble invasive carcinoma, indicating a higher likelihood of future disease progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59247 Molecular Features of Subtype-Specific Progression from Ductal Carcinoma In Situ to Invasive Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2016.06.051 {Cell reports (7.815): 10.1016/j.celrep.2016.06.051} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA254805 https://www.ebi.ac.uk/ena/browser/view/PRJNA254805 None [Overal design]One-color design, totaling 48 arrays and 41 unique tissues. Arrays consist of 4 normal controls (1 unique), 28 DCIS lesions (26 unique), and 16 small invasive breast cancers (14 unique).; [Treatment]'None'; [Growth]'None'; [Extraction]'Tumor tissues were homogenized using TRIzol Reagent (Invitrogen, Life Technologies, USA), and purified with RNeasy mini columns (Qiagen, Netherlands). The quality of RNA was assessed using NanoDrop ND-1000 Spectrophotometer, version 3.7.1 (NanoDrop Technologies, Thermo Fisher Scientific Inc, USA).'; [Cell type]'Source: ''tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 1; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 72; size (mm): 10; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 42; size (mm): 35; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Uppsala; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 57; size (mm): 13; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 47; size (mm): NA; pam50: LumB; death event: 1; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 63; source: Oslo; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): NA; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 83; size (mm): 14; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 55; size (mm): 20; pam50: Her2; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 270; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 56; size (mm): 25; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Normal breast tissue; er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: NA; age (years): NA; size (mm): NA; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: NA; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 74; size (mm): 25; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 266; source: Oslo; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 63; size (mm): 14; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 0; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 69; size (mm): 26; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 232; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 44; size (mm): NA; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): NA; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 53; size (mm): 13; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 82; size (mm): 28; pam50: Her2; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 48; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 45; size (mm): 24; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): 2; grade (eortc): NA; lymph node: 0; age (years): 52; size (mm): 9; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 244; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 49; size (mm): 35; pam50: LumB; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 51; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 48; size (mm): 60; pam50: LumA; death event: 0; iPSilateral event: 1; dmfs event: 0; recurrence event: 1; recurrence location: Ipsi situ; recurrence type: Non-Invasive; follow-up time: 37; source: Uppsala; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 40; size (mm): 15; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): NA; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 42; size (mm): 11; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 2; grade (elston): 2; grade (eortc): NA; lymph node: 0; age (years): 78; size (mm): 10; pam50: LumB; death event: 1; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 47; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 54; size (mm): 17; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 1; recurrence event: 1; recurrence location: contra invasive then liver +skeleton; recurrence type: Invasive; follow-up time: 267; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 66; size (mm): 17; pam50: Her2; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 245; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 48; size (mm): NA; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 1; grade (elston): 1; grade (eortc): NA; lymph node: 0; age (years): 40; size (mm): 10; pam50: Her2; death event: 1; iPSilateral event: 1; dmfs event: 1; recurrence event: 1; recurrence location: Skin and brain; recurrence type: Invasive; follow-up time: 51; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 1; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 66; size (mm): NA; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): NA; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 48; size (mm): 14; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 71; size (mm): 23; pam50: Basal; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 108; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 0; her2 (ihc): NA; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 78; size (mm): NA; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 1; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 50; size (mm): NA; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 241; source: Oslo; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 1; age (years): 46; size (mm): 15; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 56; size (mm): 7; pam50: Her2; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 48; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 69; size (mm): NA; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 57; size (mm): 14; pam50: Basal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 56; size (mm): NA; pam50: Her2; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 67; size (mm): 12; pam50: LumB; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Trondheim; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 0; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 55; size (mm): NA; pam50: LumB; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 50; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 72; size (mm): 19; pam50: LumA; death event: 1; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 50; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 2; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 65; size (mm): 10; pam50: LumA; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): NA; grade (elston): NA; grade (eortc): NA; lymph node: 0; age (years): 43; size (mm): NA; pam50: Normal; death event: NA; iPSilateral event: NA; dmfs event: NA; recurrence event: NA; recurrence location: NA; recurrence type: NA; follow-up time: NA; source: Akershus; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 0; pr (ihc): 0; her2 (ihc): 1; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 57; size (mm): 50; pam50: Normal; death event: 1; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 166; source: Oslo; ', 'tissue type: Invasive breast cancer (IBC); er (ihc): 1; pr (ihc): 1; her2 (ihc): 1; grade (combined): 1; grade (elston): 1; grade (eortc): NA; lymph node: 0; age (years): 72; size (mm): 10; pam50: LumA; death event: 1; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 33; source: Oslo; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): 1; pr (ihc): 1; her2 (ihc): 0; grade (combined): 3; grade (elston): NA; grade (eortc): 3; lymph node: 0; age (years): 42; size (mm): 35; pam50: LumB; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 40; source: Uppsala; ', 'tissue type: Ductal carcinoma in situ (DCIS); er (ihc): NA; pr (ihc): NA; her2 (ihc): NA; grade (combined): 2; grade (elston): NA; grade (eortc): 2; lymph node: 0; age (years): 65; size (mm): 10; pam50: LumA; death event: 0; iPSilateral event: 0; dmfs event: 0; recurrence event: 0; recurrence location: NA; recurrence type: NA; follow-up time: 47; source: Uppsala; ' GSE133987 Homo sapiens 6 Expression profiling by array GPL16686 SUM159 BrCa Decitabine Gene Expression 2019-07-08 Dysregulation of DNA methylation is an established feature of breast cancers. DNA demethylating therapies like decitabine are proposed for the treatment of triple-negative breast cancers (TNBCs) and indicators of response need to be identified. For this purpose, we characterized the effects of decitabine in a panel of 10 breast cancer cell lines and observed a range of sensitivity to decitabine that was not subtype-specific. Knockdown of potential key effectors demonstrated the requirement of deoxycytidine kinase (DCK) for decitabine response in breast cancer cells. In treatment-naive breast tumors, DCK was higher in TNBCs, and DCK levels were sustained or increased post chemotherapy treatment. This suggests that limited DCK levels will not be a barrier to response in TNBC patients treated with decitabine as a second line treatment or in a clinical trial. Methylome analysis revealed that genome-wide, region-specific, tumor suppressor gene-specific methylation, and decitabine-induced demethylation did not predict response to decitabine. Gene set enrichment analysis (GSEA) of transcriptome data demonstrated that decitabine induced genes within apoptosis, cell cycle, stress, and immune pathways in decitabine treated cells. Induced genes included those characterized by the viral mimicry response; however knockdown of key effectors of the pathway did not affect decitabine sensitivity suggesting that breast cancer growth suppression by decitabine is independent of viral mimicry. Finally, taxol-resistant breast cancer cells expressing high levels of multidrug resistance transporter ABCB1 remained sensitive to decitabine, suggesting that the drug could be used as second-line treatment for chemoresistant patients. We used microarrays to determine genome-wide expression changes induced by DNA de-methylating agent decitabine in breast cancer cell lines https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE133987 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA553252 https://www.ebi.ac.uk/ena/browser/view/PRJNA553252 None [Overal design]72 hours treated with 1uM decitabine versus NT; [Treatment]"SUM159 cells were treated with 1µM 5'-deoxy-azacytidine (Sigma) for 72 hours with media refreshed daily"; [Growth]'SUM159 cells were cultured in F-12 Ham’s Nutrient Mix Medium supplemented with 5% fetal bovine serum (Invitrogen, Gibco), 1X Antibiotic-Antimycotic (Invitrogen, Gibco), 1µM 4-(2-Hydroxyethyl) piperazine-1-ethanesulfonic acid (HEPES; Invitrogen), 0.01µg/mL human insulin (Sigma), 0.05µg/mL hydrocortisone (Invitrogen). Cells were cultured in a humidified 37C incubator with 5% CO.'; [Extraction]'Cells were collected in Trizol (Invitrogen) and RNA was purified using a PureLink RNA kit (Invitrogen Thermo Fisher Scientific) following the manufacturer’s instructions'; [Cell type]'Source: ''cell line: SUM159 Breast cancer cells; treatment: NT; ', 'cell line: SUM159 Breast cancer cells; treatment: DAC; ' GSE112517 Homo sapiens 2 Expression profiling by array GPL10558 A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway (KLHDC7B knockdown) 2018-03-30 Kelch domain-containing 7B (KLHDC7B) was revealed hypermethylated at promoter but upregulated in breast cancer. And we identified a long non-coding RNA, ST8SIA6-AS1 (STAR1), of which expression was highly associated with KLHDC7B in breast cancer (r = 0.5887). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112517 A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway. Scientific reports 4.011 https://doi.org/10.1038/s41598-018-31306-8 {Scientific reports (4.011): 10.1038/s41598-018-31306-8} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA448060 https://www.ebi.ac.uk/ena/browser/view/PRJNA448060 None [Overal design]Control sample is transfected RNA using si negative control and Test sample is a knockdown using KLHDC7B's siRNA. Both sample RNA is extracted from breast cancer cell MCF-7; [Treatment]'transfection using lipofectamin and siRNA'; [Growth]'RPMI1640 medium supplemented with 10% FBS and 1% Penicillin-Streptomycin at 37℃ containing 5% CO2'; [Extraction]'RNA was extracted and purified from MCF-10A using ZR Dyet DNA/RNA kit (Zymo research) according to standard instructions'; [Cell type]'breast cancer''cell line: MCF7; cell type: breast cancer; gender: female; tissue: adenocarcinoma; ' GSE144393 Mus musculus 12 Expression profiling by high throughput sequencing GPL19057 RNA-Seq of 2 lung metastatic breast cancer cell lines and their Nfib Kos. 2020-01-28 Next Generation Sequencing was applied to investigate molecular mechanisms underlying the increased metastatic colonization driven by Nfib. Global transcriptional profiling of the lung metastatic cell lines and respective KOs allowed to identify Ero1l as a mediator of metastasis upon Nfib upregulation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144393 The NFIB-ERO1A axis promotes breast cancer metastatic colonization of disseminated tumour cells. EMBO molecular medicine 10.624 https://doi.org/10.15252/emmm.202013162 {EMBO molecular medicine (10.624): 10.15252/emmm.202013162} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA603549 https://www.ebi.ac.uk/ena/browser/view/PRJNA603549 https://www.ncbi.nlm.nih.gov/sra?term=SRP245628 [Overal design]RNA-Seq in 2 different lung metastatic breast cancer cell lines and respective KOs to investigate NFIB signalling role in metastasic colonitazion.; [Treatment]'None'; [Growth]'LM1, LM9, LM1 Nfib KO, and LM9 Nfib KO cells were plated in ultra-low attachment plates (Corning) for six days at 10,000 cells per mL in DMEM:F12 supplemented with 1x B27 (Gibco, Invitrogen), 20 ng/mL human or mouse EGF (PeproTech), 20 ng/mL basic FGF (PeproTech), and 1x penicillin/ streptomycin (Gibco, Invitrogen). Primary tumourspheres were dissociated with 0.05% trypsin and collected.'; [Extraction]'Total RNA was extracted using a Qiagene, RNeasy Plus Mini kit (cat. number 74136)\nThe library was prepared using Illumina TruSeq stranded mRNA-seq preparation kit (according to recommendations from the manufacturer)'; [Cell type]'Source: ''breast cancer model: LM1; ', 'breast cancer model: LM1KO; ', 'breast cancer model: LM9; ', 'breast cancer model: LM9KO; ' GSE47861 Homo sapiens 161 Expression profiling by array GPL17279 Expression profiling of peripheral blood gene expression of women with hereditary breast cancer and controls (set 2) 2013-06-11 We obtained peripheral blood samples for women from Utah (USA) and Ontario (Canada) who had a family history of breast cancer (or did not), who carried a BRCA1/2 mutation (or did not), and who had developed breast cancer (or had not). We classified the women into two groups: [1] those who had a family history of breast cancer (irrespective of BRCA1/2 mutation status) and had developed an early-onset breast tumor and [2] those who had a family history of breast cancer but had not developed a breast tumor or who did not have a family history of breast cancer (some of whom had developed sporadic breast cancer and and others who had not). We then used machine-learning methods to assess how well we could classify these women into either group. The Utah samples served as a training set, and the Ontario samples served as an independent validation set from a geographically distinct population. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47861 Integrative analyses reveal signaling pathways underlying familial breast cancer susceptibility. Molecular systems biology 9.800 https://doi.org/10.15252/msb.20156506 {Molecular systems biology (9.800): 10.15252/msb.20156506} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA208224 https://www.ebi.ac.uk/ena/browser/view/PRJNA208224 None [Overal design]For the Utah cohort, there are 124 samples total: 16 who had a family history of breast cancer and carried a BRCA mutation and had developed breast cancer, 23 with a family history of breast cancer but did not carry a BRCA1/2 mutation and had developed breast cancer, 22 with a family history of breast cancer and carried a BRCA1/2 mutation but had not developed breast cancer, 22 with a family history of breast cancer but did not carry a BRCA1/2 mutation and had not developed breast cancer, 22 with no family history of breast cancer and had developed breast cancer, and 19 with no family history of breast cancer and had not developed breast cancer. The Ontario cohort included 73 samples: 11 who had a family history of breast cancer and carried a BRCA mutation and had developed breast cancer, 17 with a family history of breast cancer but did not carry a BRCA1/2 mutation and had developed breast cancer, 14 with a family history of breast cancer and carried a BRCA1/2 mutation but had not developed breast cancer, 18 with a family history of breast cancer but did not carry a BRCA1/2 mutation and had not developed breast cancer, 8 with no family history of breast cancer and had developed breast cancer, and 5 with no family history of breast cancer and had not developed breast cancer. 36 of the Ontario samples were scanned and processed at Duke University; the remaining 37 samples were handled at Boston University. The batch-adjustment process was repeated twice independently: [1] all 124 Utah samples were adjusted jointly with the 36 Ontario samples that had been processed at Duke University (set 1) and [2] all 124 Utah samples were adjusted jointly with the 37 Ontario samples that had been processed at Boston University (set 2). This dataset represents set 2.; [Treatment]'Not applicable.'; [Growth]'Not applicable.'; [Extraction]'RNA was extracted using the RiboPure RNA Isolation Kit.'; [Cell type]'peripheral blood mononuclear cells''cell type: peripheral blood mononuclear cells; breast_cancer_family_history: no; developed_breast_cancer: no; cohort: Utah; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: no; developed_breast_cancer: yes; cohort: Utah; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: no; cohort: Utah; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: yes; cohort: Utah; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: yes; cohort: Utah; carries_brca_mutation: yes; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: no; cohort: Utah; carries_brca_mutation: yes; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: yes; cohort: Ontario; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: no; cohort: Ontario; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: no; developed_breast_cancer: no; cohort: Ontario; carries_brca_mutation: no; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: yes; cohort: Ontario; carries_brca_mutation: yes; ', 'cell type: peripheral blood mononuclear cells; breast_cancer_family_history: yes; developed_breast_cancer: no; cohort: Ontario; carries_brca_mutation: yes; ' GSE17040 Homo sapiens 57 Expression profiling by array GPL887 Functional ER alpha transcriptional regulatory network for cell cycle in an ER(+) breast cancer subgroup 2009-07-10 To better characterize group IE like human breast cancer based on the gene profiles of estrogen actions through estrogen receptor alpha (ER alpha), we identified an ER alpha transcriptional regulatory network for cell cycle in silico. We used two datasets from cell line (Data 1) and clinical samples (Data 2), respectively. Analyses on Data 1 via trajectory clustering and Pathway-Express confirmed the significant estrogen effect on up-regulating cell cycle activities. The gene expression relationships between ER alpha and cell cycle genes were re-identified in Data 2 by three statistical methods – Galton-Pearson’s correlation coefficient, Student’s t-test and the coefficient of intrinsic dependence. They were mostly (56.09%)(46/82) re-confirmed by literature search. E2F1 was found to be the major ER alpha target in regulating cell cycle gene expressions (83.72%)(36/43) via suppressive mode. However, enhanced cell cycle progression via up-regulating some cell cycle genes was predicted in silico possibly involving E2F2, in part. Both tumorigenic and tumor suppressing activities indicated by this network were predicted. This network clearly provides a robust way for uncovering estrogen actions in an ER(+) subtype specific manner. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17040 Identifying gene set association enrichment using the coefficient of intrinsic dependence. PloS one 2.776 https://doi.org/10.1371/journal.pone.0058851 {PloS one (2.776): 10.1371/journal.pone.0058851} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA117841 https://www.ebi.ac.uk/ena/browser/view/PRJNA117841 None [Overal design]Two clinical datasets were used in this study. One, the 37 clinical arrays (abbreviated as 37A) consist of 26 A for patients positive in estrogen receptor alpha (ER) and in progesterone receptor (PR) immunohistochemical stain (IHC) and 11A for patients negative in ER IHC. This dataset was designated as Data 2. The 31 clinical arrays (31A) consist of 20A for patients positive in ER status but negative in PR status and 11A which are the same as in 37A. This dataset was used for data comparison. All the signals from the mRNA profile of each sample in the experiments were normalized using the internal control RNA- Stratagene's human common reference RNA via statistical method 'rank consistant lowess. Finally, those ratios were transformed by Log2.; [Treatment]'The surgical removed tumors and non-tumor part of breast specimens were excised, collected and snap-frozen in liquid nitrogen immediately before RNA extraction.'; [Growth]'The fresh samples used for this study were immediately frozen by liquid nitrogen without any additional growth procedure applied before RNA extraction.'; [Extraction]'Trizol reagent combined with Rneasy mini kit'; [Cell type]'Source: ''gender: female; tissue: primary tumor; estrogen receptor status: ER(+); progesterone receptor status: PR(+); ', "reference: Stratagene's human common reference RNA; ", 'gender: female; tissue: primary tumor; estrogen receptor status: ER(+); progesterone receptor status: PR(-); ', 'er/pr/her status: ER(-)PR(-)HER(+); gender: female; tissue: primary tumor; estrogen receptor status: ER(-); progesterone receptor status: PR(-); ', 'er/pr/her status: ER(-) PR(-)HER(-); gender: female; tissue: primary tumor; estrogen receptor status: ER(-); progesterone receptor status: PR(-); ', 'er/pr/her status: ER(-)PR(+)HER(-); gender: female; tissue: primary tumor; estrogen receptor status: ER(-); progesterone receptor status: PR(-); ', 'gender: female; tissue: recurrent tumor; estrogen receptor status: ER(+); progesterone receptor status: PR(-); ', 'er/pr/her status: ER(-) PR(+)HER(+); gender: female; tissue: primary tumor; estrogen receptor status: ER(-); progesterone receptor status: PR(-); ' GSE40837 Homo sapiens 8 Expression profiling by array GPL570 A phase II study of adding the multikinase inhibitor sorafenib to endocrine therapy in patients with metastatic ER-positive breast cancer. 2012-09-12 Growth factor signaling and angiogenesis may promote endocrine-resistance in breast cancer and blocking these pathways can overcome resistance in preclinical models. We conducted a phase-II study of adding the VEGFR/Ras/Raf/MAPK inhibitor sorafenib to endocrine therapy in metastatic ER-positive breast cancer, either upon progression or after maximal response with measurable residual disease. Tumor biopsies and serum were collected on days 1 and 28. Primary endpoint was response by RECIST after 3 months and secondary endpoints included safety, time to progression (TTP), and biomarker assessment. Planned sample size was 43 patients but the study closed after 11 patients because of slow accrual. 8 patients had progressive disease (PD) on entry and 3 had stable disease (SD). One patient with SD discontinued sorafenib after 2-weeks because of grade 3 rash. Of the 10 remaining patients after adding sorafenib, 7 had SD (70%), 3 had PD (30%) and median TTP was 6.1-months. Of the 8 patients who entered the study with PD on endocrine therapy, 5 converted to SD (62%) with a median TTP of 6.4-months. Notably, patients on tamoxifen had a median TTP of 8.4-months. The most common adverse events were hypophosphatemia, hypokalemia, and rash, and the majority were grade 1&2 with no grade 4 toxicities. There was a significant reduction in serum VEGFR2 and PDGFR-α on day-28 (p-values 0.0035 and 0.017, respectively). Both serum VEGF and sVEGFR-1 were increased on day-28, but the differences were not statistically significant (p-values 0.3223 and 0.084, respectively). Microarray analysis identified 32 suppressed genes with an FDR of <0.20 and at least a 2-fold change with no induced genes and 29 KEGG pathways were enriched on day-28. Our study suggests that sorafenib can restore endocrine sensitivity, particularly tamoxifen, and this strategy of adding novel agents in patients progressing on endocrine therapy should be examined in future trials. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE40837 Impact of adding the multikinase inhibitor sorafenib to endocrine therapy in metastatic estrogen receptor-positive breast cancer. Future oncology (London, England) 2.279 https://doi.org/10.2217/fon.14.99 {Future oncology (London, England) (2.279): 10.2217/fon.14.99} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA175060 https://www.ebi.ac.uk/ena/browser/view/PRJNA175060 None [Overal design]This was a single-institution, phase II study of adding sorafenib to existing endocrine therapy. On study entry, eligible patients underwent serum sample collection and core biopsy of accessible disease (if applicable) on endocrine therapy and prior to starting sorafenib. Serum and a second biopsy were then collected on day 28. Sorafenib dose was 400mg orally twice daily along with continuing the same endocrine agent. Patients were followed monthly for clinical and toxicity evaluation. Disease response by RECIST criteria was assessed after 3 months by appropriate scans and these were obtained every 2 months thereafter until progression. Sorafenib and the endocrine agent were continued until disease progression or unacceptable toxicity; [Treatment]'After day 1 biopsy on endocrine therapy alone, sorafenib was added and a second biopsy was obtained on day 28.'; [Growth]'None'; [Extraction]'Trizol extraction'; [Cell type]'Source: ''tissue: breast tumor; age: 44; er status: Positive; pgr status: Positive; endocrine agent: Tamoxifen; status on endocrine agent: Progressive disease (PD); response to sorafenib: N/A; ', 'tissue: breast tumor; age: 44; er status: Positive; pgr status: Positive; endocrine agent: Tamoxifen; status on endocrine agent: N/A; response to sorafenib: Stable disease (SD); ', 'tissue: breast tumor; age: 41; er status: Positive; pgr status: Positive; endocrine agent: Tamoxifen; status on endocrine agent: Stable disease (SD); response to sorafenib: N/A; ', 'tissue: breast tumor; age: 41; er status: Positive; pgr status: Positive; endocrine agent: Tamoxifen; status on endocrine agent: N/A; response to sorafenib: Stable disease (SD); ', 'tissue: breast tumor; age: 45; er status: Positive; pgr status: Positive; endocrine agent: Tamoxifen; status on endocrine agent: Progressive disease (PD); response to sorafenib: N/A; ', 'tissue: breast tumor; age: 45; er status: Positive; pgr status: Positive; endocrine agent: Tamoxifen; status on endocrine agent: N/A; response to sorafenib: Progressive disease (PD); ', 'tissue: breast tumor; age: 63; er status: Positive; pgr status: Negative; endocrine agent: Letrozole; status on endocrine agent: Progressive disease (PD); response to sorafenib: N/A; ', 'tissue: breast tumor; age: 63; er status: Positive; pgr status: Negative; endocrine agent: Letrozole; status on endocrine agent: N/A; response to sorafenib: Stable disease (SD); ' GSE11506 Homo sapiens 9 Expression profiling by array GPL570 Novel Estrogen Receptor-{alpha} Binding Sites and Estradiol Target Genes Identified by ChIP Cloning in Breast Cancer. 2008-05-20 Estrogen receptor-{alpha} (ER{alpha}) and its ligand estradiol play critical roles in breast cancer growth and are important therapeutic targets for this disease. Using chromatin immunoprecipitation (ChIP)-on-chip, ligand-bound ER{alpha} was recently found to function as a master transcriptional regulator via binding to many cis-acting sites genome-wide. Here, we used an alternative technology (ChIP cloning) and identified 94 ER{alpha} target loci in breast cancer cells. The ER{alpha}-binding sites contained both classic estrogen response elements and nonclassic binding sequences, showed specific transcriptional activity in reporter gene assay, and interacted with the key transcriptional regulators, including RNA polymerase II and nuclear receptor coactivator-3. The great majority of the binding sites were located in either introns or far distant to coding regions of genes. Forty-three percent of the genes that lie within 50 kb to an ER{alpha}-binding site were regulated by estradiol. Most of these genes are novel estradiol targets encoding receptors, signaling messengers, and ion binders/transporters. mRNA profiling in estradiol-treated breast cancer cell lines and tissues revealed that these genes are highly ER{alpha} responsive both in vitro and in vivo. Among estradiol-induced genes, Wnt11 was found to increase cell survival by significantly reducing apoptosis in breast cancer cells. Taken together, we showed novel genomic binding sites of ER{alpha} that regulate a novel set of genes in response to estradiol in breast cancer. Our findings suggest that at least a subset of these genes, including Wnt11, may play important in vivo and in vitro biological roles in breast cancer. Keywords: time course https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE11506 Novel estrogen receptor-alpha binding sites and estradiol target genes identified by chromatin immunoprecipitation cloning in breast cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-06-3696 {Cancer research (8.378): 10.1158/0008-5472.CAN-06-3696} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA106331 https://www.ebi.ac.uk/ena/browser/view/PRJNA106331 None [Overal design]This Series currently contains the gene expression data accompanying Zhihong Lin et al. Cancer Research 67,5017-5024(2007). MCF7 cells were treated with vehicle or E2 at a concentration of 10E-9 mol/L for 3 and 6 h. All experiments were performed in triplicate.; [Treatment]'After MCF-7 cells were grown to 75% to 80% confluence in MEM supplemented with 10% FBS, the cells were serum starved in DMEM/F-12 without phenol red (Invitrogen) and FBS for 24 h. MCF-7 cells were then treated with vehicle or E2 at a concentration of 10–9 mol/L for 3 and 6 h. All experiments were performed in triplicate.'; [Growth]'MCF-7 cells (American Type Culture Collection) were maintained in MEM (Invitrogen) containing 25 units/mL penicillin, 25 units/mL streptomycin, and 10% fetal bovine serum (FBS) at 37°C and 5% CO2.'; [Extraction]"Total RNA was extracted from the MCF-7 breast cancer cell line using Tri-Reagent (Sigma) according to the manufacturer's instruction. Total RNA samples were treated with DNase I (Ambion) for 20 min at 37°C according to the product manual."; [Cell type]'Source: ''' GSE147901 Homo sapiens 3 Expression profiling by high throughput sequencing GPL16791 RNA-seq of ERINA knockdown T47D cell lines 2020-04-01 We identified an intergenic lncRNA ERINA (estrogen inducible lncRNA) as a novel lncRNA that is associated with chemo-resistance and highly expressed in multiple cancer types, especially in estrogen receptor (ER) positive breast cancers. Functional characterizations based on RNA-seq analyses established ERINA as an oncogenic lncRNA, because knockdown of ERINA in breast cancer cells inhibits cell cycle progression and tumor cell proliferation in vitro and xenograft tumor growth in vivo. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE147901 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA622513 https://www.ebi.ac.uk/ena/browser/view/PRJNA622513 https://www.ncbi.nlm.nih.gov/sra?term=SRP254905 [Overal design]Investigation of gene alterations after knocking down ERINA.; [Treatment]'None'; [Growth]'ERINA and shRNA expressing vectors were separately co-transfected with psPAX2 and Pmd2G vectors into cells. Supernatant was collected at 48 hours post-transfection. The culture medium containing the lentiviruses was filtered through a 0.45 μm filter. Target cells were infected with viruses in the presence of polybrene and selected using puromycin to establish stable cells.'; [Extraction]'Total RNA was extracted using the RNAeasy mini Kit (Qiagen, 74104).\nReverse transcription from 1 µg RNA to cDNA was performed using the High-capacity cDNA reverse transcription kit (Applied Biosystems, 4368813). Real-time PCR was performed with Power SYBR Green PCR Master Mix (Applied Biosystems, 4367659) on a QuantStudio 6 Flex Real-Time PCR System (Applied Biosystems).'; [Cell type]'breast cancer cell line''cell line: T47D; cell type: breast cancer cell line; genotype: control; shRNA: None; ', 'cell line: T47D; cell type: breast cancer cell line; genotype: ERINA knockdown; shRNA: shRNA1; ', 'cell line: T47D; cell type: breast cancer cell line; genotype: ERINA knockdown; shRNA: shRNA2; ' GSE54855 Homo sapiens 8 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Transient ER binding and p300 redistribution support a physiological squelching model for immediate ER-repressed genes 2014-02-10 Selective transcriptional activation and repression of genes throughout signaling cascades and development are poorly understood. Transcription factors (TF) orchestrate patterns and magnitude of transcriptional response, but TF action, or inaction, is highly dependent upon TF kinetics, distance from genes, chromatin architecture, and the local occupancy of other TFs. We integrated genomic transcription, chromosome looping, TF binding, and chromatin structure data to analyze the molecular cascade that results from estradiol-induced (E2) signaling in human MCF-7 breast cancer cells and addressed the context-specific nature of gene regulation. We analyzed kinetic ChIP-seq that profiled the master regulator of the E2-mediated response, estrogen receptor (ER), and found that transient ER binding sites are specifically associated with enhancers of repressed genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54855 Transient estrogen receptor binding and p300 redistribution support a squelching mechanism for estradiol-repressed genes. Molecular endocrinology (Baltimore, Md.) 3.628 https://doi.org/10.1210/me.2014-1130 {Molecular endocrinology (Baltimore, Md.) (3.628): 10.1210/me.2014-1130} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA237893 https://www.ebi.ac.uk/ena/browser/view/PRJNA237893 https://www.ncbi.nlm.nih.gov/sra?term=SRP037572 [Overal design]We performed replicate ChIP-seq experiments prior to estrogen treatment and 2min, 5min, 10min, 40min, and 160min after E2 treatment.; [Treatment]'Cells were treated with 100nM estradiol for the indicated time points.'; [Growth]'MCF-7 cells were grown in DMEM supplemented with fetal bovine serum to a final concentration of 10%. Cells were cultured in charcoal-dextran FBS for the three days prior to 100nM E2 stimulation.'; [Extraction]'To achieve high temporal resolution, ChIP crosslinking concentration of formaldehyde was 2% and crosslinking was quenched after 1 minute with 250mM glycine. The ER antibody we used for IP was Santa Cruz: sc-542.\nThe ends of the ChIP DNA were blunted and phosphorylated in 1X END Repair Buffer (Epicentre Biotechnologies, #ER0720), 250nM dNTPs, 1mM ATP, and 1X END-IT enzyme mix (Epicentre Biotechnologies, #ER0720) for 45 minutes. An A overhang was achieved in 1xNEB2 buffer, 200nM dATP (Invitrogen), 3units of Klenow (3¢-5¢ exo-) 5U/ml (from New England BioLabs), in 50ul volume for 30 minutes. 10nM of adapter was ligated to the DNA in 1X ligation buffer, 5ml (3000units) of UltraPure Ligase from enzymatics (Enzymatics T4 DNA Ligase #L603-HC-L) in a total volume of 50ul. Thirteen cycles of PCR with Phusion polymerase were performed to acquire the final library.'; [Cell type]'Source: ''cell line: MCF-7; treatment: 100nM estradiol 0 min; antibody: ER (Santa Cruz, sc-542); ', 'cell line: MCF-7; treatment: 100nM estradiol 2 mins; antibody: ER (Santa Cruz, sc-542); ', 'cell line: MCF-7; treatment: 100nM estradiol 5 mins; antibody: ER (Santa Cruz, sc-542); ', 'cell line: MCF-7; treatment: 100nM estradiol 10 mins; antibody: ER (Santa Cruz, sc-542); ', 'cell line: MCF-7; treatment: 100nM estradiol 40 mins; antibody: ER (Santa Cruz, sc-542); ', 'cell line: MCF-7; treatment: 100nM estradiol1 60 mins; antibody: ER (Santa Cruz, sc-542); ', 'cell line: MCF-7; antibody: none; ', 'cell line: MCF-7; antibody: IgG; ' GSE156970 Homo sapiens 196 Methylation profiling by genome tiling array; Non-coding RNA profiling by high throughput sequencing GPL13534; GPL16791 Genome-wide DNA methylation and expression patterns of microRNAs in relation to breast cancer subtypes among American women of African and European ancestry 2020-08-27 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE156970 Differential methylation and expression patterns of microRNAs in relation to breast cancer subtypes among American women of African and European ancestry. PloS one 2.776 https://doi.org/10.1371/journal.pone.0249229 {PloS one (2.776): 10.1371/journal.pone.0249229} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA659706 https://www.ebi.ac.uk/ena/browser/view/PRJNA659706 None [Overal design]Refer to individual Series; [Treatment]'NA'; [Growth]'NA'; [Extraction]'DNA was extracted using a MasterPure DNA purification kit (Epicentre).', 'RNA extracted using RNeasy Mini Kit (Qiagen)\nNEBNext Multiplex Small RNA kit for small RNA cDNA library preparation'; [Cell type]'Source: ''gender: Female; tissue: Flash frozen breast tumor tissue; ', 'tissue: breast tumor tissue; age: 83; gender: Female; race: Caucasian; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 68; gender: Female; race: Caucasian; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 72; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 39; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 33; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 90; gender: Female; race: African American; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 50; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 39; gender: Female; race: Caucasian; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 71; gender: Female; race: African American; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 46; gender: Female; race: African American; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 82; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 73; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 92; gender: Female; race: Caucasian; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 38; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 50; gender: Female; race: African American; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 41; gender: Female; race: African American; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 75; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 47; gender: Female; race: African American; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 45; gender: Female; race: Caucasian; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 31; gender: Female; race: Caucasian; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 46; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 42; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 51; gender: Female; race: Caucasian; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 63; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 29; gender: Female; race: Caucasian; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 76; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 63; gender: Female; race: African American; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 69; gender: Female; race: Caucasian; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 65; gender: Female; race: African American; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 69; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 44; gender: Female; race: African American; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 53; gender: Female; race: African American; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 53; gender: Female; race: African American; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 62; gender: Female; race: African American; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 68; gender: Female; race: African American; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 65; gender: Female; race: African American; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 59; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 49; gender: Female; race: African American; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 75; gender: Female; race: African American; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 81; gender: Female; race: African American; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 48; gender: Female; race: African American; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 70; gender: Female; race: African American; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 59; gender: Female; race: Caucasian; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 76; gender: Female; race: African American; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 60; gender: Female; race: African American; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 80; gender: Female; race: African American; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 73; gender: Female; race: African American; er: Negative; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 87; gender: Female; race: Caucasian; er: Positive; molecule subtype: miRNA; ', 'tissue: breast tumor tissue; age: 79; gender: Female; race: Caucasian; er: Negative; molecule subtype: miRNA; ' GSE173664 Homo sapiens 40 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL16791 Transcriptional reprogramming by oxidative stress occurs within a predefined chromatin accessibility landscape 2021-04-30 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE173664 Transcriptional reprogramming by oxidative stress occurs within a predefined chromatin accessibility landscape. Free radical biology & medicine 5.657 https://doi.org/10.1016/j.freeradbiomed.2021.05.016 {Free radical biology & medicine (5.657): 10.1016/j.freeradbiomed.2021.05.016} 'polyA RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA726553 https://www.ebi.ac.uk/ena/browser/view/PRJNA726553 None [Overal design]Refer to individual Series; [Treatment]'MCF7 cells were seeded (125,000 cells/ml) in 6 well plates and grown at 37°C for 24 hrs, after which cells were treated with the growth media supplemented with either 0.1% ethanol, 10 μM MEN, or 80 μM TBOOH for 0, 1, 8, or 24 hrs.'; [Growth]'MCF7 cells were grown and maintained in IMEM culture media (Phenol-red free, Gibco) supplemented with 5% fetal bovine serum, 1% penicillin/streptomycin (Invitrogen-Life technologies), 11.25 nM bovine insulin (Sigma-Aldrich) and 2.5 μg/L Plasmocin prophylactic (InvivoGen, San Diego, CA) in humidified air with ~20% oxygen and 5% carbon dioxide.'; [Extraction]'After treatment, cells were harvested, maintained on wet ice, pelleted and flash frozen in liquid nitrogen. Samples were kept on dry ice until Qiagen Rneasy kit (Qiagen, cat no. 74104) was utilized to extract total RNA for RNA-seq. Samples were stored at -20°C until library preparation and sequencing.\nRNA libraries were prepared using standard Illumina protocols, including oligo-dT purification', 'After treatment, cells were harvested, maintained on wet ice, and counted. 50000 cells / ml was used: first washed in ice cold PBS and resuspended in 50 μL ice cold lysis buffer. Cells were centrifuged at 500 x G for 10 min at 4°C to generate crude nuclei pellets. The crude nuclei pellet was resuspended in 50 μL Nextera Tn5 reaction buffer and transposase (Nextera cat no 15027865-6). They were then incubated at 37°C for 30 min at 250 RPM, purified with Qiagen MinElute PCR Purification Kit, eluted in 50 μL buffer EB and stored at -20°C until library preparation and sequencing.\nDNA libraries were prepared using standard Illumina protocols for Nextera-tagged DNA'; [Cell type]'Source: ''cell line: MCF7; treatment: untreated; time point: 0 hours; replicate: 1; ', 'cell line: MCF7; treatment: untreated; time point: 0 hours; replicate: 2; ', 'cell line: MCF7; treatment: 0.1% ethanol; time point: 1 hour; replicate: 1; ', 'cell line: MCF7; treatment: 0.1% ethanol; time point: 1 hour; replicate: 2; ', 'cell line: MCF7; treatment: 10 uM menadione; time point: 1 hour; replicate: 1; ', 'cell line: MCF7; treatment: 10 uM menadione; time point: 1 hour; replicate: 2; ', 'cell line: MCF7; treatment: 80 uM tert-butyl hydroperoxide; time point: 1 hour; replicate: 1; ', 'cell line: MCF7; treatment: 80 uM tert-butyl hydroperoxide; time point: 1 hour; replicate: 2; ', 'cell line: MCF7; treatment: 0.1% ethanol; time point: 8 hours; replicate: 1; ', 'cell line: MCF7; treatment: 0.1% ethanol; time point: 8 hours; replicate: 2; ', 'cell line: MCF7; treatment: 10 uM menadione; time point: 8 hours; replicate: 1; ', 'cell line: MCF7; treatment: 10 uM menadione; time point: 8 hours; replicate: 2; ', 'cell line: MCF7; treatment: 80 uM tert-butyl hydroperoxide; time point: 8 hours; replicate: 1; ', 'cell line: MCF7; treatment: 80 uM tert-butyl hydroperoxide; time point: 8 hours; replicate: 2; ', 'cell line: MCF7; treatment: 0.1% ethanol; time point: 24 hours; replicate: 1; ', 'cell line: MCF7; treatment: 0.1% ethanol; time point: 24 hours; replicate: 2; ', 'cell line: MCF7; treatment: 10 uM menadione; time point: 24 hours; replicate: 1; ', 'cell line: MCF7; treatment: 10 uM menadione; time point: 24 hours; replicate: 2; ', 'cell line: MCF7; treatment: 80 uM tert-butyl hydroperoxide; time point: 24 hours; replicate: 1; ', 'cell line: MCF7; treatment: 80 uM tert-butyl hydroperoxide; time point: 24 hours; replicate: 2; ' GSE130397 Homo sapiens 21 Expression profiling by high throughput sequencing GPL16791 RNA-seq from archival FFPE Breast Cancer samples: Molecular Pathway Fidelity and Novel Discovery 2019-04-26 Archival Formalin-Fixed Paraffin Embedded (FFPE) tissue represents an abundant and more easily transferable source of patient tissue than live specimens. Furthermore cancer FFPE tissue deposited at major cancer research institutes is often paired with survival data increasing the value of biomarker and prediction based research from these samples. However the known fragility of RNA and artifacts introduced through the processes of tissue preservation and storage introduce the possibility of unfaithful RNA expression signatures from these sources. To evaluate this we established an RNA isolation, library prepration and data analysis pipeline at Oregon Health and Science University to evaluate the fidelity of RNA expression profiles from FFPE tissues utilizing gene and pathway expression comparisons between ER positive and ER negative samples in archival FFPE specimens compared to those obtained from public available data sets of fresh specimens. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130397 RNA-seq from archival FFPE breast cancer samples: molecular pathway fidelity and novel discovery. BMC medical genomics 2.568 https://doi.org/10.1186/s12920-019-0643-z {BMC medical genomics (2.568): 10.1186/s12920-019-0643-z} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA539981 https://www.ebi.ac.uk/ena/browser/view/PRJNA539981 https://www.ncbi.nlm.nih.gov/sra?term=SRP194001 [Overal design]Two Breast Cancer ER+ FFPE samples prepared by two different RNA expression library methodologies (Illumina-Access, and Nugen-Ovation) and sequenced in triplicate. 3 ER positive and 3 ER negative FFPE derived Breast Cancer specimens prepared by Illumina Access RNA Expression library and sequenced in singlet on HiSeq2000, with four samples per lane permitting approximately 70 million reads per sample.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted from single 10um FFPE section utilizing miRNeasy FFPE kit (Qiagen, Valencia, CA)\n75ng input of FFPE derived RNA was used for TruSeq RNA Access Library Prep Kit (Illumina, San Diego, CA) (Illumina-Acc), an input of 150 ng of total FFPE RNA was used with the Ovation Human FFPE RNA-seq Library System (NuGEN Technologies, San Carlos, CA)'; [Cell type]'Source: ''source (fresh or ffpe): FFPE; tissue: breast cancer - mammary gland; year_of_diagnosis_year_of_ffpe block: 2009; erstatus_by_ihc: positive; ', 'source (fresh or ffpe): FFPE; tissue: breast cancer - mammary gland; year_of_diagnosis_year_of_ffpe block: 2010; erstatus_by_ihc: positive; ', 'source (fresh or ffpe): FFPE; tissue: breast cancer - mammary gland; year_of_diagnosis_year_of_ffpe block: 2002; erstatus_by_ihc: positive; ', 'source (fresh or ffpe): FFPE; tissue: breast cancer - mammary gland; year_of_diagnosis_year_of_ffpe block: 2005; erstatus_by_ihc: positive; ', 'source (fresh or ffpe): FFPE; tissue: breast cancer - mammary gland; year_of_diagnosis_year_of_ffpe block: 1997; erstatus_by_ihc: negative; ', 'source (fresh or ffpe): FFPE; tissue: breast cancer - mammary gland; year_of_diagnosis_year_of_ffpe block: 2011; erstatus_by_ihc: negative; ', 'source (fresh or ffpe): FFPE; tissue: breast cancer - mammary gland; year_of_diagnosis_year_of_ffpe block: 2009; erstatus_by_ihc: negative; ' GSE70210 Mus musculus 12 Expression profiling by high throughput sequencing GPL13112 An essential role for the Gai2 protein in Smoothened-stimulated mammary epithelial cell proliferation 2015-06-24 Hedgehog (Hh) signaling is critical for organogenesis, tissue homeostasis, and stem cell maintenance. Smoothened (SMO), the primary effector of Hh signaling, is expressed ectopically in human breast cancer, as well as in other cancers. Constitutive activation of SMO in mouse mammary glands leads to paracrine stimulation of proliferation, as well as hyperplasia. In canonical signaling, SMO functions via GLI transcription factor activation. However, recent data from Drosophila and mammalian cell lines indicate that SMO can function non-canonically as a G-protein coupled receptor (GPCR) by coupling to heterotrimeric G proteins, particularly those in the pertussis toxin (PTX)-sensitive G-alpha-i (Gai) class. Whether SMO functions as a GPCR in mammalian tissues in vivo is not known. Using genetically modified mouse models, we demonstrate here that SMO-induced stimulation of proliferation is PTX sensitive, and requires Gai2, but not Gai1 or Gai3. Our findings provide evidence for a non-canonical GPCR function of activated SMO in vivo, a finding that may have clinical significance given that most SMO-targeted agents were selected based largely on their ability to block canonical GLI-mediated transcription. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE70210 An essential role for Gα(i2) in Smoothened-stimulated epithelial cell proliferation in the mammary gland. Science signaling 6.481 https://doi.org/10.1126/scisignal.aaa7355 {Science signaling (6.481): 10.1126/scisignal.aaa7355} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA287876 https://www.ebi.ac.uk/ena/browser/view/PRJNA287876 https://www.ncbi.nlm.nih.gov/sra?term=SRP059824 [Overal design]Primary mammary epithelial cell RNA was deep-sequenced from mT-mG/SmoM2;MMTV-Cre (EGFP), mT-mG/SmoM2;MMTV-Cre (tdTomato), and mT-mG/SmoM2;+ cells to examine the effects of SmoM2 overexpression in the mammary gland.; [Treatment]'None'; [Growth]'None'; [Extraction]"Primary mammary epithelial cells were extracted and purified using FACS sorting. Cells were collected, spun down to remove media and flash frozen in liquid nitrogen as pellets. Total RNA was isolated using Qiagen's miRNeasy kit according to the manufacture's protocol.\nRNA libraries were prepared for sequencing using standard Illumina protocols"; [Cell type]'MEC''background strain: 129X1/SvJ, C57BL/6, and Swiss Webster; age: Nine weeks; Sex: Female; developmental stage: Adult; genotype/variation: mT-mG/SmoM2;MMTV-Cre (SmoM2 positive); cell type: MEC; ', 'background strain: 129X1/SvJ, C57BL/6, and Swiss Webster; age: Nine weeks; Sex: Female; developmental stage: Adult; genotype/variation: mT-mG/SmoM2;MMTV-Cre (SmoM2 negative); cell type: MEC; ', 'background strain: 129X1/SvJ, C57BL/6, and Swiss Webster; age: Nine weeks; Sex: Female; developmental stage: Adult; genotype/variation: mT-mG/SmoM2;+ (wild type); cell type: MEC; ' GSE93759 Homo sapiens 22 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL11154 UBR7 is a novel E3 ubiquitin ligase for H2BK120 and acts as a tumor-suppressor in breast cancer 2017-01-18 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93759 Atypical plant homeodomain of UBR7 functions as an H2BK120Ub ligase and breast tumor suppressor. Nature communications 11.878 https://doi.org/10.1038/s41467-019-08986-5 {Nature communications (11.878): 10.1038/s41467-019-08986-5} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA362300 https://www.ebi.ac.uk/ena/browser/view/PRJNA362300 None [Overal design]Refer to individual Series; [Treatment]'shRNA plasmids for UBR7 with pLKO.1-puro backbone (Sigma Aldrich) were screened for efficient knock-down.Two out seven shRNAs were selected for subsequent experiments. Four micrograms of shRNA and packaging vectors were transfected as described previously (ref). Cells were selected using puromycin (10 μg / ml) (Sigma) for 3days.', 'shRNA plasmids for UBR7 with pLKO.1-puro backbone (Sigma Aldrich) were screened for efficient knock-down.Two out seven shRNAs were selected for subsequent experiments. Four micrograms of shRNA and packaging vectors were transfected and cells were selected using puromycin (10 μg / ml) (Sigma) for 3 days.'; [Growth]'MCF10A cells were maintained in DMEM / Ham’s F12 supplemented with 5% horse serum (Gibco), EGF, insulin, hydrocortisone, cholera toxin (Sigma) and 1% antibiotic-antimycotic.'; [Extraction]'Histone-DNA complexes were isolated using antibodies described from Control and UBR7-shRNA sonicated nuclei.\nLibraries for Illumina sequencing were generated following the New England BioLabs NEBNext Ultra DNA Library Prep Kit protocol. A total of 10x cycles were used during PCR amplification for the generation of all ChIP-seq libraries. Amplified ChIP DNA was purified using double-sided AMPure XP to retain fragments ~200 to 500bp and quantified using the Qubit 2000 and Bioanalyzer 1000 before multiplexing.', 'Total RNA was extracted using the Qiagen RNeasy Mini Kit and quantified using a Bioanalyzer 1000.\nLibraries for Illumina sequencing were generated using the TruSeq RNA Library Prep Kit according to manufacturers instructions.'; [Cell type]'Human mammary epithelial cell line''cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H2BK120ub Millipore 17-650; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H3K4me1 Abcam ab8895; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H3K9me3 Abcam ab8898; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H3K27ac Abcam ab4729; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H3K79me2 Abcam ab3594; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H3K4me3 Abcam/Millipore ab; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: H3K27me3 Abcam ab6002; ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; chip-antibody: none (input); ', 'cell line: MCF10A; cell type: Human mammary epithelial cell line; ' GSE71729 Homo sapiens 357 Expression profiling by array GPL20769 Virtual Microdissection of Pancreatic Ductal Adenocarcinoma Reveals Tumor and Stroma Subtypes. 2015-08-04 Pancreatic ductal adenocarcinoma (PDAC) remains a lethal disease with a 5-year survival of 4%. A key hallmark of PDAC is extensive stromal involvement, which makes capturing precise tumor-specific molecular information difficult. Here, we have overcome this problem by applying blind source separation to a diverse collection of PDAC gene expression microarray data, which includes primary, metastatic, and normal samples. By digitally separating tumor, stroma, and normal gene expression, we have identified and validated two tumor-specific subtypes including a “basal-like” subtype which has worse outcome, and is molecularly similar to basal tumors in bladder and breast cancer. Furthermore, we define 'normal' and 'activated' stromal subtypes which are independently prognostic. Our results provide new insight into the molecular composition of PDAC which may be used to tailor therapies or provide decision support in a clinical setting where the choice and timing of therapies is critical. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE71729 Virtual microdissection identifies distinct tumor- and stroma-specific subtypes of pancreatic ductal adenocarcinoma. Nature genetics 25.455 https://doi.org/10.1038/ng.3398 {Nature genetics (25.455): 10.1038/ng.3398} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA293520 https://www.ebi.ac.uk/ena/browser/view/PRJNA293520 None [Overal design]Analysis of the landscape of gene expression in pancreatic adenocarcinoma. Data include 145 primary and 61 metastatic PDAC tumors, 17 cell lines, 46 pancreas and 88 distant site adjacent normal samples. Arrays represent distinct samples. The SPOT column in the raw data file (linked to each sample record) contains Agilent feature extraction numbers (included in the 'GPL4133-20424.txt' linked to the platform records).; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen Rneasy Kit'; [Cell type]'Source: ''sample type: Stratagene Human reference RNA; ', 'cell line/tissue: BXPC3; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Capan1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Capan2; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: CFPAC; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: HPAC; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: HPAFII; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Hs766T; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: HUPT3; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: LymphNode; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Diaphragm; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Fat; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Liver; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Liver; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Lung; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Colon; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Peritoneal; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: AbWall; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: LymphNode; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Liver; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: LymphNode; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Peritoneal; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Fat; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Colon; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Duo; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Peritoneal; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Peritoneal; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Liver; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Diaphragm; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Diaphragm; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: LymphNode; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Liver; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: LymphNode; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Liver; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: AbWall; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Duo; tissue type: Metastasis; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: MiaPaca2; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Liver; tissue type: Normal; tumor_subtype_0na_1classical_2basal: 0; stroma_subtype_0na_1low_2normal_3activated: 0; ', 'cell line/tissue: LymphNode; tissue type: Normal; tumor_subtype_0na_1classical_2basal: 0; stroma_subtype_0na_1low_2normal_3activated: 0; ', 'cell line/tissue: Lung; tissue type: Normal; tumor_subtype_0na_1classical_2basal: 0; stroma_subtype_0na_1low_2normal_3activated: 0; ', 'cell line/tissue: Fat; tissue type: Normal; tumor_subtype_0na_1classical_2basal: 0; stroma_subtype_0na_1low_2normal_3activated: 0; ', 'cell line/tissue: Pancreas; tissue type: Normal; tumor_subtype_0na_1classical_2basal: 0; stroma_subtype_0na_1low_2normal_3activated: 0; ', 'cell line/tissue: Spleen; tissue type: Normal; tumor_subtype_0na_1classical_2basal: 0; stroma_subtype_0na_1low_2normal_3activated: 0; ', 'cell line/tissue: Peritoneal; tissue type: Normal; tumor_subtype_0na_1classical_2basal: 0; stroma_subtype_0na_1low_2normal_3activated: 0; ', 'cell line/tissue: Diaphragm; tissue type: Normal; tumor_subtype_0na_1classical_2basal: 0; stroma_subtype_0na_1low_2normal_3activated: 0; ', 'cell line/tissue: PelvicWall; tissue type: Normal; tumor_subtype_0na_1classical_2basal: 0; stroma_subtype_0na_1low_2normal_3activated: 0; ', 'cell line/tissue: Vessel; tissue type: Normal; tumor_subtype_0na_1classical_2basal: 0; stroma_subtype_0na_1low_2normal_3activated: 0; ', 'cell line/tissue: HPNE; tumor_subtype_0na_1classical_2basal: 0; stroma_subtype_0na_1low_2normal_3activated: 0; ', 'cell line/tissue: Panc0203; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Panc0327; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Panc1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Panc1005; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 7; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 11; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 47; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 10; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 1; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 6; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 2; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 2; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 17; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 49; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 52; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 55; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 8; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 19; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 52; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 18; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 29; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 43; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 6; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 42; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 20; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 35; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 13; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 21; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 30; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 33; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 31; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 35; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 13; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 8; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 18; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 4; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 22; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 10; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 25; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 18; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 19; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 21; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 23; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 15; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 11; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 4; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 13; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 1; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 10; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 59; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 21; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 41; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 23; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 7; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 1; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 18; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 15; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 28; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 1; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 1; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 33; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 7; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 45; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 16; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 18; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 9; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 12; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 32; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 0; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 0; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 7; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 3; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 3; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 26; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 33; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 4; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 15; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 4; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 10; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 2; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 8; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 7; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 8; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 17; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 2; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 14; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 29; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 1; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 8; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 54; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 6; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 15; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 22; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 25; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 6; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 14; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 1; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 6; death_event_1death_0censor: 0; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 19; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 17; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 3; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 20; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 2; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: Pancreas; tissue type: Primary; survival_months: 24; death_event_1death_0censor: 1; tumor_subtype_0na_1classical_2basal: 1; stroma_subtype_0na_1low_2normal_3activated: 2; ', 'cell line/tissue: SW1990; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ', 'cell line/tissue: T3M4; tumor_subtype_0na_1classical_2basal: 2; stroma_subtype_0na_1low_2normal_3activated: 1; ' GSE42529 Homo sapiens 12 Expression profiling by array GPL10558 High-throughput 3D screening reveals differences in drug sensitivities between culture models of JIMT1 breast cancer cells. 2012-11-27 The traditional method for studying cancer in vitro is to grow immortalized cancer cells in two-dimensional (2D) monolayers on plastic. However, many cellular features are impaired in these unnatural conditions and big alterations in gene expression in comparison to tumors have been reported. Three-dimensional (3D) cell culture models have become increasingly popular and are suggested to be better models than 2D monolayers due to improved cell-to-cell contacts and structures that resemble in vivo architecture. The aim of this study was to develop a simple high-throughput 3D drug screening method and to compare drug responses in JIMT1 breast cancer cells when grown in 2D, in polyHEMA coated anchorage independent 3D models and in Matrigel on-top 3D cell culture models. We screened 102 compounds with multiple concentrations and biological replicates for their effects on cell proliferation. The cells were either treated immediately upon plating or they were allowed to grow in 3D for four days prior to the drug treatment. Big variations in drug responses were observed between the models indicating that comparisons of culture model influenced drug sensitivities cannot be made based on effects of a single drug. However, we show with the 63 most prominent drugs that, in general, JIMT1 cells grown on Matrigel were significantly more sensitive to drugs than cells grown in 2D cultures, while responses of cells grown in polyHEMA resembled those of 2D. Furthermore, comparison of gene expression profiles of the cell culture models to xenograft tumors indicated that cells cultured in Matrigel and as xenografts most closely resembled each other. In this study we also suggest that 3D cultures can provide a platform for systematic experimentation of larger compound collections in a high-throughput mode and be used as alternatives for traditional 2D screens towards better comparability to in vivo state. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE42529 High-throughput 3D screening reveals differences in drug sensitivities between culture models of JIMT1 breast cancer cells. PloS one 2.776 https://doi.org/10.1371/journal.pone.0077232 {PloS one (2.776): 10.1371/journal.pone.0077232} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA182210 https://www.ebi.ac.uk/ena/browser/view/PRJNA182210 None [Overal design]Gene expression analysis of JIMT1 breast cancer cells cultured as xenografts for 43 days, in two dimensional cultures for seven days (2D7d), in polyHEMA three dimensional cell culture models for four and seven days (PH7d and PH7d), and in Matrigel three dimensional cultures for four and seven days (MG4d and MG7d). Two biological replicates was included for each sample.; [Treatment]'For gene expression studies JIMT1 cell were grown in 6 well plates in 2D (7d), PH (4 and 7 days) or MG (4 and 7 days) models. Matrigel was dissolved prior to RNA isolation using Dispase (BD Biosciences). To obtain xenograft tumors of JIMT1 cells, the fat pads of BALB/C-nude mice were injected with 1*10-6 JIMT1 cells in 25 ml of medium and 25 ml of Matrigel. The tumors were collected 43 days after injection at 99 - 158 mm2. Tumor size was calculated from palpation results using (lenght/2 * width/2) * π. PolyHEMA plates were coated prior to use with 2.3 ml/well of PolyHEMA (poly (2-hydroxyethyl methacrylate), Polysciences Inc.), ethanol (>99 %) and sterile water in a 4:90:6 ratios. The plates were left to dry for 7 days at 37oC (or until the wells were dry).The Matrigel membrane was created by pipetting of ice-cold Matrigel dilution (1/2 Matrigel (Basement Membrane Matrix Growth Factor Reduced, BD Biosciences) and 1/2 Opti-MEM® (Life technologies)) to 6-well plates. The membrane was left to polymerize to cell culture inbubator for 20 minutes, after which the cells in cell culture medium were added on top.'; [Growth]'JIMT1 cells were cultivated in a 1:1 mixture of Ham’s F-12 + glutamax medium (Gibco Invitrogen, USA) and Dulbecco’s modified Eagles medium (DMEM, glucose 4.5 g/l; Sigma Aldrich), with 10 % FBS, 2 mM L-glutamine, 0.01 mg/ml insulin, and 1 % penicillin/streptomycin. JIMT1 (DSMZ GmbH, Germany) is a HER2+, ER-, PR-, epithelial-like cell line established from a pleural effusion of a 62-year-old female with trastuzumab-resistant ductal breast cancer (Tanner et al. 2004).'; [Extraction]'RNA isolation was done using mirVana™ (Life technologies) kit according to manufacturer’s instructions. Quality control was performed with Agilent Bioanalyser. Gene expression was analyzed using illumina HumanHT-12 v 4.0 Expression BeadChip (>47\xa0000 probes). Two biological replicates were used for each sample.'; [Cell type]'breast cancer cells''cell line: JIMT1; cell type: breast cancer cells; culture method: 2D monolayer cell culture; ', 'cell line: JIMT1; cell type: breast cancer cells; culture method: Matrigel on-top 3D culture for four days; ', 'cell line: JIMT1; cell type: breast cancer cells; culture method: Matrigel on-top 3D culture for seven days; ', 'cell line: JIMT1; cell type: breast cancer cells; culture method: polyHEMA anchorage independent 3D culture for four days; ', 'cell line: JIMT1; cell type: breast cancer cells; culture method: polyHEMA anchorage independent 3D culture for seven days; ', 'cell line: JIMT1; cell type: breast cancer cells; culture method: as xenografts in the fat pads of BALB/C-nude mice; ' GSE159448 Homo sapiens 11 Expression profiling by high throughput sequencing GPL16791 RNA-Seq analysis identifies to GATA3-AS1 as a lncRNA associated with resistance to neoadjuvant chemotherapy in locally advanced breast cancer patients 2020-10-13 Purpose: Identified the expression profile of lncRNA associated to neoadjuvant chemotherapy response in 11 tumor of locally advanced breast cancer patients Methods: We implemented the transcriptomic analysis from 11 breast cancer samples by paired-end RNA-Seq, as a case-control study (responders vs nonresponders group). Differential expression analysis for lncRNA and mRNA were made to identify lncRNA as predictive biomarkers. Results: We identified the over-expressed lncRNA GATA3-AS1 in nonresponders group. Additionally, we identified the pathways were differentially expressed lncRNA and mRNA are associated in neoadjuvant chemotherapy response. Conclusion: we propose lncRNA GATA3-AS1 as a potential predictive biomarker for patients with LABC luminal B-like subtype that will not respond to neoadjuvant chemotherapy https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE159448 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA668985 https://www.ebi.ac.uk/ena/browser/view/PRJNA668985 https://www.ncbi.nlm.nih.gov/sra?term=SRP287248 [Overal design]Transcriptomic analysis of 11 tumor samples from locally advanced breast cancer mexican patients in a case-control study (responders vs nonresponders group), in order to identify lncRNA associated to neoadjuvant chemotherapy response.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was isolated using the AllPrep kit (QIAGEN, No. 80204); RNA concentration and quality analysis (RIN value) were performed by Tape Station 2200 bioanalyzer (Agilent Technologies)\n1 ug of RNA with RIN associated greater than 8.0 were used to generate sequencing libraries using the TruSeq Stranded mRNA library prep kit from illumina according to the manufacturer’s instruction'; [Cell type]'Source: ''treatment: Neoadjuvant Chemotherapy; disease: Breast Cancer; molecular subtype: Luminal B; group: Nonresponder; ', 'treatment: Neoadjuvant Chemotherapy; disease: Breast Cancer; molecular subtype: Luminal B; group: Responder; ' GSE149720 Homo sapiens 348 Protein profiling by protein array GPL23632 17 Models: Buparlisib-treated Patient Derived Xenograft (PDX) Reversed Phase Protein Array (RPPA) Data 2020-05-01 Aberrant activation of PI3K pathway is frequently observed in triple negative breast cancer (TNBC). However single agent PI3K inhibitors have shown limited anti-tumor activity. To investigate biomarkers of response and resistance mechanisms, we tested 17 TNBC patient-derived xenograft (PDX) models representing diverse genomic backgrounds and varying degrees of PI3K pathway signaling activities for their tumor growth response to the pan-PI3K inhibitor BKM120. Baseline and post-treatment PDX tumors harvested following 3 days of BKM120 or vehicle administration were subjected to reverse phase protein array (RPPA) to identify protein markers associated with tumor growth response. While BKM120 consistently reduced PI3K pathway activity, as demonstrated by reduced levels of phosphorylated AKT, percentage tumor growth inhibition (%TGI) ranged from 35% in the least sensitive to 84% in the most sensitive PDX model at the completion of approximately 3-4 weeks of treatment. Several biomarkers showed significant association with resistance, including elevated baseline levels of growth factor receptors (EGFR, pHER3 Y1197), PI3Kp85 regulatory subunit, anti-apoptotic protein BclXL, EMT (Vimentin, MMP9, IntegrinaV), NFKB pathway (IkappaB, RANKL), and intracellular signaling molecules including Caveolin, CBP, and KLF4, as well as treatment-induced increase in the levels of phosphorylated forms of Aurora kinases. Sensitivity to BKM120 was associated with higher baseline levels of proapoptotic markers (Bak and Caspase 3) and a greater number of markers differentially changed following BKM120 therapy. Interestingly, markers indicating PI3K pathway signaling activation or PTEN loss at baseline were not significantly correlated to %TGI. These results provide important insights into biomarker development for PI3K inhibitors in TNBC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE149720 None None None None None 'protein' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA629800 https://www.ebi.ac.uk/ena/browser/view/PRJNA629800 None [Overal design]17 PDX models were analyzed under 2 treatment conditions: 50hr buparlisib treatment vs. 3 day vehicle. 3 bioreplicates and 3 technical replicates were analyzed when possible.; [Treatment]'None'; [Growth]'None'; [Extraction]'Protein lysates were prepared with modified tissue protein extraction reagent (TPER; Pierce) and a cocktail of protease and phosphatase inhibitors (Roche Life Science).'; [Cell type]'Source: ''tissue: pulverized tumor tissue from human:mouse xenograft; ' GSE112855 Homo sapiens 45 Expression profiling by high throughput sequencing GPL18573 Next generation sequencing profiling experimental circulating tumor cells-derived metastatic variants [RNA-seq] 2018-04-09 Hematogenous metastasis is initiated by a subset of circulating tumor cells (CTCs) shed from primary or metastatic tumors into the blood circulation. Thus, CTCs provide a unique patient biopsy resource to decipher the cellular subpopulations that initiate metastasis and their molecular properties. However, one crucial question is whether CTCs derived from patients recapitulate human metastatic disease in an animal model. Here, we show that CTC lines established from breast cancer patients are capable of generating metastases in mice with a pattern recapitulating most major organs from corresponding patients. Genome-wide sequencing analyses of metastatic variants identified novel organ tropism-associated markers identified from CTCs and facilitate the development of potential therapies targeting metastatis initiating cells in circulation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112855 Circulating Tumor Cells Exhibit Metastatic Tropism and Reveal Brain Metastasis Drivers. Cancer discovery 26.370 https://doi.org/10.1158/2159-8290.CD-19-0384 {Cancer discovery (26.370): 10.1158/2159-8290.CD-19-0384} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA449340 https://www.ebi.ac.uk/ena/browser/view/PRJNA449340 https://www.ncbi.nlm.nih.gov/sra?term=SRP139040 [Overal design]Profiling of 4 breast cancer CTC lines (4-5 replicates each) and -derived metastatic variants from brains (8 samples), bones (7 samples), lungs (5 samples), ovaries (5 samples) and kidney (1 sample); [Treatment]'None'; [Growth]'CTC lines were cultured in ultra-low attachment plates with RPMI 1640 medium, supplemented with EGF (20ng/ml), bFGF (20ng/ml), 1X B27 and 1X antibiotic/antimycotic, in 4% O2 and 5% CO2. Metastatic tumors were established by inoculation of 100,000 GFP-LUC labeled CTCs in 100 µl of PBS into the left cardiac ventricles of 6-8 weeks old female NSG mice supplemented with subcutaneous slow release estrogen pills. Metastatic lesions were further dissociated into single-cell suspension by automated dissociation. CTC-derived metastatic cells (GFP+ cells) were sorted for RNA sequencing.'; [Extraction]'Sorted cells were collected into a pre-chilled tube maintained at 4°C containing PBS with 1% BSA. RNA was collected from 50,000 sorted cells, according to the manufacturer’s instructions (Quick RNA, Zymo). RNA integrity was measured using Bioanalyzer (Agilent).'; [Cell type]'Source: ''cell line: Brx07; parental or metastasis?: parental CTC; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: NA; generation: NA; ', 'cell line: Brx07; parental or metastasis?: parental CTC undergone dissociation protocol; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: lung_dissociation; generation: NA; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: Kidney; grown_in_culture: yes; dissociation_protocol: lung_dissociation; generation: 1; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: lung; grown_in_culture: no; dissociation_protocol: lung_dissociation; generation: 2; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: lung; grown_in_culture: yes; dissociation_protocol: lung_dissociation; generation: 2; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: lung; grown_in_culture: yes; dissociation_protocol: lung_dissociation; generation: 1; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: lung; grown_in_culture: no; dissociation_protocol: lung_dissociation; generation: 1; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: ovary; grown_in_culture: yes; dissociation_protocol: lung_dissociation; generation: 1; ', 'cell line: Brx07; parental or metastasis?: metastatic sample; metastatic site: ovary; grown_in_culture: no; dissociation_protocol: lung_dissociation; generation: 2; ', 'cell line: Brx42; parental or metastasis?: metastatic sample; metastatic site: brain; grown_in_culture: no; dissociation_protocol: brain_dissociation; generation: 1; ', 'cell line: Brx42; parental or metastasis?: parental CTC; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: NA; generation: NA; ', 'cell line: Brx42; parental or metastasis?: parental CTC undergone dissociation protocol; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: brain_dissociation; generation: NA; ', 'cell line: Brx42; parental or metastasis?: metastatic sample; metastatic site: ovary; grown_in_culture: no; dissociation_protocol: lung_dissociation; generation: 1; ', 'cell line: Brx50; parental or metastasis?: metastatic sample; metastatic site: bone; grown_in_culture: no; dissociation_protocol: bone_dissociation; generation: 2; ', 'cell line: Brx50; parental or metastasis?: metastatic sample; metastatic site: brain; grown_in_culture: no; dissociation_protocol: brain_dissociation; generation: 3; ', 'cell line: Brx50; parental or metastasis?: metastatic sample; metastatic site: brain; grown_in_culture: yes; dissociation_protocol: brain_dissociation; generation: 3; ', 'cell line: Brx50; parental or metastasis?: metastatic sample; metastatic site: brain; grown_in_culture: no; dissociation_protocol: brain_dissociation; generation: 2; ', 'cell line: Brx50; parental or metastasis?: parental CTC; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: NA; generation: NA; ', 'cell line: Brx50; parental or metastasis?: parental CTC undergone dissociation protocol; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: brain_dissociation; generation: NA; ', 'cell line: Brx68; parental or metastasis?: metastatic sample; metastatic site: bone; grown_in_culture: yes; dissociation_protocol: bone_dissociation; generation: 1; ', 'cell line: Brx68; parental or metastasis?: metastatic sample; metastatic site: bone; grown_in_culture: no; dissociation_protocol: bone_dissociation; generation: 1; ', 'cell line: Brx68; parental or metastasis?: metastatic sample; metastatic site: bone; grown_in_culture: no; dissociation_protocol: bone_dissociation; generation: 2; ', 'cell line: Brx68; parental or metastasis?: metastatic sample; metastatic site: brain; grown_in_culture: yes; dissociation_protocol: brain_dissociation; generation: 1; ', 'cell line: Brx68; parental or metastasis?: parental CTC; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: NA; generation: NA; ', 'cell line: Brx68; parental or metastasis?: parental CTC undergone dissociation protocol; metastatic site: n/a; grown_in_culture: yes; dissociation_protocol: bone_dissociation; generation: NA; ', 'cell line: Brx68; parental or metastasis?: metastatic sample; metastatic site: lung; grown_in_culture: yes; dissociation_protocol: lung_dissociation; generation: 1; ' GSE43216 Mus musculus 17 Expression profiling by array GPL6246; GPL8321 Sustained expression of cyclin D1 or cyclin D1/KE in mouse mammary gland 2012-12-31 Analysis of mammary glands from tet-inducible(rtTA) transgenic mice expressing cyclin D1 using Affymetrix Mouse Gene 1.0 ST GeneChip arrays. MMTV-rtTA transgenic mice (MMTV-Mouse Mammary Tumor Virus promoter) were cross-mated to cyclin D1 transgenic mice under control of tet operon. 8-week-old tetracycline-inducible cyclin D1/rtTA bi-transgenic pregnant female mice (12 days postcoitus) were treated with doxycycline through drinking water supplementation at a final concentration of 2 mg/ml. Control mice were rtTA transgenics alone and treated in the same manner. After 7 days of doxycycline treatment, the mice were sacrificed and mammary glands taken for RNA isolation. Results provide insight into the in vivo gene expression pattern regulated by cyclin D1 through acute induction. Analysis of mammary glands from MMTV-cyclin D1/WT and MMTV-cyclin D1/KE using Affymetrix Mouse 430A v2.0 GeneChip arrays. Cyclin D1 point mutant, cyclin D1/KE K112E (K112E) contains a lysine to glutamine substitution at amino acid position 112. cyclin D1. The cyclin D1/KE mutant fails to induce cyclin D1-dependent kinase activity. Female MFD1, MFD1-KE, and WT mice were monitored twice weekly, up to 760 days, for the development of palpable tumors. Those developing palpable tumors were sacrificed within a week of tumor detection. Tumors were dissected and portions snap frozen for RNA isolation. Results provide insight into the in vivo gene expression pattern regulated by cyclin D1 that is kinase independent. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43216 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA184999 https://www.ebi.ac.uk/ena/browser/view/PRJNA184999 None [Overal design]Two separate control mice were positive for MMTV-rtTA transgene compared to 3 separate cyclin D1/rtTA bitransgenic female mice and 3 separate cyclin D1 KE mutant/rtTA bitransgenic female mice (Mouse Gene 1.0 ST arrays). Three separate control WT FvBmice were compared to three MMTV-cyclin D1/WT and 3 MMTV-cyclin D1/KE mice (Mouse 430A v2.0 arrays).; [Treatment]'rtTA/CCND1 KE mutant samples underwent 7 days of doxycycline treatment'; [Growth]'No specific growth protocol'; [Extraction]"Total RNA extracted using Trizol reagent (Invitrogen) as per manufacturers' guidelines."; [Cell type]'Source: ''strain: FvB/N; tissue: mammary gland; transgenic mouse: rtTA; ', 'strain: FvB/N; tissue: mammary gland; transgenic mouse: rtTA/CCND1; ', 'strain: FvB/N; tissue: mammary gland; transgenic mouse: rtTA/CCND1 KE mutant; ', 'strain: FvB/N; tissue: Mammary Tumor; transgenic mouse: MMTV-CCND/WT; ', 'strain: FvB/N; tissue: Mammary Tumor; transgenic mouse: MMTV-CCND/KE; ', 'strain: FvB; tissue: Mammary gland; transgenic mouse: WT; ' GSE105020 Homo sapiens 4 Expression profiling by array GPL18451 Expression analysis of breast cancer cell lines SKBR-3 and ZR-75-1 upon treatment of LMO2 overexpression or knocking-down 2017-10-16 Investigation of whole genome gene expression level changes in ZR-75-1 cells with knocking-down of LMO2, and in SKBR-3 cells with overexpression of LMO2, compared to their relative control cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE105020 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA414433 https://www.ebi.ac.uk/ena/browser/view/PRJNA414433 None [Overal design]A total of 4 microarray assays were performed with total RNA from ZR-75-1_ctrl, ZR-75-1_sh-LMO2, SKBR-3_LMO2 and SKBR-3_ctrl cells. Samples were compared between each treatment and control in each cell lines.; [Treatment]'Cells were infected by packaged LMO2 overexpression, control or LMO2-shRNA lentivirus for 24 hrs. Stable cell strains were selected in medium supplemented with 2 μg/mL puromycin three days after lentiviral infection and maintained in medium supplemented with 1 μg/mL puromycin till harvested.'; [Growth]'Cells were regularly cultured in RPMI 1640 medium supplied with 10% FBS.'; [Extraction]'total RNA extraction with Trizol reagent (Invitrogen, Austin, TX, USA)'; [Cell type]'breast cancer cell line''cell type: breast cancer cell line; ' GSE165898 Homo sapiens 6 Expression profiling by high throughput sequencing GPL28337 IL13Rα2 promotes the proliferative switch required for outgrowth of breast cancer brain metastases 2021-02-01 The survival of women with brain metastases (BM) from breast cancer remains very poor, and more than 80% will die within a year of their diagnosis. Here we define the function of IL13Rα2 in outgrowth of breast cancer brain metastases (BCBM) in vitro and in vivo, and postulate IL13Rα2 as a suitable therapeutic target for BM. Experimental design: We performed IHC staining of IL13Rα2 in BCBM to define its prognostic value. Using inducible-shRNAs in TNBC and HER2+ breast-brain metastatic models we assessed IL13Rα2 function in vitro and in vivo. We performed RNAseq and functional studies to define the molecular mechanisms underlying IL13Rα2 function in BCBM. Results: High IL13Rα2 expression in BCBM predicted worse survival after BM diagnoses. IL13Rα2 was essential for cancer-cell survival, promoting proliferation while repressing invasion. IL13Rα2 KD resulted in repression of cell cycle and proliferation mediator Cyclin D2 and upregulation of Ephrin B1 signaling. Ephrin-B1 (i) promoted invasion of BC cells in vitro, (ii) marked micrometastasis and invasive fronts in BCBM, (iii) predicted shorter disease-free survival (DFS) and BM-free survival (BMFS) in breast primary tumors known to metastasize to the brain. In experimental metastases models, which bypass early tumor invasion, downregulation of IL13Rα2 prior or after tumor seeding and brain intravasation decreased BMs, suggesting that IL13Rα2 and a switch to a more proliferative phenotype is critical to BM outgrowth. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE165898 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA698556 https://www.ebi.ac.uk/ena/browser/view/PRJNA698556 https://www.ncbi.nlm.nih.gov/sra?term=SRP304115 [Overal design]RNA-seq profiling of 231BR treated with either shEV or shIL13RA2.; [Treatment]'Cells were induced for shRNA expression for 96 hr with 1ug/ml doxy'; [Growth]'231BR cells expressing shEV or shRNA-8523 (0.5 million) were plated in triplicate in 10 cm plates in DMEM 10% FBS'; [Extraction]'Cells were collected in 1ml Trizol and isolated total RNA was further purified with RNeasy MinElute Cleanup Kit (Qiagen).\nlibrary was constructed by BGI Global genomic services'; [Cell type]'MDA-MB-231 derived''trophism: Brain trophic; cell type: MDA-MB-231 derived; tissue: mammary gland/breast; derived from metastatic site; treatment: Expressing empty vector; ', 'trophism: Brain trophic; cell type: MDA-MB-231 derived; tissue: mammary gland/breast; derived from metastatic site; treatment: Expressing shRNA targeting IL13Ralpha2; ' GSE77661 Homo sapiens 26 Expression profiling by high throughput sequencing; Other GPL11154 RNA Sequencing Facilitates Quantitative Analysis of Transcriptomes in Human Normal and Cancerous Tissues 2016-02-08 Circular RNAs (circRNAs) represent a novel class of widespread and diverse endogenous RNAs that may regulate gene expression in eukaryotes. However, the regulation and function of human circRNAs remain largely unknown. Here we generate ribosomal-depleted RNA sequencing data from six normal tissues and seven cancers, and detect at least 27,000 circRNA candidates. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE77661 Circular RNA profiling reveals an abundant circHIPK3 that regulates cell growth by sponging multiple miRNAs. Nature communications 11.878 https://doi.org/10.1038/ncomms11215 {Nature communications (11.878): 10.1038/ncomms11215} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA311161 https://www.ebi.ac.uk/ena/browser/view/PRJNA311161 https://www.ncbi.nlm.nih.gov/sra?term=SRP069760 [Overal design]RNA profiles of six normal tissues and seven cancers were generated by deep sequencing, using Illumina HiSeq 2000.; [Treatment]'None'; [Growth]'None'; [Extraction]'Tissues were removed, flash frozen on liquid nitrogen, and RNA was harvested using Trizol reagent. NEBNext® Ultra™ Directional RNA Library Prep Kit for Illumina (Cat#E7420L) was used with 3 ug of total RNA for the construction of sequencing libraries.\nStrand-specific RNA-seq libraries were prepared using the NEBNext® Ultra™ Directional RNA Library Prep Kit for Illumina (Cat#E7420L) following the manufacturer’s instructions.'; [Cell type]'Source: ''tissue: Brain; ', 'tissue: Colon; ', 'tissue: Heart; ', 'tissue: Liver; ', 'tissue: Lung; ', 'tissue: Stomach; ', 'tissue: Normal tissue adjacent to bladder urothelial carcinoma; ', 'tissue: Normal tissue adjacent to breast cancer; ', 'tissue: Normal tissue adjacent to colorectal cancer; ', 'tissue: Normal tissue adjacent to gastric cancer; ', 'tissue: Normal tissue adjacent to hepatocellular carcinoma; ', 'tissue: Normal tissue adjacent to clear cell carcinoma; ', 'tissue: Normal tissue adjacent to prostate cancer; ', 'tissue: Bladder urothelial carcinoma; ', 'tissue: Breast cancer; ', 'tissue: Colorectal cancer; ', 'tissue: Gastric cancer; ', 'tissue: Hepatocellular carcinoma; ', 'tissue: Clear cell carcinoma; ', 'tissue: Prostate cancer; ' GSE16441 Homo sapiens 68 Expression profiling by array; Non-coding RNA profiling by array GPL6480; GPL8659 Identifying mRNA targets of microRNA in clear cell renal cell carcinoma 2009-06-04 A bioinformatic approach to identify targets of microRNA in cancer. Keywords: Patient sample study https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE16441 Identification of biological targets of therapeutic intervention for clear cell renal cell carcinoma based on bioinformatics approach. Cancer cell international 3.439 https://doi.org/10.1186/s12935-016-0291-8 {BMC systems biology (2.048) doi:10.1186/1752-0509-4-51}; {Cancer cell international (3.439) doi:10.1186/s12935-016-0291-8}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA116271 https://www.ebi.ac.uk/ena/browser/view/PRJNA116271 None [Overal design]Samples GSM413237-GSM413270: Total RNA from 17 RCC tumors and 17 corresponding non-tumor samples was hybridized against a common reference RNA (Perou CM, Sorlie T, Eisen MB, et al. Molecular portraits of human breast tumours. Nature 2000;406:747-752) for gene expression analysis. Samples GSM413271-GSM413304: MicroRNA from 17 RCC tumors and 17 corresponding non-tumor samples were hybridized on a single channel platform for miRNA expression analysis.; [Treatment]'None'; [Growth]'None'; [Extraction]"Frozen RCCs were obtained through University of North Carolina - Chapel Hill's Tissue Procurement Facility. H&E was performed on tumor tissue samples to confirm clear cell or normal histopathology.\nRNA was extracted with Qiagen RNeasy kit.\nRNA quality was determined using an Agilent LabChip Bioanalyzer.", "Frozen RCCs were obtained through University of North Carolina - Chapel Hill's Tissue Procurement Facility. H&E was performed on tumor tissue samples to confirm clear cell or normal histopathology.\nTotal RNA was extracting with Qiagen miRNeasy kit.\nRNA quality was determined using an Agilent LabChip Bioanalyzer."; [Cell type]'Source: ''identifier: 3; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'biosourcetype: Cancer cell lines; cell line: various cancer cell lines (reference); ', 'identifier: 6; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: 21; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: 25; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: 27; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: A11; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: A13; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: A16; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: A18; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: A27; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: A30; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: A31; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: A4; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: A5; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: C1; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: C13; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: C5; tissue: kidney; histology: Clear Cell; disease state: Clear Cell Carcinoma; biosourcetype: Frozen Sample; ', 'identifier: 3; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: 6; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: 21; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: 25; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: 27; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: A11; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: A13; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: A16; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: A18; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: A27; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: A30; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: A31; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: A4; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: A5; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: C1; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: C13; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ', 'identifier: C5; tissue: kidney; histology: Normal; disease state: Normal; biosourcetype: Frozen Sample; ' GSE18070 Homo sapiens 9 Expression profiling by array GPL570 Smad signaling is required for maintenance of epigenetic gene silencing during breast cancer progression 2009-09-11 In this study, we took advantage of a previously established breast cancer progression cell line model system, which consists of a parental MCF10A (MI) spontaneously immortalized mammary epithelial cell line and two of its derivatives: 1) MCF10ATk.cl2 (MII), a MCF10A H-Ras transformed cell line and 3) MCF10CA1h (MIII), derived from a xenograft of the MII cells in nude mice that progressed to carcinoma (1, 2). These cell lines were previously reported to exhibit distinct tumorigenic properties when re-implanted in nude mice; MI is non-tumorigenic, MII forms benign hyperplastic lesions and MIII forms low-grade, well differentiated carcinomas (2, 3). The advantage of this system is that these cell lines were derived from a common genetic background (MCF10A) and accumulated distinct genetic/epigenetic alterations in vivo enabling them to acquire a range of non-tumorigenic to carcinogenic properties. Our initial studies showed that MIII cells, but not MI or MII, exhibit an EMT phenotype, promoter DNA hypermethylation of epithelial genes and highly invasive properties in vitro. To investigate the role of TGFβ pathway in these processes, we disrupted the TGFβ downstream signaling events in MIII, by stably overexpressing the inhibitory Smad7, and analyzed the gene expression profiles of MII, MIII and MIIISmad7 cells using microarray analysis. Total RNA was isolated from three biological replicates corresponding to MIIpB, MIIIpB and MIIIpB-Smad7 cells using Trizol (Invitrogen) according to the manufacturer’s protocol, and the RNeasy mini-kit (Qiagen) was used to clean-up the RNA. Labeled cRNA fragments derived from the samples were hybridized onto human genome U133 plus 2.0 arrays (Affymetrix). Gene-expression estimates and a measure of sequence-specificity of the hybridization intensities were both determined using standard settings in MAS5 (Affymetrix). Probesets that did not exhibit sequence-specific hybridization in any sample were excluded from subsequent analysis. Differential expression between MIIpB and MIIIpB as well as between MIIIpB and MIIIpBSmad7 was assessed using Student’s t-test. Genes with a false discovery rate (FDR) < 0.05 and a greater than 2-fold difference in expression between the two cell lines were considered to be differentially expressed. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE18070 Smad signaling is required to maintain epigenetic silencing during breast cancer progression. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-09-1872 {Cancer research (8.378): 10.1158/0008-5472.CAN-09-1872} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA119337 https://www.ebi.ac.uk/ena/browser/view/PRJNA119337 None [Overal design]expression profiles of MII, MIII and MIIISmad7 cells; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was isolated from three biological replicates corresponding to MIIpB, MIIIpB and MIIIpB-Smad7 cells using Trizol (Invitrogen) according to the manufacturer’s protocol, and the RNeasy mini-kit (Qiagen) was used to clean-up the RNA'; [Cell type]'Source: ''cell line: MCF10A H-Ras transformed cell line; ', 'cell line: cell line derived from a xenograft of the MII cells in nude mice that progressed to carcinoma; ', 'cell line: MIII overexpressing the inhibitory Smad7; ', 'cell line: MIII overexpressing the inhibitory Smad8; ', 'cell line: MIII overexpressing the inhibitory Smad9; ' GSE77200 Homo sapiens 6 Expression profiling by array GPL15207 Expression data in MDA-MB-231 breast cancer cell lines with Histone deacetylase SAHA treatment 2016-01-25 Analysis of gene expression change after 8hr's treatment with 5μM SAHA, which is a histone deacetylase inhibitor, in MDA-MB-231 cell lines. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE77200 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA309697 https://www.ebi.ac.uk/ena/browser/view/PRJNA309697 None [Overal design]two sample, one is control, one is SAHA treatment. Each sample is triplicated.; [Treatment]"8hr's treatment with 5μM SAHA or DMSO"; [Growth]'DMEM/F12 medium with 10%FBS'; [Extraction]"Total RNA was extracted using TRIZOL Reagent (Cat#15596-18Life technologies,Carlsbad, CA, US)following the manufacturer's instructions and checked for a RIN number to inspect RNA integrity by an Agilent Bioanalyzer 2100 (Agilent technologies, Santa Clara, CA, US).Qualified total RNA was further purified by RNeasy micro kit (Cat#74004, QIAGEN, GmBH, Germany) and RNase-Free DNase Set (Cat#79254, QIAGEN, GmBH, Germany)."; [Cell type]'Source: ''cell line: MDA-MB-231; ' GSE28583 Homo sapiens 20 Expression profiling by array GPL570 Differentially expressed genes after treatment with chemotherapy in breast cancer and their correlation with pathologic mid-response (Miller & Payne grade 3) 2011-04-13 The aim of this study was to compare the gene expression profile changes breast tumors after the treatment with Anthracyclines and Taxanes. To this end, an oligonucleotide microarray was performed (Affymetrix’s HG-U133 Plus 2.0 array). This gene expression study was carried out on the biopsied tumor samples previous being treated with chemotherapy, and subsequently compared with themselves once treatment schedule ended. The post-chemotherapy biopsy was obtained from the surgical piece. The goal of this study was the finding of several genes related to apoptosis, proliferation, differentiation, survival and transformation-related genes and correlating their differences in expression with the degree of response to chemotherapy, determined by the Miller and Payne histological grading system. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28583 Transcriptional shift identifies a set of genes driving breast cancer chemoresistance. PloS one 2.776 https://doi.org/10.1371/journal.pone.0053983 {PloS one (2.776): 10.1371/journal.pone.0053983} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA153935 https://www.ebi.ac.uk/ena/browser/view/PRJNA153935 None [Overal design]After informed consent, patients with a histologically confirmed diagnosis of breast cancer and scheduled chemotherapy treatment based on Anthracyclines and Taxanes (Treatment A: Epirubicin 90 mg/m2-Cyclophosphamide 600 mg/m2, 3 cycles bi-weekly and Paclitaxel 150 mg/m2-Gemcitabine 2500 mg/m2, 6 cycles bi-weekly ± weekly Herceptin 4 mg/Kg during the first week, 2 mg/Kg for the remaining 11 cycles; Treatment B: Doxorubicin 60 mg/m2-Pemetrexed 500 mg/m2, 4 cycles tri-weekly and Docetaxel 100 mg/m2, 4 cycles tri-weekly; Treatment C: Doxorubicin 60 mg/m2-Cyclophosphamide 600 mg/m2, 4 cycles tri-weekly and Docetaxel 100 mg/m2, 4 cycles tri-weekly ) were recruited for this study. Pre-chemotherapy and post-chemotherapy biopsies were examined by a pathologist who determined the Miller & Payne grade for each patient. Matching pairs of pre-chemotherapy and post-chemotherpy samples were divided into 3 groups according to Miller & Payne grade: group of bad response (Miller & Payne grades 1 and 2), group of mid response (Miller & Payne grade 3) and group of good response (Miller & Payne grades 4 and 5). Gene expression analysis was performed in paired samples as follows: mid response group post-chemotherapy biopsy vs pre-chemotherapy biopsy (Mid final vs initial). For this assay were necessary 20 samples being chosen according to histopathologic criteria (Miller & Payne grade 3). Other comparisons in which this group of samples was involved include: Initial Good vs Mid, Initial Bad vs Mid, Final Bad vs Mid and Final Good vs Mid. This gene expression profiling was carried out making use of Affymetrix’s GeneChip technology, with the Affymetrix’s HG-U133 Plus 2.0 array from this provider. All the protocols and apparatus were recommended by Affymetrix. Total RNA from frozen mammary tumors was directly extracted by a RNeasy Mini kit and homogenized by QIAshredder columns under manufacturer’s instructions. The quality and quantity of the obtained RNA, was checked out through agarose electrophoresis and later spectrophotometry at 260/280 nm. Biotinylated cRNA was synthesized following the IVT labeling kit from Affymetrix and purified by the GeneChip Sample Cleanup Module from Affymetrix. Once again, the quality and quantity of the obtained cRNA, was checked out through agarose electrophoresis and posterior spectrophotometry at 260/280 nm. After hybridization, slides were washed and scanned following the manufacturer’s standard protocol. Intensity values were normalized by Robust Multichip Average method and subsequently these were filtered for remove the control sequences and those with a hybridization signal near to background. The spike controls were: BioB, BioC, BioD and Cre; because BioB was the less presented in the samples, it was used to estimate the sensitivity of the experiment. The housekeeping control was GAPDH. After non-supervised PCA analysis and clustering, gene expression statistical significances were identified by two regression models taking into account the pathologic response to chemotherapy and if the sample was obtained before or after chemotherapy treatment. Supervised PCA analysis and clustering were performed with processed data. Partek Genomics Suite v7.3.1 (Partek) software was employed for the statistic analysis and clustering.; [Treatment]'RNA processing: snap frozen in liquid nitrogen and preserved at -80ºC. Before RNA extraction protocol, samples were sectioned in a cryostat to evalute the celularity', 'RNA processing: snap frozen in liquid nitrogen and preserved at -80ºC. Before RNA extraction protocol, samples were sectioned in a cryostat to evalute the celularity.'; [Growth]'None'; [Extraction]'Total RNA was extracted using using an RNeasy minikit from Qiagen. Quality and quantity was assessed by agarose electrophoresis and spectrophotometric analysis (Absorbance 260/280 nm)'; [Cell type]'Source: ''age: 39; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE128; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 70; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE134; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 58; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE140; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 69; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE152; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 42; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE158; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 55; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE170; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 48; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE172; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 58; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE178; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 53; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE188; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 53; gender: female; tissue: breast tumor; trucut biopsy: 3.5 cm x 1.75 mm; tumor biopsy acquisition: Such biopsy was taken at diagnosis; treatment: none (Prechemotherapy); sample_id: 08SE275; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 39; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: C; sample_id: 08SE129; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 70; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE135; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 58; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE141; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 69; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: C; sample_id: 08SE153; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 42; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: C; sample_id: 08SE159; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 55; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE171; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 48; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: B; sample_id: 08SE173; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 58; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: C; sample_id: 08SE179; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 53; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE189; pathologic response to chemotherapy (miller & payne grade): 3; ', 'age: 53; gender: female; tissue: breast tumor; tumor biopsy acquisition: Such biopsy was taken from surgery specimen and selected by the pathologist in charge within 30 min. after tumor removal; treatment: A; sample_id: 08SE276+08SE277; pathologic response to chemotherapy (miller & payne grade): 3; ' GSE30805 Mus musculus 17 Expression profiling by array GPL8321 Expression data from low expressing T58A Mutant Myc Induced Tumors 2011-07-20 We used microarrays to futher characterize the effects of T58A mutation in Myc on mammary tumorigenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE30805 A mouse model with T58A mutations in Myc reduces the dependence on KRas mutations and has similarities to claudin-low human breast cancer. Oncogene 6.634 https://doi.org/10.1038/onc.2012.142 {Oncogene (6.634): 10.1038/onc.2012.142} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA144205 https://www.ebi.ac.uk/ena/browser/view/PRJNA144205 None [Overal design]17 MMTV-Myc T58A mammary tumors were used for RNA extraction and hybridization on Affymetrix microarrays.; [Treatment]'NA'; [Growth]'Animal use and husbandry was in accordance with institutional and federal guidelines.'; [Extraction]'Total RNA from mouse mammary tumors was extracted using the Qiagen RNeasy Midi kit.'; [Cell type]'Source: ''strain: FVB; tissue type: Mammary Tumor; histology: T58A Low Expressing, Squamous; ', 'strain: FVB; tissue type: Mammary Tumor; histology: T58A Low Expressing, EMT; ', 'strain: FVB; tissue type: Mammary Tumor; histology: T58A Low Expressing, Papillary; ', 'strain: FVB; tissue type: Mammary Tumor; histology: T58A Low Expressing, Microacinar; ' GSE74391 Homo sapiens 26 Expression profiling by array GPL570 High CDK6 protects cells from fulvestrant-mediated apoptosis and is a predictor of resistance to fulvestrant in estrogen receptor-positive metastatic breast cancer 2015-10-27 Purpose: Resistance to endocrine therapy in estrogen receptor-positive (ER+) breast cancer remains a major clinical problem. Recently, the CDK4/6 inhibitor palbociclib combined with letrozole was approved for treatment of ER+ advanced breast cancer, and other CDK4/6 inhibitors are being investigated in combination with different endocrine treatments. However, the role of CDK4/6 in endocrine resistance and their potential as predictive biomarkers of endocrine treatment response remains undefined. Experimental Design: We investigated the specific role of increased CDK6 expression in fulvestrant-resistant cells by gene knockdown and treatment with palbociclib, and evaluated the effect in cell proliferation, apoptosis and kinase activity. Furthermore, we evaluated CDK6 expression in metastatic samples from breast cancer patients treated or not with fulvestrant. Results: We found increased expression of CDK6 in two fulvestrant-resistant cell models vs. sensitive cells. Reduction of CDK6 expression impaired fulvestrant-resistant cell growth and induced apoptosis by reducing p70 ribosomal S6 kinase 2 activity. Treatment with palbociclib re-sensitized fulvestrant-resistant cells to fulvestrant through alteration of retinoblastoma phosphorylation. High CDK6 levels in metastatic samples from breast cancer patients treated with fulvestrant (N=45) correlated significantly with shorter progression-free survival (PFS) (p=0.0006), while no association was observed in patients receiving other endocrine treatments (N=41, p=0.874). Conclusions: Our results indicate that upregulation of CDK6 may be an important mechanism in overcoming fulvestrant-mediated growth inhibition in breast cancer cells. Patients with advanced ER+ breast cancer exhibiting high CDK6 expression in the metastatic lesions show shorter PFS upon fulvestrant treatment and thus may benefit from the addition of CDK4/6 inhibitors in their therapeutic regimens. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74391 High CDK6 Protects Cells from Fulvestrant-Mediated Apoptosis and is a Predictor of Resistance to Fulvestrant in Estrogen Receptor-Positive Metastatic Breast Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-15-1984 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-15-1984} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA300266 https://www.ebi.ac.uk/ena/browser/view/PRJNA300266 None [Overal design]The array included 20 fulvestrant resistant MCF7 cell lines named as ICI182 and ICI164 and 6 fulvestrant sensitive MCF7/S0.5. Ten biological replicates of each of ICI182 and ICI164 as well as 6biological replicates of parental fulvestrant sensitive cell lines were used in the study.; [Treatment]'FulvR cells were treated with 10^-7M fulvestrant prior to RNA extraction'; [Growth]'The human breast cancer cell line MCF-7 was originally obtained from The Breast Cancer Task Force Cell Culture Bank, Mason Research Institute (Edinburgh, UK). The MCF-7 cells were gradually adapted to grow in low serum concentration and the fulvestrant-sensitive subline MCF-7/S0.5 was used to establish the four fulvestrant resistant cell lines: MCF-7/ICI164R1 (ICI164R6), MCF-7/ICI182R1 (ICI182R1) and MCF-7/ICI182R6 (ICI182R6) and MCF- by long-term treatment with 10-7Mfulvestrant. Cells were kept within 10 passages throughout the experiments to reduce variability between experimental results.'; [Extraction]'Total RNA was extracted by lysing cells in Trizol and total RNA was precipitated using 75% ethanol.'; [Cell type]'ER+ breast cancer cell line''cell line source: MCF7; cell subline: MCF-7/ICI164R4; cell type: ER+ breast cancer cell line; subline cell type: fulvestrant resistant; ', 'cell line source: MCF7; cell subline: MCF-7/ICI164R1; cell type: ER+ breast cancer cell line; subline cell type: fulvestrant resistant; ', 'cell line source: MCF7; cell subline: MCF-7/ICI182R1; cell type: ER+ breast cancer cell line; subline cell type: fulvestrant resistant; ', 'cell line source: MCF7; cell subline: MCF-7/ICI182R6; cell type: ER+ breast cancer cell line; subline cell type: fulvestrant resistant; ', 'cell line source: MCF7; cell subline: MCF-7/S0.5; cell type: ER+ breast cancer cell line; subline cell type: fulvestrant sensitive; ' GSE64716 Homo sapiens 4 Expression profiling by array GPL10558 Effect of MEL-18 knockdown on estrogen-sensitive MCF7 breast cancer cells 2015-01-07 Gene expression analysis of MEL-18-silenced MCF7 cell lines. MEL-18 is a component of the polycomb repressive complex (PRC)-1, which is a critical epigenetic modulator of stem cell regulation and normal and cancerous development. Accumulating studies have suggested that MEL-18 might act as a tumor suppressor in several human tumors, including breast cancer. Results provide insight into the functional role of MEL-18 in estrogen-dependent breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64716 MEL-18 loss mediates estrogen receptor-α downregulation and hormone independence. The Journal of clinical investigation 12.282 https://doi.org/10.1172/JCI73743 {The Journal of clinical investigation (12.282): 10.1172/JCI73743} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA271730 https://www.ebi.ac.uk/ena/browser/view/PRJNA271730 None [Overal design]MCF7 cells stably infected with lentiviruses encoding either control (shCon) or MEL-18 shRNA (shMEL) were cultured in phenol-red free DMEM supplemented with 10% FBS for 48 h. Total RNA was isolated from the cultures using Trizol reagent. For each of the 2 conditions, 2 biological replicates were included. In total, 4 microarray samples were analyzed; 2 controls and 2 shRNA MEL-18 knockdowns. All labeling, hybridization and scanning steps were performed according to the manufacturers’ instructions.; [Treatment]'MCF7 cells were infected with lentiviruses encoding either control or MEL-18 shRNA'; [Growth]'Cells were cultured in phenol-red free DMEM supplemented with 10% FBS'; [Extraction]"RNA was extracted with Trizol reagent following the manufacturer's instructions. Quality control was peformed with Agilent Bioanalyzer."; [Cell type]'Source: ''cell line: MCF7; treatment: control shRNA; ', 'cell line: MCF7; treatment: MEL-18 shRNA; ' GSE7904 Homo sapiens 62 Expression profiling by array GPL570 Expression data from human breast tissue 2007-05-25 bulk breast tumor RNA from patient Abstract: Sporadic basal-like cancers (BLC) are a distinct class of human breast cancers that are phenotypically similar to BRCA1-associated cancers. Like BRCA1-deficient tumors, most BLC lack markers of a normal inactive X chromosome (Xi). Duplication of the active X chromosome and loss of Xi characterized almost half of BLC cases tested. Others contained biparental but nonheterochromatinized X chromosomes or gains of X chromosomal DNA. These abnormalities did not lead to a global increase in X chromosome transcription but were associated with overexpression of a small subset of X chromosomal genes. Other, equally aneuploid, but non-BLC rarely displayed these X chromosome abnormalities. These results suggest that X chromosome abnormalities contribute to the pathogenesis of BLC, both inherited and sporadic. total 62 sample incudes 43 tumor, 7 normal breast and 12 normal organelle Keywords: disease state analysis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7904 X chromosomal abnormalities in basal-like human breast cancer. Cancer cell 23.916 https://doi.org/10.1016/j.ccr.2006.01.013 {Cancer cell (23.916): 10.1016/j.ccr.2006.01.013} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA100077 https://www.ebi.ac.uk/ena/browser/view/PRJNA100077 None [Overal design]compare expression of tumor to normal breast tissue; [Treatment]'RNA extration, cRNA synthesis and hyb performed according to J. Clin. Invest. 110(2002), pp. 633-641 and Cancer Res. 64 (2004), pp. 64-72'; [Growth]'RNA extration, cRNA synthesis and hyb performed according to J. Clin. Invest. 110(2002), pp. 633-641 and Cancer Res. 64 (2004), pp. 64-71'; [Extraction]'RNA extration, cRNA synthesis and hyb performed according to J. Clin. Invest. 110(2002), pp. 633-641 and Cancer Res. 64 (2004), pp. 64-73'; [Cell type]'Source: ''' GSE28330 Homo sapiens 107 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL13270; GPL13362 Telomeric Allelic Imbalance Indicates Defective DNA Repair and Sensitivity to DNA-Damaging Agents 2011-04-01 DNA repair competency is one determinant of sensitivity to certain chemotherapy drugs, such as cisplatin. Cancer cells with intact DNA repair can avoid the accumulation of genome damage during growth and also can repair platinum-induced DNA damage. We sought genomic signatures indicative of defective DNA repair in cell lines and tumors and correlated these signatures to platinum sensitivity. The number of subchromosomal regions with allelic imbalance extending to the telomere (NtAI) predicted cisplatin sensitivity in vitro and pathologic response to preoperative cisplatin treatment in patients with triple-negative breast cancer (TNBC). In serous ovarian cancer treated with platinum-based chemotherapy, higher levels of NtAI forecast a better initial response. We found an inverse relationship between BRCA1 expression and NtAI in sporadic TNBC and serous ovarian cancers without BRCA1 or BRCA2 mutation. Thus, accumulation of telomeric allelic imbalance is a marker of platinum sensitivity and suggests impaired DNA repair. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28330 Telomeric allelic imbalance indicates defective DNA repair and sensitivity to DNA-damaging agents. Cancer discovery 26.370 https://doi.org/10.1158/2159-8290.CD-11-0206 {Cancer discovery (26.370): 10.1158/2159-8290.CD-11-0206} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA139475 https://www.ebi.ac.uk/ena/browser/view/PRJNA139475 None [Overal design]SNP data from 27 and 40 primary triple negative breast cancer tumor samples from two clinical trials treated with cisplatin and cisplatin + bevacizumab. Labeling, hybridization and data processing was performed by Affymetrix using 70k MIP arrays and 330k MIP arrays. In the cisplatin trial, matched normal samples based on blood from all patients and an additional three samples based on FFPE negative lymph nodes were used as references (30 normal references in total). In the cisplatin+bevacizumab trial, mathed normal samples based on blood from 10 patients were used as references.; [Treatment]'None'; [Growth]'None'; [Extraction]'genomic DNA was extracted with phenolchloroform followed by ethanol precipitation. Normal reference were from blood, FFPE normal reference were from negative lymph nodes.'; [Cell type]'Source: ''er: negative; pr: negative; her2: negative; miller-payne response: 3; neoadjuvant therapy: Cisplatin; brca1 methylation: pos; brca1 mutation: N; age: 59; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 5; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: NSM; age: 39; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 1; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: MSM; age: 68; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 5; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: Y; p53 status: MSM; age: 44; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 1; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: MSM; age: 62; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 4; neoadjuvant therapy: Cisplatin; brca1 methylation: pos; brca1 mutation: N; p53 status: NSM; age: 39; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 4; neoadjuvant therapy: Cisplatin; brca1 methylation: pos; brca1 mutation: N; p53 status: MSM; age: 51; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 5; neoadjuvant therapy: Cisplatin; brca1 mutation: N; age: 31; grade: III; tissue: Primary FFPE breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 4; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: NSM; age: 43; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 3; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: WT; age: 41; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 1; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: WT; age: 53; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 1; neoadjuvant therapy: Cisplatin; brca1 mutation: N; age: 56; grade: III; tissue: Primary FFPE breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 2; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: MSM; age: 43; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: P; neoadjuvant therapy: Cisplatin; brca1 methylation: pos; brca1 mutation: N; age: 57; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 1; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: WT; age: 45; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 5; neoadjuvant therapy: Cisplatin; brca1 methylation: pos; brca1 mutation: N; p53 status: WT; age: 52; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 5; neoadjuvant therapy: Cisplatin; brca1 mutation: Y; age: 48; grade: III; tissue: Primary FFPE breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 2; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; age: 69; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: P; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: MSM; age: 59; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 2; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: MSM; age: 67; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 3; neoadjuvant therapy: Cisplatin; brca1 methylation: pos; brca1 mutation: N; p53 status: NSM; age: 29; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 2; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: MSM; age: 50; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 3; neoadjuvant therapy: Cisplatin; brca1 methylation: pos; brca1 mutation: N; p53 status: NSM; age: 40; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: P; neoadjuvant therapy: Cisplatin; brca1 methylation: pos; brca1 mutation: N; age: 39; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: P; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; age: 63; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 2; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: WT; age: 60; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 5; neoadjuvant therapy: Cisplatin; brca1 methylation: neg; brca1 mutation: N; p53 status: NSM; age: 44; grade: III; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'tissue: Blood; disease state: normal; ', 'tissue: FFPE negative lymph node; disease state: normal; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 4; neoadjuvant therapy: cisplatin + bevacizumab; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 5; neoadjuvant therapy: cisplatin + bevacizumab; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 1; neoadjuvant therapy: cisplatin + bevacizumab; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 3; neoadjuvant therapy: cisplatin + bevacizumab; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: P; neoadjuvant therapy: cisplatin + bevacizumab; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; neoadjuvant therapy: cisplatin + bevacizumab; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ', 'er: negative; pr: negative; her2: negative; miller-payne response: 2; neoadjuvant therapy: cisplatin + bevacizumab; tissue: Primary frozen breast cancer tumor tissue; disease state: breast cancer; ' GSE45965 Homo sapiens 67 Expression profiling by array GPL16998; GPL16999; GPL17000 Isolation and expression profiling of circulating tumor cells in breast cancer patients 2013-04-10 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE45965 Expression profiling of circulating tumor cells in metastatic breast cancer. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-014-3215-0 {Breast cancer research and treatment (3.471): 10.1007/s10549-014-3215-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA196752 https://www.ebi.ac.uk/ena/browser/view/PRJNA196752 None [Overal design]Refer to individual Series; [Treatment]'All blood specimens were processed immediately by IE/FC'; [Growth]'Ten to 20 mL of peripheral blood (PB) were drawn from female Stage IV breast cancer patients yielding a range of 9-993 captured CTCs. Normal breast and skin samples were collected as a core and punch biopsy was performed, respectively.'; [Extraction]'Arcturus RiboAmp HS linear RNA amplification was used and it allowed microarray analysis from as low as 250 pg total RNA'; [Cell type]'Source: ', 'pure circulating tumor cells''tissue: normal peripheral blood; ', 'sample type: Stratagene Universal Human Pooled Reference RNA; ', 'tissue: breast cancer tumor; ', 'tissue: healthy epithelia; ', 'cell type: pure circulating tumor cells; ', 'tissue: blood of breast cancer patient; ', 'tissue: Breast Tissue; ' GSE84149 Homo sapiens 22 Expression profiling by high throughput sequencing GPL16791 Regulation of cellular heterogeneity and rates of symmetric and asymmetric divisions in triple-negative breast cancer 2016-07-07 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE84149 Regulation of Cellular Heterogeneity and Rates of Symmetric and Asymmetric Divisions in Triple-Negative Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2018.08.053 {Cell reports (7.815): 10.1016/j.celrep.2018.08.053} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA328149 https://www.ebi.ac.uk/ena/browser/view/PRJNA328149 None [Overal design]Refer to individual Series; [Treatment]'For staining of cells for differentiation markers by FACS, the cells were detached by trypsin-EDTA, fixed and permeabilized for 10 min in 100% methanol on ice, and stained with antibodies against K18 (sc-31700, Santa Cruz), K14, and vimentin (NCL-L-VIM- V9, Novocastra), followed by conjugated secondary antibodies.', 'Cells were infected with the indicated shRNA or treated as indicated'; [Growth]'Cell lines were obtained from ATCC. HCC70 cells were grown in RPMI medium containing 10% FBS, and MDA-MB-468 cells in Leibovitz L15 medium containing 10% FBS and supplemented with penicillin and streptomycin.', 'Cell lines were obtained from ATCC. HCC70 cells were grown in 96 well plates with RPMI medium containing 10% FBSand supplemented with penicillin and streptomycin.'; [Extraction]'To extract RNA from fixed and stained cell subpopulations isolated by FACS from cell lines and mRNA was extracted using the Recover All Total Nucleic Acid Isolation Kit (Ambion).\nLibraries were prepared and libraries were prepared and sequenced using Illumina’s RNA sequencing protocol', 'RNA was extracted using the Single Cell RNA Purification Kit (Norgen) and 3’ cDNA was synthesized and barcoded in batches of 12 samples, followed by RNA synthesis and amplification by in vitro transcription based on the CELseq protocol DOI: 10.1186/s13059-016-0938-8. Some samples were ran a second time due to low representation in the first run.\nLibraries were prepared and libraries were prepared and sequenced using Illumina’s RNA sequencing protocol.'; [Cell type]'Source: ''cell line: HCC70 breast cancer cell line; cell population: Keratin 18+; ', 'cell line: HCC70 breast cancer cell line; cell population: Keratin 18+ Keratin14+; ', 'cell line: HCC70 breast cancer cell line; cell population: Keratin 18+ Vimentin+; ', 'cell line: MDA-MB-468 breast cancer cell line; cell population: Keratin 18+; ', 'cell line: MDA-MB-468 breast cancer cell line; cell population: Keratin 18+ Keratin14+; ', 'cell line: MDA-MB-468 breast cancer cell line; cell population: Keratin 18+ Vimentin+; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000208001; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000000000; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000013637; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000280340; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000016207; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000016203; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000014681; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000274124; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000072209; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000072212; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000072236; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000072240; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000072250; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000072256; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000014881; ', 'cell line: HCC70; shRNA id/treatment: TRCN0000358448; ' GSE105793 Homo sapiens 4 Genome binding/occupancy profiling by high throughput sequencing GPL11154 T47D Breast cancer cell line ChIP-seq data 2017-10-23 We performed genome-wide PADI2 ChIP seq experiments in T47D cell lines and also RNP2 ChIP seq in T47D cells only expressing HA Tagged amanitin resistant wild type in comparison to R1810A mutant form of RNAP2. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE105793 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA415426 https://www.ebi.ac.uk/ena/browser/view/PRJNA415426 https://www.ncbi.nlm.nih.gov/sra?term=SRP120980 [Overal design]We designed experiment to perform genome wide PADI2 ChIP sequencing in T47D cells as in biological replicates .We find that PADI2 deiminates R1810 at CTD (C-terminal domian ) of RNAP2 , Therefore in order to investigate precise effect of the RNAP2 R1810A mutantion , we performed the RNAP2 ChIP seq by using the HA tagged antibody after expressing the amanitin resistant HA - tagged wild type and mutant form of RNAP2 .; [Treatment]'Using standard protocol of Lipofectamine 3000 transfection, T47D–MMTVL cells were transfected with \uf061-amanitin resistant HA-tagged either wild type (WTr) or R1810Ar mutant RNAP2 for 24 hours followed by \uf061-amanitin treatment (6µg/ml) for 12hours before chromatin prepration. There was no treatmnet for PADI2 ChIP sequencing.'; [Growth]'T47D carrying a single copy of luciferase reporter gene driven by MMTV promoter (T47D-MTVL), were grown in RPMI-1640 medium without phenol red supplemented with 10% dextran coated charcoal treated FBS (DCC/FBS), 2mM L-glutamine, 100U/ml penicillin-streptomycin at 37C with 5% CO2.'; [Extraction]'PADI2 was immunoprecipitated with 6μg of PADI2 antibody (z-22):sc-133877 lot number E1214 and H0715 by 50 μg of chromatin and 42μl of Protein A-Agarose Beads (Diagenode).\nT47D-MTVL cells, without treatment or transfected with \uf061-amanitin resistant HA-tagged wild type (WTr) versus R1810Ar mutant RNAP2 were cross-linked for 10 minutes with 1% formaldehyde. Lysate were sonicated to a DNA fragment size range of 200-300bp using a Biorupter sonicator (Diagenode). PADI2 was immunoprecipitated with 6μg of PADI2 antibody (z-22):sc-133877 lot number E1214 and H0715 by 50 μg and for RNAP2, 150 μg chromatin was incubated with 20μg of anti-HA (ab9110) antibody followed by 42μl of Protein A-Agarose Beads (Diagenode).\nLibraries were prepared using standadr Illumina instruction of NEBNext® ChIP-Seq Library Prep Reagent.', 'For RNAP2, 150 μg chromatin was incubated with 20μg of antibody anti-HA (ab9110) followed by 42μl of Protein A-Agarose Beads (Diagnose) .\nT47D-MTVL cells, without treatment or transfected with \uf061-amanitin resistant HA-tagged wild type (WTr) versus R1810Ar mutant RNAP2 were cross-linked for 10 minutes with 1% formaldehyde. Lysate were sonicated to a DNA fragment size range of 200-300bp using a Biorupter sonicator (Diagenode). PADI2 was immunoprecipitated with 6μg of PADI2 antibody (z-22):sc-133877 lot number E1214 and H0715 by 50 μg and for RNAP2, 150 μg chromatin was incubated with 20μg of anti-HA (ab9110) antibody followed by 42μl of Protein A-Agarose Beads (Diagenode).\nLibraries were prepared using standadr Illumina instruction of NEBNext® ChIP-Seq Library Prep Reagent.'; [Cell type]'Source: ''cell line: T47D; r5020 treatment: Untreated; chip antibody: PADI2 antibody (z-22); chip antibody vendor: Santa Cruz; chip antibody cat. #: sc-133877; chip antibody lot/batch #: E1214; ', 'cell line: T47D; r5020 treatment: Untreated; chip antibody: PADI2 antibody (z-22); chip antibody vendor: Santa Cruz; chip antibody cat. #: sc-133877; chip antibody lot/batch #: H0715; ', 'cell line: T47D; r5020 treatment: Untreated; chip antibody: anti-HA; chip antibody vendor: Abcam; chip antibody cat. #: ab9110; chip antibody lot/batch #: GR304617-2; ' GSE43837 Homo sapiens 38 Expression profiling by array GPL1352 A BRCA1 Deficient-Like Signature is Enriched in Breast Cancer Brain Metastases 2013-01-28 Purpose: There is an unmet clinical need for biomarkers to identify breast cancer patients who are at increased risk of developing brain metastases. The objective is to identify gene signatures and biological pathways associated with HER2+ brain metastasis. Experimental Design: Gene expression of 19 HER2+ breast cancer brain metastases was compared with HER2+ nonmetastatic primary tumors. Gene Set Enrichment Analysis was used to identify a signature, which was evaluated for correlation with BRCA1 mutation status and clinical outcome using published microarray datasets and for correlation with pharmacological inhibition by a PARP inhibitor and temozolomide using published microarray datasets of breast cancer cell lines. Results: A BRCA1 Deficient-Like (BD-L) gene signature is significantly correlated with HER2+ metastases in both our and an independent cohort. BD-L signature is enriched in BRCA1 mutation carrier primary tumors and HER2-/ER- sporadic tumors, but high values are found in a subset of ER+ and HER2+ tumors. Elevated BD-L signature in primary tumors is associated with increased risk of overall relapse, brain relapse, and decreased survival. The BD-L signature correlates with pharmacologic response to PARP inhibitor and temozolomide in two independent microarray datasets, and the signature outperformed four published gene signatures of BRCA1/2 deficiency. Conclusions: The BD-L signature is enriched in breast cancer brain metastases and identifies a subset of primary tumors with increased propensity for brain metastasis. Furthermore, this signature may serve as a biomarker to identify sporadic breast cancer patients who could benefit from a therapeutic combination of PARP inhibitor and temozolomide. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43837 A BRCA1 deficient-like signature is enriched in breast cancer brain metastases and predicts DNA damage-induced poly (ADP-ribose) polymerase inhibitor sensitivity. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr3625 {Breast cancer research : BCR (5.676): 10.1186/bcr3625} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA187530 https://www.ebi.ac.uk/ena/browser/view/PRJNA187530 None [Overal design]Gene expression of 19 HER2+ human breast cancer brain metastases was compared with gene expression of 19 HER2+ nonmetastatic primary human breast tumors.; [Treatment]'The 19 HER2+ breast cancer brain metastatic specimens were fresh-frozen biopsies obtained from the M.D. Anderson Cancer Center between 1998 and 2001. The HER2+ primary breast cancer specimens were fresh-frozen biopsies obtained from the Massachusetts General Hospital in 2006.'; [Growth]'Not applicable.'; [Extraction]'4,000–5,000 malignant epithelial cells were procured by laser capture microdissection using a PixCell IIe system (Molecular Devices, Mountain View, CA, USA) as described in PubMed ID: 19187537. Total RNA was isolated from captured cells using the PicoPure RNA isolation kit (Molecular Devices), then amplified by T7 RNA amplification (RiboAmp; Molecular Devices).'; [Cell type]'Source: ''disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 51 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER+; her2 status: Her2+; age: 52.8 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 55.4 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 43.7 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER+; her2 status: Her2+; age: 42.6 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER+; her2 status: Her2+; age: 55.5 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 37.6 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 71.7 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 51.5 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 58.8 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 43.2 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 66 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 40.7 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 38.5 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 57.2 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 49.1 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER-; her2 status: Her2+; age: 43.6 yr; ', 'disease state: brain metastatic breast cancer; tissue: brain metastasis; er status: ER+; her2 status: Her2+; age: 50.4 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 51 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER+; her2 status: Her2+; age: 50 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 56 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 44 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER+; her2 status: Her2+; age: 46 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER+; her2 status: Her2+; age: 54 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 32 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 73 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 60 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 71 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 66 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 41 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 61 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 57 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 50 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 47 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER-; her2 status: Her2+; age: 53 yr; ', 'disease state: nonmetastatic breast cancer; tissue: primary breast tumor; er status: ER+; her2 status: Her2+; age: 51 yr; ' GSE117309 Homo sapiens 10 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL18573; GPL19415; GPL22245 High-throughput single-cell ChIP-seq identifies heterogeneity of chromatin states in breast cancer 2018-07-18 The dynamic nature of chromatin and transcription plays a critical role in normal differentiation and is expected to contribute to tumor evolution. Studying chromatin heterogeneity with single-cell resolution is mandatory to understand the role of epigenetic plasticity in cancer. Here, we describe a droplet microfluidics system that enables the profiling of chromatin marks of individual cells with an average coverage of up to 10,000 loci per cell. In patient-derived xenograft (PDX) models of breast cancer with acquired drug resistance, single-cell chromatin immunoprecipitation followed by sequencing (scChIP-seq) identified rare populations of cells in untreated, drug-sensitive tumors with chromatin features that match those of resistant cells. Loci depleted for transcriptional repressive mark H3K27me3 included genes know to promote resistance to chemotherapy, highlighting the potential to discover new drug targets. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE117309 High-throughput single-cell ChIP-seq identifies heterogeneity of chromatin states in breast cancer. Nature genetics 25.455 https://doi.org/10.1038/s41588-019-0424-9 {Nature genetics (25.455): 10.1038/s41588-019-0424-9} 'genomic DNA', 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA481734 https://www.ebi.ac.uk/ena/browser/view/PRJNA481734 https://www.ncbi.nlm.nih.gov/sra?term=SRP154341 [Overal design]Single-cell ChIP-seq and single-cell RNA-seq in patient-derived xenograft models of breast cancer with acquired drug resistance; [Treatment]'None'; [Growth]'Human Jurkat and Ramos cell lines were grown in RPMI medium supplemented with 10% heat inactivated bovine serum and 1% Penicillin-Streptomycin.', 'Female Swiss nude mice were purchased from Charles River Laboratories and maintained under specific pathogen-free conditions. Their care and housing were in accordance with institutional guidelines and the rules of the French Ethics Committee (project authorization no. 02163.02). A PDX model of luminal breast cancer (HBCx-22) was previously established at Institut Curie from untreated early-stage luminal breast cancer with informed consent from the patient (Cottu et al, Breast Cancer Research Treatment, 2012). Acquisition of a resistant phenotype for a derivative of HBCx-22, HBCx-22-TamR, was previously established and maintained as previously described in Cottu et al, Clinical Cancer Research 2014. A PDX from a residual triple negative breast cancer post neo-adjuvant chemotherapy (HBCx-95) was previously established at Institut Curie with informed consent from the patient (Marangoni et al, Clinical Cancer Research, 2018). HBCx-95 xenografts were treated with Capecitabine (Xeloda, Roche Laboratories) orally at a dose of 540 mg/kg/day, 5 days a week for 6 weeks. Relative tumor volumes (RTV, mm^3) were calculated as previously described (Marangoni et al, Clinical Cancer Research, 2007). Mice with recurrent tumors were treated for a second round of Capecitabine when PDX reached a volume of over 200 mm^3. Mouse which did not respond to Capecitabine and PDX specimen was extracted at 1100mm^3 and tagged as HBCx-95-CapaR.'; [Extraction]'Prior scChIP-seq and scRNA-seq, PDX were digested at 37°C for 2h with a cocktail of Collagenase I (Roche, # 11088793001) and Hyaluronidase (Sigma, # H3506) as previously described (Petit et al, Lab Investigation 2013). Cells were further individualized at 37°C using a cocktail of 0.25% trypsin/Versen (ThermoFisher Scientific, #15040-033), Dispase II (Sigma, # D4693) and Dnase I (Roche, # 11284932001). Red Blood Cell lysis buffer (ThermoFisher Scientific, # 00-4333-57) was then added to degrade red blood cells. To increase the viability of the cell suspension, we removed dead cells using a Dead Cell Removal kit (Miltenyi Biotec). Cells were re-suspended in PBS/0.04% BSA (ThermoFisher Scientific, # AM2616).\nAfter immunoprecipitation targeting H3K4me3 or H3K27me3, scChIP-seq libraries were prepared as following: barcoded-nucleosomes were amplified by in vitro transcription using the T7 MegaScript kit (ThermoFisher Scientific). The resulting amplified RNA was purified using 1x RNAClean XP beads (Beckman) and reverse transcribed by random priming in cDNA. After RNA digestion, DNA was amplified by PCR using with Illumina Primers for 12 cycles and library fragments ranging from 300 to 600 bp (single-cell barcode plus nucleosomal sequence + PCR primer sequence) were size-selected on an agarose gel. Single-cell ChIP-seq libraries were sequenced on Illumina NextSeq 500 MidOutput 150 cycles', "Prior scChIP-seq and scRNA-seq, PDX were digested at 37°C for 2h with a cocktail of Collagenase I (Roche, # 11088793001) and Hyaluronidase (Sigma, # H3506) as previously described (Petit et al, Lab Investigation 2013). Cells were further individualized at 37°C using a cocktail of 0.25% trypsin/Versen (ThermoFisher Scientific, #15040-033), Dispase II (Sigma, # D4693) and Dnase I (Roche, # 11284932001). Red Blood Cell lysis buffer (ThermoFisher Scientific, # 00-4333-57) was then added to degrade red blood cells. To increase the viability of the cell suspension, we removed dead cells using a Dead Cell Removal kit (Miltenyi Biotec). Cells were re-suspended in PBS/0.04% BSA (ThermoFisher Scientific, # AM2616).\nscRNA-seq libraries were prepared with Chromium Single cell 3' reagent v2 kit according to manufacturer's recommendations (10X Genomics)."; [Cell type]'Source: ''tissue: Jurkat and Ramos cell lines; ', 'tissue: mouse PDX human tumor; ' GSE47635 Mus musculus 11 Genome variation profiling by genome tiling array GPL17131 Copy number variations in mouse mammary tumours driven by mutant Pik3ca^H1047R expression 2013-06-04 Profiling of mouse mammary tumours that have developed in a mouse model expressing mutant Pik3ca^H1047R at endogenous level under control of the MMTV promoter (Tikoo et al., PLoS one 2012). Copy number variations in tumours (compared to matching liver DNA) were detected using Agilent Sureprint microarrays. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47635 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA206990 https://www.ebi.ac.uk/ena/browser/view/PRJNA206990 None [Overal design]DNA samples prepared from 11 tumours developed in Pik3ca^H1047R mice (biological replicates). For each sample the reference is the matching liver DNA of each animal.; [Treatment]'None'; [Growth]'None'; [Extraction]"Genomic DNA extraction using QIAgen DNEasy blood and tissue kit, according to the manufacturer's instructions"; [Cell type]'Source: ''strain: Mixed FVBN/Bl6; tissue: Mammary tumor; ', 'strain: Mixed FVBN/Bl6; tissue: Liver; ' GSE69902 Mus musculus 27 Genome variation profiling by SNP array GPL13147 Copy number variation data in malignant mouse mammary cell lines 2015-06-15 Many preclinical therapy studies have focused on a small number of well-described mouse allograft or human xenograft models that poorly represent the heterogeneity of human disease. Here we have assembled a panel of mouse mammary cell lines derived from spontaneously-arising mouse mammary tumors or from mammary tumors arising in genetically engineered mouse models. We used the Affymetrix Mouse Diversity Genotyping Array to address DNA copy number variation in the genomes of the cell lines of this panel. The resulting information about regions of amplification and deletion should help inform biological analyses as well as provide a reference for cell line authentication/identification. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE69902 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA287047 https://www.ebi.ac.uk/ena/browser/view/PRJNA287047 None [Overal design]Affymetrix Mouse Diversity Genotyping arrays were used according to manufacturer's directions to analyze gDNA extracted from 27 mouse mammary cell lines of varying malignancy.; [Treatment]'None'; [Growth]'Cells were cultured in their recommended growth media using standard procedures'; [Extraction]"RNA-free DNA was prepared from the cell lines using the Gentra Puregene Cell Kit (Qiagen) according to manufacturer's protocol and resuspended in low EDTA TE buffer. DNA quantity was assessed using PicoGreen fluorometry and integrity was assessed by agarose gel electrophoresis. Qualified gDNA samples were normalized to 50ng/ul."; [Cell type]'Source: ''cell line: 2508; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: Not tested; ', 'cell line: 2855; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: Not tested; ', 'cell line: 4TO7; mouse strain: BALB/c; cell line origin: Spontaneous mammary tumor; malignancy status: Malignant; metastatic ability: Low; ', 'cell line: 4T1; mouse strain: BALB/c; cell line origin: Spontaneous mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: 67NR; mouse strain: BALB/c; cell line origin: Spontaneous mammary tumor; malignancy status: Malignant; metastatic ability: None; ', 'cell line: 6DT1; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: 780; mouse strain: C57BL/6:FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: Not tested; ', 'cell line: c-Myc; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: D2.0R; mouse strain: BALB/c; cell line origin: Spontaneous mammary tumor; malignancy status: Malignant; metastatic ability: Low; ', 'cell line: D2A1; mouse strain: BALB/c; cell line origin: Spontaneous mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: Db-7; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: Low; ', 'cell line: E0771; mouse strain: C57BL/6; cell line origin: Spontaneous mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: EMT6; mouse strain: BALB/c; cell line origin: Spontaneous mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: EpH4; mouse strain: BALB/c; cell line origin: Spontaneously immortalized mammary epithelium; malignancy status: Non-malignant; metastatic ability: None; ', 'cell line: F3II; mouse strain: BALB/c; cell line origin: Spontaneous mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: HRM-1; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: M6; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: Met-1; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: MVT1; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: MVT2; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: Myc83; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: Not tested; ', 'cell line: NIC WT; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: Not tested; ', 'cell line: NK; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: r3T; mouse strain: 129S1; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: TM15; mouse strain: FVB/N:129Sv; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: TS1; mouse strain: FVB/N; cell line origin: Genetically engineered mouse mammary tumor; malignancy status: Malignant; metastatic ability: High; ', 'cell line: TS/A-E1; mouse strain: BALB/c; cell line origin: Spontaneous mammary tumor; malignancy status: Malignant; metastatic ability: High; ' GSE72252 Homo sapiens 57 Genome binding/occupancy profiling by high throughput sequencing GPL11154; GPL18573 DNaseI hypersensitivity assay and ER, GR, and FoxA1 binding patterns in breast cancer cells 2015-08-20 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72252 Steroid Receptors Reprogram FoxA1 Occupancy through Dynamic Chromatin Transitions. Cell 36.216 https://doi.org/10.1016/j.cell.2016.02.067 {Cell (36.216): 10.1016/j.cell.2016.02.067} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA293468 https://www.ebi.ac.uk/ena/browser/view/PRJNA293468 None [Overal design]Refer to individual Series; [Treatment]'Cells were plated for experiments in phenol red free growth medium supplemented with 10% charcoal-dextran serum twenty-four hours before hormone treatment. Cells were left untreated or induced with 100nM dexamethasone or 100nM estradiol for 30 minutes.'; [Growth]'see additional columns of the SAMPLES section'; [Extraction]'Lysates were clarified from sonicated nuclei and GR/DNA, ER/DNA, of FoxA1/DNA complexes were isolated with antibody.', 'Lysates were digested with DNase-I and DNA fragments of 100-500bp were purified using a sucrose gradient.'; [Cell type]'Pleural effusion from an adenocarcinoma of the breast', 'Ascites from a ductal carcinoma of the breast', 'Pleural effusion from a ductal carcinoma of the breast''cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: Dexamethasone and 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: Dexamethasone and 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: GR E-20X sc-1003 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: ER cocktail: Ab-10 Thermo Scientific Lab Vision, HC-20 sc-543 Santa Cruz; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: T-47D; cell type: Pleural effusion from a ductal carcinoma of the breast; treatment: Dexamethasone and 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; antibody: FoxA1 ab23738 Abcam; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: MCF-7; cell type: Pleural effusion from an adenocarcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; growth proptocol: For maintenance cells were cultured in DMEM supplemented 10% calf serum, 2mM L-glutamine, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 1; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: untreated; time: 30 minutes; replicate: replicate 2; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 1; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: Dexamethasone; concentration: 100nM; time: 30 minutes; replicate: replicate 2; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 1; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ', 'cell line: ZR-75-1; cell type: Ascites from a ductal carcinoma of the breast; treatment: 17β-estradiol; concentration: 100nM; time: 30 minutes; replicate: replicate 2; growth proptocol: For maintenance cells were cultured in RPMI containing 2mM L-glutamine supplemented 10% calf serum, 1mM sodium pyruvate, 1X non-essential amino acids, and 1% penicillin-streptomycin; ' GSE93815 Mus musculus 26 Expression profiling by array GPL11383 Cell fate and adhesion dynamics rely on Ror2-mediated alternative Wnt signaling during tumor progression 2017-01-18 Cellular heterogeneity in breast cancer encompasses many features, yet an understanding of the coexistence and regulation of various tumor cell subpopulations remains a significant challenge in cancer biology. In the current study, we approached tumor cell heterogeneity from the perspective of Wnt pathway biology to address how different modes of Wnt signaling shape the behaviors of diverse cell populations within a heterogeneous tumor landscape. Using a syngeneic TP53 null mouse model of breast cancer, we identified distinctions in the topology of canonical Wnt b-catenin dependent signaling activity and noncanonical b-catenin independent Ror2-mediated Wnt signaling across subtypes and within tumor cell subpopulations in vivo. We further discovered an antagonistic role for Ror2 in regulating canonical Wnt/b-catenin activity in vivo, where lentiviral shRNA depletion of Ror2 expression augmented canonical Wnt/b-catenin signaling activity across multiple basal-like models. Depletion of Ror2 expression yielded distinct phenotypic outcomes and divergent alterations in gene expression programs among different tumors, despite all sharing basal-like features. Notably, we uncovered cell state plasticity and adhesion dynamics regulated by Ror2, where Ras Homology Family Member A (RhoA) and Rho-Associated Coiled-Coil Kinase 1 (ROCK1) activity downstream of Dishevelled-2 (Dvl2) were implicated. Collectively, these studies illustrate the integration and collaboration of Wnt pathways in basal-like breast cancer, where Ror2 provides a spatiotemporal function to regulate the balance of Wnt signaling and cellular heterogeneity during tumor progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93815 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA362571 https://www.ebi.ac.uk/ena/browser/view/PRJNA362571 None [Overal design]Total RNA from murine p53null mammary tumors was hybridized to agilent microarrays for gene expression analysis; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA isolated using a Qiagen RNeasy Kit'; [Cell type]'Source: ''sample type: Reference RNA from C57Bl6/J and 129 male and female Day1 pups; ', 'sample type: P53null 2225L; strain: Balbc; lentivirus: shLuc; ', 'sample type: P53null 2225L; strain: Balbc; lentivirus: shRor2; ', 'sample type: P53null T1; strain: Balbc; lentivirus: shLuc; ', 'sample type: P53null T1; strain: Balbc; lentivirus: shRor2; ', 'sample type: P53null T2; strain: Balbc; lentivirus: shLuc; ', 'sample type: P53null T2; strain: Balbc; lentivirus: shRor2; ' GSE148748 Homo sapiens 82 Methylation profiling by genome tiling array GPL21145 DNA methylation profiling of 82 triple negative breast cancers with BRCA1 promoter methylation or BRCA1 mutation using the Illumina EPIC 850K platform. 2020-04-15 Genome-wide DNA methylation profiles for 82 triple negative breast cancer (TNBC) samples from the Swedsh Cancerome Analysis Network - Breast (SCAN-B) cohort. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148748 Comprehensive molecular comparison of BRCA1 hypermethylated and BRCA1 mutated triple negative breast cancers. Nature communications 11.878 https://doi.org/10.1038/s41467-020-17537-2 {Nature communications (11.878): 10.1038/s41467-020-17537-2} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA625555 https://www.ebi.ac.uk/ena/browser/view/PRJNA625555 None [Overal design]Genomic DNA from 82 triple negative breast cancer (TNBC) samples was treated with bisulfite and hybridized to Illumina EPIC 850K arrays using standard protocols. Raw iDat files were processed using the minfi-package in R as well as custom R-scripts to produce normalized beta values. Both raw intensity values from minfi and the final normalized data are included for each sample.; [Treatment]'None'; [Growth]'None'; [Extraction]'Standard DNA extraction protocol according to SCAN-B workflow'; [Cell type]'Source: ''subtype: TNBC; brca1-status: Hypermethylated; gender: female; ', 'subtype: TNBC; brca1-status: BRCA1_null; gender: female; ' GSE69290 Mus musculus 28 Expression profiling by array GPL11180 Reactivation of multipotency by oncogenic PIK3CA induces breast tumor heterogeneity 2015-05-27 Breast cancer is the most frequent cancer in women and consists of heterogeneous types of tumours that are classified into different histological and molecular subtypes1-3. Pik3ca and p53 are the two most frequently mutated genes and are associated with different types of human breast cancers4. The cellular origin and the mechanisms leading to Pik3ca-induced tumour heterogeneity remain unknown. Here, we used a genetic approach in mice to define the cellular origin of Pik3ca-derived tumours and its impact on tumour heterogeneity. Surprisingly, oncogenic Pik3ca-H1047R expression at physiological levels5 in basal cells (BCs) using K5CREERT2 induced the formation of luminal ER+PR+ tumours, while its expression in luminal cells (LCs) using K8CREERT2 gave rise to luminal ER+PR+ tumours or basal-like ER-PR- tumours. Concomitant deletion of p53 and expression of Pik3ca-H1047R accelerated tumour development and induced more aggressive mammary tumours. Interestingly, expression of Pik3ca-H1047R in unipotent BCs gave rise to luminal-like cells, while its expression in unipotent LCs gave rise to basal-like cells before progressing into invasive tumours. Transcriptional profiling of cells that have undergone cell fate transition upon Pik3ca-H1047R expression in unipotent progenitors demonstrate a profound oncogene-induced reprogramming of these newly formed cells and identified gene signatures, characteristic of the different cell fate switches that occur upon Pik3ca-H1047R expression in BC and LCs, which correlated with the cell of origin, tumour type and different clinical outcomes. Altogether our study identifies the cellular origin of Pik3ca-induced tumours and reveals that oncogenic Pik3ca-H1047R activates a multipotent genetic program in normally lineage-restricted populations at the early stage of tumour initiation, setting the stage for future intratumoural heterogeneity. These results have important implications for our understanding of the mechanisms controlling tumour heterogeneity and the development of new strategies to block PIK3CA breast cancer initiation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE69290 Reactivation of multipotency by oncogenic PIK3CA induces breast tumour heterogeneity. Nature 43.070 https://doi.org/10.1038/nature14665 {Nature (43.070): 10.1038/nature14665} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA285089 https://www.ebi.ac.uk/ena/browser/view/PRJNA285089 None [Overal design]Luminal and basal cells, or tumour cells, from mice in which expression of PIK3CA-H1047R and YFP (and in some conditions loss of p53) was targeted in basal cells using K5CREERT2 or in luminal cells using K8CREERT2 were FACS isolated and RNA was extracted before being hybridized Affymetrix microarrays.; [Treatment]'Female mice were injected with 3 times with 5 mg of tamoxifen every three days starting at age of 4-5 week. Mice were sacrified at the indicated time point and mammary gland was digested in Collagenase+hyaluronidase. Single cells were stained with the appropriate antibodies and FACS sorted before RNA extraction.'; [Growth]'Mice were maintained in a certified animal house according to European guidelines'; [Extraction]'Qiagen Rneasy Micro'; [Cell type]'Mouse mammary gland FACS purified luminal cells', 'Mouse mammary gland FACS purified basal cells', 'Mouse mammary gland FACS purified tumour cells''cell type: Mouse mammary gland FACS purified luminal cells; ', 'cell type: Mouse mammary gland FACS purified basal cells; ', 'cell type: Mouse mammary gland FACS purified tumour cells; ' GSE4292 Homo sapiens 6 Expression profiling by array GPL96 PTHrP-responsive genes in breast cancer 2006-02-23 Parathyroid hormone-related protein (PTHrP) is overexpressed in many cancer types. This secretory protein can induce hypercalcaemia of malignancy by mimicking the action of calcium-regulating parathyroid hormone (PTH). PTHrP may also be involved in the regulation of migration, invasion, proliferation and apoptosis. It can either stimulate signal cascades, such as the cAMP pathway, or act on not yet defined targets in the nucleus. In this study, we analyzed the effect of PTHrP-specific siRNA on gene expression in MDA-MB-231 breast cancer cells. MDA-MB-231 cells were either transfected with the PTHrP-specific siRNA (siPTHrP) or a control siRNA (siLuc). Differences in gene expression pattern in siPTHrP- vs. siLuc-treated cells were measured by microarray analysis. More than 200 differentially expressed genes were found. Some of these genes have important functions in carcinogenesis. Keywords: siRNA knock-down analysis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE4292 Parathyroid hormone-related protein regulates tumor-relevant genes in breast cancer cells. The Journal of biological chemistry 4.106 https://doi.org/10.1074/jbc.M510527200 {The Journal of biological chemistry (4.106): 10.1074/jbc.M510527200} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA94789 https://www.ebi.ac.uk/ena/browser/view/PRJNA94789 None [Overal design]Three independent transfection experiments were performed. Cells were transfected with siPTHrP or siLuc by electroporation, grown for three days and harvested for isolation of total RNA. RNAs were subjected to microarray analysis. The RNAs of experiment 1 are designated as siLuc 1 and siPTHrP 1, those of experiment 2 as siLuc 2 and siPTHrP 2 etc.. To identify siPTHrP-responsive genes, the siPTHrP- and siLuc-RNAs of the same experiment were compared.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNeasy'; [Cell type]'Source: ''Cell line: MDA-MB-231; ' GSE125215 Homo sapiens 335 Expression profiling by high throughput sequencing GPL21697 Digital gene expression (DGE) based transcript profiling of CDK inhibitors 2019-01-16 We compare differences in gene expression induced after 6 hours of exposure to one of three CDK4/6 inhibitors or a pan-CDK inhibitor https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE125215 Multiomics Profiling Establishes the Polypharmacology of FDA-Approved CDK4/6 Inhibitors and the Potential for Differential Clinical Activity. Cell chemical biology 6.762 https://doi.org/10.1016/j.chembiol.2019.05.005 {Cell chemical biology (6.762): 10.1016/j.chembiol.2019.05.005} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA515531 https://www.ebi.ac.uk/ena/browser/view/PRJNA515531 https://www.ncbi.nlm.nih.gov/sra?term=SRP179781 [Overal design]mRNA levels for 7 breast cancer cell lines or PDX models treated with one of three CDK4/6 inhibitors (abemaciclib, palbociclib, or ribociclib) at 4 concentrations (0.1, 0.3, 1, 3 um) or the pan-CDK inhibitor alvocidib at 2 concentrations (0.1, 1 um) in triplicate.; [Treatment]'24 hours after seeding cells, CDK4/6 inhibitors were added. Cells were lysed in the plates after 6 hours.'; [Growth]'Cells were plated at densitieis ranging from 500 to 2000 cells per well in a 384-well plate and allowed to adhere for 24 hours'; [Extraction]'RNA was extracted using TCL lysis buffer, samples were using universal adapters, barcodes, unique molecular identifiers, and a template switching reverse transcriptase.\nLibraries were prepared using Nextera DNA kit (Illumina).\nDigitial gene expression (DGE)'; [Cell type]'BT549 breast cancer cell line', 'PDX1258 breast cancer PDX', 'HCC1806 breast cancer cell line', 'Hs578T breast cancer cell line', 'MCF7 breast cancer cell line', 'PDXHCI002 breast cancer PDX', 'T47D breast cancer cell line''cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Palbociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: DMSO; concentration (um): 0; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Palbociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Palbociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: DMSO; concentration (um): 0; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Palbociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Palbociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: DMSO; concentration (um): 0; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Palbociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Palbociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: DMSO; concentration (um): 0; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Palbociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Palbociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: DMSO; concentration (um): 0; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Palbociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Palbociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: DMSO; concentration (um): 0; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Palbociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Palbociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: DMSO; concentration (um): 0; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Palbociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Ribociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Abemaciclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Palbociclib; concentration (um): 1; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Ribociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Abemaciclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Palbociclib; concentration (um): 1; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Ribociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Abemaciclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Palbociclib; concentration (um): 1; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Ribociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Abemaciclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Palbociclib; concentration (um): 1; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Ribociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Abemaciclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Palbociclib; concentration (um): 1; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Ribociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Abemaciclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Palbociclib; concentration (um): 1; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Ribociclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Abemaciclib; concentration (um): 0.3; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Palbociclib; concentration (um): 1; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Ribociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Abemaciclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Ribociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Abemaciclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Ribociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Abemaciclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Ribociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Abemaciclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Ribociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Abemaciclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Ribociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Abemaciclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Ribociclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Abemaciclib; concentration (um): 3.16; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Palbociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Alvocidib; concentration (um): 1; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Palbociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Alvocidib; concentration (um): 1; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Palbociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Alvocidib; concentration (um): 1; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Palbociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Alvocidib; concentration (um): 1; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Palbociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Alvocidib; concentration (um): 1; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Palbociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Alvocidib; concentration (um): 1; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Palbociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Alvocidib; concentration (um): 1; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Abemaciclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Ribociclib; concentration (um): 1; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Abemaciclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Ribociclib; concentration (um): 1; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Abemaciclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Ribociclib; concentration (um): 1; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Abemaciclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Ribociclib; concentration (um): 1; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Abemaciclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Ribociclib; concentration (um): 1; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Abemaciclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Ribociclib; concentration (um): 1; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Abemaciclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Ribociclib; concentration (um): 1; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Ribociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Ribociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Ribociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Ribociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Ribociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Ribociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Ribociclib; concentration (um): 0.1; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Alvocidib; concentration (um): 0.1; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Alvocidib; concentration (um): 0.1; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Alvocidib; concentration (um): 0.1; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Alvocidib; concentration (um): 0.1; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Alvocidib; concentration (um): 0.1; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Alvocidib; concentration (um): 0.1; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Alvocidib; concentration (um): 0.1; time (hours): 6; ', 'cell type: BT549 breast cancer cell line; cell line: BT549; drug treatment: Abemaciclib; concentration (um): 1; time (hours): 6; ', 'cell type: PDX1258 breast cancer PDX; cell line: PDX1258; drug treatment: Abemaciclib; concentration (um): 1; time (hours): 6; ', 'cell type: HCC1806 breast cancer cell line; cell line: HCC1806; drug treatment: Abemaciclib; concentration (um): 1; time (hours): 6; ', 'cell type: Hs578T breast cancer cell line; cell line: Hs578T; drug treatment: Abemaciclib; concentration (um): 1; time (hours): 6; ', 'cell type: MCF7 breast cancer cell line; cell line: MCF7; drug treatment: Abemaciclib; concentration (um): 1; time (hours): 6; ', 'cell type: PDXHCI002 breast cancer PDX; cell line: PDXHCI002; drug treatment: Abemaciclib; concentration (um): 1; time (hours): 6; ', 'cell type: T47D breast cancer cell line; cell line: T47D; drug treatment: Abemaciclib; concentration (um): 1; time (hours): 6; ' GSE48905 Homo sapiens 42 Expression profiling by array GPL570 The NEWEST trial 2013-07-16 The NEWEST (Neoadjuvant Endocrine Therapy for Women with Estrogen-Sensitive Tumours) trial compared the clinical and biological activity of fulvestrant 500 mg vs 250 mg in the neoadjuvant setting. In this multi-centre phase II study, post-menopausal women with operable, locally advanced (T2, 3, 4b; N0-3; M0) ER-positive breast tumours were randomised to receive neoadjuvant treatment with either dose of fulvestrant for 16 weeks before surgery. Tumour core biopsies were obtained at baseline, 4 weeks and at surgery for assessment of changes in biomarker expression. Tumour volumes were measured by 3-D ultrasound at the same timepoints. In this trial, the percentage of patients who showed a reduction in tumour volume or stabilisation of disease (using RECIST criteria) after treatment with fulvestrant 500 mg was 36% (26 out of 69 patients). Therefore, within a population of endocrine-therapy naive patients whose tumours were confirmed as being ER-positive at the time of study entry, there is a subgroup who gained particular clinical benefit from fulvestrant treatment. These clinical response data together with the availability of biological response information and frozen tumour tissue from participants makes the NEWEST trial an attractive setting in which to investigate the potential of new markers of response to fulvestrant. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48905 Development and validation of a gene expression score that predicts response to fulvestrant in breast cancer patients. PloS one 2.776 https://doi.org/10.1371/journal.pone.0087415 {PloS one (2.776): 10.1371/journal.pone.0087415} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA212260 https://www.ebi.ac.uk/ena/browser/view/PRJNA212260 None [Overal design]42 samples; [Treatment]'None'; [Growth]'None'; [Extraction]'Rneasy'; [Cell type]'Source: ''Sex: female; rmh lab code: 004; trtlong: Faslodex 250mg; ki67wk0: 22; ki67wk4: 19; erhswk0: 180; erhswk4: 145; prhswk0: 4.5; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 014; trtlong: Faslodex 250mg; ki67wk0: 65; ki67wk4: 6; ki67wk16: 3; erhswk0: 230; erhswk4: 170; erhswk16: 2.5; prhswk0: 125; prhswk4: 80; prhswk16: 55; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 015; trtlong: Faslodex 250mg; ki67wk0: 56; ki67wk4: 5; ki67wk16: 37; erhswk0: 150; erhswk4: 155; erhswk16: 125; prhswk0: 150; prhswk4: 0; prhswk16: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 018; trtlong: Faslodex 500mg; ki67wk0: 66; ki67wk4: 3; erhswk0: 182.5; erhswk4: 100; prhswk0: 50; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 019; trtlong: Faslodex 250mg; ki67wk0: 37; ki67wk4: 7; erhswk0: 190; erhswk4: 180; prhswk0: 225; prhswk4: 170; histtype: Infiltrating Ductal Carcinoma; tgrade: Poorly Differentiated(G3); responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 020; trtlong: Faslodex 500mg; her2hsw0: 200; her2hsw4: 200; ki67wk0: 77; ki67wk4: 1; erhswk0: 239; erhswk4: 220; prhswk0: 110; prhswk4: 12; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 021; trtlong: Faslodex 250mg; her2hsw0: 200; ki67wk0: 45; ki67wk4: 71; erhswk0: 1; erhswk4: 8.5; prhswk0: 0; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Poorly Differentiated(G3); responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 024; trtlong: Faslodex 250mg; her2hsw4: 100; ki67wk0: 100; ki67wk4: 97; erhswk0: 0; erhswk4: 0; prhswk0: 0; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: PD; best response (if different): SD; ', 'Sex: female; rmh lab code: 025; trtlong: Faslodex 250mg; ki67wk0: 50; ki67wk4: 10; erhswk0: 150; erhswk4: 110; prhswk0: 65; prhswk4: 9.5; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 027; trtlong: Faslodex 500mg; her2hsw0: 194; her2hsw4: 200; ki67wk0: 19; ki67wk4: 4; erhswk0: 195; erhswk4: 125; prhswk0: 165; prhswk4: 75; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 028; trtlong: Faslodex 250mg; ki67wk0: 56; ki67wk4: 36; erhswk0: 157.5; erhswk4: 107.5; prhswk0: 132.5; prhswk4: 18.5; histtype: Infiltrating Ductal Carcinoma; tgrade: Poorly Differentiated(G3); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 005; trtlong: Faslodex 500mg; ki67wk0: 1; ki67wk4: 2; erhswk0: 90; erhswk4: 80; prhswk0: 30; prhswk4: 30; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 029; trtlong: Faslodex 500mg; ki67wk0: 69; ki67wk4: 18; erhswk0: 152.5; erhswk4: 130; prhswk0: 180; prhswk4: 105; histtype: Infiltrating Ductal Carcinoma; tgrade: Poorly Differentiated(G3); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 030; trtlong: Faslodex 250mg; ki67wk0: 28; ki67wk4: 5; erhswk0: 152.5; erhswk4: 112.5; prhswk0: 60; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 031; trtlong: Faslodex 500mg; her2hsw0: 21; ki67wk0: 5; ki67wk4: 1; ki67wk16: 2; erhswk0: 180; erhswk4: 140; erhswk16: 152.5; prhswk0: 100; prhswk4: 40; prhswk16: 1.5; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 033; trtlong: Faslodex 250mg; her2hsw0: 100; her2hsw4: 200; ki67wk0: 3; ki67wk4: 29; ki67wk16: 2; erhswk0: 175; erhswk4: 195; erhswk16: 135; prhswk0: 5; prhswk4: 75; prhswk16: 7.5; histtype: Infiltrating Ductal Carcinoma; tgrade: Well Differentiated(G1); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 036; trtlong: Faslodex 500mg; ki67wk0: 51; ki67wk4: 4; erhswk0: 207.5; erhswk4: 167.5; prhswk0: 65; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 037; trtlong: Faslodex 250mg; ki67wk0: 59; ki67wk4: 3; erhswk0: 160; erhswk4: 90; prhswk0: 0; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Unassessable(GX); responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 039; trtlong: Faslodex 250mg; her2hsw4: 34; ki67wk0: 69; ki67wk4: 57; erhswk0: 195; erhswk4: 195; prhswk0: 32.5; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Not Done; responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 040; trtlong: Faslodex 500mg; ki67wk0: 33; ki67wk4: 22; erhswk0: 147.5; erhswk4: 82.5; prhswk0: 195; prhswk4: 17.5; histtype: Infiltrating Ductal Carcinoma; tgrade: Not Done; responder status (us)at last visit: PD; best response (if different): PR; ', 'Sex: female; rmh lab code: 041; trtlong: Faslodex 250mg; ki67wk0: 61; ki67wk4: 15; erhswk0: 0; erhswk4: 107.5; prhswk0: 0; prhswk4: 42.5; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 006; trtlong: Faslodex 500mg; ki67wk0: 44; ki67wk4: 17; erhswk0: 125; erhswk4: 37.5; prhswk0: 60; prhswk4: 15; histtype: Infiltrating Lobular Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 042; trtlong: Faslodex 500mg; ki67wk0: 50; ki67wk4: 10; erhswk0: 195; erhswk4: 122.5; prhswk0: 3; prhswk4: 3; histtype: Infiltrating Lobular Carcinoma; tgrade: Unassessable(GX); responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 044; trtlong: Faslodex 500mg; ki67wk0: 91; ki67wk4: 15; erhswk0: 200; erhswk4: 125; prhswk0: 0; prhswk4: 0; histtype: Undifferentiated Carcinoma; tgrade: Not Done; responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 047; hstlo_s: CARCINOMA MUCINOUS; trtlong: Faslodex 500mg; ki67wk0: 17; ki67wk4: 3; ki67wk16: 2; erhswk0: 155; erhswk4: 1; erhswk16: 0; prhswk0: 117.5; prhswk4: 0; prhswk16: 0; histtype: Other; tgrade: Not Done; responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 048; trtlong: Faslodex 500mg; ki67wk0: 55; erhswk0: 162.5; erhswk4: 0; prhswk0: 142.5; prhswk4: 0; histtype: Infiltrating Lobular Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 049; trtlong: Faslodex 500mg; ki67wk0: 26; ki67wk4: 11; erhswk0: 160; erhswk4: 125; prhswk0: 0; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: NE; ', 'Sex: female; rmh lab code: 050; trtlong: Faslodex 250mg; ki67wk0: 6; ki67wk4: 11; erhswk0: 100; erhswk4: 67.5; erhswk16: 35; prhswk0: 125; prhswk4: 13; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 051; trtlong: Faslodex 500mg; her2hsw0: 30; ki67wk0: 34; ki67wk4: 22; erhswk0: 127.5; erhswk4: 95; prhswk0: 0; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Poorly Differentiated(G3); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 053; trtlong: Faslodex 250mg; her2hsw4: 96; ki67wk0: 18; ki67wk4: 45; ki67wk16: 91; erhswk0: 145; erhswk4: 47.5; erhswk16: 60; prhswk0: 52.5; prhswk4: 0; prhswk16: 0; histtype: Infiltrating Lobular Carcinoma; tgrade: Unassessable(GX); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 054; trtlong: Faslodex 500mg; her2hsw4: 200; ki67wk0: 17; ki67wk4: 19; erhswk0: 95; erhswk4: 60; prhswk0: 0; prhswk4: 0; histtype: Infiltrating Lobular Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 055; trtlong: Faslodex 250mg; ki67wk0: 61; ki67wk4: 4; erhswk0: 220; erhswk4: 157.5; prhswk0: 3; prhswk4: 1; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 007; trtlong: Faslodex 250mg; ki67wk0: 46; ki67wk4: 11; erhswk0: 185; erhswk4: 105; prhswk0: 60; prhswk4: 22.5; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 056; trtlong: Faslodex 250mg; her2hsw0: 96; her2hsw4: 55; ki67wk0: 30; ki67wk4: 28; erhswk0: 65; erhswk4: 55; prhswk0: 0; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: NE; best response (if different): SD; ', 'Sex: female; rmh lab code: 057; trtlong: Faslodex 500mg; ki67wk0: 8; ki67wk4: 7; ki67wk16: 1; erhswk0: 190; erhswk4: 145; erhswk16: 100; prhswk0: 0; prhswk4: 0; prhswk16: 5; histtype: Infiltrating Ductal Carcinoma; tgrade: Poorly Differentiated(G3); responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 058; trtlong: Faslodex 500mg; ki67wk0: 13; ki67wk4: 1; erhswk0: 140; erhswk4: 75; prhswk0: 192.5; prhswk4: 40; histtype: Infiltrating Ductal Carcinoma; tgrade: Poorly Differentiated(G3); responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 059; trtlong: Faslodex 500mg; her2hsw0: 80; her2hsw4: 100; ki67wk0: 18; ki67wk4: 7; ki67wk16: 13; erhswk0: 127.5; erhswk4: 75; erhswk16: 105; prhswk0: 127.5; prhswk4: 29; prhswk16: 25; histtype: Infiltrating Lobular Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 062; trtlong: Faslodex 500mg; ki67wk0: 68; ki67wk4: 4; ki67wk16: 2; erhswk0: 165; erhswk4: 145; erhswk16: 135; prhswk0: 7.5; prhswk4: 7.5; prhswk16: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Poorly Differentiated(G3); responder status (us)at last visit: NE; best response (if different): PR; ', 'Sex: female; rmh lab code: 008; trtlong: Faslodex 500mg; ki67wk0: 89; ki67wk4: 5; erhswk0: 200; erhswk4: 124; prhswk0: 27.5; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Moderately Differentiated(G2); responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 009; trtlong: Faslodex 250mg; her2hsw4: 0; ki67wk0: 75; ki67wk4: 25; erhswk0: 190; erhswk4: 140; prhswk0: 20.5; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Poorly Differentiated(G3); responder status (us)at last visit: SD; ', 'Sex: female; rmh lab code: 010; trtlong: Faslodex 500mg; ki67wk0: 34; ki67wk4: 3; erhswk0: 205; erhswk4: 80; prhswk0: 100; prhswk4: 2.5; histtype: Infiltrating Ductal Carcinoma; tgrade: Not Done; responder status (us)at last visit: PR; ', 'Sex: female; rmh lab code: 013; trtlong: Faslodex 250mg; her2hsw4: 41; ki67wk0: 22; ki67wk4: 86; erhswk0: 137.5; erhswk4: 180; prhswk0: 75; prhswk4: 0; histtype: Infiltrating Ductal Carcinoma; tgrade: Not Done; responder status (us)at last visit: PR; ' GSE102377 Homo sapiens 6 Expression profiling by high throughput sequencing GPL18573 Metastasis in triple negative breast cancer is dependent on ΔNp63/CXCL2/CCL22-mediated recruitment of myeloid-derived suppressor cells 2017-08-08 Gene expression analysis of the knockdown of ΔNP63 in two different human breast cancer cell lines using RNA-Seq https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE102377 ΔNp63-driven recruitment of myeloid-derived suppressor cells promotes metastasis in triple-negative breast cancer. The Journal of clinical investigation 12.282 https://doi.org/10.1172/JCI99673 {The Journal of clinical investigation (12.282): 10.1172/JCI99673} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA397593 https://www.ebi.ac.uk/ena/browser/view/PRJNA397593 https://www.ncbi.nlm.nih.gov/sra?term=SRP115049 [Overal design]RNA was collected and analyzed for biological replicates of each condition (shΔNP63 vs Vector) from two different human breast cancer cell lines (HCC1806 and SUM1315); [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was isolated from the cell lines using the Invitrogen RNA extraction kit in accordance with the manufacturer’s instructions.\nRNA-Sequencing libraries were prepared using the Kapa Stranded mRNA-Seq Kit Illumina Librabry Prep Kit, multiplexed and sequenced on the Illumina NextSeq 500.'; [Cell type]'Source: ''cell line: HCC1806RR; shRNA: shΔNP63; ', 'cell line: HCC1806RR; shRNA: Vector; ', 'cell line: SUM1315; shRNA: shΔNP63; ', 'cell line: SUM1315; shRNA: Vector; ' GSE153509 Homo sapiens 647 Expression profiling by high throughput sequencing GPL18573 Acquired FGFR and FGF alterations confer resistance to estrogen receptor (ER) targeted therapy in ER+ metastatic breast cancer 2020-06-29 Beyond acquired mutations in the estrogen receptor (ER), mechanisms of resistance to ER-directed therapies in ER+ breast cancer have not been clearly defined. We conducted a genome-scale functional screen spanning 10,135 genes to investigate genes whose overexpression confer resistance to selective estrogen receptor degraders. Pathway analysis of candidate resistance genes demonstrated that the FGFR, ERBB, insulin receptor, and MAPK pathways represented key modalities of resistance. In parallel, we performed whole exome sequencing in paired pre-treatment and post-resistance biopsies from 60 patients with ER+ metastatic breast cancer who had developed resistance to ER-targeted therapy. The FGFR pathway was altered via FGFR1, FGFR2, or FGF3/FGF4 amplifications or FGFR2 mutations in 24 (40%) of the post-resistance biopsies. In 12 of the 24 post-resistance tumors exhibiting FGFR/FGF alterations, these alterations were not detected in the corresponding pre-treatment tumors, suggesting that they were acquired or enriched under the selective pressure of ER-directed therapy. In vitro experiments in ER+ breast cancer cells confirmed that FGFR/FGF alterations led to fulvestrant resistance as well as cross-resistance to the CDK4/6 inhibitor palbociclib, through activation of the MAPK pathway. The resistance phenotypes were reversed by FGFR inhibitors and, to a lesser extent, MEK inhibitors, suggesting potential treatment strategies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE153509 Acquired FGFR and FGF Alterations Confer Resistance to Estrogen Receptor (ER) Targeted Therapy in ER+ Metastatic Breast Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-19-3958 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-19-3958} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA642877 https://www.ebi.ac.uk/ena/browser/view/PRJNA642877 https://www.ncbi.nlm.nih.gov/sra?term=SRP269262 [Overal design]Examination of the transcriptional output (mRNA) of the FGFR activation, with T47D cells perturbed to overexpress FGFR pathway activation including FGFR1, FGFR2 (WT, K660N, M538I and N550K), and FGF3, as well as GFP and parental as a control. DMSO, fulvestrant (100 nM), palbociclib (1 uM), FIIN-3 (100 nM), and trametinib (500 nM) as single agent and in combinations for 24 hours. All experimental conditions were done in 6 replicates; [Treatment]'Cell were then treated with DMSO, fulvestrant (100 nM), palbociclib (1 uM), FIIN-3 (100 nM), and trametinib (500 nM) as single agent and in combinations for 24 hours'; [Growth]'T47D cells were infected de novo with lentivirus encoding FGFR1, FGFR2 mutants, FGF3 and controls in the pLX307 plasmid. Cells were plated in 96-well plates in for 48 hours.'; [Extraction]'Plates with cell lysates were thawed and purified with 2.2x RNAClean SPRI beads (Beckman Coulter Genomics). The RNA captured beads were air-dried and processed immediately for RNA secondary structure denaturation (72˚C for three minutes) and cDNA synthesis. We performed SMART-Seq2 following the published protocol\nSmart-seq 2'; [Cell type]'Source: ''cell line: T47D; lentivirus: parental; replicate: 6; treatment: DMSO; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: FIIN-3+FGF2; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: Fulv+Palbo+FGF2; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: Fulv; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: FGF2; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: Fulv+FGF2; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: Fulv+FGF2+Tram; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: Fulv+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: Fulv+Palbo+FGF2; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: DMSO; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: Fulv; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: FGF2; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: Fulv+FGF2; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: Fulv+FGF2+Tram; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: Fulv+Palbo+FGF2; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: DMSO; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: Fulv; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: FGF2; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: Fulv+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: Fulv+FGF2+Tram; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: Fulv+Palbo+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: DMSO; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: Fulv; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: FGF2; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: Fulv+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: Fulv+FGF2+Tram; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: Fulv+Palbo+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: DMSO; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: Fulv; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: FGF2; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: Fulv+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: Fulv+FGF2+Tram; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: Fulv+Palbo+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: DMSO; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: Fulv; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: FGF2; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: Fulv+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: Fulv+FGF2+Tram; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: Fulv+Palbo+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: DMSO; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: Fulv; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: FGF2; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: Fulv+FGF2; ', 'cell line: T47D; lentivirus: FGF3; replicate: 6; treatment: DMSO; ', 'cell line: T47D; lentivirus: FGF3; replicate: 6; treatment: Fulv; ', 'cell line: T47D; lentivirus: FGF3; replicate: 6; treatment: FIIN-3; ', 'cell line: T47D; lentivirus: FGF3; replicate: 6; treatment: Fulv+FIIN-3; ', 'cell line: T47D; lentivirus: FGF3; replicate: 6; treatment: Fulv+Tram; ', 'cell line: T47D; lentivirus: FGF3; replicate: 6; treatment: Fulv+Palbo; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: Fulv+FGF2+Tram; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: FIIN-3+FGF2; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: Fulv+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: FIIN-3+FGF2; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: Fulv+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: FIIN-3+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: Fulv+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: FIIN-3+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: Fulv+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: FIIN-3+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: Fulv+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: FIIN-3+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: Fulv+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: Fulv+FIIN-3; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: Palbo; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: Fulv+Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: FIIN-3; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: Fulv+Palbo+FGF2+Tram; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: Palbo; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: Palbo+FGF2; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: FIIN-3; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: Fulv+Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: GFP; replicate: 6; treatment: Fulv+Palbo+FGF2+Tram; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: Palbo; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: Palbo+FGF2; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: FIIN-3; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: Fulv+Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR1; replicate: 6; treatment: Fulv+Palbo+FGF2+Tram; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: Palbo; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: Palbo+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: Fulv+Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_WT; replicate: 6; treatment: Fulv+Palbo+FGF2+Tram; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: Palbo; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: Palbo+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: Fulv+Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_M538I; replicate: 6; treatment: Fulv+Palbo+FGF2+Tram; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: Palbo; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: Palbo+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: Fulv+Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_N550K; replicate: 6; treatment: Fulv+Palbo+FGF2+Tram; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: Palbo; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: Palbo+FGF2; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: Fulv+Palbo+FGF2+FIIN-3; ', 'cell line: T47D; lentivirus: FGFR2_K660N; replicate: 6; treatment: Fulv+Palbo+FGF2+Tram; ', 'cell line: T47D; lentivirus: FGF3; replicate: 6; treatment: control; ', 'cell line: T47D; lentivirus: FGF3; replicate: 6; treatment: Palbo; ', 'cell line: T47D; lentivirus: FGF3; replicate: 6; treatment: Palbo+FIIN-3; ', 'cell line: T47D; lentivirus: FGF3; replicate: 6; treatment: Fulv+Palbo+FIIN3; ', 'cell line: T47D; lentivirus: FGF3; replicate: 6; treatment: Fulv+Palbo+Tram; ', 'cell line: T47D; lentivirus: parental; replicate: 6; treatment: Palbo+FGF2; ' GSE68681 Mus musculus 43 Expression profiling by array GPL13188 Cell density, Her2 and progesterone signaling regulate dissemination of breast cancer cells [Gene expression] 2015-05-08 Disseminated breast cancer cells display genotypes disparate from the predominant clone of the primary tumor before manifestation of metastasis, suggesting that cancer cell dissemination occurs preferentially early; however, the underlying molecular mechanisms are unknown. Investigating metastasis in a Her2-driven mouse model, we found that the progesterone-induced paracrine cytokines Wnt4 and Rankl induced migration and early dissemination shortly after Her2 activation. Once tumorigenic growth was established, progesterone receptor (PgR) expression was lost and Wnt4/Rankl induced proliferation. The altered response from migration to proliferation was determined by cell density involving miRNA-regulated PgR expression and was reversible. Cells from early, low-density lesions displayed more functional stemness traits than cells from dense, advanced tumors, migrated more and founded significantly more metastases. The data suggest that many metastases are derived from early-disseminated cancer cells, implying that our concepts for systemic therapy need to be revised. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE68681 Early dissemination seeds metastasis in breast cancer. Nature 43.070 https://doi.org/10.1038/nature20785 {Nature (43.070): 10.1038/nature20785} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA283390 https://www.ebi.ac.uk/ena/browser/view/PRJNA283390 None [Overal design]Gene expression analysis was performed for 10 normal, 7 ADH, 19 primary tumor and 7 lung metastatic tissue samples.; [Treatment]'Transgenic Balb-NeuT mouse model of breast cancer (untreated)'; [Growth]'not applicable'; [Extraction]'Laser microdissection (PALM MicroBeam from Carl Zeiss MicroImaging GmbH) was performed to dissect metastatic lesions from lung, primary tumors, epithelial layers of mammary glands of BALB-NeuT mice at the time point of ADH, and BALB/c mice at different age. Small pieces summing up to 100,000 um2 for each sample were catapulted into a cap with 10 ul paramagnetic oligo-dT bead suspension and lysis buffer. The extraction of mRNA and microarray experiments were performed as described previously (Klein et al., 2002).'; [Cell type]'Source: ''source: ADH tissue; ', 'source: normal tissue; ', 'source: tumor margin tissue; ', 'source: tumor center tissue; ', 'source: tumor tissue; ', 'source: lung metastasis tissue; ' GSE181585 Homo sapiens 4 Other GPL25389 Gene expression in human cell lines reproducing breast cancer progression 2021-08-06 We looked for difference in genetic expression in 4 cell lines that have the same genetic background but reproduce breast cancer progression. Especially, we identied genes that were overexpressed in late cancer progression (MCFT1 and MCFCA1) but not in early stages (MCF10A and MCFNeoT). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE181585 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA752604 https://www.ebi.ac.uk/ena/browser/view/PRJNA752604 None [Overal design]Total RNA was extracted from 4 human cell lines : MCF10A, MCFNeoT, MCFT1 and MCFCA1 and used to performed a Nanostring array (NanoString nCounter Immunology Panel (Human V2).; [Treatment]'no treatment was applied'; [Growth]'RNA was extracted from a confluent 10cm2 plate'; [Extraction]'RNA was extracted using RNAeasy mini kit from Qiagen'; [Cell type]'Source: ''cell line: MCF10A; ', 'cell line: MCFCA1; ', 'cell line: MCFNeoT; ', 'cell line: MCFT1; ' GSE148847 Homo sapiens 6 Expression profiling by array GPL17077 Gene expression profiling of MDA-MB-231 cells transfected with hsa-miR-205-5p and hsa-miR-214-3p compared to scrambled miRNA precursors 2020-04-17 We have employed whole genome microarray to identify changes in gene expression in MDA-MB-231 cells transfected with hsa-miR-205-5p and hsa-miR-214-3p compared to scrambled miRNA precursors at 72 hours after transfection. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148847 MicroRNA Expression Profiling on Paired Primary and Lymph Node Metastatic Breast Cancer Revealed Distinct microRNA Profile Associated With LNM. Frontiers in oncology 4.137 https://doi.org/10.3389/fonc.2020.00756 {Frontiers in oncology (4.137): 10.3389/fonc.2020.00756} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA625956 https://www.ebi.ac.uk/ena/browser/view/PRJNA625956 None [Overal design]We have employed whole genome microarray to identify changes in gene expression in MDA-MB-231 cells transfected with hsa-miR-205-5p and hsa-miR-214-3p compared to scrambled miRNA precursors at 72 hours after transfection.; [Treatment]'MDA-MB-231 cells (0.168 x 10e6 cells/ml) were transfected with the selected miRNA precursors (pre-miR–negative control, hsa-miR-205-5p and hsa-miR-214-3p) purchased from Ambion. Cell transfection was conducted employing a reverse transfection protocol.'; [Growth]'MDA-MB-231 cells were grown in DMEM supplemented with 10% fetal bovine serum, 1% NEAA, 1% L-glutamine, 100 mg/l penicillin, and 100 mg/l streptomycin.'; [Extraction]'Total RNA were isolated from control and treated cells using Total RNA Purification Kit (Norgen-Biotek Corp., Canada) according to the manufacturer’s instructions. The concentrations of total RNA were measured using NanoDrop 2000 (Thermo-Scientific).'; [Cell type]'Breast cancer cell line''cell line: MDA-MB-231; cell type: Breast cancer cell line; miRNA: has-miR-205-5p precursor; ', 'cell line: MDA-MB-231; cell type: Breast cancer cell line; miRNA: has-miR-214-3p precursor; ', 'cell line: MDA-MB-231; cell type: Breast cancer cell line; miRNA: scrambled microRNA; ' GSE72652 Homo sapiens 36 Genome variation profiling by genome tiling array GPL9128 Mapping alterations spatially and temporally during early stages of breast tumourigenesis [aCGH] 2015-09-02 Identifying genomic alterations that precede tumourigenesis of breast tumours will allow us to better understand tumour development and heterogeneity. In particular, by obtaining and profiling normal-epithelium samples at various distances from the tumour, we can draft both a spatial and temporal map of the genomic events and transcriptomic alterations that occur along the mammary duct (leading up to and including the tumour). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72652 Mapping genomic and transcriptomic alterations spatially in epithelial cells adjacent to human breast carcinoma. Nature communications 11.878 https://doi.org/10.1038/s41467-017-01357-y {Nature communications (11.878): 10.1038/s41467-017-01357-y} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA294597 https://www.ebi.ac.uk/ena/browser/view/PRJNA294597 None [Overal design]Dataset consisting of 9 patients with breast cancer, from which multiple normal epithelium samples were obtained from along the duct leading to the tumour, one sample from the contralateral duct, and a sample from the tumor itself; [Treatment]'Fifteen patients undergoing mastectomy for biopsy-proven carcinoma were recruited at the Princess Margaret Cancer Center, University Health Network (Toronto, ON, Canada) from 2005 to 2008. Inclusion criteria were defined as tumours at least 2cm in largest diameter as measured by imaging, and located at least 3cm from the nipple. During surgery, prior to removal of the breast, a ductoscopy procedure was performed using a 0.7mm mammary ductoscope (MF2-707, MD Fibertech Co, Japan). The duct leading to the tumour was identified by visual inspection and identification of the tumour. Methylene blue dye was injected to identify the involved duct for tissue sampling. Immediately after the mastectomy procedure, tissue sampling was performed. Two samples were taken along the duct between the tumour and the nipple (previously dye stained) (T1 and T2) and one from the opposite duct within the same breast (as a normal control) (T3). A sample from the tumour was also obtained (T4). All tissues obtained were bisected, with one half snap frozen and the other half formalin-fixed and paraffin-embedded. Normal skin tissue was also obtained for control DNA.'; [Growth]'n/a'; [Extraction]'Snap frozen tissues were sectioned at 8 micron thickness using a microtome and lightly stained with hematoxylin. Histological identification of tumour and normal ducts was confirmed by a pathologist. Needle-microdissection was performed under a dissecting microscope for both tumour and ducts to ensure minimal stromal contamination of epithelial cells. DNA was extracted from microdissected tissue using the Qiagen Allprep RNA/DNA Micro Kit (Qiagen, Mississauga, ON, Canada).'; [Cell type]'Source: ''location: T1; tissue: breast; ', 'reference: Pooled lymph node tissue; ', 'location: T2; tissue: breast; ', 'location: T3; tissue: breast; ', 'location: T4; tissue: breast; ' GSE58027 Homo sapiens 8 Non-coding RNA profiling by array GPL15446 miRNA expression profile of cells and exosomes 2014-05-28 We hypothesized that miRNAs in the bone maroow mesenchymal stem cells (BM-MSC)-derived exosomes contributed to the phenotype change of breast cancer cells through exosome transfer. We analyzed the miRNA expression signature in BM-MSC-derived exosomes. We compared the miRNA expression levels in exosomes between BM-MSCs and adult fibroblasts (as a control). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58027 Exosomes from bone marrow mesenchymal stem cells contain a microRNA that promotes dormancy in metastatic breast cancer cells. Science signaling 6.481 https://doi.org/10.1126/scisignal.2005231 {Science signaling (6.481): 10.1126/scisignal.2005231} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA248726 https://www.ebi.ac.uk/ena/browser/view/PRJNA248726 None [Overal design]In this study, miRNA expression including in bone-marrow mesenchymal cell (BM-MSC)-derived exosomes was examined, and compared with that of exosomes derived from adult fibroblast cells or the BM-MSC cells. In addition, miRNA expression of BM-MSC exosomes was also compared with that of breast cancer cells with or without cancer stem cell marker.; [Treatment]'After incubation of cells for 2–3 days, the medium was collected and centrifuged at 2,000 x g for 15 minutes at room temperature. To thoroughly remove the cellular debris, the supernatant was filtered using a 0.22-µm filter unit (Millipore). The CM was then ultracentrifuged at 110,000 x g for 70 minutes at 4°C. The pellets were washed with 11 ml PBS, ultracentrifuged, and resuspended in PBS.'; [Growth]'The Bone marrow mesenchymal stem cells and adult fibroblast cells were cultured in a reduced-serum (2%) medium (MesenPRO RS, Invitrogen) or StemPro (Invitrogen) containing Glutamax (Invitrogen) and an antibiotic-antimycotic (Invitrogen) at 37°C in 5% CO2.'; [Extraction]'RNA samples were extracted from cells using miRNesy mini kit (Quiagen).'; [Cell type]'Source: ''gender: male; ', 'gender: female; ' GSE138536 Homo sapiens 1902 Expression profiling by high throughput sequencing GPL18573 Single-cell transcriptional diversity is a hallmark of developmental potential 2019-10-07 Single-cell RNA sequencing (scRNA-seq) is a powerful approach for reconstructing cellular differentiation trajectories. However, inferring both the state and direction of differentiation is challenging. Here, we demonstrate a simple, yet robust, determinant of developmental potential—the number of expressed genes per cell—and leverage this measure of transcriptional diversity to develop a computational framework (CytoTRACE) for predicting differentiation states from scRNA-seq data. When applied to diverse tissue types and organisms, CytoTRACE outperformed previous methods and nearly 19,000 annotated gene sets for resolving 52 experimentally determined developmental trajectories. Additionally, it facilitated the identification of quiescent stem cells and revealed genes that contribute to breast tumorigenesis. This study thus establishes a key RNA-based feature of developmental potential and a platform for delineation of cellular hierarchies (https://cytotrace.stanford.edu). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE138536 Single-cell transcriptional diversity is a hallmark of developmental potential. Science (New York, N.Y.) 41.037 https://doi.org/10.1126/science.aax0249 {Science (New York, N.Y.) (41.037): 10.1126/science.aax0249} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA576262 https://www.ebi.ac.uk/ena/browser/view/PRJNA576262 None [Overal design]Single-cell RNA-sequencing (Smart-seq2) profiles (n = 1,902 cells) of human basal (tumor: n = 294, adjacent normal: n = 366), luminal progenitor (tumor: n = 213, adjacent normal: n = 319), and mature luminal cells (tumor: n = 354, adjacent normal: n = 356) from 8 human breast cancer patients (luminal-like: n = 6; basal-like: n = 2) ----------------------------------------- The authors state that they will "upload the remaining raw data to dbGap".; [Treatment]'None'; [Growth]'None'; [Extraction]'6 tumor biopsies from patients with luminal-like breast cancer and 2 tumor biopsies from patients with basal-like breast cancer were obtained from the primary site during surgical resection of breast tumors at Stanford Hospital and City of Hope National Medical Center. Samples were mechanically dissociated into < 1-2 mm3 pieces with a razor blade and then digested at 37 oC with 1500 U collagenase and 500 U hyaluronidase in Advanced DMEM/F12 (Thermo Fisher Scientific), 2 mM Glutamax (Invitrogen), and an antibiotic/antimycotic mix containing 120 μg/ml penicillin, 100 μg/ml streptomycin, and 0.25 μg/ml amphotericin-B (PSA) for 4-6 hrs with hourly pipetting for 5 min. After digestion, cells were treated with ACK lysis buffer to deplete red blood cells and then incubated with 10 U dispase to further dissociate the tissue into single cells and 1000 U DNase I to prevent cell clumping. Cells were filtered through a 70 μm nylon mesh and washed with staining buffer containing 2% fetal bovine serum (FBS) and PSA in Hank’s Balanced Salt Solution (HBBS). Single cell suspensions of fresh breast tissue were then stained with fluorescent antibodies to prepare for FACS. To reduce nonspecific antibody binding, single cells were blocked with 10 μg/mL rat IgG on ice for 10 minutes. Cells were then stained, in the dark, on ice for 30 minutes. FACS was performed with a 130 μm nozzle on a BD FACSAria II with BD FACSDiva software. Side scatter and forward scatter profiles (area and width) were used to eliminate debris and cell doublets. Dead cells were eliminated by excluding 4’,6-diamidino-2-phenylindole (DAPI) positive cells. Breast epithelial cells were enriched by negative gating of lineage cells expressing CD45, CD31, CD3, CD16, or CD64. Human breast basal cells were then gated as CD49fhighEPCAMmed-low, luminal progenitors as CD49fhighEPCAMhigh, and mature luminal cells as CD49flowEPCAMhigh. Single human breast cells were then sorted into 96-well plates of lysis buffer.\ncDNA libraries were constructed using a modified Smart-seq2 protocol and machine-automated pipeline by the Stanford Functional Genomic Facility (SFGF), as described previously (PMIDs: 24385147 and 30241615). Notably, 27 cycles of PCR amplification were required to obtain cDNA amounts within range of the recommended concentrations (0.05 – 0.32 ng/μL) for downstream tagmentation. Wells with over-amplified cDNA were diluted. Libraries were prepared using the Nextera XT DNA Library Prep (Illumina) kit and sequenced on a NextSeq 500 (Illumina) to obtain 2x76 or 2x151 bp paired-end reads.'; [Cell type]'Source: ''patient: SU2; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Basal; er status: NA; pr status: NA; her status: NA; ', 'patient: SU2; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Mature luminal; er status: NA; pr status: NA; her status: NA; ', 'patient: SU2; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Luminal progenitor; er status: NA; pr status: NA; her status: NA; ', 'patient: SU2; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Luminal progenitor; er status: NA; pr status: NA; her status: NA; ', 'patient: SU2; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Basal; er status: NA; pr status: NA; her status: NA; ', 'patient: SU2; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Mature luminal; er status: NA; pr status: NA; her status: NA; ', 'patient: SU20; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Basal; er status: Pos; pr status: NA; her status: NA; ', 'patient: SU20; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Mature luminal; er status: Pos; pr status: NA; her status: NA; ', 'patient: SU20; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Luminal progenitor; er status: Pos; pr status: NA; her status: NA; ', 'patient: SU58; clinical subtype: Basal; tissue: Tumor; celltype by seurat cluster: Mature luminal; er status: Neg; pr status: Neg; her status: Neg; ', 'patient: SU58; clinical subtype: Basal; tissue: Tumor; celltype by seurat cluster: Basal; er status: Neg; pr status: Neg; her status: Neg; ', 'patient: SU58; clinical subtype: Basal; tissue: Tumor; celltype by seurat cluster: Luminal progenitor; er status: Neg; pr status: Neg; her status: Neg; ', 'patient: SU58; clinical subtype: Basal; tissue: Adjacent normal; celltype by seurat cluster: Basal; er status: Neg; pr status: Neg; her status: Neg; ', 'patient: SU20; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Mature luminal; er status: Pos; pr status: NA; her status: NA; ', 'patient: SU20; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Basal; er status: Pos; pr status: NA; her status: NA; ', 'patient: SU20; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Luminal progenitor; er status: Pos; pr status: NA; her status: NA; ', 'patient: SU4; clinical subtype: Basal; tissue: Tumor; celltype by seurat cluster: Mature luminal; er status: Neg; pr status: Neg; her status: Neg; ', 'patient: SU4; clinical subtype: Basal; tissue: Tumor; celltype by seurat cluster: Basal; er status: Neg; pr status: Neg; her status: Neg; ', 'patient: SU4; clinical subtype: Basal; tissue: Adjacent normal; celltype by seurat cluster: Basal; er status: Neg; pr status: Neg; her status: Neg; ', 'patient: SU4; clinical subtype: Basal; tissue: Adjacent normal; celltype by seurat cluster: Mature luminal; er status: Neg; pr status: Neg; her status: Neg; ', 'patient: SU4; clinical subtype: Basal; tissue: Adjacent normal; celltype by seurat cluster: Luminal progenitor; er status: Neg; pr status: Neg; her status: Neg; ', 'patient: SU4; clinical subtype: Basal; tissue: Tumor; celltype by seurat cluster: Luminal progenitor; er status: Neg; pr status: Neg; her status: Neg; ', 'patient: SU17; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Basal; er status: Pos; pr status: Pos; her status: Neg; ', 'patient: SU17; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Luminal progenitor; er status: Pos; pr status: Pos; her status: Neg; ', 'patient: SU21; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Mature luminal; er status: Pos; pr status: Pos; her status: NA; ', 'patient: SU21; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Basal; er status: Pos; pr status: Pos; her status: NA; ', 'patient: SU21; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Luminal progenitor; er status: Pos; pr status: Pos; her status: NA; ', 'patient: SU9; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Basal; er status: Pos; pr status: Pos; her status: Neg; ', 'patient: SU17; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Basal; er status: Pos; pr status: Pos; her status: Neg; ', 'patient: SU17; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Mature luminal; er status: Pos; pr status: Pos; her status: Neg; ', 'patient: SU17; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Luminal progenitor; er status: Pos; pr status: Pos; her status: Neg; ', 'patient: SU17; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Mature luminal; er status: Pos; pr status: Pos; her status: Neg; ', 'patient: SU9; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Mature luminal; er status: Pos; pr status: Pos; her status: Neg; ', 'patient: SU9; clinical subtype: Luminal; tissue: Adjacent normal; celltype by seurat cluster: Luminal progenitor; er status: Pos; pr status: Pos; her status: Neg; ', 'patient: SU9; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Basal; er status: Pos; pr status: Pos; her status: Neg; ', 'patient: SU9; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Mature luminal; er status: Pos; pr status: Pos; her status: Neg; ', 'patient: SU9; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Luminal progenitor; er status: Pos; pr status: Pos; her status: Neg; ', 'patient: SU21; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Basal; er status: Pos; pr status: Pos; her status: NA; ', 'patient: SU21; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Mature luminal; er status: Pos; pr status: Pos; her status: NA; ', 'patient: SU21; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Luminal progenitor; er status: Pos; pr status: Pos; her status: NA; ', 'patient: COH69; clinical subtype: Luminal; tissue: Tumor; celltype by seurat cluster: Luminal progenitor; er status: Pos; pr status: NA; her status: NA; ' GSE64720 Homo sapiens 100 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL18224 Post-zygotic structural variants in histologically normal breast tissue may predispose to sporadic breast cancer [SET 2] 2015-01-07 Sporadic breast cancer (SBC) is a common and heterogeneous disease. There is no reliable way of early prediction of risk for SBC in the general population. We studied 282 females with SBC concentrating on copy number aberrations in tumor-free breast tissue (uninvolved margin, UM) outside the area of primary tumor (PT). Totally 1162 UMs (1-14 per breast) were studied. PT and blood/skin as control was also analyzed. Comparative analysis between genetic profiles for UM(s), PT(s) and blood/skin from the same patient is the core of study design. We identified 108 patients with at least one aberrant UM specimen, representing 38.3% of all cases. Gains were the dominating mutations in microscopically normal breast cells and gain of ERBB2, with overexpression of HER2 protein, was the most common aberration in normal cells. Five additional receptor genes (EGFR, FGFR1, IGF1R, LIFR and NGFR) also showed gains, and these were occasionally present in combination with the gain of ERBB2. Up to 67.6% of patients showed gain of one or more of these genes in normal cells. The aberrations found in normal cells from UMs were previously described in cancer literature, which suggest their causative, driving role in this disease. We demonstrate that analysis of normal cells from cancer-bearing patients leads to identification of genetic signatures that may predispose to SBC. Early detection of signals suggesting a predisposition towards development of SBC, long before detectable tumors are formed, is a key to the anticipated shift into a preventive paradigm of personalized medicine of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64720 Signatures of post-zygotic structural genetic aberrations in the cells of histologically normal breast tissue that can predispose to sporadic breast cancer. Genome research 9.944 https://doi.org/10.1101/gr.187823.114 {Genome research (9.944): 10.1101/gr.187823.114} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA271743 https://www.ebi.ac.uk/ena/browser/view/PRJNA271743 None [Overal design]We studied 282 female breast cancer patients that were assessed as affected by sporadic disease at the time of diagnosis and all underwent mastectomy. In total, 1162 UMs (uninvolved margin tissues), ranging from 1 to 14 UMs per patient, taken outside the location of clinically characterized index primary tumor, were analyzed on Illumina arrays. For each subject, DNA from at least one control tissue was also analyzed, which was predominantly blood DNA, alternatively skin-derived DNA. We also studied primary tumor (PT), or up to 3 primary tumor foci from patients with diagnosis of multifocal disease. This GEO project contains the genotyping profiles (processed and normalized data including Log R Ratio and B allele frequency) for these 1162 UMs used in the study. Information on phenotypes (age at diagnosis, tumor focality, tumor grade, tumor molecular phenotype) is also provided, whenever available. The first 100 samples out of 811 experiments runned on platform GPL18224 (Infinium HumanOmniExpressExome); [Treatment]'None'; [Growth]'None'; [Extraction]'The tissues were stored at -70 degrees C prior to DNA extraction. The solid tissues were homogenized with a Tissuerupter (Qiagen). Proteinase K and Sarcosine was then added and the sample was incubated at 50oC over-night. The samples were transferred to PhaseLock Gel tubes and the DNA was purified with phenol/chloroform extraction. Due to very rich content of fat in UMs, phenol/chloroform extraction was repeated 6 times for all UMs, and 3 times for PTs and control samples from skin. The purified DNA was precipitated with sodium acetate, pH 5.4 and 95% ethanol. The DNA precipitate was dried before dissolving in water. Control samples of blood were extracted with QIAmp DNA Blood Maxi Kit (Qiagen).'; [Cell type]'Source: ''subject_code: 004JJ; gender: female; age at cancer diagnosis (yrs): 71; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 006MK; gender: female; age at cancer diagnosis (yrs): 51; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 015SK; gender: female; age at cancer diagnosis (yrs): 72; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 017KM; gender: female; age at cancer diagnosis (yrs): 82; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 029LN; gender: female; age at cancer diagnosis (yrs): 81; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 036CS; gender: female; age at cancer diagnosis (yrs): 57; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: unifocal; ', 'subject_code: 038ALZ; gender: female; age at cancer diagnosis (yrs): 58; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: unifocal; ', 'subject_code: 039BW; gender: female; age at cancer diagnosis (yrs): 62; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: 040HM; gender: female; age at cancer diagnosis (yrs): 72; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: unifocal; ', 'subject_code: 041JS; gender: female; age at cancer diagnosis (yrs): 48; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 042JL; gender: female; age at cancer diagnosis (yrs): 78; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: 043WB; gender: female; age at cancer diagnosis (yrs): 79; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: 044JD; gender: female; age at cancer diagnosis (yrs): 74; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 045EK; gender: female; age at cancer diagnosis (yrs): 54; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: 046MU; gender: female; age at cancer diagnosis (yrs): 66; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: 047MS; gender: female; age at cancer diagnosis (yrs): 68; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: 048EB; gender: female; age at cancer diagnosis (yrs): 71; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: 049ASZ; gender: female; age at cancer diagnosis (yrs): 61; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: 050RW; gender: female; age at cancer diagnosis (yrs): 50; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: multifocal?; ', 'subject_code: 051AZ; gender: female; age at cancer diagnosis (yrs): 82; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: 052JW; gender: female; age at cancer diagnosis (yrs): 42; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: multifocal; ', "subject_code: 053KS; gender: female; age at cancer diagnosis (yrs): 57; tumor grade: ductal ca. in situ + Paget's ca.; tumor focality: multifocal ductal ca. in situ; " GSE28049 Homo sapiens 9 Expression profiling by array GPL571 Gene expression data from MDA-MB231 cells stably transduced with lentiviral vectors encoding a control shRNA (shscramble) or two shRNAs targeting Coco (shco2 and shco4) 2011-03-21 Metastatic relapse of breast cancer and other tumor types usually occurs several years after surgical resection of the primary tumor. Early dissemination of tumor cells followed by an extended period of dormancy is thought to explain this prevalent clinical behavior. By using a gain-of-function retroviral cDNA screen in the mouse, we found that Coco, a secreted antagonist of TGF-beta ligands, induces solitary mammary carcinoma cells that have extravasated in the lung stroma to exit from dormancy. Mechanistic studies demonstrate that Coco awakens dormant metastasis-initiating cells by blocking stroma-derived Bone Morphogenetic Proteins. Inhibition of canonical BMP signaling reverses the commitment to differentiation of these cells and enhances their self-renewal and tumor-initiation capacity. Expression of Coco induces a discrete gene expression signature strongly associated with metastatic relapse to the lung but not to the bone or brain in primary patients’ samples. Accordi ngly, silencing of Coco does not inhibit metastasis to the bone or brain in mouse models. These findings suggest that metastasis-initiating cells require the self-renewal capability typically associated with stem cells in order to exit from dormancy and identify Coco as a master regulator of this process. The Affymetrix HG-U133A and Agilent platforms, which were used to build MSK82 [GSE2603], EMC192 [GSE12276], EMC286 [GSE2034], and NKI295 [van 't Veer et al., 2002; van de Vijver et al.,2002; Fan et al., 2006] datasets, do not contain probes for Coco, preventing a direct analysis of the correlation of the expression of Coco with metastatic relapse. We therefore examined the changes in gene expression caused by silencing of Coco in MDA-MB231 cells in vitro and used the resulting signature as a proxy of Coco expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28049 The BMP inhibitor Coco reactivates breast cancer cells at lung metastatic sites. Cell 36.216 https://doi.org/10.1016/j.cell.2012.06.035 {Cell (36.216): 10.1016/j.cell.2012.06.035} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA139765 https://www.ebi.ac.uk/ena/browser/view/PRJNA139765 None [Overal design]Compare the gene expression profile between shscramble with shCoco knockingdown MDA-MB231 cells Coco shRNA #2 corresponds to TRCN0000149666 and Coco shRNA #4 corresponds to TRCN0000148148.; [Treatment]'The lentivirus pLKO vector expression Coco shRNAs (TRCN0000149666 and TRCN0000148148) was used to make stable cell line knocking down Coco.'; [Growth]'10% fetal bovine serum with DMEM media, 37 degree 5% CO2 incubator'; [Extraction]'RNA extraction plus kit was used to isolate RNA, and cDNA was made with invitrogen superscriptase.'; [Cell type]'Source: ''cell line: MDA-MB231; lentiviral vector transduction: control shRNA (shscramble); genotype/variation: control; ', 'cell line: MDA-MB231; lentiviral vector transduction: shco2 shRNA targeting Coco; genotype/variation: Coco knock down; ', 'cell line: MDA-MB231; lentiviral vector transduction: shco4 shRNA targeting Coco; genotype/variation: Coco knock down; ' GSE75946 Mus musculus 6 Expression profiling by high throughput sequencing GPL13112 Proteolysis - hallmark of tumor-initiating cells in polyoma-middle-T-oncogene induced murine mammary carcinomas. 2015-12-11 Tumor initiating cells (TIC) have been identified and functionally characterized in hematological malignancies as well as in solid tumors such as breast cancer. In addition to their high tumor-initiating potency, TICs are important for metastasis formation and involved in chemotherapy resistance. Here we explored the molecular pathways that enable the tumor initiating potential of a cancer cell subset of the transgenic MMTV-PyMT mouse model for metastasizing breast cancer. The cell population, characterized by the marker profile CD24+CD90+CD45-, revealed a high tumorigenicity compared to CD24-CD90- cancer cells in colony formation assays as well as upon orthotopic transplantation into the mammary fad pad of mice. In addition, these orthotropically grown CD24+CD90+ TICs metastasized to the lungs. Upon cell sorting from primary tumors the transcriptome of TICs was compared with that of CD24-CD90- cancer cells by RNAseq. In addition to more established TIC signatures, such as epithelial-to-mesenchymal transition or mitogen signaling, an upregulated gene set comprising several classes of proteolytic enzymes was uncovered in CD24+CD90+TICs. Accordingly, TICs showed a high intra- and extracellular proteolytic activity. Application of a broad range of protease inhibitors to TICs in a colony formation assay reduced anchorage independent growth and had an impact on the colony morphology in 3D cell culture assays. Proteases have been frequently implicated in tumor growth and progression by shaping the extracellular environment and liberating growth factors, cytokines and chemokines. We conclude that CD24+CD90+ cells of the MMTV- PyMT mouse model possess an upregulated proteolytic signature that is likely to represent a functional hallmark of metastatic TICs of mammary carcinomas. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE75946 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA305759 https://www.ebi.ac.uk/ena/browser/view/PRJNA305759 https://www.ncbi.nlm.nih.gov/sra?term=SRP067282 [Overal design]The transcriptome of TICs was compared with that of CD24-CD90- cancer cells by RNAseq.; [Treatment]'None'; [Growth]'None'; [Extraction]'Primary sorted breast cancer cells were collected via FACS sorting and RNA was isolated using the RNA Nanoprep kit (Agilent Technologies). RNA quality was assessed using the Agilent Bioanalyzer 2100. 120ng of total RNA per sample was used for the construction of the sequencing libraries\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'breast cancer cell''strain: FVB/N-TgN(MMTVPyVT)634Mul/J; tissue: Breast; cell type: breast cancer cell; ' GSE50109 Homo sapiens 74 Protein profiling by protein array GPL15317; GPL15318; GPL15319; GPL17612; GPL17613; GPL17812 Targeted inhibition of three human breast cancer cell lines as model systems of ERBB2-positive breast cancer 2013-08-22 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50109 Boolean ErbB network reconstructions and perturbation simulations reveal individual drug response in different breast cancer cell lines. BMC systems biology 2.048 https://doi.org/10.1186/1752-0509-8-75 {BMC systems biology (2.048): 10.1186/1752-0509-8-75} 'protein' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA216087 https://www.ebi.ac.uk/ena/browser/view/PRJNA216087 None [Overal design]Refer to individual Series; [Treatment]'The inhibitors trastuzumab (10 ng/µL), pertuzumab (10 ng/µL), and erlotinib (1 µM) (Roche, Penzberg, Germany) were added to cells in starvation medium either alone or in combinations 1 h prior to stimulation with EGF or HRG (5 nM) for 0, 4, 8, 12, 16, 20, 30, 40, 50 and 60 min. After stimulation, medium was removed and ice-cold PBS was added to the plates.', 'The inhibitors trastuzumab (10\xa0ng/µL), pertuzumab (10\xa0ng/µL), and erlotinib (1\xa0µM) (Roche, Penzberg, Germany) were added to cells in full growth medium either alone (erlotinib) or in combinations. After inhibition medium was removed and ice-cold PBS was added to the plates.', 'The inhibitors trastuzumab (10\xa0ng/µL), pertuzumab (10\xa0ng/µL), and erlotinib (1\xa0µM) (Roche, Penzberg, Germany) were added to cells in starvation medium either alone or in combinations 1\xa0h prior to stimulation with EGF or HRG (5\xa0nM) for 0, 4, 8, 12, 16, 20, 30, 40, 50 and 60 min. After stimulation, medium was removed and ice-cold PBS was added to the plates.', 'The inhibitors trastuzumab (10 ng/µL), pertuzumab (10 ng/µL), and erlotinib (1 µM) (Roche, Penzberg, Germany) were added to cells in full growth medium either alone (erlotinib) or in combinations. After inhibition medium was removed and ice-cold PBS was added to the plates.'; [Growth]'Cells were seeded in 6-well plates, cultivated for 24h, and serum-starved for additional 24h.', 'Cells were seeded in 6-well plates, cultivated for 24h prior to addition of the inhibitors.', 'Cells were seeded in 6-well plates and serum-starved for 24h.'; [Extraction]'Medium was replaced by ice-cold PBS, transferred on ice, and cells were harvested manually by scraping in M-PER lysis buffer (Pierce, Bonn, Germany) containing protease inhibitor Complete Mini and phosphatase inhibitor PhosSTOP (Roche, Mannheim, Germany). Cells were lyzed for 20\xa0min on an end-over-end shaker and lysates were cleared at 16,000\xa0x\xa0g by centrifugation.', 'Medium was replaced by ice-cold PBS, transferred on ice, and cells were harvested by scraping in M-PER lysis buffer (Pierce, Bonn, Germany) containing protease inhibitor Complete Mini and phosphatase inhibitor PhosSTOP (Roche, Mannheim, Germany). Cells were lyzed for 20 min on an end-over-end shaker and lysates were cleared at 13,000 rpm for 10 min by centrifugation.', 'Medium was replaced by ice-cold PBS, transferred on ice, and cells were harvested manually by scraping in M-PER lysis buffer (Pierce, Bonn, Germany) containing protease inhibitor Complete Mini and phosphatase inhibitor PhosSTOP (Roche, Mannheim, Germany). Cells were lyzed for 20 min on an end-over-end shaker and lysates were cleared at 16,000 x g by centrifugation.'; [Cell type]'Source: ''protein target: phospho-ERK1/2; phospho site: T202Y204; antibody id: CST 4370; ', 'protein target: phospho-AKT; phospho site: S473; antibody id: CST 9271; ', 'protein target: phospho-RPS6; phospho site: S235/236; antibody id: CST 4858; ', 'protein target: phospho-RB; phospho site: S807/811; antibody id: CST 9308; ', 'protein target: phospho-ERK1/2; phospho site: T202Y204; antibody id: CST 9106, 4370; ', 'protein target: phospho-p70S6K; phospho site: T389; antibody id: CST 9206; ', 'protein target: phospho-RB; phospho site: S807S811; antibody id: CST 9308; ', 'protein target: phospho-RPS6; phospho site: S235S236; antibody id: CST 4858; ', 'protein target: phospho-ERBB1; phospho site: Y1086; antibody id: CST 2220; ', 'protein target: phospho-ERBB2; phospho site: Y1221Y1222; antibody id: CST 2243; ', 'protein target: phospho-MEK1/2; phospho site: S217S221; antibody id: Sigma M7683; ', 'protein target: phospho-PLCgamma; phospho site: S1248; antibody id: CST 4510; ', 'protein target: phospho-PKCalpha; phospho site: S657Y658, S657; antibody id: Abcam ab23513, Millipore 06-822; ', 'protein target: phospho-mTOR; phospho site: S2481; antibody id: Millipore 09-343; ', 'protein target: phospho-ERBB3; phospho site: Y1289; antibody id: CST 4791; ', 'protein target: phospho-ERBB1; phospho site: Y1068; antibody id: CST 2236; ', 'protein target: phospho-ERBB2; phospho site: Y1248; antibody id: Millipore 06-229; ', 'protein target: phospho-PKCalpha; phospho site: S657Y658; antibody id: Abcam ab23513; ', 'protein target: phospho-mTOR; phospho site: S2448; antibody id: CST 2971; ', 'protein target: phospho-PDK1; phospho site: S241; antibody id: CST 3438; ', 'protein target: total-BAX; phospho site: none; antibody id: CST 2772; ', 'protein target: phospho-cJUN; phospho site: S63; antibody id: BD 558036; ', 'protein target: phospho-cRAF; phospho site: S338; antibody id: CST 9427; ', 'protein target: total-CyclinB1; phospho site: none; antibody id: DLN 09016; ', 'protein target: total-CyclinD1; phospho site: none; antibody id: CST 2922; ', 'protein target: phospho-ERBB1; phospho site: Y1173; antibody id: CST 4407; ', 'protein target: phospho-FoxO1/3a; phospho site: T24T32; antibody id: CST 9464; ', 'protein target: phospho-GSK3alpha/beta; phospho site: Y279Y216; antibody id: Epitomics 2309-1; ', 'protein target: phospho-NFkB; phospho site: S536; antibody id: CST 3033; ', 'protein target: phospho-p38; phospho site: T180Y182; antibody id: CST 9211; ', 'protein target: total-p53; phospho site: none; antibody id: SC 126; ', 'protein target: phospho-PRAS; phospho site: T246; antibody id: CST 2997; ', 'protein target: total-PTEN; phospho site: none; antibody id: CST 9552; ', 'protein target: phospho-TSC2; phospho site: T1462; antibody id: CST 3617; ' GSE97326 Homo sapiens 110 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL18573 Resetting the Epigenetic Balance of Polycomb/COMPASS Function at Enhancers for Cancer Therapy 2017-04-03 MLL3/KMT2C is a COMPASS family member and tumor suppressor that functions as a histone H3K4 mono-methyltransferase at enhancers. Human cancer genome sequencing studies have identified frequent MLL3 point mutations, however, the question of how these mutations alter MLL3 function and contribute to oncogenesis remains unanswered. Here, we have characterized a cancer mutational hot spot in the MLL3 Plant Homeo Domain (PHD) repeats that correlates with poor patient survival. Cancer-associated mutations in the MLL3-PHD disrupt interaction with the BAP1 deubiquitinase complex. BAP1 loss-of-function in cancer cells significantly reduces MLL3 recruitment to enhancers regions, resulting in reduced H3K4me1 and increased H3K27me3 levels at these loci. Notably, we find that increased H3K27me3 levels in BAP1 null cells are due to decreased MLL3/UTX/COMPASS occupancy. Reducing H3K27me3 through PRC2 catalytic inhibition resets the pattern of gene expression in cells with defective MLL3- BAP1-UTX activity and impairs tumor proliferation in cancer cells with MLL3 mutations. This study provides a molecular mechanism to explain the role of MLL3 PHD mutations in cancer pathogenesis. Therefore, based on these observations, we propose a potential therapeutic strategy for cancers harboring MLL3/COMPASS mutations by resetting the Polycomb/COMPASS epigenetic balanced state of gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE97326 Resetting the epigenetic balance of Polycomb and COMPASS function at enhancers for cancer therapy. Nature medicine 30.641 https://doi.org/10.1038/s41591-018-0034-6 {Nature medicine (30.641): 10.1038/s41591-018-0034-6} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA381421 https://www.ebi.ac.uk/ena/browser/view/PRJNA381421 https://www.ncbi.nlm.nih.gov/sra?term=SRP108473 [Overal design]To examine changes in histone modification and gene expression after depletion of MLL3/BAP1/UTX or EZH2 inhibition in human cell lines.; [Treatment]'None'; [Growth]'Cell medium was composed as follow: DMEM 1X (Thermo Fisher), 10% serum (Corning), 1X glutamine (Life Technologies), 1X penicillin/streptomycin (Life Technologies), cells were grown in a CO2 incubator (5% CO2) at 37˚C', 'Cell medium was composed as follows: DMEM 1X (Thermo Fisher), 10% serum (Corning), 1X glutamine (Life Technologies), 1X penicillin/streptomycin (Life Technologies), cells were grown in a CO2 incubator (5% CO2) at 37˚C'; [Extraction]'RNA was extracted using QIAGEN RNeasy kit. DNA after ChIP protocol was isolated using QIAGEN PCR purification kit.\nChIP-sequencing libraries were prepared using the KAPA HTP Library Preparation Kit complemented with NEXTflex DNA Barcodes from Bioo Scientific. 10 ng of DNA was used as starting material for input and ip samples. Libraries were amplified using 13 cycles on the thermocycler. Post amplification libraries were size selected at 250- 450bp in length using Agencourt AMPure XP beads from Beckman Coulter. Libraries were validated using the Agilent High Sensitivity DNA Kit. RNA-sequencing libraries were prepared using the Illumina TruSeq Stranded Total RNA Preparation Kit with Ribo-Depletion. Input RNA quality was validated using the Agilent RNA 6000 Nano Kit. 200ng-1 µg of total RNA was used as starting material. Libraries were validated using the Agilent DNA 1000 Kit'; [Cell type]'breast cancer cell', 'Kidney cell line', 'Kidney cell''cell type: breast cancer cell; passages: Low passages (6-10); sample type: BAP1_FL_CAL51_BAP1_KO_R1; chip antibody: BAP1_FL (homemade); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: BAP1_FL_CAL51_BAP1_KO_R2; chip antibody: BAP1_FL (homemade); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: BAP1_FL_CAL51_BAP1_WT_R1; chip antibody: BAP1_FL (homemade); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: BAP1_FL_CAL51_BAP1_WT_R2; chip antibody: BAP1_FL (homemade); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: BAP1_NTD_CAL51_BAP1_KO; chip antibody: BAP1_NTD (homemade); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: BAP1_NTD_CAL51_BAP1_WT; chip antibody: BAP1_NTD (homemade); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_BAP1_KO_R1; genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_BAP1_KO_R2; genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_BAP1_WT_R1; genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_BAP1_WT_R2; genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_H3K27Ac; chip antibody: H3K27Ac (CST); ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_H3K4me1; chip antibody: H3K4me1 (homemade); ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_H3K4me3; chip antibody: H3K4me3 (homemade); ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_MLL3_KO_Clone1_R1; genotype/variation: MLL3 deletion Clone1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_MLL3_KO_Clone1_R2; genotype/variation: MLL3 deletion Clone1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_MLL3_KO_Clone2_R1; genotype/variation: MLL3 deletion Clone2; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_MLL3_KO_Clone2_R2; genotype/variation: MLL3 deletion Clone2; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_MLL3_KO_Clone3_R1; genotype/variation: MLL3 deletion Clone3; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_MLL3_KO_Clone3_R2; genotype/variation: MLL3 deletion Clone3; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_MLL3_WT_R1; genotype/variation: wild type MLL3; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_MLL3_WT_R2; genotype/variation: wild type MLL3; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_Pol II; chip antibody: Pol II (CST); ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_UTX_KO_R1; genotype/variation: UTX deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_UTX_KO_R2; genotype/variation: UTX deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_UTX_WT_R1; genotype/variation: wild type UTX; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_UTX_WT_R2; genotype/variation: wild type UTX; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H2AUb_CAL51_BAP1_KO_R1; chip antibody: H2AK119Ub (CST); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H2AUb_CAL51_BAP1_KO_R2; chip antibody: H2AK119Ub (CST); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H2AUb_CAL51_BAP1_WT_R1; chip antibody: H2AK119Ub (CST); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H2AUb_CAL51_BAP1_WT_R2; chip antibody: H2AK119Ub (CST); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H3K27me3_CAL51_BAP1_KO_R1; chip antibody: H3K27me3 (CST); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H3K27me3_CAL51_BAP1_KO_R2; chip antibody: H3K27me3 (CST); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H3K27me3_CAL51_BAP1_WT_R1; chip antibody: H3K27me3 (CST); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H3K27me3_CAL51_BAP1_WT_R2; chip antibody: H3K27me3 (CST); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H3K27me3_CAL51_UTX_KO; chip antibody: H3K27me3 (CST); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H3K27me3_CAL51_UTX_WT; chip antibody: H3K27me3 (CST); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H3K4me1_CAL51_BAP1_KO; chip antibody: H3K4me1 (homemade); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H3K4me1_CAL51_BAP1_WT; chip antibody: H3K4me1 (homemade); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H3K4me3_CAL51_BAP1_KO; chip antibody: H3K4me3 (homemade); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: H3K4me3_CAL51_BAP1_WT; chip antibody: H3K4me3 (homemade); genotype/variation: wild type BAP1; ', 'cell type: Kidney cell line; passages: Low passages (6-10); sample type: HEK293T_BAP1_KO_Clone46_R1; genotype/variation: BAP1 deletion; ', 'cell type: Kidney cell line; passages: Low passages (6-10); sample type: HEK293T_BAP1_KO_Clone53_R1; genotype/variation: BAP1 deletion; ', 'cell type: Kidney cell line; passages: Low passages (6-10); sample type: HEK293T_BAP1_WT; genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: Input_CAL51; antibody: none; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: Input_CAL51_BAP1_KO; antibody: none; genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: Input_CAL51_BAP1_WT; antibody: none; genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); cell line: MCF7; treatment: BAP1 shRNA-1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); cell line: MCF7; treatment: BAP1 shRNA-2; ', 'cell type: breast cancer cell; passages: Low passages (6-10); cell line: MCF7; treatment: luciferase shRNA; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: MLL3_CAL51_BAP1_KO_R1; chip antibody: MLL3_MR (homemade); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: MLL3_CAL51_BAP1_KO_R2; chip antibody: MLL3_MR (homemade); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: MLL3_CAL51_BAP1_WT_R1; chip antibody: MLL3_MR (homemade); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: MLL3_CAL51_BAP1_WT_R2; chip antibody: MLL3_MR (homemade); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: Suz12_CAL51_BAP1_KO; chip antibody: Suz12(CST); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: Suz12_CAL51_BAP1_WT; chip antibody: Suz12(CST); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: UTX_CAL51_BAP1_KO_R1; chip antibody: UTX (homemade); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: UTX_CAL51_BAP1_KO_R2; chip antibody: UTX (homemade); genotype/variation: BAP1 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: UTX_CAL51_BAP1_WT_R1; chip antibody: UTX (homemade); genotype/variation: wild type BAP1; ', 'cell type: breast cancer cell; passages: Low passages (6-10); sample type: UTX_CAL51_BAP1_WT_R2; chip antibody: UTX (homemade); genotype/variation: wild type BAP1; ', 'cell line: 293T; cell type: Kidney cell; passages: Low passages (6-10); sample type: 293T-G368V-KI-Rep1; genotype/variation: G368V-KI; ', 'cell line: 293T; cell type: Kidney cell; passages: Low passages (6-10); sample type: 293T-G368V-KI-Rep2; genotype/variation: G368V-KI; ', 'cell line: 293T; cell type: Kidney cell; passages: Low passages (6-10); sample type: 293T-W383L-KI-Rep1; genotype/variation: W383L-KI; ', 'cell line: 293T; cell type: Kidney cell; passages: Low passages (6-10); sample type: 293T-W383L-KI-Rep2; genotype/variation: W383L-KI; ', 'cell line: 293T; cell type: Kidney cell; passages: Low passages (6-10); sample type: 293T-WT-Rep1; genotype/variation: WT; ', 'cell line: 293T; cell type: Kidney cell; passages: Low passages (6-10); sample type: 293T-WT-Rep2; genotype/variation: WT; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_MLL3_Exon8_KO_Rep1; genotype/variation: MLL3_Exon8_KO; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_MLL3_Exon8_KO_Rep2; genotype/variation: MLL3_Exon8_KO; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_MLL3_Exon8_WT_Rep1; genotype/variation: MLL3_Exon8_WT; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: CAL51_MLL3_Exon8_WT_Rep2; genotype/variation: MLL3_Exon8_WT; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: H3K4me1_CAL51_MLL3_KO; chip antibody: H3K4me1 (homemade); genotype/variation: MLL3_KO; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: H3K4me1_CAL51_MLL3_WT; chip antibody: H3K4me1 (homemade); genotype/variation: MLL3_WT; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: Input_CAL51_MLL3_Exon8_KO; chip antibody: none; genotype/variation: MLL3_Exon8_KO; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: Input_CAL51_MLL3_KO; chip antibody: none; genotype/variation: MLL3_KO; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: Input_CAL51_MLL3_WT; chip antibody: none; genotype/variation: MLL3_WT; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: Input_CAL51_UTX_KO; chip antibody: none; genotype/variation: UTX_KO; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: Input_CAL51_UTX_WT; chip antibody: none; genotype/variation: UTX_WT; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: MLL3_CAL51_MLL3_Exon8_KO; chip antibody: MLL3_MR (homemade); genotype/variation: MLL3_Exon8_KO; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: UTX_CAL51_UTX_KO; chip antibody: UTX (homemade); genotype/variation: UTX_KO; ', 'cell line: CAL51; cell type: breast cancer cell; passages: Low passages (6-10); sample type: UTX_CAL51_UTX_WT; chip antibody: UTX (homemade); genotype/variation: UTX_WT; ', 'cell type: breast cancer cell; passages: Low passages (6-10); chip antibody: H3K27me3 (homemade); cell line: CAL51; genotype/variation: wild type MLL3; ', 'cell type: breast cancer cell; passages: Low passages (6-10); chip antibody: H3K27me3 (homemade); cell line: CAL51; genotype/variation: MLL3 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); chip antibody: H3K27me3 (homemade); drug treatment: DMSO; cell line: CAL51; genotype/variation: MLL3 deletion; ', 'cell type: breast cancer cell; passages: Low passages (6-10); chip antibody: H3K27me3 (homemade); drug treatment: GSK126; cell line: CAL51; genotype/variation: MLL3 deletion; ', 'cell type: Kidney cell line; passages: Low passages (6-10); chip antibody: H3K27me3 (homemade); cell line: HEK293T; genotype/variation: wild type MLL3; ', 'cell type: Kidney cell line; passages: Low passages (6-10); chip antibody: H3K27me3 (homemade); cell line: HEK293T; genotype/variation: MLL3 G368V mutation; ', 'cell type: Kidney cell line; passages: Low passages (6-10); chip antibody: H3K27me3 (homemade); cell line: HEK293T; genotype/variation: MLL3 W383L mutation; ', 'cell type: Kidney cell line; passages: Low passages (6-10); cell line: HEK293T; genotype/variation: wild type MLL3; ', 'cell type: Kidney cell line; passages: Low passages (6-10); cell line: HEK293T; genotype/variation: MLL3 depletion; ', 'cell type: Kidney cell line; passages: Low passages (6-10); cell line: HEK293T; genotype/variation: MLL3 G368V mutation; ', 'cell type: Kidney cell line; passages: Low passages (6-10); cell line: HEK293T; genotype/variation: MLL3 W383L mutation; ' GSE161762 Homo sapiens 30 Expression profiling by high throughput sequencing GPL16791 Persistent inflammatory stimulation drives the transition of MSCs to inflammatory CAFs that promote pro-metastatic characteristics in breast cancer cells 2020-11-18 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE161762 Persistent Inflammatory Stimulation Drives the Conversion of MSCs to Inflammatory CAFs That Promote Pro-Metastatic Characteristics in Breast Cancer Cells. Cancers 6.162 https://doi.org/10.3390/cancers13061472 {Cancers (6.162): 10.3390/cancers13061472} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA679307 https://www.ebi.ac.uk/ena/browser/view/PRJNA679307 None [Overal design]Refer to individual Series; [Treatment]'Samples were either treated with IL1 and TNFa or untreated controls', 'Samples were treated with either IL1β, TNFa, IL1β+TNFa or remained untreated, for duration of 2 days or 14 days in MEM alpha medium'; [Growth]'Human primary BM-derived MSCs were kept in culture for up to 9 passages. The cells were grown in mesenchymal stem cells growth medium.'; [Extraction]'Total RNA was isolated using Qiagen miRNeasy Mini Kit\n500ng of total RNA were fragmented followed by reverse transcription and second strand cDNA synthesis. The double strand cDNA was subjected to end repair, A base addition, adapter ligation and PCR amplification to create libraries'; [Cell type]'primary bone marrow-derived MSCs''cell type: primary bone marrow-derived MSCs; tissue: Bone marrow; treatment: untreated; ', 'cell type: primary bone marrow-derived MSCs; tissue: Bone marrow; treatment: treated with IL1 and TNF; ', 'cell type: primary bone marrow-derived MSCs; tissue: Bone marrow; treatment: treated with IL1 for 2 days; ', 'cell type: primary bone marrow-derived MSCs; tissue: Bone marrow; treatment: treated with TNF for 2 days; ', 'cell type: primary bone marrow-derived MSCs; tissue: Bone marrow; treatment: treated with IL1 and TNF for 2 days; ', 'cell type: primary bone marrow-derived MSCs; tissue: Bone marrow; treatment: treated with IL1 for 14 days; ', 'cell type: primary bone marrow-derived MSCs; tissue: Bone marrow; treatment: treated with TNF for 14 days; ', 'cell type: primary bone marrow-derived MSCs; tissue: Bone marrow; treatment: treated with IL1 and TNF for 14 days; ' GSE36771 Homo sapiens 107 Expression profiling by array GPL570 Expression data from primary breast tumors (Auckland) 2012-03-23 Frozen tissue specimens from primary breast tumors were collected and profiled using Affymetrix U133 plus 2 expression microarrays. A publication describing the generation of these data is not yet available. However, these data can be used alongside other Affymetrix breast tumour data sets to form large meta-cohorts for breast cancer research, as was done in Lasham et. al. J Natl Cancer Inst. 2012 Jan 18;104(2):133-146. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36771 Cyclin E2 overexpression is associated with endocrine resistance but not insensitivity to CDK2 inhibition in human breast cancer cells. Molecular cancer therapeutics 4.856 https://doi.org/10.1158/1535-7163.MCT-11-0963 {Molecular cancer therapeutics (4.856): 10.1158/1535-7163.MCT-11-0963} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA156847 https://www.ebi.ac.uk/ena/browser/view/PRJNA156847 None [Overal design]Frozen tumor tissues comprising of >60% tumor cellularity were extracted for total RNA and hybridized on Affymetrix microarrays.; [Treatment]'None'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''tumour histological grade: G3; estrogen receptor status: ER+; progesterone receptor status: PgR-; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G3; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G3; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G3; estrogen receptor status: ER-; progesterone receptor status: PgR-; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G3; estrogen receptor status: ER-; progesterone receptor status: PgR-; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G3; estrogen receptor status: ER+; progesterone receptor status: PgR-; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER+; progesterone receptor status: NA; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G1; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G1; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER-; progesterone receptor status: PgR-; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER+; progesterone receptor status: PgR+; lymph node metastasis: N/A; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER+; progesterone receptor status: PgR-; lymph node metastasis: LN-; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G3; estrogen receptor status: ER-; progesterone receptor status: PgR-; lymph node metastasis: N/A; tissue: primary breast tumor; disease state: breast cancer; ', 'tumour histological grade: G2; estrogen receptor status: ER+; progesterone receptor status: PgR-; lymph node metastasis: LN+; tissue: primary breast tumor; disease state: breast cancer; ' GSE14753 Mus musculus 6 Expression profiling by array GPL1261 Mammary tumors from K14-cre; ApcCKO/+ mice vs control mammary glands 2009-02-09 Many components of Wnt/β-catenin signaling pathway also play critical roles in mammary tumor development. To study the role of Apc in mammary tumorigensis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-Cre (progenitor) and WAP-cre (lactaing luminal) transgenic mice. Only the K14-cre mediated Apc heterozygosity developed mammary adenocarcinomas demonstrating histological and molecular heterogeneity, suggesting the progenitor cell origin of these tumors. These tumors harbored truncation mutation in a very defined region in the remaining wild-type allele of Apc that would retain some down-regulating activity of β-catenin signaling. Our results suggest that not only the epithelial origin but also a certain Apc mutations are selected to achieve a specific level of β-catenin signaling optimal for mammary tumor development. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE14753 Genetic mechanisms in Apc-mediated mammary tumorigenesis. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1000367 {PLoS genetics (5.224): 10.1371/journal.pgen.1000367} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA112245 https://www.ebi.ac.uk/ena/browser/view/PRJNA112245 None [Overal design]We have compared 3 mammary tumors from K14-cre; ApcCKO/+ mice with 3 control mammary glands.; [Treatment]'None'; [Growth]'None'; [Extraction]"RNA was extracted by homogenizing tumors and tissues in 3 ml Trizol reagent (Invitrogen). After phase separation, an equal volume of 70% ethanol was added to the aqueous phase and purified through PureLink Micro-to-Midi Total RNA Purification System (Invitrogen), following manufacturer's instruction."; [Cell type]'Source: ''' GSE169016 Homo sapiens 6 Expression profiling by high throughput sequencing GPL18573 Continuous inflammatory stimulation leads via metabolic plasticity to a pro-metastatic phenotype in triple-negative breast cancer cells I 2021-03-16 Chronic inflammation promotes cancer progression by affecting the tumor cells and their microenvironment. Here, we demonstrate that the continuous stimulation (6 weeks) of triple-negative breast tumor cells (TNBC) by the potent pro-inflammatory cytokines tumor necrosis factor α (TNFα) and interleukin 1β (IL-1β) had a robust effect on gene expression, demonstrating that the cancer cells have been skewed to strong pro-inflammatory phenotype. Moreover, continuous TNFα + IL-1β stimulation has reduced cell-to-cell contacts in the cancer cells and has induced metabolic plasticity in TNBC cells: this was exemplified by increase in active mitochondria area and elevations in the glycolytic as well as mitochondrial respiratory potential of the cancer cells (OXPHOS). Glycolysis has induced p65 activation and has led to increased transcription and expression of pro-metastatic chemokines such as CXCL8, CXCL1 and CCL2 and sICAM-1; agreeing with the ability of these chemokines to induce the recruitment of deleterious myeloid cells to tumors, mainly inhibition of glycolysis has given rise to reduced monocytic cell migration, in vitro and in vivo, in response to cancer cell supernatants obtained following continuous TNFα + IL-1β stimulation. Such inflammation-induced metabolic plasticity, which promotes metastatic cascades in TNBC, may have important clinical implications in the treatment of TNBC patients https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE169016 Continuous Inflammatory Stimulation Leads via Metabolic Plasticity to a Prometastatic Phenotype in Triple-Negative Breast Cancer Cells. Cells 5.656 https://doi.org/10.3390/cells10061356 {Cells (5.656): 10.3390/cells10061356} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA714905 https://www.ebi.ac.uk/ena/browser/view/PRJNA714905 https://www.ncbi.nlm.nih.gov/sra?term=SRP310883 [Overal design]To explore this important aspect of inflammation-driven effects on breast tumor cells, we chose to study the most aggressive subtype of breast cancer, namely triple-negative breast cancer (TNBC). The TNBC subtype account for 15-20% of breast cancer cases, demonstrating high degree of recurrence and poor survival [19-21]. In view of the large versatility of pro-metastatic functions demonstrated by TNBC cells, it was of major interest to determine if a continuous stimulation by TNFα + IL-1β will further potentiate some of these activities or even lead to acquisition of novel pro-metastatic capabilities by TNBC cells.; [Treatment]'TNBC cells were stimulated by 10ng/ml recombinant human (rh) TNFα (#300-01A, PeproTech, NJ, USA) and 0.4ng/ml rhIL-1β (#200-01B, PeproTech) for 6 weeks in the presence of the two cytokines together (replaced twice a week)'; [Growth]'cells were grown in DMEM (4,500 mg/liter glucose) media, supplemented with 10% fetal bovine serum (FBS), 2% L-glutamine and 1% penicillin-streptomycin solution'; [Extraction]'total RNA was isolated using miRNeasy Mini Kit (Cat# 217004; QIAGEN, Hilden, Germany) according to manufacturer’s protocols\nLibraries were prepared at the INCPM from the RNAs using in-house protocol.'; [Cell type]'Source: ''treatment: control; ', 'treatment: treatment; ' GSE30821 Homo sapiens 6 Expression profiling by array GPL6480 Integration of BRCA1-mediated miRNA and mRNA signatures reveal miR-146a, miR-99b and miR-205 regulation of the TRAF2 and NFkB pathways (mRNA dataset) 2011-07-20 BRCA1 deregulation is a frequent event in the pathogenesis of breast as well as other cancers. In addition to the DNA repair functions of BRCA1, it is involved in a wide range of cellular processes such as cell cycle, chromatin remodeling or transcription. However, the molecular events underlying BRCA1-associated tumorigenesis are still largely unknown. In order to deepen our understanding of BRCA1-associated tumorigenesis, we integrated data from mRNA and miRNA microarray experiments on the HCC1937 breast cancer cell line, and the isogenic HCC1937 stably expressing BRCA1, to obtain significant miRNA-mRNA relationships associated to the presence of the BRCA1 gene. Our results demonstrate that integration of mRNA and miRNA associated to BRCA1 expression was useful to discover new miRNA-gene interactions as molecular events underlying BRCA1-mediated tumorigenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE30821 Integration of BRCA1-mediated miRNA and mRNA profiles reveals microRNA regulation of TRAF2 and NFκB pathway. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-011-1905-4 {Breast cancer research and treatment (3.471): 10.1007/s10549-011-1905-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA154567 https://www.ebi.ac.uk/ena/browser/view/PRJNA154567 None [Overal design]Transcriptional profiling of the BRCA1-null HCC1937 cell line and HCC1937 cells after stable transfection of BRCA1. Two-condition experiment: Universal Human Reference RNA (Stratagene, catalog #740000) (Cy3) vs. cell line (Cy5). Biological replicates: 3 HCC1937, 3 BRCA1-transfected HCC1937 cells.; [Treatment]'None'; [Growth]'Cell lines were cultured in DMEM medium supplemented with 10%FBS, 0.08% Fungizone and 100units/mL penicillin/streptomycin, and maintained at 37ºC in 5% CO2.'; [Extraction]'Total RNA was extracted from cell lines using Trizol (Invitrogen) according to the instructions of the manufacturer.'; [Cell type]'Source: ', 'breast cancer cells''sample description: pool of total RNA from 10 human cell lines; ', 'cell line: BRCA1-transfected HCC1937; cell type: breast cancer cells; brca1 expression: yes; ', 'cell line: HCC1937; cell type: breast cancer cells; brca1 expression: no; ' GSE101961 Homo sapiens 121 Methylation profiling by genome tiling array GPL13534 Epigenome analysis of normal breast samples 2017-07-27 Despite known age-related DNA methylation (aDNAm) changes in breast tumors, little is known about aDNAm in normal breast tissues. Breast tissues from a cross-sectional study of 121 cancer-free women, were assayed for genome-wide DNA methylation. mRNA expression was assayed by microarray technology. Analysis of covariance was used to identify aDNAm’s. Altered methylation was correlated with expression of the corresponding gene and with DNA methyltransferase protein DNMT3A, assayed by immunohistochemistry. Publically-available TCGA data were used for replication. 1,214 aDNAm’s were identified; 97% with increased methylation, and all on autosomes. Sites with increased methylation were predominantly in CpG lslands and non-enhancers. aDNAm’s with decreased methylation were generally located in intergenic regions, non-CpG Islands, and enhancers. Of the aDNAm’s identified, 650 are known to be involved in cancer, including ESR1 and beta-estradiol responsive genes. Expression of DNMT3A was positively associated with age. Two aDNAm’s showed significant associations with DNMT3A expression; KRR1 (OR 6.57, 95% CI: 2.51-17.23) and DHRS12 (OR 6.08, 95% CI: 2.33-15.86). A subset of aDNAm’s co-localized within vulnerable regions for somatic mutations in breast cancer. Expression of C19orf48 was inversely and significantly correlated with its methylation level. In the TCGA dataset, 84% and 64% of the previously identified aDNAm’s were correlated with age in both normal-adjacent and tumor breast tissues, with differential associations by histological subtype. Given the similarity of findings in the breast tissues of healthy women and breast tumors, and the effects on gene expression, aDNAm’s may be one pathway for increased breast cancer risk with age. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE101961 Landscape of genome-wide age-related DNA methylation in breast tissue. Oncotarget None https://doi.org/10.18632/oncotarget.22754 {Oncotarget (None): 10.18632/oncotarget.22754} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA396020 https://www.ebi.ac.uk/ena/browser/view/PRJNA396020 None [Overal design]Bisulphite converted DNA from the 121 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchips; [Treatment]'None'; [Growth]'None'; [Extraction]'genomic DNA was extracted and purified from dissected frozen fresh breast tissues using MasterPure DNA purificationKit according to standard instructions (Epicenter, Madison, WI)'; [Cell type]'Source: ''age: 18; race: white; bmi: 22.71; ', 'age: 30; race: black; bmi: 31.01; ', 'age: 24; race: white; bmi: 20.80; ', 'age: 19; race: white; bmi: 39.85; ', 'age: 52; race: white; bmi: 28.83; ', 'age: 33; race: white; bmi: 31.00; ', 'age: 20; race: white; bmi: 25.84; ', 'age: 26; race: white; bmi: 30.89; ', 'age: 45; race: black; bmi: 31.00; ', 'age: 55; race: black; bmi: 31.74; ', 'age: 76; race: white; bmi: 37.70; ', 'age: 27; race: white; bmi: 42.76; ', 'age: 45; race: black; bmi: 41.01; ', 'age: 46; race: white; bmi: 28.90; ', 'age: 48; race: white; bmi: 28.34; ', 'age: 56; race: white; bmi: 44.12; ', 'age: 33; race: black; bmi: 32.12; ', 'age: 42; race: black; bmi: 31.61; ', 'age: 28; race: black; bmi: 39.30; ', 'age: 43; race: white; bmi: 25.74; ', 'age: 41; race: black; bmi: 39.93; ', 'age: 25; race: black; bmi: 33.45; ', 'age: 39; race: white; bmi: 23.08; ', 'age: 37; race: white; bmi: 25.79; ', 'age: 36; race: black; bmi: 35.02; ', 'age: 36; race: black; bmi: 29.05; ', 'age: 42; race: white; bmi: 23.17; ', 'age: 25; race: white; bmi: 20.78; ', 'age: 25; race: white; bmi: 36.02; ', 'age: 33; race: white; bmi: 21.25; ', 'age: 50; race: white; bmi: 23.63; ', 'age: 21; race: white; bmi: 29.95; ', 'age: 45; race: black; bmi: 24.80; ', 'age: 29; race: black; bmi: 26.15; ', 'age: 56; race: white; bmi: 23.43; ', 'age: 49; race: black; bmi: 28.24; ', 'age: 47; race: white; bmi: 28.52; ', 'age: 48; race: black; bmi: 34.33; ', 'age: 25; race: black; bmi: 28.13; ', 'age: 31; race: black; bmi: 33.45; ', 'age: 31; race: black; bmi: 39.22; ', 'age: 31; race: black; bmi: 32.69; ', 'age: 37; race: black; bmi: 39.93; ', 'age: 24; race: white; bmi: 22.96; ', 'age: 53; race: black; bmi: 36.31; ', 'age: 37; race: white; bmi: 20.59; ', 'age: 54; race: white; bmi: 25.29; ', 'age: 64; race: white; bmi: 30.22; ', 'age: 27; race: black; bmi: 25.69; ', 'age: 30; race: white; bmi: 30.18; ', 'age: 18; race: white; bmi: 26.52; ', 'age: 40; race: white; bmi: 24.80; ', 'age: 36; race: white; bmi: 28.91; ', 'age: 48; race: white; bmi: 21.45; ', 'age: 38; race: black; bmi: 42.13; ', 'age: 31; race: black; bmi: 35.42; ', 'age: 53; race: white; bmi: 25.40; ', 'age: 29; race: white; bmi: 22.80; ', 'age: 28; race: white; bmi: 33.65; ', 'age: 49; race: white; bmi: 32.19; ', 'age: 41; race: white; bmi: 26.14; ', 'age: 53; race: white; bmi: 25.39; ', 'age: 52; race: white; bmi: 26.92; ', 'age: 39; race: white; bmi: 21.77; ', 'age: 47; race: white; bmi: 26.63; ', 'age: 62; race: white; bmi: 30.23; ', 'age: 25; race: black; bmi: 33.20; ', 'age: 38; race: white; bmi: 45.48; ', 'age: 40; race: white; bmi: 25.24; ', 'age: 51; race: white; bmi: 23.69; ', 'age: 35; race: black; bmi: 31.01; ', 'age: 43; race: white; bmi: 27.46; ', 'age: 60; race: white; bmi: 27.29; ', 'age: 23; race: white; bmi: 28.24; ', 'age: 22; race: white; bmi: 23.96; ', 'age: 43; race: white; bmi: 25.70; ', 'age: 38; race: black; bmi: 31.30; ', 'age: 17; race: white; bmi: 25.68; ', 'age: 39; race: black; bmi: 29.18; ', 'age: 31; race: black; bmi: 28.66; ', 'age: 50; race: white; bmi: 27.44; ', 'age: 26; race: black; bmi: 43.40; ', 'age: 22; race: white; bmi: 29.05; ', 'age: 35; race: white; bmi: 34.33; ', 'age: 33; race: white; bmi: 38.26; ', 'age: 48; race: white; bmi: 31.31; ', 'age: 30; race: black; bmi: 34.21; ', 'age: 22; race: black; bmi: 41.97; ', 'age: 57; race: white; bmi: 28.53; ', 'age: 40; race: white; bmi: 38.45; ', 'age: 35; race: black; bmi: 33.28; ', 'age: 31; race: black; bmi: 33.12; ', 'age: 49; race: white; bmi: 25.82; ', 'age: 41; race: white; bmi: 28.89; ', 'age: 29; race: white; bmi: 25.85; ', 'age: 58; race: white; bmi: 29.45; ', 'age: 21; race: white; bmi: 25.29; ', 'age: 29; race: black; bmi: 30.66; ', 'age: 20; race: white; bmi: 23.69; ', 'age: 55; race: white; bmi: 27.25; ', 'age: 38; race: black; bmi: 33.32; ', 'age: 26; race: white; bmi: 23.67; ', 'age: 47; race: white; bmi: 21.58; ', 'age: 55; race: white; bmi: 25.82; ', 'age: 17; race: white; bmi: 22.59; ', 'age: 37; race: black; bmi: 37.76; ', 'age: 41; race: white; bmi: 22.96; ', 'age: 35; race: white; bmi: 36.31; ', 'age: 50; race: white; bmi: 27.45; ', 'age: 34; race: black; bmi: 33.65; ', 'age: 50; race: white; bmi: 30.66; ', 'age: 44; race: white; bmi: 23.99; ', 'age: 28; race: white; bmi: 24.89; ', 'age: 48; race: black; bmi: 25.74; ', 'age: 23; race: white; bmi: 24.20; ', 'age: 45; race: black; bmi: 43.26; ', 'age: 25; race: white; bmi: 30.23; ', 'age: 54; race: white; bmi: 28.90; ', 'age: 55; race: white; bmi: 21.08; ', 'age: 29; race: white; bmi: 29.95; ', 'age: 51; race: white; bmi: 29.70; ' GSE22937 Homo sapiens 16 Expression profiling by array GPL8444 An ESRP-regulated splicing program is abrogated during the Epithelial Mesenchymal Transition 2010-07-14 Alternative splicing achieves coordinated changes in post-transcriptional gene expression programs through the activities of diverse RNA binding proteins. Epithelial Splicing Regulatory Proteins 1 and 2 (ESRP1 and ESRP2) are cell type-specific regulators of transcripts that switch splicing during the Epithelial Mesenchymal Transition (EMT). To define a comprehensive program of alternative splicing that is regulated during the EMT, we identified an extensive ESRP-regulated splicing network of hundreds of alternative splicing events within numerous genes with roles in cell-cell adhesion, polarity, and migration. Loss of this global ESRP-regulated epithelial splicing program induces the phenotypic changes in cell morphology that are observed during the EMT. Components of this splicing signature provide novel molecular markers that can be used to characterize the EMT. Bioinformatics and experimental approaches revealed a high affinity ESRP binding motif and a predictive RNA map that governs their activity. This work establishes the ESRPs as coordinators of a complex alternative splicing network that adds an important post-transcriptional layer to the changes in gene expression that underlie epithelial-mesenchymal transitions during development and disease. Keywords: control / knockdown comparison and control / ectopic expression comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22937 An ESRP-regulated splicing programme is abrogated during the epithelial-mesenchymal transition. The EMBO journal 11.227 https://doi.org/10.1038/emboj.2010.195 {The EMBO journal (11.227): 10.1038/emboj.2010.195} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA127941 https://www.ebi.ac.uk/ena/browser/view/PRJNA127941 None [Overal design]siRNA knockdown of ESRP1 and ESRP2 in human prostate epithelial cells PNT2 and ectopic expression of mEsrp1 in human breast cancer cells MDA-MB-231 as described before (Warzecha et al., 2009, Molecular Cell 33:591 - 601). The efficiency of ESRP knockdown and ectopic expression was monitored by western blot using a monoclonal antibody which recognizes both proteins (Clone 23A7) prepared by Rockland Immunochemicals, Inc. (Gilbertsville, PA) using our GST-Esrp1 recombinant protein. We conducted HJAY exon and exon junction array profiling on RNAs from four siESRP1 + siESRP2 treated PNT2 samples vs. four siGFP treated PNT2 samples and four samples of MDA-MB-231 cells transduced with retrovirus expressing a cDNA for mEsrp1 vs. four samples of MDA-MB-231 cells transduced with retrovirus expressing a control empty vector.; [Treatment]'siRNA knockdown of ESRP1 and ESRP2 in human prostate epithelial cells PNT2 and ectopic expression of mEsrp1 in human breast cancer cells MDA-MB-231 as described before (Warzecha et al., 2009, Molecular Cell 33:591 - 601).'; [Growth]'PNT2 cells were grown in RPMI1640 media supplemented with 10% FBS (Thermo Scientific) and Glutamax (Invitrogen). MDA-MB-231 cells were grown in DMEM media supplemented with 10% FBS (Thermo Scientific), 10ug/ml Insulin (Sigma), and Glutamax (Invitrogen). Selection for expression of ectopic Esrp1 used 0.5 ug/ml Puromycin (Sigma).'; [Extraction]'Total RNA was collected from adherent tissue culture cells using Trizol (Invitrogen) according to the manufacturer’s instructions. RNA was quantified (A260) using a Nanodrop-1000 spectrophotometer (Nanodrop Technologies).'; [Cell type]'Source: ''cell line: PNT2; ', 'cell line: MDA-MB-231; ' GSE33776 Homo sapiens 2 Expression profiling by high throughput sequencing GPL9115 A novel post-translational mechanism controlling the oncogenic activity of c-Myc is enhanced in poor outcome breast cancer 2011-11-17 Examination of Pin1-regulated Myc target genes in a human breast epithelial cell line. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE33776 Pin1 regulates the dynamics of c-Myc DNA binding to facilitate target gene regulation and oncogenesis. Molecular and cellular biology 3.735 https://doi.org/10.1128/MCB.01455-12 {Molecular and cellular biology (3.735): 10.1128/MCB.01455-12} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA148595 https://www.ebi.ac.uk/ena/browser/view/PRJNA148595 https://www.ncbi.nlm.nih.gov/sra?term=SRP009374 [Overal design]Two samples: control GFP-expressing MCF10A-Myc cells and Pin1-expressing MCF10A-Myc cells.; [Treatment]'Cells were infected with AdGFP (control) or AdPin1 for 18 hrs and Myc was turned on in both with Doxycycline for 4 hrs before RNA extraction.'; [Growth]'Stable expression of Doxycycline-inducible c-Myc by lentiviral infection. Cells were grown to sub-confluence in DMEM/F12.'; [Extraction]'Total RNA was purified and reverse transcribed with oligo dT. Second strand DNA was synthesized and ligated to proprietary indexed adapters. Ligated material was amplified using Illumina genomic primers and sequenced on an Illumina GAII sequencer.'; [Cell type]'normal breast epithlial''cell type: normal breast epithlial; cell line: MCF10A-Myc; phenotype: GFP-expressing; ', 'cell type: normal breast epithlial; cell line: MCF10A-Myc; phenotype: Pin1-expressing; ' GSE107476 Homo sapiens 6 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Transition of breast cancer cells from luminal to basal-like phenotype engages a shift from genomic to non-genomic activities of estrogen receptor-alpha activity 2017-11-29 Estrogen receptor (ERα) is central in driving the development of hormone-dependent breast cancers. A major challenge in treating these cancers is to understand and struggle endocrine resistance. We have previously shown that the Megakaryoblastic Leukemia 1 (MKL1) protein, a master regulator of actin dynamic and cellular motile functions, directs down-regulation of ERα and hormonal escape of estrogen-responsive breast cancer cell lines. In the present study, we decipher the underlining mechanisms by tracking functional changes in ERα activity. We demonstrate through gene expression microarray analysis that the constitutive activation of MKL1 in ERα-positive MCF7 breast cancer cells induces a transition from a luminal to a basal-like phenotype and suppresses almost all regulations of gene expression by estrogen. Chromatin immunoprecipitation of DNA coupled to high-throughput sequencing (ChIP-Seq) shows a profound reprogramming in ERα cistrome associated with a massive loss of ERα binding sites (ERBSs) generally associated with lower ERα-binding activity. Novel ERBSs appear to be associated with EGF and RAS signaling pathways. ERα dynamic was further impacted by a displacement of its monomer/dimer equilibrium towards its monomer state, associated with a redistribution of the normally nuclear ERα protein to the entire cell volume. We next show that the combination of these remodeled dynamics of ERα alters its interactions with genomic and non-genomic partners. In particular, the formation of ERα/kinase complexes was promoted by the constitutive activation of MKL1. Hence, MKL1-induced transition of ER-positive breast cancer cells from luminal to basal-like phenotype shifts ERα activities from genomic to non-genomic function. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE107476 Nuclear accumulation of MKL1 in luminal breast cancer cells impairs genomic activity of ERα and is associated with endocrine resistance. Biochimica et biophysica acta. Gene regulatory mechanisms 4.599 https://doi.org/10.1016/j.bbagrm.2020.194507 {Biochimica et biophysica acta. Gene regulatory mechanisms (4.599): 10.1016/j.bbagrm.2020.194507} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA420212 https://www.ebi.ac.uk/ena/browser/view/PRJNA420212 https://www.ncbi.nlm.nih.gov/sra?term=SRP125813 [Overal design]Whole-genome analysis of estrogen receptor (ER) binding events in MCF-7 cells ectopically expressing a dominant form of the MKL1 protein and associated control cells.; [Treatment]'15.10E6 MCF-7 control or MCF-7 MKL1ΔN200 cells were cultivated for 48h in DMEM/10% serum followed by 3 days of culture in DMEM/2.5% charcoal-stripped serum (BioWest). Expression of the MKL1 ΔN200 transgene in MCF-7 MKL1D200 cells was induced 48h before the E2 treatment by adding Tetracycline (Sigma) at a final concentration of 1 microg/ml. Cells were treated for 50 minutes with 10-8M final estradiol and fixed for 10 min at room temperature in a PBS solution containing 1.5% formaldehyde (ACROS). After a 5 min quenching with 0.125M glycine, cells were washed twice in ice-cold PBS and collected in 1 ml of cold buffer (100 mM Tris-HCl [pH 9.4] and 100 mM DTT).'; [Growth]'Cells were maintained in DMEM (Gibco, Invitrogen)/10% FCS (BioWest) supplemented or not with selection antibiotics for integrated vectors ( 5 µg/ml blasticidin, 75 µg/ml Zeocin ).'; [Extraction]"Cells were and lysed for 10 min in ice in 300 µl of lysis buffer [10 mM EDTA, 50 mM Tris-HCl (pH 8.0), 0.1% SDS, 0.5% Empigen BB (Sigma)]. Crosslinked chromatin was sheared to an average size of 400 bp by sonication for 15 min with 30secs on/off cycles at full power in a BioRuptor apparatus (Diagenode). Following 10 minutes of centrifugation at 10,000 x g, 30 µl were kept as input fraction and the remainder diluted 5 fold in IP buffer (2 mM EDTA, 100 mM NaCl, 20 mM Tris-HCl [pH 8.1], and 0.5%Triton X-100) before proceeding to immunoprecipitation overnight at 4°C under rocking using 2 µg of antibodies and 5 µg of yeast tRNAs. Complexes were recovered after 3 hr incubation at 4°C with 5 µg of yeast tRNAs and 100 µl of a 50% protein A or protein G-Sepharose beads slurry (Amersham Pharmacia Biosciences). Precipitates were then serially washed, using 500 µl of Washing Buffers (WB) I [2 mM EDTA, 20 mM Tris-HCl (pH 8.1), 0.1% SDS, 1% Triton X-100, 150 mM NaCl], WB II [2 mM EDTA, 20 mM Tris-HCl (pH 8.1), 0.1% SDS, 1% Triton X-100, 500 mM NaCl], WB III [1 mM EDTA, 10 mM Tris-HCl (pH 8.1), 1% NP-40, 1% Deoxycholate, 0.25 M LiCl] and then twice with 1 mM EDTA, 10 mM Tris-HCl (pH 8.1). Precipitated complexes were removed from the beads through two sequential incubations of 10 min with 50 µl of 1% SDS, 0.1 M NaHCO3. Crosslink was reversed by an overnight incubation at 65°C with 50 µg of Proteinase K (Sigma). Following a subsequent incubation of the samples with 2.5 µg RNAse (Sigma) for 1h at 37°C, the DNA was then purified on NucleoSpin™ columns (Macherey-Nagel) using NTB buffer and eluted in 40 µl of elution buffer. Efficiency of the ChIP assay was evaluated using qPCR positive and negative controls before proceeding to subsequent steps. For each ChIP conditions, from 18 to 20 individually prepared samples were pooled and submitted for library preparation.\nLibraries were prepared according to Illumina's instructions by IGBMC sequencing facility (Strasbourg, France)"; [Cell type]'Source: ''cell line: MCF-7; integrated vectors: pcDNA6/TR and pcDNA4/TO, Invitrogen; hormone treatment: Ethanol (0.01% final); chip antibody: HC-20, sc-543, Santa Cruz Biotechnology; ', 'cell line: MCF-7; integrated vectors: pcDNA6/TR and pcDNA4/TO, Invitrogen; hormone treatment: 10-8M Estradiol (Sigma); chip antibody: HC-20, sc-543, Santa Cruz Biotechnology; ', 'cell line: MCF-7; integrated vectors: pcDNA6/TR and pcDNA4/TO -MKL1 deltaN200, Invitrogen; hormone treatment: Ethanol (0.01% final); chip antibody: HC-20, sc-543, Santa Cruz Biotechnology; ', 'cell line: MCF-7; integrated vectors: pcDNA6/TR and pcDNA4/TO -MKL1 deltaN200, Invitrogen; hormone treatment: 10-8M Estradiol (Sigma); chip antibody: HC-20, sc-543, Santa Cruz Biotechnology; ', 'cell line: MCF-7; integrated vectors: pcDNA6/TR and pcDNA4/TO, Invitrogen; hormone treatment: Ethanol (0.01% final); chip antibody: none; ', 'cell line: MCF-7; integrated vectors: pcDNA6/TR and pcDNA4/TO, Invitrogen; hormone treatment: 10-8M Estradiol (Sigma); chip antibody: none; ' GSE93662 Saccharomyces cerevisiae; Homo sapiens 62 Genome binding/occupancy profiling by high throughput sequencing GPL13821; GPL18573; GPL19756 Genome-wide determinants of sequence-specific DNA binding 2017-01-16 DNA binding protein are generally thought to bind specific DNA sequences through selective interactions with DNA bases. However, it is now becoming more widely appreciated that DNA shape, which may not be specified by a unique base sequence, also contributes to site-specific binding. Here we elucidate how DNA sequence and shape confer site specificity on a genomic scale, and relate this to specificity imparted indirectly through occlusion of sequences by the in vivo environment. For simplicity, we focus on the set of General Regulatory Factors (GRFs) that do not rely on other factors for binding. They also serve a related function in organizing chromatin. Remarkably, we find that GRFs will not bind to their cognate motif if the DNA surrounding that sequence lacks a specific shape. While proper DNA sequence/shape properties tend to be restricted to promoter regions, weaker sites that are still binding-competent reside in gene bodies, but are prevented from binding by resident chromatin. Thus, site-specificity is achieved across a genome in vivo by the combined action of favorable DNA sequence and shape interactions, and occlusion by chromatin. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93662 Genome-wide determinants of sequence-specific DNA binding of general regulatory factors. Genome research 9.944 https://doi.org/10.1101/gr.229518.117 {Genome research (9.944): 10.1101/gr.229518.117} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA361490 https://www.ebi.ac.uk/ena/browser/view/PRJNA361490 https://www.ncbi.nlm.nih.gov/sra?term=SRP096827 [Overal design]Genome-wide analysis of yeast general regulatory factors using an in vitro version of ChIP-exo; [Treatment]'For PB-exo and WhIP-exo, reactions were crosslinked with formaldehyde to a final concentration of 0.05%.\nFor ChIP-exo, cells were crosslinked with formaldehyde to a final concentration of 1.0%.\nFor Native PB-seq, reactions were not cross-linked'; [Growth]'For ChIP-exo, cells were grown to an O.D600 of 0.8 - 1.0 at 25°C.'; [Extraction]'For PB-exo, WhIP-exo, and Native PB-seq, lysates were clarified from sonicated genomic DNA and protein-DNA complexes were isolated with antibody.\nFor ChIP-exo, lysates were clarified from sonicated nuclei and protein-DNA complexes were isolated with IgG antibody.\nChIP-exo libraries were prepared for sequencing using standard SOLiD & Illumina protocols with a minor modification; Reference paper:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3813302/'; [Cell type]'Source: ''chip antibody: Abf1-TAP (Genescript A00683, Lot 12D000473); cell description: GRF88, MATa his4-38, S288C background; strain: BY4741; ', 'chip antibody: Abf1-TAP (Sigma i5006-100MG, Lot#SLBM2617V); cell description: GRF88, MATa his4-38, S288C background; strain: BY4741; ', 'chip antibody: Cbf1-TAP (Genescript A00683, Lot 12D000473); cell description: GRF88, MATa his4-38, S288C background; strain: BY4741; ', 'chip antibody: Cbf1-TAP (Sigma i5006-100MG, Lot#SLBM2617V); cell description: GRF88, MATa his4-38, S288C background; strain: BY4741; ', 'chip antibody: Mcm1-TAP (Genescript A00683, Lot 12D000473); cell description: GRF88, MATa his4-38, S288C background; strain: BY4741; ', 'chip antibody: Mcm1-TAP (Sigma i5006-100MG, Lot#SLBM2617V); cell description: GRF88, MATa his4-38, S288C background; strain: BY4741; ', 'chip antibody: Pho4-HA (Abcam ab9108, Lot#GR133543-5); cell description: GRF88, MATa his4-38, S288C background; strain: BY4741; ', 'chip antibody: Rap1-TAP (Genescript A00683, Lot 12D000473); cell description: GRF88, MATa his4-38, S288C background; strain: BY4741; ', 'chip antibody: Rap1-TAP (Sigma i5006-100MG, Lot#SLBM2617V); cell description: GRF88, MATa his4-38, S288C background; strain: BY4741; ', 'chip antibody: Rap1-TAP (Genescript A00683, Lot 12D000473); cell description: cell ine established from 69 year old female with breast cancer; strain: MCF7; ', 'chip antibody: Reb1-TAP (Sigma i5006-100MG, Lot#SLBM2617V); cell description: GRF88, MATa his4-38, S288C background; strain: BY4741; ', 'chip antibody: None specific antibody; cell description: GRF88, MATa his4-38, S288C background; strain: BY4741; ', 'chip antibody: Ume6-TAP (Sigma i5006-100MG, Lot#SLBM2617V); cell description: GRF88, MATa his4-38, S288C background; strain: BY4741; ' GSE27567 Mus musculus; Homo sapiens 255 Expression profiling by array GPL570; GPL1261 Integrating Factor Analysis and a Transgenic Mouse Model to Reveal a Peripheral Blood Predictor of Breast Tumors 2011-02-28 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE27567 Integrating factor analysis and a transgenic mouse model to reveal a peripheral blood predictor of breast tumors. BMC medical genomics 2.568 https://doi.org/10.1186/1755-8794-4-61 {BMC medical genomics (2.568): 10.1186/1755-8794-4-61} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA138405 https://www.ebi.ac.uk/ena/browser/view/PRJNA138405 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA from peripheral blood mononuclear cells was isolated using the Ambion Ribopure™-Blood kit (Ambion, Austin, TX).', 'Samples were collected using the submandibular (cheekpouch) method. Briefly, the vein that drains the face and cheek area was punctured by a lancet (GoldenRod animal lancet, MEDIpoint, Inc., Mineola, NY) and blood was captured in BD Microtainer™ tubes with potassium-EDTA anticoagulant (Becton Dickinson, Franklin Lakes, NJ). Tubes were immediately inverted 10-12 times and placed on ice.\nFollowing erythrocyte lysis, total RNA was isolated from the leukocyte pellet using the QIAamp RNA Blood Mini Kit (Qiagen, Valencia, CA). Alternatively, the leukocyte pellet was immediately lysed, homogenized and stored at -80°C. RNA was isolated at a later date using the protocol described above or the adapted protocol associated with the QIAamp RNA Blood Mini Kit for use in the QIAcube (Qiagen, Valencia, CA).'; [Cell type]'Source: ''phenotype: Normal; tissue: peripheral blood mononuclear cells; data set: training; ', 'phenotype: Malignant; tissue: peripheral blood mononuclear cells; data set: training; ', 'phenotype: Benign; tissue: peripheral blood mononuclear cells; data set: validation; ', 'phenotype: Ectopic; tissue: peripheral blood mononuclear cells; data set: validation; ', 'phenotype: Ectopic; tissue: peripheral blood leukocytes; data set: validation; ', 'phenotype: Normal; tissue: peripheral blood mononuclear cells; data set: validation; ', 'phenotype: Malignant; tissue: peripheral blood mononuclear cells; data set: validation; ', 'phenotype: Pre-Surgery (aka Malignant); tissue: peripheral blood mononuclear cells; data set: validation; ', 'phenotype: Post-Surgery; tissue: peripheral blood mononuclear cells; data set: validation; ', 'strain: FVB/NJ; genotype/variation: wild type; phenotype: tumor-free control; tissue: total white blood cells (WBCs); data set: training; ', 'strain: FVB/NJ; genotype/variation: MMTV/c-MYC transgenic; phenotype: tumor-bearing transgenic mouse; tissue: total white blood cells (WBCs); data set: training; ', 'strain: FVB/NJ; genotype/variation: wild type; phenotype: tumor-free control; tissue: total white blood cells (WBCs); data set: validation; ', 'strain: FVB/NJ; genotype/variation: MMTV/c-MYC transgenic; phenotype: tumor-bearing transgenic mouse; tissue: total white blood cells (WBCs); data set: validation; ' GSE24185 Homo sapiens 103 Expression profiling by array GPL96 Gene transcription signature of obesity in breast cancer 2010-09-17 Obesity is thought to contribute to worse disease outcome in breast cancer as a result of increased levels of adipocyte-secreted endocrine factors, insulin, and insulin-like growth factors (IGFs) that accelerate tumor cell proliferation and impair treatment response. We examined the effects of patient obesity on primary breast tumor gene expression, by profiling transcription of a set of tumors for which the patients’ body mass index (BMI) was ascertained. Sample profiles were stratified according to patients’ obesity phenotype defined as normal (BMI <25), overweight (BMI 25-29.9), or obese (BMI>30). Widespread alterations in gene expression were evident in breast tumors from obese patients as compared to tumors from other patients, allowing us to define an obesity-associated cancer transcriptional signature of 662 genes. Keywords: two group comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24185 A gene transcription signature of obesity in breast cancer. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-011-1595-y {Breast cancer research and treatment (3.471): 10.1007/s10549-011-1595-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA130113 https://www.ebi.ac.uk/ena/browser/view/PRJNA130113 None [Overal design]Primary breast tumor specimens were obtained from patients. Study volunteers completed questionnaires used to define historically normal (BMI<=24.9), overweight (BMI 25-29.9), or obese (BMI>=30) patient categories according to established WHO criteria.; [Treatment]'None'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''disease state: breast cancer; age: 44; race: w; menopause: PRE; bmi: 19.92; bmi status: normal; grade: 1/3; lymph: y; er: N; pr: N; her2: P; ', 'disease state: breast cancer; age: 45; race: w; menopause: PRE; bmi: 19.72; bmi status: normal; grade: 2/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 42; race: w; menopause: PRE; bmi: 23.74; bmi status: normal; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 33; race: w; menopause: PRE; bmi: 23.88; bmi status: normal; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 72; race: w; menopause: POST; bmi: 24.91; bmi status: normal; grade: 1/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 41; race: b; menopause: PRE; bmi: 24.06; bmi status: normal; grade: 1/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 38; race: a; menopause: PRE; bmi: 20.4; bmi status: normal; grade: 3/3; lymph: n; er: P; pr: P; her2: P; ', 'disease state: breast cancer; age: 41; race: a; menopause: PRE; bmi: 22.06; bmi status: normal; grade: 3/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 45; race: w; menopause: PERI; bmi: 24.45; bmi status: normal; grade: 2/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 57; race: a; menopause: POST; bmi: 24; bmi status: normal; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 49; race: w; menopause: PRE; bmi: 23.05; bmi status: normal; grade: 1/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 44; race: w; menopause: PRE; bmi: 22.27; bmi status: normal; grade: 2/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 38; race: w; menopause: PRE; bmi: 19.1; bmi status: normal; grade: 3/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 47; race: w; menopause: PRE; bmi: 23.34; bmi status: normal; grade: 2/3; lymph: n; er: N; pr: N; her2: P; ', 'disease state: breast cancer; age: 61; race: w; menopause: POST; bmi: 24.69; bmi status: normal; grade: 2/3; lymph: y; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 39; race: w; menopause: PRE; bmi: 24.06; bmi status: normal; grade: 1/3; lymph: n; er: P; pr: N; her2: U; ', 'disease state: breast cancer; age: 47; race: w; menopause: PRE; bmi: 23.83; bmi status: normal; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 38; race: w; menopause: PRE; bmi: 23.53; bmi status: normal; grade: 2/3; lymph: n; er: P; pr: U; her2: U; ', 'disease state: breast cancer; age: 50; race: w; menopause: POST; bmi: 23.71; bmi status: normal; grade: 2/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 55; race: w; menopause: POST; bmi: 22.76; bmi status: normal; grade: 1/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 54; race: w; menopause: POST; bmi: 22.41; bmi status: normal; grade: 3/3; lymph: n; er: N; pr: N; her2: U; ', 'disease state: breast cancer; age: 40; race: w; menopause: PRE; bmi: 22.58; bmi status: normal; grade: 3/3; lymph: y; er: N; pr: N; her2: U; ', 'disease state: breast cancer; age: 57; race: b; menopause: POST; bmi: 22.59; bmi status: normal; grade: 2/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 50; race: w; menopause: POST; bmi: 24.61; bmi status: normal; grade: 3/3; lymph: n; er: P; pr: P; her2: P; ', 'disease state: breast cancer; age: 63; race: w; menopause: POST; bmi: 21.64; bmi status: normal; grade: 1/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 32; race: w; menopause: PRE; bmi: 28.84; bmi status: normal; grade: 3/3; lymph: n; er: N; pr: N; her2: U; ', 'disease state: breast cancer; age: 42; race: w; menopause: PRE; bmi: 22.76; bmi status: normal; grade: 3/3; lymph: n; er: N; pr: N; her2: U; ', 'disease state: breast cancer; age: 61; race: w; menopause: POST; bmi: 21.64; bmi status: normal; grade: 3/3; lymph: n; er: U; pr: U; her2: U; ', 'disease state: breast cancer; age: 54; race: w; menopause: POST; bmi: 23.11; bmi status: normal; grade: 3/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 50; race: w; menopause: PRE; bmi: 24.17; bmi status: normal; grade: 2/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 40; race: w; menopause: PRE; bmi: 21.72; bmi status: normal; grade: 2/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 58; race: w; menopause: POST; bmi: 23.14; bmi status: normal; grade: 3/3; lymph: n; er: N; pr: N; her2: U; ', 'disease state: breast cancer; age: 62; race: w; menopause: POST; bmi: 21.26; bmi status: normal; grade: 2/3; lymph: n; er: N; pr: N; her2: U; ', 'disease state: breast cancer; age: 31; race: w; menopause: PRE; bmi: 20.28; bmi status: normal; grade: 2/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 57; race: w; menopause: POST; bmi: 24.92; bmi status: normal; grade: 3/3; lymph: n; er: P; pr: N; her2: U; ', 'disease state: breast cancer; age: 32; race: w; menopause: PRE; bmi: 24.02; bmi status: normal; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 45; race: w; menopause: PRE; bmi: 28.26; bmi status: overweight; grade: 3/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 39; race: w; menopause: PRE; bmi: 26.35; bmi status: overweight; grade: 2/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 43; race: w; menopause: PRE; bmi: 28.13; bmi status: overweight; grade: 3/3; lymph: y; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 49; race: w; menopause: POST; bmi: 26.99; bmi status: overweight; grade: 1/3; lymph: y; er: P; pr: N; her2: N; ', 'disease state: breast cancer; age: 46; race: w; menopause: PRE; bmi: 26.64; bmi status: overweight; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 46; race: w; menopause: PRE; bmi: 27.64; bmi status: overweight; grade: 3/3; lymph: y; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 59; race: b; menopause: POST; bmi: 25.85; bmi status: overweight; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 65; race: w; menopause: POST; bmi: 27.64; bmi status: overweight; grade: 2/3; lymph: y; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 37; race: w; menopause: PRE; bmi: 26.35; bmi status: overweight; grade: 2/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 58; race: w; menopause: POST; bmi: 27.92; bmi status: overweight; grade: 1/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 57; race: a; menopause: POST; bmi: 29.21; bmi status: overweight; grade: 3/3; lymph: n; er: N; pr: N; her2: P; ', 'disease state: breast cancer; age: 61; race: w; menopause: POST; bmi: 29.48; bmi status: overweight; grade: 2/3; lymph: n; er: P; pr: N; her2: N; ', 'disease state: breast cancer; age: 30; race: w; menopause: PRE; bmi: 27.18; bmi status: overweight; grade: 3/3; lymph: y; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 42; race: w; menopause: PRE; bmi: 25.59; bmi status: overweight; grade: 2/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 66; race: w; menopause: POST; bmi: 26.18; bmi status: overweight; grade: 1/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 48; race: w; menopause: PRE; bmi: 27.61; bmi status: overweight; grade: 1/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 58; race: w; menopause: POST; bmi: 28.25; bmi status: overweight; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 45; race: w; menopause: PRE; bmi: 27.34; bmi status: overweight; grade: 3/3; lymph: n; er: N; pr: N; her2: U; ', 'disease state: breast cancer; age: 57; race: a; menopause: POST; bmi: 29.86; bmi status: overweight; grade: 2/3; lymph: n; er: P; pr: N; her2: N; ', 'disease state: breast cancer; age: 48; race: w; menopause: POST; bmi: 27.1; bmi status: overweight; grade: 3/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 54; race: w; menopause: POST; bmi: 25.56; bmi status: overweight; grade: 3/3; lymph: n; er: P; pr: N; her2: U; ', 'disease state: breast cancer; age: 42; race: w; menopause: PRE; bmi: 25.81; bmi status: overweight; grade: 2/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 59; race: w; menopause: POST; bmi: 29; bmi status: overweight; grade: 2/3; lymph: n; er: N; pr: P; her2: U; ', 'disease state: breast cancer; age: 38; race: w; menopause: PRE; bmi: 27.34; bmi status: overweight; grade: 2/3; lymph: y; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 40; race: w; menopause: PRE; bmi: 29.75; bmi status: overweight; grade: 2/3; lymph: n; er: P; pr: U; her2: P; ', 'disease state: breast cancer; age: 62; race: a; menopause: POST; bmi: 29.82; bmi status: overweight; grade: 2/3; lymph: n; er: N; pr: N; her2: U; ', 'disease state: breast cancer; age: 44; race: w; menopause: PRE; bmi: 25.06; bmi status: overweight; grade: 3/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 51; race: w; menopause: POST; bmi: 25.34; bmi status: overweight; grade: 2/3; lymph: n; er: N; pr: N; her2: U; ', 'disease state: breast cancer; age: 47; race: a; menopause: PERI; bmi: 26.77; bmi status: overweight; grade: 3/3; lymph: n; er: U; pr: U; her2: U; ', 'disease state: breast cancer; age: 63; race: a; menopause: POST; bmi: 32.89; bmi status: obese; grade: 3/3; lymph: y; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 50; race: b; menopause: PRE; bmi: 37.25; bmi status: obese; grade: 2/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 50; race: b; menopause: POST; bmi: 30.82; bmi status: obese; grade: 2/3; lymph: n; er: P; pr: N; her2: P; ', 'disease state: breast cancer; age: 38; race: w; menopause: PRE; bmi: 30.67; bmi status: obese; grade: 3/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 59; race: w; menopause: POST; bmi: 31.89; bmi status: obese; grade: 3/3; lymph: y; er: N; pr: N; her2: P; ', 'disease state: breast cancer; age: 49; race: w; menopause: POST; bmi: 36.73; bmi status: obese; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 38; race: b; menopause: PRE; bmi: 48.27; bmi status: obese; grade: 2/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 42; race: w; menopause: PRE; bmi: 33.65; bmi status: obese; grade: 3/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 40; race: w; menopause: POST; bmi: 58.47; bmi status: obese; grade: 3/3; lymph: y; er: P; pr: P; her2: P; ', 'disease state: breast cancer; age: 51; race: b; menopause: POST; bmi: 35.94; bmi status: obese; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 48; race: w; menopause: PERI; bmi: 40.26; bmi status: obese; grade: 3/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 42; race: b; menopause: PRE; bmi: 46.62; bmi status: obese; grade: 3/3; lymph: y; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 53; race: w; menopause: POST; bmi: 34.72; bmi status: obese; grade: 3/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 47; race: b; menopause: PERI; bmi: 31.18; bmi status: obese; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 51; race: b; menopause: PRE; bmi: 31.49; bmi status: obese; grade: 2/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 59; race: b; menopause: POST; bmi: 32.25; bmi status: obese; grade: 3/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 47; race: b; menopause: PERI; bmi: 31.02; bmi status: obese; grade: 2/3; lymph: n; er: N; pr: N; her2: P; ', 'disease state: breast cancer; age: 67; race: w; menopause: POST; bmi: 42.24; bmi status: obese; grade: 1/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 56; race: b; menopause: POST; bmi: 40.53; bmi status: obese; grade: 3/3; lymph: y; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 62; race: w; menopause: POST; bmi: 31.35; bmi status: obese; grade: 1/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 44; race: w; menopause: PERI; bmi: 33.06; bmi status: obese; grade: 3/3; lymph: n; er: N; pr: N; her2: P; ', 'disease state: breast cancer; age: 54; race: a; menopause: POST; bmi: 32.69; bmi status: obese; grade: 1/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 40; race: b; menopause: PRE; bmi: 37.5; bmi status: obese; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 57; race: b; menopause: POST; bmi: 40.4; bmi status: obese; grade: 3/3; lymph: n; er: P; pr: N; her2: N; ', 'disease state: breast cancer; age: 68; race: w; menopause: POST; bmi: 35.26; bmi status: obese; grade: 2/3; lymph: n; er: P; pr: N; her2: N; ', 'disease state: breast cancer; age: 47; race: w; menopause: PRE; bmi: 34.41; bmi status: obese; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 61; race: w; menopause: POST; bmi: 30.44; bmi status: obese; grade: 2/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 44; race: b; menopause: PERI; bmi: 30.04; bmi status: obese; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 46; race: w; menopause: PRE; bmi: 30.12; bmi status: obese; grade: 2/3; lymph: n; er: P; pr: P; her2: N; ', 'disease state: breast cancer; age: 63; race: w; menopause: POST; bmi: 32.03; bmi status: obese; grade: 3/3; lymph: n; er: U; pr: U; her2: U; ', 'disease state: breast cancer; age: 49; race: a; menopause: PRE; bmi: 30; bmi status: obese; grade: 3/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 46; race: w; menopause: PRE; bmi: 31.2; bmi status: obese; grade: 2/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 50; race: w; menopause: PRE; bmi: 33.12; bmi status: obese; grade: 2/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 33; race: w; menopause: PRE; bmi: 38.19; bmi status: obese; grade: 3/3; lymph: n; er: N; pr: N; her2: N; ', 'disease state: breast cancer; age: 49; race: w; menopause: PERI; bmi: 35.55; bmi status: obese; grade: 2/3; lymph: n; er: N; pr: N; her2: P; ', 'disease state: breast cancer; age: 34; race: w; menopause: PRE; bmi: 30.11; bmi status: obese; grade: 3/3; lymph: n; er: N; pr: N; her2: U; ', 'disease state: breast cancer; age: 52; race: w; menopause: PERI; bmi: 31.6; bmi status: obese; grade: 3/3; lymph: n; er: P; pr: P; her2: U; ', 'disease state: breast cancer; age: 56; race: w; menopause: POST; bmi: 46.48; bmi status: obese; grade: 3/3; lymph: n; er: P; pr: P; her2: U; ' GSE57935 Homo sapiens 24 Expression profiling by array GPL6244 Expression data for Control and SMRT-Depleted MCF-7 Cells 2014-05-23 Estrogens are an important regulator of breast cancer disease progression, and they function by binding the estrogen receptor-α (ERα) to regulate changes in gene expression. ERα is able to both activate and inhibit gene transcription in a gene-specific manner and do so by binding target DNA sequences and recruiting coactivators and corepressors which can modulate the chromatin environment. Silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) is known to act as coactivator and corepressor of ERα in a gene-specific manner. We used a microarray analysis to examine the gene expression changes that occur when the coregulator SMRT is depleted from the ERα positive MCF-7 breast cancer cell line. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE57935 The SMRT coregulator enhances growth of estrogen receptor-α-positive breast cancer cells by promotion of cell cycle progression and inhibition of apoptosis. Endocrinology 3.800 https://doi.org/10.1210/en.2014-1002 {Endocrinology (3.800): 10.1210/en.2014-1002} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA251372 https://www.ebi.ac.uk/ena/browser/view/PRJNA251372 None [Overal design]We sought to determine the genes that are regulated by depletion of the coregulator SMRT using Affymetrix Human Gene 1.0 ST Array. To this end, we transfected MCF-7 cells with control siRNA or SMRT-targeting siRNA for 48 h and treated for an additional 4 or 24 h with vehicle (0.1% EtOH) or 1 nM estradiol (E2). A total of 24 samples were analyzed, separated into eight groups each with three experimental replicates in each group, siControl-Veh 4 h, siControl -E2 4 h, siSMRT-Veh 4 h, siSMRT-E2 4 h, siControl-Veh 24 h, siControl-E2 24 h, siSMRT-Veh 24 h, siSMRT-E2 24 h.; [Treatment]'Cells were plated DME supplemented with 10% FBS 24 h prior to transfection. The transfection was conducted in Opti-MEM using oligofectamine. Media was changed after transfection to phenol red-free DME medium supplemented with 10% charcoal stripped fetal bovine serum and 1% L-Glutamine. After 48 h cells were treated with vehicle (0.1% EtOH) or 1 nM E2 for an additional 4 or 24 h.'; [Growth]"We routinely grow MCF-7 cells in Dublecco's Modified Eagle Medium (DME) supplemented with 10% fetal bovine serum (FBS)."; [Extraction]'RNA was isolated using the RNeasy kit from Qiagen.'; [Cell type]'breast cancer cell line''cell line: MCF-7; cell type: breast cancer cell line; transfected with: control siRNA; treated with: vehicle (0.1% EtOH) for 4hrs; ', 'cell line: MCF-7; cell type: breast cancer cell line; transfected with: control siRNA; treated with: 1 nM estradiol (E2) for 4hrs; ', 'cell line: MCF-7; cell type: breast cancer cell line; transfected with: SMRT-targeting siRNA; treated with: vehicle (0.1% EtOH) for 4hrs; ', 'cell line: MCF-7; cell type: breast cancer cell line; transfected with: SMRT-targeting siRNA; treated with: 1 nM estradiol (E2) for 4hrs; ', 'cell line: MCF-7; cell type: breast cancer cell line; transfected with: control siRNA; treated with: vehicle (0.1% EtOH) for 24hrs; ', 'cell line: MCF-7; cell type: breast cancer cell line; transfected with: control siRNA; treated with: 1 nM estradiol (E2) for 24hrs; ', 'cell line: MCF-7; cell type: breast cancer cell line; transfected with: SMRT-targeting siRNA; treated with: vehicle (0.1% EtOH) for 24hrs; ', 'cell line: MCF-7; cell type: breast cancer cell line; transfected with: SMRT-targeting siRNA; treated with: 1 nM estradiol (E2) for 24hrs; ' GSE41995 Homo sapiens 238 Genome binding/occupancy profiling by genome tiling array GPL4910; GPL4911; GPL4912; GPL4913; GPL4914; GPL4915; GPL4916 ChIP-chip of 38 nuclear receptors and NR co-factors in breast cancer cell line MCF7 2012-11-01 Altered gene expression patterns in human diseases reflect perturbations in the transcriptional networks that regulate cellular state. In breast cancer, Nuclear Receptors (NRs) play a prominent role in governing gene expression. NRs have prognostic utility and are therapeutically important targets. Here we describe a complete regulatory map for twenty-four NR proteins that are expressed in the breast cancer cell line MCF-7, as well as fourteen additional breast cancer associated transcription factors (TFs) and six key chromatin state markers. The CEL files for the 38 NRs ChIP-chip presented in the paper are included, together with the results bar files, except 5 previsouly published ones: ER [GSE10800], RARA, RARG, FOXA1, GATA3 [GSE15244]. The supplementary bed file contains all 200,140 binding sites of all 38 TFs reported in the paper. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41995 A comprehensive nuclear receptor network for breast cancer cells. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2013.01.004 {Cell reports (7.815): 10.1016/j.celrep.2013.01.004} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA178695 https://www.ebi.ac.uk/ena/browser/view/PRJNA178695 None [Overal design]Input DNA was used as control against all 38 ChIPchip samples. All samples are done in triplicates. We mapped the binding sites in the bacterial artificial chromosome (BAC) transgenic MCF7 cells in which we tagged the transcription factors with a modified LAP (localization and affinity purification) tag containing green fluorescent protein (GFP). Goat anti-GFP (raised against His-tagged full-length eGFP and affinity-purified with GST-tagged full-length eGFP) was used to perform ChIP experiments in those transgenic lines. *Bed files for binding sites of each of 38 factors (TR2L and TR2S are two isoforms of TR2) were provided as additional results files. Please note that the folllowing data files are re-processed from Dr. Sujun Hua's GSE10800 and GSE15244 uploads. ESR1.bed FOXA1.bed GATA3.bed RARA.bed RARG.bed Since the authors have updated the analysis pipeline and presented the changed results in the associated publication, these updated results are included in the records (Dr. Sujun is one of the contributors in this work).; [Treatment]'According to the standard chromatin extraction protocol (Shang et al., 2000).'; [Growth]"MCF7 breast cancer cells (ATCC HTB-22) were grown in phenol-free Dulbecco's modified Eagles's medium, 10% fetal bovine serum, with supplemental bovine insulin (0.01 mg/ml), 2 mM L-glutamine, and antibiotics at 37oC in a 5% CO2 humidified atmosphere.\nFor each NR with known ligand, MCF7 Cells were hormone-deprived for 3 days and then were treated with 100 nM NR ligand at 80% confluence. ~5x10^6 cells per ChIP were cross-linked with 1% formaldehyde for 10 minutes at 37oC then quenched with 125 mM glycine. For orphan NRs and NR-cofactors, no ligand was used and ChIP was performed with cells growing in phenol-free Dulbecco's modified Eagles's medium, 10% fetal bovine serum, with supplemental bovine insulin (0.01 mg/ml)."; [Extraction]'ChIPed DNA was amplified using linker-mediated PCR amplification method. 2mM dUTP was added to the 10mM dNTP mix during the amplification.'; [Cell type]'transgenic MCF7''cell type: transgenic MCF7; transcription factor: AR; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; ', 'cell type: transgenic MCF7; transcription factor: ATF1; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: CREB1; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: ELK; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: FOS; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: FOSB; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: FOSL1; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: FOSL2; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: NR3C1; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: JUN; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: JUNB; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: JUND; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: NR1H2; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: NR1D1; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: NR1D2; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: NR2F1; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: NR2F2; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: NR4A1; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: NR4A2; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: PGR; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: PPARA; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: PPARD; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: PPARG; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: RORA; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: RORC; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: RXRA; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: RXRB; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: SPDEF; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: THRA; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: NR2C1-L; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: NR2C1-S; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: NR2C2; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: VDR; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ', 'cell type: transgenic MCF7; transcription factor: XBP1; tag: modified LAP (localization and affinity purification) tag containing GFP; chip antibody: Goat anti-GFP; ' GSE40925 Mus musculus 18 Genome variation profiling by array GPL9906 Cooperativity of Rb, Brca1, and p53 and malignant breast cancer evolution (MFT121 p53f/f Brca1f/f) 2012-09-17 Breast cancers that are “triple-negative” for the clinical markers ESR1, PGR, and HER2 typically belong to the Basal-like molecular subtype. Defective Rb, p53, and Brca1 pathways are each associated with triple-negative and Basal-like subtypes. Our mouse genetic studies demonstrate that the combined inactivation of Rb and p53 pathways is sufficient to suppress the physiological cell death of mammary involution. Furthermore, concomitant inactivation of all three pathways in mammary epithelium has an additive effect on tumor latency and predisposes highly penetrant, metastatic adenocarcinomas. The tumors are poorly differentiated and have histologic features that are common among human Brca1-mutated tumors, including heterogeneous morphology, metaplasia, and necrosis. Gene expression analyses demonstrate that the tumors share attributes of both Basal-like and Claudin-low signatures, two molecular subtypes encompassed by the broader, triple-negative class defined by clinical markers. These studies establish a unique animal model of aggressive forms of breast cancer for which there are no effective, targeted treatments. Rb, p53, and Brca1 are associated with inherited forms of cancer, but defects in these pathways are also found together in a subset of breast cancer patients without a family history of the disease. Simultaneous inactivation of all three pathways causes more aggressive disease than do pair-wise combinations, indicating that the pathways play non-overlapping roles in tumor prevention. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE40925 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA175373 https://www.ebi.ac.uk/ena/browser/view/PRJNA175373 None [Overal design]We investigated the effect of perturbation of Rb family pathways, p53, and/or Brca1 in mouse mammary epithelium. Eighteen tumors were compared to normal spleen DNA.; [Treatment]'Tissues were flash frozen in liquid nitrogen.'; [Growth]'None'; [Extraction]'Genomic DNA was isolated using commercial silica columns and standard techniques.'; [Cell type]'Source: ''tissue: adenocarcinoma; genotype: MFT121,p53f/f; sample type: tumor; genetic background: FVB; ', 'genotype: MFT121,p53f/f; sample type: reference; tissue: normal spleen; genetic background: FVB; ', 'tissue: adenocarcinoma; genotype: MFT121,p53f/f Brca1f/f; sample type: tumor; genetic background: FVB; ', 'genotype: MFT121,p53f/f Brca1f/f; sample type: reference; tissue: normal spleen; genetic background: FVB; ' GSE115255 Homo sapiens 8 Expression profiling by high throughput sequencing GPL16791 RNA sequence analysis of stable versus reversible EMT events and the resultant metastases 2018-06-03 The ability of breast cancer cells to transiently transition between epithelial and mesenchymal states is critical to complete the metastatic process. In contrast, induction of epithelial-mesenchymal transition (EMT) through the acquisition of drug persistence is a more stable event. Herein, we utilize Her2 transformed human mammary epithelial (HMLE) cells to compare a reversible model of EMT induced by TGF-beta to a stable mesenchymal phenotype induced by chronic exposure to the ErbB kinase inhibitor, lapatinib. Indeed, only a TGF-beta cells capable of returning to an epithelial phenotype resulted in long bone metastasis (BM). These four cell populations were anylzed by RNA sequencing. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115255 Spleen Tyrosine Kinase-Mediated Autophagy Is Required for Epithelial-Mesenchymal Plasticity and Metastasis in Breast Cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-18-2636 {Cancer research (8.378): 10.1158/0008-5472.CAN-18-2636} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA474381 https://www.ebi.ac.uk/ena/browser/view/PRJNA474381 https://www.ncbi.nlm.nih.gov/sra?term=SRP149630 [Overal design]The Her2 transformed HMLE cells are referred to as the parental (Par) cell line and serves as the control. These cells were treated with TGF-beta every three days for a period of 4 weeks to induce EMT (TGFB). Alternatively, the parental cells were treated with 1 micromolar of lapatinib every three days also for 4 weeks and a proliferative drug resistant population (LAPR) emerged. The TGF-beta treated cells were engrafted onto the mammary fatpad and resultant long bone metasases (BM) were isolated and subcluted ex-vivo.; [Treatment]'To generate TGFB population, the parental cells were treated with TGF-beta (5ng/ml) every three days for 4 weeks. To generate LAPR cells the parental population was treated with 1 micromolar lapatinib every three days for 4 weeks. The TGFB population was engrafted onto the mammary fat pad and a metastsis was isolated from the tibia BM cell population was'; [Growth]'All cells were cultured in DMEM high glucose including 10% FBS and pen/strep. All cells expression firefly luciferase under blasticidin selection and Her2 under puromycin selection'; [Extraction]'E.Z.N.A. Total RNA kit from Omega bio-tek. RNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'Source: ''subtype: Her2 transformation model; culture conditions: In vitro; cell line: Her2 transformed HMLE cells; group: Parental cell line; ', 'subtype: Her2 transformation model; culture conditions: In vitro; cell line: Her2 transformed HMLE cells; group: TGFB; ', 'subtype: Her2 transformation model; culture conditions: In vitro; cell line: Her2 transformed HMLE cells; group: LAPR; ', 'subtype: Her2 transformation model; culture conditions: ex vivo; cell line: Her2 transformed HMLE cells; group: BM; ' GSE52687 Homo sapiens 9 Expression profiling by high throughput sequencing GPL9052 The RON receptor tyrosine kinase promotes metastasis by triggering epigenetic reprogramming through the thymine glycosylase MBD4 (RNA-Seq) 2013-11-23 Metastasis is the major cause of death in cancer patients, yet the genetic/epigenetic programs that drive metastasis are poorly understood. Here, we report a novel epigenetic reprogramming pathway that is required for breast cancer metastasis. Concerted differential DNA methylation is initiated by activation of the RON receptor tyrosine kinase by its ligand, macrophage stimulating protein (MSP). Through PI3K signaling, RON/MSP promotes expression of the G:T mismatch-specific thymine glycosylase MBD4. RON/MSP and MBD4-dependent aberrant DNA methylation results in misregulation of a specific set of genes. Knockdown of MBD4 reverses methylation at these specific loci, and blocks metastasis. We also show that the MBD4 glycosylase catalytic residue is required for RON/MSP-driven metastasis. Analysis of human breast cancers using a set of specific genes that are regulated by RON/MSP through MBD4-directed aberrant DNA methylation revealed that this epigenetic program is significantly associated with poor clinical outcome. Furthermore, inhibition of Ron kinase activity with a new pharmacological agent prevents activation of the RON/MBD4 pathway and blocks metastasis of patient-derived breast tumor grafts in vivo. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE52687 The RON receptor tyrosine kinase promotes metastasis by triggering MBD4-dependent DNA methylation reprogramming. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2013.12.010 {Cell reports (7.815): 10.1016/j.celrep.2013.12.010} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA229803 https://www.ebi.ac.uk/ena/browser/view/PRJNA229803 https://www.ncbi.nlm.nih.gov/sra?term=SRP033282 [Overal design]Examination of 3 cell types.; [Treatment]'None'; [Growth]"MCF-7 cells were cultured in Dulbecco's modified Eagle's medium (DME/F-12, Thermo Scientific) supplemented with 1% penicillin/streptomycin (Thermo Scientific), 10 µg/ml insulin (Gibco), and 10% heat inactivated fetal bovine serum (Thermo Scientific) at 37°C in 5% CO2. T47D cells were cultured in the same conditions in RPMI1640 (RPMI1640, Thermo Scientific) supplemented with 1% penicillin/streptomycin (Thermo Scientific) and 10% heat inactivated fetal bovine serum. RON and MSP were stably expressed in MCF7 cells by retroviral infection (Liu et al., 2011). MCF7-RON/MSP cells were maintained in MCF7 medium supplemented with 0.2 µg/ml puromycin and 50 µg/ml hygromycin. MCF7 and T47D cell lines were infected with lentiviral constructs that direct the synthesis of shRNA (based on PLKO.1 but with a neo resistant cassette substituted for the puromycin resistant cassette) and selected by the addition of 1 mg/mL G418 48 hours later."; [Extraction]'Total RNA for gene expression analysis was isolated with the RNeasy Kit (Qiagen) and tested for integrity on RNA 6000 NanoChips using an Agilent 2100 Bioanalyzer.\nIllumina TruSeq Stranded RNA Sample Prep with RiboZero treatment'; [Cell type]'breast cancer cell line''cell type: breast cancer cell line; passages: 4-8; cell line: MCF-7; ', 'cell type: breast cancer cell line; passages: 4-8; cell line: MCF-7; treatment: RON and MSP; ', 'cell type: breast cancer cell line; passages: 4-8; cell line: MCF-7; treatment: RON and MSP and shMBD4; ' GSE17460 Homo sapiens 9 Expression profiling by array GPL5175 Expression data from MCF-7 cells transfected with miR-26a and treated or not with estradiol 2009-07-31 Altered expression of microRNAs (miRNAs), an abundant class of small non-protein-coding RNAs that mostly function as negative regulators of protein-coding gene expression, is common in cancer. Here we analyze the regulation of miRNA expression in response to estrogen, a steroid hormone that is involved in the development and progression of breast carcinomas and that is acting via the estrogen receptors (ER) transcription factors. We set out to thoroughly describe miRNA expression, by using miRNA microarrays and real time RTPCR experiments, in various breast tumor cell lines in which estrogen signaling has been induced by 17β-estradiol (E2). We show that the expression of a broad set of miRNAs decreases following E2 treatment in an ER-dependent manner. We further show that enforced expression of several of the repressed miRNAs reduces E2-dependent cell growth, thus linking expression of specific miRNAs with estrogen-dependent cellular response. In addition, a transcriptome analysis revealed that the E2-repressed miR-26a and miR-181a regulate many genes associated with cell growth and proliferation, including the progesterone receptor gene, a key actor in estrogen signaling. Strikingly, miRNA expression is also regulated in breast cancers of women who had received antiestrogen neoadjuvant therapy thereby showing an estrogen-dependent in vivo regulation of miRNA expression. Overall, our data indicates that the extensive alterations in miRNA regulation upon estrogen signalling pathway plays a key role in estrogen-dependent functions and highlights the utility of considering miRNA expression in the understanding of antiestrogen resistance of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17460 Widespread estrogen-dependent repression of micrornas involved in breast tumor cell growth. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-09-2206 {Cancer research (8.378): 10.1158/0008-5472.CAN-09-2206} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA118737 https://www.ebi.ac.uk/ena/browser/view/PRJNA118737 None [Overal design]9 samples analyzed. Triplicates were done. MCF-7+miR26a+E2 (n=1 to 3) ; MCF7+miRctrl+E2 (n=1 to 3) ; MCF7+miRctrl+vehicle (n=1 to 3). We generated pairwise comparisons using EASANA from GenoSplice technology: MCF-7+miR26a+E2 versus MCF7+miRctrl+E2 and MCF-7+miRctrl+E2 versus MCF7+miRctrl+vehicle. Fold change ≥1.5 were selected.; [Treatment]'MCF-7 cells plated at 30% of confluence were grown 3 days in DMEM w/o red phenol and supplemented with 5% of dextran-coated charcoal-treated fetal calf serum. At day 3, 5 nM of indicated miRNA were transfected with INTERFERin (PolyPlus Transfection) and stimulated with 10 nM of 17-beta-estradiol( E2). Total RNA were extracted 48 h after E2 stimulation.'; [Growth]'MCF-7 cells were maintained in DMEM supplemented with 5% fetal calf serum at 37°C, 5% CO2 in a humidified atmosphere.'; [Extraction]'Trizol (Invitrogen) was used to extract total RNA from 1X PBS-rinsed cells.'; [Cell type]'Source: ''cell line: MCF-7; ' GSE32667 Homo sapiens 8 Expression profiling by array GPL570 Time-course effect of estradiol and estradiol-BSA on early gene expression in MCF-7 cells 2011-10-06 Estrogens have been reported to activate several processes via membrane binding to either classic estrogen receptors (ERs) or GPR30. We have used either estradiol or BSA-conjugated estradiol in order to initiate membrane-initiated actions and ICI 172,780 (ICI) or G15 to explore ER- and GPR30-related transcription. Our results show that the majority of G15-inhibited transcription is depending on ERs, as it is also inhibited by ICI. However, a small number of transcripts, related to specific actions/pathways is either exclusively inhibited by G15, providing evidence about a specific GPR30 signature, or not inhibited by ICI or G15 suggesting the existence of another, yet unidentified estrogen receptor. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32667 Early membrane initiated transcriptional effects of estrogens in breast cancer cells: First pharmacological evidence for a novel membrane estrogen receptor element (ERx). Steroids 2.136 https://doi.org/10.1016/j.steroids.2012.02.011 {Steroids (2.136) doi:10.1016/j.steroids.2012.02.011}; {Steroids (2.136) doi:10.1016/j.steroids.2011.11.005}; {Steroids (2.136) doi:10.1016/j.steroids.2011.12.016}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA154469 https://www.ebi.ac.uk/ena/browser/view/PRJNA154469 None [Overal design]Cells after a 4h incubation with medium containing 10% charcoal stripped FBS were incubated with or without E2-BSA (10-6M) in the presence or absence of specific antagonists, in DMEM/F12 (1:1) supplemented with 10% charcoal stripped FBS, for 3 hours. Total RNA was isolated using Nucleospin II columns (Macheray-Nagel, Dttren, Germany), according to the manufacturer’s instructions. RNA was labeled and hybridized according to the Affymetrix protocol (Affymetrix Gene-Chip Expression Analysis Technical Manual), using the HGU133A plus 2 chip, analyzing a total of 54675 transcripts. Signals were detected by an Affymetrix microarray chip reader.; [Treatment]'MCF-7 cells were incubated with or without Estradiol, E2-BSA or combinations of E2-BSA with ICI or G15 for 3 hours after preincubation for 4 hours with medium containing 10% charcoal stripped FBS.'; [Growth]'The human breast cancer cell line MCF-7 was obtained from DSMZ (Braunschweig, Germany) and cultured in DMEM/F12 (1:1) supplemented with 10% fetal bovine serum, at 37 °C, 5% CO2.'; [Extraction]'Total RNA was isolated using Nucleospin II columns (Macheray-Nagel, Dttren, Germany), according to the manufacturer’s instructions.'; [Cell type]'breast cancer derived cells''cell line: MCF-7; cell type: breast cancer derived cells; ' GSE135514 Homo sapiens 32 Expression profiling by high throughput sequencing GPL20301 Transcriptomic insight into salinomycin mechanisms in breast cancer cell lines: synergistic effects with dasatinib and induction of estrogen receptor beta 2019-08-07 Purpose:The use of a single-drug to encounter cancer progression is generally ineffective due to the tumors heterogeneity. To improve the clinical outcome, multiple drugs of distinctive mechanisms but complementary anticancer activities (combination therapy) are often used to enhance antitumor efficacy and minimize the risk of acquiring drug resistance. In this study, we proposed to use a combination of salinomycin (which targets anticancer stem cells) and dasatinib (an Src kinase inhibitor) for the treatment of breast cancer. The use of a RNA-seq is a combinatorial technique that allows to quantify global gene expression in biological samples. We employed this next generation sequencing technique to provide an initial insight into how Sal and Das alone, as well as in combination, modulated gene expression in the MDA-MB-468 human triple negative breast cancer cell line. Method: mRNA profiles of MDA-MB-468 cells treated with PBS (control), salinomycin, dasatinib, or the drug combination Sal + Das were generated by deep sequencing, in quadruplicate, using HiSeq4000 sequencer with single-end 50 bps reads. The results were validated by RT-qPCR analysis using StepOnePlus Real-timePCR system and SYBR Green assays. Results: RNA-seq data revealed that both salinomycin and dasatinib inhibit the expression of many downstream targeted genes of the STAT3, Wnt/beta-catenin, and hedgehog cell signaling pathways. The drug combination exhibited synergism through suppression of multiple pathways, leading to a promotion of cell cycle arrest at the G1/S phase mainly via the estrogen-mediated S-phase entry pathway, and partially via the BRCA1 and DNA damage response pathway. We also identified new salinomycin mechanisms involved in upregulating transcription factor 2. The study further led to a discovery of a new drug-induced targeting of estrogen receptor beta approach for triple-negative breast cancer treatment. Conclusion: Using RNA-seq, we identified for the first time the responsible pathways, including the estrogen-mediated S-phase entry pathway, that contributed to the synergistic effects of the drug combination Sal + Das. The discoveries of potential therapeutic targets, such as E2F2 as well as a novel drug-induced targeting of estrogen receptor beta (ESR2) approach were also described herein.We believe that using next generation approach to study drug mechanisms will allow us to identify more specific disease-relevant biomarkers for precision treatment of breast cancer, as well as other cancers in the future. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE135514 Transcriptomic insight into salinomycin mechanisms in breast cancer cell lines: synergistic effects with dasatinib and induction of estrogen receptor β. BMC cancer 2.933 https://doi.org/10.1186/s12885-020-07134-3 {BMC cancer (2.933): 10.1186/s12885-020-07134-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA559155 https://www.ebi.ac.uk/ena/browser/view/PRJNA559155 https://www.ncbi.nlm.nih.gov/sra?term=SRP217701 [Overal design]mRNA profiles of MDA-MB-468 cells treated with PBS (control), salinomycin, dasatinib, or the drug combination Sal + Das were generated by deep sequencing, in quadruplicate, using HiSeq4000 sequencer with single-end 50 bps reads.; [Treatment]'Cells were seeded on a T25 culture flask (1 million cells per flask) overnight and then treated with PBS (control), the drugs alone (salinomycin or dasatinib), or the drug combination (Sal + Das) for 24 or 72 h.'; [Growth]'MDA-MB-468 cells were cultured in RPMI 1640 medium supplemented with 10% (v/v) fetal bovine serum (FBS), penicillin (50,000 units/L), and streptomycin (50 mg/mL), and then maintained in 5% of CO2 at 37˚C.'; [Extraction]"The total RNA was extracted and purified using the Rneasy Mini Kit (Qiagen), according to the manufacturer's instructions. The final RNAs were quality controlledusing Agilent 2100 Bioanalyzer and quantified by absorbance using NanoDrop, prior RNA-seq analysis.\nLibrary was constructed on the purified RNAs obtained from the PBS- or drug-treated MDA-MB-468 cells (4 biological replicates per condition), using Illumina TruSeq RNA preparation kit."; [Cell type]'Source: ''cell line: MDA-MB-468; tissue: Triple negative breast tumor; drug incubation time: 24 h; drug concentration: -; ', 'cell line: MDA-MB-468; tissue: Triple negative breast tumor; drug incubation time: 24 h; drug concentration: 0.5 microM; ', 'cell line: MDA-MB-468; tissue: Triple negative breast tumor; drug incubation time: 24 h; drug concentration: 15 microM; ', 'cell line: MDA-MB-468; tissue: Triple negative breast tumor; drug incubation time: 24 h; drug concentration: 15.5 microM; ', 'cell line: MDA-MB-468; tissue: Triple negative breast tumor; drug incubation time: 72 h; drug concentration: -; ', 'cell line: MDA-MB-468; tissue: Triple negative breast tumor; drug incubation time: 72 h; drug concentration: 0.5 microM; ', 'cell line: MDA-MB-468; tissue: Triple negative breast tumor; drug incubation time: 72 h; drug concentration: 15 microM; ', 'cell line: MDA-MB-468; tissue: Triple negative breast tumor; drug incubation time: 72 h; drug concentration: 15.5 microM; ' GSE115173 Mus musculus 16 Expression profiling by array GPL11180 Translational regulation of RANKL by CPEB2 regulates mammary gland development and luminal tumorigenesis (Affymetrix Microarrays) 2018-05-31 Here we show that the RNA-binding protein CPEB2 controls synthesis of RANKL, thereby modulating epithealial proliferation, differentiation and breast cancer outcome https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115173 The RNA binding protein CPEB2 regulates hormone sensing in mammary gland development and luminal breast cancer. Science advances 12.804 https://doi.org/10.1126/sciadv.aax3868 {Science advances (12.804): 10.1126/sciadv.aax3868} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA474002 https://www.ebi.ac.uk/ena/browser/view/PRJNA474002 None [Overal design]Mouse array in duplicates of freshly sorted mammary epithelial populations: myoepithelial (Epcam_low and CD49f_high) and luminal (Epcam_high and CD49f_low). The sorted luminal subpopulations were non-clonogenic luminal (Sca1+CD49b-), ductal progenitors (Sca1+CD49b+) and alveolar progenitors (Sca1-Cd49b+).; [Treatment]'No specific treatment was used.'; [Growth]'Freshly sorted mammary epithelial cells'; [Extraction]'Trizol extraction'; [Cell type]'Source: ''tissue: Mammary gland; mouseid: 318; color: black; Sex: Female; age (weeks(days)): 10(2); line: DMI; genotype: Sox2-Cre +/+ ; Cpeb2 -/-; strain: C57BL/6J 129; fatherid: 182; motherid: 163; ', 'tissue: Mammary gland; mouseid: 319; color: black; Sex: Female; age (weeks(days)): 10(2); line: DMI; genotype: Sox2-Cre +/+ ; Cpeb2 +/+; strain: C57BL/6J 129; fatherid: 182; motherid: 163; ', 'tissue: Mammary gland; mouseid: 326; color: black; Sex: Female; age (weeks(days)): 10(2); line: DMI; genotype: Sox2-Cre +/+ ; Cpeb2 -/-; strain: C57BL/6J 129; fatherid: 220; motherid: 233; ', 'tissue: Mammary gland; mouseid: 327; color: black; Sex: Female; age (weeks(days)): 10(2); line: DMI; genotype: Sox2-Cre +/+ ; Cpeb2 +/+; strain: C57BL/6J 129; fatherid: 220; motherid: 233; ' GSE76271 Homo sapiens 10 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL11154 TRIM28 interacts with EZH2 and SWI/SNF to activate genes that promote mammosphere formation 2015-12-22 EZH2 is generally associated with H3K27 methylation and gene silencing. Mass spectrometry of the EZH2-interactome in MCF7 cells revealed EZH2-interactions with SWI/SNF subunits and TRIM28, which formed a complex with EZH2 distinct from PRC2. Transcriptome profiling showed that EZH2 primarily activates transcription in MCF7 cells and with TRIM28 co-regulates a set of genes associated with stem cell maintenance and poor survival of breast cancer patients. TRIM28 depletion repressed EZH2 recruitment and expression of this gene set, in parallel with decreased CD44hi/CD24lo mammosphere formation. These results support PRC2-independent functions of EZH2 and TRIM28 in mammary stem cell enrichment and maintenance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76271 TRIM28 interacts with EZH2 and SWI/SNF to activate genes that promote mammosphere formation. Oncogene 6.634 https://doi.org/10.1038/onc.2016.453 {Oncogene (6.634): 10.1038/onc.2016.453} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA306771 https://www.ebi.ac.uk/ena/browser/view/PRJNA306771 https://www.ncbi.nlm.nih.gov/sra?term=SRP067706 [Overal design]TRIM28 ChIP-seq, EZH2 KD RNA-seq and TRIM28 KD RNA-seq in MCF7 cells; [Treatment]'None'; [Growth]'The breast cancer cell line MCF7 was obtained from the American Type Culture Collection (ATCC) and grown in suggested media conditions. EZH2 and TRIM28 knockdown was achieved by using stable pGIPZ short-hairpin interfering RNA in lentivirus (clone: V2LHS_17507, Open Biosystems). A lentiviral scrambled plasmid was used as control for transfection and virus packaging. The stable EZH2 and TRIM28 depleted clones were maintained with Puromycin (Sigma).'; [Extraction]'For ChIP-seq, MCF7 lysates with were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody. For RNA-seq, RNA was harvested using Trizol reagent from control, EZH2, and TRIM28 depleted MCF7 cells.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''cell line: MCF7; treatment: Control; ', 'cell line: MCF7; treatment: Control; antibody: TRIM28; ', 'cell line: MCF7; treatment: EZH2 Knock Down; ', 'cell line: MCF7; treatment: TRIM28 Knock Down; ' GSE175513 Homo sapiens 2 Expression profiling by array; Other GPL17077 Identify metastasis-associated lncRNAs in MDA-MB-231 cell (microarray) 2021-05-25 The objective of this study is to unravel the metastasis-associated lncRNAs involved in the regulation of cell migration and invasion in breast cancer cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE175513 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA732677 https://www.ebi.ac.uk/ena/browser/view/PRJNA732677 None [Overal design]The cDNA probes derived from paired RNA samples from MDA-MB-231 cells and MDA-MB-231-IV2-1 cell. The expression levels of protein-coding gene or lncRNAs were examined by using a microarray approach (Agilent SurePrint G3 Human V2 GE); [Treatment]'When cells growth with 70 percent confluence, cells were subjected for RNA extraction.'; [Growth]'MDA-MB-231 cells and IV2-1 cells were culturein in Dulbecco’s modified Eagle’s medium supplemented with 10% inactivated FBS'; [Extraction]'Total RNA of breast cancer cells was prepared using TRIZOL (Invitrogen, Carlsbad, CA, USA) according to the manufacturer’s protocol.'; [Cell type]'breast cancer cell line''cell type: breast cancer cell line; treatment: Parental; ', 'cell type: breast cancer cell line; treatment: highly metastatic breast cancer cells derived from MDA-MB-231-P; ' GSE146012 Mus musculus 8 Expression profiling by high throughput sequencing GPL17021 Gene expression of primary tumor and lung metastases in 4T1 mouse mammry tumor model 2020-02-26 We sorted GFP-labeled 4T1 cells from primary tumor and lung metastases and performed mRNA sequencing. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE146012 Induction of DNMT3B by PGE2 and IL6 at Distant Metastatic Sites Promotes Epigenetic Modification and Breast Cancer Colonization. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-19-3339 {Cancer research (8.378): 10.1158/0008-5472.CAN-19-3339} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA608973 https://www.ebi.ac.uk/ena/browser/view/PRJNA608973 https://www.ncbi.nlm.nih.gov/sra?term=SRP250874 [Overal design]Identify differentially expressed genes between primary tumor and lung metastases; [Treatment]'None'; [Growth]'None'; [Extraction]'ZR-Duet DNA/RNA miniprep\nUltra Low Input RNA - v3\nIllumina TruSeq V4.0'; [Cell type]'Source: ''cell line: 4T1 mammary tumor cell; tissue source: Primary tumor; strain: BALB/c; ', 'cell line: 4T1 mammary tumor cell; tissue source: Lung metastases; strain: BALB/c; ' GSE59006 Homo sapiens 5 Expression profiling by array GPL10558 Fluvastatin-induced differential global gene expression in human malignant MCF-7 breast cancer cells 2014-07-02 The current study analyzed the altered expression profiles of genes that are responsible for fluvastatin-induced breast cancer cell death in MCF-7 cells (ER+ve luminal breast cancer cells). Some of these altered gene expressions were further inter connceted to various pathways which may eventually be recognised as drug targets/ biomarkers in statin-sensitve breast cancer patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59006 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA254100 https://www.ebi.ac.uk/ena/browser/view/PRJNA254100 None [Overal design]To understand the differential gene expression profile in fluvastatin treated (24 h) malignant breast cancer cells with untreated malignant breast cancer cells.; [Treatment]'MCF-7 cells were treated with sterile water for a period of 24h as a mock control'; [Growth]'MCF-7 cells were grown in DMEM supplemented with 10 % Foetal Bovine Serum, 2mM glutamine and Pen-Strep'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'ER+ve luminal breast cancer cells''cell line: MCF-7; cell type: ER+ve luminal breast cancer cells; treated with: water for 24hrs (mock-control); ', 'cell line: MCF-7; cell type: ER+ve luminal breast cancer cells; treated with: fluvastatin for 24hrs; ' GSE173663 Homo sapiens 20 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Transcriptional reprogramming by oxidative stress occurs within a predefined chromatin accessibility landscape [ATAC-seq] 2021-04-30 Reactive oxygen species (ROS) are important signalling molecules in many physiological processes, yet excess ROS leads to cell damage and can lead to pathology. Accordingly, cells need to maintain tight regulation of ROS levels, and ROS-responsive transcriptional reprogramming is central to this process. Although it has long been recognized that oxidative stress leads to rapid, significant changes in gene expression, the impact of oxidative stress on the underlying chromatin accessibility landscape remained unclear. Here, we asked whether ROS-responsive transcriptional reprogramming is accompanied by reprogramming of the chromatin environment in MCF7 human breast cancer cells. Using a time-course exposure to multiple inducers of oxidative stress, we determined that the widespread ROS-responsive changes in gene expression induced by ROS occur with minimal changes to the chromatin environment. While we did observe changes in chromatin accessibility, these changes were: (1) far less numerous than gene expression changes after oxidative stress, and (2) occur within pre-existing regions of accessible chromatin. TF footprinting analysis identified 5 TFs or TF families with evidence for ROS-responsive changes in DNA binding: NRF2, AP-1, p53, NFY, and SP/KLF. Importantly, several of these (AP-1, NF- Y, and SP/KLF factors) have not been previously implicated as widespread regulators in the response to ROS. In summary, we have characterized genome-wide changes in gene expression and chromatin accessibility in response to ROS treatment of MCF7 cells, and we have found that regulation of the large-scale transcriptional response to excess ROS is primarily constrained by the cell’s pre-existing chromatin landscape. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE173663 Transcriptional reprogramming by oxidative stress occurs within a predefined chromatin accessibility landscape. Free radical biology & medicine 5.657 https://doi.org/10.1016/j.freeradbiomed.2021.05.016 {Free radical biology & medicine (5.657): 10.1016/j.freeradbiomed.2021.05.016} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA726557 https://www.ebi.ac.uk/ena/browser/view/PRJNA726557 https://www.ncbi.nlm.nih.gov/sra?term=SRP318033 [Overal design]ATAC-seq of MCF7 cells at 0, 1, 8 and 24 hrs treatment with ethanol vehicle control (EtOH), menadione (MEN) or tert-butyl hydroperoxide (TBOOH), 2 replicates each.; [Treatment]'MCF7 cells were seeded (125,000 cells/ml) in 6 well plates and grown at 37°C for 24 hrs, after which cells were treated with the growth media supplemented with either 0.1% ethanol, 10 μM MEN, or 80 μM TBOOH for 0, 1, 8, or 24 hrs.'; [Growth]'MCF7 cells were grown and maintained in IMEM culture media (Phenol-red free, Gibco) supplemented with 5% fetal bovine serum, 1% penicillin/streptomycin (Invitrogen-Life technologies), 11.25 nM bovine insulin (Sigma-Aldrich) and 2.5 μg/L Plasmocin prophylactic (InvivoGen, San Diego, CA) in humidified air with ~20% oxygen and 5% carbon dioxide.'; [Extraction]'After treatment, cells were harvested, maintained on wet ice, and counted. 50000 cells / ml was used: first washed in ice cold PBS and resuspended in 50 μL ice cold lysis buffer. Cells were centrifuged at 500 x G for 10 min at 4°C to generate crude nuclei pellets. The crude nuclei pellet was resuspended in 50 μL Nextera Tn5 reaction buffer and transposase (Nextera cat no 15027865-6). They were then incubated at 37°C for 30 min at 250 RPM, purified with Qiagen MinElute PCR Purification Kit, eluted in 50 μL buffer EB and stored at -20°C until library preparation and sequencing.\nDNA libraries were prepared using standard Illumina protocols for Nextera-tagged DNA'; [Cell type]'Source: ''cell line: MCF7; treatment: untreated; time point: 0 hours; replicate: 1; ', 'cell line: MCF7; treatment: untreated; time point: 0 hours; replicate: 2; ', 'cell line: MCF7; treatment: 0.1% ethanol; time point: 1 hour; replicate: 1; ', 'cell line: MCF7; treatment: 0.1% ethanol; time point: 1 hour; replicate: 2; ', 'cell line: MCF7; treatment: 10 uM menadione; time point: 1 hour; replicate: 1; ', 'cell line: MCF7; treatment: 10 uM menadione; time point: 1 hour; replicate: 2; ', 'cell line: MCF7; treatment: 80 uM tert-butyl hydroperoxide; time point: 1 hour; replicate: 1; ', 'cell line: MCF7; treatment: 80 uM tert-butyl hydroperoxide; time point: 1 hour; replicate: 2; ', 'cell line: MCF7; treatment: 0.1% ethanol; time point: 8 hours; replicate: 1; ', 'cell line: MCF7; treatment: 0.1% ethanol; time point: 8 hours; replicate: 2; ', 'cell line: MCF7; treatment: 10 uM menadione; time point: 8 hours; replicate: 1; ', 'cell line: MCF7; treatment: 10 uM menadione; time point: 8 hours; replicate: 2; ', 'cell line: MCF7; treatment: 80 uM tert-butyl hydroperoxide; time point: 8 hours; replicate: 1; ', 'cell line: MCF7; treatment: 80 uM tert-butyl hydroperoxide; time point: 8 hours; replicate: 2; ', 'cell line: MCF7; treatment: 0.1% ethanol; time point: 24 hours; replicate: 1; ', 'cell line: MCF7; treatment: 0.1% ethanol; time point: 24 hours; replicate: 2; ', 'cell line: MCF7; treatment: 10 uM menadione; time point: 24 hours; replicate: 1; ', 'cell line: MCF7; treatment: 10 uM menadione; time point: 24 hours; replicate: 2; ', 'cell line: MCF7; treatment: 80 uM tert-butyl hydroperoxide; time point: 24 hours; replicate: 1; ', 'cell line: MCF7; treatment: 80 uM tert-butyl hydroperoxide; time point: 24 hours; replicate: 2; ' GSE43825 Mus musculus 31 Expression profiling by array GPL1261 Gene expression profiles from mammary tissue of control mice, small K5ΔNβcat hyperplasia, large K5ΔNβcat hyperplasia and K5ΔNβcat tumor 2013-01-28 Basal-like breast cancer is a heterogeneous disease characterised by the expression of basal cell markers, no oestrogen or progesterone receptor expression and a lack of HER2 overexpression. Recent studies have linked activation of the Wnt/beta-catenin pathway to basal-like breast cancer. Transgenic mice expressing N-terminally truncated stabilised beta-catenin in the mammary basal/myoepithelial cell layer (K5deltaNbetacat strain) develop mammary hyperplasias that progress to invasive carcinomas. Histological and microarray analyses of these lesions have revealed their high similarity to a subset of basal-like human breast tumours with squamous differentiation. As in human basal-like carcinomas, the Myc pathway was found to be activated in the mammary lesions of K5deltaNbetacat mice. Mammosphere and transplantation assays showed that a basal cell population with stem/progenitor characteristics was amplified in K5deltaNbetacat mouse preneoplastic glands. Myc deletion from the mammary basal layer of K5deltaNbetacat mice abolished both basal cell regenerative capacity and tumorigenesis. These results show that Myc is essential for beta-catenin-induced stem cell amplification and tumorigenesis and that basal stem/progenitor cells may be at the origin of a subset of basal-like breast tumours. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43825 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA187503 https://www.ebi.ac.uk/ena/browser/view/PRJNA187503 None [Overal design]mammary tissue from K5ΔNβcat mice were dissected at successive stages of development (small hyperplasia (n=5), large hyperplasia (n=5), tumor (n=11) and control (n=4)) for RNA extraction and hybridization on Affymetrix microarrays; [Treatment]'None'; [Growth]'Experiments were conducted in accordance with French veterinary guidelines and those formulated by the Council of Europe for experimental animal use'; [Extraction]'Total RNA was extracted from mammary tissues using Trizol Reagent (Invitrogen) followed by DNAse treatment and a clean-up step in miRNeasy Micro-columns (Qiagen).'; [Cell type]'Source: ''strain: C57BL6; genotype/variation: K5ΔNβcat; tumor stage: tumor; label protocol: Affymetrix; ', 'strain: C57BL6; genotype/variation: K5ΔNβcat; tumor stage: small hyperplasia; label protocol: Affymetrix; ', 'strain: C57BL6; genotype/variation: K5ΔNβcat; tumor stage: large hyperplasia; label protocol: Affymetrix; ', 'strain: C57BL6; genotype/variation: control; tumor stage: control tissue; label protocol: Affymetrix; ', 'strain: C57BL6; genotype/variation: control; tumor stage: basal mammary cells; label protocol: Nugen; ', 'strain: C57BL6; genotype/variation: K5creMycL/L; tumor stage: basal mammary cells; label protocol: Nugen; ' GSE85108 Homo sapiens 18 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL11154 CTCF modulates Estrogen Receptor function through specific chromatin and nuclear matrix interactions 2016-08-02 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE85108 CTCF modulates Estrogen Receptor function through specific chromatin and nuclear matrix interactions. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkw785 {Nucleic acids research (11.147): 10.1093/nar/gkw785} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA336182 https://www.ebi.ac.uk/ena/browser/view/PRJNA336182 None [Overal design]Refer to individual Series; [Treatment]'In 6-well plates, MCF7 cells were transfected with siRNA targeting CTCF (ON-TARGET J-010319-05-0005, Thermo Fisher Scientific) and siControl Non-targeting (siNT) (AllStars, Qiagen) using Lipofectamine RNAiMax (Life technologies) to a final concentration of 40 nM. Upon hormone deprivation, cells were treated either with 100 nM 17-beta-estradiol for 0h or 3h.', 'Upon hormone deprivation, MCF7 cells were treated either with 100 nM 17-beta-estradiol for 0h, 45 min or 3h.'; [Growth]'MCF7 cells were hormone deprived for 72 h in DMEM 5% Charcoal stripped Fetal Bovine Serum.'; [Extraction]'Total RNA was isolated with the total RNA isolation kit (RNeasy, Qiagen) according to the manufacturer’s protocol. RNA yield was assessed spectrophotometrically (NanoDrop 2000). Quantification and quality control for RNA-seq libraries were performed by Agilent Bioanalyzer (RNA nano 6000, Agilent).\nThe libraries were prepared at Norwegian Sequencing Center (NSC, Oslo). The instructions from TruSeq RNA-seq strand-specific sample protocol were followed.', 'For each ChIP-seq, 2 plates 70-80% confluent (around total 20 millions MCF7 cells) were lysed in SDS buffer (1% SDS, 10 mM EDTA, 50 mM Tris-HCl (pH 8.0)) and sonicated for 20 cycles 30 sec ON 30 sec OFF in Bioruptor sonicator (Diagenode). Subsequently, chromatin was diluted in dilution buffer (10 mM Tris-HCl pH 8.0, 0.5 mM EGTA pH 8.0, 1% Triton-X-100, 140 mM NaCl) and incubated over night with 10 ug of antibody coupled with magnetic beads. Afterwards, beads were washed 7 times with RIPA buffer (50mM HEPES pH7.6, 1mM EDTA pH8, 0.7% Na-deoxycholate, 1% NP-40, 0.5 M LiCl2) and reverse cross-linked at 65 degrees overnight in Elution buffer (50 mM Tris-HCl pH8, 1 mM EDTA pH8, 1% SDS). RNA was digested at 37 degrees in RNAse A (Ambion), and proteins were digested with proteinase K (Life Technologies) at 56 degrees. DNA was isolated by Phenol-chloroform extraction followed by Ethanol precipitation.\nLibrary preparation for sequencing was done following the instructions of TruSeq DNA sample preparation kit from Illumina.'; [Cell type]'Source: ''cell line: MCF-7; transfection: siNT; treatment: 0h Estrogen; ', 'cell line: MCF-7; transfection: siCTCF; treatment: 0h Estrogen; ', 'cell line: MCF-7; transfection: siNT; treatment: 3h Estrogen; ', 'cell line: MCF-7; transfection: siCTCF; treatment: 3h Estrogen; ', 'cell line: MCF-7; chip antibody: CTCF: Millipore 07-729 (lot #2453497); treatment: control; time: 0h; ', 'cell line: MCF-7; chip antibody: CTCF: Millipore 07-729 (lot #2453497); treatment: estrogen; time: 45min; ', 'cell line: MCF-7; chip antibody: CTCF: Millipore 07-729 (lot #2453497); treatment: estrogen; time: 3h; ', 'cell line: MCF-7; chip antibody: ER-alpha: Santa Cruz Biotechnology sc-543 (lot #F1215); treatment: control; time: 0h; ', 'cell line: MCF-7; chip antibody: ER-alpha: Santa Cruz Biotechnology sc-543 (lot #F1215); treatment: estrogen; time: 45min; ', 'cell line: MCF-7; chip antibody: ER-alpha: Santa Cruz Biotechnology sc-543 (lot #F1215); treatment: estrogen; time: 3h; ', 'cell line: MCF-7; chip antibody: FOXA1 AbCam ab5089 (lot #GK122110-17) and ab23738 (lot #GK176970-1); treatment: control; time: 0h; ', 'cell line: MCF-7; chip antibody: FOXA1 AbCam ab5089 (lot #GK122110-17) and ab23738 (lot #GK176970-1); treatment: estrogen; time: 45min; ', 'cell line: MCF-7; chip antibody: FOXA1 AbCam ab5089 (lot #GK122110-17) and ab23738 (lot #GK176970-1); treatment: estrogen; time: 3h; ', 'cell line: MCF-7; chip antibody: LaminB (c-20) Santa Cruz Biotechnology sc-6216 (lot #F1715); treatment: control; time: 0h; ', 'cell line: MCF-7; chip antibody: LaminB (c-20) Santa Cruz Biotechnology sc-6216 (lot #F1715); treatment: estrogen; time: 45min; ', 'cell line: MCF-7; chip antibody: LaminB (c-20) Santa Cruz Biotechnology sc-6216 (lot #F1715); treatment: estrogen; time: 3h; ', 'cell line: MCF-7; chip antibody: ER-alpha: Santa Cruz Biotechnology sc-543 (lot #F1215); treatment: siCTCF; ', 'cell line: MCF-7; chip antibody: ER-alpha: Santa Cruz Biotechnology sc-543 (lot #F1215); treatment: siNT; ' GSE70745 Homo sapiens 6 Expression profiling by array GPL15207 SAPORIN-EpCAM antibody conjugates for targeted therapy 2015-07-10 Saporin (SAP) is an Ribosomal inactivation protein (RIP) toxin molecule. Conjugating SAP with EpCAM Antibody will direct the toxin pay loads to the EpCAM positive cancer cells as a targeted therapy We used microarrays to detail the global gene expression to understand the pathways involved in EpCAM-mediated SAP drug delivery in breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE70745 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA289480 https://www.ebi.ac.uk/ena/browser/view/PRJNA289480 None [Overal design]MCF-7 breast cancer cells were cultured and treated with Saporin and Saporin-EpCAM Antibody conjugate for the duration of 24h. RNA was extracted from cells and hybridized onto Affymetrix Human PrimeView arrays. To understand the changes in the transcriptome, we have included untreated MCF-7 cells (Controls; C1, C2- were taken from our own data Accession number:GSE69160) along with treated cells (SAP_1, SAP_2, SAP-CONJ_1, SAP CONJ_2).; [Treatment]'Cells were treated with Saporin (Sigma) and Saporin-EpCAM Antibody conjugate (using EDC-NHS cross linker) and incubated for 24 h, cells with out treatment was maintained as a control'; [Growth]'MCF-7 Breast cancer cell line (ATCC) was maintained with DMEM culture media supplemented with 10% FBS, in a humidified Co2 incubator.'; [Extraction]'RNA was extracted frm the cells using Qiagen RNAeasy mini kit'; [Cell type]'Source: ''cell line: MCF7; ', 'cell line: MCF7 cells with same passage number; ' GSE95294 Homo sapiens 13 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL11154 KDM4 inhibition targets breast cancer stem cells 2017-02-23 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95294 KDM4 Inhibition Targets Breast Cancer Stem-like Cells. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-17-1754 {Cancer research (8.378): 10.1158/0008-5472.CAN-17-1754} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA376573 https://www.ebi.ac.uk/ena/browser/view/PRJNA376573 None [Overal design]Refer to individual Series; [Treatment]'BCSC1 cells were treated with 10nm KDM4(i) for 18 hours or infected with shRNA for 3 days', 'BCSC1 cells were treated with 10nm KDM4(i) for 18 hours'; [Growth]'BCSC1 cells were grown in MSC medium under low-oxygen conditions'; [Extraction]'Metzger, E., et al. Phosphorylation of histone H3 at threonine 11 establishes a novel chromatin mark for transcriptional regulation. Nat Cell Biol 10, 53-60 (2008), Drosophila Spike in Chromatin was added in H3K9me3 control and H3K9me3 (i) samples.\nLibraries were prepared from immunoprecipitated DNA according to standard methods. ChIP-seq libraries were sequenced using a HiSeq 2000 (Illumina) and mapped to the hg19 reference genome using bowtie 2', 'RNA was harvested from BCSC1 cells using Trizol reagent. Illumina TruSeq RNA Sample Prep Kit (Cat#FC-122-1001) was used with 1 ug of total RNA for the construction of sequencing libraries.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''cell line: breast triple negative tumor cell line BCSC1; treatment: vehicle; chip antibody: none; ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: vehicle; chip antibody: H3K9me3 (Diagenode, #C15410056, lotA1675-001P); ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: 10 nM kDM4(i) for 18 hours; chip antibody: none; ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: 10 nM kDM4(i) for 18 hours; chip antibody: H3K9me3 (Diagenode, #C15410056, lotA1675-001P); ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: shRNA control; chip antibody: none; ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: shRNA control; chip antibody: KDM4A (Schuele Lab; #5766, lot 21110); ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: shRNA KDM4A; chip antibody: none; ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: shRNA KDM4A; chip antibody: KDM4A (Schuele Lab; #5766, lot 21110); ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: vehicle; ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: 10 nM kDM4(i) for 18 hours; ' GSE131306 Mus musculus 4 Expression profiling by high throughput sequencing GPL21493 The effects of chemokines CXCL1/2/8 on mouse lung fibroblasts 2019-05-16 Our preliminary data show that the primary triple-negative breast tumor-derived chemokines CXCL1/2/8 promote migration and tube formation of mouse lung endothelial cells, which is mediated by lung fibroblasts. To explore the molecular events underlying this mediator function of lung fibroblasts, we treated freshly-isolated lung fibroblasts with chemokines CXCL1/2/8 and performed RNA-Seq assay. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131306 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA543226 https://www.ebi.ac.uk/ena/browser/view/PRJNA543226 https://www.ncbi.nlm.nih.gov/sra?term=SRP198602 [Overal design]Freshly-isolated mouse lung fibroblasts were treated with recombinant human CXCL1 (8 nM)/2 (2 nM)/8 (20 nM) proteins for 3 hours.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was isolated from the using RNeasy Mini kit (Qiagen, Germany).\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'fibrolasts''strain: BALB/c; genotype: wild-type; tissue: lung; cell type: fibrolasts; age: 4 weeks; treatment: control; ', 'strain: BALB/c; genotype: wild-type; tissue: lung; cell type: fibrolasts; age: 4 weeks; treatment: chemokines CXCL1/2/8; ' GSE121443 Homo sapiens 6 Other GPL21290 Intrinsic dynamics of an endogenous human gene reveal the basis of expression heterogeneity 2018-10-18 Transcriptional regulation in metazoans occurs through long range genomic contacts between enhancers and promoters, and most genes are transcribed in episodic ‘bursts’ of RNA synthesis. The relationship between these two phenomena and the dynamic regulation of genes in response to upstream signals is unknown. Here, we describe the use of live-cell RNA imaging coupled with Hi-C measurements to dissect the regulation of the estrogen-responsive TFF1 gene under endogenous regulation. Although this gene is highly induced, we observe short active periods and variable inactive periods ranging from minutes to days. The heterogeneity in inactive times gives rise to the widely-observed ‘noise’ in human gene expression and explains the distribution of protein levels in human tissue. We derive a mathematical model of regulation that relates transcription, chromosome structure, and the cell’s ability to ‘sense’ changes in estrogen and predicts that hypervariability is largely dynamic and does not reflect a stable biological state. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE121443 Intrinsic Dynamics of a Human Gene Reveal the Basis of Expression Heterogeneity. Cell 36.216 https://doi.org/10.1016/j.cell.2018.11.026 {Cell (36.216): 10.1016/j.cell.2018.11.026} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA497364 https://www.ebi.ac.uk/ena/browser/view/PRJNA497364 https://www.ncbi.nlm.nih.gov/sra?term=SRP166061 [Overal design]We used 3e HiC to look at the estradiol induced entropy changes for ER bound enhancers.; [Treatment]'Cells were hormone depleted by washing cells twice in Phenol free media supplemented with 10% Charcoal/Dextran Treated FBS (Atlanta Biologicals), 2mM Glutamine and 1X Penstrep (hormone depleted media). Cells were returned to incubator and an hour later hormone depleted media was replaced. This step was performed again. After 4 days, media was replaced with hormone depleted media supplemented with the specific concentration of E2 or complete media for the Saturated E2 sample. Cells were allowed to reach steady state for 3 days.'; [Growth]'MCF7 cells in 10cm dishes were grown in MEM media (Corning) supplemented with 2mM Glutamine (Hyclone SH30034), 1X Penicillin/Strep (100units/mL Penicillin, 100micrograms/mL Streptomycin), and 10% FBS (Sigma). This media is denoted in the text as complete media or Saturated E2.'; [Extraction]'fresh MCF7 cells were cross-linked with 1% formaldehyde for 10 minutes at 25°C. 2-5 X 106 cells were lysed in 10 ml lysis buffer (10 mM Tris-HCl pH8.0, 10 mM NaCl, 0.2% NP40; 10 μl protease inhibitors (Sigma)) with rotation at 4°C for 60 minutes. The cells were then treated with 400 μl 1X NEB cutsmart buffer with 0.1% SDS at 65°C for 10 minutes, followed by addition of 44 μl 10% Triton X-100 to quench SDS. Chromatin was subsequently digested with 20 Units CviQ I (NEB), and 20 Units CviA II (NEB) at 25°C for 20 minutes, then with 20 Units Bfa I (NEB) at 37°C for 20 minutes. The reaction was stopped by washing the cells twice with 600 \uf06dl wash buffer (10mM NaCl, 1mM EDTA, 0.1% triton-100). The DNA ends were blunted and labeled with biotin by Klenow enzyme in the presence of dCTP, dGTP, dTTP, biotin-14-dATP, followed by ligation using T4 DNA ligase. After reverse crosslinking, the samples were treated with T4 DNA polymerase to remove biotin labels at the DNA ends.\nDNA was fragmented to 300-500 bp by sonication with a Bioruptor sonicator (Diagenode UCD-200). Next, The DNA was end-repaired, followed by A-addition as described previously (Lieberman-Aiden et al., 2009). The remaining biotinylated DNA fragments were then captured using Dynabeads MyOne Streptavin C1 Beads (Invitrogen) by incubating for 30 minutes at 25°C with rotation. The DNA on beads was ligated to the Illumina Paired End Adaptors. Following PCR-amplification of the libraries, DNA fragments from 300 to 700 bp were purified from 2% E-gel and sequenced on Hi-Seq 3000.'; [Cell type]'Source: ''cell line: MCF7; tissue: breast cancer; gender: female; ' GSE48924 Homo sapiens 46 Expression profiling by array GPL10558 Stimulation of endogenous FGFR1b and FGFR2b 2013-07-16 Genome-wide association studies for breast cancer have identified over 80 different risk regions in the genome, with the FGFR2 locus consistently identified as the most strongly associated locus. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Here we use a systems biology approach to elucidate the regulatory networks operating in breast cancer and examine the role of FGFR2 in mediating risk. Using model systems we identify FGFR2-regulated genes and, combining variant set enrichment and eQTL analysis, show that these are preferentially linked to breast cancer risk loci. Our results support the concept that cancer-risk associated genes cluster in pathways https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48924 Master regulators of FGFR2 signalling and breast cancer risk. Nature communications 11.878 https://doi.org/10.1038/ncomms3464 {Nature communications (11.878): 10.1038/ncomms3464} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA212326 https://www.ebi.ac.uk/ena/browser/view/PRJNA212326 None [Overal design]The data consists of 46 microarray samples from MCF-7 cells treated under different conditions, at 3 time points (0, 6 and 24 h) in order to perturb FGFR 1b and 2b signalling. The data have been pre-processed in R using the beadarray package, and are presented in the form of log2 expression values. The experiment was carried out on 4 Humanv4 arrays using 12 samples per array. The original arrays contain 48324 features, with an average of 22 beads per feature (Standard Deviation of 5); [Treatment]'Estrogen deprived cells were stimulated with 1nM estradiol (Sigma); 100ng/mL FGF10 (Invitrogen); 100ng/mL PD173074 (Sigma-Aldrich)'; [Growth]'MCF7 human breast cancer cells were cultured in DMEM supplemented with 10% HI-FCS and antibiotics. Cell synchronisation via estrogen deprivation was carried out for at least 3 days in phenol red-free DMEM (Invitrogen) supplemented with 5% charcoal dextran-treated HI-FBS (Hyclone) and 1% penicillin-streptomycin. All cells were grown at 37oC in 5% CO2'; [Extraction]'RNA was extracted using the miRNeasy spin column kit (Qiagen) and quality checked using an RNA 6000 Nano chip on a 2100 Bioanalyser (Agilent). 250ng RNA (RIN>7) was used for cRNA amplification and labelling using the Illumina TotalPrep-96 kit (Ambion 4397949)'; [Cell type]'Source: ''cell line: MCF-7; treatment duration (hs): 0; ', 'cell line: MCF-7; treatment duration (hs): 6; ', 'cell line: MCF-7; treatment duration (hs): 24; ' GSE93057 Homo sapiens 12 Expression profiling by high throughput sequencing GPL16791 RNAseq analysis of patient-derived luminal breast cancer xenografts treated with progestins 2017-01-03 Primary breast cancer xenografts https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93057 Breast Cancer Suppression by Progesterone Receptors Is Mediated by Their Modulation of Estrogen Receptors and RNA Polymerase III. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-16-3541 {Cancer research (8.378): 10.1158/0008-5472.CAN-16-3541} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA359750 https://www.ebi.ac.uk/ena/browser/view/PRJNA359750 https://www.ncbi.nlm.nih.gov/sra?term=SRP095932 [Overal design]Two primary xenografts with different treatments in triplicate; [Treatment]'Chronic E2/E2+MPA treatment upon transplant'; [Growth]'Xenografts were grown in NOD/SCID/Il2rgnull mice'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions.\nRNA libraries were prepared for sequencing using the Illumina TruSeq Stranded mRNA LT Sample Prep Kit at the University of Colorado Denver Genomics and Microarray Core facility."; [Cell type]'Source: ''xenograft: UCD4; treatment: estrogen; ', 'xenograft: UCD4; treatment: estrogen+MPA; ', 'xenograft: UCD65; treatment: estrogen; ', 'xenograft: UCD65; treatment: estrogen+MPA; ' GSE3178 Homo sapiens 48 Expression profiling by array GPL885; GPL887 Gene expression patterns associated with p53 status in breast cancer 2005-08-23 Breast cancer subtypes identified in genomic studies have different underlying genetic defects. Mutations in the tumor suppressor p53 occur more frequently in estrogen receptor (ER) negative, basal-like and HER2-amplified tumors than in luminal, ER positive tumors. Thus, because p53 mutation status is tightly linked to other characteristics of prognostic importance, it is difficult to identify p53's independent prognostic effects. The relation between p53 status and subtype can be better studied by combining data from primary tumors with data from isogenic cell line pairs (with and without p53 function). In this study, the p53-dependent gene expression signatures of four cell lines (MCF-7, ZR-75-1, and two immortalized human mammary epithelial cell lines) were identified by comparing p53-RNAi transduced cell lines to their parent cell lines. Cell lines were treated with vehicle only or doxorubicin to identify p53 responses in both non-induced and induced states. Each cell line displayed unique patterns of gene expression, but cell type specific trends were evident. A common gene expression signature associated with p53 loss across all four cell lines was identified. This signature showed overlap with the signature of p53 loss in primary breast tumors and predicted relapse-free survival and overall survival in independent test data sets. Keywords: untreated x treated https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE3178 Gene expression patterns associated with p53 status in breast cancer. BMC cancer 2.933 https://doi.org/10.1186/1471-2407-6-276 {BMC cancer (2.933): 10.1186/1471-2407-6-276} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA92723 https://www.ebi.ac.uk/ena/browser/view/PRJNA92723 None [Overal design]We analyzed 48 arrays performed using 48 polyA RNA samples. RNAs were collected from cell lines treated with an IC50 dose of doxorubicin hydrochloride or with a feeding control. Each cell line had its own reference which represented the second sample on the dual channel array. These untreated RNAs were prepared by pooling four harvests of that cell line at 60-80% confluence and 48h after feeding; [Treatment]'None'; [Growth]'None', 'Cells grown for to 60-80% confluence in MEGM media (Clonetics), harvested 48 hours after feeding, 4 harvests were pooled', 'Cells grown for to 60-80% confluence in RPMI 1640 media, harvested 48 hours after feeding, 4 harvests were pooled'; [Extraction]'Harvest cells by scraping, use invitrogen Micro-FastTrack to extract mRNA'; [Cell type]'Source: ''' GSE130462 Homo sapiens 7 Expression profiling by array GPL26593 Unlocking the transcriptomic potential of formalin-fixed paraffin embedded clinical tissues: Comparison of gene expression profiling approaches [Nanostring] 2019-04-29 Background: High-throughput transcriptomics has matured into a very well established and widely utilised research tool over the last two decades since the first mRNA profiling microarrays. Clinical datasets generated on a range of different platforms continue to be deposited in public repositories provide an ever-growing, valuable resource for reanalysis. Cost and tissue availability normally preclude processing samples across multiple technologies, making it difficult to directly evaluate performance, reliability and to what extent gene expression data from different platforms can be compared or integrated. Purpose: In this study, we describe our experiences using nine new and established mRNA profiling techniques including Lexogen QuantSeq, Qiagen QiaSeq, BioSpyder TempO-Seq, Ion AmpliSeq, Nanostring, Affymetrix Clariom S or U133A, Illumina BeadChip and Ion Total RNA-seq of formalin-fixed paraffin embedded (FFPE) and fresh frozen (FF) sequential patient-matched breast tumour samples. Results: The number of genes represented and reliability were found to vary between the platforms, but overall all methods provided data which were largely comparable. Crucially we found that it is possible to integrate data for combined analyses across FFPE/FF and platforms using established batch correction methods as required to increase cohort sizes. However, some platforms appear to be better suited to FFPE samples, particularly archival material. Overall, we illustrate that technology selection is a balance between required resolution, sample quality, availability and cost. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130462 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA540864 https://www.ebi.ac.uk/ena/browser/view/PRJNA540864 None [Overal design]Sequencing of patient-matched sets of human breast cancer biopsy samples using 9 different mRNA profiling platforms. We assess the feasibility of integrating data from FFPE or FF tissue sequenced using different platforms and compare these different technoolgies.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted from fresh frozen tissue using the Qiagen miRNeasy kit.'; [Cell type]'Source: ''tissue: breast cancer; time point: pre-treatment biopsy; ', 'tissue: breast cancer; time point: late on-treatment biopsy; ', 'tissue: breast cancer; time point: later on-treatment biopsy; ', 'tissue: breast cancer; time point: early on-treatment biopsy; ' GSE8828 Mus musculus 6 Expression profiling by array GPL1261 Isolation and molecular characterization of cancer stem cells in MMTVWnt-1 murine breast tumors 2007-08-20 In human breast cancers, a phenotypically distinct minority population of tumorigenic cancer (TG) cells (sometimes referred to as cancer stem cells) drives tumor growth when transplanted into immunodeficient mice. Our objective was to identify a mouse model of breast cancer stem cells that could have relevance to studying human breast cancer. To do so, we utilized breast tumors of the MMTVWnt-1 mice. MMTV-Wnt-1 breast tumors were harvested, dissociated into single cell suspensions, and FACS sorted on Thy1, CD24, and CD45. FACS sorted cells were then injected into recipient background FBV/NJ female mice. Thy1+CD24+ cancer cells, which constitute approximately 1-4% of tumor cells were highly enriched for cells capable of regenerating new tumors when compared to cells of the tumor that did not fit this profile (“Not Thy1+CD24+”). Resultant tumors were of the same phenotypic diversity as the original tumor and behaved in a similar manner when passaged. Microarray analysis comparing Thy1+CD24+ tumor cells to “Not Thy1+CD24+” cells identified a list of differentially expressed genes. Orthologs of these differentially expressed genes predicted survival of human breast cancer patients from two different study groups. These studies suggest that there is a cancer stem cell compartment in the MMTV-Wnt-1 murine breast tumor and that there is a clinical utility of this model for the study of cancer stem cells. Keywords: cell type comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE8828 Isolation and molecular characterization of cancer stem cells in MMTV-Wnt-1 murine breast tumors. Stem cells (Dayton, Ohio) 5.614 https://doi.org/10.1634/stemcells.2007-0440 {Stem cells (Dayton, Ohio) (5.614): 10.1634/stemcells.2007-0440} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA102157 https://www.ebi.ac.uk/ena/browser/view/PRJNA102157 None [Overal design]Expression profling were performed on 3 tumorigenic and 3 non tumorigenic samples of MMTV-Wnt-1 breast tumors. A gene signature was derived by comparing the gene expressions of 3 tumorigenic samples with 3 nontumorigenic samples; [Treatment]'None'; [Growth]'None'; [Extraction]'Using RNAqueous-Micro (Ambion #1931).'; [Cell type]'Source: ''' GSE75570 Homo sapiens 18 Expression profiling by array GPL15207 Expression data from MCF-7 breast cancer cells treated with CNTs, ginsenosides (Rb1 and Rg1) and conjugates (Rb-CNTs and Rg-CNTs) 2015-12-01 To investigate the effects of ginsenosides-CNTs conjugtaes on total expression profile of MCF-7 breast cancer cells, we conjugated ginsenoides Rb1 and Rg1 with multi-walled carbon nanotubes in a 5:1 ratio. Objectives for this study included the identification of genes that were up or down-regulated at the transcriptional level in MCF-7 cells treated with ginsenoside-CNTs conjugates and compare it to the ginsenosides alone (Rb1 and Rg1) https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE75570 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA304617 https://www.ebi.ac.uk/ena/browser/view/PRJNA304617 None [Overal design]MCF-7 breast cancer cells were incubated with CNTs (8 ug/ml), Rb1 (2 ug/ml), Rg1 (2 ug/ml), Rb-CNTs (10 ug/ml) and Rg-CNTs (10 ug/ml) for 24 hours and selected for RNA extraction and hybridization on Affymetrix microarrays. type: cell death responses; [Treatment]'No special treatments before harvesting were carried out.'; [Growth]'Cells were maintained in Dulbecco’s Modified Eagle’s Medium (DMEM) supplemented with 10% fetal calf serum, 2% glutamine, 1% penicillin and 1% streptomycin stock solutions. Cells were incubated at 37°C/ 95% air/ 5% CO2 and the media was changed every two days.'; [Extraction]'Cells were washed 3 times using PBS and total RNA was collected from adherent tissue culture cells using Trizol (Invitrogen) according to the manufacturer’s instructions. RNA was quantified (A260) using a Nanodrop-1000 spectrophotometer (Nanodrop Technologies).'; [Cell type]'breast cancer''cell line: MCF-7; cell type: breast cancer; gender: female; ' GSE160955 Homo sapiens 12 Expression profiling by high throughput sequencing GPL20301 Effect of a SNRPA1-interacting RNA structural element on alternative splicing 2020-11-05 Assessing the influence of RNA structural and sequence variations on SNRPA1-mediated regulation of alternative splicing https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE160955 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA674898 https://www.ebi.ac.uk/ena/browser/view/PRJNA674898 https://www.ncbi.nlm.nih.gov/sra?term=SRP291358 [Overal design]A SNRPA1-interacting RNA structural element (WT sequence hg38: chr8:143925142-143925188), along with sequence and structure mutants of this element, was transfected into human breast cancer cells and then RNA-seq was used to assess the resulting changes in alternative splicing. Mock-transfected cells were used as a control. The sequence of the WT and variant structural RNA are available in the file "structural_RNA_sequence_with_variants.txt" at the foot of this record.; [Treatment]"Each well of cells was transfected with 100pmol of the indicated RNA using lipofectamine 2000 (thermo) per the manufacturer's protocol. Mock transfected cells were treated identically except RNA was excluded from the transfection mix."; [Growth]'48 hours before transfection MDA-LM2 cancer cells were seeded at 1x10^5 per well in 6-well plates. Cells were grown in a 37degC 5% CO2 humidified incubator. Cells were grown in DMEM media supplemented with 10% FBS, glucose (4.5g/L), L-glutamine (4mM), sodium pyruvate (1mM), penicillin (100 units/mL), streptomycin (100 ug/mL) and amphotericin (1ug/mL).'; [Extraction]'48 hours after transfection, total RNA was harvested using the zymo research RNA quick prep kit, including an on-column DNase-treatment step.\nThe Takara SMARTer stranded total RNA-seq V2-pico input mammalian kit (634411) was used to prepare libraries from the total RNA.'; [Cell type]'Source: ''cell line: MDA-LM2; rep: 1; synthetic rna oligo: loopN; ', 'cell line: MDA-LM2; rep: 2; synthetic rna oligo: loopN; ', 'cell line: MDA-LM2; rep: 1; synthetic rna oligo: loopN+unstructured; ', 'cell line: MDA-LM2; rep: 2; synthetic rna oligo: loopN+unstructured; ', 'cell line: MDA-LM2; rep: 1; synthetic rna oligo: mock; ', 'cell line: MDA-LM2; rep: 2; synthetic rna oligo: mock; ', 'cell line: MDA-LM2; rep: 1; synthetic rna oligo: structured; ', 'cell line: MDA-LM2; rep: 2; synthetic rna oligo: structured; ', 'cell line: MDA-LM2; rep: 1; synthetic rna oligo: unstructured; ', 'cell line: MDA-LM2; rep: 2; synthetic rna oligo: unstructured; ', 'cell line: MDA-LM2; rep: 1; synthetic rna oligo: WT; ', 'cell line: MDA-LM2; rep: 2; synthetic rna oligo: WT; ' GSE153251 Homo sapiens 89 Genome binding/occupancy profiling by high throughput sequencing GPL20301; GPL24676 TET2 is a component of the ER complex and controls 5mC to 5hmC conversion at ER cis-regulatory regions [ChIP-Seq] 2020-06-25 Estrogen receptor-a (ER) drives tumour development and metastasis in ER positive (ER+) breast cancer. GATA3 is a transcription factor that has been closely linked to ER function, but the role of GATA3 in ER transcriptional activity is not clear. We sought to identify the contribution of GATA3 to the ER complex by conducting quantitative multiplexed rapid immunoprecipitation mass spectrometry of endogenous proteins (qPLEX-RIME) to assess changes to the ER complex in response to GATA3 depletion. Unexpectedly, very few proteins were dissociated from the ER complex in the absence of GATA3, with the only major change being depletion of TET2 from the ER complex. In breast cancer cells and Patient-Derived Xenograft (PDX) tissue, TET2 binding events were shown to constitute a near-total subset of ER binding events, and loss of TET2 was functionally associated with reduced activation of proliferative pathways. To investigate the TET2-ER relationship, the role of TET2 in regulating DNA modifications in ER+ breast cancer cells was examined. TET2 knockdown did not appear to result in changes to global DNA methylation, however, oxidation of methylated DNA to 5-hydroxymethylcytosine (5hmC) was significantly reduced after TET2 depletion and these events occurred at ER enhancers. These findings implicate TET2 in the production and maintenance of 5hmC at ER sites, providing a potential mechanism for TET2-mediated regulation of ER target genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE153251 TET2 is a component of the estrogen receptor complex and controls 5mC to 5hmC conversion at estrogen receptor cis-regulatory regions. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2021.108776 {Cell reports (7.815): 10.1016/j.celrep.2021.108776} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA641868 https://www.ebi.ac.uk/ena/browser/view/PRJNA641868 https://www.ncbi.nlm.nih.gov/sra?term=SRP268807 [Overal design]ChIP-seq in breast cancer cell lines, either untreated, or in response to TET2 knockdown or fulvestrant treatment. Additionally, ChIP-seq in untreated PDX samples.; [Treatment]'For the siRNA-mediated knockdown, cells were transfected with ON-TARGETplus SMARTPools (Dharmacon) targeting ER or TET2. A non-targeting siRNA pool was used as a control. For fulvestrant (ICI 182 780, "ICI") treatment, cells were treated with 100nM compound or vehicle for 3 hours.'; [Growth]'MCF7 cells were grown in DMEM supplemented with 10% FBS, 2mM L-glutamine, 50 U/ml penicillin, 50 ug/ml streptomycin. ZR75-1 cells were grown in RPMI supplemented with 10% FBS, 2mM L-glutamine and 50 U/ml penicillin and 50 ug/ml streptomycin.'; [Extraction]"Cells were crosslinked with 2mM DSG for 20 min followed by crosslinking in 1% formaldehyde for 10 min and then quenched in 100mM glycine. Nuclear enrichment was performed followed by sonication for 15 minutes (Bioruptor plus, Diagenode). Chromatin was immunoprecipitated over night using specific antibodies. Beads were washed six times in RIPA buffer and eluted from beads using SDS buffer. After RNase and proteinase K treatment, DNA was purified by phenol/chloroform extraction.\nLibraries were prepared using the Thruplex kit (Illumina) according to the manufacturer's instructions."; [Cell type]'Breast cancer''cell line: MCF7; cell type: Breast cancer; treatment: No treatment; chip antibody: input; ', 'cell line: ZR75-1; cell type: Breast cancer; treatment: No treatment; chip antibody: input; ', 'cell line: MCF7; cell type: Breast cancer; treatment: No treatment; chip antibody: ab3575 (Abcam)/06-935 (Millipore); ', 'cell line: MCF7; cell type: Breast cancer; treatment: No treatment; chip antibody: ab94580 (Abcam); ', 'cell line: ZR75-1; cell type: Breast cancer; treatment: No treatment; chip antibody: ab3575 (Abcam)/06-935 (Millipore); ', 'cell line: ZR75-1; cell type: Breast cancer; treatment: No treatment; chip antibody: ab94580 (Abcam); ', 'cell line: STG195; cell type: Breast cancer; treatment: No treatment; chip antibody: input; ', 'cell line: AB555; cell type: Breast cancer; treatment: No treatment; chip antibody: input; ', 'cell line: STG195; cell type: Breast cancer; treatment: No treatment; chip antibody: ab3575 (Abcam)/06-935 (Millipore); ', 'cell line: AB555; cell type: Breast cancer; treatment: No treatment; chip antibody: ab3575 (Abcam)/06-935 (Millipore); ', 'cell line: STG195; cell type: Breast cancer; treatment: No treatment; chip antibody: ab94580 (Abcam); ', 'cell line: AB555; cell type: Breast cancer; treatment: No treatment; chip antibody: ab94580 (Abcam); ', 'cell line: MCF7; cell type: Breast cancer; treatment: Control siRNA 72hr; chip antibody: ab3575 (Abcam); ', 'cell line: MCF7; cell type: Breast cancer; treatment: TET2 siRNA 72hr; chip antibody: ab3575 (Abcam); ', 'cell line: MCF7; cell type: Breast cancer; treatment: Control siRNA 48hr; chip antibody: ab94580 (Abcam); ', 'cell line: MCF7; cell type: Breast cancer; treatment: TET2 siRNA 48hr; chip antibody: ab94580 (Abcam); ', 'cell line: MCF7; cell type: Breast cancer; treatment: Control siRNA 48hr; chip antibody: input; ', 'cell line: MCF7; cell type: Breast cancer; treatment: siRNA control; chip antibody: input; ', 'cell line: MCF7; cell type: Breast cancer; treatment: Control siRNA 72hr; chip antibody: input; ', 'cell line: MCF7; cell type: Breast cancer; treatment: Control 3hr; chip antibody: ab94580 (Abcam); ', 'cell line: MCF7; cell type: Breast cancer; treatment: 100nM Fulvestrant 3hr; chip antibody: ab94580 (Abcam); ', 'cell line: MCF7; cell type: Breast cancer; treatment: Control 3hr; chip antibody: input; ', 'cell line: MCF7; cell type: Breast cancer; treatment: 100nM Fulvestrant 3hr; chip antibody: input; ', 'cell type: Breast cancer; treatment: Vehicle; genotype/variation: wild type; chip antibody: none; ', 'cell type: Breast cancer; treatment: Vehicle; genotype/variation: mutant; chip antibody: none; ', 'cell type: Breast cancer; treatment: Vehicle; genotype/variation: wild type; chip antibody: mix_of_millipore_06_935_&_ab3575; ', 'cell type: Breast cancer; treatment: Vehicle; genotype/variation: mutant; chip antibody: mix_of_millipore_06_935_&_ab3575; ', 'cell type: Breast cancer; treatment: Vehicle; genotype/variation: wild type; chip antibody: ab94580; ', 'cell type: Breast cancer; treatment: Vehicle; genotype/variation: mutant; chip antibody: ab94580; ', 'cell type: Breast cancer; treatment: Vehicle; genotype/variation: wild type; chip antibody: sc268; ', 'cell type: Breast cancer; treatment: Vehicle; genotype/variation: mutant; chip antibody: sc268; ' GSE113379 Mus musculus 3 Expression profiling by high throughput sequencing GPL11002 A Syngeneic ErbB2 Mammary Cancer Model for Preclinical Immunotherapy Trials [RNA-seq] 2018-04-19 A cell line was derived from a mammary carcinoma in the transgenic FVB/N-Tg(MMTV-ErbB2)NDL2-5Mul mouse. The line, referred to as “NDL(UCD)” is adapted to standard cell culture and can be transplanted into syngeneic FVB/N mice. The line maintains a stable phenotype over multiple in vitro passages and rounds of in vivo transplantation. The cell line exhibits high expression of ErbB2 and ErbB3 and signaling molecules downstream from ErbB2. The line was previously shown to be reactive to anti-immune checkpoint therapy with responses conducive to immunotherapy studies. Here, using both histology/immunophenotyping and gene expression/microarray analysis, we show that the syngeneic transplant tumors elicit an immune reaction in the adjacent stroma, with additional tumor infiltrating lymphocytes. We also show that this immune activating effect is greater in the syngeneic transplants than in the primary tumors arising in the native transgenic mouse. We further analyzed the PD-1 and PD-L-1 expression in the model and found PD-L1 expression in the tumors and in vitro. In conclusion these data document the validity and utility of this cell line for in vivo preclinical immunotherapy trials. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113379 A Syngeneic ErbB2 Mammary Cancer Model for Preclinical Immunotherapy Trials. Journal of mammary gland biology and neoplasia 2.758 https://doi.org/10.1007/s10911-019-09425-3 {Journal of mammary gland biology and neoplasia (2.758): 10.1007/s10911-019-09425-3} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA450988 https://www.ebi.ac.uk/ena/browser/view/PRJNA450988 https://www.ncbi.nlm.nih.gov/sra?term=SRP141163 [Overal design]Flash frozen NDL(UCD) cell line tumor transplants were sampled and whole-transcriptome analysis was performed by next-generation sequencing (NGS)-based RNA-Sequencing. This series includes three biological replicates of the same cell line grown in three different (but same strain) mouse.; [Treatment]'None'; [Growth]'The NDL(UCD) transplantable mouse mammary tumor cell line was propagated in vitro and then injected as a bolus (0.1 – 2.0 x 10^6 cells) bilaterally into the uncleared #2, #3, and #4 mammary fat pads of 6- to 8-week-old female FVB/NJ mice. Tumors were harvested when they reached a maximum width of 5-10 mm, cut into 1-2mm sections, and then immediately snap-frozen.'; [Extraction]'RNA was isolated from frozen samples using the miRNeasy FFPE Kit (Qiagen) according to the manufacturer’s protocols. Total RNA was eluted from the columns in nuclease-free water and stored at -80°C.\nTotal RNA-Seq sequencing libraries were prepared from both intact RNA derived from flash-frozen samples and severely fragmented RNA isolated from FFPE samples. Briefly, rRNA-depleted RNA was prepared from total RNA input (1-5 ug) using the Ribo-Zero rRNA Removal Kit (Epicentre), which selectively depletes rRNA by hybridization to biotinylated capture probes followed by microsphere bead capture. Subsequently, directional Total RNA-Seq libraries were prepared from rRNA-depleted RNA (50 ng) using the ScriptSeq v2 RNA-Seq Library Preparation Kit (Epicentre) according to the manufacturer’s protocol. Briefly, 5’,3’-di-tagged cDNA was synthesized using tagged random hexamer-primed cDNA synthesis primers followed by annealing of 3’-terminal-tagging oligo (TTO) and extension with DNA Polymerase. The cDNA was then purified with Agencourt AMPure XP beads (Beckman Coulter, Inc.) or with the MinElute PCR Purification Kit (Qiagen), depending upon the source of RNA from flash-frozen or FFPE samples respectively. Illumina adaptor sequences and indexes were then incorporated during library amplification with the appropriate PCR primers and high-fidelity FailSafe PCR Enzyme Mix. Subsequently, the libraries were purified in a similar manner to that described above for the cDNA preparations. The ScriptSeq v2 libraries were then quantitated with the Qubit fluorometer (Invitrogen Life Sciences) and insert sizes determined with the Agilent 2100 Bioanalyzer. The molar concentration of PCR-competent sequencing templates in the libraries was then determined using by quantitative PCR with the KAPA Library Quantification Kit (Kapa Biosystems, Inc.).'; [Cell type]'Source: ''tissue: mammary tumor; strain: FVB/N; gender: female; ' GSE67867 Mus musculus; Homo sapiens 48 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing GPL16791; GPL17021 Competition between DNA methylation and transcription factors determines binding of NRF1 2015-04-14 Eukaryotic transcription factors (TFs) are key determinants of gene activity, yet they bind only a fraction of their corresponding DNA sequence motifs in any given cell type. Chromatin has the potential to restrict accessibility of binding sites; however, in which context chromatin states are instructive for TF binding remains mainly unknown. To explore the contribution of DNA methylation to constrained TF binding, we mapped DNase-I-hypersensitive sites in murine stem cells in the presence and absence of DNA methylation. Methylation-restricted sites are enriched for TF motifs containing CpGs, especially for those of NRF1. In fact, the TF NRF1 occupies several thousand additional sites in the unmethylated genome, resulting in increased transcription. Restoring de novo methyltransferase activity initiates remethylation at these sites and outcompetes NRF1 binding. This suggests that binding of DNA-methylationsensitive TFs relies on additional determinants to induce local hypomethylation. In support of this model, removal of neighbouring motifs in cis or of a TF in trans causes local hypermethylation and subsequent loss of NRF1 binding. This competition between DNA methylation and TFs in vivo reveals a case of cooperativity between TFs that acts indirectly via DNA methylation. Methylation removal by methylation-insensitive factors enables occupancy of methylation-sensitive factors, a principle that rationalizes hypomethylation of regulatory regions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE67867 Competition between DNA methylation and transcription factors determines binding of NRF1. Nature 43.070 https://doi.org/10.1038/nature16462 {Nature (43.070): 10.1038/nature16462} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA281090 https://www.ebi.ac.uk/ena/browser/view/PRJNA281090 https://www.ncbi.nlm.nih.gov/sra?term=SRP057157 [Overal design]DNase-seq (2 replicates) in mouse embryonic stem cells with (WT) and without DNA methylation (DNMT TKO). RNA-seq (3 replicates) in WT and DNMT TKO cells and in DNMT TKO cells after treatment with control siRNA or siRNA targeting Nrf1. H3K27ac ChIP-seq (2 replicates) in WT and DNMT TKO cells. NRF1 ChIP-seq (2 replicates) in WT and DNMT TKO cells, in WT upon culture in different conditions (adaptation to 2i and back to serum), upon transient overexpression of NRF1 and after differentiation into neuronal progenitor cells (NP). Whole-genome bisulfite sequencing in DNMT TKO cells and in WT upon culture in different conditions (adaptation to 2i and back to serum). NRF1 ChIP-seq (2 replicates) in human HMEC and HCC1954 cells.; [Treatment]'None', 'For transient overexpression of NRF1, a plasmid containing Nrf1 under the control of the CAG promoter was reverse transfected into 159 cells 12 h prior to harvesting\nFor transient overexpression of NRF1, a plasmid containing Nrf1 under the control of the CAG promoter was reverse transfected into 159 cells 12 h prior to harvesting', 'For transient overexpression of NRF1, a plasmid containing Nrf1 under the control of the CAG promoter was reverse transfected into 159 cells 12 h prior to harvesting', 'Negative control siRNA for 72h (Qiagen, AllStars Negative Control siRNA, SI03650318)\nNegative control siRNA for 72h (Qiagen, AllStars Negative Control siRNA, SI03650318)', 'siRNA targeting Nrf1 for 72h (Qiagen, Mm_Nrf1_7 FlexiTube siRNA, SI05183738)\nsiRNA targeting Nrf1 for 72h (Qiagen, Mm_Nrf1_7 FlexiTube siRNA, SI05183738)'; [Growth]'Mouse embryonic stem cells were cultivated without feeders on 0.2% gelatine-coated dishes in DMEM, supplemented with 15% fetal calf serum, 1× non-essential amino acids, 2 mM L-glutamine, LIF and 0.001% β-mercaptoethanol (37°C, 7% CO2).', 'Mouse embryonic stem cells were cultivated without feeders on 0.2% gelatine-coated dishes in DMEM, supplemented with 15% fetal calf serum, 1× non-essential amino acids, 2 mM L-glutamine, LIF and 0.001% β-mercaptoethanol (37°C, 7% CO2). Serum-free cultivation was performed in N2B27 medium, supplemented with 1× non-essential amino acids, 2 mM L-glutamine, LIF and 0.001% β-mercaptoethanol as well as MEK inhibitor PD0325901 (1 µM) and GSK3 inhibitor CHIR99021 (3 µM), together known as 2i. For reversal between culturing conditions, cells were cultured for at least three weeks under the new conditions prior to performing downstream experiments.', 'WT mouse ES cells (159) were differentiated to neuronal progenitors as previously described (Bibel et al. Nature Protocols 2007).', "HMECs were purchased from Lonza (CC-2551), cultivated according to the distributor's instructions and harvested after two passages.", 'HCC1954 cells were cultured in RPMI 1640 medium supplemented with 10% fetal calf serum, 1× nonessential amino acids and 1× L-glutamine (37°C, 5% CO2).'; [Extraction]'DNase treatment was performed essentially as previously described, with some modifications (John et al. Curr Prot Mol Biol 2013). Briefly, intact nuclei were extracted using 0.03% NP-40 in an isotonic buffer. After NP-40 removal, batches of 5 million nuclei were incubated for 4 min at 37°C with a range of DNase I (DPRF, Worthington) concentrations in the presence of Ca2+. The digestion was stopped by addition of EDTA/SDS and the samples were treated with proteinase K and RNase A. Phenol-chloroform extracted DNA was separated on a 5-30% sucrose gradient by ultracentrifugation for 24 h and fractionated with a Gilson fraction Collector FC 203B. Fractions were precipitated with ethanol and resuspended in TE buffer. Both successful digestion and size separation were verified by agarose gel electrophoresis. Low-coverage sequencing of a bar-coded pool of samples derived from different fractions of the sucrose gradient and treated with different DNase concentrations was used to select the sample with the highest information content.\nLibrary Construction Protocol: Libraries for DNase-seq were prepared essentially according to standard Illumina protocols, using 40 ng of the precipitated fractions of the sucrose gradient as starting material. To reduce amplification bias, end-repaired, A-tailed and adapter ligated DNA was amplified in 6 cycles of PCR with KAPA HiFi Hot Start polymerase. Adapter dimers were subsequently removed with Agencourt AMPure XP beads (Beckman Coulter). Quality of the libraries and size distribution was assessed on an Agilent 2100 Bioanalyzer (Agilent Technologies). Sequencing was performed on an Illumina HiSeq 2500 machine (50 bp read length, single end) according to Illumina standards.', 'RNA was isolated with the RNeasy Mini kit (Qiagen) with on-column DNA digestion. Two micrograms of total RNA were depleted from ribosomal RNA using the Ribo-Zero rRNA removal kit (Epicentre).\nLibrary Construction Protocol: Strand-specific libraries for RNA-seq were prepared using the ScriptSeq v2 protocol (Epicentre). Quality of the libraries and size distribution was assessed on an Agilent 2100 Bioanalyzer (Agilent Technologies). Sequencing was performed on an Illumina HiSeq 2500 machine (50 bp read length, single end) according to Illumina standards.', 'Chromatin immunoprecipitation (ChIP) was carried out essentially as previously described (Jermann et al. PNAS 2014).\nLibrary Construction Protocol: Libraries for ChIP-seq were prepared according to standard Illumina library preparation protocols. Twelve cycles of PCR (NEB Q5 Hot Start HiFi PCR) were performed on end-repaired, A-tailed and adapter-ligated DNA prior to gel size-selection. Quality of the libraries and size distribution was assessed on an Agilent 2100 Bioanalyzer (Agilent Technologies). Sequencing was performed on an Illumina HiSeq 2500 machine (50 bp read length, single end) according to Illumina standards.', 'DNA was isolated by phenol chloroform extraction, followed by ethanol precipitation.\nLibrary Construction Protocol: 5 μg of sonicated genomic DNA were end repaired and 3′-end adenylated using the Illumina TruSeq DNA LT Sample Preparation kit (Illumina 15025064). Paired-end adapters were ligated to the DNA fragments and adaptor-ligated DNA was purified by 2% agarose gel electrophoresis. The gel-purified DNA was converted with the EpiTect Bisulfite kit (Qiagen). Converted libraries were enriched by 10 cycles of PCR using PfuTurbo Cx Hotstart DNA Polymerase (Agilent) and purified using AMPure XP beads. Quality of the libraries and size distribution was assessed on an Agilent 2100 Bioanalyzer (Agilent Technologies). Sequencing was performed on an Illumina HiSeq 2500 machine (100 bp read length, paired end) according to Illumina standards.'; [Cell type]'Source: ''strain: 159 (mixed 129-C57Bl/6); genotype: WT; growth condition: serum; ', 'strain: 159 (mixed 129-C57Bl/6); genotype: DNMT TKO; growth condition: serum; ', 'strain: 159 (mixed 129-C57Bl/6); genotype: WT; growth condition: adaptation to 2i (> 3 weeks); chip antibody: NRF1 (Abcam, ab55744); ', 'strain: 159 (mixed 129-C57Bl/6); genotype: WT; growth condition: adaptation to 2i (> 3 weeks); chip antibody: none; ', 'strain: 159 (mixed 129-C57Bl/6); genotype: WT; growth condition: adaptation from 2i back to serum (3 weeks); chip antibody: NRF1 (Abcam, ab55744); ', 'strain: 159 (mixed 129-C57Bl/6); genotype: WT; growth condition: adaptation from 2i back to serum (3 weeks); chip antibody: none; ', 'strain: 159 (mixed 129-C57Bl/6); genotype: WT; growth condition: serum; chip antibody: NRF1 (Abcam, ab55744); ', 'strain: 159 (mixed 129-C57Bl/6); genotype: WT; growth condition: serum; chip antibody: none; ', 'strain: 159 (mixed 129-C57Bl/6); genotype: WT; growth condition: serum; chip antibody: none (input); ', 'strain: 159 (mixed 129-C57Bl/6); genotype: DNMT TKO; growth condition: serum; chip antibody: NRF1 (Abcam, ab55744); ', 'strain: 159 (mixed 129-C57Bl/6); genotype: DNMT TKO; growth condition: serum; chip antibody: none (input); ', 'strain: 159 (mixed 129-C57Bl/6); genotype: WT; chip antibody: NRF1 (Abcam, ab55744); ', 'strain: 159 (mixed 129-C57Bl/6); genotype: WT; chip antibody: none (input); ', 'strain: 159 (mixed 129-C57Bl/6); genotype: WT; growth condition: serum; chip antibody: H3K27ac (Abcam, ab4729); ', 'strain: 159 (mixed 129-C57Bl/6); genotype: DNMT TKO; growth condition: serum; chip antibody: H3K27ac (Abcam, ab4729); ', 'cell line: HMEC; genotype: WT; chip antibody: NRF1 (Abcam, ab55744); ', 'cell line: HMEC; genotype: WT; chip antibody: none (input); ', 'cell line: HCC1954; genotype: WT; chip antibody: NRF1 (Abcam, ab55744); ', 'cell line: HCC1955; genotype: WT; chip antibody: NRF1 (Abcam, ab55744); ', 'cell line: HCC1956; genotype: WT; chip antibody: none (input); ', 'strain: 159 (mixed 129-C57Bl/6); genotype: WT; growth condition: adaptation to 2i (> 3 weeks); ', 'strain: 159 (mixed 129-C57Bl/6); genotype: WT; growth condition: adaptation from 2i back to serum (3 weeks); ' GSE21657 Homo sapiens 4 Expression profiling by array GPL201 BP1 Expression Promotes Tumorigenesis and Aggression in MCF-7 Breast Cancer Cells 2010-05-04 This study was designed to identify genes that are differentially expressed when BP1 homeobox gene is overexpressed in MCF-7 breast cancer cells. The goal is to understand the functional role of BP1 in breast tumorigenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE21657 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA125887 https://www.ebi.ac.uk/ena/browser/view/PRJNA125887 None [Overal design]MCF-7 overexpressing pcDNA3.2-BP1 clones, O1 and O4 as replicates vs. MCF-7 transfected with pcDNA3.2 vector clones, V1 and V2 as replicates; [Treatment]'None'; [Growth]'None'; [Extraction]'Trizol reagent (Invitrogen) and RNeasy kit (Qiagen) was used to isolate and purify total RNA'; [Cell type]'Source: ''cell line: MCF-7; expression: Control; ', 'cell line: MCF-7; expression: BP1-overexpressor; ' GSE100529 Homo sapiens 23 Genome variation profiling by SNP array GPL23668 Genome-wide multi-omics profiling reveals extensive genetic complexity in 8p11-p12 amplified breast carcinomas [SNP_genotyping] 2017-06-27 SNP genotyping of human breast tumors https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE100529 Genome-wide multi-omics profiling of the 8p11-p12 amplicon in breast carcinoma. Oncotarget None https://doi.org/10.18632/oncotarget.25329 {Oncotarget (None): 10.18632/oncotarget.25329} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA392039 https://www.ebi.ac.uk/ena/browser/view/PRJNA392039 None [Overal design]High-resolution copy number analysis of 8p11-p12 amplified breast carcinomas; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA was isolated from fresh-frozen tissue specimens using the Wizard Genomic DNA extraction kit, including proteinase K treatment followed by phenol chloroform purification'; [Cell type]'Source: ''8p11-p12 amplification: Amplified; age: 82; pt status: pT3; lymph node status: pN0; er status: pos; pgr status: pos; her2 status: pos; ', '8p11-p12 amplification: Amplified; age: 76; pt status: pT3; lymph node status: pN1; er status: pos; pgr status: pos; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 52; pt status: pT2; lymph node status: pN0; er status: neg; pgr status: neg; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 83; pt status: pT3; lymph node status: NA; er status: pos; pgr status: pos; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 73; pt status: NA; lymph node status: NA; er status: pos; pgr status: neg; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 79; pt status: NA; lymph node status: pN0; er status: pos; pgr status: neg; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 78; pt status: pT3; lymph node status: pN1; er status: neg; pgr status: neg; her2 status: pos; ', '8p11-p12 amplification: Amplified; age: 63; pt status: pT1; lymph node status: pN1; er status: pos; pgr status: pos; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 88; pt status: NA; lymph node status: NA; er status: pos; pgr status: pos; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 83; pt status: pT3; lymph node status: pN1; er status: pos; pgr status: neg; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 65; pt status: pT2; lymph node status: pN0; er status: pos; pgr status: neg; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 39; pt status: pT2; lymph node status: pN1; er status: pos; pgr status: neg; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 54; pt status: pT1; lymph node status: pN0; er status: pos; pgr status: neg; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 72; pt status: NA; lymph node status: NA; er status: pos; pgr status: pos; her2 status: pos; ', '8p11-p12 amplification: Amplified; age: 84; pt status: pT3; lymph node status: pN1; er status: pos; pgr status: pos; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 46; pt status: pT2; lymph node status: pN1; er status: pos; pgr status: pos; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 86; pt status: NA; lymph node status: NA; er status: pos; pgr status: pos; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 64; pt status: pT3; lymph node status: pN1; er status: pos; pgr status: pos; her2 status: neg; ', '8p11-p12 amplification: Amplified; age: 61; pt status: pT3; lymph node status: pN1; er status: neg; pgr status: neg; her2 status: pos; ', '8p11-p12 amplification: Amplified; age: 57; pt status: pT2; lymph node status: pN0; er status: pos; pgr status: neg; her2 status: neg; ' GSE92281 Homo sapiens 12 Expression profiling by array GPL10558 Level of FACT defines the transcriptional landscape and aggressive phenotype of breast cancer cells 2016-12-12 FACT inhibition, via small molecule or shRNA, lead to reduced growth and viability of all BrCa cells tested. Phenotypic changes were more severe in high FACT cells (death or growth arrest) than in low FACT cells (decreased proliferation). Though inhibition had no effect on the rate of general transcription, expression of individual genes was changed in a cell-specific manner. Initially distinct transcriptional profiles of BrCa cells became almost identical via equalizing FACT expression. We found that in “high-FACT” cells FACT supports expression of genes involved in the regulation of cell cycle, DNA replication, maintenance of undifferentiated cell state and regulated by the activity of proto-oncogenes, such as Hras, cMyc, E2F family ets. In “low-FACT” cells presence of FACT reduces expression of genes coding enzymes of steroid metabolism characteristic for the differentiated mammary epithelia. Inhibition of FACT leads to the shift from more aggressive transcriptional program to more benign, accompanied with similar type of phenotypical changes. Thus we propose FACT as a marker to predict aggressiveness of BrCa and as a target to either kill aggressive BrCa cells or to convert them to a less aggressive phenotype. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE92281 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA357086 https://www.ebi.ac.uk/ena/browser/view/PRJNA357086 None [Overal design]MCF7, MCF7v.1 and T47D cells were transduced with lentiviral vectors encoding control shRNA or two shRNAs to SSRP1 subunit of FACT. RNA was isolated from cells at 72 hrs post-transduction and used for microarray hybridization.; [Treatment]'lentiviral transduction with control shRNA (scrambled) or shRNAs to SSRP1. 72 hours after transduction.'; [Growth]'standard growth conditions in DMEM + 5% FBS + antibiotic solution'; [Extraction]'Trizol reagent'; [Cell type]'Source: ''condition: Control; cell line: MCF7v1; ', 'condition: Treatment; cell line: MCF7v1; ', 'condition: Control; cell line: T47D; ', 'condition: Treatment; cell line: T47D; ', 'condition: Control; cell line: MCF7; ', 'condition: Treatment; cell line: MCF7; ' GSE17945 Saccharomyces cerevisiae 44 Expression profiling by array GPL9143 tRNA Over-Expression in Breast Cancer 2009-09-02 Increased proliferation and elevated levels of protein synthesis are characteristic of transformed and tumor cells. Though components of the translation machinery are often misregulated in cancers, how tRNA plays a role in cancer cells has not been explored. We compare genome-wide tRNA expression in tumorigenic versus non-tumorigenic breast cell lines, as well as tRNA expression in breast tumors versus normal breast tissues. In tumorigenic versus non-tumorigenic cell lines, nuclear-encoded tRNAs increase by up to 3-fold and mitochondrial-encoded tRNAs increase by up to 5-fold. In tumors versus normal breast tissues, both nuclear and mitochondrial-encoded tRNAs increase by up to 10-fold. This tRNA over-expression is selective and coordinates with the properties of cognate amino acids. Nuclear- and mitochondrial-encoded tRNAs exhibit distinct expression patterns, indicating that tRNAs can be used as biomarkers for breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17945 tRNA over-expression in breast cancer and functional consequences. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkp787 {Nucleic acids research (11.147): 10.1093/nar/gkp787} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA119953 https://www.ebi.ac.uk/ena/browser/view/PRJNA119953 None [Overal design]We analyzed tRNA expression levels in 2 non-tumorigenic breast cell lines, 6 tumorigenic breast cancer cell lines, 3 normal breast tissue samples, and 9 breast tumor samples. We used a non-tumorigenic breast cell line (MCF10A) as a reference sample in all hybridizations. All data is dye-swapped.; [Treatment]'Deacylation: 0.25µg/µl total RNA premixed with three tRNA standards (E. coli tRNALys, E. coli tRNATyr, and yeast tRNAPhe) at 0.2µM each was incubated in 100mM Tris-HCl (pH 9.0) at 37°C for 30 minutes. The solution was neutralized by the addition of an equal volume of 100mM Na-acetate/acetic acid (pH 4.8) plus 100mM NaCl, followed by ethanol precipitation. Deacylated total RNA was dissolved in water, and its integrity verified by agarose gel electrophoresis.'; [Growth]'All cell lines were purchased from American Type Culture Collection (ATCC, Manassas, VA) and maintained according to ATCC recommendations. MCF7 cells were cultured in DMEM medium (Invitrogen, 11965-092) supplemented with 10% FBS and 1% penicillin/streptomycin (P/S). MCF10A cells were cultured in 1:1 (+I factor, Vectro)-DMEM/F12 (Invitrogen, 11330-032) supplemented with 10% FBS, 1% P/S, 5μg/mL insulin, 10ng/mL EGF, and 0.5μg/mL hydrocortisone. All other cell lines were cultured in RPMI 1640 1X medium (Mediatech, 10-040-CV) supplemented with 10% FBS and 1% P/S.'; [Extraction]'Cell lines: total RNA for each cell line was obtained at 80-90% confluency using the mirVanaTM miRNA Isolation Kit (Ambion, AM1560). This procedure isolates RNA species as short as 15 nucleotides and is therefore not biased against tRNA. Normal breast: two samples of human breast total RNA were purchased from Ambion (FirstChoice® Human Breast Total RNA, AM6952, lot numbers 0808001 and 0812006). An additional sample of human breast total RNA was purchased from Stratagene (MVP Total RNA Human Breast, 540045, lot number 0380023). Both providers certify small RNA content in total RNA samples and provide relevant donor information. Breast tumors: Breast tumor samples were obtained from the Human Tissue Resource Center (HTRC) at the University of Chicago. Pathology reports were provided for all samples. All breast tumor samples were obtained frozen and embedded in OCT (optimal cutting temperature compound). Following removal of the surrounding OCT and tissue pulverization, total RNA was isolated using TRIzol reagent (Invitrogen, 15596-018). In all cases, total RNA quality was checked on agarose gels.'; [Cell type]'Source: ''total rna source: 80-90% confluent cell culture; source type: Cell line; tumor type: Fibrocystic disease; receptor status: ER-, PR-, HER2-; ', 'total rna source: 80-90% confluent cell culture; source type: Cell line; tumor type: Invasive ductal carcinoma (ascites); receptor status: ER+, PR+, HER2-; ', 'total rna source: 80-90% confluent cell culture; source type: Cell line; tumor type: Ductal carcinoma (primary); receptor status: ER+, PR-, HER2-; ', 'total rna source: 80-90% confluent cell culture; source type: Cell line; tumor type: Adenocarcinoma (pleural effusion); receptor status: ER-, PR-, HER2-; ', 'total rna source: 80-90% confluent cell culture; source type: Cell line; tumor type: Invasive ductal carcinoma (pleural effusion); receptor status: ER+, PR+, HER2-; ', 'total rna source: 80-90% confluent cell culture; source type: Cell line; tumor type: Invasive ductal carcinoma (primary); receptor status: ER+, PR+, HER2+; ', 'total rna source: 80-90% confluent cell culture; source type: Cell line; tumor type: Normal; receptor status: ER-, PR-, HER2-; ', 'total rna source: Ambion FirstChoice human breast total RNA; source type: Tissue sample; tumor type: Normal; receptor status: ND; ', 'total rna source: Stratagene MVP total RNA, human breast; source type: Tissue sample; tumor type: Fibrocystic disease; receptor status: ND; ', 'total rna source: OCT-embedded tumor sample; source type: Tissue sample; tumor type: Invasive ductal carcinoma; receptor status: ER-, PR-, HER2-; ', 'total rna source: OCT-embedded tumor sample; source type: Tissue sample; tumor type: Ductal carcinoma in situ; receptor status: ER-, PR-, HER2-; ', 'total rna source: OCT-embedded tumor sample; source type: Tissue sample; tumor type: Ductal breast carcinoma; receptor status: ER-, PR-, HER2+; ', 'total rna source: OCT-embedded tumor sample; source type: Tissue sample; tumor type: Unknown; receptor status: ER+, PR+, HER2-; ', 'total rna source: OCT-embedded tumor sample; source type: Tissue sample; tumor type: Ductal carcinoma in situ; receptor status: ER+, PR+, HER2-; ', 'total rna source: OCT-embedded tumor sample; source type: Tissue sample; tumor type: Ductal carcinoma in situ; receptor status: ER+, PR-, HER2+; ' GSE53300 Homo sapiens 2 Expression profiling by high throughput sequencing GPL9052 Gene expression profiling of breast cancer cells with knockdown of PTEN 2013-12-13 Activation of the PI3K pathway in estrogen receptor α (ER)-positive (+) breast cancer is associated with reduced ER expression and activity, luminal B subtype, and poor outcome. PTEN is a negative regulator of the PI3K pathway typically lost in ER-negative (-) breast cancer. To clarify the effect of PTEN down-regulation on the response of ER+/HER2- breast cancer to endocrine therapy, we established reduced PTEN cell models using inducible knockdown. We found that only moderate PTEN reduction is sufficient to enhance PI3K signaling, generate a gene signature associated with luminal B subtype, and cause endocrine resistance. Combining endocrine therapy with mTOR, AKT, or MEK inhibitors improves antitumor activity, but the efficacy varies by type of endocrine therapy and the specific inhibitor. Fulvestrant plus an AKT inhibitor is the most potent combination when PTEN is reduced, inducing apoptosis and tumor regression. This combination deserves further study in patients with PI3K pathway activation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53300 Overcoming endocrine resistance due to reduced PTEN levels in estrogen receptor-positive breast cancer by co-targeting mammalian target of rapamycin, protein kinase B, or mitogen-activated protein kinase kinase. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-014-0430-x {Breast cancer research : BCR (5.676): 10.1186/s13058-014-0430-x} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA231626 https://www.ebi.ac.uk/ena/browser/view/PRJNA231626 https://www.ncbi.nlm.nih.gov/sra?term=SRP034017 [Overal design]Gene expression profiles (by RNA-seq) were taken of a cell model with or without reduced PTEN (using inducible knockdown).; [Treatment]'pINDUCER Lentiviral System to reduced PTEN was carried out as previously described (PMID:21307310).'; [Growth]'Human breast cancer cell line MCF7L (from Dr. Marc Lippman) were all authenticated and maintained in RPMI/1640 medium supplemented with 10% heat-inactivated FBS and 1% penicillin/streptomycin/glutamine, and incubated at 37°C in 5% CO2.'; [Extraction]'Invitrogen Trizol\nIllumina TruSeq RNA, according to standard protocol'; [Cell type]'Source: ''genotype/variation: control; ', 'genotype/variation: reduced PTEN; ' GSE158398 Homo sapiens 2 Genome binding/occupancy profiling by high throughput sequencing GPL24676 single-cell ATAC sequencing reveals the mechanism of human breast cancer metastasis 2020-09-22 To obtain more information about the lymph node metastasis of breast cancer cells, we selected the matched positive lymph nodes (PL), and negative lymph nodes (NL) of the same patient to perform integrated analysis. The PL, NL samples were analysed with single-cell ATAC sequencing. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE158398 Integrative analyses of scRNA-seq and scATAC-seq reveal CXCL14 as a key regulator of lymph node metastasis in breast cancer. Human molecular genetics 4.544 https://doi.org/10.1093/hmg/ddab042 {Human molecular genetics (4.544): 10.1093/hmg/ddab042} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA665069 https://www.ebi.ac.uk/ena/browser/view/PRJNA665069 https://www.ncbi.nlm.nih.gov/sra?term=SRP285031 [Overal design]Single cell ATACseq was performed using the 10X Genomics platform per the manufacturers instructions.; [Treatment]'None'; [Growth]'None'; [Extraction]'The concentration of single-cell suspension was adjusted to 1×105 cells/mL in PBS. Cell suspension was transferred to 2-ml tube and centrifuged (300rcf,5 min) to remove supernatant. Then added lysis buffer (Tris-HCl (pH 7.4): 10 mM, NaCl: 10mM, MgCl2: 3mM, Tween-20: 0.1%, Nonidet P40 Substitute: 0.1%, Digitonin: 0.01%, BSA: 1%, right amount nuclease-free waster) to pellet and mixed. Incubated the mixture on ice (3~5min). After that, added wash buffer (Tris-HCl (pH 7.4): 10mM, NaCl: 10mM, MgCl2: 3mM, Tween-20: 0.1%, BSA: 1%, right amount nuclease-free waster) to the mixture, mixed and centrifuged (500 rcf, 5min). The supernatant was removed, and resuspended the pellet by diluted nuclei buffer (10x Genomics, 2000153/2000207). After nuclei concentration was determined by Countess II FL Automated Cell Counter, the resulting nuclei solution was used for library construction immediately.\nThe scATAC libraries were constructed according to the user guide of Chromium Next GEM Single Cell ATAC Reagent Kits v1.1.\nscATAC-seq'; [Cell type]'Source: ''treatment: untreated; tnm stage: T3N2M0; molecular typing: luminal B; ' GSE113288 Homo sapiens 30 Expression profiling by high throughput sequencing GPL9115 WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [RNA-seq PDX] 2018-04-17 The core subunit of the COMPASS-like complex, WD Repeat Domain 5 (WDR5) has a prominent role in reprogramming and Epithelial-to-Mesenchymal transition (EMT) in different tumor types. Our evidences support a model in which WDR5 is prominent for EMT and metastasis dissemination in breast cancer patient-derived xenografts and cell lines. Moreover, WDR5 silencing abrogates TGFB pathway activation and reverts mesenchymal into epithelial phenotype, by inhibiting transcription of main master regulators of EMT (CDH2, TWIST1, SNAI1, SNAI2 and ZEB1). Our data suggest that WDR5 inhibition may be a successful approach to prevent progression of metastatic BC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113288 WDR5 inhibition halts metastasis dissemination by repressing the mesenchymal phenotype of breast cancer cells. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-019-1216-y {Breast cancer research : BCR (5.676): 10.1186/s13058-019-1216-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA450653 https://www.ebi.ac.uk/ena/browser/view/PRJNA450653 https://www.ncbi.nlm.nih.gov/sra?term=SRP140715 [Overal design]Total RNA from human breast cancer metastatic patient-derived xenografts (PDXs) line was processed for multiparallel sequencing. Experiments were carried out in shLuc (control) and WDR5 silenced cells; [Treatment]'See additional columns of the SAMPLES section'; [Growth]'See additional columns of the SAMPLES section'; [Extraction]'2.5x10^4 cells are lysed and processed according to TRUSeq RNA Sample Prep Kit Illumina protocol. Briefly, after cell lysis the poly-A containing mRNA molecules were purified using oligo-dT attached magnetic beads. Following purification, the mRNA is fragmented into small pieces using divalent cations under elevated temperature. The cleaved RNA fragments are copied into first strand cDNA using reverse transcriptase and random primers. Second strand cDNA synthesis follows, using DNA Polymerase I and RNase H. The cDNA fragments then go through an end repair process, the addition of a single ‘A’ base, and then ligation of the adapters. The products are then purified and enriched with PCR to create the final cDNA library for HiSeq 2000 Illumina sequencing.'; [Cell type]'Human Breast Cancer PDXs primary cells''cell type: Human Breast Cancer PDXs primary cells; growth protocol: DMEM supplemented with 10% Fetal Bovine Serum, 2mM L-Glutamine, 1% Pen/Strep, 10mM HEPES, 5 µg/ml Insulin, 0.5 µg/ml Hydrocortisone, 10 ng/ml EGF, 10 NG/ML Cholera Toxin; treatment: Cells were infected with pRSI-U6-shLuc-UbiC-TagRFP-2A-Puro vector and selectioned with 3µg/ml of Puromycin; ', 'cell type: Human Breast Cancer PDXs primary cells; growth protocol: DMEM supplemented with 10% Fetal Bovine Serum, 2mM L-Glutamine, 1% Pen/Strep, 10mM HEPES, 5 µg/ml Insulin, 0.5 µg/ml Hydrocortisone, 10 ng/ml EGF, 10 NG/ML Cholera Toxin; treatment: Cells were infected with pRSI-U6-shWDR5-UbiC-TagRFP-2A-Puro vector and selectioned with 3µg/ml of Puromycin; ' GSE53752 Homo sapiens 76 Expression profiling by array; Third-party reanalysis GPL7264 Molecular characteristics and metastasis predictor genes of triple-negative breast cancer (II) 2014-01-02 This microarray dataset contains 51 triple-negative breast cancers, 25 normal breast tissues, and 106 luminal breast cancers (reanalyzed data from Series GSE24124, GSE9309, and GSE17040). Keywords: Expression profiling by array https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53752 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA232811 https://www.ebi.ac.uk/ena/browser/view/PRJNA232811 None [Overal design]Specimens of breast cancer tissue were collected and snap-frozen from breast cancer patients who had surgery between 1995 and 2008 at National Taiwan University Hospital (NTUH, Taipei, Taiwan). Clinicopathological information was obtained for all breast cancer patients along with informed consent. The AJCC/UICC TNM system was used for breast cancer staging classification.; [Treatment]'The breast tumor samples were excised, collected, and snap-frozen in liquid nitrogen immediately before RNA extraction.'; [Growth]'The breast tumor samples were immediately frozen by liquid nitrogen without any additional growth procedure before RNA extraction.'; [Extraction]'Trizol reagent combined with RNAeasy mini kit'; [Cell type]'Infiltrating Ductal Carcinoma (IDC)', 'Source: ''tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 1453; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 50; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 5.32; event of distant metastasis: 0; event of death: 0; ', 'sample type: Commercially-available reference; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 1621; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 49; ajcc stage: IIIA; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 3; distant metastasis-free (years): 2.54; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 1657; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 56; ajcc stage: IIIA; lymph node metastasis: 1; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 2; tumor size: 2; distant metastasis-free (years): 4.97; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 1661; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 47; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.84; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 1683; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 54; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 2; tumor size: 1; distant metastasis-free (years): 4.95; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 2461; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 60; ajcc stage: IIIA; lymph node metastasis: 1; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 1.24; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4353; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 45; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 0.00; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4355; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 53; ajcc stage: IIB; lymph node metastasis: 1; lymphovascular invasion: 0; grade: 2; mitotic count: 3; nuclear pleomorphism: 2; tubule formation: 2; tumor size: 2; distant metastasis-free (years): 3.30; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4359; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 69; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 6.15; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4361; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 85; ajcc stage: IIIA; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 3; distant metastasis-free (years): 1.20; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4363; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 56; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 5.42; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4365; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 33; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 0.39; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4367; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 66; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 2; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 2; tumor size: 1; distant metastasis-free (years): 0.00; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4369; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 27; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.59; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4371; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 54; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 2; mitotic count: 2; nuclear pleomorphism: 2; tubule formation: 2; tumor size: 1; distant metastasis-free (years): 4.67; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4373; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 52; ajcc stage: IIB; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 3; distant metastasis-free (years): 4.80; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4375; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 54; ajcc stage: IIA; lymph node metastasis: 1; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.76; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4377; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 55; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 4.46; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4379; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 60; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 4.47; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4381; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 57; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 2; mitotic count: 1; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 4.17; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4383; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 55; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.18; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4385; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 51; ajcc stage: IIIC; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 2; tumor size: 3; distant metastasis-free (years): 4.26; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4387; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 44; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.17; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4389; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 37; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 1.79; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4391; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 62; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 2; mitotic count: 2; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.14; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4393; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 51; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 2; mitotic count: 2; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 4.04; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4395; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 63; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.13; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4397; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 68; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 3.95; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4399; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 63; ajcc stage: IIIC; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 3; distant metastasis-free (years): 3.75; event of distant metastasis: 1; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4401; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 61; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 0.71; event of distant metastasis: 1; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4403; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 46; ajcc stage: IIB; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 3.82; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4405; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 65; ajcc stage: IIB; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 3.86; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4407; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 41; ajcc stage: IIIC; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 3; distant metastasis-free (years): 3.06; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4409; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 54; ajcc stage: IIB; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 1.64; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4411; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 58; ajcc stage: IIB; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 2; tumor size: 2; distant metastasis-free (years): 2.11; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4413; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 49; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 2.82; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5307; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 61; ajcc stage: IIIB; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 1.04; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5317; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 83; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 3.53; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5323; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 38; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 2.86; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5325; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 52; ajcc stage: IIA; lymph node metastasis: 1; lymphovascular invasion: N/A; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 2.76; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5327; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 54; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 2.79; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5329; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 51; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 1; grade: N/A; mitotic count: N/A; nuclear pleomorphism: N/A; tubule formation: N/A; tumor size: 2; distant metastasis-free (years): 2.89; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5345; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 63; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 2.87; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5347; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 55; ajcc stage: IIB; lymph node metastasis: 1; lymphovascular invasion: N/A; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 2; tumor size: 2; distant metastasis-free (years): 1.45; event of distant metastasis: 1; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5357; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 57; ajcc stage: IIIC; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 5.53; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5393; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 38; ajcc stage: IIIC; lymph node metastasis: 1; lymphovascular invasion: N/A; grade: N/A; mitotic count: N/A; nuclear pleomorphism: N/A; tubule formation: N/A; tumor size: 2; distant metastasis-free (years): 7.05; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5399; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 40; ajcc stage: IIIC; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 3.96; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 8571; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 54; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: N/A; grade: N/A; mitotic count: N/A; nuclear pleomorphism: N/A; tubule formation: N/A; tumor size: 2; distant metastasis-free (years): 3.08; event of distant metastasis: 1; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 8573; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 41; ajcc stage: IV; lymph node metastasis: 0; lymphovascular invasion: N/A; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 0.13; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 8575; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 53; ajcc stage: IV; lymph node metastasis: 1; lymphovascular invasion: 1; grade: N/A; mitotic count: N/A; nuclear pleomorphism: N/A; tubule formation: N/A; tumor size: 3; distant metastasis-free (years): 0.11; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 8577; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 57; ajcc stage: IV; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 3; distant metastasis-free (years): 0.00; event of distant metastasis: 1; event of death: 1; ', 'gender: female; tissue: normal breast tissue; ' GSE102776 Homo sapiens 4 Expression profiling by array GPL571 Protein acyltransferase DHHC3 regulates breast tumor growth, oxidative stress and senescence. 2017-08-17 Protein acyltransferase DHHC3 is upregulated in malignant and metastatic human breast cancer, and its elevated expression correlates with diminished survival not only in human breast cancer but also in six other cancer types. In a direct demonstration of pro-tumor DHHC3 function, ZDHHC3 ablation diminished both MDA-MB-231 mammary cell xenografts growth and the size of metastatic lung colonies. Gene array data and fluorescence dye assays documented increased oxidative stress and senescence in ZDHHC3-ablated cells. Consistent with increased senescence, ZDHHC3-ablated tumors showed enhanced recruitment of innate immune cells (anti-tumor macrophages, NK cells) associated with clearance of senescent tumors. ZDHHC3-ablation effects (decreased tumor growth, increased oxidative stress, increased senescence) were reversed upon reconstitution with wildtype, but not enzyme active site-deficient DHHC3. ZDHHC3-ablation effects on oxidative stress/senescence were also substantially reversed upon concomitant ablation of upregulated oxidative stress driver TXNIP. Diminished DHHC3-dependent palmitoylation of ERGIC3 protein likely plays a key role in TXNIP upregulation. In conclusion, through its palmitoylation activity, DHHC3 supports in vivo breast tumor growth by a mechanism involving negative modulation of tumor cell oxidative stress and senescence. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE102776 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA398659 https://www.ebi.ac.uk/ena/browser/view/PRJNA398659 None [Overal design]The MDA-MB-231 cells stably ablated for control and DHHC3 protein expression were injected into nude mice (10 injections each with control and D3 ablated cells), and the tumor volumes were assessed over a 30-day period. Subsequently, the mice were sacrificed, followed by excision of tumors. The small portion of the excised tumors were used for RNA extraction and eventually DNA microarray analysis (two replicates each from control and DHHC3 ablated tumors).; [Treatment]'None'; [Growth]'Orthotopic tumor were generated by injecting MDA-MB-231 cells, ablated for control and DHHC3 expression, into mammary fat pads of nude mice'; [Extraction]'Total RNA from xenograft tumors were extracted using Qiagen RNA isolation kit'; [Cell type]'Source: ''host strain: athymic nude mice; host strain gender: female; host strain genotype/variation: Crl:NU(NCr)-Foxn1nu; injected with: MDA-MB-231 cells; genotype/variation: ablated with control shRNA; tissue: xenograft tumor after 35 days; ', 'host strain: athymic nude mice; host strain gender: female; host strain genotype/variation: Crl:NU(NCr)-Foxn1nu; injected with: MDA-MB-231 cells; genotype/variation: ablated with DHHC3 shRNA; tissue: xenograft tumor after 35 days; ' GSE87419 Mus musculus; Homo sapiens 64 Expression profiling by high throughput sequencing GPL11154; GPL13112; GPL18573 Enhancer Remodeling During Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacological Targeting of the P-TEFb Complex (RNA-seq) 2016-09-28 Targeting the dysregulated BRaf-MEK-ERK pathway in cancer has increasingly emerged in clinical trial design. Despite clinical responses in specific cancers using inhibitors targeting BRaf and MEK, resistance develops often involving non-genomic adaptive bypass mechanisms. Inhibition of MEK1/2 by trametinib in triple negative breast cancer (TNBC) patients induced dramatic transcriptional responses, including upregulation of receptor tyrosine kinases (RTKs) comparing tumor samples before and after one week of treatment. In preclinical models MEK inhibition induced genome-wide enhancer formation involving the seeding of BRD4, MED1, H3K27 acetylation and p300 that drives transcriptional adaptation. Inhibition of P-TEFb associated proteins BRD4 and CBP/p300 arrested enhancer seeding and RTK upregulation. BRD4 bromodomain inhibitors overcame trametinib resistance, producing sustained growth inhibition in cells, xenografts and syngeneic mouse TNBC models. Pharmacological targeting of P-TEFb members in conjunction with MEK inhibition by trametinib is an effective strategy to durably inhibit epigenomic remodeling required for adaptive resistance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE87419 Enhancer Remodeling during Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacologic Targeting of the P-TEFb Complex. Cancer discovery 26.370 https://doi.org/10.1158/2159-8290.CD-16-0653 {Cancer discovery (26.370): 10.1158/2159-8290.CD-16-0653} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA344725 https://www.ebi.ac.uk/ena/browser/view/PRJNA344725 https://www.ncbi.nlm.nih.gov/sra?term=SRP090547 [Overal design]64 experimental samples; replicates are indicated in sample title; [Treatment]'None'; [Growth]'culture media: F12 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone, 10 mM HEPES', 'culture media: RPMI 1640 supplemented with 10% FBS', 'culture media: DMEM/F12 1:1 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone'; [Extraction]'Total RNA was isolated using Qiagen RNeasy Plus kit.\n2 µg total RNA and 15 cycles of amplification were used for libraries constructed with Illumina TruSeq RNA Library Prep Kit v2. 4 µg total RNA and 10 cycles of amplification (using 0.5X recommended DNA template) were used for libraries constructed with KAPA Stranded mRNAseq kit or Illumina TruSeq RNA library kit v2.\nlibrary preparation kit: Illumina TruSeq RNA library kit v2', 'Total RNA was isolated using Qiagen RNeasy Plus kit.\n2 µg total RNA and 15 cycles of amplification were used for libraries constructed with Illumina TruSeq RNA Library Prep Kit v2. 4 µg total RNA and 10 cycles of amplification (using 0.5X recommended DNA template) were used for libraries constructed with KAPA Stranded mRNAseq kit or Illumina TruSeq RNA library kit v2.\nlibrary preparation kit: KAPA Stranded mRNAseq kit', 'Total RNA was isolated using Qiagen RNeasy Plus kit.\n2 µg total RNA and 15 cycles of amplification were used for libaries constructed with Illumina TruSeq RNA Library Prep Kit v2. 4 µg total RNA and 10 cycles of amplification (using 0.5X recommended DNA template) were used for libraries constructed with KAPA Stranded mRNAseq kit.'; [Cell type]'Source: ''cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f positive subpopulation; treatment: DMSO; time: 24h; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f positive subpopulation; treatment: 30nM trametinib; time: 24h; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f negative subpopulation; treatment: DMSO; time: 24h; ', 'cell line: SUM229 breast carcinoma cell line, EpCAM/CD49f negative subpopulation; treatment: 30nM trametinib; time: 24h; ', 'cell line: T11 orthotopic serial transplant cell line; treatment: DMSO; time: 24h; ', 'cell line: T11 orthotopic serial transplant cell line; treatment: 500nM trametinib; time: 24h; ', 'cell line: C3TAg GEMM cell line; treatment: DMSO; time: 24h; ', 'cell line: C3TAg GEMM cell line; treatment: 500nM trametinib; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: DMSO; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 300nM JQ1; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 300nM JQ1; time: 24h; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: DMSO; time: 48h; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: 10nM trametinib; time: 48h; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: 300nM JQ1; time: 48h; ', 'cell line: HCC1806 breast carcinoma cell line; treatment: 10nM trametinib 300nM JQ1; time: 48h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 3uMSGCCBP30; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 3uMSGCCBP30; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 500nM IBET151; time: 24h; ', 'cell line: SUM159 breast carcinoma cell line; treatment: 100nM trametinib 500nM IBET151; time: 24h; ', 'xenograft: SUM159 breast carcinoma cell line xenograft; treatment: 2mpk trametinib; time: 48h; ', 'xenograft: SUM159 breast carcinoma cell line xenograft; treatment: 2mpk trametinib 30mpkIBET151; time: 48h; ', 'xenograft: SUM159 breast carcinoma cell line xenograft; treatment: 30mpkIBET151; time: 48h; ', 'xenograft: SUM159 breast carcinoma cell line xenograft; treatment: control; time: 48h; ', 'cell line: HCC1806 breast carcinoma cell line; culture media: RPMI 1640 supplemented with 10% FBS; library preparation kit: KAPA Stranded mRNAseq kit; ', 'cell line: EpCAM/CD49f positive SUM149 breast carcinoma subpopulation; culture media: HuMEC supplemented with 5% FBS and Gibco defined HuMEC supplements; library preparation kit: KAPA Stranded mRNAseq kit; ', 'cell line: MDAMB468 breast carcinoma cell line; culture media: RPMI 1640 supplemented with 10% FBS; library preparation kit: KAPA Stranded mRNAseq kit; ', 'cell line: SUM159 breast carcinoma cell line; culture media: DMEM/F12 1:1 supplemented with 5% FBS, 5 µg/ml insulin, 1 µg/ml hydrocortisone; library preparation kit: KAPA Stranded mRNAseq kit; ', 'cell line: HS578T breast carcinoma cell line; culture media: RPMI 1640 supplemented with 10% FBS; library preparation kit: KAPA Stranded mRNAseq kit; ', 'cell line: PDX breast carcinoma cell line; culture media: RPMI 1640 supplemented with 10% FBS; library preparation kit: KAPA Stranded mRNAseq kit; ' GSE110153 Homo sapiens 11 Expression profiling by array GPL16699 Transcriptomic profiling of triple-negative breast cancer (TNBC) patient-derived xenografts (PDX) sensitive and resistant to docetaxel. 2018-02-05 SurePrint G3 Human Gene Expression Microarray v2 was used to obtain gene expression profiles of two different TNBC PDX models sensitive to docetaxel and in the docetaxel resistant TNBC PDX models derived from both initially sensitive. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE110153 The Altered Transcriptome and DNA Methylation Profiles of Docetaxel Resistance in Breast Cancer PDX Models. Molecular cancer research : MCR 4.484 https://doi.org/10.1158/1541-7786.MCR-19-0040 {Molecular cancer research : MCR (4.484): 10.1158/1541-7786.MCR-19-0040} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA432960 https://www.ebi.ac.uk/ena/browser/view/PRJNA432960 None [Overal design]RNA was isolated from frozen tumors of two different TNBC PDXs models sensitive to docetaxel and from the docetaxel resistant-derived TNBC PDX models. DNAse treated RNA from each sample (n=22) was hybridized to the SurePrint G3 Human Gene Expression Microarray v2 (ID 039494). The Two-Color Microarray-Based Gene Expression Analysis v. 6.5 (Agilent) was used for the labeling.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was isolated by standard procedures using TriPure (Roche, #11667165001)'; [Cell type]'Source: ''tissue: tumor; pdx model: IDB-01S model; sensitivity to docetaxel: Sensitive; ', 'tissue: tumor; pdx model: IDB-01R model; sensitivity to docetaxel: Resistant; ', 'tissue: tumor; pdx model: IDB-02S model; sensitivity to docetaxel: Sensitive; ', 'tissue: tumor; pdx model: IDB-02R model; sensitivity to docetaxel: Resistant; ' GSE67806 Mus musculus 6 Expression profiling by array GPL16570 Expression data from mouse breast cancer tissue: Serglycin heterozygous and knock-out conditions 2015-04-13 Serglycin proteoglycans contribute to proper storage and secretion of inflammatory mediators in hematopoietic cells. Serglycin is also expressed in cancer cells where increased expression has been linked to poor prognosis. In the present study we report that serglycin proteoglycan is absolutely required for metastasis in the MMTV-PyMT-driven mouse breast cancer model. Serglycin seems to play a role in promoting epithelial to mesenchymal transition, cancer-related inflammation and extravasation. Our results suggest that serglycin and serglycin-dependent mediators are potential drug targets to prevent metastatic disease/dissemination of cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE67806 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA280964 https://www.ebi.ac.uk/ena/browser/view/PRJNA280964 None [Overal design]6 total breast tumor samples were analyzed. 3 of SG+/- and 3 of SG-/- tumour tissue. Raw data was normalized using the robust multi-array average (RMA) method. To identify potential serglycin-regulated mediators of metastasis, we performed a microarray expression analysis of RNA isolated from SG+/- and SG-/- breast tumor tissue. The expression analysis identified 672 genes with a significantly altered expression level, at log2 fold >±1,2. Strikingly, only six genes were up-regulated in the SG-/- PyMT+ tumor cells compared to SG+/- PyMT+ tumor cells while 666 were significantly down-regulated.; [Treatment]'None'; [Growth]'Breast tumour tissue snap freezed in liquid nitrogen'; [Extraction]'All samples were snap frozen in liquid N2 and genotyped. Trizol RNA extraction, RNA concentration was measured with ND-1000 spectrophotometer (NanoDrop Technologies, Wilmington, DE) and RNA quality was evaluated using the Agilent 2100 Bioanalyzer system (Agilent Technologies Inc, Palo Alto, CA).'; [Cell type]'Source: ''tissue: Breast tumor; genotype/variation: PyMT+ SG-/-; ', 'tissue: Breast tumor; genotype/variation: PyMT+ SG+/-; ' GSE55688 Homo sapiens 3 Expression profiling by array GPL570 ZEB1 expression prevents DNA replication stress in cancer stem cells and delays chromosomal instability [Affymetrix] 2014-03-07 Aberrant cell proliferation, a hallmark of most cancers, requires the escape from intrinsic antitumour barriers. Primary among these is the DNA damage response (DDR). In both cell culture-models and in early stages of tumorigenesis in vivo, activated oncogenes induce DNA replication stress and DNA double-strand breaks (DSBs), leading to DDR activation and p53-dependent apoptosis and/or senescence. The means by which tumour-initiating cells, also termed cancer stem cells (CSCs), circumvent this oncosuppressive response is unknown. Here we demonstrate that the ZEB1 transcription factor provides breast CSCs with the ability to withstand an aberrant mitogenic activity. Its forced expression in human mammary epithelial cells is sufficient to alleviate DNA replicative stress and to decrease the production of reactive oxygen species, an important contributor to DDR and oncogene-induced senescence. Consistently, human breast cancer cells with endogenous ZEB1 expression show two characteristic features: low levels of DSBs and DDR markers, reflecting mitigation of the DNA replication stress, and a low p53 mutation frequency, reflecting a weak selective pressure for inactivation. Using high-throughput sequencing analysis of controlled cellular models, we further demonstrate that ZEB1 delays the onset of structural chromosomal instability (CIN), a known consequence of replicative stress and prevents the emergence of chromosome 8p deletions and 8q amplifications, two prevalent abnormalities in high-grade breast cancers. Supporting these findings, ZEB1 expression discriminates human breast tumours by their copy number alterations (CNAs) and chromosome 8 aberrations. We propose that the tumorigenic potential of CSCs relies upon their unique capacity to tolerate oncogenic stimuli through the alleviation of DNA replication stress. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55688 A stemness-related ZEB1-MSRB3 axis governs cellular pliancy and breast cancer genome stability. Nature medicine 30.641 https://doi.org/10.1038/nm.4323 {Nature medicine (30.641): 10.1038/nm.4323} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA240556 https://www.ebi.ac.uk/ena/browser/view/PRJNA240556 None [Overal design]Immortalized human mammary epithelial cells were infected with retrovirus expressing H-RASV12 with or without a retrovirus expressing ZEB1.; [Treatment]'HMEC hTERT immortalized cells were infected with retrovirus expressing H-RASV12 with or without a retrovirus expressing ZEB1.'; [Growth]"Primary human mammary epithelial cells (HMECs) immortalized by-hTert, called HME, were cultured in 1:1 Dulbecco's Modified Eagle's Medium (DMEM)/HAMF12 medium (Invitrogen) complemented with 10% FBS (Cambrex), 100 U/ml penicillin-streptomycin (Invitrogen), 2 mM L glutamine (Invitrogen), 10 ng/ml human epidermal growth factor (EGF) (PromoCell), 0.5 mg/ml hydrocortisone (Sigma) and 10 mg/ml insulin (Actrapid)."; [Extraction]"Total RNAs were extracted with the Qiagen RNeasy minikit (Qiagen), then 100 ng of total RNAs were amplified using Kit GeneChip 3' IVT Express (Affymetrix)."; [Cell type]'immortalized human mammary epithelial cells''cell type: immortalized human mammary epithelial cells; state: immortalized; ', 'cell type: immortalized human mammary epithelial cells; retrovirus expression: HRasG12V; state: non-transformed; ', 'cell type: immortalized human mammary epithelial cells; retrovirus expression: HRasG12V and Zeb1; state: transformed; ' GSE70905 Homo sapiens 137 Expression profiling by array GPL4133 Age and estrogen-dependent inflammation in breast adenocarcinoma and normal breast tissue [cohort_1] 2015-07-14 Chronic inflammation promotes breast tumor growth and invasion by accelerating angiogenesis and tissue remodeling in the tumor microenvironment. The relationship between inflammation and estrogen, which drives the growth of 70 percent of breast tumors, is complex. Low levels of estrogen exposure stimulate macrophages and other inflammatory cell populations, but very high levels are immune suppressive. Breast tumor incidence is increased by obesity and age, which interact to influence inflammatory cell populations in normal breast tissue. The molecular impact of these factors on tumor initiation and growth is not well-understood. We modeled the difference in gene expression between 195 breast adenocarcinomas and 195 matched adjacent normal breast tissue samples, using age, body mass index (BMI), and tumor subtype as covariates. Age and BMI were independently associated with inflammation in normal tissue but not tumors. Older patients with ER-positive disease had tumors with higher levels of Estrogen Receptor (ER) signaling compared to adjacent normal tissue and had lower relative levels of tumor macrophage expression. We developed a novel statistic to quantify the rewiring of gene co-expression networks and demonstrate that in ER-positive tumors basal gene networks are rewired even though their expression levels of these genes are not significantly different from those in adjacent normal tissue. Patient age influences the molecular profile of ER-positive breast tumors. Our data support an immunosuppressive effect of estrogen signaling in the breast tumor microenvironment, suggesting this effect contributes to the greater presence of prognostic and therapeutically relevant immune cells in ER-negative tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE70905 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA289897 https://www.ebi.ac.uk/ena/browser/view/PRJNA289897 None [Overal design]137 total samples: 43 mammaplastic reduction, 47 breast adenocarcinoma, 47 paired adjacent normal breast tissue; [Treatment]'None'; [Growth]'None'; [Extraction]'Tissue samples were stabilized with RNAlater at the time of surgery. After surgery, RNAlater was removed and tissue was stored at -80°C. RNA was extracted with TRIzol (Invitrogen, Carlsbad CA) or TRI reagent (Life Technologies, Gaithersburg MD) and further purified on RNeasy columns in combination with the RNeasy Mini Kit (Qiagen, Valenca, CA). RNA was quantified using a NanoDrop ND-1000 spectrophotometer (Thermo Scientific, Wilmington DE) and quality checked with an Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA).'; [Cell type]'Source: ''sample id: CM1N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 62; bmi: 29.4; tumor_size_cm: 6.5; array_scan_date: 2008-09-23; ', 'sample id: CM9N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 39; bmi: 21; tumor_size_cm: 4.5; array_scan_date: 2008-09-23; ', 'sample id: CM10N; tissue: normal; er: neg; her2: neg; cohort: cohort_1; age_in_years: 48; bmi: 26.5; tumor_size_cm: 5; array_scan_date: 2008-09-23; ', 'sample id: CM11N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 76; bmi: 25.1; tumor_size_cm: 2.6; array_scan_date: 2009-01-20; ', 'sample id: CM13N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 45; bmi: 25.9; tumor_size_cm: 1.5; array_scan_date: 2008-09-23; ', 'sample id: CM15N; tissue: normal; er: neg; her2: neg; cohort: cohort_1; age_in_years: 76; bmi: 23.5; tumor_size_cm: 1.9; array_scan_date: 2009-01-20; ', 'sample id: CM18N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 64; bmi: 22.9; tumor_size_cm: 4; array_scan_date: 2008-09-23; ', 'sample id: CM19N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 61; bmi: 22.5; tumor_size_cm: 1.6; array_scan_date: 2008-06-24; ', 'sample id: CM21N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 64; bmi: 34.4; tumor_size_cm: 1.7; array_scan_date: 2008-09-23; ', 'sample id: CM23N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 69; bmi: 27.3; tumor_size_cm: 1; array_scan_date: 2008-09-23; ', 'sample id: CM26N; tissue: normal; er: neg; her2: pos; cohort: cohort_1; age_in_years: 58; bmi: 21; tumor_size_cm: 3.3; array_scan_date: 2008-09-23; ', 'sample id: CM31N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 83; bmi: 33.4; tumor_size_cm: 2.5; array_scan_date: 2008-09-23; ', 'sample id: CM32N; tissue: normal; er: pos; her2: pos; cohort: cohort_1; age_in_years: 54; bmi: 24.8; tumor_size_cm: 4.3; array_scan_date: 2008-06-24; ', 'sample id: CM33N; tissue: normal; er: neg; her2: neg; cohort: cohort_1; age_in_years: 43; bmi: 21.1; tumor_size_cm: 0.6; array_scan_date: 2008-09-23; ', 'sample id: CM34N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 56; bmi: 28; tumor_size_cm: 1.5; array_scan_date: 2008-09-23; ', 'sample id: CM35N; tissue: normal; er: pos; her2: pos; cohort: cohort_1; age_in_years: 57; bmi: 25.3; tumor_size_cm: 1.1; array_scan_date: 2008-09-23; ', 'sample id: CM38N; tissue: normal; er: neg; her2: neg; cohort: cohort_1; age_in_years: 42; bmi: 23.9; tumor_size_cm: 4.8; array_scan_date: 2008-06-24; ', 'sample id: CM40N; tissue: normal; er: neg; her2: pos; cohort: cohort_1; age_in_years: 75; bmi: 22.2; tumor_size_cm: 2.5; array_scan_date: 2009-06-10; ', 'sample id: CM41N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 67; bmi: 28.1; tumor_size_cm: 3.5; array_scan_date: 2008-06-24; ', 'sample id: CM44N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 68; bmi: 24.5; tumor_size_cm: 2.1; array_scan_date: 2009-01-20; ', 'sample id: CM46N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 82; bmi: NA; tumor_size_cm: 1.8; array_scan_date: 2008-07-30; ', 'sample id: CM47N; tissue: normal; er: neg; her2: pos; cohort: cohort_1; age_in_years: 52; bmi: 22.2; tumor_size_cm: 2; array_scan_date: 2008-07-30; ', 'sample id: CM53N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 53; bmi: NA; tumor_size_cm: 5; array_scan_date: 2008-09-23; ', 'sample id: CM54N; tissue: normal; er: pos; her2: pos; cohort: cohort_1; age_in_years: 68; bmi: 19.1; tumor_size_cm: 1.3; array_scan_date: 2008-07-30; ', 'sample id: CM56N; tissue: normal; er: neg; her2: neg; cohort: cohort_1; age_in_years: 76; bmi: 26; tumor_size_cm: 1.4; array_scan_date: 2008-07-30; ', 'sample id: CM64N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 59; bmi: 23.4; tumor_size_cm: 2; array_scan_date: 2009-12-16; ', 'sample id: CM65N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 57; bmi: 18.9; tumor_size_cm: 2.5; array_scan_date: 2009-12-16; ', 'sample id: CM81N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 70; bmi: NA; tumor_size_cm: 0.9; array_scan_date: 2009-12-16; ', 'sample id: CM110N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 77; bmi: 31.6; tumor_size_cm: 2.6; array_scan_date: 2009-12-16; ', 'sample id: CM112N; tissue: normal; er: neg; her2: pos; cohort: cohort_1; age_in_years: 61; bmi: 20.9; tumor_size_cm: 2.5; array_scan_date: 2009-12-16; ', 'sample id: CM114N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 93; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-11-11; ', 'sample id: CM115N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 64; bmi: NA; tumor_size_cm: 2.5; array_scan_date: 2010-10-27; ', 'sample id: CM125N; tissue: normal; er: neg; her2: pos; cohort: cohort_1; age_in_years: 96; bmi: 25.7; tumor_size_cm: 4.2; array_scan_date: 2009-12-16; ', 'sample id: CM128N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 86; bmi: NA; tumor_size_cm: 3.1; array_scan_date: 2010-11-11; ', 'sample id: CM137N; tissue: normal; er: pos; her2: pos; cohort: cohort_1; age_in_years: 63; bmi: 22.6; tumor_size_cm: 3.5; array_scan_date: 2010-10-27; ', 'sample id: CM148N; tissue: normal; er: pos; her2: pos; cohort: cohort_1; age_in_years: 79; bmi: 18.8; tumor_size_cm: 2.3; array_scan_date: 2009-12-16; ', 'sample id: CM159N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 74; bmi: 26.6; tumor_size_cm: 5; array_scan_date: 2010-10-27; ', 'sample id: CM160N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 50; bmi: NA; tumor_size_cm: 1.1; array_scan_date: 2010-10-27; ', 'sample id: CM161N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 62; bmi: 24.1; tumor_size_cm: 2.3; array_scan_date: 2010-10-27; ', 'sample id: CM170N; tissue: normal; er: pos; her2: pos; cohort: cohort_1; age_in_years: 84; bmi: NA; tumor_size_cm: 4.5; array_scan_date: 2010-10-27; ', 'sample id: CM175N; tissue: normal; er: pos; her2: neg; cohort: cohort_1; age_in_years: 70; bmi: 25.4; tumor_size_cm: 2.3; array_scan_date: 2009-12-16; ', 'sample id: CM198N; tissue: normal; er: pos; her2: pos; cohort: cohort_1; age_in_years: 59; bmi: NA; tumor_size_cm: 0.8; array_scan_date: 2010-10-27; ', 'sample id: CMG15N; tissue: normal; er: pos; her2: NA; cohort: cohort_1; age_in_years: 76; bmi: NA; tumor_size_cm: 1.5; array_scan_date: 2010-10-27; ', 'sample id: CMG23N; tissue: normal; er: pos; her2: NA; cohort: cohort_1; age_in_years: 84; bmi: NA; tumor_size_cm: 0.8; array_scan_date: 2010-11-11; ', 'sample id: CMG24N; tissue: normal; er: pos; her2: NA; cohort: cohort_1; age_in_years: 79; bmi: 24.8; tumor_size_cm: 3.4; array_scan_date: 2008-06-24; ', 'sample id: CMG28N; tissue: normal; er: pos; her2: NA; cohort: cohort_1; age_in_years: 74; bmi: NA; tumor_size_cm: 1.8; array_scan_date: 2010-11-11; ', 'sample id: CMG43N; tissue: normal; er: pos; her2: NA; cohort: cohort_1; age_in_years: 68; bmi: NA; tumor_size_cm: 2.5; array_scan_date: 2008-06-24; ', 'sample id: CM1T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 62; bmi: 29.4; tumor_size_cm: 6.5; array_scan_date: 2008-09-23; ', 'sample id: CM9T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 39; bmi: 21; tumor_size_cm: 4.5; array_scan_date: 2008-09-23; ', 'sample id: CM10T; tissue: tumor; er: neg; her2: neg; cohort: cohort_1; age_in_years: 48; bmi: 26.5; tumor_size_cm: 5; array_scan_date: 2008-09-23; ', 'sample id: CM11T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 76; bmi: 25.1; tumor_size_cm: 2.6; array_scan_date: 2009-01-20; ', 'sample id: CM13T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 45; bmi: 25.9; tumor_size_cm: 1.5; array_scan_date: 2008-09-23; ', 'sample id: CM15T; tissue: tumor; er: neg; her2: neg; cohort: cohort_1; age_in_years: 76; bmi: 23.5; tumor_size_cm: 1.9; array_scan_date: 2009-06-10; ', 'sample id: CM18T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 64; bmi: 22.9; tumor_size_cm: 4; array_scan_date: 2008-09-23; ', 'sample id: CM19T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 61; bmi: 22.5; tumor_size_cm: 1.6; array_scan_date: 2008-06-24; ', 'sample id: CM21B; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 64; bmi: 34.4; tumor_size_cm: 1.7; array_scan_date: 2008-09-23; ', 'sample id: CM23B; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 69; bmi: 27.3; tumor_size_cm: 1; array_scan_date: 2008-09-23; ', 'sample id: CM26T; tissue: tumor; er: neg; her2: pos; cohort: cohort_1; age_in_years: 58; bmi: 21; tumor_size_cm: 3.3; array_scan_date: 2008-09-23; ', 'sample id: CM31T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 83; bmi: 33.4; tumor_size_cm: 2.5; array_scan_date: 2008-09-23; ', 'sample id: CM32T; tissue: tumor; er: pos; her2: pos; cohort: cohort_1; age_in_years: 54; bmi: 24.8; tumor_size_cm: 4.3; array_scan_date: 2008-06-24; ', 'sample id: CM33B; tissue: tumor; er: neg; her2: neg; cohort: cohort_1; age_in_years: 43; bmi: 21.1; tumor_size_cm: 0.6; array_scan_date: 2008-09-23; ', 'sample id: CM34B; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 56; bmi: 28; tumor_size_cm: 1.5; array_scan_date: 2008-09-23; ', 'sample id: CM35B; tissue: tumor; er: pos; her2: pos; cohort: cohort_1; age_in_years: 57; bmi: 25.3; tumor_size_cm: 1.1; array_scan_date: 2008-09-23; ', 'sample id: CM38T; tissue: tumor; er: neg; her2: neg; cohort: cohort_1; age_in_years: 42; bmi: 23.9; tumor_size_cm: 4.8; array_scan_date: 2008-06-24; ', 'sample id: CM40T; tissue: tumor; er: neg; her2: pos; cohort: cohort_1; age_in_years: 75; bmi: 22.2; tumor_size_cm: 2.5; array_scan_date: 2009-06-10; ', 'sample id: CM41T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 67; bmi: 28.1; tumor_size_cm: 3.5; array_scan_date: 2008-06-24; ', 'sample id: CM44T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 68; bmi: 24.5; tumor_size_cm: 2.1; array_scan_date: 2009-01-20; ', 'sample id: CM46T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 82; bmi: NA; tumor_size_cm: 1.8; array_scan_date: 2008-07-30; ', 'sample id: CM47T; tissue: tumor; er: neg; her2: pos; cohort: cohort_1; age_in_years: 52; bmi: 22.2; tumor_size_cm: 2; array_scan_date: 2008-07-30; ', 'sample id: CM53B; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 53; bmi: NA; tumor_size_cm: 5; array_scan_date: 2008-09-23; ', 'sample id: CM54T; tissue: tumor; er: pos; her2: pos; cohort: cohort_1; age_in_years: 68; bmi: 19.1; tumor_size_cm: 1.3; array_scan_date: 2008-07-30; ', 'sample id: CM56T; tissue: tumor; er: neg; her2: neg; cohort: cohort_1; age_in_years: 76; bmi: 26; tumor_size_cm: 1.4; array_scan_date: 2008-07-30; ', 'sample id: CM64B; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 59; bmi: 23.4; tumor_size_cm: 2; array_scan_date: 2009-12-16; ', 'sample id: CM65B; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 57; bmi: 18.9; tumor_size_cm: 2.5; array_scan_date: 2009-12-16; ', 'sample id: CM81T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 70; bmi: NA; tumor_size_cm: 0.9; array_scan_date: 2009-12-16; ', 'sample id: CM110T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 77; bmi: 31.6; tumor_size_cm: 2.6; array_scan_date: 2009-12-16; ', 'sample id: CM112T; tissue: tumor; er: neg; her2: pos; cohort: cohort_1; age_in_years: 61; bmi: 20.9; tumor_size_cm: 2.5; array_scan_date: 2009-12-16; ', 'sample id: CM114T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 93; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-10-27; ', 'sample id: CM115B; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 64; bmi: NA; tumor_size_cm: 2.5; array_scan_date: 2010-11-11; ', 'sample id: CM125T; tissue: tumor; er: neg; her2: pos; cohort: cohort_1; age_in_years: 96; bmi: 25.7; tumor_size_cm: 4.2; array_scan_date: 2009-12-16; ', 'sample id: CM128B; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 86; bmi: NA; tumor_size_cm: 3.1; array_scan_date: 2010-11-11; ', 'sample id: CM137B; tissue: tumor; er: pos; her2: pos; cohort: cohort_1; age_in_years: 63; bmi: 22.6; tumor_size_cm: 3.5; array_scan_date: 2010-10-27; ', 'sample id: CM148T; tissue: tumor; er: pos; her2: pos; cohort: cohort_1; age_in_years: 79; bmi: 18.8; tumor_size_cm: 2.3; array_scan_date: 2009-12-16; ', 'sample id: CM159T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 74; bmi: 26.6; tumor_size_cm: 5; array_scan_date: 2010-10-27; ', 'sample id: CM160T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 50; bmi: NA; tumor_size_cm: 1.1; array_scan_date: 2010-10-27; ', 'sample id: CM161T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 62; bmi: 24.1; tumor_size_cm: 2.3; array_scan_date: 2010-10-27; ', 'sample id: CM170T; tissue: tumor; er: pos; her2: pos; cohort: cohort_1; age_in_years: 84; bmi: NA; tumor_size_cm: 4.5; array_scan_date: 2010-10-27; ', 'sample id: CM175T; tissue: tumor; er: pos; her2: neg; cohort: cohort_1; age_in_years: 70; bmi: 25.4; tumor_size_cm: 2.3; array_scan_date: 2009-12-16; ', 'sample id: CM198B; tissue: tumor; er: pos; her2: pos; cohort: cohort_1; age_in_years: 59; bmi: NA; tumor_size_cm: 0.8; array_scan_date: 2010-10-27; ', 'sample id: CMG15T; tissue: tumor; er: pos; her2: NA; cohort: cohort_1; age_in_years: 76; bmi: NA; tumor_size_cm: 1.5; array_scan_date: 2010-10-27; ', 'sample id: CMG23T; tissue: tumor; er: pos; her2: NA; cohort: cohort_1; age_in_years: 84; bmi: NA; tumor_size_cm: 0.8; array_scan_date: 2010-11-11; ', 'sample id: CMG24T; tissue: tumor; er: pos; her2: NA; cohort: cohort_1; age_in_years: 79; bmi: 24.8; tumor_size_cm: 3.4; array_scan_date: 2008-06-24; ', 'sample id: CMG28T; tissue: tumor; er: pos; her2: NA; cohort: cohort_1; age_in_years: 74; bmi: NA; tumor_size_cm: 1.8; array_scan_date: 2010-11-11; ', 'sample id: CMG43T; tissue: tumor; er: pos; her2: NA; cohort: cohort_1; age_in_years: 68; bmi: NA; tumor_size_cm: 2.5; array_scan_date: 2008-06-24; ', 'sample id: RP1; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2008-10-15; ', 'sample id: RP2; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2008-10-15; ', 'sample id: RP3; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2008-10-15; ', 'sample id: RP4; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2008-10-15; ', 'sample id: RP5; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2008-10-15; ', 'sample id: RP6; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2008-10-15; ', 'sample id: RP10; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2008-10-15; ', 'sample id: RP11; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2008-10-15; ', 'sample id: RP13; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2008-10-15; ', 'sample id: RP14; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2008-10-15; ', 'sample id: RP16; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2008-10-15; ', 'sample id: RP17; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2008-10-15; ', 'sample id: RP20; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-10-13; ', 'sample id: RP22; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-10-13; ', 'sample id: RP23; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-10-13; ', 'sample id: RP24; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-10-13; ', 'sample id: RP26; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-10-13; ', 'sample id: RP28; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-10-13; ', 'sample id: RP33; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-01-20; ', 'sample id: RP35; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-01-20; ', 'sample id: RP36; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-01-20; ', 'sample id: RP37; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-11-11; ', 'sample id: RP38; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-10-13; ', 'sample id: RP39; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-11-11; ', 'sample id: RP40; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-01-21; ', 'sample id: RP45; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-10-27; ', 'sample id: RP46; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-04-08; ', 'sample id: RP47; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-04-08; ', 'sample id: RP48; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-04-08; ', 'sample id: RP50; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-12-16; ', 'sample id: RP51; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-11-11; ', 'sample id: RP53; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-01-21; ', 'sample id: RP54; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-12-16; ', 'sample id: RP55; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-10-27; ', 'sample id: RP57; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-01-21; ', 'sample id: RP58; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-12-16; ', 'sample id: RP62; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2009-06-10; ', 'sample id: RP63; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-01-21; ', 'sample id: RP64; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-01-21; ', 'sample id: RP65; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-01-21; ', 'sample id: RP66; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-01-21; ', 'sample id: RP67; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-01-21; ', 'sample id: RP70; tissue: reduction; er: NA; her2: NA; cohort: cohort_1; age_in_years: NA; bmi: NA; tumor_size_cm: NA; array_scan_date: 2010-01-21; ' GSE32670 Homo sapiens 38 Expression profiling by array GPL570 Time-course effect of estradiol and estradiol-BSA on early gene expression 2011-10-06 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32670 Early membrane initiated transcriptional effects of estrogens in breast cancer cells: First pharmacological evidence for a novel membrane estrogen receptor element (ERx). Steroids 2.136 https://doi.org/10.1016/j.steroids.2012.02.011 {Steroids (2.136) doi:10.1016/j.steroids.2012.02.011}; {Steroids (2.136) doi:10.1016/j.steroids.2011.11.005}; {Steroids (2.136) doi:10.1016/j.steroids.2011.12.016}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA147037 https://www.ebi.ac.uk/ena/browser/view/PRJNA147037 None [Overal design]Refer to individual Series; [Treatment]'T47D cells were incubated with or without Estradiol, E2-BSA, ICI, G15 or combinations of E2-BSA with ICI or G15 for 3 hours after preincubation for 4 hours with medium containing 10% charcoal stripped FBS', 'MCF-7 cells were incubated with or without Estradiol, E2-BSA or combinations of E2-BSA with ICI or G15 for 3 hours after preincubation for 4 hours with medium containing 10% charcoal stripped FBS.', 'MDA-MB-231 cells were incubated with or without Estradiol, E2-BSA, ICI, G15 or combinations of E2-BSA with ICI or G15 for 3 hours after preincubation for 4 hours with medium containing 10% charcoal stripped FBS.', 'SKBR3 cells were incubated with or without Estradiol, E2-BSA, ICI, G15 or combinations of E2-BSA with ICI or G15 for 3 hours after preincubation for 4 hours with medium containing 10% charcoal stripped FBS.'; [Growth]'The human breast cancer cell line T47D was obtained from DSMZ (Braunschweig, Germany) and cultured in RPMI 1640 supplemented with 10% fetal bovine serum, at 37 °C, 5% CO2.', 'The human breast cancer cell line MCF-7 was obtained from DSMZ (Braunschweig, Germany) and cultured in DMEM/F12 (1:1) supplemented with 10% fetal bovine serum, at 37 °C, 5% CO2.', 'The human breast cancer cell line MDA-MB-231 was obtained from DSMZ (Braunschweig, Germany) and cultured in RPMI 1640 supplemented with 10% fetal bovine serum, at 37 °C, 5% CO2.', 'The human breast cancer cell line SKBR3 was obtained from DSMZ (Braunschweig, Germany) and cultured in McCoy′s 5A supplemented with 10% fetal bovine serum, at 37 °C, 5% CO2.'; [Extraction]"Total RNA was isolated using Nucleospin II columns (Macheray-Nagel, Dttren, Germany), according to the manufacturer's instructions.", 'Total RNA was isolated using Nucleospin II columns (Macheray-Nagel, Dttren, Germany), according to the manufacturer’s instructions.'; [Cell type]'breast cancer derived cells''cell line: T47D; cell type: breast cancer derived cells; ', 'cell line: MCF-7; cell type: breast cancer derived cells; ', 'cell line: MDA-MB-231; cell type: breast cancer derived cells; ', 'cell line: SKBR3; cell type: breast cancer derived cells; ' GSE72687 Homo sapiens 12 Expression profiling by array GPL571 RNA expression in MDA-MB-231 cells transfected with scramble, LSD1 or HDAC5 shRNA (HG-U133A_2) 2015-09-03 We performed gene expression microarray to examine the potential effect that depletion of HDAC5 (an important HDAC isozyme) or LSD1 (an FAD-dependent histone lysine demethylase) has on the triple-negative breast cancer transcriptome. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72687 HDAC5-LSD1 axis regulates antineoplastic effect of natural HDAC inhibitor sulforaphane in human breast cancer cells. International journal of cancer 4.982 https://doi.org/10.1002/ijc.31419 {International journal of cancer (4.982): 10.1002/ijc.31419} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA294669 https://www.ebi.ac.uk/ena/browser/view/PRJNA294669 None [Overal design]Twelve samples were subject to microarray anaylsis: 3 biological replicates were treated with 1) scramble shRNA, 2) HDAC5 shRNA, 3) scramble shRNA, or 4) LSD1 shRNA.; [Treatment]"shRNA Lentiviral Particles were purchased from Santa Cruz Biotecnology and transduced according to manufacturer's protocol (http://www.scbt.com/protocols.html?protocol=shrna_lentiviral_particles_transduction)"; [Growth]'normal culturing conditions for MDA-MB-231'; [Extraction]'QIAgen RNeasy Mini (Animal Cells Spin protocol, w/DNase I digest performed on homogenized lysate prior to applying lysate to column for purification)'; [Cell type]'breast cancer cell line''cell line: MDA-MB-231; cell type: breast cancer cell line; transfected with: scramble shRNA; ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; transfected with: HDAC5 shRNA; ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; transfected with: LSD1 shRNA; ' GSE160566 Homo sapiens 20 Other GPL20301 Impact of the bone microenvironment on phenotypic plasticity of ER+ breast cancer cells [Evolving Barcode] 2020-10-31 Evolving barcode was used to evaluate clonal expansion in bone metastases induced by intra-iliac artery injection. The assocoation of these results with ER expression revealed a non-genomic effect of the bone microenvironment on ER heterogeneity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE160566 The bone microenvironment increases phenotypic plasticity of ER+ breast cancer cells. Developmental cell 9.190 https://doi.org/10.1016/j.devcel.2021.03.008 {Developmental cell (9.190): 10.1016/j.devcel.2021.03.008} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA673694 https://www.ebi.ac.uk/ena/browser/view/PRJNA673694 https://www.ncbi.nlm.nih.gov/sra?term=SRP290686 [Overal design]ER-positive breast cancer cells (MCF7) with hgRNA-A21 and inducible Cas9 expression were inejcted to hind limb of nude mice. Cas9 expression was induced weekly and laser capture microdissection (LCM) was employed to collect independent bone lesions for targeted sequencing at week 3. All samples were processed using the TraceQC package; [Treatment]'None'; [Growth]'MCF7 cells were maintained in DMEM 10% FBS'; [Extraction]'For DNA collection we used the quick-dna/rna microprep plus kit from Zymo (#D7005)\nhgRNA was amplified using the KAPA SYBR FAST qPCR Kit before library preparation with the NEBNext Multiplex oligos for illumina (Dual Index Primers set1) kit (#NEB E7600S)'; [Cell type]'Source: ''cell line: MCF-7; collection process: LCM-derived; ', 'cell line: MCF-7; collection process: Parental; ' GSE55024 Homo sapiens 16 Non-coding RNA profiling by array; Expression profiling by array GPL4133; GPL7731; GPL14767 miRNA and mRNA profiling of tumor-educated macrophages 2014-02-13 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55024 Integrated miRNA and mRNA profiling of tumor-educated macrophages identifies prognostic subgroups in estrogen receptor-positive breast cancer. Molecular oncology 5.962 https://doi.org/10.1016/j.molonc.2014.07.023 {Molecular oncology (5.962): 10.1016/j.molonc.2014.07.023} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA238262 https://www.ebi.ac.uk/ena/browser/view/PRJNA238262 None [Overal design]Refer to individual Series; [Treatment]'The ER+ and PR+ human breast cancer cell line MCF-7 was purchased from DSMZ and maintained in RPMI-1640 medium (PAA Laboratories Inc., Cölbe, Germany) supplemented with 10% fetal calf serum (FCS, Invitrogen, Karlsruhe, Germany). Human macrophages were derived from mononuclear peripheral blood cells. Briefly, monocytes were obtained from buffy coats of healthy donors through double-density-gradient isolation. Macrophages were differentiated by culturing monocytes in fluorinated ethylene propylene-coated cell culture bags (CellGenix, Freiburg, Germany) in the presence of M-CSF (Immunotools, Friesoythe, Germany) for 7 days. For indirect co-culture experiments, macrophages were seeded in hanging cell culture inserts (0.4µm pore size, PET; Millipore, Billerica, MA, USA) and co-cultured with MCF-7 cells at a ratio of 2:1 under normoxia for 24 hours.'; [Growth]'None'; [Extraction]'Total RNA for array experiments was isolated using TRIZOL reagent according to the manufacturer’s instructions (Invitrogen, Carlsbad, CA). RNA integrity for each sample was confirmed with the Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA). Samples used for microarray experiments exhibited a RIN number greater than 7.5. Each RNA sample was then split into two aliquots that were either processed for the miRNA or the mRNA microarray.'; [Cell type]'Source: ''coculture: control; patient: 1; ', 'coculture: control; patient: 2; ', 'coculture: control; patient: 4; ', 'coculture: coculture with MCF-7; patient: 1; ', 'coculture: coculture with MCF-7; patient: 2; ', 'coculture: coculture with MCF-7; patient: 4; ', 'coculture: control; patient: 3; ', 'coculture: coculture with MCF-7; patient: 3; ' GSE50512 Homo sapiens 56 Genome variation profiling by genome tiling array GPL17668 High-resolution genomic profiling of male breast cancer reveals differences hidden behind the similarities with female breast cancer. 2013-08-30 Male breast cancer (MBC) is extremely rare and poorly characterized on the molecular level. Using high-resolution genomic data, we aimed to characterize MBC by genomic imbalances and to compare it with female breast cancer (FBC), and further to investigate whether the genomic profiles hold any prognostic infor- mation. Fifty-six fresh frozen MBC tumors were analyzed using high-resolution tiling BAC arrays. Significant regions in common between cases were assessed using Genomic Identification of Significant Targets in Cancer (GISTIC) analysis. A publicly available genomic data set of 359 FBC tumors was used for reference purposes. The data revealed a broad pattern of aberrations, confirming that MBC is a heterogeneous tumor type. Genomic gains were more common in MBC than in FBC and often involved whole chromosome arms, while losses of genomic material were less frequent. The most common aberrations were similar between the genders, but high-level amplifications were more common in FBC. We identified two genomic subgroups among MBCs; male-complex and male-simple. The male-complex subgroup displayed striking similarities with the previously reported luminal-complex FBC sub- group, while the male-simple subgroup seems to represent a new subgroup of breast cancer occurring only in men. There are many similarities between FBC and MBC with respect to genomic imbalances, but there are also distinct differ- ences as revealed by high-resolution genomic profiling. MBC can be divided into two comprehensive genomic subgroups, which may be of prognostic value. The male- simple subgroup appears notably different from any geno- mic subgroup so far defined in FBC. Male breast cancer (MBC) is extremely rare and poorly characterized on the molecular level. Using high-resolution genomic data, we aimed to characterize MBC by genomic imbalances and to compare it with female breast cancer (FBC), and further to investigate whether the genomic profiles hold any prognostic infor- mation. Fifty-six fresh frozen MBC tumors were analyzed using high-resolution tiling BAC arrays. Significant regions in common between cases were assessed using Genomic Identification of Significant Targets in Cancer (GISTIC) analysis. A publicly available genomic data set of 359 FBC tumors was used for reference purposes. The data revealed a broad pattern of aberrations, confirming that MBC is a heterogeneous tumor type. Genomic gains were more common in MBC than in FBC and often involved whole chromosome arms, while losses of genomic material were less frequent. The most common aberrations were similar between the genders, but high-level amplifications were more common in FBC. We identified two genomic subgroups among MBCs; male-complex and male-simple. The male-complex subgroup displayed striking similarities with the previously reported luminal-complex FBC sub- group, while the male-simple subgroup seems to represent a new subgroup of breast cancer occurring only in men. There are many similarities between FBC and MBC with respect to genomic imbalances, but there are also distinct differ- ences as revealed by high-resolution genomic profiling. MBC can be divided into two comprehensive genomic subgroups, which may be of prognostic value. The male- simple subgroup appears notably different from any geno- mic subgroup so far defined in FBC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50512 The landscape of candidate driver genes differs between male and female breast cancer. PloS one 2.776 https://doi.org/10.1371/journal.pone.0078299 {PloS one (2.776): 10.1371/journal.pone.0078299} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA217798 https://www.ebi.ac.uk/ena/browser/view/PRJNA217798 None [Overal design]Tumor cellularity was determined on H&E-stained sections and only tumors with high tumor cell content were included. DNA was extracted from fresh frozen tissue using a modification of a back-extraction protocol from the organic phase of the Qiagen Lipid mini RNA kit (Qiagen, Valencia, CA) as follows: 1 M Tris-buffer containing 4 M Guanidine Thiocyanate and 50 mM Sodium Citrate, followed by glycogen precipitation. DNA quality was assessed with a BioAnalyzer. Sufficient good quality DNA from 56 fresh frozen MBC tumors was available for high-resolution tiling BAC aCGH. BAC arrays, containing about 32,000 BAC clones mapped to the UCSC Human Genome build 17, were produced at the SCIBLU Genomics Resource Center, Lund University, Sweden. The aCGH data were normalized using PopLowess. Circular binary segmentation (CBS) was used for breakpoint analysis with an a of 0.01 and segments containing at least four probes were used in subsequent analyses.; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA was extracted from fresh frozen tissue using a modification of a back-extraction protocol from the organic phase of the Qiagen Lipid mini RNA kit (Qiagen, Valencia, CA) as follows: 1 M Tris-buffer containing 4 M Guanidine Thiocyanate and 50 mM Sodium Citrate, followed by glycogen precipitation.'; [Cell type]'Source: ''age_at_diagnosis: 91; size: 40; year_of_diagnosis: 1988; pr: positive; ', 'sample type: reference; ', 'age_at_diagnosis: 83; size: 40; nhg: II; year_of_diagnosis: 1995; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 79; size: 22; nhg: II; year_of_diagnosis: 1992; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 85; size: 42; year_of_diagnosis: 1997; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 85; size: 30; nhg: III; year_of_diagnosis: 1998; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 92; size: 18; nhg: II; year_of_diagnosis: 2005; her2: negative; er: positive; ', 'age_at_diagnosis: 88; size: 23; nhg: II; year_of_diagnosis: 2001; her2: negative; er: positive; pr: negative; ', 'age_at_diagnosis: 68; size: 25; year_of_diagnosis: 1983; pr: positive; ', 'age_at_diagnosis: 73; size: 20; year_of_diagnosis: 1989; pr: positive; ', 'age_at_diagnosis: 77; size: 25; year_of_diagnosis: 1994; her2: positive; er: positive; pr: negative; ', 'age_at_diagnosis: 72; size: 20; year_of_diagnosis: 1989; pr: positive; ', 'age_at_diagnosis: 75; year_of_diagnosis: 1993; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 78; size: 25; nhg: III; year_of_diagnosis: 1997; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 83; size: 25; nhg: II; year_of_diagnosis: 2001; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 66; size: 29; nhg: III; year_of_diagnosis: 1985; pr: negative; ', 'age_at_diagnosis: 70; size: 22; nhg: III; year_of_diagnosis: 1990; pr: positive; ', 'age_at_diagnosis: 80; size: 16; nhg: III; year_of_diagnosis: 2001; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 72; size: 24; year_of_diagnosis: 1996; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 77; size: 25; nhg: III; year_of_diagnosis: 2001; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 63; size: 19; nhg: II; year_of_diagnosis: 1988; pr: positive; ', 'age_at_diagnosis: 61; size: 28; nhg: II; year_of_diagnosis: 1988; pr: positive; ', 'age_at_diagnosis: 78; size: 20; nhg: II; year_of_diagnosis: 2005; her2: negative; pr: positive; ', 'age_at_diagnosis: 72; size: 30; nhg: III; year_of_diagnosis: 1999; her2: negative; er: positive; pr: negative; ', 'age_at_diagnosis: 70; size: 17; nhg: II; year_of_diagnosis: 1997; pr: positive; ', 'age_at_diagnosis: 70; size: 28; nhg: II; year_of_diagnosis: 1997; pr: positive; ', 'age_at_diagnosis: 70; size: 50; nhg: II; year_of_diagnosis: 1998; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 70; size: 28; nhg: III; year_of_diagnosis: 1997; her2: negative; er: positive; ', 'age_at_diagnosis: 61; size: 17; year_of_diagnosis: 1989; pr: positive; ', 'age_at_diagnosis: 71; size: 25; nhg: II; year_of_diagnosis: 2000; her2: negative; er: positive; ', 'age_at_diagnosis: 58; size: 25; nhg: III; year_of_diagnosis: 1988; pr: positive; ', 'age_at_diagnosis: 73; size: 17; nhg: II; year_of_diagnosis: 2003; her2: positive; er: positive; pr: positive; ', 'age_at_diagnosis: 58; size: 15; year_of_diagnosis: 1989; pr: positive; ', 'age_at_diagnosis: 73; size: 50; nhg: I; year_of_diagnosis: 2004; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 57; size: 22; year_of_diagnosis: 1989; pr: positive; ', 'age_at_diagnosis: 58; size: 15; year_of_diagnosis: 1991; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 62; size: 19; nhg: II; year_of_diagnosis: 1996; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 65; size: 26; nhg: II; year_of_diagnosis: 2000; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 71; size: 60; nhg: III; year_of_diagnosis: 2007; pr: positive; ', 'age_at_diagnosis: 70; size: 28; nhg: III; year_of_diagnosis: 2008; er: positive; pr: negative; ', 'age_at_diagnosis: 49; size: 22; nhg: III; year_of_diagnosis: 1989; ', 'age_at_diagnosis: 54; size: 38; year_of_diagnosis: 1996; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 58; year_of_diagnosis: 2000; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 58; size: 19; nhg: II; year_of_diagnosis: 2001; her2: negative; er: positive; pr: negative; ', 'age_at_diagnosis: 60; nhg: II; year_of_diagnosis: 2004; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 60; size: 12; nhg: II; year_of_diagnosis: 2005; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 42; size: 12; nhg: II; year_of_diagnosis: 1989; pr: positive; ', 'age_at_diagnosis: n/a; size: n/a; nhg: n/a; year_of_diagnosis: n/a; her2: n/a; er: n/a; pr: n/a; ', 'age_at_diagnosis: 58; size: 25; nhg: II; year_of_diagnosis: 2006; her2: negative; er: positive; pr: positive; ', 'age_at_diagnosis: 47; size: 40; nhg: II; year_of_diagnosis: 2000; her2: negative; er: positive; pr: negative; ', 'age_at_diagnosis: 49; size: 26; nhg: II; year_of_diagnosis: 2001; pr: positive; ', 'age_at_diagnosis: 42; size: 25; nhg: I; year_of_diagnosis: 2002; her2: negative; er: positive; pr: negative; ' GSE120313 Homo sapiens 3 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Dynamic incorporation of histone H3 variants into chromatin is essential for acquisition of aggressive traits and metastatic colonization 2018-09-21 Carcinomas can acquire metastatic potential by undergoing a cellular program referred to as epithelial-to-mesenchymal transition (EMT). During EMT, the genome undergoes major epigenetic changes required for the expression of genes that promote cell motility, invasiveness, and survival under stress. While recent data point to a crucial role of chromatin remodeling in this process, little is known about the nature of this remodeling and the signals that trigger it. Here we show that metastasis-inducing pathways regulate histone chaperones to reduce canonical histone incorporation into chromatin. This triggers deposition of H3.3 to the promoters of EMT-inducing transcription factors and poor prognosis genes, a phenomenon that is sufficient and necessary for the induction of EMT and metastasis. Together, we have discovered histone H3.3 variant as a major regulator of cell fate during tumorigenesis and histone chaperones as valuable therapeutic targets for metastatic disease. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE120313 Dynamic Incorporation of Histone H3 Variants into Chromatin Is Essential for Acquisition of Aggressive Traits and Metastatic Colonization. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2019.08.006 {Cancer cell (23.916): 10.1016/j.ccell.2019.08.006} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA492482 https://www.ebi.ac.uk/ena/browser/view/PRJNA492482 https://www.ncbi.nlm.nih.gov/sra?term=SRP162347 [Overal design]Examination of chromatin enrichment of histone H3 variants in a highly metastatic cell line.; [Treatment]'None'; [Growth]'MDA-MB-231 LM2 clones were obtained from Dr. Massague’s lab and were maintained in high glucose DMEM (Gibco) supplemented with 10% FBS (Sigma-Aldrich) and penicillin-streptomycin (Gibco).'; [Extraction]'Lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody.\nIllumina sequencing libraries were prepared from the ChIP and Input DNAs by the standard consecutive enzymatic steps of end-polishing, dA-addition, and adaptor ligation. After a final PCR amplification step, the resulting DNA libraries were quantified and sequenced on Illumina’s NextSeq 500 (75 nt reads, single end).'; [Cell type]'Source: ''cell line: MDA-MB-231 LM2 cells; chip antibody: H3.1/3,2: 61629 Active Motif, Lot#: 31814001; antibody amount: 4 microgram; ', 'cell line: MDA-MB-231 LM2 cells; chip antibody: H3.3: 17-10245, Millipore, Lot#: 2914462; antibody amount: 6 microgram; ', 'cell line: MDA-MB-231 LM2 cells; chip antibody: none (input); antibody amount: n/a; ' GSE32291 Homo sapiens 414 Genome variation profiling by genome tiling array GPL4091 Regional complexity in breast tumors reveals patterns of prognostic value 2011-09-21 Genomic complexity in breast tumors has been associated with aggressive disease and less favorable outcome. Recently, we developed an algorithm to calculate complexity scores per chromosome arm in order to sub-classify breast tumors with respect to progression paths and prognosis. We have further developed this method to calculate probe-focused complexity scores per sample, enabling identification of regions with recurrent complexities and grouping of tumors according to genome-wide complexity patterns. Probe-focused complexity scores were calculated based on data derived from aCGH analyses of 394 invasive ductal breast carcinomas. These continuous complexity scores (CCI) were used to identify regions with recurrent high level complexity, and the regional complexity scores were correlated to clinicopathological variables and survival data. A total of 25 recurrent regions with high level complexity were identified. Regional complexities on chromosome arms 8p, 11q and 17q were each associated with clinical parameters associated with aggressive disease. Complexity patterns were different between tumors of different gene expression subtypes. Multivariate Cox analysis revealed that regional complexity on 17q21.32-q21.33 was significantly associated with shorter survival, independent of established clinical variables. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32291 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA146361 https://www.ebi.ac.uk/ena/browser/view/PRJNA146361 None [Overal design]394 invasive ductal breast carcinomas were analyzed using whole genome CGH arrays from Agilent. In addition 20 normal breast biopsies were included as controls, a total of 414 samples. All samples were hybridized to the arrays together with a commercial female reference sample from Promega.; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA was isolated from snap frozen tumor tissue using chloroform/phenol extraction followed by ethanol precipitation (Nucler Acid Extractor 340A; Applied Biosystems, Foster City, CA, USA). Some of the normal breast tissue samples were preserved in ethanol prior to extraction.'; [Cell type]'Source: ''gender: Female; age at onset: 57; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; ', 'gender: Female; age at onset: 65; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 44; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT3; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 55; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 51; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 52; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 69; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT3; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 55; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 59; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 46; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 66; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 68; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 55; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 46; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 52; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 67; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 55; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 52; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 36; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 68; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 45; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 43; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 38; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 31; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 39; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 41; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 45; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 46; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT3; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 61; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 39; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 68; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 64; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 50; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 46; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 38; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 58; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 64; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 61; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 51; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 58; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 57; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 66; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 66; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 65; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 58; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 68; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 53; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 59; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 61; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 66; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 38; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 54; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 36; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 67; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 51; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 53; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 31; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 65; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 65; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 53; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 69; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 67; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 55; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 45; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 46; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 50; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 45; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 51; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 43; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 61; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 51; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 59; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 58; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 65; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 59; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 51; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 26; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 30; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 41; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 53; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 45; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 56; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 51; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 45; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 44; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 44; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 44; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 57; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 73; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 53; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 90; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 55; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 50; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 67; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 55; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 58; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 39; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: NA; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 59; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 41; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 36; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 90; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 58; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 56; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 76; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 74; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 85; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 54; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: NA; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 28; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 44; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 57; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 54; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 78; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 61; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 72; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 68; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 56; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 71; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 68; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 50; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 52; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 70; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 72; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 44; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 40; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: ERBB2 +; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 52; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 38; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 50; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 82; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: NA; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 86; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 71; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 51; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: NA; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 73; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 52; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 38; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 59; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 84; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: NA; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 77; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 55; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 56; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 75; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 66; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 67; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: NA; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 59; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 59; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 73; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 73; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 64; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 69; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 45; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN3; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 53; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 64; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 66; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 87; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: NA; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 44; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 79; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 69; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: NA; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 37; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 56; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 66; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 57; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 70; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 55; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 67; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 65; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 51; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 68; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 71; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 56; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 76; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 81; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN3; estrogen receptor status: positive; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT4; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 46; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 37; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT4; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 33; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 56; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 39; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 70; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN3; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 38; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN3; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 41; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT3; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 76; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 52; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 71; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: NA; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 51; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: NA; lymph node status: pN3; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 65; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 57; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 65; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Normal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 71; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 64; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 64; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 70; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Normal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 69; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 56; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 72; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 88; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 66; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 79; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 61; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 81; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 79; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 76; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 67; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 55; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 28; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT3; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 74; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 40; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN2; estrogen receptor status: NA; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 71; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: NA; lymph node status: pN1; estrogen receptor status: NA; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 76; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 78; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 75; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 85; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 82; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 61; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 78; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN3; estrogen receptor status: positive; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 77; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 33; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 84; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 78; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 85; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 64; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 43; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 28; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 65; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 40; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 58; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 59; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT4; lymph node status: pN3; estrogen receptor status: negative; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 66; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 52; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 84; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 57; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 69; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 55; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 81; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT4; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 64; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 66; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil B; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 61; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN0; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 45; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 73; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 87; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 44; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 60; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 64; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 69; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 48; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN0; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 79; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 74; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 76; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT4; lymph node status: pN3; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 75; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN3; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 51; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN3; estrogen receptor status: negative; gene expression subtype: ERBB2+; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 36; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 55; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 46; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT3; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 28; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 46; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 73; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: NA; gene expression subtype: Lumil B; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 71; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: NA; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 78; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: NA; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 77; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN0; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 58; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 32; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 73; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT4; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: Basal-like; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 78; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 59; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 49; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT3; lymph node status: pN0; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 63; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 44; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 67; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 1; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN3; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 64; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: Lumil A; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 58; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 71; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 64; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 85; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT3; lymph node status: NA; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 70; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 51; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 62; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 35; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT3; lymph node status: pN3; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 34; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN2; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 80; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT3; lymph node status: pN3; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 37; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 90; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: NA; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT2; lymph node status: pN1; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 47; histology: IDC; histologic grade: G3; histologic grade and genomic grade combin ed: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: negative; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 80; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 36; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN2; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 74; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: mutated; ', 'gender: Female; age at onset: 71; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT1; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 75; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 80; histology: IDC; histologic grade: G1; histologic grade and genomic grade combined: 1; tumor size: pT1; lymph node status: pN1; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 52; histology: IDC; histologic grade: G2; histologic grade and genomic grade combined: NA; tumor size: pT2; lymph node status: pN1; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 79; histology: IDC; histologic grade: G3; histologic grade and genomic grade combined: 3; tumor size: pT1; lymph node status: pN0; estrogen receptor status: positive; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 49; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 31; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: NA; ', 'gender: Female; age at onset: NA; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 60; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: NA; ', 'gender: Female; age at onset: 53; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 3; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 46; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 55; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 42; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: NA; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 50; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 22; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: NA; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 40; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 22; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 62; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 56; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 31; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 51; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 24; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 43; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ', 'gender: Female; age at onset: 36; histology: Normal; histologic grade: NA; histologic grade and genomic grade combined: 1; tumor size: Normal; lymph node status: NA; estrogen receptor status: NA; gene expression subtype: NA; tp53 mutation status: wild-type; ' GSE103165 synthetic RNA; Homo sapiens 20 Other GPL18573; GPL25479 Global Profiling of hnRNP A2/B1-RNA Interactions on Chromatin Suggests Additional Roles Outside of Splicing 2017-08-28 Long noncoding RNAs (lncRNAs) often carry out their functions through associations with adaptor proteins. We recently identified heterogeneous ribonucleoprotein (hnRNP) A2/B1 as an adaptor of the human HOTAIR lncRNA. hnRNP A2 and B1 are splice isoforms of the same gene. Spliced HOTAIR preferentially associates with the B1 isoform, which may contribute to a mechanism matching lncRNAs with RNA transcripts of target genes. In this study we used enhanced cross-linking immunoprecipitation (eCLIP) to map the complete set of direct interactions between A2/B1 and RNA in breast cancer cells. We identified multiple additional sites of isoform specificity that correlate with differences in binding motif enrichment. Surprisingly, a strong A2/B1 binding site occurs in the third intron of HOTAIR, which interrupts a known RNA-RNA interaction hotspot and is retained at a higher frequency than other HOTAIR introns. In vitro eCLIP experiments suggest that A2/B1 may redistribute to exonic binding sites once this intron is spliced. A2/B1 associates with multiple lncRNAs at regions that may contribute to downstream regulation and function of the lncRNA. Finally, we performed cellular fractionation experiments to characterize the pattern of RNA association of A2/B1 in chromatin, nucleoplasm, and cytoplasm and find that a majority of interactions occur on chromatin, even those that do not contribute to co-transcriptional splicing. Our data characterize the multiple functions of a repurposed splicing factor, including isoform-biased interactions, and highlight that the vast majority of these functions occur on chromatin-associated RNA. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE103165 Global profiling of hnRNP A2/B1-RNA binding on chromatin highlights LncRNA interactions. RNA biology 5.477 https://doi.org/10.1080/15476286.2018.1474072 {RNA biology (5.477): 10.1080/15476286.2018.1474072} 'nuclear RNA', 'other', 'cytoplasmic RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA400384 https://www.ebi.ac.uk/ena/browser/view/PRJNA400384 https://www.ncbi.nlm.nih.gov/sra?term=SRP116309 [Overal design]eCLIP-seq in human MCF7 and MCF10A cells; [Treatment]'None'; [Growth]'MCF7 cells were grown in RPMI supplemeted with 10% FBS and 1% penicillin/streptomycin', 'MCF10A cells were grown in DMEM/F12 with 5% horse serum, 20 ng/mL EGF, 0.5 µg/mL hydrocortisone, 100 ng/mL cholera toxin, 10 µg/mL insulin, and 1x penicillin/streptomycin'; [Extraction]'eCLIP-seq was performed as previously described (Van Nostrand et al. 2016) with minor modifications. Briefly, confluent cells were UV-crosslinked at 150 mJ and 254 nm wavelength in 13 mL of PBS in 15 cm plates; these cells were then spun down, flash frozen in liquid nitrogen, and stored at –80ºC. Nuclear isolation was performed as previously described (Kung et al. 2015), followed by further digestion by Bioruptor, RNase I, and Turbo DNase as specified in the original eCLIP protocol. Overnight immunoprecipitation was performed using 2 mg Protein G Dynabeads per 10 µg antibody, and appropriate antibodies for hnRNP A2/B1 (Abcam ab31645, 9 µg/IP), hnRNP B1 (IBL 18941, 2.5 µg/IP), or IgG (Novus NB810-56910, 5 µg/IP). Following end repair and 3′ adaptor ligation (using X1A and X1B adaptors as previously described), size selection was carried out using Nupage 4-12% Bis-Tris protein gels followed by overnight transfer at 30V to nitrocellulose membranes.\nProtein-RNA complexes on nitrocellulose were then digested with Proteinase K (Roche) and reverse transcribed using SuperScript IV (Thermo Fisher). These cDNAs were then prepared for sequencing as described using Illumina TruSeq HT dual indexed primers, and sequenced on an Illumina NextSeq 500 for high-output 2x75 bp run.', 'eCLIP-seq was performed as previously described (Van Nostrand et al. 2016) with minor modifications. Briefly, confluent cells were UV-crosslinked at 150 mJ and 254 nm wavelength in 13 mL of PBS in 15 cm plates; these cells were then spun down, flash frozen in liquid nitrogen, and stored at –80ºC. Cellular fractionation was performed as previously described (Wysocka et al. 2001). Each fraction was raised to 1 mL final volume using Buffer D (20 mM HEPES pH 7.5, 210 mM NaCl, 7.5% glycerol, 0.75 mM MgCl2, 0.25 mM PMSF, and 1x proteinase inhibitor) then incubated with TURBO DNase (40U for chromatin sample, 10U for soluble samples) for 30 minutes at 37ºC, then quenched with 10 mM EDTA. Fractions were then further digested with Bioruptor and RNase (but no additional DNase) as specified in the original eCLIP protocol, then immunoprecipitated overnight with antibody to hnRNP B1(IBL 18941, 2.5 µg/IP). Following end repair and 3′ adaptor ligation (using X1A and X1B adaptors as previously described), size selection was carried out using Nupage 4-12% Bis-Tris protein gels followed by overnight transfer at 30V to nitrocellulose membranes.\nProtein-RNA complexes on nitrocellulose were then digested with Proteinase K (Roche) and reverse transcribed using SuperScript IV (Thermo Fisher). These cDNAs were then prepared for sequencing as described using Illumina TruSeq HT dual indexed primers, and sequenced on an Illumina NextSeq 500 for high-output 2x75 bp run.', 'Cloning and purification of recombinant hnRNP B1 was performed as previously described (Meredith et al. 2016). HOTAIR and antisense luciferase control RNA (see (Meredith et al. 2016) for sequence details) were in vitro transcribed using the MEGAscript T7 Transcription Kit, treated with TURBO DNase, and purified with RNeasy Qiagen Kit. In a 1:10 RNA:protein molar ratio, 1.2 ug of control or HOTAIR RNA was incubated with recombinant B1 in 100 µL RNA refolding buffer (20 mM HEPES-KOH pH 7.9, 100 mM KCl, 0.2 EDTA pH 8.0. 20% Glycerol, 0.5 mM PMSF, 0.5 DTT) for 20 minutes at room temperature. The mixture was diluted to 250 µL in refolding buffer and UV-crosslinked twice in one well of a 24-well plate at 250 mJ and 254 nm wavelength, with mixing by pipette in between. B1-RNA crosslinked and non-crosslinked samples were treated with 0.1 ng RNase A for 3 minutes at 37ºC and 1200 rpm, then stopped with 200 U Murine RNase Inhibitor (NEB).\nProtein-RNA complexes on nitrocellulose were then digested with Proteinase K (Roche) and reverse transcribed using SuperScript IV (Thermo Fisher). These cDNAs were then prepared for sequencing as described using Illumina TruSeq HT dual indexed primers, and sequenced on an Illumina NextSeq 500 for high-output 2x75 bp run.'; [Cell type]'Source: ''cell line: MCF7; antibody: hnRNP A2/B1; antibody vendor: abcam; antibody catalog number: ab31645; ', 'cell line: MCF7; antibody: none; antibody vendor: none; antibody catalog number: none; ', 'cell line: MCF7; antibody: hnRNP B1; antibody vendor: IBL; antibody catalog number: 18941; ', 'cell line: MCF10A; antibody: hnRNP A2/B1; antibody vendor: abcam; antibody catalog number: ab31645; ', 'cell line: MCF10A; antibody: none; antibody vendor: none; antibody catalog number: none; ', 'cell line: MCF10A; antibody: hnRNP B1; antibody vendor: IBL; antibody catalog number: 18941; ', 'antibody: hnRNP B1; antibody vendor: IBL; antibody catalog number: 18941; ' GSE49952 Homo sapiens 11 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Genome-wide maps of XBP1 binding sites in different breast cancer cell lines [ChIP-Seq] 2013-08-18 We report the application of ChIP-seq, which combines chromatin immunoprecipitation (ChIP) with massively parallel DNA sequencing, to map genome-wide XBP1 binding sites in different breast cancer cell lines. We showed that HIF1α motif was enriched in XBP1 binding sites in triple negative breast cancer (TNBC) cell lines, but not enriched in ER positive breast cancer cell line. We also demonstrated that different breast cancer cell lines of the same sub-type had similar XBP1 binding sites, whereas different breast cancer sub-types had majorly different XBP1 binding sites. Finally, a model was applied to integrate XBP1 ChIP-seq data with expression data to predict XBP1's direct targets in TNBC cell line; the predicted direct targets were shown to be predictive of patient survival, and the prediction power was specific to TNBC patients. The above evidence indicates that XBP1 performs important functions in TNBC by interacting with HIF1α, and such regulation mechanism is specific to TNBC, which is later proved by follow-up experiments.This study represents the first detailed anaysis of XBP1 binding sites in different breast cancer cell lines. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE49952 XBP1 promotes triple-negative breast cancer by controlling the HIF1α pathway. Nature 43.070 https://doi.org/10.1038/nature13119 {Nature (43.070): 10.1038/nature13119} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA221365 https://www.ebi.ac.uk/ena/browser/view/PRJNA221365 https://www.ncbi.nlm.nih.gov/sra?term=SRP033364 [Overal design]Examination of XBP1 binding sites in 2 cell types (3 cell lines).; [Treatment]'For all hypoxia experiments, cells were maintained in an anaerobic chamber (Coy laboratory) with 0.1% O2. For glucose deprivation experiments, cells were maintained in DMEM without glucose medium (Gibco) with 10% FBS (Gibco) and 50 units/ml of penicillin/streptomycin.'; [Growth]'All breast cancer cells were cultured according to Neve et al. (Cancer Cell 2006). Following retroviral or lentiviral infection, cells were maintained in the presence of puromycin (2 ug/ml) (Sigma).'; [Extraction]'ChIP was performed as previously described by Chen et al. (Cell 2008).\nThe ChIP-seq library was prepared using ChIP-Seq DNA Sample Prep Kit (Illumina) according to the manufacturer’s instructions.'; [Cell type]'triple negative breast cancer cells', 'ER positive breast cancer cells''cell type: triple negative breast cancer cells; chip antibody: XBP1 (Biolegend, 619502); cell line: MDA-MB-231; ', 'cell type: triple negative breast cancer cells; chip antibody: none; cell line: MDA-MB-231; ', 'cell type: ER positive breast cancer cells; chip antibody: XBP1 (Biolegend, 619502); cell line: T47D; ', 'cell type: ER positive breast cancer cells; chip antibody: none; cell line: T47D; ', 'cell type: triple negative breast cancer cells; chip antibody: XBP1 (Biolegend, 619502); cell line: HS578T; ', 'cell type: triple negative breast cancer cells; chip antibody: none; cell line: HS578T; ' GSE22169 Homo sapiens 7 Expression profiling by array GPL6480; GPL10487 Comparison of CD44+/CD24- sorted fraction with 'rest' fraction of NBLE cells and primary breast cancer-derived cells 2010-06-07 TSV40ER and hTERT immortalized mammospheres undergo transformation in culture to generate breast cancer stem cells The stem cell hypothesis of cancer predicts that cancers arise from the transformation of normal stem/progenitor cells present within adult tissues. However, the molecular mechanisms that lead to the transformation of these cells remain largely unknown, mainly owing to the lack of suitable model systems. In this study, we have generated an immortalized breast epithelial cell line, NBLE, by over-expressing the SV40 Early Region and the catalytic domain of human telomerase into mammosphere-derived cells that are enriched in breast stem/progenitor cells. While primary mammospheres fail to grow beyond four passages in suspension culture, NBLE cells propagated continuously generating spheres at a high frequency of 35%. These cells also expressed stemness-related genes, and differentiated into both luminal and myoepithelial lineages. Interestingly, after around 135 population doublings in culture, the late passage cells exhibited a mesenchymal morphology and contained >90% of CD44+/CD24Low/- cells resembling breast cancer stem cells. When injected subcutaneously into nude mice, the late passage NBLEs formed invasive tumors closely resembling breast adenocarcinomas, the most common type of breast cancer. The transformed NBLE cells showed hyperactivation of Wnt, Hh and TGFbeta pathways, suggesting that the deregulation of these self-renewal pathways may have in part contributed to tumorigenesis. Gene expression analysis further revealed a high degree of similarity with breast cancer stem cells. Thus, our study provides a unique model system to study signaling pathways involved in self-renewal, differentiation, and transformation of breast stem/progenitor cells. Additionally, the NBLE cells can be utilized for screening drugs specifically targeting breast cancer stem cells. NBLE cells were generated by over-expressing SV40ER and hTERT into mammosphere-derived cells. These cells harnored CD44+/CD24- fraction that resembled breast cancer stem cells. To understand the unique gene expression of this fraction we performed microarray on CD44+/CD24- versus rest fractions from NBLE cells (Rep 1 and Rep 2). To see if this gene profile has any similarity with breast cancer stem cells, we performed CD44+/CD24- versus rest microarray on two primary breast tumors (CB272 and CB258-Rep1 andRep2). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22169 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA127687 https://www.ebi.ac.uk/ena/browser/view/PRJNA127687 None [Overal design]Whole genome gene expression profiling microarray based comparison of immortalized and transformed mammospheres derived cells. Two-color experiment, NBLE-CD44+/CD24- labelled with Cy5 and NBLE-Rest labelled with Cy3; [Treatment]'None', 'Not Applicable- CD44+/CD24- and rest fractions were flow sorted and RNA was extracted'; [Growth]'None', 'NBLE cells were grown in low attachment condition in the absence of serum for 6 days to form mammospheres. The media was supplemented with B27, EGF, insulin, hydrocortisone and heparin along with pen/strep/fungizone. Primary cancer cells were sorted immidiately without growing.'; [Extraction]'The mammospheres were used for RNA isolation by using Qiagen Rneasy Minikit (Cat No: 74106) as per the manufacturer’s instructions . The RNA was eluted in 30 µl of RNase free water (Ambion, AM9939). RNA concentration and purity was determined at an optical density ratio of 260/280 using the Nanodrop® ND-1000 spectrophotometer (NanoDrop Technologies, Wilmington, DE) and the integrity of total RNA was verified on an Agilent 2100 Bioanalyzer using the RNA 6000 Nano LabChip (Agilent Technologies). RNA was stored at −80 °C until use.', 'Total RNA was extracted using Qiagen Rneasy mini columns'; [Cell type]'immortalized mammosphere derived cells', 'transformed mammosphere derived cells', 'Sorted CD44+/CD24- fractions from immortalized mammosphere-derived cells grown as spheres', 'Sorted rest fractions from immortalized mammosphere-derived cells grown as spheres', 'Sorted CD44+/CD24- fractions from primary breast cancer (CB272)-derived cells', 'Sorted rest fractions from primary breast cancer (CB272)-derived cells', 'Sorted CD44+/CD24- fractions from primary breast cancer (CB258)-derived cells', 'Sorted rest fractions from primary breast cancer (CB258)-derived cells''cell type: immortalized mammosphere derived cells; passage: early; ', 'cell type: transformed mammosphere derived cells; passage: late; ', 'cell type: Sorted CD44+/CD24- fractions from immortalized mammosphere-derived cells grown as spheres; ', 'cell type: Sorted rest fractions from immortalized mammosphere-derived cells grown as spheres; ', 'cell type: Sorted CD44+/CD24- fractions from primary breast cancer (CB272)-derived cells; ', 'cell type: Sorted rest fractions from primary breast cancer (CB272)-derived cells; ', 'cell type: Sorted CD44+/CD24- fractions from primary breast cancer (CB258)-derived cells; ', 'cell type: Sorted rest fractions from primary breast cancer (CB258)-derived cells; ' GSE109666 Homo sapiens 33 Other GPL14767 RIP-Chip analysis supports different roles for AGO2 and GW182 proteins in recruiting and processing microRNA targets (microRNA) 2018-01-25 MicroRNAs are small non-coding RNA molecules mediating the translational repression and degradation of target mRNAs in the cell. Mature miRNAs are used as a template by the RNA-induced silencing complex (RISC) to recognize the complementary mRNAs to be regulated. To discern further RISC complex functions, we analyzed the activities of two RISC proteins, AGO2 and GW182, in the MCF-7 human breast cancer cell line. We performed three RIP-Chip experiments using either anti-AGO2 or anti-GW182 antibody and compiled a dataset made up of the miRNA and mRNA expression profiles of three samples for each experiment. Specifically, we analyzed the input sample, the immunoprecipitated fraction and the unbound sample resulting from the RIP experiment. We used the expression profile of the input sample to compute several variables, using formulae capable of integrating the information on predicted miRNA binding sites, both in the 3’UTR and coding regions, with miRNA and mRNA expression level profiles. We compared immunoprecipitated vs unbound samples to determine the differentially expressed genes, independently for AGO2 and GW182 related samples. For each of the two proteins, we trained and tested several support vector machine algorithms able to predict the differentially expressed genes that were experimentally detected. The most efficient algorithm for predicting the over-expressed genes in AGO2 immunoprecipitated samples was trained by using variables involving the number of binding sites in both the 3’UTR and coding region, integrated with the miRNA expression profile, as expected for miRNA targets. On the other hand, we found that the best variable for predicting over-expressed genes in the GW182 immunoprecipitated sample was the length of the coding region. Due to the major role of GW182 in GW/P-bodies, our data suggests that the AGO2-GW182 RISC complex recruits genes based on miRNA binding sites in the 3’UTR and coding region, but only the longer mRNAs remain sequestered in GW/P-bodies, functioning as a repository for translationally silenced RNAs. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE109666 RIP-Chip analysis supports different roles for AGO2 and GW182 proteins in recruiting and processing microRNA targets. BMC bioinformatics 2.511 https://doi.org/10.1186/s12859-019-2683-y {BMC bioinformatics (2.511): 10.1186/s12859-019-2683-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA431617 https://www.ebi.ac.uk/ena/browser/view/PRJNA431617 None [Overal design]We performed three independent RIP-Chip experiment for each of the two protein AGO2 and GW182 in MCF-7 human breast cancer cell line. In each experiment we analyzed three samples: the Input sample (IN), the immunoprecipitated fraction (IP) and the unbound sample resulting from the RIP experiment (FT). Each sample was analyzed with human whole genome microarray and microRNA microarray, mostly in two replicates.; [Treatment]'Immunoprecipitation (IP) of RISC proteins was performed using mouse monoclonal anti-AGO2 (clone 1B1-E2H5, RN003M), rabbit anti-GW182 (TNRC6A, RN033P) and the RIP-Assay Kit for microRNA (MBL International corporation). Briefly, cells (1.5x107) were suspended in 0.3 ml of miLysis buffer supplemented with protease and RNase inhibitors, after incubation on ice for 10min and one freeze-thaw cycle, the lysate was diluted five-times with lysis buffer and the cytoplasmic fraction was isolated by centrifugation at 12,000xg at 4 °C for 5 min. To eliminate nonspecific binding the lysate was incubated with protein A/G-agarose beads (SantaCruz) at 4 °C for 1 hour. The precleared lysates were then mixed with anti-AGO2 or anti-GW182 (25 ug of Ab/mg of lysate) armed beads, the use of preimmune mouse IgG isotype and rabbit IgG assessed the specificity of the precipitated immunocomplexes. After incubation overnight at 4 °C on a rocking platform, AGO2-IP and GW182-IP beads were washed three times with ice cold wash buffer.'; [Growth]'The MCF-7 human breast cancer cell line was purchased from American Type Culture Collection (ATCC, Rockville, MD, USA). Cells were cultured in Dulbecco’s modified Eagle Medium (DMEM) supplemented with 10% heat-inactivated fetal bovine serum (FBS), glutamine (4 mM) and penicillin/streptomycin (100 μg/ml).'; [Extraction]'Total RNA (i.e. including mRNAs and microRNAs ) was extracted from IP fractions following the two-step method described in the RIP-Assay Kit, while total and unbound fractions were processed using TRIzol LS (ThermoFisher Scientific Inc.) according to the manufacturer’s instructions. In some cases, total RNA was isolated using the miRNeasy Mini Kit from Qiagen. RNA was quantified by NanoDrop (ThermoFisher Scientific Inc.) and RNA integrity and quality were assessed using the 2100 Agilent Bioanalyzer.'; [Cell type]'Source: ''protein: AGO2; fraction: IN; ', 'protein: AGO2; fraction: FT; ', 'protein: AGO2; fraction: IP; ', 'protein: GW182; fraction: IN; ', 'protein: GW182; fraction: FT; ', 'protein: GW182; fraction: IP; ' GSE107966 Homo sapiens 1 Methylation profiling by high throughput sequencing GPL11154 Unliganded Progesterone Receptor Governs Estrogen Receptor Gene Expression by Regulating DNA Methylation in Breast Cancer Cells 2017-12-12 How breast cancers respond to endocrine therapy strongly depends on the expression of the estrogen and progesterone receptors (ER and PR, respectively), with doublenegative ER-/PR- breast cancers having worse clinical outcome than ER+/PR+ breast cancers. Although much is known about ERα gene (ESR1) regulation after hormonal stimulation, how it is regulated in the absence of hormones is not fully understood. We used ER+/PR+ positive breast cancer cells to investigate the role of PR in ESR1 gene regulation in the absence of hormones. We show that PR binds to the low-methylated ESR1 promoter and maintains both gene expression and the DNA methylation profile of the ESR1 locus in hormone-deprived breast cancer cells. Depletion of PR reduces ESR1 expression, with a concomitant increase in gene promoter methylation. The high amount of DNA methylation in the ESR1 promoter of PR-depleted cells persists after the stable re-expression of PR and inhibits PR binding to this genomic region. Consequently, the rescue of PR expression in PR-depleted cells is insufficient to restore ESR1 expression. Consistent with these data, DNA methylation impedes PR binding to consensus progesterone responsive elements in vitro. These findings help us understand the complex crosstalk between PR and ER, and suggest that the analysis of DNA methylation of ESR1 promoter in breast cancer cells can help to design the appropriate targeted therapies for different types of breast cancer patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE107966 Unliganded Progesterone Receptor Governs Estrogen Receptor Gene Expression by Regulating DNA Methylation in Breast Cancer Cells. Cancers 6.162 https://doi.org/10.3390/cancers10100371 {Cancers (6.162): 10.3390/cancers10100371} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA422054 https://www.ebi.ac.uk/ena/browser/view/PRJNA422054 https://www.ncbi.nlm.nih.gov/sra?term=SRP126550 [Overal design]DNA methylation analysis in hormone-deprived T47D breast cancer cells; [Treatment]'None'; [Growth]'None'; [Extraction]'Hormone-deprived T47D cell pellet has been resuspended in Tris-EDTA and 20 μg of proteinase K was added. The mix has been then incubated at 55°C for 16 hours and DNA was extracted using first 1 volume of phenol and the 1 volume of chloroform. The DNA was precipitated with ethanol and sodium acetate and then resuspended in Tris-EDTA containing 20 μg/ml RNAse A\nThe library has been prepared using NEBNext Ultra DNA Library Prep Kit for Illumina (E7370L) following manufacturer’s instructions.'; [Cell type]'Source: ''tissue: T47D breast cancer cells; ' GSE23118 Homo sapiens 16 Expression profiling by array GPL6884 Cellular response to protein-conjugated nanoparticles 2010-07-23 Interaction of nanomaterials with the mammalian cells remains to be poorly understood at the molecular level. Here we report the first synthesis of hybrid nanomaterial termed phage mimetic nanorods (PMN’s) inspired from filamentous bacteriophage present in nature. We emulate filamentous bacteriophage structure by combining two separate nanoscale entities, one functionalized gold nanorods and the other is coat proteins isolated from filamentous bacteriophage obtained through landscape phage screening. Utilizing biochemical interactions between a phage-derived protein and functionalized gold nanorods, we synthesized novel phage mimetic nanorods. The resulting nanovectors showed excellent multi functional properties including target specificity, imaging and photo destruction ability in a model SKBR-3 breast cancer cells. In addition, to gain insight into the molecular interactions involved during internalization of PMNs by SKBR-3 cells, we performed gene expression profiling of cells exposed to PMNs as compared with naive cells. We identified 70 upregulated and 26 downregulated genes responding to PMNs. Heparin binding internalization was identified as most plausible mechanisms of PMNs entry. Members of Major Histocompatibility complex I (MHC class I) were activated by PMNs, leading to enhanced lysosome and proteasome activity. Seven members of poorly annotated G antigen family (GAGE) of genes were upregulated, and may represent novel mechanism of PMNs entry recognition by cells. In summary, we present a versatile technique of PMNs production as any protein isolated from phage libraries selected against any in vitro and in vivo cells can be used as a source to synthesize PMN’s. This study also opens new avenues to understand the role of nanomaterials at the molecular level. Investigate the effect of phage mimetic nanorods onto SKBT-3 cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23118 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA131509 https://www.ebi.ac.uk/ena/browser/view/PRJNA131509 None [Overal design]Two groups were compared, three biological replicates each. One group was control cells and the other was test.; [Treatment]'Normally cultured cells were compared with cells treated with our designed phage mimetic nanorods', 'H441 cells were seeded in 6-well tissue culture plates at a density of 1x106 cells per well. The cells were allowed to attach and grow overnight. CLEFMA was solubilized in dimethyl sulfoxide (DMSO), filtered through 0.2 µm nylon filter and added to the treated wells (n=4) at 1 µM concentration in culture medium supplemented with 5% FBS. The DMSO concentration was maintained at 0.1% per well. Control wells (n=4) received equivalent volume of DMSO without any test compound. The cells were allowed to remain in the treatment medium for 12 hours.'; [Growth]'The SKBR-3 cells were cultured in DMEM F-12 medium supplemented with fetal bovine serum (10%) and 100μg/ml streptomycin', "Human lung adenocarcinoma cell line NCI-H441 (ATCC Number: HTB-174) was obtained from the American Type Culture Collection (Manassas, VA). H441 cells were maintained at 37 °C with 5% CO2 in McCoy's 5A Medium (Invitrogen, Carlsbad, California) supplemented with 5% heat-inactivated fetal bovine serum (FBS). All media contained gentamicin at 50 µg/ml (GIBCO Laboratories, Grand Island, NY)."; [Extraction]'The total RNA was isolated using RNeasy Kit (Qiagen, USA) according to the manufacturer’s instructions.', "After 12 h of treatment with CLEFMA (1 µM), the cells were washed twice with Dulbecco’s PBS. The total RNA was extracted using RNAeasy kit (Qiagen, CA) as per the manufacturer’s instructions. The quality of RNA was ascertained by Nanodrop 2000. A total of 250 ng of total RNA from three biological replicates of untreated H441 cells and cells treated with CLEFMA were labeled using the Illumina Total Prep RNA Amplification Kit following manufacturer's directions (Ambion, Austin. TX)."; [Cell type]'Source: ', 'lung adenocarcinoma cells''cell line: SKBR-3; treatment: Untreated; ', 'cell line: SKBR-3; treatment: Treated; ', 'cell type: lung adenocarcinoma cells; cell line: NCI-H441 (ATCC Number: HTB-174); treatment: Untreated; ', 'cell type: lung adenocarcinoma cells; cell line: NCI-H441 (ATCC Number: HTB-174); treatment: Treated; ' GSE130421 Homo sapiens 3 Other GPL15520 BART-Seq: cost-effective massively parallelized targeted sequencing for genomics, transcriptomics, and single cell analysis [Genotyping] 2019-04-29 We describe a novel workflow named Barcode Assembly foR Targeted Sequencing, which is a highly sensitive, quantitative, and inexpensive technique for targeted sequencing of transcript cohorts (rBART-Seq) or genomic regions (gBART-Seq) from thousands of bulk samples or single cells in parallel. Multiplexing is based on a simple method that produces extensive matrices of diverse DNA barcodes attached to invariant primer sets, for generating amplicons with dual indices. Here, we used the gBART-Seq for genetic screening of breast cancer patients and identified BRCA mutations with very high precision. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130421 BART-Seq: cost-effective massively parallelized targeted sequencing for genomics, transcriptomics, and single-cell analysis. Genome biology 14.028 https://doi.org/10.1186/s13059-019-1748-6 {Genome biology (14.028): 10.1186/s13059-019-1748-6} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA540229 https://www.ebi.ac.uk/ena/browser/view/PRJNA540229 https://www.ncbi.nlm.nih.gov/sra?term=SRP194114 [Overal design]10 regions from BRCA1 and BRCA2 genes were co-amplified from genomic DNA samples of 96 breast cancer patients. The amplicons are barcoded using the BART-seq method, and multiplexed for sequencing.; [Treatment]'None'; [Growth]'None'; [Extraction]'Patient gDNAs were received from the Hadassah Medical Center.\nAdapted protocol from NEBNext® ChIP-Seq Library Prep Master Mix Set for Illumina® (provided with the BART-Seq method)'; [Cell type]'patient samples', 'Source: ''cell type: patient samples; target genes: BRCA1, BRCA2; sample size: 96; ', 'cell line: MCF7; target genes: BRCA1, BRCA2; ' GSE132424 Homo sapiens 20 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer [ATAC-seq] 2019-06-10 Estrogen receptor alpha (ESR1) mutations have been identified in hormone therapy resistant breast cancer and primary endometrial cancer. Analyses in breast cancer suggests that mutant ESR1 exhibits estrogen independent activity. In endometrial cancer, ESR1 mutations are associated with worse outcomes and less obesity, however experimental investigation of these mutations has not been performed. Using a unique CRISPR/Cas9 strategy, we introduced the D538G mutation, a common endometrial cancer mutation that alters the ligand binding domain of ESR1, while epitope tagging the endogenous locus. We discovered estrogen-independent mutant ESR1 genomic binding that is significantly altered from wildtype ESR1. The D538G mutation impacted expression, including a large set of non-estrogen regulated genes, and chromatin accessibility, with most affected loci bound by mutant ESR1. Mutant ESR1 is unique from constitutive ESR1 activity as mutant-specific changes are not recapitulated with prolonged estrogen exposure. Overall, D538G mutant ESR1 confers estrogen-independent activity while causing additional regulatory changes in endometrial cancer cells that are distinct from breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132424 Estrogen-independent molecular actions of mutant estrogen receptor 1 in endometrial cancer. Genome research 9.944 https://doi.org/10.1101/gr.244780.118 {Genome research (9.944): 10.1101/gr.244780.118} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA548065 https://www.ebi.ac.uk/ena/browser/view/PRJNA548065 https://www.ncbi.nlm.nih.gov/sra?term=SRP200986 [Overal design]ATAC-seq was used to study the effects of the D538G ESR1 mutation on chromatin accessibility; [Treatment]'Media was changed 1 day prior to inductions and cells were treated with either DMSO (vehicle) or 10 nM (estradiol) E2 for 1 hour or 8 hours. For prolonged estrogen samples, wildtype cell lines were cultured in phenol-red free RPMI with 10% charcoal-dextran stripped fetal bovine serum and 1% pen-strep for up to 25 days. Cells were treated with 10 nM E2 every 2 days with media changes, and cell lysates were collected at the following time points: day 10, day 15, day 20, day 25.'; [Growth]'Ishikawa ESR1 LBD mutant and wildtype cells were cultured in full media: RPMI-1640 with 10% fetal bovine serum and 1% penicillin-streptomycin. Cells were incubated at 37°C with 5% CO2 for the duration of all experiments. At least 5 days prior to inductions, cells were placed in hormone deprived media: phenol-red free RPMI-1640 media (Thermo Fisher Scientific), since phenol-red is estrogenic, with 10% charcoal-dextran stripped fetal bovine serum (Thermo Fisher Scientific) and 1% penicillin-streptomycin.'; [Extraction]'After treatments, cells were trypsinized and isolated by centrifugation.\nATAC-seq was performed as originally described in Buenrostro et al. 2013'; [Cell type]'Source: ''cell line: Ishikawa WT ESR1 clone 1; genotype: WT ESR1; treatment: 0.1% DMSO; time: 1 hr; ', 'cell line: Ishikawa WT ESR1 clone 1; genotype: WT ESR1; treatment: 10nM E2; time: 1 hr; ', 'cell line: Ishikawa WT ESR1 clone 1; genotype: WT ESR1; treatment: 10nM E2; time: 8 hrs; ', 'cell line: Ishikawa WT ESR1 clone 2; genotype: WT ESR1; treatment: 0.1% DMSO; time: 1 hr; ', 'cell line: Ishikawa WT ESR1 clone 2; genotype: WT ESR1; treatment: 10nM E2; time: 1 hr; ', 'cell line: Ishikawa WT ESR1 clone 2; genotype: WT ESR1; treatment: 10nM E2; time: 8 hrs; ', 'cell line: Ishikawa WT ESR1 clone 1; genotype: WT ESR1; treatment: 10nM E2; time: 10 days; ', 'cell line: Ishikawa WT ESR1 clone 1; genotype: WT ESR1; treatment: 10nM E2; time: 15 days; ', 'cell line: Ishikawa WT ESR1 clone 1; genotype: WT ESR1; treatment: 10nM E2; time: 20 days; ', 'cell line: Ishikawa WT ESR1 clone 1; genotype: WT ESR1; treatment: 10nM E2; time: 25 days; ', 'cell line: Ishikawa WT ESR1 clone 2; genotype: WT ESR1; treatment: 10nM E2; time: 10 days; ', 'cell line: Ishikawa WT ESR1 clone 2; genotype: WT ESR1; treatment: 10nM E2; time: 15 days; ', 'cell line: Ishikawa WT ESR1 clone 2; genotype: WT ESR1; treatment: 10nM E2; time: 20 days; ', 'cell line: Ishikawa WT ESR1 clone 2; genotype: WT ESR1; treatment: 10nM E2; time: 25 days; ', 'cell line: Ishikawa D538G ESR1 clone 1; genotype: D538G ESR1; treatment: 0.1% DMSO; time: 1 hr; ', 'cell line: Ishikawa D538G ESR1 clone 1; genotype: D538G ESR1; treatment: 10nM E2; time: 1 hr; ', 'cell line: Ishikawa D538G ESR1 clone 2; genotype: D538G ESR1; treatment: 0.1% DMSO; time: 1 hr; ', 'cell line: Ishikawa D538G ESR1 clone 2; genotype: D538G ESR1; treatment: 10nM E2; time: 1 hr; ', 'cell line: Ishikawa D538G ESR1 clone 3; genotype: D538G ESR1; treatment: 0.1% DMSO; time: 1 hr; ', 'cell line: Ishikawa D538G ESR1 clone 3; genotype: D538G ESR1; treatment: 10nM E2; time: 1 hr; ' GSE67129 synthetic construct 2 Non-coding RNA profiling by array GPL19117 Establishment and miRNA expression characterization of a canine mammary gland tumor cell line 2015-03-20 Canine mammary gland tumors (CMGTs) are the most common neoplasms in sexually intact female dogs. CMGTs have been suggested as a model for studying human breast cancer because of several similarities, including the relative age of onset, risk factors, incidence, histological and molecular features, biological behavior, metastatic pattern, and responses to therapy. In the present study, we established a new cell line, the SNP cell line, from a CMGT. A tumor formed in each NOD.CB17-Prkdcscid/J mouse at the site of subcutaneous SNP cell injection, with an average size at 7 days after inoculation of 49.9 mm3. SNP cells are characterized by proliferation in a tubulopapillary pattern. Moreover, we examined miRNA expression in the cultured cells and found that the expression values of miRNA-143 and miRNA-138a showed the greatest increase and decrease, respectively, of all miRNAs observed. These miRNAs might therefore play a significant role in the malignancy of SNP cells. SNP cells might serve as a model for future genetic analysis and clinical treatments of human breast tumors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE67129 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA279018 https://www.ebi.ac.uk/ena/browser/view/PRJNA279018 None [Overal design]SNP cells or normal mammary gland tissue were freshly frozen within 30 minutes of harvesting or surgical excision and stored at -80 °C until further use for an Affymetrix® GeneChip® miRNA array. An Agilent 2100 Bioanalyzer (Agilent Technologies, Inc.) was used to assess the quality of total RNA (1,000 ng). The biotin-labeled sample was prepared with a Flash TagTM Biotin HSR RNA Labeling Kit (Affymetrix, Inc.) according to the manufacturer’s protocol, and 21.5 µl of biotin-labeled sample was combined with 110.5 μl of Hybridization Master Mix. The array was incubated at 48 °C and 60 rpm for 18 hours in a GeneChip® Hybridization Oven 645 (Affymetrix, Inc.) according to the manufacturer’s protocol. A GeneChip® Fluidics Station 450 (Affymetrix, Inc.) was used to wash the array according to the manufacturer’s protocol before scanning with a GeneChip® Scanner 3000 7G (Affymetrix, Inc.) following the protocol in the Affymetrix® GeneChip® Command Console User Manual.; [Treatment]'Establishment of the cell line.The tumor cells were prepared under aseptic conditions for cell culture. The cells were cultured in 35-mm diameter petri dishes (Nunc, Ltd., Roskilde, Denmark) in RPMI 1640 medium (Invitrogen, Carlsbad, CA) supplemented with 10% heat-inactivated fetal bovine serum (Nichirei Biosciences Inc., Tokyo, Japan) and PSN (5 mg/ml penicillin, 5 mg/ml streptomycin, and 10 mg/ml neomycin) solution (Invitrogen), then incubated in 5% CO2 at 37 °C. The cells were subcultured by washing with phosphate-buffered saline. Then, the cells were harvested from near-confluent cultures by brief exposure to a solution containing 0.25% trypsin and 1 mmol/l tetrasodium ethylenediaminetetraacetic acid solution with phenol red (Invitrogen). Trypsinization was stopped using RPMI 1640 containing 10% fetal bovine serum. Trypsinized cells were transferred to a new petri dish.'; [Growth]'For clonal experiments, we serially diluted cell suspensions and plated them onto 96-well plates. We marked wells containing one single cell after microscopic confirmation. A colony was then sub-cultured from each marked well into a 12-well plate. Cloning was repeated two times. Cell lines were maintained in continuous culture over 60 passages, and we designated the established cell line as SNP cells.'; [Extraction]'miRNeasy® Mini Kit was used.'; [Cell type]'Source: ''gender: female; age: 10-year-old; tissue: tumor cells in the pleural effusion; ', 'gender: female; age: 10-year-old; tissue: normal mammary gland tissue; ' GSE129929 Homo sapiens 5 Genome binding/occupancy profiling by high throughput sequencing GPL18573 The Androgen Receptor is a Tumor Suppressor in Estrogen Receptor Positive Breast Cancer [T-47D cell line ChIP-seq] 2019-04-17 The role of the androgen receptor (AR) in estrogen receptor alpha (ER) positive breast cancer is controversial, constraining implementation of AR-directed therapies. Using a diverse, clinically relevant panel of cell-line and patient-derived models, we demonstrate that AR activation, not suppression, exerts potent anti-tumor activity in multiple disease contexts, including resistance to standard-of-care ER and CDK4/6 inhibitors. Importantly, AR agonists combined with standard-of-care agents enhanced therapeutic responses. Mechanistically, agonist activation of AR altered the genomic distribution of ER and essential co-activators (p300, SRC-3), resulting in repression of ER-regulated cell cycle genes and up-regulation of AR target genes, including known tumor suppressors. A gene signature of AR activity positively predicted disease survival in multiple clinical ER+ breast cancer cohorts. These findings provide unambiguous evidence that AR has a tumor suppressor role in ER+ breast cancer and support AR agonism as the optimal AR-directed treatment strategy, revealing a rational therapeutic opportunity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE129929 The androgen receptor is a tumor suppressor in estrogen receptor-positive breast cancer. Nature medicine 30.641 https://doi.org/10.1038/s41591-020-01168-7 {Nature medicine (30.641): 10.1038/s41591-020-01168-7} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA533222 https://www.ebi.ac.uk/ena/browser/view/PRJNA533222 https://www.ncbi.nlm.nih.gov/sra?term=SRP192818 [Overal design]ChIP-seq for AR and ERα in T-47D cells cultured in steroid-depleted conditions and treated for 4 hours with E2 or E2+DHT (10 nM each).; [Treatment]'T-47D cells were treated for 4 h with either 10 nM E2 or 10 nM E2 + 10 nM DHT'; [Growth]'T-47D cells were grown in hormone-deplete conditions (phenol red-free RPMI-1640 + 5% dextran-coated charcoal-stripped FBS) for 72h'; [Extraction]"T-47D cells were fixed with formaldehyde for 10m prior to quenching. Chromatin was prepared and subsequently sheared by the Diagenode BioRuptor Plus for 10 cycles (30 sec on, 30 sec off) on ice. Sheared chromatin was immunoprecipitated with 10µg of AR or ERα antibody overnight, after coupling to Protein A Dynabeads (10002D). DNA was purified using phenol:chloroform:isoamyl alcohol extraction.\nLibraries were prepared according to manufacturer's instructions accompanying the Qiagen Ultralow Input Library Kit (Part# 180495).\nChIP-Seq; Illumina NextSeq500 (High Output v2) single-end 75 bp reads."; [Cell type]'Source: ''cell line: T-47D; passages: 14-16 (where replicates represent sequential passages); chip antibody: AR (N-20) (Santa Cruz SC-816); treatment: E2; ', 'cell line: T-47D; passages: 14-16 (where replicates represent sequential passages); chip antibody: AR (N-20) (Santa Cruz SC-816); treatment: E2+DHT; ', 'cell line: T-47D; passages: 14-16 (where replicates represent sequential passages); chip antibody: ERα (HC-20)X (Santa Cruz SC-543X); treatment: E2; ', 'cell line: T-47D; passages: 14-16 (where replicates represent sequential passages); chip antibody: ERα (HC-20)X (Santa Cruz SC-543X); treatment: E2+DHT; ', 'cell line: T-47D; passages: 14-16 (where replicates represent sequential passages); chip antibody: Pooled input; treatment: Pooled input; ' GSE127859 Mus musculus; Homo sapiens 8 Genome binding/occupancy profiling by high throughput sequencing GPL16791; GPL17021 ERα over-expression does not accelerate development of p53-deficient mammary tumors in mice [ChIP-Seq] 2019-03-05 About 75% of all breast cancers express the nuclear hormone receptor oestrogen receptor α (ERα). However, the majority of mammary tumors from genetically engineered mouse models are ERα-negative. To model ERα-positive breast cancer in mice, we exogenously introduced expression of mouse and human ERα in an existing p53-deficiency driven breast cancer mouse model. After initial ERα expression during development of the mammary gland, expression was reduced or lost in adult glands and p53-deficient mammary tumors. ChIP-sequencing analysis of primary mouse mammary epithelial cells (MMECs) derived from these models, in which expression of the ERα constructs was induced in vitro, confirmed interaction of ERα with the DNA. In human breast and endometrial cancer, the pioneer factor FOXA1 is known to be essential to facilitate ERα/DNA binding. Surprisingly, the ERα binding sites identified in primary MMECs, but also in mouse mammary gland and uterus, showed a high enrichment of ERE motifs, but were devoid of Forkhead motifs. Furthermore, exogenous introduction of FOXA1 and GATA3 in ERα-expressing MMECs was not sufficient to promote ERα-responsiveness of these cells. Together, this suggests that species-specific differences in ERα-cistromes between mouse and human are dictated by the DNA sequence, resulting in ERα-dependencies in mice that are not FOXA1 driven and potentially not tumorigenic. These species-specific differences in ERα-biology can limit the use of mouse models in ERα-positive breast cancer research. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE127859 Exogenous ERα Expression in the Mammary Epithelium Decreases Over Time and Does Not Contribute to p53-Deficient Mammary Tumor Formation in Mice. Journal of mammary gland biology and neoplasia 2.758 https://doi.org/10.1007/s10911-019-09437-z {Journal of mammary gland biology and neoplasia (2.758): 10.1007/s10911-019-09437-z} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA525658 https://www.ebi.ac.uk/ena/browser/view/PRJNA525658 https://www.ncbi.nlm.nih.gov/sra?term=SRP187558 [Overal design]Binding of ERa in MCF7 cells and HA-tagged human ERa or HA-tagged mouse ERa in primary MMECs profiled by ChIP-seq (Chromatin Immunoprecipitation followed by deep sequencing).; [Treatment]'None'; [Growth]'None'; [Extraction]'Chromatin immunoprecipitations were performed as described previously, with adaptations (Schmidt et al., 2009). In short, cells were crosslinked in solution A (pH 7.4, 50mM Hepes, 100mM NaCl, 1mM EDTA, 0.5M EGTA) containing 2mM DSG for 35 minutes, then formaldehyde was added to a final concentration of 1% and incubated for another 10 minutes. After addition of Glycine to a final concentration of 125mM to quench the crosslinking reaction and washing with PBS, cells were collected. The Bioruptor Pico (Diagenode) was used for sonication. For ChIP, antibodies were used to detect the HA-tag (25ug, 05-904, Millipore) and ERa (10ug, sc-543, Santa Cruz) with 100 ml Protein A magnetic beads (Thermo Scientific).\nImmunoprecipitated DNA was processed for library preparation (Part# 0801-0303, KAPA biosystems kit).'; [Cell type]'Primary MMECs', 'Breast cancer cells''strain: FVB; cell type: Primary MMECs; genotype: WcrH;P53F/F; chip antibody: aHA (Millipore, catalog# 05-904); treatment: AdCre transduction, harvested after 72hrs; ', 'strain: FVB; cell type: Primary MMECs; genotype: WcrH;P53F/F;HA-hERa; chip antibody: aHA (Millipore, catalog# 05-904); treatment: AdCre transduction, harvested after 72hrs; ', 'strain: FVB; cell type: Primary MMECs; genotype: WcrH;P53F/F;HA-mERa; chip antibody: aHA (Millipore, catalog# 05-904); treatment: AdCre transduction, harvested after 72hrs; ', 'cell line: MCF7; cell type: Breast cancer cells; chip antibody: aERa (Santa Cruz, catalog# sc-543); treatment: Full medium; ' GSE116876 Homo sapiens 87 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other GPL18573 Oncogenic Notch promotes long-range regulatory interactions within hyperconnected 3D cliques 2018-07-10 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE116876 Oncogenic Notch Promotes Long-Range Regulatory Interactions within Hyperconnected 3D Cliques. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2019.01.006 {Molecular cell (14.548): 10.1016/j.molcel.2019.01.006} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA480468 https://www.ebi.ac.uk/ena/browser/view/PRJNA480468 None [Overal design]Refer to individual Series; [Treatment]'Cells were treated with the GSI compound E (1 μM, Calbiochem cat# 565790) for 72 hours, washed, and then cultured for 5 hours in media containing 1μM GSI (mock washout) or DMSO (washout) as previously described (Weng et al., 2006).', 'Untreated.', 'Cells were treated with the GSI compound E (1 μM, Calbiochem cat# 565790) for 72 hours.', 'Cells were treated with the GSI compound E (1 μM, Calbiochem cat# 565790) for 72 hours, washed, and then cultured for 3 days in media containing DMSO.'; [Growth]'MB157 (female) cells were grown in DMEM (Corning, cat# 10-013-CV) supplemented with 10% fetal bovine serum (Hyclone, cat# SH30070.03) and 100 U/mL and 100 μg/mL penicillin/streptomycin (Corning, cat# 30-002-CI). When passaged cells were detached with 0.25% trypsin, EDTA-free (Gibco, cat# 15090-046) to avoid activation of Notch signaling.', 'HCC1599 (female) cells were grown in RPMI 1640 (Corning, cat# 10-040-CM) supplemented with 10% fetal bovine serum (Hyclone, cat# SH30070.03), 2 mM L-glutamine (Corning, cat# 25-005-CI), 100 U/mL and 100 μg/mL penicillin/streptomycin (Corning, cat# 30-002-CI), 100 mM nonessential amino acids (Gibco, cat# 11140-050), 1mM sodium pyruvate (Gibco, cat#11360-070) and 0.1mM of 2-mercaptoethanol (Sigma, cat# M6250).', 'DND41 (male) cells were grown in RPMI 1640 (Corning, cat# 10-040-CM) supplemented with 10% fetal bovine serum (Hyclone, cat# SH30070.03), 2 mM L-glutamine (Corning, cat# 25-005-CI), 100 U/mL and 100 μg/mL penicillin/streptomycin (Corning, cat# 30-002-CI), 100 mM nonessential amino acids (Gibco, cat# 11140-050), 1mM sodium pyruvate (Gibco, cat#11360-070) and 0.1mM of 2-mercaptoethanol (Sigma, cat# M6250).', 'Rec-1 (male) cells were grown in RPMI 1640 (Corning, cat# 10-040-CM) supplemented with 10% fetal bovine serum (Hyclone, cat# SH30070.03), 2 mM L-glutamine (Corning, cat# 25-005-CI), 100 U/mL and 100 μg/mL penicillin/streptomycin (Corning, cat# 30-002-CI), 100 mM nonessential amino acids (Gibco, cat# 11140-050), 1mM sodium pyruvate (Gibco, cat#11360-070) and 0.1mM of 2-mercaptoethanol (Sigma, cat# M6250).', 'Rec-1 (female) cells were grown in RPMI 1640 (Corning, cat# 10-040-CM) supplemented with 10% fetal bovine serum (Hyclone, cat# SH30070.03), 2 mM L-glutamine (Corning, cat# 25-005-CI), 100 U/mL and 100 μg/mL penicillin/streptomycin (Corning, cat# 30-002-CI), 100 mM nonessential amino acids (Gibco, cat# 11140-050), 1mM sodium pyruvate (Gibco, cat#11360-070) and 0.1mM of 2-mercaptoethanol (Sigma, cat# M6250).'; [Extraction]'Cells from GSI and washout conditions were washed with 1 x PBS (Corning, cat# 21031CV) and lysed with 350 μl RLT Plus buffer (Qiagen) supplemented with 10% 2-mercaptoethanol (Sigma, cat# M6250), vortexed briefly, snap-frozen on dry ice, and stored at -80°C. Subsequently, total RNA was isolated using the RNeasy Plus Micro Kit (Qiagen, cat# 74034).\nRNA integrity numbers were determined using TapeStation 2200 (Agilent), and all samples used for RNA-seq library preparation had RIN numbers greater than 9.5. 800 ng of total RNA was used and libraries were prepared using the SMARTer Standard Total RNA Sample Prep Kit-HI Mammalian (Clontech, cat# 634873). Libraries were single-end sequenced (75 bp) on a NextSeq 550.', 'ChIP-seq was performed as previously described (Ryan et al., 2017). Briefly, chromatin samples prepared from appropriate number of fixed cells (10^7 for histone modifications and 4 x 10^7 for transcription factors) were sonicated and cleared with recombinant protein G–conjugated Agarose beads (Invitrogen, cat# 15920-010) and subsequently immunoprecipitated with antibodies recognizing Notch1 (Wang et al., 2014), RBPJ (D10A4) (CST, cat# 5313), H3K27ac (Active Motif, cat# 39133), H3K27me3 (EMD Millipore cat# 07-449), H3K4me1 (Abcam, cat# ab8895), Smc1a (Bethyl, cat# A300-055A) and CTCF (EMD Millipore cat# 07-729). Antibody-chromatin complexes were captured with recombinant protein G–conjugated Agarose beads, washed with Low Salt Wash Buffer, High Salt Wash Buffer, LiCl Wash Buffer and TE buffer with 50mM NaCl and eluted. Input sample was prepared by the same approach without immunoprecipitation. After reversal of cross-linking, RNase and Proteinase K (Invitrogen, cat# 25530-049) treatment were performed and DNA was purified with QIAquick PCR Purification Kit (Qiagen, cat# 28106).\nLibraries were then prepared using the NEBNext Ultra II DNA library Prep Kit for Illumina (NEB, cat# E7645S). Two replicates were performed for each condition. Indexed libraries were validated for quality and size distribution using a TapeStation 2200 (Agilent). Single end sequencing (75 bp) or Paired-end sequencing (38 bp+38 bp) was performed on a NextSeq 550.', 'ChIP-seq was performed as previously described (Ryan et al., 2017). Briefly, chromatin samples prepared from appropriate number of fixed cells (107 for histone modifications and 4 x 107 for transcription factors) were sonicated and cleared with recombinant protein G–conjugated Agarose beads (Invitrogen, cat# 15920-010) and subsequently immunoprecipitated with antibodies recognizing Notch1 (Wang et al., 2014), RBPJ (D10A4) (CST, cat# 5313), H3K27ac (Active Motif, cat# 39133), H3K27me3 (EMD Millipore cat# 07-449), H3K4me1 (Abcam, cat# ab8895), Smc1a (Bethyl, cat# A300-055A) and CTCF (EMD Millipore cat# 07-729). Antibody-chromatin complexes were captured with recombinant protein G–conjugated Agarose beads, washed with Low Salt Wash Buffer, High Salt Wash Buffer, LiCl Wash Buffer and TE buffer with 50mM NaCl and eluted. Input sample was prepared by the same approach without immunoprecipitation. After reversal of cross-linking, RNase and Proteinase K (Invitrogen, cat# 25530-049) treatment were performed and DNA was purified with QIAquick PCR Purification Kit (Qiagen, cat# 28106).\nLibraries were then prepared using the NEBNext Ultra II DNA library Prep Kit for Illumina (NEB, cat# E7645S). Two replicates were performed for each condition. Indexed libraries were validated for quality and size distribution using a TapeStation 2200 (Agilent). Single end sequencing (75 bp) or Paired-end sequencing (38 bp+38 bp) was performed on a NextSeq 550.', 'HiChIP was performed as described (Mumbach et al., 2016) using antibody against Smc1 (Bethyl, cat# A300-055A). Briefly, 2 x 10^7 cells were crosslinked with 1% formaldehyde (Thermo Scientific, cat# 28908) for 10 min and subsequently quenched with 0.125M glycine (Invitrogen, cat# 15527-013). Chromatin was digested using MboI restriction enzyme (NEB, Cat#R0147), followed by biotin incorporation with Biotin-14-dATP (Invitrogen, 19524-016) in end-repair step, ligation, and sonication. Sheared chromatin was 4-fold diluted with ChIP dilution buffer (16.7mM Tris pH 7.5, 167mM NaCl, 1.2mM EDTA, 0.01% SDS, 1.1% Triton X-100) and cleared and then incubated with anti-Smc1 antibody at 4°C for overnight. Chromatin-antibody complexes were captured by Protein-A magnetic beads (Pierce, cat# 88846) and subsequently washed with Low Salt Wash Buffer, High Salt Wash Buffer, LiCl Wash Buffer and eluted.\nDNA was purified with MinElute PCR Purification Kit (Qiagen, cat# 28004) and quantified using Qubit dsDNA HS Assay Kit (Invitrogen, cat# Q32851). 50-150ng was used for capture with Dynabeads MyOne Streptavidin C-1 (Invitrogen, cat# 65001) and an appropriate amount of Tn5 enzyme was added to captured DNA to generate sequencing library. Paired-end sequencing (38 bp+38 bp) was performed on a NextSeq 550.'; [Cell type]'Triple-negative breast cancer cell line', 'T-ALL cell line', 'Mantle cell lymphoma cell line''cell line: MB157; cell type: Triple-negative breast cancer cell line; drug treatment: GSI-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; drug treatment: GSI-mock-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: H3K27ac; drug treatment: GSI-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: H3K27ac; drug treatment: GSI-mock-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: H3K4me1; drug treatment: GSI-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: H3K4me1; drug treatment: GSI-mock-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: H3K27me3; drug treatment: GSI-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: H3K27me3; drug treatment: GSI-mock-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: NICD1; drug treatment: GSI-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: NICD1; drug treatment: GSI-mock-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: RBPJ; drug treatment: GSI-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: RBPJ; drug treatment: GSI-mock-washout; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: SMC1a; drug treatment: untreated; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: CTCF; drug treatment: untreated; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: input; drug treatment: untreated; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: SMC1a; drug treatment: GSI-treated; ', 'cell line: MB157; cell type: Triple-negative breast cancer cell line; chip antibody: SMC1a; drug treatment: GSI-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; drug treatment: GSI-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; drug treatment: GSI-mock-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: H3K27ac; drug treatment: GSI-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: H3K27ac; drug treatment: GSI-mock-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: H3K4me1; drug treatment: GSI-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: H3K4me1; drug treatment: GSI-mock-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: H3K27me3; drug treatment: GSI-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: H3K27me3; drug treatment: GSI-mock-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: NICD1; drug treatment: GSI-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: NICD1; drug treatment: GSI-mock-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: RBPJ; drug treatment: GSI-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: RBPJ; drug treatment: GSI-mock-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: input; drug treatment: untreated; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: input; drug treatment: GSI-mock-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: input; drug treatment: GSI-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: SMC1a; drug treatment: untreated; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; chip antibody: SMC1a; drug treatment: GSI-treated; ', 'cell line: DND41; cell type: T-ALL cell line; drug treatment: GSI-washout; ', 'cell line: DND41; cell type: T-ALL cell line; drug treatment: GSI-mock-washout; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: H3K27me3; drug treatment: GSI-washout; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: H3K27me3; drug treatment: GSI-mock-washout; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: H3K27ac; drug treatment: GSI-washout; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: H3K27ac; drug treatment: GSI-mock-washout; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: input; drug treatment: untreated; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: input; drug treatment: GSI-mock-washout; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: input; drug treatment: GSI-washout; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: SMC1a; drug treatment: untreated; ', 'cell line: Rec-1; cell type: Mantle cell lymphoma cell line; chip antibody: SMC1a; drug treatment: GSI-treated; ' GSE131977 Homo sapiens 174 Genome variation profiling by high throughput sequencing GPL18573 Acquired resistance to combined BET and CDK4/6 inhibition in triple-negative breast cancer [Barcode] 2019-05-30 BET inhibitors are promising therapeutic agents for the treatment of triple-negative breast cancer (TNBC), but the rapid emergence of resistance necessitates investigation of combination therapies and their effects on tumor evolution. Here, we show that palbociclib, a CDK4/6 inhibitor, and paclitaxel, a microtubule inhibitor, synergize with the BET inhibitor JQ1 in TNBC lines. High-complexity DNA barcoding and mathematical modeling indicate a high rate of de novo acquired resistance to these drugs relative to pre-existing resistance. We demonstrate that the combination of JQ1 and palbociclib induces cell division errors, which can increase the chance of developing aneuploidy. Characterizing acquired resistance to combination treatment at single cell level shows heterogeneous mechanisms including activation of G1-S and senescence pathways. Our results establish a rationale for further investigation of combined BET and CDK4/6 inhibition in TNBC and suggest novel mechanisms of action for these drugs, and new vulnerabilities in cells after emergence of resistance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE131977 Acquired resistance to combined BET and CDK4/6 inhibition in triple-negative breast cancer. Nature communications 11.878 https://doi.org/10.1038/s41467-020-16170-3 {Nature communications (11.878): 10.1038/s41467-020-16170-3} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA545507 https://www.ebi.ac.uk/ena/browser/view/PRJNA545507 https://www.ncbi.nlm.nih.gov/sra?term=SRP199904 [Overal design]Barcode-seq of SUM159 breast cancer cell line treated in vivo and in vitro with JQ1, palbociclib, paclitaxel, and combinations; [Treatment]'Cells were grown in vitro in the presence of DMSO, JQ1 (100 nM), paclitaxel (0.6 nM), palbociclib (160 nM), JQ1+paclitaxel, or JQ1+palbociclib, in triplicates, for up to 18 passages. Mice were treated for up to 2 weeks with vehicle, JQ1 (30-50 mg/kg daily), palbociclib (75 mg/kg daily), paclitaxel (10 mg/kg twice weekly), JQ1+palbociclib, or JQ1+paclitaxel, with 5 mice per group.'; [Growth]'Cells were lentivirally infected with the ClonTracer barcode library (Bhang et al., 2015). Barcoded cells were passaged in vitro in the presence of drug or injected orthotopically into mammary fat pads of NOG mice to produce xenografts.'; [Extraction]'DNA was extracted from frozen cultured cells and xenografts using the AllPrep DNA/RNA Mini Kit or the QIAamp DNA Mini Kit (Qiagen).\nPCR was used to amplify barcodes and introduce Illumina adaptors along with a 5 bp index sequence for multiplexing as described (Bhang et al., 2015). 2 µg of genomic DNA was used as template, and 15-16 samples were multiplexed. PCR products were run on 0.8% agarose NGS E-Gels (Invitrogen) to verify the correct library size, and bands were purified using the MinElute Gel Extraction Kit (Qiagen).'; [Cell type]'Source: ''cell line: SUM159; treatment: vehicle; time point: 2 wk; replicate: 1; ', 'cell line: SUM159; treatment: vehicle; time point: 2 wk; replicate: 2; ', 'cell line: SUM159; treatment: vehicle; time point: 2 wk; replicate: 3; ', 'cell line: SUM159; treatment: vehicle; time point: 2 wk; replicate: 4; ', 'cell line: SUM159; treatment: JQ1; time point: 2 wk; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: 2 wk; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: 2 wk; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: 2 wk; replicate: 4; ', 'cell line: SUM159; treatment: palbociclib; time point: 2 wk; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; time point: 2 wk; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; time point: 2 wk; replicate: 3; ', 'cell line: SUM159; treatment: palbociclib; time point: 2 wk; replicate: 4; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: 2 wk; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: 2 wk; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: 2 wk; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: 2 wk; replicate: 4; ', 'cell line: SUM159; treatment: pre-treatment; time point: 0 wk; replicate: 1; ', 'cell line: SUM159; treatment: pre-treatment; time point: 0 wk; replicate: 2; ', 'cell line: SUM159; treatment: pre-treatment; time point: 0 wk; replicate: 3; ', 'cell line: SUM159; treatment: pre-treatment; time point: 0 wk; replicate: 4; ', 'cell line: SUM159; treatment: vehicle; time point: 1 wk; replicate: 1; ', 'cell line: SUM159; treatment: vehicle; time point: 1 wk; replicate: 2; ', 'cell line: SUM159; treatment: vehicle; time point: 1 wk; replicate: 3; ', 'cell line: SUM159; treatment: vehicle; time point: 1 wk; replicate: 4; ', 'cell line: SUM159; treatment: JQ1; time point: 1 wk; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: 1 wk; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: 1 wk; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: 1 wk; replicate: 4; ', 'cell line: SUM159; treatment: paclitaxel; time point: 1 wk; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; time point: 1 wk; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; time point: 1 wk; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: 1 wk; replicate: 4; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 1 wk; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 1 wk; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 1 wk; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 1 wk; replicate: 4; ', 'cell line: SUM159; treatment: paclitaxel; time point: 2 wk; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; time point: 2 wk; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; time point: 2 wk; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: 2 wk; replicate: 4; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 2 wk; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 2 wk; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 2 wk; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: 2 wk; replicate: 4; ', 'cell line: SUM159; treatment: pre-treatment; time point: passage 0; replicate: 1; ', 'cell line: SUM159; treatment: pre-treatment; time point: passage 0; replicate: 2; ', 'cell line: SUM159; treatment: pre-treatment; time point: passage 0; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 2; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 2; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 2; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 4; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 4; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 4; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 6; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 6; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 6; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 11; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 11; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 11; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 18; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 18; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 18; replicate: 3; 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treatment: JQ1; time point: passage 18; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: passage 18; replicate: 3; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 2; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 2; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 2; replicate: 3; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 4; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 4; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 4; replicate: 3; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 6; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 6; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 6; replicate: 3; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 11; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 11; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 11; replicate: 3; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 18; replicate: 1; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 18; replicate: 2; ', 'cell line: SUM159; treatment: palbociclib; time point: passage 18; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 2; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 2; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 2; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 4; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 4; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 4; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 6; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 6; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 6; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 7; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 11; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 11; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 18; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+palbociclib; time point: passage 18; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 1; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 1; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 1; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 7; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 7; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 7; replicate: 3; ', 'cell line: SUM159; treatment: DMSO; time point: passage 14; replicate: 1; ', 'cell line: SUM159; treatment: DMSO; time point: passage 14; replicate: 2; ', 'cell line: SUM159; treatment: DMSO; time point: passage 14; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: passage 7; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: passage 7; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: passage 7; replicate: 3; ', 'cell line: SUM159; treatment: JQ1; time point: passage 14; replicate: 1; ', 'cell line: SUM159; treatment: JQ1; time point: passage 14; replicate: 2; ', 'cell line: SUM159; treatment: JQ1; time point: passage 14; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 2; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 2; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 2; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 4; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 4; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 4; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 6; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 6; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 6; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 7; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 7; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 7; replicate: 3; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 14; replicate: 1; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 14; replicate: 2; ', 'cell line: SUM159; treatment: paclitaxel; time point: passage 14; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 2; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 2; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 2; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 4; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 4; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 4; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 7; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 7; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 7; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 9; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 9; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 9; replicate: 3; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 14; replicate: 1; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 14; replicate: 2; ', 'cell line: SUM159; treatment: JQ1+paclitaxel; time point: passage 14; replicate: 3; ' GSE63610 Homo sapiens 10 Expression profiling by high throughput sequencing GPL11154 The effect of REST and its alternatively spliced transcript, REST-003, on breast cancer invasiveness 2014-11-25 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE63610 Non-coding RNAs derived from an alternatively spliced REST transcript (REST-003) regulate breast cancer invasiveness. Scientific reports 4.011 https://doi.org/10.1038/srep11207 {Scientific reports (4.011): 10.1038/srep11207} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA268443 https://www.ebi.ac.uk/ena/browser/view/PRJNA268443 None [Overal design]Refer to individual Series; [Treatment]'Lipofectamine 2000 (Invitrogen) was used for mt- or wt-REST cDNA plasmid transfection experiments. For siRNA transfection, we used DharmaFect (Thermo Scientific) or RNAiMax (Invitrogen) according to the manufacturer’s instructions.', 'For siRNA transfection, we used DharmaFect (Thermo Scientific) or RNAiMax (Invitrogen) according to the manufacturer’s instructions.'; [Growth]'MDA-MB-231 and MCF-7 cancer cell lines were maintained in a modified complete medium (RPMI, 10% FBS, 10mM HEPES, 2 mM L-glutamine, 1mM sodium-pyruvate, 0.05mM 2-mercaptoethanol, 11 mM D-glucose).', 'MDA-MB-231 cancer cell lines were maintained in a modified complete medium (RPMI, 10% FBS, 10mM HEPES, 2 mM L-glutamine, 1mM sodium-pyruvate, 0.05mM 2-mercaptoethanol, 11 mM D-glucose).'; [Extraction]'Total RNAs were isolated from cell lines using Trizol (Invitrogen) and digested with Turbo DNase (Ambion) to remove genomic DNA, according to the manufacturer’s instructions.\nLibraries from rRNA-depleted samples were prepared using a TruSeq RNA Sample Preparation kit v2 (Illumina) following the recommended protocol starting from the RNA fragmentation stage. Purification of polyadenylated RNA was omitted. Libraries were pooled (4 samples per pool), clustered on cBOT (Illumina), and sequenced on HiSeq2000, each pool in one lane. We performed single-end 100 bp reads. Reads were mapped using TopHat followed by data analysis using Cufflinks and Cuffdiff software, as well as our own pipeline.', 'Total RNAs were isolated from cell lines using Trizol (Invitrogen) and digested with Turbo DNase (Ambion) to remove genomic DNA, according to the manufacturer’s instructions.\nLibraries from rRNA-depleted samples were prepared using a TruSeq RNA Sample Preparation kit v2 (Illumina) following the recommended protocol starting from the RNA fragmentation stage. Purification of polyadenylated RNA was omitted. Libraries were pooled (4 samples per pool), clustered on cBOT (Illumina), and sequenced on HiSeq2000, each pool in one lane. We performed single-end 100 bp reads. Reads were mapped using TopHat followed by data analysis using Cufflinks and Cuffdiff software, as well as our own pipeline.'; [Cell type]'weakly invasive', 'highly invasive', 'Breast cancer cell line''cell line: MCF-7; cell type: weakly invasive; transfected with: si-GAPDH (control); genotype/variation: control; ', 'cell line: MCF-7; cell type: weakly invasive; transfected with: si-REST; genotype/variation: Downregulation of REST; ', 'cell line: MDA-MB-231; cell type: highly invasive; transfected with: EGFP (control); genotype/variation: EGFP control; ', 'cell line: MDA-MB-231; cell type: highly invasive; transfected with: mt-REST; genotype/variation: overexpression of mutant REST; ', 'cell line: MDA-MB-231; cell type: highly invasive; transfected with: wt-REST; genotype/variation: overexpression of wild type REST; ', 'cell line: MDA-MB-231; cell type: Breast cancer cell line; cell type: highly invasive; transfected with: control siRNA; ', 'cell line: MDA-MB-231; cell type: Breast cancer cell line; cell type: highly invasive; transfected with: REST-003 siRNA; ' GSE36565 Homo sapiens 10 Expression profiling by array GPL10558 Whole genome expression after modulation of miR-30a expression 2012-03-16 A subset of breast cancer cells displays increased ability to self-renew and reproduce breast cancer heterogeneity (so called, breast tumour-initiating cells or BT-ICs). As microRNAs (miRNAs) control developmental programs in stem cells, BT-ICs may also rely on specific miRNA profiles for their sustained activity. We analyzed miRNA expression in a model of putative BT-ICs and found that miR-30 family regulates growth under “stemness” conditions. A target screening revealed that miR-30 family modulates the expression of apoptosis and proliferation-related genes. The importance of miR-30 in tumour progression and breast cancer stemness was demonstrated in vivo using a mouse mammary cancer model. This is the first analysis of target prediction in a whole family of microRNAs potentially involved in survival of putative BT-ICs. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36565 MicroRNA miR-30 family regulates non-attachment growth of breast cancer cells. BMC genomics 3.501 https://doi.org/10.1186/1471-2164-14-139 {BMC genomics (3.501): 10.1186/1471-2164-14-139} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA153719 https://www.ebi.ac.uk/ena/browser/view/PRJNA153719 None [Overal design]Total RNA from cells transfected with Pre-miR-30 and KD-miR-30 family and control KD-miR-159 was extracted and reverse-transcribed and hybrized on HT12 Human bead chips; [Treatment]'Pre-miR mature microRNA (Pre-miR-30a) sequence (Applied Biosystems) and knock-down (miR-30 family-KD) locked nucleic acid (LNA) (Exiqon) were used for overexpression and inhibition of miR-30a, respectively. miR-159 LNA was used as negative control.'; [Growth]'Breast cancer cell lines (American Type Culture Collection) were grown in standard (10% fetal calf serum, 1% penicillin/streptomycin, 1% sodium pyruvate and 1% glutamine) medium. Supernatant from confluent cells was centrifuged and plated in mammosphere conditions, as previously described (Hernandez-Vargas et al., 2011).'; [Extraction]'Total RNA was extracted using TRIzol (Sigma) according to the manufacturer’s instructions.'; [Cell type]'breast cancer''cell line: MCF7; cell type: breast cancer; ' GSE174717 Homo sapiens 4 Expression profiling by high throughput sequencing GPL11154 Sequencing of human breast cancer cell line MDA-MB-231 and its highly pulmonary metastatic subline MDA-MB-231-LM2 2021-05-19 Purpose: Tumor metastasis is the main cause of death from breast cancer patients and cell migration plays a critical role in metastasis. Recent studies have shown long non-coding RNAs (lncRNAs) play an essential role in the initiation and progression of cancer. In the present study, the role of a LncRNA, Rho GTPase Activating Protein 5- Antisense 1 (ARHGAP5-AS1) in breast cancer was investigated. Methods: RNA sequencing was performed to find out dysregulated LncRNAs in MDA-MB-231-LM2 cells. Transwell migration assays and F-actin staining were utilized to estimate cell migration ability. RNA pulldown assays and RNA immunoprecipitation were used to prove the interaction between ARHGAP5-AS1 and SMAD7. Western blot and immunofluorescence imaging were used to examine the protein levels. Dual luciferase reporter assays were performed to evaluate the activation of TGF-β signaling. Results: Compared to MDA-MB-231 cells, the expression of LncRNA ARHGAP5-AS1 (NR_027263) was significantly suppressed in its highly metastatic subtype MDA-MB-231-LM2 cells. Functional study showed ARHGAP5-AS1 could inhibit cell migration via suppression of stress fibers in breast cancer cell lines. Afterwards, SMAD7 was further identified to interact with ARHGAP5-AS1 by its PY motif and thus its ubiquitination and degradation was blocked due to reduced interaction with E3 ligase SMURF1 and SMURF2. Moreover, ARHGAP5-AS1 could inhibit TGF-β signaling pathway due to its inhibitory role on SMAD7. Conclusion: Overall, these findings demonstrate that ARHGAP5-AS1 inhibits breast cancer cell migration and could serve as a novel biomarker for breast cancer metastasis and a potent target for the treatment in the future. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE174717 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA731178 https://www.ebi.ac.uk/ena/browser/view/PRJNA731178 https://www.ncbi.nlm.nih.gov/sra?term=SRP320552 [Overal design]Whole RNA profiles of MDA-MB-231 and MDA-MB-231-LM2 cells.; [Treatment]'None'; [Growth]'MDA-MB-231 was cultured in Leibovitz L-15 medium (Gibco) supplemented with 10% FBS, MDA-MB-231-LM2 was cultured in DMEM medium (Hyclone) supplemented with 10% FBS.'; [Extraction]'RNA was harvested using Trizol reagent.\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'Source: ''cell line: MDA-MB-231; metastatic ability: parental; ', 'cell line: MDA-MB-231-LM2; metastatic ability: highly pulmonary metastatic; ' GSE152102 Homo sapiens 54 Expression profiling by high throughput sequencing GPL16791 Transciptome profiling of 18 breast cancer cell llines 2020-06-09 Transciptome profiling of 18 breast cancer cell llines as part of a drug screen to identify mechanisms of response and resistance for each compound and find biomarkers doi: 10.7554/eLife.57894 https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE152102 PTEN and DNA-PK determine sensitivity and recovery in response to WEE1 inhibition in human breast cancer. eLife 7.551 https://doi.org/10.7554/eLife.57894 {eLife (7.551): 10.7554/eLife.57894} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA638351 https://www.ebi.ac.uk/ena/browser/view/PRJNA638351 https://www.ncbi.nlm.nih.gov/sra?term=SRP266607 [Overal design]18 different breast cancer cell lines analysed in biological triplicates; [Treatment]'Untreated'; [Growth]'Panel of breast cancer cell lines consisting of HCC1419, MCF7, CAMA, HCC1428, T47D, HCC38, HCC70, HCC1569, MDA-MB-157, HCC1143, BT20, MDA-MB-231, MDA-MB-468, BT549, SUM159PT, Cal51 were purchased from the American Type Culture Collection (ATCC). Cell lines were maintained in RPMI1640 (Gibco, Thermo Fisher) supplemented with 10% FBS (Gibco, Thermo Fisher) and 2 mM L-glutamine (Gibco, Thermo Fisher), 10 mM HEPES (Gibco, Thermo Fisher), and 1 mM Sodium Pyruvate (Gibco, Thermo Fisher).'; [Extraction]'RNA was first isolated using Trizol reagent (Invitrogen, Life technologies), followed by RNeasy Mini Kit (Qiagen)\nIllumina TruSeq Stranded total RNA, Illumina RiboZero'; [Cell type]'Breast cancer cell line''cell line: BT20; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: BT549; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: CAL51; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: HCC1143; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: HCC1187; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: HCC1419; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: HCC1569; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: HCC1397; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: HCC1954; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: HCC38; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: HCC70; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: LCC2; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: MCF7; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: MCF7_HJ; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: MDAMB157; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: SKBR3; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: SUM149PT; cell type: Breast cancer cell line; treatment: Untreated; ', 'cell line: T47D; cell type: Breast cancer cell line; treatment: Untreated; ' GSE9187 Homo sapiens 12 Expression profiling by array GPL4133 Human breast cancer LM2 cell lines: control vs. MTDH knockdown 2007-09-27 Transcriptional profiling of human breast cancer cell line LM2, a subline of MDA-MB-231 highly metastatic to lung when injected to nude mice, to identify the genes that are regulated after the metastasis gene metadherin is knocked down. Keywords: Genetic modification https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE9187 MTDH activation by 8q22 genomic gain promotes chemoresistance and metastasis of poor-prognosis breast cancer. Cancer cell 23.916 https://doi.org/10.1016/j.ccr.2008.11.013 {Cancer cell (23.916): 10.1016/j.ccr.2008.11.013} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA102757 https://www.ebi.ac.uk/ena/browser/view/PRJNA102757 None [Overal design]Empty pSuper vector control cells were compared to the cells transfected with the MTDH knockdown shRNA construct. Two cultured conditions were studied: the LM2 cancer cells were cultured alone or on top of a monolayer of human lung endothelial HMVEC-L cells. Three arrays for each sample.; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA extracted using Qiagen RNAeasy mini kit following manufacturer's instructions. In the co-culture condition, LM2 cells were labeled with GFP, and HMVEC-L cells were labeled with SNARF before co-culture. LM2 cells were isolated by FACS 48 hours after co-culture."; [Cell type]'Source: ''' GSE134405 Homo sapiens 12 Expression profiling by high throughput sequencing GPL16791 Temporal dissection of breast cancer brain metastases 2019-07-17 The goal of this study was to identify temporal changes to breast cancer cells as they adapt to the brain metastatic microenvironment. MDA-MB-231-tdTomato human breast cancer cells were injected into the carotid artery of Rag1-/- mice and dissected at 7 or 40 days post injection for RNA-sequencing. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE134405 Rab11b-mediated integrin recycling promotes brain metastatic adaptation and outgrowth. Nature communications 11.878 https://doi.org/10.1038/s41467-020-16832-2 {Nature communications (11.878): 10.1038/s41467-020-16832-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA555055 https://www.ebi.ac.uk/ena/browser/view/PRJNA555055 https://www.ncbi.nlm.nih.gov/sra?term=SRP215018 [Overal design]3 samples were analyzed at 7 days post injection, and 9 samples were analyzed at 40 days post injection; [Treatment]'None'; [Growth]'MDA-MB-231-tdTomato cells were routinely cultured in DMEM/F-12 supplemented with 10% fetal bovine serum and pen/strep'; [Extraction]"Total RNA was isoalted using the Acturus PicoPure RNA isolation kit (Life Technologies) according to the manufacturer's instructions\nSequencing libraries were constructed using the Ovation Single Cell RNA-Seq System (NuGEN)."; [Cell type]'breast cancer cells were injected into the carotid artery of Rag1-/- mice''cell type: breast cancer cells were injected into the carotid artery of Rag1-/- mice; timepoint: 7; cell line: MDA-MB-231-tdTomato; ', 'cell type: breast cancer cells were injected into the carotid artery of Rag1-/- mice; timepoint: 40; cell line: MDA-MB-231-tdTomato; ' GSE30931 Homo sapiens 12 Expression profiling by array GPL10558 Proteasome inhibition blocks estrogen-dependent gene transcription by decreasing histone H2B monoubiquitination in human breast cancer cells 2011-07-25 The estrogen receptor-alpha (ERα) determines breast cancer cell phenotype and is a prognostic indicator. A better understanding of the mechanisms controlling ERα function may uncover improved strategies for the treatment of breast cancer. Proteasome inhibition was previously reported to regulate estrogen-induced transcription but the mechanisms by which it influences ERα function remain controversial. In this study we investigated the transcriptome-wide effects of the proteasome inhibitor Velcade on estrogen-regulated transcription in MCF7 human breast cancer cells and demonstrate a specific global decrease in estrogen-induced transcription. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE30931 Estrogen-dependent gene transcription in human breast cancer cells relies upon proteasome-dependent monoubiquitination of histone H2B. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-11-1896 {Cancer research (8.378): 10.1158/0008-5472.CAN-11-1896} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA146281 https://www.ebi.ac.uk/ena/browser/view/PRJNA146281 None [Overal design]This set contains 12 microarray samples. 3 controls, 3 estrogen stimulated, 3 Bortezomib stimulated, 3 Bortezomib + estrogen stimulated; [Treatment]'Where indicated, cells were pretreated with 50 nM Bortezomib for 15 minutes followed by 10 nM 17- -estradiol for 6 hours.'; [Growth]'Cells were grown in phenol-red free DMEM containing 5% charcoal-dextran treated FBS for 48 hours prior to treatment with Bortezomib or estrogen.'; [Extraction]"Total RNA was extracted using Qiazol (Qiagen) according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MCF7; treatment: none; ', 'cell line: MCF7; treatment: estrogen stimulated; ', 'cell line: MCF7; treatment: velcade stimulated; ', 'cell line: MCF7; treatment: estrogen (6h) + velcade stimulated; ' GSE13671 Homo sapiens 14 Expression profiling by array GPL570 Expression data from mammary epithelial cells from BRCA1 mutation carriers and non BRCA1 mutation carriers 2008-11-19 Female BRCA1 mutation carriers have a nearly 80% probability of developing breast cancer during their life-time. We hypothesized that the breast epithelium at risk in BRCA1 mutation carriers harbors mammary epithelial cells (MECs) with altered proliferation and differentiation properties. Microarray studies revealed that PMEC colonies from BRCA1 mutation carriers anticipate expression profiles found in BRCA1-related tumors, and that the EGFR pathway is upregulated in BRCA1 mutation carriers compared ton non BRCA1 mutation carriers. Keywords: Class comparison and pathway analysis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE13671 Altered proliferation and differentiation properties of primary mammary epithelial cells from BRCA1 mutation carriers. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-08-2954 {Cancer research (8.378): 10.1158/0008-5472.CAN-08-2954} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA110413 https://www.ebi.ac.uk/ena/browser/view/PRJNA110413 None [Overal design]10 colonies were collected and RNA was isolated using the Absolutely RNA Nanoprep kit, Stratagene. The arrays included duplicates from four normal controls and from two BRCA1 mutation carriers and single arrays from another two BRCA1 mutation carriers.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted using the Absolutely RNA Nanoprep kit, Stratagene'; [Cell type]'Source: ''' GSE125607 Homo sapiens 6 Expression profiling by high throughput sequencing GPL21290 A non-canonical role of YAP/TEAD is required for activation of estrogen-regulated enhancers in breast cancer [GRO-seq] 2019-01-24 Estrogen and estrogen receptor alpha (ERα) signaling plays an essential role in ERα-positive breast cancer. ERα mainly occupies on distal enhancers within genome and requires the cooperation of additional co-factors to tune the enhancer activity. Through in vivo proximity-dependent labeling technique BioID, we identified YAP1 and TEAD4 protein as novel co-regulators of ERα. YAP and TEAD are nuclear effectors of the Hippo pathway regulating cell proliferation, organ size and tumorigenesis. Their non-canonical function as transcriptional co-regulators for other signals have been reported but remains under investigated. Our ChIP-seq data in both MCF7 and T47D breast cancer cell lines indicated that YAP1 and TEAD4 co-bind to the strongest estrogen-responsive ERα-bound enhancers, and their bindings are augmented upon E2 stimulation. Knockdown of YAP1 or TEAD4 showed a global effect on the induction of E2/ERα target genes as examined by RNA-seq, also on E2-induced oncogenic growth of ER-positive breast cancer cells. We used Global Run-on sequencing (GRO-seq) assays to test the expression of enhancer non-coding RNAs (eRNAs), which are sensitive markers for estrogen-induced enhancer activation. Our results supported our hypothesis that the recruitment YAP/TEAD to ERα-bound enhancers is required for enhancer activation. Further studies revealed that the binding of YAP1 on ERα enhancers is a prerequisite for the recruitment of the enhancer activation machinery component MED1. These findings indicate that ERα collaborates with YAP1 and TEAD4 to activate or maintain its enhancer activity. Our data reveals a non-canonical function of YAP1 and TEAD4, which is independent of their canonical target genes, in regulating cancer growth, highlighting the potential of YAP1 and TEAD4 as actionable drug targets for ERα-positive breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE125607 A Non-canonical Role of YAP/TEAD Is Required for Activation of Estrogen-Regulated Enhancers in Breast Cancer. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2019.06.010 {Molecular cell (14.548): 10.1016/j.molcel.2019.06.010} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA516912 https://www.ebi.ac.uk/ena/browser/view/PRJNA516912 https://www.ncbi.nlm.nih.gov/sra?term=SRP181911 [Overal design]Global Run On (GRO) assay followed by high-throughput sequencing (GRO-seq).; [Treatment]'For knockdown of TEAD4 and YAP1, MCF7 cells were infected with shRNA lentiviruses and selected by puromycin (1 ug/ml) for 3 days to establish TEAD4 or YAP knockdown MCF7 stable cell lines. Before experiment, the MCF7 cells were hormone-stripped in phenol red-free DMEM medium plus 5% charcoal-treated FBS for 3 days, followed by treatment of either 100 nM 17β-estradiol (E2) or ethanol as vehicle control for 1 hour.'; [Growth]'MCF7 obtained from ATCC were cultured in DMEM media supplemented with 10% FBS in a 5% CO2 humidified incubator at 37°C.'; [Extraction]'MCF7 cells were subjected to nuclear run-on for 5 minutes at 30°C with BrU labeling. The run-on RNAs were pulled down by BrU beads and subjected to library preparation for deep sequencing.\nWe followed a previous published protocol (Ingolia et al., 2009 Science; Wang et al., 2011 Nature). Briefly, the run-on RNA were first added with a polyA tracts by RNA polyA polymerase. This polyA tail enables the run-on RNA to be reverse transcribed into single strand cDNA by Reverse Transcriptase. The cDNA was circularized by CircLigase (Epicentre) and re-linearized by APE I, subsequently subjected to PCR amplification and deep sequencing.'; [Cell type]'Breast cancer cell line''cell line: MCF7; cell type: Breast cancer cell line; shRNA: shCtrl; treatment: Veh, 1 hr; ', 'cell line: MCF7; cell type: Breast cancer cell line; shRNA: shCtrl; treatment: 100 nM E2, 1hr; ', 'cell line: MCF7; cell type: Breast cancer cell line; shRNA: shTEAD4; treatment: Veh, 1 hr; ', 'cell line: MCF7; cell type: Breast cancer cell line; shRNA: shTEAD4; treatment: 100 nM E2, 1hr; ', 'cell line: MCF7; cell type: Breast cancer cell line; shRNA: shYAP1; treatment: Veh, 1 hr; ', 'cell line: MCF7; cell type: Breast cancer cell line; shRNA: shYAP1; treatment: 100 nM E2, 1hr; ' GSE132031 Mus musculus 18 Expression profiling by high throughput sequencing GPL17021 Alterations in Wnt- and/or STAT3 signaling pathways and the immune microenvironment during metastatic progression 2019-05-31 Metastatic breast cancer is an extremely complex disease with limited treatment options due to the lack of information about the major characteristics of metastatic disease. There is an urgent need, therefore, to understand the changes in cellular complexity and dynamics that occur during metastatic progression. In the current study, we analyzed the cellular and molecular differences between primary tumors and paired lung metastases using a syngeneic p53-null mammary tumor model of basal-like breast cancer. Distinct subpopulations driven by the Wnt- and/or STAT3 signaling pathways were detected in vivo using a lentiviral Wnt- and STAT3 signaling reporter system. A significant increase in the overlapping populations driven by both the Wnt- and STAT3 signaling pathways was observed in the lung metastases as compared to the primary tumors. Furthermore, STAT3 signaling activity was markedly enhanced in the metastatic lesions relative to the primary tumors with minimal changes observed in Wnt reporter activity. An analysis of the unique molecular features of the lung metastases revealed a significant association with immune response signatures. Specifically, Foxp3 gene expression was markedly increased and elevated levels of Foxp3+ Treg cells were detected in close proximity to lung metastases. Collectively, these studies illustrate the importance of analyzing intratumoral heterogeneity, changes in population dynamics and the immune microenvironment during metastatic progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132031 Alterations in Wnt- and/or STAT3 signaling pathways and the immune microenvironment during metastatic progression. Oncogene 6.634 https://doi.org/10.1038/s41388-019-0852-0 {Oncogene (6.634): 10.1038/s41388-019-0852-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA545701 https://www.ebi.ac.uk/ena/browser/view/PRJNA545701 None [Overal design]The breast tumor cells are transplanted into the mammary fat pad to establish primary tumor nodules. The primary tumor can then be surgically removed as in human breast cancer patient Comment: There are 8 additional samples in the processed file which have already been uploaded in the study GSE124821 (see below relations).; [Treatment]'All RNA was purified from tissue chunks of 3 primary tumors, 3 lung metastases, 8 normal lung and 12 normal mammary gland tissues following the manufacturer’s protocol (PicoPure RNA Isolation Kit, ThermoFisher Scientific)'; [Growth]'We used primary tumors and metastases using a lentiviral-based signaling reporter system in conjunction with the basal-like p53-null syngeneic mouse models of TNBC. Tumors were collected as indicated in the methods section.'; [Extraction]'Cell line lysate was prepared using QIAshredder tubes (QIAGEN). RNA was isolated using the RNeasy Mini Kit (QUIAGEN) according to manufacturer protocol. Isolated RNA was quantified using a NanoDrop® Spectrophotometer.\nmRNA libraries were made from total RNA using the Illumina TruSeq mRNA sample preparation kit\nSamples were equenced on an Illumina HiSeq 2000/2500 using a 2x50bp configuration with an average of 136 million read pairs per sample'; [Cell type]'Source: ''tissue: Orthotopic mouse breast tumor; ', 'tissue: Metastatic mouse breast tumor; ', 'tissue: Mouse mammary gland tissue; ', 'tissue: Mouse Lung tissue; ' GSE124646 Homo sapiens 100 Expression profiling by array GPL96 Breast cancer and normal breast tissue samples to estimate the effect of contamination of breast cancer samples with normal breast tissue 2019-01-03 PURPOSE: To estimate the effect of contamination with normal breast tissue for the development of gene signatures robust to pre-analytical conditions. METHODS: We evaluated the effect of contamination with normal breast tissue on gene signatures by comparing microarray profiles of breast cancer samples contaminated with increasing amounts of normal breast tissue. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124646 SETER/PR: a robust 18-gene predictor for sensitivity to endocrine therapy for metastatic breast cancer. NPJ breast cancer 32.43 https://doi.org/10.1038/s41523-019-0111-0 {NPJ breast cancer (32.43): 10.1038/s41523-019-0111-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA512930 https://www.ebi.ac.uk/ena/browser/view/PRJNA512930 None [Overal design]A set of 10 breast cancer samples were mixed with increasing amounts of 10 individual normal breast tissue samples. Samples were contaminated with 0, 10, 25, 50, 75, 80, 85, 90, 95 and 100 % of normal breast tissue, respectively.; [Treatment]'Patients prospectively consented to a research biopsy by fine needle aspiration (FNA).'; [Growth]'None'; [Extraction]'Total RNA was extracted from tissue using Qiagen Rneasy columns.'; [Cell type]'Source: ''breast cancer sample id: 1; normal breast tissue sample id: NA; ', 'breast cancer sample id: 1; normal breast tissue sample id: 1; ', 'breast cancer sample id: NA; normal breast tissue sample id: 1; ', 'breast cancer sample id: 2; normal breast tissue sample id: NA; ', 'breast cancer sample id: 2; normal breast tissue sample id: 2; ', 'breast cancer sample id: NA; normal breast tissue sample id: 2; ', 'breast cancer sample id: 3; normal breast tissue sample id: NA; ', 'breast cancer sample id: 3; normal breast tissue sample id: 3; ', 'breast cancer sample id: NA; normal breast tissue sample id: 3; ', 'breast cancer sample id: 4; normal breast tissue sample id: NA; ', 'breast cancer sample id: 4; normal breast tissue sample id: 4; ', 'breast cancer sample id: NA; normal breast tissue sample id: 4; ', 'breast cancer sample id: 5; normal breast tissue sample id: NA; ', 'breast cancer sample id: 5; normal breast tissue sample id: 5; ', 'breast cancer sample id: NA; normal breast tissue sample id: 5; ', 'breast cancer sample id: 6; normal breast tissue sample id: NA; ', 'breast cancer sample id: 6; normal breast tissue sample id: 6; ', 'breast cancer sample id: NA; normal breast tissue sample id: 6; ', 'breast cancer sample id: 7; normal breast tissue sample id: NA; ', 'breast cancer sample id: 7; normal breast tissue sample id: 7; ', 'breast cancer sample id: NA; normal breast tissue sample id: 7; ', 'breast cancer sample id: 8; normal breast tissue sample id: NA; ', 'breast cancer sample id: 8; normal breast tissue sample id: 8; ', 'breast cancer sample id: NA; normal breast tissue sample id: 8; ', 'breast cancer sample id: 9; normal breast tissue sample id: NA; ', 'breast cancer sample id: 9; normal breast tissue sample id: 9; ', 'breast cancer sample id: NA; normal breast tissue sample id: 9; ', 'breast cancer sample id: 10; normal breast tissue sample id: NA; ', 'breast cancer sample id: 10; normal breast tissue sample id: 10; ', 'breast cancer sample id: NA; normal breast tissue sample id: 10; ' GSE20611 Homo sapiens 12 Expression profiling by array GPL96 VCAM1 promotes outbreak from dormant bone metastasis 2010-03-03 A weakly bone metastatic variant of the breast cancer cell line MDA-MB-231, SCP6, gave rise to highly bone metastatic sublines (PD1, PD2A-E) after long time dormancy in vivo. These cell lines were subjected to microarray analysis with data drawn from previous studies (Kang et al., 2003; Minn et al. 2005; Lu and Kang 2009; Lu and Kang 2010). Keywords: Cell type comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE20611 VCAM-1 promotes osteolytic expansion of indolent bone micrometastasis of breast cancer by engaging α4β1-positive osteoclast progenitors. Cancer cell 23.916 https://doi.org/10.1016/j.ccr.2011.11.002 {Cancer cell (23.916): 10.1016/j.ccr.2011.11.002} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA124789 https://www.ebi.ac.uk/ena/browser/view/PRJNA124789 None [Overal design]12 cell lines (parental MDA-MB-231 with biological repeats; weakly bone metastasis variants: SCP3, SCP4 and SCP6; post-dormancy sublines of SCP6: PD1, PD2A, PD2B, PD2C, PD2D, PD2E and PD2R) were cultured and subjected to Affymetrix microarray analysis. Data were analysed with Genespring software.; [Treatment]'Cells were grown to sub-confluency before harvesting RNA.'; [Growth]'Cell lines were maintained in DMEM with 10% FBS and antibiotics.'; [Extraction]"Total RNA extracted using Qiagen RNAeasy mini kit following manufacturer's instructions."; [Cell type]'Source: ''cell line: MDA-MB-231; cell derivative: breast cancer; ', 'cell line: PD1; cell derivative: breast cancer; ', 'cell line: PD2A; cell derivative: breast cancer; ', 'cell line: PD2B; cell derivative: breast cancer; ', 'cell line: PD2C; cell derivative: breast cancer; ', 'cell line: PD2D; cell derivative: breast cancer; ', 'cell line: PD2E; cell derivative: breast cancer; ', 'cell line: PD2R; cell derivative: breast cancer; ', 'cell line: SCP3; cell derivative: breast cancer; ', 'cell line: SCP4; cell derivative: breast cancer; ', 'cell line: SCP6; cell derivative: breast cancer; ' GSE63627 Mus musculus 28 Expression profiling by array GPL1261 Global gene expression profiling of primary tumors and lung metastases using a mouse model of spontaneous metastatic mammary carcinoma 2014-11-25 In this study, we explored the molecular basis of site-specific metastasis of breast cancer to the lungs in a clinically relevant model based on the JygMC(A) cell line. In this dataset, we include expression data from JygMC(A) primary mammary tumors, lung metastases, normal mammary glands and normal lung parenchyma. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE63627 Adaptation of Laser Microdissection Technique for the Study of a Spontaneous Metastatic Mammary Carcinoma Mouse Model by NanoString Technologies. PloS one 2.776 https://doi.org/10.1371/journal.pone.0153270 {PloS one (2.776) doi:10.1371/journal.pone.0153270}; {Oncotarget (None) doi:10.18632/oncotarget.4182}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA268496 https://www.ebi.ac.uk/ena/browser/view/PRJNA268496 None [Overal design]In total, 28 samples were analyzed. We generated the following pairwise comparisons using Partek Genomic Suite 6.6 (PGS, Version 6.6, Partek Inc.): PT vs. NMG; PT vs. LM; LM vs. NL; LM vs. NMG. Genes with an FDR-adjusted p-value < 0.05 and a fold-change > 2 were selected.; [Treatment]'n/a'; [Growth]'Balb/C nude mice were inoculated subcutaneously with 50,000 JygMC(A) cells into the 4th mammary gland, which resulted in tumor growth and subsequent metastasis to the lungs. Mouse mammary primary tumor were dissected 30 days after the cell injection, while lung nodules were collected 50 days after the injection. Normal tissue samples were harvested from healthy Balb/C nude mice.'; [Extraction]"All tissue samples were snap frozen in liquid nitrogen. RNAs were extracted using TRIzol reagent according to the manufacturer's recommendations (Invitrogen, Carlsbad, CA). Total RNA from cells in culture was isolated and purified using the RNeasy Mini Kit and subjected to DNAse treatment (Qiagen, Gaithersburg, MD) in accordance to manufacturer’s instructions. Following, 1ug of total RNA was reverse transcribed using the RETROscript® kit (Ambion, Carlsbad, CA) according to the manufacturer's recommendations."; [Cell type]'Source: ''tissue: Cell line; date: 2012-08-29; strain: BalbC nude; ', 'tissue: Lung metastasis; date: 2012-08-29; strain: BalbC nude; ', 'tissue: Lung metastasis; date: 2013-02-12; strain: BalbC nude; ', 'tissue: Mammary Primary tumor; date: 2012-08-29; strain: BalbC nude; ', 'tissue: Mammary Primary tumor; date: 2013-02-12; strain: BalbC nude; ', 'tissue: normal lung parenchyma; date: 2013-05-14; strain: BalbC nude; ', 'tissue: normal mammary gland; date: 2013-05-16; strain: BalbC nude; ' GSE26454 Homo sapiens 12 Expression profiling by array GPL11219 Gene expression profiles of CARM1 overexpression in MCF7 2011-01-05 The goal of this study is to identify ERalpha-target genes affected by overexpression of the histone arginine methyltransferase CARM1 in breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 overexpressing MCF7 cell line where CARM1 is overexpressed by 2 fold to determine the created a Dox-inducible CARM1 overexpressing MCF7 cells for evaluation of the global effects of CARM1 on Eralpha-target gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26454 CARM1 is an important determinant of ERα-dependent breast cancer cell differentiation and proliferation in breast cancer cells. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-10-2426 {Cancer research (8.378): 10.1158/0008-5472.CAN-10-2426} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA136557 https://www.ebi.ac.uk/ena/browser/view/PRJNA136557 None [Overal design]MCF7-tet-on-CARM1 clone 13 were treated under 4 conditions: DMSO; Dox; E2 (10nM); Dox+E2. In Dox+E2 condition, cells were pre-treated with Dox for 5 days before treating with E2 for 4 hours. 3 biological replicates were included and total of 12 samples were analyzed.; [Treatment]'When the cells were treated with Dox, they were treated with 1ug/ml Dox for 4 days to induce CARM1 expression. The medium were changed to phenol-red free DMEM+charcoal stripped FBS for 2 days before treating with E2 (10nM)'; [Growth]'MCF7-tet-on-CARM1 cells were grown in DMEM in 10% FBS. Two days before E2 treatment, the cells were switched to phenol-red free DMEM with 5% 6X charcoal stripped FBS.'; [Extraction]'mRNA were extracted from cells using Qiagen Rneasy Kit'; [Cell type]'breast cancer cell line''cell type: breast cancer cell line; cell line: MCF7-tet-on-CARM1 clone 13; treatment: DMSO; ', 'cell type: breast cancer cell line; cell line: MCF7-tet-on-CARM1 clone 13; treatment: E2; ', 'cell type: breast cancer cell line; cell line: MCF7-tet-on-CARM1 clone 13; treatment: Dox and D2; ', 'cell type: breast cancer cell line; cell line: MCF7-tet-on-CARM1 clone 13; treatment: Dox; ' GSE17802 Homo sapiens 4 Expression profiling by array GPL6106 The role of vimentin in regulating genes related to EMT 2009-08-25 To study the biological and functional role of vimentin in maintenance of the mesenchymal phenotype of mammary epithelial cells, vimentin was silenced in the non-transformed MCF10A cells and vimentin-dependent changes in gene expression were analyzed. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE17802 Vimentin regulates EMT induction by Slug and oncogenic H-Ras and migration by governing Axl expression in breast cancer. Oncogene 6.634 https://doi.org/10.1038/onc.2010.509 {Oncogene (6.634): 10.1038/onc.2010.509} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA118337 https://www.ebi.ac.uk/ena/browser/view/PRJNA118337 None [Overal design]Scrambled is the siScr-transfected control with two replicates; KD the sample with vimentin knockdown, also two replicates.; [Treatment]"An siRNA targeting vimentin (siGENOME SMARTpoolTM M-003551-01-005: Dharmacon, Inc.) or a scrambled control siRNA (AllStars Negative Control siRNA; Qiagen) was transfected to cells using Lipofectamine 2000 (Invitrogen) according to the manufacturer's instructions."; [Growth]"MCF10A cells were grown in 1:1 DMEM:Ham's F-12 supplemented with 5 % horse serum, 10 µg/ml insulin, 0.5 µg/ml hydrocortisone, 20 ng/ml EGF, and 100 ng/ml choleratoxin."; [Extraction]'Three days after vimentin siRNA transfection, RNA was extracted with Trizol reagent. To ensure sufficient purity of the cellular RNA, the samples were further processed with RNeasy Mini kit (QIAGEN). The purity of the cellular RNA was controlled and the material was considered to be sufficiently pure when A260/A280 > 1.8.'; [Cell type]'MCF10A''cell type: MCF10A; ' GSE41970 Homo sapiens 329 Non-coding RNA profiling by array; Expression profiling by array GPL16231; GPL16299 Integrated microRNA and mRNA Signatures Associated with Survival in Triple Negative Breast Cancer 2012-11-01 Triple negative breast cancer (TNBC) includes basal and non-basal subclasses. To further stratify TNBC we determined microRNA (miRNA) and mRNA expression profiles, linked specific miRNA signatures to patient survival and used miRNA/mRNA anti-correlations to identify TNBC subclasses associated with expression of canonical signal pathways https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41970 Protective role of miR-155 in breast cancer through RAD51 targeting impairs homologous recombination after irradiation. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1402604111 {PloS one (2.776) doi:10.1371/journal.pone.0055910}; {Proceedings of the National Academy of Sciences of the United States of America (9.580) doi:10.1073/pnas.1402604111}; {PloS one (2.776) doi:10.1371/journal.pone.0088525}; {Oncotarget (None) doi:10.18632/oncotarget.1682}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA178625 https://www.ebi.ac.uk/ena/browser/view/PRJNA178625 None [Overal design]RNA was isolated from formalin-fixed paraffin-embedded tissue cores of 165 primary tumors, 59 adjacent normal and 54 lymph node metastatic samples and expression of 664 miRNAs and 230 cancer-associated mRNAs was assessed for each sample using the nanoString nCounter platform. Kaplan-Meier distant-disease free and overall survival curves were compared using the log-rank test. Cox proportional hazard regression and risk score analysis were used to identify miRNAs for classification of patients with significantly different prognoses.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was isolated from FFPE tissue using Recover ALL kit (Ambion)'; [Cell type]'Source: ''tissue: Breast; status: primary triple negative cancer; ', 'tissue: Lymph Node; status: Metastatic; gender: Female; age at diagnosis: NA; best stage: NA; grade: NA; ', 'tissue: Breast; status: normal; gender: Female; age at diagnosis: NA; best stage: NA; grade: NA; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 34; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 36; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 70; best stage: 1; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 56; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 50; best stage: 2A; grade: 9; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 61; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: NA; best stage: NA; grade: NA; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 37; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 52; best stage: 1; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 84; best stage: 3C; grade: 9; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 27; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 29; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 40; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 39; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 45; best stage: 3C; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 68; best stage: 3C; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 37; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 54; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 24; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 52; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 60; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 51; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 48; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 51; best stage: 3C; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 53; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 56; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 44; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 67; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 39; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 57; best stage: 3A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 65; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 47; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 48; best stage: 3A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 55; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 56; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 46; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 51; best stage: 3A; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 33; best stage: 3A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 35; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 62; best stage: 3A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 84; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 66; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 47; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 42; best stage: 2A; grade: 1; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 48; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 46; best stage: 3C; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 59; best stage: 2A; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 42; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 70; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 39; best stage: 3A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 67; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 52; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 57; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 45; best stage: 2A; grade: 4; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 47; best stage: 3A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 81; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 42; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 49; best stage: 2A; grade: 4; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 45; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 55; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 53; best stage: 3B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 67; best stage: 3B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 54; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 43; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 31; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 66; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 33; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 64; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 30; best stage: 3B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 78; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 41; best stage: 1; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 60; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 59; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 52; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 58; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 47; best stage: 2A; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 52; best stage: 3A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 58; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 79; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 43; best stage: 3B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 38; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 46; best stage: 2A; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 40; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 20; best stage: 3A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 50; best stage: 2B; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 68; best stage: 3B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 46; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 48; best stage: 1; grade: 9; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 34; best stage: 3A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 36; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 63; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 44; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 76; best stage: 1; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 28; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 28; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 63; best stage: 2B; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 35; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 48; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 61; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 36; best stage: 2B; grade: 9; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 58; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 74; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 49; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 46; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 43; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 50; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 48; best stage: 3B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 44; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 55; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 69; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 61; best stage: 2A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 70; best stage: 2A; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 53; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 72; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 59; best stage: 1; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 66; best stage: 1; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 72; best stage: 2B; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 77; best stage: 1; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 44; best stage: 1; grade: 9; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 67; best stage: 3A; grade: 3; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 39; best stage: 2B; grade: 2; ', 'tissue: Breast; status: primary triple negative cancer; gender: Female; age at diagnosis: 34; best stage: 1; grade: 3; ' GSE115607 Homo sapiens 11 Genome binding/occupancy profiling by high throughput sequencing GPL18573 ChIP-Seq analysis of estrogen deprived MCF7 cells treated with H3B-5942 and standards of care compounds 2018-06-11 The goal of this experiment was to interrogate the potential transcriptional impact of H3B-5942 by investigating its influence on genome-wide DNA-binding modes of ERa in MCF7 cells using chromatin immunoprecipitation followed by high-throughput DNA sequencing (ChIP-Seq). Affects of H3B-5942 on chromatin recruitment were compared to results from treatment with E2, 4-OHT, and fulvestrant. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115607 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA475564 https://www.ebi.ac.uk/ena/browser/view/PRJNA475564 https://www.ncbi.nlm.nih.gov/sra?term=SRP150236 [Overal design]A total of 5 treatments were analyzed. These included H3B-5942, E2, reference compounds 4-OHT and fulvestrant, and DMSO as control. Material from two plates per treatment were pooled and then analyzed.; [Treatment]'Cells were treated with indicated compounds for 45 minutes before harvesting.'; [Growth]'MCF cell were maintained in DMEM supplemented with 10% FBS, 4 mM L-glutamine and 1x non-essential amino acids. Cells were then washed 3 times in PBS and cultured for 72 hours in phenol red-free DMEM media supplemented with 10% charcoal-stripped serum prior to treatment.'; [Extraction]'Cells were formaldehyde fixed for 15 minutes (1% formaldehyde, 100 mM NaCl, 0.1 mM EDTA pH8.0, 5 mM Hepes pH 7.9). Fixation was stopped with 2.5M glycine and cells were washed 2X in PBS/0.5% Igepal CA-630. Cell pellets were snap frozen and chromatin was isolated by the addition of lysis buffer, followed by disruption with a Dounce homogenizer. Lysates were sonicated and the DNA sheared to an average length of 300-500 bp. Genomic DNA (Input) was prepared by treating aliquots of chromatin with RNase, proteinase K and heat for de-crosslinking, followed by ethanol precipitation.\nIllumina sequencing libraries were prepared from the ChIP and Input DNAs by the standard consecutive enzymatic steps of end-polishing, dA-addition, and adaptor ligation. After a final PCR amplification step, the resulting DNA libraries were quantified and sequenced on Illumina’s NextSeq 500 (75 nt reads, single end).'; [Cell type]'breast cancer cell line''cell line: MCF7; chip antibody: Estrogen Receptor alpha (Santa Cruz, sc-543, lot F1716); cell type: breast cancer cell line; treatment: DMSO; ', 'cell line: MCF7; chip antibody: Estrogen Receptor alpha (Santa Cruz, sc-543, lot F1716); cell type: breast cancer cell line; treatment: H3B-6545; ', 'cell line: MCF7; chip antibody: Estrogen Receptor alpha (Santa Cruz, sc-543, lot F1716); cell type: breast cancer cell line; treatment: Saturated H3B-6545; ', 'cell line: MCF7; chip antibody: Estrogen Receptor alpha (Santa Cruz, sc-543, lot F1716); cell type: breast cancer cell line; treatment: 800; ', 'cell line: MCF7; chip antibody: Estrogen Receptor alpha (Santa Cruz, sc-543, lot F1716); cell type: breast cancer cell line; treatment: Rad1901; ', 'cell line: MCF7; chip antibody: Estrogen Receptor alpha (Santa Cruz, sc-543, lot F1716); cell type: breast cancer cell line; treatment: H3B-5942; ', 'cell line: MCF7; chip antibody: Estrogen Receptor alpha (Santa Cruz, sc-543, lot F1716); cell type: breast cancer cell line; treatment: Saturated H3B-5942; ', 'cell line: MCF7; chip antibody: Estrogen Receptor alpha (Santa Cruz, sc-543, lot F1716); cell type: breast cancer cell line; treatment: Tamoxifen; ', 'cell line: MCF7; chip antibody: Estrogen Receptor alpha (Santa Cruz, sc-543, lot F1716); cell type: breast cancer cell line; treatment: Fulvestrant; ', 'cell line: MCF7; chip antibody: Estrogen Receptor alpha (Santa Cruz, sc-543, lot F1716); cell type: breast cancer cell line; treatment: E2; ', 'cell line: MCF7; chip antibody: none; cell type: breast cancer cell line; treatment: none; ' GSE155239 Mus musculus 21 Expression profiling by array GPL2881; GPL10732 Understanding BRCA1 function in INK4-RB deficient tumors 2020-07-27 Most BRCA1-deficient BLBCs carry a dysfunctional INK4-RB pathway. Thus, we have created genetically engineered mice with Brca1 loss and deletion of p16INK4A, or separately p18INK4C, to model the deficient INK4-RB signaling in human BLBC. By using these mutant mice and human BRCA1 deficient and proficient breast cancer tissues and cells, we tested if there exists a druggable target in BRCA1 deficient breast cancers. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE155239 PDGFRβ is an essential therapeutic target for BRCA1-deficient mammary tumors. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-021-01387-x {Breast cancer research : BCR (5.676): 10.1186/s13058-021-01387-x} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA655906 https://www.ebi.ac.uk/ena/browser/view/PRJNA655906 None [Overal design]Gene expression microarray analysis of mouse mammary tumors.; [Treatment]'NA'; [Growth]'Mammary tumors were harvested for gene expression analysis.'; [Extraction]'RNA was extracted using Qiagen RNeasy kits.', 'Reference'; [Cell type]'Source: ''strain: Balbc; tissue: mammary tumor; genotype: p18het; ', 'sample type: reference; genotype: normal; ', 'strain: Balbc; tissue: mammary tumor; genotype: p18null; ', 'strain: Balbc; tissue: mammary tumor; genotype: p18null_BRCA1het; ' GSE11293 Homo sapiens 3 Expression profiling by array GPL6780 Investigation of gene expression signature induced by Alk5TD (active type I TGF-beta receptor) 2008-04-29 BT474 cells stably expressing Alk5TD or vector (BT474-Alk5TD and BT474-pBMN, respectively) were compared for gene expression. Genes that were differentially expressed between the two cell lines were collected as the signature induced by Alk5TD expression. Keywords: Comparison of two cell types (BT474-Alk5TD and BT474-pBMN). BT474-pBMN was used as the reference line. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE11293 Transforming growth factor beta engages TACE and ErbB3 to activate phosphatidylinositol-3 kinase/Akt in ErbB2-overexpressing breast cancer and desensitizes cells to trastuzumab. Molecular and cellular biology 3.735 https://doi.org/10.1128/MCB.00787-08 {Molecular and cellular biology (3.735): 10.1128/MCB.00787-08} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA106711 https://www.ebi.ac.uk/ena/browser/view/PRJNA106711 None [Overal design]RNA samples extracted from the two cell lines (BT474-Alk5TD and BT474-pBMN) were differentially labeled (BT474-Alk5TD with Cy5 and BT474-pBMN with Cy3) and analyzed. The experiment was performed in triplicate with independent samples.; [Treatment]'No treatment. Both cell types were harvested when they reached 70-80% confluency in 100 mm dishes'; [Growth]'BT474-pBMN and BT474-Alk5TD cells were grown in IMEM with 10% FBS'; [Extraction]'Total RNA was isolated from one 100 mm cell culture dish of each cell lines using Trizol Reagent (Invitrogen) followed by RNeasy Mini Kit (Qiagen, Valencia, CA) and RNase-Free DNase Set (Qiagen, Valencia, CA) according to the manufacturer’s instructions. To elute RNA from columns at final elution, 30-40 ul water were used to get about 30-50 ug total RNA.'; [Cell type]'Source: ''BT474 human breast cancer cells (Organ: mammary gland; breast, Tissue: duct, Disease: ductal carcinoma, Age: 60 years adult, Gender: female); ' GSE107542 Homo sapiens 4 Expression profiling by high throughput sequencing GPL20301 RNA G-quadruplex secondary structure promotes alternative splicing via the RNA binding protein hnRNPF 2017-11-30 It is generally thought that splicing factors regulate alternative splicing through binding to RNA consensus sequences. In addition to these linear motifs, RNA secondary structure is emerging as an important layer in splicing regulation. Here we demonstrate that RNA elements with G-quadruplex forming capacity promote exon inclusion. Destroying G-quadruplex forming capacity while keeping G-tracts intact abrogates exon inclusion. Analysis of RNA binding protein footprints revealed that G-quadruplexes are enriched in hnRNPF-binding sites and near hnRNPF-regulated alternatively spliced exons in the human transcriptome. Moreover, hnRNPF regulates an EMT-associated CD44 isoform switch in a G-quadruplex-dependent manner, which results in inhibition of EMT. Mining breast cancer TCGA datasets, we demonstrate that hnRNPF negatively correlates with an EMT gene signature and positively correlates with patient survival. These data suggest a critical role for RNA G-quadruplexes in regulating alternative splicing. Modulation of G-quadruplex structural integrity may control cellular processes important for tumor progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE107542 RNA G-quadruplex secondary structure promotes alternative splicing via the RNA-binding protein hnRNPF. Genes & development 8.990 https://doi.org/10.1101/gad.305862.117 {Genes & development (8.990): 10.1101/gad.305862.117} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA420499 https://www.ebi.ac.uk/ena/browser/view/PRJNA420499 https://www.ncbi.nlm.nih.gov/sra?term=SRP125893 [Overal design]PolyA-RNA-sequencing of two non-specific shRNA and two shhnRNPF HMLE cell lines; [Treatment]'Cell lines stably expressing the relevant shRNA were generated using lentiviral vectors using standard infection protocols'; [Growth]'The maintenance of immortalized human mammary epithelial cells HMLE was conducted as previously described (Brown et al., 2011)'; [Extraction]'Total RNA was extracted using standard Trizol extraction procedures\nStranded paired-end polyA-purified RNA sequencing libraries were prepared using Illumina TruSeq protocols'; [Cell type]'Immortalized breast epithelial cells''cell type: Immortalized breast epithelial cells; cell line: HMLE; treatment: Non-specific shRNA treated; ', 'cell type: Immortalized breast epithelial cells; cell line: HMLE; treatment: hnRNPF shRNA treated; ' GSE66159 Homo sapiens 76 Expression profiling by array GPL570 Biomarkers of dietary energy restriction in women at increased risk of breast cancer 2015-02-20 Dietary energy restriction (DER) reduces risk of spontaneous mammary cancer in rodents. In humans, DER in premenopausal years seems to reduce risk of postmenopausal breast cancer. Markers of DER are required to develop acceptable DER regimens for breast cancer prevention. We therefore examined markers of DER in the breast, adipose tissue, and serum. Nineteen overweight or obese women at moderately increased risk of breast cancer (lifetime risk, 1 in 6 to 1 in 3) ages between 35 and 45 were randomly allocated to DER [liquid diet, 3,656 kJ/d (864 kcal/d); n = 10] or asked to continue their normal eating patterns (n = 9) for one menstrual cycle. Biopsies of the breast and abdominal fat were taken before and after the intervention. RNA was extracted from whole tissues and breast epithelium (by laser capture microdissection) and hybridized to Affymetrix GeneChips. Longitudinal plasma and urine samples were collected before and after intervention, and metabolic profiles were generated using gas chromatography-mass spectrometry. DER was associated with significant reductions in weight [-7.0 (+/-2.3) kg] and in alterations of serum biomarkers of breast cancer risk (insulin, leptin, total and low-density lipoprotein cholesterol, and triglycerides). In both abdominal and breast tissues, as well as isolated breast epithelial cells, genes involved in glycolytic and lipid synthesis pathways (including stearoyl-CoA desaturase, fatty acid desaturase, and aldolase C) were significantly down-regulated. We conclude that reduced expressions of genes in the lipid metabolism and glycolytic pathways are detectable in breast tissue following DER, and these may represent targets for DER mimetics as effective chemoprophylactic agents Transcriptomic and Metabolomic intervention study of continuous energy restriction in 19 participants https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE66159 Biomarkers of dietary energy restriction in women at increased risk of breast cancer. Cancer prevention research (Philadelphia, Pa.) 3.866 https://doi.org/10.1158/1940-6207.CAPR-09-0008 {Cancer prevention research (Philadelphia, Pa.) (3.866): 10.1158/1940-6207.CAPR-09-0008} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA275989 https://www.ebi.ac.uk/ena/browser/view/PRJNA275989 None [Overal design]10 Participants were randomised to DER, 9 to control. Samples were taken before DER and once menstrual cycle later from adopsie fat and breast tissue; [Treatment]'Participants were randomly allocated to dietary energy restriction [liquid diet, 3,656 kJ/d (864 kcal/d); n = 10] or asked to continue their normal eating patterns (n = 9) for one menstrual cycle.'; [Growth]'Human breast tissue was biopsied from women with a dense glandular breast pattern under radiographic guidance (n = 7). A single-coned craniocaudal mammogram of the breast was obtained at the time of biopsy and done with the breast immobilized under the compression device. In women with a diffusely fatty breast pattern (n = 12), biopsies were done without radiological guidance. After infiltration of 2% lidocaine, a small incision was made in the skin at the biopsy site through which a 14-gauge biopsy needle was inserted to a depth estimated by the operator. Between seven and nine biopsy samples were obtained through the same skin incision, although the direction of the needle was altered for each sample. Three to five milliliters of subcutaneous abdominal adipose tissue were obtained by suction biopsy under local anesthesia from the anterior abdominal wall, midway between the anterior superior iliac spine and the umbilicus. The first biopsies were taken from either the left or right breast/abdominal side chosen by computer randomization (independently) and repeat biopsies on the opposite side to eliminate gene expression changes due to the healing process. One half of two separate breast cores were fixed in 4% formalin and embedded in paraffin blocks; the remaining tissue was immediately snap frozen in liquid nitrogen and stored at −80°C.'; [Extraction]"20 to 50 mg of breast tissue were ground to a fine powder under liquid nitrogen; RNA was isolated with 600 μL of Qiazol reagent (Qiagen Ltd.), which was passed through a commercially available RNA shearing device (QiaShredder, Qiagen); and 200 μL chloroform was added, incubated at room temperature for 5 min, and centrifuged at 12,000 rpm for 15 min. The aqueous phase was removed to a clean tube and 350 μL of 70% ethanol were added. The mixture was placed in an RNeasy Micro column (Qiagen) and the protocol for the RNeasy Micro kit was followed to completion. Abdominal adipose tissue total RNA was isolated using Trizol reagent (Invitrogen). RNA samples were purified using RNeasy Mini columns (Qiagen) according to the manufacturer's protocols."; [Cell type]'Source: ''tissue: breast; participant number: 5766; diet: DER; timepoint: before; ', 'tissue: breast; participant number: 5766; diet: DER; timepoint: after; ', 'tissue: breast; participant number: 2732; diet: Control; timepoint: before; ', 'tissue: breast; participant number: 2978; diet: DER; timepoint: after; ', 'tissue: breast; participant number: 333; diet: Control; timepoint: before; ', 'tissue: breast; participant number: 333; diet: Control; timepoint: after; ', 'tissue: breast; participant number: 2978; diet: DER; timepoint: before; ', 'tissue: breast; participant number: 5533; diet: DER; timepoint: before; ', 'tissue: breast; participant number: 5533; diet: DER; timepoint: after; ', 'tissue: breast; participant number: 4412; diet: Control; timepoint: before; ', 'tissue: breast; participant number: 4412; diet: Control; timepoint: after; ', 'tissue: breast; participant number: 7147; diet: Control; timepoint: before; ', 'tissue: breast; participant number: 7147; diet: Control; timepoint: after; ', 'tissue: breast; participant number: 2732; diet: Control; timepoint: after; ', 'tissue: breast; participant number: 4416; diet: DER; timepoint: before; ', 'tissue: breast; participant number: 4416; diet: DER; timepoint: after; ', 'tissue: breast; participant number: 5030; diet: Control; timepoint: before; ', 'tissue: breast; participant number: 5030; diet: Control; timepoint: after; ', 'tissue: breast; participant number: 5027; diet: DER; timepoint: before; ', 'tissue: breast; participant number: 5027; diet: DER; timepoint: after; ', 'tissue: breast; participant number: 3714; diet: Control; timepoint: before; ', 'tissue: breast; participant number: 3714; diet: Control; timepoint: after; ', 'tissue: breast; participant number: 1372; diet: DER; timepoint: before; ', 'tissue: breast; participant number: 1372; diet: DER; timepoint: after; ', 'tissue: breast; participant number: 2292; diet: DER; timepoint: before; ', 'tissue: breast; participant number: 2292; diet: DER; timepoint: after; ', 'tissue: breast; participant number: 6858; diet: DER; timepoint: before; ', 'tissue: breast; participant number: 6858; diet: DER; timepoint: after; ', 'tissue: breast; participant number: 6268; diet: Control; timepoint: before; ', 'tissue: breast; participant number: 6268; diet: Control; timepoint: after; ', 'tissue: breast; participant number: 132; diet: DER; timepoint: before; ', 'tissue: breast; participant number: 132; diet: DER; timepoint: after; ', 'tissue: breast; participant number: 6843; diet: Control; timepoint: before; ', 'tissue: breast; participant number: 6843; diet: Control; timepoint: after; ', 'tissue: breast; participant number: 8539; diet: DER; timepoint: before; ', 'tissue: breast; participant number: 8539; diet: DER; timepoint: after; ', 'tissue: breast; participant number: 8232; diet: Control; timepoint: before; ', 'tissue: breast; participant number: 8232; diet: Control; timepoint: after; ', 'tissue: adipose; participant number: 5766; diet: DER; timepoint: after; ', 'tissue: adipose; participant number: 5533; diet: DER; timepoint: before; ', 'tissue: adipose; participant number: 5533; diet: DER; timepoint: after; ', 'tissue: adipose; participant number: 4412; diet: Control; timepoint: before; ', 'tissue: adipose; participant number: 4412; diet: Control; timepoint: after; ', 'tissue: adipose; participant number: 7147; diet: Control; timepoint: before; ', 'tissue: adipose; participant number: 7147; diet: Control; timepoint: after; ', 'tissue: adipose; participant number: 2978; diet: DER; timepoint: after; ', 'tissue: adipose; participant number: 5030; diet: Control; timepoint: before; ', 'tissue: adipose; participant number: 5030; diet: Control; timepoint: after; ', 'tissue: adipose; participant number: 3714; diet: Control; timepoint: before; ', 'tissue: adipose; participant number: 3714; diet: Control; timepoint: after; ', 'tissue: adipose; participant number: 5027; diet: DER; timepoint: before; ', 'tissue: adipose; participant number: 5027; diet: DER; timepoint: after; ', 'tissue: adipose; participant number: 4416; diet: DER; timepoint: before; ', 'tissue: adipose; participant number: 4416; diet: DER; timepoint: after; ', 'tissue: adipose; participant number: 1372; diet: DER; timepoint: before; ', 'tissue: adipose; participant number: 1372; diet: DER; timepoint: after; ', 'tissue: adipose; participant number: 2292; diet: DER; timepoint: before; ', 'tissue: adipose; participant number: 2292; diet: DER; timepoint: after; ', 'tissue: adipose; participant number: 6858; diet: DER; timepoint: before; ', 'tissue: adipose; participant number: 6858; diet: DER; timepoint: after; ', 'tissue: adipose; participant number: 6268; diet: DER; timepoint: before; ', 'tissue: adipose; participant number: 6268; diet: DER; timepoint: after; ', 'tissue: adipose; participant number: 2978; diet: DER; timepoint: before; ', 'tissue: adipose; participant number: 2732; diet: Control; timepoint: before; ', 'tissue: adipose; participant number: 2732; diet: Control; timepoint: after; ', 'tissue: adipose; participant number: 333; diet: Control; timepoint: before; ', 'tissue: adipose; participant number: 333; diet: Control; timepoint: after; ', 'tissue: adipose; participant number: 5766; diet: DER; timepoint: before; ', 'tissue: adipose; participant number: 132; diet: DER; timepoint: before; ', 'tissue: adipose; participant number: 132; diet: DER; timepoint: after; ', 'tissue: adipose; participant number: 6843; diet: Control; timepoint: before; ', 'tissue: adipose; participant number: 6843; diet: Control; timepoint: after; ', 'tissue: adipose; participant number: 8539; diet: DER; timepoint: before; ', 'tissue: adipose; participant number: 8539; diet: DER; timepoint: after; ', 'tissue: adipose; participant number: 8232; diet: Control; timepoint: before; ', 'tissue: adipose; participant number: 8232; diet: Control; timepoint: after; ' GSE29327 Homo sapiens 6 Expression profiling by array GPL570 Gene expression profiling of MCF10A (miR-221/222 vs control) 2011-05-16 Analysis of gene expression of MCF10A to identify the targets of miR-221 and miR-222 Keywords: MCF10, miR-221, miR-222 https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE29327 TRPS1 targeting by miR-221/222 promotes the epithelial-to-mesenchymal transition in breast cancer. Science signaling 6.481 https://doi.org/10.1126/scisignal.2001538 {Science signaling (6.481): 10.1126/scisignal.2001538} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA140123 https://www.ebi.ac.uk/ena/browser/view/PRJNA140123 None [Overal design]RNA profiles of human MCF10A cell line; [Treatment]'Three biological replicates of MCF10A cell lines transfected with either miR-221/222 or miR-control'; [Growth]'None'; [Extraction]'total cellular RNA were extracted with mirVanaTM miRNA Isolation Kit (Ambion, Austin, TX).'; [Cell type]'Source: ''cell line: MCF10A; treatment: miR-221/222; ', 'cell line: MCF10A; treatment: miR-control; ' GSE31432 Homo sapiens 23 Expression profiling by array GPL6947 Defining the molecular response to trastuzumab, pertuzumab and combination therapy in ovarian cancer 2011-08-17 The purpose of this study was to characterise the effects of trastuzumab and pertuzumab, either as single agents or as combination therapy on gene and protein expression in human ovarian cancer in vivo. Illumina BeadChips were used to profile the transcriptome after four days treatment of SKOV3 tumor xenografts. Although genes involved with HER2, MAP-kinase and p53 signaling pathways were commonly induced by all treatments, a greater number and variety of genes were differentially expressed by the complementary combination therapies compared to either drug on its own. The protein level of the CDK-inhibitors p21 and p27 were increased in response to both agents alone and further by the combination; pERK signaling was inhibited by all treatments; but only pertuzumab alone inhibited pAkt signaling. The expression of proliferation, apoptosis, cell division and cell cycle markers was distinct in a panel of primary ovarian cancer xenografts, suggesting heterogeneity of response in ovarian cancer and the need to establish biomarkers of response. This first comprehensive study of the molecular response to trastuzumab, pertuzumab and combination therapy in vivo highlights that there are both common and distinct downstream effects to different HER2 antibodies and that pathways may be invoked more strongly or in a different manner by a combination of agents. Some of the in vivo results for ovarian tumors differ from previous in vitro studies in breast cancer cells, emphasizing that the molecular response to anti-cancer agents involves variable and complex disease-specific interactions of signaling mechanisms. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE31432 Defining the molecular response to trastuzumab, pertuzumab and combination therapy in ovarian cancer. British journal of cancer 5.416 https://doi.org/10.1038/bjc.2012.176 {British journal of cancer (5.416): 10.1038/bjc.2012.176} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA145793 https://www.ebi.ac.uk/ena/browser/view/PRJNA145793 None [Overal design]SCOV3 Ovarian cell line xenografts treated with Trastuzumab, pertuzumab or combination after 4 days; [Treatment]'The mice were treated with trastuzumab (20 mg/kg), pertuzumab (20 mg/kg) and trastuzumab + pertuzumab (20 mg/kg each)'; [Growth]'Adult female nu/nu mice were implanted subcutaneously with SKOV3 tumor fragments (previously established from the cell line) or primary ovarian tumor fragments in the flanks and allowed to grow to 4–6 mm in diameter (over a period of approximately 1 month).'; [Extraction]'Total RNA was prepared from 10-50 mg of frozen tissue after 4 days of treatment, preincubated with RNAlater-ICE (Ambion, Austin, TX) using the miRNeasy Mini kit (Qiagen) and TissueRuptor (Qiagen) following the manufacturers’ instructions'; [Cell type]'Source: ''cell line: SCOV3; ' GSE59772 Homo sapiens 9 Expression profiling by array GPL6244 Analysis of compartment-specific gene expression in breast cancer tumors 2014-07-25 Triple-negative primary breast cancer tumors, rich in inflammatory stroma, were laser microdissected and global mRNA expression was analyzed in stroma compartment, cancer cell compartment, and in total tumor tissue. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59772 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA256180 https://www.ebi.ac.uk/ena/browser/view/PRJNA256180 None [Overal design]Three FFPE breast cancer tumors wer laser microdissected and the cancer cell and stroma compartments were collected. A piece of t; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen AllPrep DNA/RNA FFPE kit'; [Cell type]'Source: ''tissue: Cancer cells; ', 'tissue: Stroma; ', 'tissue: Total tumor; ' GSE60125 Homo sapiens 11 Expression profiling by array GPL570 SAHA Induced Dynamics of a Human Histone Deacetylase Protein Interaction Network 2014-08-05 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60125 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA257520 https://www.ebi.ac.uk/ena/browser/view/PRJNA257520 None [Overal design]Refer to individual Series; [Treatment]'ING2 expression is knocked down in human breast cancer cells (MDA-MB-231 cell line) using siRNA #116981 (Ambion) and Dharmafect 1 (Dharmacon). RNA was collected 4 days post-transfection.', 'SAHA or DMSO was added directly to the culture media for a final concentration of 2 uM, and cells were collected after 30 hrs of incubation.'; [Growth]'MDA-MB-231 cells were obtained from the American Type Culture Collection. All cell lines were maintained in DMEM (GIBCO) supplemented with 10% FBS, Pen/Strep, and Glutamax (GIBCO) in a humidified atmosphere at 370C with 5% CO2.'; [Extraction]'Cells were lysed in Trizol (Invitrogen) three days after transfection, RNA was extracted and then processed through an RNeasy column (QIAGEN) using the RNA clean-up protocol.'; [Cell type]'human breast cancer cell line''cell line: MDA-MB-231; cell type: human breast cancer cell line; sirna: non-targeting; ', 'cell line: MDA-MB-231; cell type: human breast cancer cell line; sirna: ING2 targeting; ', 'cell line: MDA-MB-231; cell type: human breast cancer cell line; drug: DMSO; ', 'cell line: MDA-MB-231; cell type: human breast cancer cell line; drug: suberoylanilide hydroxamic acid (SAHA); ' GSE161760 Homo sapiens 6 Expression profiling by high throughput sequencing GPL16791 Persistent inflammatory stimulation drives the transition of MSCs to inflammatory CAFs that promote pro-metastatic characteristics in breast cancer cells [I] 2020-11-18 The pro-inflammatory cytokines tumor necrosis factor α (TNFα) and interleukin 1β (IL-1β) are expressed simultaneously and have tumor-promoting roles in breast cancer. In parallel, mesenchymal stem cells (MSCs) undergo transition at the tumor site to cancer-associated fibroblasts (CAFs), which are generally connected to enhanced tumor progression. Here, we determined the impact of consistent inflammatory stimulation on stromal cell plasticity. MSCs that were persistently stimulated by TNFα+IL-1β (2-3 weeks) gained a CAF-like morphology, accompanied by prominent changes in gene expression, including in stroma/fibroblast-related genes. These CAF-like cells expressed elevated levels of vimentin and fibroblast activation protein (FAP) and demonstrated significantly increased ability to contract collagen gels. Moreover, they have gained the phenotype of inflammatory CAFs, as indicated by reduced expression of α smooth muscle actin (αSMA), increased proliferation and elevated expression of inflammatory genes and proteins, primarily inflammatory chemokines. These inflammatory CAFs released factors that enhanced tumor cell detachment, spreading and migration; the inflammatory CAF-derived factors elevated cancer cell migration by stimulating the chemokine receptors CCR2, CCR5 and CXCR1/2 and Ras-activating receptors, expressed by the cancer cells. Together, these novel findings demonstrate that chronic inflammation, per se, can induce MSC-to-CAF transition, leading to generation of tumor-promoting inflammatory CAFs. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE161760 Persistent Inflammatory Stimulation Drives the Conversion of MSCs to Inflammatory CAFs That Promote Pro-Metastatic Characteristics in Breast Cancer Cells. Cancers 6.162 https://doi.org/10.3390/cancers13061472 {Cancers (6.162): 10.3390/cancers13061472} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA679309 https://www.ebi.ac.uk/ena/browser/view/PRJNA679309 https://www.ncbi.nlm.nih.gov/sra?term=SRP293134 [Overal design]To determine transcriptome alterations upon persistent cytokine stimulation, genome-wide expression analysis was performed on MSCs stimulated by TNFα and IL-1β or by vehicle controls, for 14 days.; [Treatment]'Samples were either treated with IL1 and TNFa or untreated controls'; [Growth]'Human primary BM-derived MSCs were kept in culture for up to 9 passages. The cells were grown in mesenchymal stem cells growth medium.'; [Extraction]'Total RNA was isolated using Qiagen miRNeasy Mini Kit\n500ng of total RNA were fragmented followed by reverse transcription and second strand cDNA synthesis. The double strand cDNA was subjected to end repair, A base addition, adapter ligation and PCR amplification to create libraries'; [Cell type]'primary bone marrow-derived MSCs''cell type: primary bone marrow-derived MSCs; tissue: Bone marrow; treatment: untreated; ', 'cell type: primary bone marrow-derived MSCs; tissue: Bone marrow; treatment: treated with IL1 and TNF; ' GSE120478 Mus musculus; Homo sapiens 32 Expression profiling by array; Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL6246; GPL18573; GPL19057 PTEN interacts with the transcription machinery on chromatin and regulates RNA polymerase II-mediated transcription 2018-09-25 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE120478 PTEN interacts with the transcription machinery on chromatin and regulates RNA polymerase II-mediated transcription. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkz272 {Nucleic acids research (11.147): 10.1093/nar/gkz272} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA493120 https://www.ebi.ac.uk/ena/browser/view/PRJNA493120 None [Overal design]Refer to individual Series; [Treatment]'None', 'For deletion of Pten, primary MEFs, that have loxP sites flanking exon 5 inserted into the endogenous locus of Pten, were infected with adenovirus Adeno-CMV-Cre-recombinase (Vector Biolabs) or Adeno-CMV-Null (Vector Biolabs) as a control.'; [Growth]'None', 'grown in DMEM supplemented with 10% FBS, penicillin and streptomycin, and 2mM L-glutamine'; [Extraction]'ChIP-seq: Lysates were clarified from sonicated nuclei and prtein-DNA complexes were isolated with antibody\nRNA-seq: RNA was extracted from cell pellets using Qiagen RNeasy Kit.\nChIP-seq: 2-10 ng of DNA were subject to end-repair, A-tailing, and ligation with Illumina Truseq adapters using NEB enzymes (NEB), followed by size-selection of 300-400 bp and amplification for 10-15 cycles using the KAPA HiFi Library Amplification Kit (Kapa Biosystems).\nRNA-seq: Illumina TruSeq RNALibrary Prep Kit v2 (RS 122-2001) was used with 1 ug of total RNA for the construction of sequencing libraries', 'RNA was extracted from MEFs 4 passages after infection with Adeno-CMV-Cre or Adeno-CMV-Null virus using the Qiagen RNeasy Kit.'; [Cell type]'HeLa', 'primary mouse embryonic fibroblasts (passage 6-8)', 'mouse breast tumor cells', 'Source: ''cell type: HeLa; growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: CRISPR-PTEN KO; ', 'cell type: HeLa; chip antibody: PTEN 6H2.1 (Millipore, 04-035); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; chip antibody: PTEN 138G6 (Cell Signaling, 9559); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; chip antibody: RNAPII (Santa Cruz, Sc-899); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; chip antibody: RNAPII Ser2P (abcam, ab5095); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; chip antibody: RNAPII Ser5P (abcam, ab5408); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; chip antibody: SPT5 (Bethyl Laboratories, A300-868A); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; chip antibody: PTEN 6H2.1 (Millipore, 04-035) and PTEN 138G6 (Cell Signaling, 9559); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: CRISPR-PTEN KO; ', 'cell type: HeLa; chip antibody: RNAPII (Santa Cruz, Sc-899); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: CRISPR-PTEN KO; ', 'cell type: HeLa; chip antibody: RNAPII Ser2P (abcam, ab5095); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: CRISPR-PTEN KO; ', 'cell type: HeLa; chip antibody: RNAPII Ser5P (abcam, ab5408); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: CRISPR-PTEN KO; ', 'cell type: HeLa; chip antibody: SPT5 (Bethyl Laboratories, A300-868A); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: CRISPR-PTEN KO; ', 'cell type: primary mouse embryonic fibroblasts (passage 6-8); chip antibody: n/a; growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: Pten WT; ', 'cell type: primary mouse embryonic fibroblasts (passage 6-8); chip antibody: RNAPII (Santa Cruz, Sc-899); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin, and 2mM L-glutamine; genotype/variation: Pten WT; ', 'cell type: primary mouse embryonic fibroblasts (passage 6-8); chip antibody: RNAPII (Santa Cruz, Sc-899); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin, and 2mM L-glutamine; genotype/variation: Pten Null; ', 'cell type: mouse breast tumor cells; chip antibody: n/a; growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin, and 2mM L-glutamine; genotype/variation: Pten WT; ', 'cell type: mouse breast tumor cells; chip antibody: RNAPII (Santa Cruz, Sc-899); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin, and 2mM L-glutamine; genotype/variation: Pten WT; ', 'cell type: mouse breast tumor cells; chip antibody: RNAPII (Santa Cruz, Sc-899); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin, and 2mM L-glutamine; genotype/variation: Pten Null; ', 'passage: primary mouse embryonic fibroblasts (passage 6-8); genotype/variation: infected with Adeno-CMV-Null virus; ', 'passage: primary mouse embryonic fibroblasts (passage 6-8); genotype/variation: Pten was deleted using Adeno-CMV-Cre virus; ' GSE114737 Homo sapiens 99 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Optimized ChIP-seq procedure facilitates hormone receptor profiling in human tumors 2018-05-21 Performing ChIP-seq analyses in clinical specimens has remained largely challenging due to multiple technical limitations and low quantities of starting material, resulting in low enrichments and poor signal-to-noise ratio. Here, we refined the original protocols for transcription factor ChIP-seq analyses in breast, prostate, and endometrial tumor tissue. In addition to the standard fixative formaldehyde, a second crosslinker Disuccinimidyl glutarate (DSG) was included in the procedure. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE114737 Optimized ChIP-seq method facilitates transcription factor profiling in human tumors. Life science alliance 3.448 https://doi.org/10.26508/lsa.201800115 {Life science alliance (3.448): 10.26508/lsa.201800115} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA472620 https://www.ebi.ac.uk/ena/browser/view/PRJNA472620 https://www.ncbi.nlm.nih.gov/sra?term=SRP148757 [Overal design]AR, FOXA1, ERα, H3K27ac & H3K4me3 ChIP-seq data with and without double croslinking in celllines (LNCAP & MCF-7) and in human tissues (Prostate, Breast, Endometrium and Prostate samples from core needle biopsies).; [Treatment]'Surgical resections from Prostate, breast and endometrium tumors.'; [Growth]'fresh frozen material'; [Extraction]'Chromatin immunoprecipitations were performed as described previously with minor changes (Zwart et al., 2013). Samples were crosslinked in solution A with 2mM DSG (CovaChem) for 25 minutes at room temperature. After 25 minutes, 1% formaldehyde was added for 20 minutes and subsequently quenched with glycine. Samples were lysed as described (Schmidt et al., 2009) and sonicated for at least 10 cycles of 30s on, 30s off using a Diagenode Bioruptor Pico. For each ChIP, 5ug of antibody was conjugated with 50ul Protein A magnetic beads. Antibodies used were AR (sc-816, Santa Cruz), H3K27ac (39133, Active Motif), H3K4me3 (Ab8580, Abcam) and H3K27me3 (39155, Active Motif). Immunoprecipitated DNA was processed for library preparation (Part# 0801-0303, KAPA biosystems kit).\nImmunoprecipitated DNA was processed for library preparation (Part# 0801-0303, KAPA biosystems kit).'; [Cell type]'Source: ''chip antibody: AR (Santa Cruz; sc-816); patient id: LNCAP_AR_FA; case/control: FA; ', 'chip antibody: AR (Santa Cruz; sc-816); patient id: LNCAP_AR_DSG; case/control: DSG; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: LNCAP_FOXA1_FA; case/control: FA; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: LNCAP_FOXA1_DSG; case/control: DSG; ', 'chip antibody: H3K4me3 (Abcam; ab8580); patient id: LNCAP_H3K4me3_FA; case/control: FA; ', 'chip antibody: H3K4me3 (Abcam; ab8580); patient id: LNCAP_H3K4me3_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: LNCAP_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: LNCAP_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: MCF7_ER_FA; case/control: FA; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: MCF7_ER_DSG; case/control: DSG; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: MCF7_FOXA1_FA; case/control: FA; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: MCF7_FOXA1_DSG; case/control: DSG; ', 'chip antibody: H3K4me3 (Abcam; ab8580); patient id: MCF7_H3K4me3_FA; case/control: FA; ', 'chip antibody: H3K4me3 (Abcam; ab8580); patient id: MCF7_H3K4me3_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: MCF7_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: MCF7_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: AR (Santa Cruz; sc-816); patient id: P1_AR_FA; case/control: FA; ', 'chip antibody: AR (Santa Cruz; sc-816); patient id: P1_AR_DSG; case/control: DSG; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: P1_FOXA1_FA; case/control: FA; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: P1_FOXA1_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: P1_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: P1_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: AR (Santa Cruz; sc-816); patient id: P2_AR_FA; case/control: FA; ', 'chip antibody: AR (Santa Cruz; sc-816); patient id: P2_AR_DSG; case/control: DSG; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: P2_FOXA1_FA; case/control: FA; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: P2_FOXA1_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: P2_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: P2_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: AR (Santa Cruz; sc-816); patient id: P3_AR_FA; case/control: FA; ', 'chip antibody: AR (Santa Cruz; sc-816); patient id: P3_AR_DSG; case/control: DSG; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: P3_FOXA1_FA; case/control: FA; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: P3_FOXA1_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: P3_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: P3_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: AR (Santa Cruz; sc-816); patient id: P4_AR_FA; case/control: FA; ', 'chip antibody: AR (Santa Cruz; sc-816); patient id: P4_AR_DSG; case/control: DSG; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: P4_FOXA1_FA; case/control: FA; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: P4_FOXA1_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: P4_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: P4_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: B1_ER_FA; case/control: FA; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: B1_ER_DSG; case/control: DSG; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: B1_FOXA1_FA; case/control: FA; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: B1_FOXA1_DSG; case/control: DSG; ', 'chip antibody: H3K4me3 (Abcam; ab8580); patient id: B1_H3K4me3_FA; case/control: FA; ', 'chip antibody: H3K4me3 (Abcam; ab8580); patient id: B1_H3K4me3_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: B1_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: B1_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: B2_ER_FA; case/control: FA; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: B2_ER_DSG; case/control: DSG; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: B2_FOXA1_FA; case/control: FA; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: B2_FOXA1_DSG; case/control: DSG; ', 'chip antibody: H3K4me3 (Abcam; ab8580); patient id: B2_H3K4me3_FA; case/control: FA; ', 'chip antibody: H3K4me3 (Abcam; ab8580); patient id: B2_H3K4me3_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: B2_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: B2_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: B3_ER_FA; case/control: FA; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: B3_ER_DSG; case/control: DSG; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: B3_FOXA1_FA; case/control: FA; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: B3_FOXA1_DSG; case/control: DSG; ', 'chip antibody: H3K4me3 (Abcam; ab8580); patient id: B3_H3K4me3_FA; case/control: FA; ', 'chip antibody: H3K4me3 (Abcam; ab8580); patient id: B3_H3K4me3_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: B3_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: B3_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: B4_ER_FA; case/control: FA; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: B4_ER_DSG; case/control: DSG; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: B4_FOXA1_FA; case/control: FA; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: B4_FOXA1_DSG; case/control: DSG; ', 'chip antibody: H3K4me3 (Abcam; ab8580); patient id: B4_H3K4me3_FA; case/control: FA; ', 'chip antibody: H3K4me3 (Abcam; ab8580); patient id: B4_H3K4me3_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: B4_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: B4_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: E1_ER_FA; case/control: FA; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: E1_ER_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: E1_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: E1_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: E2_ER_FA; case/control: FA; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: E2_ER_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: E2_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: E2_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: E3_ER_FA; case/control: FA; ', 'chip antibody: ER (Santa Cruz; sc-543); patient id: E3_ER_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: E3_H3K27ac_FA; case/control: FA; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: E3_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: AR (Santa Cruz; sc-816); patient id: G1_AR_DSG; case/control: DSG; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: G1_FOXA1_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: G1_H3K27ac_DSG; case/control: DSG; ', 'chip antibody: AR (Santa Cruz; sc-816); patient id: G2_AR_DSG; case/control: DSG; ', 'chip antibody: FOXA1 (Santa Cruz; sc-6554); patient id: G2_FOXA1_DSG; case/control: DSG; ', 'chip antibody: H3K27ac (Active Motif; 39133); patient id: G2_H3K27ac_DSG; case/control: DSG; ', 'patient id: LNCAP_Input; ', 'patient id: MCF7_Input; ', 'patient id: P_Input_DSG; case/control: DSG; ', 'patient id: P_Input_FA; case/control: FA; ', 'patient id: B_Input_DSG; case/control: DSG; ', 'patient id: B_Input_FA; case/control: FA; ', 'patient id: E_Input_DSG; case/control: DSG; ', 'patient id: E_Input_FA; case/control: FA; ', 'patient id: G_Input; case/control: DSG; ' GSE124937 Homo sapiens 6 Expression profiling by array GPL570 Expression data from human lung cancer cell line NCI-H292 2019-01-10 CT45 family is abnormally overexpressed in various types of cancer. However, the molecular mechanisms of the oncogenic CT45 to trigger carcinogenesis and tumor malignant progression are largely enigmatic. We previously reported that CT45A1 functions as a proto-oncogene to promote the transcription in the human breast cancer cells, thereby escalating tumorigenesis and cancer metastasis, However, the mechanism of CT45A1-mediated concurrent overexpression of the multiple oncogenic genes in cancer is unclear. We used microarrays to study the role and mechanism of CT45A1 in gene transcriptional regulation in human lung cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124937 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA514355 https://www.ebi.ac.uk/ena/browser/view/PRJNA514355 None [Overal design]Three replicates of NCI-H292_CT45A1-overexpression VS three replicates of NCI-H292_CT45A1-negative; [Treatment]'NCI-H292 cells were stably transcfected with CT45A1-Venus or the vector Venus as a control'; [Growth]'DMEM complete medium, 10%FBS, 37 ̊C, 5% CO2'; [Extraction]'Total RNA was extracted using TRIZOL Reagent (Cat#15596-018,Life technologies, Carlsbad, CA, US)following the manufacturer’s instructions and checked for a RIN number to inspect RNA integrity by an Agilent Bioanalyzer 2100 (Agilent technologies, Santa Clara, CA, US).Qualified total RNA was further purified by RNeasy micro kit (Cat#74004, QIAGEN, GmBH, Germany) and RNase-Free DNase Set (Cat#79254, QIAGEN, GmBH, Germany).'; [Cell type]'Source: ''cell line: NCI-H292; genotype: CT45A1-overexpression; ', 'cell line: NCI-H292; genotype: CT45A1-negative; ' GSE92265 Mus musculus 10 Genome variation profiling by genome tiling array GPL10449 Copy number alteration in Murine Tumor Cells: primary inoculated tumor cells vs. out-growing tumor cells [Fig3a-b] 2016-12-12 Copy number alteration in out-growing mouse tumor cells comparing that in the original tumor cells that was primarily inoculated into the indicated mice. Goal is to determine the effects of IFN-gamma producing tumor-specific CTL on targeted tumor cell gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE92265 IFN-γ is required for cytotoxic T cell-dependent cancer genome immunoediting. Nature communications 11.878 https://doi.org/10.1038/ncomms14607 {Nature communications (11.878): 10.1038/ncomms14607} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA357066 https://www.ebi.ac.uk/ena/browser/view/PRJNA357066 None [Overal design]genomic DNA of out-growing tumor cells was compared with that of primary inoculated tumor cells by a-CGH assay; [Treatment]'Tumor cells were isolated from the out-growing tumor mass in the indicated mice and the primarily inoculated tumor cells was used as reference. Some mice were treated with HA-specific WT CTL.'; [Growth]'4T1-HAgRDN cells kept in complete RPMI1640-10% FCS medium after the establishment by dominant-negative form of IFN-gamma receptor alpha chain gene transfection into HA-expressing 4T1 (4T1-HA) tumor cells follwed by single cell cloning.'; [Extraction]"Total DNA extracted using DNeasy Blood & Tissue Kit (QUIAGEN) following manufacturer's instructions"; [Cell type]'Source: ''cell line: 4T1; tissue: mammary tumor cell line; strain: BALB/c; ' GSE134657 Homo sapiens 174 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL16791; GPL20301 Characterization of FOXA1 mutations in breast cancer 2019-07-22 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE134657 FOXA1 Mutations Reveal Distinct Chromatin Profiles and Influence Therapeutic Response in Breast Cancer. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2020.08.003 {Cancer cell (23.916): 10.1016/j.ccell.2020.08.003} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA556002 https://www.ebi.ac.uk/ena/browser/view/PRJNA556002 None [Overal design]Refer to individual Series; [Treatment]'DMSO and E2 conditions were subjected to DMSO or E2 treatment for 1h', 'DMSO and E2 conditions were subjected to DMSO or E2 treatment for 6h'; [Growth]'Cells were seeded in full media; the following day media was changed to either estrogen depleted media (for DMSO and E2 groups) or same DMEM/F12 50/50 full media (for FM); cells were incubated for 72h; the day of cell harvesting media was refreshed'; [Extraction]'Cells were deattached with accutase, spinned down, counted and 100K cells were used to perform Omni-ATAC protocol\nAmplification with barcode employing NEBNext Q5 Hot Start HiFi PCR Master Mix (prod. no: M0543L)', 'Cells were crosslinked in adherent conditions, crosslinked cells were lysed to obtain nuclear extracts, lysates were clarified from sonicated nuclei and protein-DNA complexes were isolated with antibody.\nNEBNext ChIP-Seq Library Prep Master Mix Set for Illumina (prod. no: E6240L)', 'Cells were snap frozen and RNA was extracted with RNeasy Kit from Qiagen (#74106), DNase treatment was performed during the extraction\nLibraries were performed by Genewiz'; [Cell type]'breast cancer', 'V5', 'V6', 'V7', 'V8', 'V9', 'V10', 'V11', 'V12', 'V13', 'V14', 'V15', 'V16', 'V17', 'V18', 'V19', 'V20', 'V21', 'V22', 'V23', 'V24', 'V25', 'V26', 'V27', 'V28', 'V29', 'V30', 'V31', 'V32', 'V33', 'V34', 'V35', 'V36', 'V37', 'V38', 'V39', 'V40', 'V41', 'V42', 'V43', 'V44', 'V45', 'V46', 'V47', 'V48', 'V49', 'V50', 'V51', 'V52', 'V53', 'V54', 'V55', 'V56', 'V57', 'breast cancer cell line''cell line: MCF7; cell type: breast cancer; ', 'cell line: MCF7; cell type: breast cancer; chip antibody: FOXA1 (ab23738, lot:GR3241520-1); ', 'cell line: MCF7; cell type: breast cancer; chip antibody: none (input); ', 'cell line: MCF7; cell type: V5; ', 'cell line: MCF7; cell type: V6; ', 'cell line: MCF7; cell type: V7; ', 'cell line: MCF7; cell type: V8; ', 'cell line: MCF7; cell type: V9; ', 'cell line: MCF7; cell type: V10; ', 'cell line: MCF7; cell type: V11; ', 'cell line: MCF7; cell type: V12; ', 'cell line: MCF7; cell type: V13; ', 'cell line: MCF7; cell type: V14; ', 'cell line: MCF7; cell type: V15; ', 'cell line: MCF7; cell type: V16; ', 'cell line: MCF7; cell type: V17; ', 'cell line: MCF7; cell type: V18; ', 'cell line: MCF7; cell type: V19; ', 'cell line: MCF7; cell type: V20; ', 'cell line: MCF7; cell type: V21; ', 'cell line: MCF7; cell type: V22; ', 'cell line: MCF7; cell type: V23; ', 'cell line: MCF7; cell type: V24; ', 'cell line: MCF7; cell type: V25; ', 'cell line: MCF7; cell type: V26; ', 'cell line: MCF7; cell type: V27; ', 'cell line: MCF7; cell type: V28; ', 'cell line: MCF7; cell type: V29; ', 'cell line: MCF7; cell type: V30; ', 'cell line: MCF7; cell type: V31; ', 'cell line: MCF7; cell type: V32; ', 'cell line: MCF7; cell type: V33; ', 'cell line: MCF7; cell type: V34; ', 'cell line: MCF7; cell type: V35; ', 'cell line: MCF7; cell type: V36; ', 'cell line: MCF7; cell type: V37; ', 'cell line: MCF7; cell type: V38; ', 'cell line: MCF7; cell type: V39; ', 'cell line: MCF7; cell type: V40; ', 'cell line: MCF7; cell type: V41; ', 'cell line: MCF7; cell type: V42; ', 'cell line: MCF7; cell type: V43; ', 'cell line: MCF7; cell type: V44; ', 'cell line: MCF7; cell type: V45; ', 'cell line: MCF7; cell type: V46; ', 'cell line: MCF7; cell type: V47; ', 'cell line: MCF7; cell type: V48; ', 'cell line: MCF7; cell type: V49; ', 'cell line: MCF7; cell type: V50; ', 'cell line: MCF7; cell type: V51; ', 'cell line: MCF7; cell type: V52; ', 'cell line: MCF7; cell type: V53; ', 'cell line: MCF7; cell type: V54; ', 'cell line: MCF7; cell type: V55; ', 'cell line: MCF7; cell type: V56; ', 'cell line: MCF7; cell type: V57; ', 'cell line: MCF7; cell type: breast cancer cell line; genotype: FOXA1 mutant (SY242CS) knockin; ', 'cell line: MCF7; cell type: breast cancer cell line; genotype: wild type; ', 'cell line: MCF7; cell type: breast cancer cell line; overexpression: V5-FOXA1(F266L); antibody: Anti-V5, Abcam ab9116, Lot GR3224488-6; treatment: DMSO control; ', 'cell line: MCF7; cell type: breast cancer cell line; overexpression: V5-FOXA1(F266L); antibody: Anti-V5, Abcam ab9116, Lot GR3224488-6; treatment: E2 1h Induction; ', 'cell line: MCF7; cell type: breast cancer cell line; overexpression: V5-FOXA1; antibody: Anti-V5, Abcam ab9116, Lot GR3224488-6; treatment: DMSO control; ', 'cell line: MCF7; cell type: breast cancer cell line; overexpression: V5-FOXA1; antibody: Anti-V5, Abcam ab9116, Lot GR3224488-6; treatment: E2 1h Induction; ', 'cell line: MCF7; cell type: breast cancer cell line; overexpression: V5-FOXA1(F266L); antibody: None; treatment: DMSO control; ', 'cell line: MCF7; cell type: breast cancer cell line; overexpression: V5-FOXA1(F266L); antibody: None; treatment: E2 1h Induction; ', 'cell line: MCF7; cell type: breast cancer cell line; overexpression: V5-FOXA1; antibody: None; treatment: DMSO control; ', 'cell line: MCF7; cell type: breast cancer cell line; overexpression: V5-FOXA1; antibody: None; treatment: E2 1h Induction; ' GSE85802 Homo sapiens 12 Expression profiling by array GPL17077 LCOR regulates transcription of human mammary epithelial and breast cancer cells 2016-08-18 Normal human mammary epithelial cell (HMLE) and breast cancer MDA-MB-231 cells are engineered to knockdown or enforce expression of variety of LCOR gene products. In addition to wild-type cDNA, functional domain deficient mutants were used to elucidate mechanism of LCOR incorporated transcriptional regulation. The transcriptome profiles were determined and compared. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE85802 Normal and cancerous mammary stem cells evade interferon-induced constraint through the miR-199a-LCOR axis. Nature cell biology 17.728 https://doi.org/10.1038/ncb3533 {Nature cell biology (17.728): 10.1038/ncb3533} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA339445 https://www.ebi.ac.uk/ena/browser/view/PRJNA339445 None [Overal design]Two sets of experiments: (1) LKO vector control vs LCOR-KD in two cell types to determine the outcome of LCOR deficiency. (2) LEX vector control vs. (wild-type, LSKAA mutant, △HTH mutant) LCOR to confirm the LCOR outcome (as identified by KD) and determine the functional impact of individual domain.; [Treatment]'None'; [Growth]'None'; [Extraction]'MDA-MB-231 and HMLE cells were infected with lentiviral vectors of either LKO1 vectorred shRNAs targeting LCOR or LEX vectorred variety LCOR cDNAs. Virus containing the empty vector were used as control. Cells were treated and selected with puromycin and the expression of LCOR and its variants were determined by qRT-PCR and Western blot to confirm the designed manipulation.\nTotal RNA were extracted using RNAeasy mini-prep kit from Qiagen'; [Cell type]'Source: ''cell line: MDA-MB-231; type: Breast cancer; exogenous manipulation: LKO1; ', 'cell lines: Mix of 10 human cell lines; ', 'cell line: MDA-MB-231; type: Breast cancer; exogenous manipulation: LKO1-shLCOR#1; ', 'cell line: HMLE; type: Human Mammary epithelial Cell; exogenous manipulation: LKO1; ', 'cell line: HMLE; type: Human Mammary epithelial Cell; exogenous manipulation: LKO1-shLCOR#1; ', 'cell line: HMLE; type: Human Mammary epithelial Cell; exogenous manipulation: LEX; ', 'cell line: HMLE; type: Human Mammary epithelial Cell; exogenous manipulation: LEX-LCOR; ', 'cell line: HMLE; type: Human Mammary epithelial Cell; exogenous manipulation: LEX-LCOR-LXXLL; ', 'cell line: HMLE; type: Human Mammary epithelial Cell; exogenous manipulation: LEX-LCOR-△HTH; ' GSE64731 Homo sapiens 92 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL6984 Post-zygotic structural variants in histologically normal breast tissue may predispose to sporadic breast cancer [SET 13] 2015-01-07 Sporadic breast cancer (SBC) is a common and heterogeneous disease. There is no reliable way of early prediction of risk for SBC in the general population. We studied 282 females with SBC concentrating on copy number aberrations in tumor-free breast tissue (uninvolved margin, UM) outside the area of primary tumor (PT). Totally 1162 UMs (1-14 per breast) were studied. PT and blood/skin as control was also analyzed. Comparative analysis between genetic profiles for UM(s), PT(s) and blood/skin from the same patient is the core of study design. We identified 108 patients with at least one aberrant UM specimen, representing 38.3% of all cases. Gains were the dominating mutations in microscopically normal breast cells and gain of ERBB2, with overexpression of HER2 protein, was the most common aberration in normal cells. Five additional receptor genes (EGFR, FGFR1, IGF1R, LIFR and NGFR) also showed gains, and these were occasionally present in combination with the gain of ERBB2. Up to 67.6% of patients showed gain of one or more of these genes in normal cells. The aberrations found in normal cells from UMs were previously described in cancer literature, which suggest their causative, driving role in this disease. We demonstrate that analysis of normal cells from cancer-bearing patients leads to identification of genetic signatures that may predispose to SBC. Early detection of signals suggesting a predisposition towards development of SBC, long before detectable tumors are formed, is a key to the anticipated shift into a preventive paradigm of personalized medicine of breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64731 Signatures of post-zygotic structural genetic aberrations in the cells of histologically normal breast tissue that can predispose to sporadic breast cancer. Genome research 9.944 https://doi.org/10.1101/gr.187823.114 {Genome research (9.944): 10.1101/gr.187823.114} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA271748 https://www.ebi.ac.uk/ena/browser/view/PRJNA271748 None [Overal design]We studied 282 female breast cancer patients that were assessed as affected by sporadic disease at the time of diagnosis and all underwent mastectomy. In total, 1162 UMs (uninvolved margin tissues), ranging from 1 to 14 UMs per patient, taken outside the location of clinically characterized index primary tumor, were analyzed on Illumina arrays. For each subject, DNA from at least one control tissue was also analyzed, which was predominantly blood DNA, alternatively skin-derived DNA. We also studied primary tumor (PT), or up to 3 primary tumor foci from patients with diagnosis of multifocal disease. This GEO project contains the genotyping profiles (processed and normalized data including Log R Ratio and B allele frequency) for these 1162 UMs used in the study. Information on phenotypes (age at diagnosis, tumor focality, tumor grade, tumor molecular phenotype) is also provided, whenever available. 92 experiments runned on platform GPL6984 (Human1M-Duov3_B); [Treatment]'None'; [Growth]'None'; [Extraction]'The tissues were stored at -70 degrees C prior to DNA extraction. The solid tissues were homogenized with a Tissuerupter (Qiagen). Proteinase K and Sarcosine was then added and the sample was incubated at 50oC over-night. The samples were transferred to PhaseLock Gel tubes and the DNA was purified with phenol/chloroform extraction. Due to very rich content of fat in UMs, phenol/chloroform extraction was repeated 6 times for all UMs, and 3 times for PTs and control samples from skin. The purified DNA was precipitated with sodium acetate, pH 5.4 and 95% ethanol. The DNA precipitate was dried before dissolving in water. Control samples of blood were extracted with QIAmp DNA Blood Maxi Kit (Qiagen).'; [Cell type]'Source: ''subject_code: AB007; gender: female; age at cancer diagnosis (yrs): 54; tumor grade: 2; molecular_phenotype: HER2+; tumor focality: multifocal; ', 'subject_code: AL002; gender: female; age at cancer diagnosis (yrs): 49; tumor grade: 3; molecular_phenotype: Luminal B, HER2+; tumor focality: multifocal; ', 'subject_code: BH81; gender: female; age at cancer diagnosis (yrs): 70; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: BK152; gender: female; age at cancer diagnosis (yrs): 55; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: multifocal; ', 'subject_code: BL87; gender: female; age at cancer diagnosis (yrs): 67; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: BM50; gender: female; age at cancer diagnosis (yrs): 59; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: unifocal; ', 'subject_code: BMF005; gender: female; age at cancer diagnosis (yrs): 55; tumor grade: 3; molecular_phenotype: HER2+; tumor focality: multifocal; ', 'subject_code: BMK015; gender: female; age at cancer diagnosis (yrs): 53; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; ', 'subject_code: BU97; gender: female; age at cancer diagnosis (yrs): 46; tumor grade: 2; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: CB110; gender: female; age at cancer diagnosis (yrs): 66; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: CG010; gender: female; age at cancer diagnosis (yrs): 38; tumor grade: 3; tumor focality: multifocal; ', 'subject_code: CJ112; gender: female; age at cancer diagnosis (yrs): 55; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: CM155; gender: female; age at cancer diagnosis (yrs): 61; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: DA83; gender: female; age at cancer diagnosis (yrs): 53; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: DE108; gender: female; age at cancer diagnosis (yrs): 76; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: DE137; gender: female; age at cancer diagnosis (yrs): 52; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: DH74; gender: female; age at cancer diagnosis (yrs): 40; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: DM138; gender: female; age at cancer diagnosis (yrs): 46; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: GW39; gender: female; age at cancer diagnosis (yrs): 46; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: HW82; gender: female; age at cancer diagnosis (yrs): 55; tumor grade: 2; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: IMH013; gender: female; age at cancer diagnosis (yrs): 73; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; ', 'subject_code: JB11; gender: female; age at cancer diagnosis (yrs): 57; molecular_phenotype: Triple negative; tumor focality: multifocal; ', 'subject_code: JJ144; gender: female; age at cancer diagnosis (yrs): 77; tumor grade: 2; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: JU32; gender: female; age at cancer diagnosis (yrs): 62; tumor grade: 2; molecular_phenotype: HER2+; tumor focality: unifocal; ', 'subject_code: KA15; gender: female; age at cancer diagnosis (yrs): 70; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: KB132; gender: female; age at cancer diagnosis (yrs): 64; tumor grade: 3; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; ', 'subject_code: KB80; gender: female; age at cancer diagnosis (yrs): 47; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: KE127; gender: female; age at cancer diagnosis (yrs): 44; molecular_phenotype: HER2+; tumor focality: unifocal; ', 'subject_code: KE53; gender: female; age at cancer diagnosis (yrs): 60; tumor grade: 2; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: KJ142; gender: female; age at cancer diagnosis (yrs): 75; tumor grade: 2; molecular_phenotype: HER2+; tumor focality: unifocal; ', 'subject_code: KK123; gender: female; age at cancer diagnosis (yrs): 62; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: KM136; gender: female; age at cancer diagnosis (yrs): 46; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; ', 'subject_code: KM143; gender: female; age at cancer diagnosis (yrs): 44; tumor grade: 2; tumor focality: unifocal; ', 'subject_code: KM19; gender: female; age at cancer diagnosis (yrs): 48; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ', 'subject_code: KZ54; gender: female; age at cancer diagnosis (yrs): 52; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ', 'subject_code: LEB004; gender: female; age at cancer diagnosis (yrs): 48; tumor grade: 3; molecular_phenotype: Triple negative; tumor focality: multifocal; ', 'subject_code: LK003; gender: female; age at cancer diagnosis (yrs): 64; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; ', 'subject_code: MB101; gender: female; age at cancer diagnosis (yrs): 60; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: MC109; gender: female; age at cancer diagnosis (yrs): 47; tumor grade: 2; tumor focality: unifocal; ', 'subject_code: MD106; gender: female; age at cancer diagnosis (yrs): 52; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: multifocal; ', 'subject_code: MD86; gender: female; age at cancer diagnosis (yrs): 51; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: ME114; gender: female; age at cancer diagnosis (yrs): 56; molecular_phenotype: Luminal B, HER2+; tumor focality: unifocal; ', 'subject_code: MG124; gender: female; age at cancer diagnosis (yrs): 58; tumor grade: 2; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: MH016; gender: female; age at cancer diagnosis (yrs): 53; tumor grade: 2; molecular_phenotype: Luminal B, HER2+; tumor focality: multifocal; ', 'subject_code: MK120; gender: female; age at cancer diagnosis (yrs): 57; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: ML36; gender: female; age at cancer diagnosis (yrs): 60; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: MM115; gender: female; age at cancer diagnosis (yrs): 64; molecular_phenotype: Luminal A; tumor focality: multifocal; ', 'subject_code: MM69; gender: female; age at cancer diagnosis (yrs): 27; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: multifocal; ', 'subject_code: MU154; gender: female; age at cancer diagnosis (yrs): 70; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: NJ111; gender: female; age at cancer diagnosis (yrs): 57; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: OB125; gender: female; age at cancer diagnosis (yrs): 69; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: OG93; gender: female; age at cancer diagnosis (yrs): 79; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: PE103; gender: female; age at cancer diagnosis (yrs): 62; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: PI33; gender: female; age at cancer diagnosis (yrs): 79; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: PJ121; gender: female; age at cancer diagnosis (yrs): 61; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: PJ133; gender: female; age at cancer diagnosis (yrs): 67; tumor grade: 2; molecular_phenotype: Luminal A; tumor focality: unifocal; ', 'subject_code: PM102; gender: female; age at cancer diagnosis (yrs): 65; tumor grade: 2; molecular_phenotype: Triple negative; tumor focality: unifocal; ', 'subject_code: RB84; gender: female; age at cancer diagnosis (yrs): 73; tumor grade: 2; tumor focality: unifocal; ', 'subject_code: SE135; gender: female; age at cancer diagnosis (yrs): 62; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ', 'subject_code: SJ88; gender: female; age at cancer diagnosis (yrs): 76; tumor grade: 2; molecular_phenotype: Luminal B, HER2-; tumor focality: unifocal; ' GSE51237 Homo sapiens 1 Genome variation profiling by genome tiling array GPL14965 Identification of CNA associated with bone metastatic breast cancer cells 2013-09-27 We used comparative genomic hybridization (CGH) analysis between Bone metastatic derivatives isolated in vivo and parental cells and focused on genomic changes affecting the expression of potential bone metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE51237 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA221790 https://www.ebi.ac.uk/ena/browser/view/PRJNA221790 None [Overal design]Total RNA from biological and technical replicates of parental MCF7 and BoM2 bone metastasis derivatives grown for 48 hours in regular media (see growth protocol). High-molecular DNA was isolated from in vitro cultured MCF7 and BoM2 cells using GeneElute™ Mammalian Genomic DNA Miniprep Kit (Sigma-Aldrich) following manufacture’s instructions.; [Treatment]'Cells were grown for 2 days following the growth protocol outlined above and DNA extracted'; [Growth]'MCF7 media (Control media): DMEM (Life Technologies), 1X Glutamax (Gibco 35050) and 10% FBS (Biological Industires) when passaging. See growth conditions in Tarragona et al., Journal of Biological Chemistry, 2012), for more details.'; [Extraction]'High-molecular DNA was isolated from in vitro cultured MCF7 and BoM2 cells using GeneElute™ Mammalian Genomic DNA Miniprep Kit (Sigma-Aldrich) following manufacture’s instructions. DNA quantity and quality was determined by NanoDrop ND-1000 UV-Vis Spectrophotometer and electrophoresis in 1% agarose gel.'; [Cell type]'bone metastatic derivative', 'none-bone metastatic derivative''cell type: bone metastatic derivative; ', 'cell type: none-bone metastatic derivative; ' GSE115295 Mus musculus 2 Non-coding RNA profiling by high throughput sequencing GPL11002 miR-100 maintains phenotype of tumor associated macrophages by targeting mTOR to promote tumor metastasis via Stat5a/IL-1ra pathway in mouse breast cancer 2018-06-04 Tumor-associated macrophages (TAMs),the main part of immune cells in tumor microenvironment (TME),play a potent role in promoting tumorigenesis through mechanisms such as stimulating angiogenesis, enhancing tumor migration and suppressing antitumor immunity. MicroRNAs (miRNAs) are considered as crucial regulators in multiple biological processes. The relationship between miRNAs and macrophages function has been extensively reported, but the roles that miRNAs play in regulating TAMs phenotype remains unclear. In this study, we screened highly-expressed microRNAs in TAMs, and first identified that miR-100 represented a TAMs-high expression pattern and maintained TAMs phenotype by targeting mTOR signaling pathway. Moreover, miR-100 expression level in TAMs was positively related to IL-1ra secretion, a traditional immune-suppressive cytokine, which was determined to promote tumor cells stemness via stimulating Hedgehog pathway. Mechanism study suggested that mTOR/Stat5a pathway was involved in IL-1ra transcriptional regulation process mediated by miR-100. More importantly, tumor metastasis and invasion capacity were significantly decreased in a 4T1 mouse breast cancer model injected intratumorally with miR-100 antagomir, and combination therapy with cisplatin showed much better benefit. In this study, we confirmed that highly expressed miR-100 maintains the phenotype of TAMs and promotes tumor metastasis via enhancing IL-1ra secretion. Interfering miR-100 expression of TAMs in mouse breast cancer model could inhibit TAMs pro-tumor function and reduce tumor metastasis, which suggested that miR-100 could serve as a potential therapy target to remodel tumor microenvironment in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115295 miR-100 maintains phenotype of tumor-associated macrophages by targeting mTOR to promote tumor metastasis via Stat5a/IL-1ra pathway in mouse breast cancer. Oncogenesis 5.995 https://doi.org/10.1038/s41389-018-0106-y {Oncogenesis (5.995): 10.1038/s41389-018-0106-y} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA474505 https://www.ebi.ac.uk/ena/browser/view/PRJNA474505 https://www.ncbi.nlm.nih.gov/sra?term=SRP149712 [Overal design]Tumor associated macrophages isolated from mouse breast tumor tissues were performed microRNA Solexa sequencing,using IlluminaGAIIX , macrophages from naïve healthy mice spleen were viewed as control.; [Treatment]'None'; [Growth]'None'; [Extraction]'Macrophages from mouse breast tumor or naïve mouse spleen were isolated, flash frozen on dry ice, and RNA was harvested using Trizol reagent. 3 ug of total RNA were used for the construction of sequencing libraries.\nFor small RNA library construction and deep sequencing, RNA samples were prepared by using the TruSeq Small RNA Sample Preparation Kit according to the manufacture’s protocol.'; [Cell type]'Source: ''strain: BALB/c; tissue: breast tumor; ', 'strain: BALB/c; tissue: spleen; ' GSE5460 Homo sapiens 129 Expression profiling by array GPL570 Predicting Features of Breast Cancer with Gene Expression Patterns 2006-08-04 Predictors built from gene expression data accurately predict ER, PR, and HER2 status, and divide tumor grade into high-grade and low-grade clusters; intermediate-grade tumors are not a unique group. In contrast, gene expression data cannot be used to predict tumor size or lymphatic-vascular invasion. Keywords: disease state analysis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE5460 Predicting features of breast cancer with gene expression patterns. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-007-9596-6 {Breast cancer research and treatment (3.471): 10.1007/s10549-007-9596-6} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA95969 https://www.ebi.ac.uk/ena/browser/view/PRJNA95969 None [Overal design]Microarray data from the tumors of 129 patients were analyzed for the ability to predict biomarkers (ER, PR, HER2), histologic features (grade and lymphatic-vascular invasion), and stage-related information (tumor size and lymph node metastasis). Multiple statistical predictors were used and the prediction accuracy determined by error rates of prediction and by dimensional scaling and visualization of the states under study. Models to predict lymph node metastasis were built by combinations of molecular, histologic and anatomic features. ***GSM125119.CEL and GSM125120.CEL are corrupt***; [Treatment]'The frozen bulk tumor samples were confirmed to contain at least 70% viable tumor by area on histologic thin sections.'; [Growth]'None'; [Extraction]'Total RNA extracted from frozen tissue was used to generate biotinylated cRNA target.'; [Cell type]'Source: ''ER: neg; HER2: pos; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 2.3; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 0.9; ', 'ER: neg; HER2: pos; B-R grade: III; node status: neg; LVI: pos; tumor type: Ductal; tumor size: 2.5; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 3.5; ', 'ER: neg; HER2: neg; B-R grade: III; node status: pos; LVI: n; tumor type: Ductal; tumor size: 2.1; ', 'ER: neg; HER2: pos; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 2.5; ', 'ER: neg; HER2: neg; B-R grade: III; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 1.2; ', 'ER: neg; HER2: pos; B-R grade: III; node status: neg; LVI: pos; tumor type: Ductal; tumor size: 2.1; ', 'ER: neg; HER2: neg; B-R grade: II; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 2.5; ', 'ER: neg; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 3.3; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 2.5; ', 'ER: neg; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 3.0; ', 'ER: neg; HER2: neg; B-R grade: II; node status: neg; LVI: pos; tumor type: Ductal; tumor size: 1.8; ', 'ER: neg; HER2: neg; B-R grade: III; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 4.0; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 2.1; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.0; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 2.2; ', 'ER: neg; HER2: pos; B-R grade: III; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 3.5; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: pos; tumor type: Ductal; tumor size: 2.5; ', 'ER: neg; HER2: neg; B-R grade: II; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 2.6; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 3.0; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.3; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.4; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.7; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 2.3; ', 'ER: neg; HER2: pos; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 3.4; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.5; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 2.8; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Lobular; tumor size: 3.5; ', 'ER: pos; HER2: pos; B-R grade: III; node status: neg; LVI: pos; tumor type: Ductal; tumor size: 1.0; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.7; ', 'ER: pos; HER2: pos; B-R grade: III; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 1.4; ', 'ER: pos; HER2: neg; B-R grade: II; node status: pos; LVI: pos; tumor type: Mixed; tumor size: 2.6; ', 'ER: pos; HER2: neg; B-R grade: II; node status: neg; LVI: pos; tumor type: Mixed; tumor size: 0.9; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 0.8; ', 'ER: pos; HER2: pos; B-R grade: II; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 2.2; ', 'ER: neg; HER2: pos; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.8; ', 'ER: pos; HER2: neg; B-R grade: II; node status: pos; LVI: pos; tumor type: Mixed; tumor size: 2.2; ', 'ER: pos; HER2: pos; B-R grade: III; node status: neg; LVI: pos; tumor type: Ductal; tumor size: 4.2; ', 'ER: neg; HER2: pos; B-R grade: II; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 2.5; ', 'ER: pos; HER2: neg; B-R grade: II; node status: neg; LVI: neg; tumor type: Lobular; tumor size: 2.3; ', 'ER: pos; HER2: pos; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 2.0; ', 'ER: pos; HER2: pos; B-R grade: II; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 1.7; ', 'ER: pos; HER2: neg; B-R grade: II; node status: pos; LVI: neg; tumor type: Lobular; tumor size: 1.1; ', 'ER: pos; HER2: neg; B-R grade: II; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 2.5; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 0.9; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: pos; tumor type: Ductal; tumor size: 3.0; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 2.3; ', 'ER: pos; HER2: neg; B-R grade: II; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 1.5; ', 'ER: pos; HER2: neg; B-R grade: I; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 4.0; ', 'ER: neg; HER2: pos; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.5; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: pos; tumor type: Ductal; tumor size: 1.1; ', 'ER: pos; HER2: neg; B-R grade: II; node status: pos; LVI: neg; tumor type: Mixed; tumor size: 5.5; ', 'ER: pos; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Lobular; tumor size: 2.3; ', 'ER: pos; HER2: neg; B-R grade: II; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.0; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: pos; tumor type: Ductal; tumor size: 1.1; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.1; ', 'ER: pos; HER2: neg; B-R grade: I; node status: pos; LVI: neg; tumor type: Lobular; tumor size: 2.5; ', 'ER: neg; HER2: neg; B-R grade: III; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 3.0; ', 'ER: neg; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Lobular; tumor size: 5.2; ', 'ER: pos; HER2: neg; B-R grade: II; node status: neg; LVI: neg; tumor type: Lobular; tumor size: 2.5; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.1; ', 'ER: pos; HER2: neg; B-R grade: III; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 1.7; ', 'ER: pos; HER2: neg; B-R grade: II; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 2.1; ', 'ER: pos; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 1.5; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.9; ', 'ER: pos; HER2: neg; B-R grade: II; node status: pos; LVI: pos; tumor type: Mixed; tumor size: 3.5; ', 'ER: neg; HER2: pos; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 2.2; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.5; ', 'ER: neg; HER2: neg; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 2.0; ', 'ER: pos; HER2: pos; B-R grade: II; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 1.3; ', 'ER: neg; HER2: pos; B-R grade: III; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 2.5; ', 'ER: pos; HER2: pos; B-R grade: II; node status: pos; LVI: neg; tumor type: Mixed; tumor size: 2.9; ', 'ER: neg; HER2: pos; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 3.0; ', 'ER: pos; HER2: neg; B-R grade: I; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 1.1; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Mixed; tumor size: 2.0; ', 'ER: pos; HER2: pos; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.2; ', 'ER: pos; HER2: neg; B-R grade: II; node status: pos; LVI: pos; tumor type: Lobular; tumor size: 3.5; ', 'ER: pos; HER2: pos; B-R grade: II; node status: pos; LVI: pos; tumor type: Mixed; tumor size: 3.1; ', 'ER: pos; HER2: neg; B-R grade: I; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 1.2; ', 'ER: pos; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Mixed; tumor size: 4.2; ', 'ER: pos; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 3.0; ', 'ER: pos; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 2.2; ', 'ER: pos; HER2: neg; B-R grade: I; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 1.3; ', 'ER: pos; HER2: neg; B-R grade: I; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 1.2; ', 'ER: pos; HER2: pos; B-R grade: III; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 2.0; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Mixed; tumor size: 1.1; ', 'ER: neg; HER2: pos; B-R grade: II; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 2.9; ', 'ER: pos; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 2.5; ', 'ER: pos; HER2: neg; B-R grade: III; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 2.5; ', 'ER: pos; HER2: pos; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 4.5; ', 'ER: pos; HER2: neg; B-R grade: II; node status: neg; LVI: neg; tumor type: Lobular; tumor size: 1.2; ', 'ER: pos; HER2: neg; B-R grade: I; node status: pos; LVI: pos; tumor type: Lobular; tumor size: 1.5; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Lobular; tumor size: 5.0; ', 'ER: pos; HER2: neg; B-R grade: I; node status: pos; LVI: neg; tumor type: Mixed; tumor size: 1.5; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.4; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Lobular; tumor size: 1.0; ', 'ER: pos; HER2: neg; B-R grade: II; node status: neg; LVI: pos; tumor type: Ductal; tumor size: 2.1; ', 'ER: pos; HER2: neg; B-R grade: II; node status: neg; LVI: neg; tumor type: Ductal; tumor size: 1.5; ', 'ER: pos; HER2: neg; B-R grade: I; node status: neg; LVI: neg; tumor type: Mixed; tumor size: 1.3; ', 'ER: pos; HER2: neg; B-R grade: III; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 1.9; ', 'ER: pos; HER2: pos; B-R grade: III; node status: neg; LVI: pos; tumor type: Ductal; tumor size: 2.1; ', 'ER: neg; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Mixed; tumor size: 5.5; ', 'ER: pos; HER2: neg; B-R grade: I; node status: pos; LVI: neg; tumor type: Lobular; tumor size: 3.5; ', 'ER: pos; HER2: neg; B-R grade: II; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 6.5; ', 'ER: pos; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 4.5; ', 'ER: pos; HER2: pos; B-R grade: III; node status: pos; LVI: neg; tumor type: Lobular; tumor size: 2.3; ', 'ER: neg; HER2: pos; B-R grade: III; node status: pos; LVI: pos; tumor type: Lobular; tumor size: 7.0; ', 'ER: pos; HER2: neg; B-R grade: I; node status: pos; LVI: neg; tumor type: Mixed; tumor size: 2.9; ', 'ER: pos; HER2: neg; B-R grade: II; node status: pos; LVI: pos; tumor type: Lobular; tumor size: 4.0; ', 'ER: pos; HER2: neg; B-R grade: II; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 5.5; ', 'ER: pos; HER2: neg; B-R grade: III; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 2.3; ', 'ER: pos; HER2: pos; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 4.0; ', 'ER: neg; HER2: pos; B-R grade: III; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 8.5; ', 'ER: pos; HER2: neg; B-R grade: I; node status: pos; LVI: neg; tumor type: Lobular; tumor size: 7.0; ', 'ER: pos; HER2: neg; B-R grade: II; node status: pos; LVI: neg; tumor type: Lobular; tumor size: 3.5; ', 'ER: pos; HER2: neg; B-R grade: III; node status: pos; LVI: neg; tumor type: Ductal; tumor size: 4.0; ', 'ER: pos; HER2: pos; B-R grade: II; node status: pos; LVI: pos; tumor type: Mixed; tumor size: 4.5; ', 'ER: neg; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 1.7; ', 'ER: neg; HER2: neg; B-R grade: III; node status: pos; LVI: pos; tumor type: Ductal; tumor size: 4.2; ' GSE83132 Mus musculus; Homo sapiens 41 Expression profiling by high throughput sequencing GPL11154; GPL13112 Genes that mediate leptomeningeal metastasis from breast and lung solid tumor primaries 2016-06-08 Little is understood about the gene expression changes that underlie cancer spread to the cerebrospinal fluid, or leptomeningeal metastasis. Using four cancer cell line models, we empolyed iterative in vivo selection to generate subpopulations of these cell lines able to access the leptomeningeal space and grow once there. We compared the gene expression profile of the terminally selected cells or "Lep" cells with that of the parental or "Par" cells, as well as that of an intermediate stage of in vivo selection or "Int" cells. Analyses for brain parenchymal metastatic derivatives or "BrM" cells were included for comparison. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE83132 Complement Component 3 Adapts the Cerebrospinal Fluid for Leptomeningeal Metastasis. Cell 36.216 https://doi.org/10.1016/j.cell.2017.02.025 {Cell (36.216): 10.1016/j.cell.2017.02.025} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA324845 https://www.ebi.ac.uk/ena/browser/view/PRJNA324845 https://www.ncbi.nlm.nih.gov/sra?term=SRP076297 [Overal design]Four different models were employed: Two human breast cancer cell lines, MDA-MB-231 and HCC1954 as well as one human lung cancer cell line, PC9 and a mouse non-small cell lung cancer cell line, Lewis lung carcinoma. Three technical replicates of each Par cell line, two or three biological replicates and two technical replicates of each of the Int and Lep cells were all subjected to analysis.; [Treatment]'None'; [Growth]'Parental cell lines (MDA-MB-231, HCC1954, PC9 and LLC) all stably express GFP. Mice harboring leptomeningeal metastases from MDAMB231, HCC1954, PC9 or LLC cell lines were euthanized. The leptomeningeal space was rinsed repeatedly with PBS. Cells dislodged from this space were collected and grown in culture on bare, tissue-culture treated plastic plates, in DMEM with 10% FBS, with supplemental L-glutamine and Pen-Strep (MDA, LLC cell lines and their derivatives); PC9 and HCC1954 were cultured in RPMI1640 wtih 10% FBS, L-glutamine and Pen-Strep. Derivative cells were grown in culture until a homogenous population of GFP-expressing cells was obtained. These cells were maintained in culture in media described above, and passaged three times prior to analysis.'; [Extraction]"Total RNA was extracted from cells using PrepEase RNA isolation kits (Affymetrix) according to the manufacturer's instructions.\nExtracted total RNA samples were quantified by Ribogreen and quality assessed by Agilent BioAnalyzer 2000. 500ng RNA with integrity number (RIN) > 9.5 from each sample was used for library construction with TruSeq RNA Sample Prep Kit v2 (Illumina) according to manufacturer’s instructions.\nLibraries were constructed for RNA-Seq analysis on Hi-Seq 2000 platform.\nHCC1954, PC9 and LLC: 50/50bp paired-end RNA-Seq; MDA-MB-231: 75/75bp paired-end RNA-Seq. 25-65 million (average 40 million) raw read pairs were generated for each sample."; [Cell type]'Source: ''cell line source: cell line HCC1954; cancer type: Grade III invasive ductal breast carcinoma with elevated HER2/Neu expression; ', 'cell line source: cell line LLC; cancer type: spontaneous non-small cell lung carcinoma from C57/B6 mouse; ', 'cell line source: cell line MDA-MB-231; cancer type: Grade IV invasive ductal breast carcinoma, ER-, PR-, HER2-; ', 'cell line source: cell line PC9; cancer type: Human non-small cell lung adenocarcinoma with elevated EGFR expression; ' GSE47714 Mus musculus 5 Expression profiling by array GPL1261 Osteotropism in breast cancer metastasis 2013-06-06 Breast cancer metastases develop in the bone more frequently than any other site, and are a common cause of morbidity in the form of bone pain, pathological fractures, nerve compression, and life-threatening hypercalcemia. Despite ongoing research efforts, the molecular and cellular mechanisms that regulate breast cancer cell homing to and colonization of the bone as well as resultant pathological bone alteration remain poorly understood. To identify key mediators promoting breast cancer metastasis to bone, we utilized an immunocompetent, syngeneic murine model of breast cancer metastasis employing the mammary tumor cell line NT2.5. Following intracardiac injection of NT2.5 cells in neu-N mice, metastases developed in the bone, liver, and lung, closely mimicking the anatomical distribution of metastases in breast cancer patients. Using an in vivo selection process, we established NT2.5 sub-lines demonstrating an enhanced ability to colonize the bone and liver. Genome-wide cDNA microarray analysis comparing gene expression between parental NT2.5 cells and established sub-lines was performed. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47714 Identification of prospective factors promoting osteotropism in breast cancer: a potential role for CITED2. International journal of cancer 4.982 https://doi.org/10.1002/ijc.24780 {International journal of cancer (4.982) doi:10.1002/ijc.24780}; {PloS one (2.776) doi:10.1371/journal.pone.0066752}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA207351 https://www.ebi.ac.uk/ena/browser/view/PRJNA207351 None [Overal design]Individual samples of RNA from parental NT2.5 cells, early passage (BO3 and LI1) sub-lines, and final passage (BO6 and LI3) sub-lines were compared using GeneChip® Mouse Genome 430 2.0 Arrays; [Treatment]'None'; [Growth]'None'; [Extraction]"RNeasy RNA purification kit (Qiagen) was used according to the manufacturer's instructions."; [Cell type]'Wild type NT2.5', 'NT2.5 bone sub-line, 3rd passage', 'NT2.5 bone sub-line, 6th passage', 'NT2.5 liver sub-line, 1st passage', 'NT2.5 liver sub-line, 3rd passage''cell type: Wild type NT2.5; metastatic site preference: bone, liver, lung; ', 'cell type: NT2.5 bone sub-line, 3rd passage; metastatic site preference: bone; ', 'cell type: NT2.5 bone sub-line, 6th passage; metastatic site preference: bone; ', 'cell type: NT2.5 liver sub-line, 1st passage; metastatic site preference: liver; ', 'cell type: NT2.5 liver sub-line, 3rd passage; metastatic site preference: liver; ' GSE25315 Homo sapiens 12 Expression profiling by array GPL10558 FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response (part II) 2010-11-12 Estrogen Receptor-a (ER) is the key feature in the majority of breast cancers and ER binding to the genome correlates with the Forkhead protein FOXA1 (HNF3a), but mechanistic insight is lacking. We now show that FOXA1 is the defining factor that governs differential ER-chromatin interactions. We show that almost all ER-chromatin interactions and gene expression changes are dependent on the presence of FOXA1 and that FOXA1 dictates genome-wide chromatin accessibility. Furthermore, we show that CTCF is an upstream negative regulator of FOXA1-chromatin interactions. In ER responsive breast cancer cells, the dependency on FOXA1 for tamoxifen-ER activity is absolute and in tamoxifen resistant cells, ER binding occurs independently of ligand, but in a FOXA1 dependent manner. Importantly, expression of FOXA1 in non-breast cancer cells is sufficient to alter ER binding and response to endocrine treatment. As such, FOXA1 is the primary determinant that regulates estrogen-ER activity and endocrine response in breast cancer cells and is sufficient to program ER functionality in non-breast cancer contexts. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE25315 FOXA1 is a key determinant of estrogen receptor function and endocrine response. Nature genetics 25.455 https://doi.org/10.1038/ng.730 {Nature genetics (25.455): 10.1038/ng.730} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA142547 https://www.ebi.ac.uk/ena/browser/view/PRJNA142547 None [Overal design]FoxA1 silenced breast cancer MCF-7 cell lines or control siRNA in the presence of Estrogen or a vehicle. MCF-7 cells were hormone-depleted for 3 d and treated with 100 nM estrogen for 6 h. There were three biological replicates for each of the four different groups.; [Treatment]'Estrogen was added at a final concentration of 100 nM.'; [Growth]'MCF-7 human cell lines were grown as described previously (Neve et al. 2006, Cancer Cell 10:515–527).'; [Extraction]'Total RNA was extracted using the QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. A DNase I digestion was included. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''cell: MCF-7; treatment: control siRNA and vehicle (control); ', 'cell: MCF-7; treatment: FoxA1 siRNA and vehicle (control); ', 'cell: MCF-7; treatment: control siRNA and estrogen; ', 'cell: MCF-7; treatment: FoxA1 siRNA and estrogen; ' GSE122953 Homo sapiens 4 Expression profiling by high throughput sequencing GPL18573 Thymidylate synthase maintains the de-differentiated state of triple negative breast cancers 2018-11-26 Cancer cells frequently boost nucleotide metabolism (NM) to support their increased proliferation, but the consequences of elevated NM on tumor de-differentiation are mostly unexplored. Here, we identified a role for thymidylate synthase (TS), a NM enzyme and established drug target, in cancer cell de-differentiation and investigated its clinical significance in breast cancer (BC). In vitro, TS knockdown increased the population of CD24+ differentiated cells, and attenuated migration and sphere-formation. RNA-seq profiling indicated a repression of epithelial-to-mesenchymal transition (EMT) signature genes upon TS knockdown, and TS-deficient cells showed an increased ability to invade and metastasize in vivo, consistent with the occurrence of a partial EMT phenotype. Mechanistically, TS enzymatic activity was found essential for the maintenance of the EMT/stem-like state by fueling a dihydropyrimidine dehydrogenase – dependent pyrimidine catabolism. In patient tissues, TS levels were found significantly higher in poorly differentiated and in triple negative BC, and strongly correlated with worse prognosis. The present study provides the rationale to study in-depth the role of NM at the crossroads of proliferation and differentiation, and depicts new avenues for the design of novel drug combinations for the treatment of BC https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE122953 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA506989 https://www.ebi.ac.uk/ena/browser/view/PRJNA506989 https://www.ncbi.nlm.nih.gov/sra?term=SRP170742 [Overal design]Gene expression analysis by RNAseq in Triple Negative Breast Cancer Cell Line MDA-MB-231 with knock down of Thymidylate Synthase and scrambled pLKO control.; [Treatment]'MDA-MB-231 were transduced with lentivirus to generate shTS#1 (TS knock down) and pLKO (control). Cells were selected in 3µg/ml puromycin and culture was maintained in 1µg/ml Puromycin. No other treatment was done on the cells.'; [Growth]'MDA-MB-231 (ATCC) cells were maintained in RPMI-1640 media (Sigma) supplemented with 10% FBS (Sigma), 1%Pen/Strep (Sigma) and 1%L-Glutamine (Sigma). Cells were grown at 37°C in a 5% CO 2 incubator.'; [Extraction]'Total RNA was isolated using miRNeasy Kit (Invitrogen) following the manufacturer’s instructions.\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''tissue: Breast Cancer; cell line: MDA-MB-231; genotype/variation: scrambled pLKO control; ', 'tissue: Breast Cancer; cell line: MDA-MB-231; genotype/variation: knock down of Thymidylate Synthase; ' GSE14017 Homo sapiens 29 Expression profiling by array GPL570 Metastases of breast cancer (U133plus2) 2008-12-17 Comparisons among breast cancer metastases at different organs revealed distinct microenvironments as characterized by cytokine content. Such microenvironment distinction might be important to dictate how the cancer cells adapt to survival before they successfully colonize. Keywords: Disease state analyses https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE14017 Latent bone metastasis in breast cancer tied to Src-dependent survival signals. Cancer cell 23.916 https://doi.org/10.1016/j.ccr.2009.05.017 {Cancer cell (23.916) doi:10.1016/j.ccr.2009.05.017}; {Cancer cell (23.916) doi:10.1016/j.ccell.2014.11.025}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA114533 https://www.ebi.ac.uk/ena/browser/view/PRJNA114533 None [Overal design]58 breast cancer metastases from different organs were profiled and compared by the expression level of over 400 cytokines. 29 samples were incuded in this series. 29 others as well as 7 in the present series were profiled on U133A platforms and included in series GSE14018.; [Treatment]'None'; [Growth]'None'; [Extraction]'TRIzol (GIBCO/BRL)'; [Cell type]'Source: ''' GSE141057 Mus musculus 17 Expression profiling by high throughput sequencing GPL21103 CLIC4 is essential for host competence for metastasis in murine models of breast cancer and a prognostic indicator for human breast cancer 2019-11-26 CLIC4 belongs to a family of highly conserved metamorphic proteins of the glutathione‐S‐transferase superfamily and dysregulation is implicated in pulmonary arterial hypertension, asthma, and ovarian cancer. We show that genetic ablation of host Clic4 eliminated the establishment of breast cancer lung metastases in two independent mouse models while Clic4 null tumor cells retained metastatic capability. TCGA and METABRIC data indicated that CLIC4 is elevated in human breast cancers from young women, those with poor prognosis and those with early stage metastatic disease. Experimentally, the essential Clic4 host contributions for metastatic competence depended on circulating levels of pro‐ metastatic mediators, neoangiogenesis, tumor cell attachment to lung tissue, myofibroblast differentiation, and leukocyte migration. CLIC4 was abundant in circulating extracellular vesicles (EVs) from tumor‐bearing wildtype mice but absent in EVs from tumor‐bearing Clic4 null hosts or wildtype hosts bearing Clic4 null‐tumors suggesting cross‐talk between host and tumor cells is required to deposit CLIC4 in EVs. These results illuminate CLIC4 as a critical host factor for metastatic competence, a potential prognostic marker for breast cancer patients and a target for anti‐metastatic therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE141057 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA591906 https://www.ebi.ac.uk/ena/browser/view/PRJNA591906 https://www.ncbi.nlm.nih.gov/sra?term=SRP233308 [Overal design]Examination of Clic4 KO vs WT at day 0 and 14 days in mouse lung. At day 0, we have 5 WT mice and 6 KO mice. At day 14, we have 2 WT mice and 6 KO mice.; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen Rneasy\nIllumina TruSeq v4'; [Cell type]'Source: ''strain: FVB/6DT1; tissue: lung; age: 8 weeks; genotype: Clic4 KO; time: Day 14; ', 'strain: FVB/6DT1; tissue: lung; age: 6 weeks; genotype: WT; time: Day 0; ', 'strain: FVB/6DT1; tissue: lung; age: 8 weeks; genotype: WT; time: Day 14; ', 'strain: FVB/6DT1; tissue: lung; age: 6 weeks; genotype: Clic4 KO; time: Day 0; ' GSE57281 Homo sapiens 12 Expression profiling by array GPL5188 RNA helicases DDX5 and DDX17 dynamically orchestrate transcription, microRNA and splicing programs in cell differentiation 2014-05-05 RNA helicases DDX5 and DDX17 are members of a large family of highly conserved proteins involved in gene expression regulation, although their in vivo targets and activities in biological processes like cell differentiation, that requires reprogramming of gene expression programs at multiple levels, are not well characterized. In this report, we uncovered a new mechanism by which DDX5 and DDX17 cooperate with hnRNP H/F splicing factors to define epithelial- and myoblast-specific splicing subprograms. We next observed that downregulation of DDX5 and DDX17 protein expression during epithelial to mesenchymal transdifferentiation and during myogenesis contributes to switching splicing programs during these processes. Remarkably, this downregulation is mediated by the production of microRNAs induced upon differentiation in a DDX5/DDX17-dependent manner. Since DDX5 and DDX17 also function as coregulators of master transcriptional regulators of differentiation, we propose to name these proteins “master orchestrators” of differentiation, that dynamically orchestrate several layers of gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE57281 RNA helicases DDX5 and DDX17 dynamically orchestrate transcription, miRNA, and splicing programs in cell differentiation. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2014.05.010 {Cell reports (7.815): 10.1016/j.celrep.2014.05.010} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA246163 https://www.ebi.ac.uk/ena/browser/view/PRJNA246163 None [Overal design]6 samples of MCF7 cells exposed to different treatments were analyzed: 3 x siCTRL ; 3 x si(DDX5-17) AND 6 samples of MCF10 cells exposed to different treatments were analyzed: 3 x siCTRL ; 3 x si(DDX5-17); [Treatment]'MCF7 and MCF10A were transfected for 48 h with either a control siRNA or with a single siRNA targeting a conserved region in both DDX5 and DDX17 transcripts; siRNA were used at a final concentration of 26.6 nM'; [Growth]'MCF7 cells were cultured in DMEM supplemented with 10% fetal bovine serum, MCF10A cells were cultured in 1:1 (DMEM)/HAM-F12 medium supplemented with 5% horse serum (Cambrex), 10 ng/ml human epidermal growth factor (PromoCell), 0.5 μg/ml hydrocortisone (Sigma), 10 μg/ml insulin (Sigma) and 100 ng/ml cholera toxin (Sigma).'; [Extraction]"Total RNA was extracted using Tripure isolation reagent (Roche) according to the manufacturer's protocol"; [Cell type]'non-tumorigenic mammary epithelial cell lines', 'ER+ breast cancer''cell type: non-tumorigenic mammary epithelial cell lines; cell line: MCF10A; transfection: DDX5 and DDX17; replicate: 1; ', 'cell type: non-tumorigenic mammary epithelial cell lines; cell line: MCF10A; transfection: DDX5 and DDX17; replicate: 2; ', 'cell type: non-tumorigenic mammary epithelial cell lines; cell line: MCF10A; transfection: DDX5 and DDX17; replicate: 3; ', 'cell type: non-tumorigenic mammary epithelial cell lines; cell line: MCF10A; transfection: CTRL; replicate: 1; ', 'cell type: non-tumorigenic mammary epithelial cell lines; cell line: MCF10A; transfection: CTRL; replicate: 2; ', 'cell type: non-tumorigenic mammary epithelial cell lines; cell line: MCF10A; transfection: CTRL; replicate: 3; ', 'cell type: ER+ breast cancer; cell line: MCF7; transfection: DDX5 and DDX17; replicate: 1; ', 'cell type: ER+ breast cancer; cell line: MCF7; transfection: DDX5 and DDX17; replicate: 2; ', 'cell type: ER+ breast cancer; cell line: MCF7; transfection: DDX5 and DDX17; replicate: 3; ', 'cell type: ER+ breast cancer; cell line: MCF7; transfection: CTRL; replicate: 1; ', 'cell type: ER+ breast cancer; cell line: MCF7; transfection: CTRL; replicate: 2; ', 'cell type: ER+ breast cancer; cell line: MCF7; transfection: CTRL; replicate: 3; ' GSE132749 Homo sapiens 27 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other GPL20795 The H2BE76K mutation drives breast cancer development by enhancing the transcription of ADAM19 2019-06-14 Study was conducted to understand the effect of the cancer associated H2BE76K mutation. Using CRISPR/Cas9 Knock-in cell lines expressing FLAG-tagged WT and E76K mutant H2B, we conducted gene expression profiling experiments and studied the effect of the H2BE76K mutation on H2B occupancy using CUT&RUN sequencing. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132749 The elevated transcription of ADAM19 by the oncohistone H2BE76K contributes to oncogenic properties in breast cancer. The Journal of biological chemistry 4.106 https://doi.org/10.1016/j.jbc.2021.100374 {The Journal of biological chemistry (4.106): 10.1016/j.jbc.2021.100374} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA548915 https://www.ebi.ac.uk/ena/browser/view/PRJNA548915 https://www.ncbi.nlm.nih.gov/sra?term=SRP201457 [Overal design]CRISPR/Cas9 cell lines expressing FLAG tagged Wildtype (WT) H2B and H2BE76K were generated to study the H2BE76K mutation in breast invasive carcinoma. Two WT and two mutant E76K cell lines as well as the Parental MDA-MB-231 cell lines were used for experiments. Gene expression of WT and E76K mutant lines was profiled by RNA-seq. Genomic localization of FLAG-tagged WT and E76K H2B proteins were profiled by CUT&RUN sequencing. ATAC-seq was performed to detect any difference of chromosomal accessibility between H2BE76K and WT.; [Treatment]'None', 'NT and sh94 samples: WT6 cells were either treated with NT (non-targeting) or sh94 shRNAs to knockdown NAP1L1. Cells were collected 72 hours after shRNA treatment for NAP1L1 CUT&RUN experiment.'; [Growth]'MDA-MB-231 cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% FBS. Cells were cultured at 37°C with 5% CO2.'; [Extraction]'ATAC-seq was performed according to the protocol in Buenrostro et al. (2015). 50,000 cells were suspended in cold lysis buffer (10 mM Tris-HCl pH 7.4, 10 mM NaCl, 3 mM MgCl2, 0.1% NP40). Crude nuclei were isolated by centrifugation at 500 g for 10 min and resuspended in 25 ml of TD Buffer (2x reaction buffer, Illumina). Nuclei pellet was collected (500 g, 5 min) and suspended in transposition reaction mix (25 ml, 2.5 ml TDE1, 22.5 ml l H2O). The reactions were incubated at 37ºC for 30 min with gentle mixing. DNA was immediately purified using Qiagen MinElute PCR Purification kit.\nLibraries were PCR amplified according to protocol and purified using Qiagen MinElute PCR Purification kit. Double sided bead purification (0.5x beads volume, followed by 1.3x beads volume) was performed using AMPure XP beads to enrich for fragments between 150 bp to 1000 bp. Library quality and fragment sizes were accessed using Bioanalyzer (Agilent).\nATAC-seq libraries were sequenced with 150 bp paired end sequencing on HiSeq X (Illumina).', 'Total RNA was extracted from KI cell lines (WT6, WT11, E76K1, E76K6) using the MiniBEST Universal RNA extraction kit (Takara). Ribosomal RNA was depleted removed using the NEBNext® rRNA Depletion Kit (NEB).\nRNA-seq libraries were prepared with NEBNext® Ultra™ II Directional RNA Library Prep Kit for Illumina® (NEB) according to the manufacturer’s protocol, followed by quality control using Bioanalyzer 2100.\nRNA-seq libraries were sequenced on a HiSeq X platform (Illumina) using 150 bp paired-end sequencing.', 'Cut & Run was performed according to the protocol described in Skene, P. J. & Henikoff, S. (2017) with slight modifications. All reactions were performed at 4ºC unless stated otherwise. Each centrifugation step was performed at 600 g for 3 min. 4 x 106 cells was used for each reaction. Cells were washed twice with PBS and resuspended in Buffer NE1 (20 mM HEPES-KOH pH7.9, 10 mM KCl, 0.5 mM Spermidine, 0.1% Triton X-100, 20% Glycerol, Proteinase Inhibitor). After 10 min, cells were collected and incubated in Buffer 1 (20 mM HEPES-KOH pH7.9, 150 mM NaCl, 2 mM EDTA, 0.5 mM Spermidine, 0.1% BSA, Proteinase Inhibitor) for 5 min. Cells were collected, washed once with Buffer 2 (20 mM HEPES pH 7.5, 150 mM NaCl, 0.5 mM Spermidine, 0.1% BSA, Proteinase Inhibitor) and resuspended in CUT&RUN Buffer 2. Samples were incubated with antibodies for 2 hours or overnight. Samples containing primary mouse antibodies were washed twice with Buffer 2 before incubation with anti-mouse rb IgG (Jackson ImmunoResearch, 315-005-003) for one hour. Nuclei was then collected, washed twice with Buffer 2 and incubated with pA-MNase fusion protein (150 ng) for one hour. Nuclei was washed once with Buffer 2 and once with low salt buffer (3.5 mM HEPES, Proteinase Inhibitor). Upon resuspension in low salt buffer, 10 mM CaCl2 was added to each reaction. MNase digestion was stopped after 30 min with the addition of Buffer 2 (supplemented with 10 mM EDTA, 20 mM EGTA and 28.8 pg yeast spike in). Samples were incubated for 15 min at 37 ºC. DNA was purified using NucleoSpin Gel and PCR Clean-up kit (MACHEREY-NAGEL).\nCUT&RUN libraries were prepared using Ovation Ultralow System V2 (NuGEN, 0344NB).\nCUT&RUN libraries were sequenced on a HiSeq X platform (Illumina) using paired end sequencing.'; [Cell type]'Breast cancer cell line', 'H2BE76K mutant', 'WT', 'Parental', 'Breast cancer cell line; adenocarcinoma derived''cell line: MDA-MB-231; cell type: Breast cancer cell line; genotype/variation: H2BE76K mutant; technology: ATAC-seq; ', 'cell line: MDA-MB-231; cell type: Breast cancer cell line; genotype/variation: WT; technology: ATAC-seq; ', 'strain: MDA-MB-231; cell type: H2BE76K mutant; technology: RNAseq; ', 'strain: MDA-MB-231; cell type: WT; technology: RNAseq; ', 'strain: MDA-MB-231; cell type: H2BE76K mutant; technology: CUT&RUN; ', 'strain: MDA-MB-231; cell type: Parental; technology: CUT&RUN; ', 'strain: MDA-MB-231; cell type: WT; technology: CUT&RUN; ', 'cell line: MDA-MB-231; cell type: Breast cancer cell line; adenocarcinoma derived; genotype/variation: H2BE76K mutant; ', 'cell line: MDA-MB-231; cell type: Breast cancer cell line; adenocarcinoma derived; genotype/variation: Parental; ', 'cell line: MDA-MB-231; cell type: Breast cancer cell line; adenocarcinoma derived; genotype/variation: WT; ' GSE98552 Homo sapiens 4 Other; Third-party reanalysis GPL18460 Chromatin structure and CTCF across the MCF10 breast cancer progression series (HiC) 2017-05-04 Transcription and processing of histone mRNAs occurs at subnuclear domains known as Histone Locus Bodies (HLBs). Although it is known that higher-order chromatin organization is dysregulated in cancer, structural alterations within HLB across breast cancer progression are unclear. Differential expression across known as MCF10, a basal triple negative breast cancer progression model, followed by pathway analysis demonstrated many alterations in signaling cascades known to be related to proliferation. Positional gene enrichment identified the hist1 gene locus at chromosome 6p22 as the most significantly altered cluster of genes from the normal-like MCF10A to premalignant MCF10AT1. The malignant MCF10CA1a had a more varied expression pattern across the hist1 locus. Within this region there are three subclusters of hist1 genes which were generally upregulated while intervening genes were more frequently downregulated. Extending these findings to TCGA breast tumors revealed that normal adjacent tissue had lower expression within the subclusters than their matched tumor samples. Moreover, the expression pattern within the hist1 locus comparing normal versus tumors recapitulated a very similar pattern to that comparing 10A to AT1 or CA1a. Since the hist1 locus is transcribed and processed at a specific subnuclear microenvironment, the higher order chromatin organization of this locus may be a critical component of its regulation. We addressed whether CTCF, a key chromatin organizing protein, may play a role in organizing the hist1 HLB. Immunofluorescence for CTCF along with NPAT, a protein which decorates this locus, identified that CTCF may tether the hist1 HLB to the nuclear matrix. All three subclusters reside within a single topologically associating domain wherein interacting loops are bound by CTCF. Inter-subcluster interactions are lost in the premalignant AT1. Consistent with the varied expression across the hist1 HLB in CA1a, inter-subcluster interactions are regained in the malignant state. These data suggest a transient state in highly proliferative breast cancer cells in which the hist1 HLB is dynamically reorganized. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98552 Intranuclear and higher-order chromatin organization of the major histone gene cluster in breast cancer. Journal of cellular physiology 4.522 https://doi.org/10.1002/jcp.25996 {Journal of cellular physiology (4.522): 10.1002/jcp.25996} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA385494 https://www.ebi.ac.uk/ena/browser/view/PRJNA385494 https://www.ncbi.nlm.nih.gov/sra?term=SRP106470 [Overal design]HiC ------------------------ title: MCF10A Hi-C GSM1631184 source name: mammary gland/breast epithelial cell characteristics: cell type: basal epithelial, non-tumorigenic characteristics: neoplasia type: fibrocystic disease characteristics: ATCC ID: ATCC CRL-10317 description: reanalysis of GSM1631184/SRR1909069 processed data file: MCF10A_pooled_40000_iced.matrix.gz processed data file: HiCPro_40000_matrix_coordinates.bed processed data file: MCF10A_pooled.allValidPairs.hic; [Treatment]'Cells were seeded at 1x106 cells per 100 mm dish and grown to 80-90% confluence. Cells were washed twice with phosphate buffered saline (PBS), fixed with 1% methanol free formaldehyde, and pellets stored at -80C. Hi-C was performed as previously published (belton, 2012, PMCID: PMC3874846).'; [Growth]'MCF10A and MCF10AT1 cells were grown in DMEM: F12 (Hyclone-SH30271), 5% (v/v) horse serum (Gibco #16050) + 10ug/ml human insulin (Sigma I-1882)+ 20ng/ml recombinant hEGF (Peprotech AF-100-15) + 100ng/ml Cholera toxin (Sigma C-8052) + 0.5 ug/ml Hydrocortisone (Sigma H-0888) Pen/Strep (Life Technologies) and Glutamine (Life Technologies). MCF10CA1a cells were grown in DMEM: F12 (Hyclone-SH30271) + 5% (v/v) horse serum (Gibco #16050) +Pen/Strep (Life Technologies)and Glutamine (Life Technologies) .'; [Extraction]'Total RNA was isolated from Trizol using Direct-zol RNA mini-prep kit (Zymo Research #R2050) with DNaseI digestion.\nDNA libraries were prepared for sequencing using standard Illumina TruSeq ChIP kit (Illumina #IP-202-1012)\nBarcoded libraries (Illumina TruSeq) were then loaded onto an Illumina HiSeq 1500 and paired-end 100-base (PE100) sequencing was performed at the Advanced Genome Technologies Core Massively Parallel Sequencing Facility at UVM.'; [Cell type]'basal, pre-metastatic', 'basal, metastatic''tissue: breast; cell type: basal, pre-metastatic; neoplasia type: hyperplastic; atcc id: n/a; ', 'tissue: breast; cell type: basal, metastatic; neoplasia type: tumorigenic; atcc id: n/a; ' GSE65505 Homo sapiens 62 Expression profiling by array GPL17586 Gene expression profiling in response to radiation treatment in human breast cancer 2015-02-02 Treatment-related morbidities have been linked to the large post-operative treatment volumes required for external beam partial breast irradiation (PBI). Alternative PBI techniques require equipment that is not readily available. To address these issues, we designed a phase I trial utilizing widely available technology to 1) evaluate the safety of a single radiation treatment delivered preoperatively to the small-volume, intact breast tumor and 2) identify imaging and genomic markers of radiation response. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE65505 FAS Death Receptor: A Breast Cancer Subtype-Specific Radiation Response Biomarker and Potential Therapeutic Target. Radiation research 2.779 https://doi.org/10.1667/RR14089.1 {Radiation research (2.779): 10.1667/RR14089.1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA274283 https://www.ebi.ac.uk/ena/browser/view/PRJNA274283 None [Overal design]Women 55 or older with clinically node negative, ER+ and/or PR+, HER2-, T1 invasive carcinomas or low-intermediate grade in situ disease ≤2cm were enrolled (n=32). Intensity-modulated radiotherapy was used to deliver 15 Gy (n=8, patients 01-08), 18 Gy (n=8, patients 09-16), or 21Gy (n=16, patients 17-32) to the tumor with a 1.5cm margin. Lumpectomy was performed within 10 days. Paired pre- and post-radiation MRI images and patient tumor samples were analyzed.; [Treatment]'Formalin fixed and paraffin-embedded (FFPE) samples were obtained at the time of diagnosis. Patients then received a single large dose of radiation to the intact tumor and proceeded to surgical resection within 10 days of treatment. A second post-radiation sample was obtained at the time of surgical excision.'; [Growth]'None'; [Extraction]'FFPE RNA extraction and labeling was performed using the RNeasy FFPE kit from Qiagen, and the SensationPlus™ FFPE Amplification and Labeling Kit (Affymetrix, Inc. catalog # 902312). All total RNA samples were assessed for quality using a NanoDrop ND8000 Spectrophotometer for absorbance ratios, and the Agilent Bioanalyzer 2100 for RIN scores. Whole transcriptome expression analysis was evaluated with HTA 2.0 arrays (Affymetrix, Inc. catalog # 902162).'; [Cell type]'Source: ''tissue: breast cancer; dose: none; pre or post treatment: pre; ', 'tissue: breast cancer; dose: 15 Gy; pre or post treatment: post; ', 'tissue: breast cancer; dose: 18 Gy; pre or post treatment: post; ', 'tissue: breast cancer; dose: 21Gy; pre or post treatment: post; ' GSE142387 Mus musculus 199 Other; Expression profiling by high throughput sequencing; Genome variation profiling by high throughput sequencing GPL13112; GPL17021; GPL21103 The genomic landscape of metastasis in treatment-naïve breast cancer models 2019-12-19 Exome and whole genome sequencing of matched primary tumor and lung metastases was used to identify metastasis-specific genomic events that drive metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE142387 The genomic landscape of metastasis in treatment-naïve breast cancer models. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1008743 {PLoS genetics (5.224): 10.1371/journal.pgen.1008743} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA596799 https://www.ebi.ac.uk/ena/browser/view/PRJNA596799 https://www.ncbi.nlm.nih.gov/sra?term=SRP238263 [Overal design]Primary and metastastic tumors from PyMT and Her2 genetically engineered mouse models were isolated and sequenced. Recurrent metastasis-specific copy number alterations, single nucleotide variants, and translocations within codiing regions were assessed. The metastatic driving potential of metastasis-specific single nucleotide variants was then tested using allograft models.; [Treatment]'genetically engineered mice were allowed to age until a humane endpoint was reached, no treatment was applied'; [Growth]'None'; [Extraction]'Mice were bred and allowed to age until a humane endpoint was reached. Primary tumors and lung metastases were isolated and snap frozen in cryo vials using liquid nitrogen. Tissue was stored at -80 and gDNA was later isolated using the gDNA purification using ZR-Duet DNA/RNA MiniPrep kit from Zymo Research. (cat.no. D7001)\nExome libraries were prepared using an Agilent SureSelectXT Mouse All Exon Kit for target enrichment. Libraries were barcoded and pooled before sequencing on an Illumina HiSeq3000 or HiSeq4000 to an average depth of 40x.', 'Mice were bred and allowed to age until a humane endpoint was reached. Primary tumors and lung metastases were isolated and snap frozen in cryo vials using liquid nitrogen. Tissue was stored at -80 and gDNA was later isolated using the gDNA purification using ZR-Duet DNA/RNA MiniPrep kit from Zymo Research. (cat.no. D7001)\nWhole genome sequencing library preparation was performed using the TruSeq DNA Sample Prep kit FC-121-1001. Samples were barcoded, pooled and sequenced on an Illumina HiSeq4000 to a depth of ~10x per sample. For RNA sequencing, the preparation of mRNA libraries and mRNA sequencing was performed by the Sequencing Facility using the HiSeq2500 instrument with Illumina TruSeq v4 chemistry.'; [Cell type]'Source: ''tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 9865; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 9865; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10025; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10025; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10026; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10026; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10111; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10111; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10113; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10113; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10109; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10109; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10172; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10172; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 9780; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 9780; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 9777; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 9777; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10091; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10091; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/10J x FVBn/J; mouse id: 9836; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/10J x FVBn/J; mouse id: 9836; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10238; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10238; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10000; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10000; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10062; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10062; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10061; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10061; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10048; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10048; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10047; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10047; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10049; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10049; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: CAST/EiJ x FVBn/J; mouse id: 10055; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: CAST/EiJ x FVBn/J; mouse id: 10055; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: CAST/EiJ x FVBn/J; mouse id: 10077; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: CAST/EiJ x FVBn/J; mouse id: 10077; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/10J x FVBn/J; mouse id: 9897; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/10J x FVBn/J; mouse id: 9897; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/10J x FVBn/J; mouse id: 9839; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/10J x FVBn/J; mouse id: 9839; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: CAST/EiJ x FVBn/J; mouse id: 9801; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: CAST/EiJ x FVBn/J; mouse id: 9801; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: CAST/EiJ x FVBn/J; mouse id: 9985; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: CAST/EiJ x FVBn/J; mouse id: 9985; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10208; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/6J x FVBn/J; mouse id: 10208; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10237; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10237; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10125; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10125; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 9884; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 9884; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 9994; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 9994; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 9998; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 9998; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9756; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9756; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 9879; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 9879; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: N/A; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: N/A; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10183; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10183; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10157; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10157; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10009; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10009; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10136; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10136; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10135; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10135; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9958; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9958; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10081; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 10081; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9470; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 956; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 965; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9674; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9725; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9742; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 974; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9760; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9725; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9760; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 956; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9470; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 965; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 974; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9742; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVB/NJ x FVBn/J; mouse id: 9674; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/10J x FVBn/J; mouse id: 10204; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: C57BL/10J x FVBn/J; mouse id: 10204; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10245; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10245; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10418; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10418; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10507; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10507; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10548; ', 'tissue: Primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10548; ', 'tissue: Lung metastatic tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10306; ', 'tissue: Primary tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10306; ', 'tissue: Lung metastatic tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10357; ', 'tissue: Primary tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10357; ', 'tissue: Lung metastatic tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10359; ', 'tissue: Primary tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10359; ', 'tissue: Lung metastatic tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10361; ', 'tissue: Primary tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10361; ', 'tissue: Lung metastatic tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10362; ', 'tissue: Primary tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10362; ', 'tissue: Lung metastatic tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10402; ', 'tissue: Primary tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10402; ', 'tissue: Lung metastatic tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10403; ', 'tissue: Primary tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10403; ', 'tissue: Lung metastatic tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10681; ', 'tissue: Primary tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10681; ', 'tissue: Lung metastatic tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10684; ', 'tissue: Primary tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 10684; ', 'tissue: Lung metastatic tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 11175; ', 'tissue: Primary tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 11175; ', 'tissue: Lung metastatic tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 11276; ', 'tissue: Primary tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 11276; ', 'tissue: Lung metastatic tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 11279; ', 'tissue: Primary tumor; oncogenic driver: Her2; model: Genetically engineered / Autochthonous; strain: FVBn/J x FVBn/J; mouse id: 11279; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10000; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10047; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10048; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10049; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10055; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10055; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10061; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10062; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10077; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10077; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10125; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10237; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10238; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10245; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10387; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10387; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10389; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10389; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10390; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 10390; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 2817; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 2817; ', 'tissue: Lung metastatic tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 31717; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 31717; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 9884; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 9994; ', 'tissue: primary tumor; oncogenic driver: PyMT; model: Genetically engineered / Autochthonous; strain: MOLF/EiJ x FVBn/J; mouse id: 9998; ', 'tissue: 4T1 cell line; oncogenic driver: Spontaneous / unknown; model: cell line lentivirally transduced with pDest empty vector; strain: Balb/cJ x FVBn/J; mouse id: Sample A; ', 'tissue: 4T1 cell line; oncogenic driver: Spontaneous / unknown; model: cell line lentivirally transduced with pDest empty vector; strain: Balb/cJ x FVBn/J; mouse id: Sample B; ', 'tissue: 4T1 cell line; oncogenic driver: Spontaneous / unknown; model: cell line lentivirally transduced with pDest empty vector; strain: Balb/cJ x FVBn/J; mouse id: Sample C; ', 'tissue: 4T1 cell line; oncogenic driver: Spontaneous / unknown; model: cell line lentivirally transduced with pDest Kras wildtype-myc; strain: Balb/cJ x FVBn/J; mouse id: Sample A; ', 'tissue: 4T1 cell line; oncogenic driver: Spontaneous / unknown; model: cell line lentivirally transduced with pDest Kras wildtype-myc; strain: Balb/cJ x FVBn/J; mouse id: Sample B; ', 'tissue: 4T1 cell line; oncogenic driver: Spontaneous / unknown; model: cell line lentivirally transduced with pDest Kras wildtype-myc; strain: Balb/cJ x FVBn/J; mouse id: Sample C; ', 'tissue: 4T1 cell line; oncogenic driver: Spontaneous / unknown; model: cell line lentivirally transduced with pDest Kras-G12D-myc; strain: Balb/cJ x FVBn/J; mouse id: Sample A; ', 'tissue: 4T1 cell line; oncogenic driver: Spontaneous / unknown; model: cell line lentivirally transduced with pDest Kras-G12D-myc; strain: Balb/cJ x FVBn/J; mouse id: Sample B; ', 'tissue: 4T1 cell line; oncogenic driver: Spontaneous / unknown; model: cell line lentivirally transduced with pDest Kras-G12D-myc; strain: Balb/cJ x FVBn/J; mouse id: Sample C; ' GSE25214 Homo sapiens 2 Genome binding/occupancy profiling by array GPL7765 Profiles of JARID1B target genes in MCF-7 cell line 2010-11-09 Using ChIP-DSL technology from AVIVA SYSTEMS BIOLOGY to find out the targets of JARID1B on whole genome. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE25214 Binding of the JmjC demethylase JARID1B to LSD1/NuRD suppresses angiogenesis and metastasis in breast cancer cells by repressing chemokine CCL14. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-11-1523 {Cancer research (8.378): 10.1158/0008-5472.CAN-11-1523} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA134333 https://www.ebi.ac.uk/ena/browser/view/PRJNA134333 None [Overal design]Enriched DNA from Chromatin IP of JARID1B was analyzed by arrays, normal IgG was used as negative control.; [Treatment]'None'; [Growth]'None'; [Extraction]'common cell lysate'; [Cell type]'Source: ''cell line: MCF-7 breast cancer cell line; antibody: JARID1B; antibody vendor: santa cruz; antibody lot/bach#: A0108; antibody catalog#: sc-67035; ', 'cell line: MCF-7 breast cancer cell line; ', 'cell line: MCF-7 breast cancer cell line; antibody: IgG; antibody vendor: santa cruz; antibody lot/bach#: C2210; antibody catalog#: sc-66931; ' GSE72955 Homo sapiens 9 Expression profiling by high throughput sequencing GPL11154 Retroviral Replicating Vectors Deliver Cytosine Deaminase Leading to Targeted 5-FU-Mediated Cytotoxicity in Multiple Human Cancer Types 2015-09-11 Toca 511 is a modified Retroviral Replicating Vector based on Moloney g‑retrovirus with an amphotropic envelope. As an investigational cancer treatment, Toca 511 preferentially infects cancer cells without direct cell lysis and encodes an enhanced yeast cytosine deaminase that converts the antifungal drug 5‑fluorocytosine to the anticancer drug, 5-fluorouracil. A panel of established human cancers cell lines, derived from glioblastoma, colon, and breast cancer tissue was used to evaluate parameters critical for effective anticancer activity. As part of these analyses, we profiled relative mRNA levels across these cell lines via RNA sequencing. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72955 Retroviral Replicating Vectors Deliver Cytosine Deaminase Leading to Targeted 5-Fluorouracil-Mediated Cytotoxicity in Multiple Human Cancer Types. Human gene therapy methods 2.089 https://doi.org/10.1089/hgtb.2015.106 {Human gene therapy methods (2.089): 10.1089/hgtb.2015.106} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA295406 https://www.ebi.ac.uk/ena/browser/view/PRJNA295406 https://www.ncbi.nlm.nih.gov/sra?term=SRP063620 [Overal design]mRNA expression profiles across nine human cancer cell lines.; [Treatment]'None'; [Growth]'Cells were grown in indicated media plus 10% FBS (Hyclone Lab Inc, Omaha, NE), 1 mM Sodium Pyruvate (Hyclone Lab Inc, Omaha, NE), and 2 mM Glutamax (Life Technologies, Grand Island, NY). All cells were cultured at 37°C in a humidified 5% CO₂ incubator, except MB-157 which was cultured at 37°C in a humidified atmospheric (no supplemental CO2) incubator'; [Extraction]'Media was removed and cells were lysed on the plate by addition of 1 mL of Trizol. The Trizol solution was transferred to 1.5 mL microfuge tubes and RNA was extracted by addition of chloroform to 30% final concentration. Tubes were centrifuged at 12,000 x g for 15 minutes. The aqueous phase was removed and RNA was further purified using Maxwell® 16 Total RNA Purification Kit (Promega, Madison, WI, Cat.# AS1050)\nOvation Human FFPE RNA-Seq kit (Nugen, San Carlos, CA, Cat.# 0340 and 0341)'; [Cell type]'glioblastoma', 'breast adenocarcinoma', 'colorectal primary adenocarcinoma', 'colorectal metastatic adenocarcinoma', 'human colorectal metastatic adenocarcinoma', 'breast medullary carcinoma''growth media: DMEM; cell line: U-87; cell type: glioblastoma; ', 'growth media: DMEM; cell line: T98G; cell type: glioblastoma; ', 'growth media: DMEM; cell line: 8-MG; cell type: glioblastoma; ', 'growth media: DMEM; cell line: 42-MG; cell type: glioblastoma; ', 'growth media: RPM1-1640; cell line: AU565; cell type: breast adenocarcinoma; ', 'growth media: McCoy’s 5A; cell line: HTB-38; cell type: colorectal primary adenocarcinoma; ', 'growth media: RPM1-1640; cell line: NCI-H508; cell type: colorectal metastatic adenocarcinoma; ', 'growth media: RPM1-1640; cell line: COLO 205; cell type: human colorectal metastatic adenocarcinoma; ', 'growth media: L-15 Leibovitz; cell line: MB-157; cell type: breast medullary carcinoma; ' GSE95190 Homo sapiens 8 Genome binding/occupancy profiling by high throughput sequencing GPL11154 KDM4 inhibition targets breast cancer stem cells [ChIP-Seq] 2017-02-22 We treated breast cancer stemm cells (BCSC) with a KDM4 inhibitor or performed knockdown of KDM4A https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95190 KDM4 Inhibition Targets Breast Cancer Stem-like Cells. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-17-1754 {Cancer research (8.378): 10.1158/0008-5472.CAN-17-1754} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA376389 https://www.ebi.ac.uk/ena/browser/view/PRJNA376389 https://www.ncbi.nlm.nih.gov/sra?term=SRP100520 [Overal design]BCSC1 cells were cultured in the presence and absence of KDM4(i) or infected with a shRNA KDM4A adenovirus; [Treatment]'BCSC1 cells were treated with 10nm KDM4(i) for 18 hours or infected with shRNA for 3 days'; [Growth]'BCSC1 cells were grown in MSC medium under low-oxygen conditions'; [Extraction]'Metzger, E., et al. Phosphorylation of histone H3 at threonine 11 establishes a novel chromatin mark for transcriptional regulation. Nat Cell Biol 10, 53-60 (2008), Drosophila Spike in Chromatin was added in H3K9me3 control and H3K9me3 (i) samples.\nLibraries were prepared from immunoprecipitated DNA according to standard methods. ChIP-seq libraries were sequenced using a HiSeq 2000 (Illumina) and mapped to the hg19 reference genome using bowtie 2'; [Cell type]'Source: ''cell line: breast triple negative tumor cell line BCSC1; treatment: vehicle; chip antibody: none; ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: vehicle; chip antibody: H3K9me3 (Diagenode, #C15410056, lotA1675-001P); ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: 10 nM kDM4(i) for 18 hours; chip antibody: none; ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: 10 nM kDM4(i) for 18 hours; chip antibody: H3K9me3 (Diagenode, #C15410056, lotA1675-001P); ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: shRNA control; chip antibody: none; ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: shRNA control; chip antibody: KDM4A (Schuele Lab; #5766, lot 21110); ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: shRNA KDM4A; chip antibody: none; ', 'cell line: breast triple negative tumor cell line BCSC1; treatment: shRNA KDM4A; chip antibody: KDM4A (Schuele Lab; #5766, lot 21110); ' GSE19328 Homo sapiens 28 Genome binding/occupancy profiling by genome tiling array GPL4910; GPL4911; GPL4912; GPL4913; GPL4914; GPL4915; GPL4916 Coativator Function Defines the Active Estrogen Receptor Alpha Cistrome 2009-12-04 Genome-wide ChIP-on-Chip against RNA Pol II in untreated MCF7 cells (phenol-red free media) and H3R17me2 in untreated and estrogen (45 min) treated cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE19328 Coactivator function defines the active estrogen receptor alpha cistrome. Molecular and cellular biology 3.735 https://doi.org/10.1128/MCB.00020-09 {Molecular and cellular biology (3.735): 10.1128/MCB.00020-09} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA121689 https://www.ebi.ac.uk/ena/browser/view/PRJNA121689 None [Overal design]MCF7 breast cancer cells were grown in phenol-red free media, cross-linked and processed as in (Carroll et al 2005). DNA was hybridized to GeneChip® Human Tiling 2.0R Array Set.; [Treatment]'control (ethanol) or estrogen (E2: 1x10-8M) for 45 minutes'; [Growth]'phenol-red free DMEM supplemented with 10% charcoal dextran treated serum.'; [Extraction]'according to (Carroll et al 2005)'; [Cell type]'MCF7 breast cancer cells', 'Source: ''cell type: MCF7 breast cancer cells; antibody: RNA Pol II; agent: none; ', 'cell type: MCF7 breast cancer cells; antibody: H3K17me2; agent: Estrogen; ', 'cell type: MCF7 breast cancer cells; antibody: H3K17me2; agent: none; ', 'reference: input; ' GSE24594 Mus musculus 80 Expression profiling by array GPL8321 MMTV-Myc tumor development in E2F-null backgrounds 2010-10-08 Advances in genomic signatures have begun to dissect breast cancer heterogeneity, and application of these signatures will allow the prediction of which pathways are important in tumor development. Here we used genomic signatures to predict involvement of specific E2F transcription factors in Myc-induced tumors. We genetically tested this prediction by interbreeding Myc transgenics with mice lacking various activator E2F alleles. Tumor latency decreased in the E2F1 mutant background and significantly increased in both the E2F2 and E2F3 mutants. Investigating the mechanism behind these changes revealed a reduction in apoptosis in the E2F1 knockout strain. E2F2 and E2F3 mutant backgrounds alleviated Myc effects on the mammary gland, reducing the susceptible tumor target population. Gene expression data from tumors revealed that the E2F2 knockout background resulted in fewer tumors with EMT, corresponding with a reduction in probability of Ras activation. In human breast cancer we found that a low probability of E2F2 pathway activation was associated with increased relapse-free survival time. Together these data illustrate the predictive utility of genomic signatures in deciphering the heterogeneity within breast cancer and illustrate the unique genetic requirements for individual E2Fs in mediating tumorigenesis in both mouse models and human breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24594 Prediction and genetic demonstration of a role for activator E2Fs in Myc-induced tumors. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-10-2386 {Cancer research (8.378): 10.1158/0008-5472.CAN-10-2386} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA132381 https://www.ebi.ac.uk/ena/browser/view/PRJNA132381 None [Overal design]MMTV-Myc tumors were generated in an E2F wild-type, E2F1 null, E2F2 null and E2F3 heterozygous background. When the primary tumor reached the endpoint, the tumors were flash frozen. 20 tumors from each genotype were selected for microarray analysis.; [Treatment]'Tumors were flash frozen.'; [Growth]'All tumors are from MMTV-Myc transgenics in an FVB background.'; [Extraction]'Total RNA was extracted from mouse mammary tumors using the Qiagen RNeasy Midi Kit.'; [Cell type]'Source: ''strain: FVB; genotype: wild-type; tissue: mammary gland tumor; ', 'strain: FVB; genotype: E2F1 null; tissue: mammary gland tumor; ', 'strain: FVB; genotype: E2F2 null; tissue: mammary gland tumor; ', 'strain: FVB; genotype: E2F3 heterozygous; tissue: mammary gland tumor; ' GSE92898 Homo sapiens 6 Genome binding/occupancy profiling by high throughput sequencing GPL16791 Genome-wide maps of chromatin accessibility of histone deacetylase inhibition in triple-negative breast cancer 2016-12-23 Analysis of chromatin accessibility changes after prolonged exposure of triple-negative breast cancer cell lines to low doses of Panobinostat (LBH589), a pan-histone deacetylase inhibitor. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE92898 Genome-wide chromatin accessibility, DNA methylation and gene expression analysis of histone deacetylase inhibition in triple-negative breast cancer. Genomics data 0.527 https://doi.org/10.1016/j.gdata.2017.01.002 {Genomics data (0.527): 10.1016/j.gdata.2017.01.002} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA358732 https://www.ebi.ac.uk/ena/browser/view/PRJNA358732 https://www.ncbi.nlm.nih.gov/sra?term=SRP095624 [Overal design]Examination of accessible chromatin after histone deacetylase inhibition in 2 triple-negative cell lines cell types.; [Treatment]'Control cells were maintained in full RPMI + DMSO for 28 days, treated cells were maintained for 4 cycles of 5 days incubation in full RPMI + 10nM LBH589 followed by 2 days of incubation in full RPMI + DMSO. Treated cells with drug holiday, were maintained in RPMI + DMSO for an additional period of 14 days.'; [Growth]'Cells were cultured at 37C in RPMI-1640 supplemented with 10mM HEPES, 10% heat-inactivated fetal bovine serum (FBS) and 1% penicillin-streptomycin (Full RPMI).'; [Extraction]'50,000 intact cells were lysed and the nuclei were collected by centrifugation at 500 x g for 10 min at 4°C. The pellet was then incubated with transposition reaction mix for 30 min at 37°C and then purified using the MinElute PCR Purification kit (Qiagen, Hilden, Germany).\nThe eluted transposed DNA was barcoded and amplified for 5 cycles, and then 5 µl of the product was used for a qPCR side-reaction to prevent amplification saturation.\nThe optimal amount of additional PCR cycles was determined based on the number of cycles that represented one-third of maximum fluorescence intensity in the qPCR reaction after 20 cycles. The final transposed DNA was amplified for a total of 9-11 cycles. The final amplified library was purified using MinElute PCR Purification kit and eluted in 20ul elution buffer. The ATAC libraries were sequenced on the Illumina HiSeq 2500 in Rapid Mode using 50 bp paired-end.'; [Cell type]'Source: ''cell line: HCC1806; disease subtype: Triple-negative breast cancer; treatment: DMSO for 28 days; ', 'cell line: HCC1806; disease subtype: Triple-negative breast cancer; treatment: LBH589 (10nM) for 28 days; ', 'cell line: HCC1806; disease subtype: Triple-negative breast cancer; treatment: LBH589 (10nM) for 28 days + DMSO for 14 days; ', 'cell line: MDA-MB-231; disease subtype: Triple-negative breast cancer; treatment: DMSO for 28 days; ', 'cell line: MDA-MB-231; disease subtype: Triple-negative breast cancer; treatment: LBH589 (10nM) for 28 days; ', 'cell line: MDA-MB-231; disease subtype: Triple-negative breast cancer; treatment: LBH589 (10nM) for 28 days + DMSO for 14 days; ' GSE52964 Homo sapiens 8 Genome binding/occupancy profiling by high throughput sequencing GPL11154 BAF155 methylation at R1064 creates unique chromatin association patterns 2013-12-04 CARM1, a coactivator for various cancer-relevant transcription factors, is overexpressed in breast cancer. To elucidate the functions of CARM1 in tumorigenesis, we knocked out CARM1 from several breast cancer cell lines using Zinc-Finger Nuclease technology, which resulted in drastic phenotypic and biochemical changes. The CARM1 KO cell lines enabled identification of novel CARM1 substrates, notably the SWI/SNF core subunit BAF155. Methylation of BAF155 at R1064 was found to be an independent prognostic biomarker for cancer recurrence and to regulate breast cancer cell migration and metastasis. Further, CARM1-mediated BAF155 methylation affects gene expression by directing methylated BAF155 to unique chromatin regions (e.g., c-Myc pathway genes). Collectively our studies uncover a mechanism by which BAF155 acquires tumorigenic functions via arginine methylation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE52964 CARM1 methylates chromatin remodeling factor BAF155 to enhance tumor progression and metastasis. Cancer cell 23.916 https://doi.org/10.1016/j.ccr.2013.12.007 {Cancer cell (23.916): 10.1016/j.ccr.2013.12.007} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA230559 https://www.ebi.ac.uk/ena/browser/view/PRJNA230559 https://www.ncbi.nlm.nih.gov/sra?term=SRP033492 [Overal design]Examination of methylation of BAF155 (R1064) in breast cancer cells; [Treatment]'None'; [Growth]'MCF-7 cells were obtained from ATCC, and maintained with DMEM (Gibco, Gaithersburg, MD) containing 10% FBS (Gibco)'; [Extraction]"Chromatin immunoprecipitation was performed as described previously (Meyer MB. Mol Endo. 2012)\nThe isolated DNA (or Input DNA acquired prior to precipitation) was then validated by quantitative real time PCR (qPCR) and further prepared for ChIP-seq analysis. ChIP-seq libraries were prepared using the NEBNext DNA sample prep kit (NEB, #E6000L) with the Bioo NEXTflex ChIP-seq Barcodes (Bioo Scientific, Austin, TX, #514122) according to manufacturer’s protocols, with few exceptions. During the NEBNext prep, the Illumina adapters were replaced with the Bioo Scientific Barcoded adapters according to Bioo protocols. ChIP-DNA ligated libraries were cleaned up with Agencourt AMPureXP Magnetic Beads (Beckman-Coulter, #A63881). A pre-size selection PCR was performed using Phusion polymerase, NEXTflex Primer Mix and purified ligation product for 4 cycles of PCR according to the Bioo Protocol. Libraries were size selected using Invitrogen E-gels to a size of 400-500bp. Samples were then PCR amplified for 14 cycles using Phusion polymerase, NEXTflex Primer mix and the size selected DNA as per Bioo protocol, followed by Agencourt bead clean up. Libraries were validated for integrity using the Agilent Bioanalyzer 2100 (Agilent Technologies, Santa Clara, CA). Clusters were formed and sequenced on the Illumina HiSeq2000 sequencer by the University of Wisconsin - Madison DNA Sequencing Facility in the University of Wisconsin- Madison Biotechnology Center. DNA clusters were generated using a cBot Single Read Cluster Generation kit (ver. 3) on an Illumina cBot (Illumina) according to the manufacturer's instructions, to obtain an average of 1.5×108 clusters for each lane on a flowcell. All sequencing runs for 50mers were performed on an Illumina HiSeq2000 using the Illumina Sequencing kit (ver. 3). Fluorescent images were analyzed using the CASAVA 1.8.2 (Illumina) to obtain FASTQ formatted sequence data. Twelve barcoded libraries were run per lane and this was repeated over 4 lanes. After which, the raw FASTQ for each sample was concatenated from the 4 lanes prior to mapping to create a single sample. Each ChIP sample was repeated in biological replicate in the same manner (minimum of 2 replicates). Sequences were mapped to the human genome (hg19) using BOWTIE (--best –m 1) to yield unique alignments."; [Cell type]'breast cancer cells''cell line: MCF7; cell type: breast cancer cells; passages: <20; genotype/variation: CARM1 KO; chip antibody: BAF155; chip antibody vendor: Santa cruz; chip antibody cat. #: sc-10756; ', 'cell line: MCF7; cell type: breast cancer cells; passages: <20; genotype/variation: CARM1 KO; ', 'cell line: MCF7; cell type: breast cancer cells; passages: <20; genotype/variation: wild type; chip antibody: BAF155; chip antibody vendor: Santa cruz; chip antibody cat. #: sc-10756; ', 'cell line: MCF7; cell type: breast cancer cells; passages: <20; genotype/variation: wild type; ' GSE73320 Homo sapiens 2 Genome binding/occupancy profiling by high throughput sequencing GPL9052 P21-activated kinase group II small compound inhibitor GNE-2861 perturbs estrogen receptor alpha signaling and restores tamoxifen-sensitivity in breast cancer cells 2015-09-22 Estrogen receptor alpha (ERα) is highly expressed in most breast cancers. Consequently, ERα modulators, such as tamoxifen, are successful in breast cancer treatment, although tamoxifen resistance is commonly observed. While tamoxifen resistance may be caused by altered ERα signaling, the molecular mechanisms regulating ERα signaling and tamoxifen resistance are not entirely clear. Here, we found that PAK4 expression was consistently correlated to poor patient outcome in endocrine treated and tamoxifen-only treated breast cancer patients. Importantly, while PAK4 overexpression promoted tamoxifen resistance in MCF-7 human breast cancer cells, pharmacological treatment with a group II PAK (PAK4, 5, 6) inhibitor, GNE-2861, sensitized tamoxifen resistant MCF-7/LCC2 breast cancer cells to tamoxifen. Mechanistically, we identified a regulatory positive feedback loop, where ERα bound to the PAK4 gene, thereby promoting PAK4 expression, while PAK4 in turn stabilized the ERα protein, activated ERα transcriptional activity and ERα target gene expression. Further, PAK4 phosphorylated ERα-Ser305, a phosphorylation event needed for the PAK4 activation of ERα-dependent transcription. In conclusion, PAK4 may be a suitable target for perturbing ERα signaling and tamoxifen resistance in breast cancer patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE73320 p21-activated kinase group II small compound inhibitor GNE-2861 perturbs estrogen receptor alpha signaling and restores tamoxifen-sensitivity in breast cancer cells. Oncotarget None https://doi.org/10.18632/oncotarget.6081 {Oncotarget (None): 10.18632/oncotarget.6081} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA296591 https://www.ebi.ac.uk/ena/browser/view/PRJNA296591 https://www.ncbi.nlm.nih.gov/sra?term=SRP063987 [Overal design]MCF7 cells were serum-starved for 72h and then treated with E2 for 45 min.; [Treatment]'Cells were fixed with 1% formaldehyde for 10 minutes, then glycine-quenched and harvested'; [Growth]'The human breast cancer cell line MCF7 was maintained in DMEM medium supplemented with 10% fetal bovine serum (FBS) (Invitrogen) at 37°C, under a humidified atmosphere of 5% carbon dioxide.'; [Extraction]'Standard Illumina DNA library construction\nChIP-seq libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'ERalpha-positive breast cancer cells''cell line: MCF7; cell type: ERalpha-positive breast cancer cells; chip antibody: none; ', 'cell line: MCF7; cell type: ERalpha-positive breast cancer cells; chip antibody: ERalpha (H-20, Santa Cruz); ' GSE56445 Homo sapiens 12 Expression profiling by array GPL15034 The transcriptional regulators TAZ and YAP direct Transforming Growth Factor-beta-induced tumorigenic phenotypes in breast cancer cells 2014-04-02 Uncontrolled Transforming growth factor-beta (TGFβ) signaling promotes aggressive metastatic properties in late-stage breast cancers. However, how TGFβ-mediated cues are directed to induce late-stage tumorigenic events is poorly understood, particularly given that TGFβ has clear tumor suppressing activity in other contexts. Here we demonstrate that the transcriptional regulators TAZ and YAP (TAZ/YAP), key effectors of the Hippo pathway, are necessary to promote and maintain TGFβ-induced tumorigenic phenotypes in breast cancer cells. Interactions between TAZ/YAP, TGFβ-activated SMAD2/3, and TEAD transcription factors reveal convergent roles for these factors in the nucleus. Genome-wide expression analyses indicate that TAZ/YAP, TEADs and TGFβ-induced signals coordinate a specific pro-tumorigenic transcriptional program. Importantly, genes cooperatively regulated by TAZ/YAP, TEAD, and TGFβ, such as the novel targets NEGR1 and UCA1, are necessary for maintaining tumorigenic activity in metastatic breast cancer cells. Nuclear TAZ/YAP also cooperate with TGFβ signaling to promote phenotypic and transcriptional changes in non-tumorigenic cells to overcome TGFβ repressive effects. Our work thus identifies crosstalk between nuclear TAZ/YAP and TGFβ signaling in breast cancer cells, revealing novel insight into late-stage disease-driving mechanisms. Expression profiling was conducted following the repression of the transcriptional regulators TAZ and YAP (TAZ/YAP), the TEAD family of transcription factors (TEAD1/2/3/4), or the TGFb signaling pathway (with SB-431542, an inhibitor of the TBRI recpeptor) in human MDA-MB-231-LM2 breast cancer cells treated with TGFβ1. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE56445 The transcriptional regulators TAZ and YAP direct transforming growth factor β-induced tumorigenic phenotypes in breast cancer cells. The Journal of biological chemistry 4.106 https://doi.org/10.1074/jbc.M113.529115 {The Journal of biological chemistry (4.106): 10.1074/jbc.M113.529115} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA243330 https://www.ebi.ac.uk/ena/browser/view/PRJNA243330 None [Overal design]Human MDA-MB-231-LM2-4 breast cancer cells were transfected with control siRNA, or siRNAs targeting TAZ/YAP or all four TEADs and were treated 24 hours later with 500pM TGFβ1 or 5mM SB-431542 for an additional 24 hours. Total RNA was isolated and twelve microarrays in total were performed, with each condition carried out three times on separate days. The Boston University Microarray Core generated the data using the Affymetrix Human Gene 1.0 St Array.; [Treatment]'RNA interference was performed by transfecting the indicated siRNA using Dharmafect 1 (Thermo Scientific) according to manufacturer’s protocol.'; [Growth]'MDA-MB-231-LM2-4 cells were cultured using RPMI media supplemented with 10% FBS.'; [Extraction]'Total RNA was isolated and purified by Quick-RNA MiniPrep (Zymogen Research) according to manufacturer’s protocol.'; [Cell type]'Source: ''cell line: MDA-MB-231-LM2-4 breast cancer cells; treatment: Control siRNA plus TGF-beta; ', 'cell line: MDA-MB-231-LM2-4 breast cancer cells; treatment: siRNA targetting TAZ/YAP plus TGF-beta; ', 'cell line: MDA-MB-231-LM2-4 breast cancer cells; treatment: siRNA targetting TEAD1/2/3/4 plus TGF-beta; ', 'cell line: MDA-MB-231-LM2-4 breast cancer cells; treatment: SB-431542 (an inhibitor of the TBRI recpeptor) plus TGF-beta; ' GSE117491 Homo sapiens 2 Expression profiling by array GPL21185 Effect of cold atmospheric plasma (CAP) on MCF-7 breast cancer cell (Agilent Human GE v3 8x60K Microarray) 2018-07-23 Genom-wide expression profiling of MCF-7, MCF-7 and CAP-treated MCF-7 cell. In result, cold atmospheric plasma different effect the CAP-treated MCF-7 breast cancer cell. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE117491 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA482325 https://www.ebi.ac.uk/ena/browser/view/PRJNA482325 None [Overal design]Total RNA is obtained from MCF-7 and CAP-treated MCF-7.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted and purified from MCF-7 using ZR Dyet DNA/RNA kit (Zymo research) according'; [Cell type]'Source: ''tissue: MCF-7 breast cancer cell line; gender: female; ' GSE54771 Mus musculus 6 Expression profiling by array GPL1261 Comparison of the tarnscriptome of 4T1 control cells versus shRNA NFAT1 transduced cells (mouse) 2014-02-07 4T1 is a mammary tumor cell line to which the NFAT1 transcription factor is essential for tumorigenesis and metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54771 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA237586 https://www.ebi.ac.uk/ena/browser/view/PRJNA237586 None [Overal design]control or shRNA transduced 4T1 cells growing in culture were collected and RNA was extracted from each sample and processed for hybridization to Affymetrix arrays.; [Treatment]'None'; [Growth]'4T1 adherent cell were transduced with a control vector or an shRNA NFAT1 expressing vector. After 10 days of selection cells were trypsinized and collected from culture dishes. Cells were next lysed following the Rneasy kit from QUIAGEN'; [Extraction]'Total RNA was isolated using the RNeasy kit from QIAGEN'; [Cell type]'highly tumorigenic and metastatic mammary tumor cells''cell line: 4T1; cell type: highly tumorigenic and metastatic mammary tumor cells; transduced with: control shRNA; ', 'cell line: 4T1; cell type: highly tumorigenic and metastatic mammary tumor cells; transduced with: NFAT1 shRNA; ' GSE104939 Homo sapiens 7 Expression profiling by array GPL15207 Expression data MCF-7 Breast cancer cells with Graphene Oxide and Graphene nitrite Treatments 2017-10-13 Breast cancer is one of the fatal diseases, Graphene has a property that can be used for Imaging and Therapy. Global gene expression changes leading to these changes were investigated presently in Breast cancer subtypes. The pathological staging of the cancers is compared to global gene expression profiles. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE104939 Graphitic Carbon Nitride Causes Widespread Global Molecular Changes in Epithelial and Fibroblast Cells. ACS omega 2.584 https://doi.org/10.1021/acsomega.0c05513 {ACS omega (2.584): 10.1021/acsomega.0c05513} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA414192 https://www.ebi.ac.uk/ena/browser/view/PRJNA414192 None [Overal design]Graphene Oxide and Graphene Nitrite was treated with IC25 vvalue in MCF-7 Breast cancer cell lines respectively. RNA extraction extraction and hybridization on Affymetrix microarrays were performed to under stand tumour progression with an intent to identify candidate markers for Imaging and therapy.; [Treatment]'None'; [Growth]'The cells were Trypsinized and collected after Treatments, washed thrice with 1X PBS.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MCF-7; tissue: Breast Cancer cell line; ' GSE58304 Homo sapiens 2 Expression profiling by array GPL17077 Gene expression profiling in MCF-7 cells exposed to blackcurrant extract. 2014-06-09 Blackcurrants (Ribes nigrum L., Grossulariaceae) have a high content of anthocyanin polyphenols and these have been shown to have beneficial effects on health, owing to their antioxidant and anti-carcinogenic properties. This study analyzed the constituents of blackcurrant extract (BCE) and investigated its potential phytoestrogenic effects using a breast cancer cell line (MCF-7) overexpressing the estrogen receptor (ER) α. Microarray and ingenuity pathway analysis showed that BCE activated upstream genes such as ERα and transforming growth factor beta 1, and upregulated the expression of many genes downstream of ERα. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58304 Phytoestrogenic activity of blackcurrant (Ribes nigrum) anthocyanins is mediated through estrogen receptor alpha. Molecular nutrition & food research 4.653 https://doi.org/10.1002/mnfr.201500479 {Molecular nutrition & food research (4.653): 10.1002/mnfr.201500479} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA251962 https://www.ebi.ac.uk/ena/browser/view/PRJNA251962 None [Overal design]MCF-7 cells were seeded in culture dish and maintain to confluent. Then medium replace with phenol-red-serum-free DMEM medium with or without BCE (50μg/ml). After the cells were incubated for 24 h at 37 °C 5% CO2.; [Treatment]'The medium was then replaced with phenol red- and serum-free DMEM, with or without BCE (50 μg/ml). After the cells were incubated for 24 h at 37°C with 5% CO2, they were washed twice with phosphate-buffered saline (PBS).'; [Growth]'MCF-7 cells were seeded in culture dishes in DMEM with 10% FBS and incubated at 37°C with 5% CO2 until confluent.'; [Extraction]'Total RNA was extracted by using the RNeasy mini kit (Qiagen, Tokyo, Japan).'; [Cell type]'Human mammary tumor cells''cell line: MCF-7; cell type: Human mammary tumor cells; culture media: phenol red- and serum-free DMEM (without BCE); ', 'cell line: MCF-7; cell type: Human mammary tumor cells; culture media: phenol red- and serum-free DMEM with BCE (50 μg/ml); ' GSE18773 Homo sapiens 6 Expression profiling by array GPL570 CAL-51 breast cancer side population cells 2009-10-28 Human solid tumors contain rare cancer side population (SP) cells, which expel the fluorescencent dye H33342 and display cancer stem cell characteristics. Transcriptional profiling of cancer SP cells isolated by H33342 fluorescence analysis is a newly emerging approach to discover cancer stem cell markers and aberrant differentiation pathways. Using Affymetrix expression microarrays this study investigated differential gene expression between SP and non-SP (NSP) cells isolated from the CAL-51 human mammary carcinoma cell line. Keywords: cell type comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE18773 Down-regulation of the fetal stem cell factor SOX17 by H33342: a mechanism responsible for differential gene expression in breast cancer side population cells. The Journal of biological chemistry 4.106 https://doi.org/10.1074/jbc.M109.082941 {The Journal of biological chemistry (4.106): 10.1074/jbc.M109.082941} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA121621 https://www.ebi.ac.uk/ena/browser/view/PRJNA121621 None [Overal design]To characterize differential gene expression between CAL-51 breast cancer SP and NSP cells, three consecutive cell culture passages of CAL-51 were independently subjected to H33342 labeling and dual wavelength fluorescence analysis and were then flow cytometrically sorted into SP and NSP cell fractions. Subsequently, each of the six cell preparations was subjected to global transcriptional profiling using Affymetrix HG U133 Plus 2.0 expression microarrays.; [Treatment]'Med3, 80 % confluency'; [Growth]'None'; [Extraction]'Rneasy'; [Cell type]'Source: ''tissue: breast cancer; ' GSE116117 Mus musculus 9 Expression profiling by high throughput sequencing GPL18480 The FAK-Inhibitor BI 853520 exerts anti-tumor effects in breast cancer 2018-06-21 In order to delineate the molecular mechanisms leading to the therapeutic effect of BI 853520 on primary tumor growth, mice harboring 4T1 primary tumors were treated for five days with BI 853520, and RNA extracted from total tumors was subjected to next generation sequencing. Only primary tumors with sufficient RNA quality were included into further analysis (Suppl. Fig. 2A). Gene expression correlation analysis displayed a clear separation of transcriptomic profiles derived from primary tumors of mice treated with BI 853520 or vehicle (Suppl. Fig. 2B). Comparative gene expression analysis of primary tumors of mice treated with BI 853520 versus vehicle control revealed 1293 upregulated and 475 downregulated genes (cutoffs: p-value ≤ 0.05, fold change +/- 1.5). Functional enrichment analysis for biological processes and signaling pathways indicated that the regulation of epithelial cell proliferation, positive regulation of cell cycle/cell proliferation/cell division and regulation of cell proliferation/cell division/cell growth were enriched in genes downregulated by BI 853520 treatment (Fig. 3A). In line with this finding, gene set enrichment analysis confirmed a significant reduction in the relative expression of genes important for cell cycle and positive regulation of mitotic cell cycle (including cyclin-dependent kinase 1 and 4; Cdk1: log2 fold-change= -0.4519, FDR= 4.24e-03; Cdk4: log2 fold-change= -0.3072, FDR= 0.003718), while the negative regulation of cell proliferation was increased following BI 853520 treatment (Fig. 3C; Suppl. Fig. 2C). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE116117 The FAK inhibitor BI 853520 exerts anti-tumor effects in breast cancer. Oncogenesis 5.995 https://doi.org/10.1038/s41389-018-0083-1 {Oncogenesis (5.995): 10.1038/s41389-018-0083-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA477312 https://www.ebi.ac.uk/ena/browser/view/PRJNA477312 https://www.ncbi.nlm.nih.gov/sra?term=SRP151030 [Overal design]BI 853520 was administered from day 15 post injection for five consecutive days. RNA was isolated from snap-frozen 4T1 primary tumor pieces and applied to next generation sequencing.; [Treatment]'BI 853520 was administered from day 15 post injection for five consecutive days.'; [Growth]'1,000,000 4T1 cells suspended in 100µl sterile PBS were injected into mammary fat pad number nine of anaesthetized, six to ten week- old female BALB/c mice.'; [Extraction]'Snap-frozen 4T1 mouse tumor pieces were homogenized in Trizol (Sigma-Aldrich) and total RNA was isolated with the RNeasy Lipid Tissue Mini Kit (Qiagen).\nApproximately 80 ng of total RNA were subsequently used for TruSeq Stranded mRNA Library preparation on the NeoPrep System (Illumina, San Diego, CA, USA) and sequenced on the HiSeq1500 with the paired-end 50 cycle protocol and the fast-output mode (Illumina, San Diego, CA, USA).'; [Cell type]'Source: ''agent: Natrosol; ', 'agent: BI 853520; ' GSE162804 Mus musculus 6 Expression profiling by high throughput sequencing GPL13112 ATF3-induced mammary tumors exhibit molecular features of human basal-like breast cancer 2020-12-07 Transcriptional profiling of mammary tumors that occurs in parous, BK5.ATF3 mice, compared to adjacent normal mammary tissue https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE162804 ATF3-Induced Mammary Tumors Exhibit Molecular Features of Human Basal-Like Breast Cancer. International journal of molecular sciences 4.183 https://doi.org/10.3390/ijms22052353 {International journal of molecular sciences (4.183): 10.3390/ijms22052353} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA683050 https://www.ebi.ac.uk/ena/browser/view/PRJNA683050 https://www.ncbi.nlm.nih.gov/sra?term=SRP296815 [Overal design]Two-condition experiment, BK5.ATF3-induced mammary tumors v. adjacent normal mammary glands. Biological replicates: 3 tumors, 3 paired normal glands.; [Treatment]'Females were allowed to breed and raise one litter of pups. Mammary tumors arose in most transgenic mice between 6 months and 12 months of age. When tumors reached 1.5 cm in length, animals were sacrificed under CO2 and the tumor was quickly dissected. Adjacent normal mammary glands were obtained from each tumor-bearing mouse.'; [Growth]'Transgenic female BK5.ATF3 mice were bred and raised in an A AALAC-accredited facility on standard lab chow.'; [Extraction]"Total RNA was extracted using Trizol following manufacturer's instructions.\nOvation RNA-Seq System V2 from NuGEN Technologies, Inc. was used to prepare RNA-Seq libraries following manufacturer's instructions."; [Cell type]'Source: ''tissue: mammary gland; genotype: ATF3 transgenic; tissue type: normal mammary gland; ', 'tissue: mammary gland; genotype: ATF3 transgenic; tissue type: mammary tumor; ' GSE50695 Homo sapiens 40 Expression profiling by array GPL571 Endocrine response in invasive lobular carcinoma is characterized by unique estrogen-mediated gene expression and de novo tamoxifen resistance 2013-09-09 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50695 Invasive lobular carcinoma cell lines are characterized by unique estrogen-mediated gene expression patterns and altered tamoxifen response. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-13-2779 {Cancer research (8.378): 10.1158/0008-5472.CAN-13-2779} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA218513 https://www.ebi.ac.uk/ena/browser/view/PRJNA218513 None [Overal design]Refer to individual Series; [Treatment]'Following deprivation, cells were treated for 3 or 24 hours with 1nM E2 or vehicle (0.01% EtOH).'; [Growth]'Cells were hormone deprived by replacing growth medium with IMEM+10% charcoal stripped serum for 3 days.'; [Extraction]'Following treatment, cells were lysed and RNA was harvested using the Illustra RNAspin Mini kit (GE Health)'; [Cell type]'Source: ''tissue: Cell culture; source: ATCC; cell line: MM134; treatment: baseline; time: 0hr; ', 'tissue: Cell culture; source: ATCC; cell line: MM134; treatment: vehicle; time: 3hr; ', 'tissue: Cell culture; source: ATCC; cell line: MM134; treatment: E2; time: 3hr; ', 'tissue: Cell culture; source: ATCC; cell line: MM134; treatment: vehicle; time: 24hr; ', 'tissue: Cell culture; source: ATCC; cell line: MM134; treatment: baseline; time: 24hr; ', 'tissue: Cell culture; source: Asterand; cell line: SUM44; treatment: baseline; time: 0hr; ', 'tissue: Cell culture; source: Asterand; cell line: SUM44; treatment: vehicle; time: 3hr; ', 'tissue: Cell culture; source: Asterand; cell line: SUM44; treatment: E2; time: 3hr; ', 'tissue: Cell culture; source: Asterand; cell line: SUM44; treatment: vehicle; time: 24hr; ', 'tissue: Cell culture; source: Asterand; cell line: SUM44; treatment: baseline; time: 24hr; ' GSE137326 Rattus norvegicus 6 Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing GPL24688 Transcriptional Profiling of Lumbar Spinal Cord in a Rat Model of Bone Cancer Pain 2019-09-12 Bone cancer pain (BCP), in which the majority is caused by metastasis from other cancer sites, is the most common type of chronic cancer pain. Bone cancer pain is developed accompanied by changes of numerous genes expression, from peripheral to central nervous system, which may account for this dysfunctional nociceptive perception. Although the pivotal role of lncRNA in neuropathic pain are well acknowledged, the involvement of lncRNA in bone cancer pain development are remain to be clarified. Thus, in the present study we performed transcriptome sequencing to explore changes in expression profiles of lncRNA and mRNA to provide a landscape of dysregulated lncRNA and mRNA in spinal cord of bone cancer pain. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE137326 Transcriptomic analysis of long noncoding RNAs and mRNAs expression profiles in the spinal cord of bone cancer pain rats. Molecular brain 4.051 https://doi.org/10.1186/s13041-020-00589-2 {Molecular brain (4.051): 10.1186/s13041-020-00589-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA565189 https://www.ebi.ac.uk/ena/browser/view/PRJNA565189 https://www.ncbi.nlm.nih.gov/sra?term=SRP221473 [Overal design]On the fourteenth day after tumor inoculation, total RNA was extracted from the ipsilateral side of spinal cord of bone-cancer-pained and sham-operated Wistar rats, in triplicates, and high throughput sequencing of ncRNA and mRNA was performed by Illumina HiSeq X Ten.; [Treatment]'Approximately (1-5) ×10e5 living or heat-killed Walker 256 breast cancer cells were implanted into medullary cavity of left tibia'; [Growth]'None'; [Extraction]'The lumbar enlargement spinal cord was quickly isolated out, removed the meninges, and dissected longitudinally on ice; then the ipsilateral spinal cord was snap-frozen and preserved in liquid nitrogen. Total RNA was extracted using RNeasy Mini Kit (Cat#74106, Qiagen)following the manufacturer’s instructions and checked for a RIN number to inspect RNA integrity by an Agilent Bioanalyzer 2100 (Agilent technologies, Santa Clara, CA, US).Qualified total RNA was further purified by RNAClean XP Kit (Cat A63987, Beckman Coulter,Inc.Kraemer Boulevard Brea, CA,USA)and RNase-Free DNase Set (Cat#79254, QIAGEN, GmBH, Germany).\nStrand specific libraries were prepared using the TruSeq® Stranded Total RNA Sample Preparation kit (Illumina, USA). Briefly, ribosomal RNA was removed from total RNA by Ribo-Zero rRNA removal beads. Then fragmented RNA was copied into first strand cDNA using reverse transcriptase, followed by second strand cDNA synthesis using DNA Polymerase I and RNase H. After undergoing an end repair process, the addition of a single ‘A’ base, and then ligation of the adapters, cDNA fragments were purified and enriched with PCR to create the final cDNA library.'; [Cell type]'Source: ''strain: Wistar; tissue: spinal cord; treatment: control; time: 14 days after tumor inoculation of treated samples; condition: sham; ', 'strain: Wistar; tissue: spinal cord; treatment: breast cancer cells were implanted into medullary cavity of left tibia; time: 14 days after tumor inoculation of treated samples; condition: BCP; ' GSE99536 Homo sapiens 16 Expression profiling by high throughput sequencing GPL11154 Effect of low-dose sorafenib and alkylating agents in inflammation and angiogenesis in breast cancer 2017-06-01 Molecular targeted compounds are emerging as important component to improve the efficacy of classical chemotherapeutics. In this study, we tested whether using low dose sorafenib to reduce off target inhibitions of kinases impacts the antitumor effect of alkylating agents in breast cancer models. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99536 Sorafenib improves alkylating therapy by blocking induced inflammation, invasion and angiogenesis in breast cancer cells. Cancer letters 6.508 https://doi.org/10.1016/j.canlet.2018.03.037 {Cancer letters (6.508): 10.1016/j.canlet.2018.03.037} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA388753 https://www.ebi.ac.uk/ena/browser/view/PRJNA388753 https://www.ncbi.nlm.nih.gov/sra?term=SRP108414 [Overal design]MDA-MB231 cells were treated with 1 μM sorafenib, 40 μg/mL MMS, or pre-incubated with 1 μM sorafenib for 12 h followed by 40 μg/mL MMS, each in two independent experiments. RNA was harvested 8 and 24 h, or post MMS treatment for combination treatment.; [Treatment]'Samples were treated with either vehicle (DMSO) or indicated doses of drug for indicated amout of time before extraction of RNA'; [Growth]'Cells were passaged in 10cm corningware dishes using media described in Samples section in a 37°C humidified incubator'; [Extraction]'Total RNA was extracted from sub-confluent 10cm dishes using Qiagen RNeasy kit\nRNA libraries were prepared for sequencing using Illumina TruSeq protocols'; [Cell type]'Breast cancer''cell line: MDA-MB231; cell type: Breast cancer; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: DMSO for 8 hours; ', 'cell line: MDA-MB231; cell type: Breast cancer; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: DMSO for 24 hours; ', 'cell line: MDA-MB231; cell type: Breast cancer; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: 40μM MMS for 8 hours; ', 'cell line: MDA-MB231; cell type: Breast cancer; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: 40μM MMS for 24 hours; ', 'cell line: MDA-MB231; cell type: Breast cancer; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: 1μM Sorafenib for 8 hours; ', 'cell line: MDA-MB231; cell type: Breast cancer; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: 1μM Sorafenib for 24 hours; ', 'cell line: MDA-MB231; cell type: Breast cancer; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: 1μM Sorafenib followed by 40μM MMS for 8 hours; ', 'cell line: MDA-MB231; cell type: Breast cancer; growth protocol: Cells were grown in DMEM supplemented with 10%FBS; treatment prototcol: 1μM Sorafenib followed by 40μM MMS for 24 hours; ' GSE18494 Homo sapiens 36 Expression profiling by array GPL9419 Expression profiling of hypoxic HepG2 hepatoma, U87 glioma, and MDA-MB231 breast cancer cells: time course 2009-10-09 Analysis of expression changes of cultured HepG2 hepatoma, U87 glioma, and MDA-MB231 breast cancer cells subjected to hypoxia (0.5% O2) for 0, 4, 8, 12 hours . Results provide insight to cell type-specific response to hypoxia. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE18494 Preferential binding of HIF-1 to transcriptionally active loci determines cell-type specific response to hypoxia. Genome biology 14.028 https://doi.org/10.1186/gb-2009-10-10-r113 {Genome biology (14.028): 10.1186/gb-2009-10-10-r113} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA123717 https://www.ebi.ac.uk/ena/browser/view/PRJNA123717 None [Overal design]HepG2 hepatoma, U87 glioma, and MDA-MB231 breast cancer cells were collected under normoxic conditions (~19% O2, 0 hours) and after 4, 8 and 12 hours of hypoxia treatment (0.5% O2). For each cell line, three replicates of total RNA at each time point were prepared using Trizol and submitted to the DFCI Microarray Core for labeling, hybridization to Affymetrix HG-U133Plus2 oligonucleotide arrays and image scanning.; [Treatment]'HepG2 hepatoma, U87 glioma, and MDA-MB231 breast cancer cells were collected under normoxic conditions (~19% O2, 0 hours) and after 4, 8 and 12 hours of hypoxia treatment (0.5% O2).'; [Growth]'None'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: HepG2 hepatoma; stress: normoxia; time: control; ', 'cell line: HepG2 hepatoma; stress: hypoxia; time: 4h; ', 'cell line: HepG2 hepatoma; stress: hypoxia; time: 8h; ', 'cell line: HepG2 hepatoma; stress: hypoxia; time: 12h; ', 'cell line: U87 glioma; stress: normoxia; time: control; ', 'cell line: U87 glioma; stress: hypoxia; time: 4h; ', 'cell line: U87 glioma; stress: hypoxia; time: 8h; ', 'cell line: U87 glioma; stress: hypoxia; time: 12h; ', 'cell line: MDA-MB231 breast cancer; stress: normoxia; time: control; ', 'cell line: MDA-MB231 breast cancer; stress: hypoxia; time: 4h; ', 'cell line: MDA-MB231 breast cancer; stress: hypoxia; time: 8h; ', 'cell line: MDA-MB231 breast cancer; stress: hypoxia; time: 12h; ' GSE39564 Homo sapiens 24 Expression profiling by array GPL10558 Transducin-like enhancer protein 1 mediates estrogen receptor binding and transcriptional activity in breast cancer cells 2012-07-23 Transducin-like enhancer protein 1 mediates estrogen receptor binding and transcriptional activity in breast cancer cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39564 Transducin-like enhancer protein 1 mediates estrogen receptor binding and transcriptional activity in breast cancer cells. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1018863108 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1018863108} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA171140 https://www.ebi.ac.uk/ena/browser/view/PRJNA171140 None [Overal design]TLE1 silenced breast cancer MCF-7 cell lines or control siRNA in the presence of Estrogen or a vehicle. MCF-7 cells were hormone-depleted for 3 d and treated with 100 nM estrogen (or vehicle) for 6 h. There were six biological replicates for each of the four different groups.; [Treatment]'Estrogen was added at a final concentration of 100 nM for 6 hours.'; [Growth]'MCF-7 human cell lines were grown as described previously (Neve et al. 2006, Cancer Cell 10:515–527).'; [Extraction]'Total RNA was extracted using the QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. A DNase I digestion was included. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''cell line: MCF-7; ' GSE84578 Homo sapiens 6 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Integrated analyses identify phenotype specific BMP4 signaling in breast cancer [Dnase-seq] 2016-07-19 Bone morphogenetic protein 4 (BMP4) plays an important role in cancer pathogenesis. In breast cancer, it reduces proliferation and increases migration in a cell line-dependent manner. To characterize the transcriptional mediators of these phenotypes, we performed RNA-seq and DNase-seq analyses after BMP4 treatment in MDA-MB-231 and T-47D breast cancer cells that respond to BMP4 with enhanced migration and decreased cell growth, respectively. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE84578 Integrated RNA-seq and DNase-seq analyses identify phenotype-specific BMP4 signaling in breast cancer. BMC genomics 3.501 https://doi.org/10.1186/s12864-016-3428-1 {BMC genomics (3.501): 10.1186/s12864-016-3428-1} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA329671 https://www.ebi.ac.uk/ena/browser/view/PRJNA329671 https://www.ncbi.nlm.nih.gov/sra?term=SRP078932 [Overal design]We characterized the Dnase I hypersensitive sites BMP4 treated and non-treated MDA-MB-231 and T-47D cells using Dnase-seq; [Treatment]'Cells were treated either with 100 ng/ml recombinant human BMP4 protein (BM4 treatment) or BMP4 dilution solution (non-treated vehicle) for 3h'; [Growth]'Cells were seeded and were grown to 80-90% confluency before treatment'; [Extraction]'The nuclei were extracted using protocol similar to Song and Crawford 2010 and the DNase I digestion was done according to Ling and Waxman 2013.\nThe library preparation was done according to library construction protocol of BGI'; [Cell type]'Source: ''datatype: DnaseSeq; cell line: MDA-MB_231; cell karyotype: breast cancer; treatment: BMP4 (100 ng/ml); treatment description: 3 hours treatment with BMP4 (100 ng/ml); ', 'datatype: DnaseSeq; cell line: MDA-MB_231; cell karyotype: breast cancer; treatment: None; treatment description: None; ', 'datatype: InputDNA; cell line: MDA-MB_231; cell karyotype: breast cancer; treatment: BMP4 (100 ng/ml); treatment description: 3 hours treatment with BMP4 (100 ng/ml); ', 'datatype: DnaseSeq; cell line: T-47D; cell karyotype: breast cancer; treatment: BMP4 (100 ng/ml); treatment description: 3 hours treatment with BMP4 (100 ng/ml); ', 'datatype: DnaseSeq; cell line: T-47D; cell karyotype: breast cancer; treatment: None; treatment description: None; ', 'datatype: InputDNA; cell line: T-47D; cell karyotype: breast cancer; treatment: None; treatment description: None; ' GSE16511 Homo sapiens 47 Genome variation profiling by genome tiling array GPL4560 CGH profiles of BRCA2-mutated breast tumors 2009-06-09 Prediction of BRCA2-association in hereditary breast carcinomas with array-CGH https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE16511 Prediction of BRCA2-association in hereditary breast carcinomas using array-CGH. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-010-1016-7 {Breast cancer research and treatment (3.471): 10.1007/s10549-010-1016-7} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA116067 https://www.ebi.ac.uk/ena/browser/view/PRJNA116067 None [Overal design]Chromosomal aberrations in BRCA2 samples; [Treatment]'None'; [Growth]'None'; [Extraction]'As decribed in:\nPrediction of BRCA1-association in hereditary non-BRCA1/2 breast carcinomas with array-CGH.\nJoosse SA, van Beers EH, Tielen IH, Horlings H, Peterse JL, Hoogerbrugge N, Ligtenberg MJ, Wessels LF, Axwijk P, Verhoef S, Hogervorst FB, Nederlof PM.\nBreast Cancer Res Treat. 2008 Aug 14', 'Prediction of BRCA1-association in hereditary non-BRCA1/2 breast carcinomas with array-CGH.\nJoosse SA, van Beers EH, Tielen IH, Horlings H, Peterse JL, Hoogerbrugge N, Ligtenberg MJ, Wessels LF, Axwijk P, Verhoef S, Hogervorst FB, Nederlof PM.\nBreast Cancer Res Treat. 2008 Aug 14', 'As decribed in:\nPrediction of BRCA1-association in hereditary non-BRCA1/2 breast carcinomas with array-CGH.\nJoosse SA, et al.\nBreast Cancer Res Treat. 2008 Aug 14', 'Prediction of BRCA1-association in hereditary non-BRCA1/2 breast carcinomas with array-CGH.\nJoosse SA, et al.\nBreast Cancer Res Treat. 2008 Aug 14'; [Cell type]'Source: ', 'peripheral blood lymphocytes''organ: mammary gland; disease: infiltrating ductal carcinoma; genotype: mutation in the BRCA2 gene; ', 'sample: A pool of DNA from peripheral blood lymphocytes, from 7 apparently healty women.; disease: healthy appearing; cell type: peripheral blood lymphocytes; ' GSE124347 Homo sapiens 42 Expression profiling by array GPL570 TP53 wild type cells are resistant to arsenic trioxide induced dynamic transcriptional changes 2018-12-25 Previous and our results show that cells with mutant p53 are more sensitive to arsenic trioxide (ATO) induced cell growth inhibition. To explore the underling mechanisms, we conduct a detailed analysis of the globe transcriptional profiles of ATO regulated genes in breast, colon and lung cancer cells with different p53 status. We find p53 wild type cells are resistant to ATO induced globe dynamic transcriptional changes, thus resistant to ATO induced cell growth inhibition. P53 inhibitor PFTα releases p53 mediated transcriptional resistance and increases the sensitivity of ATO in p53 wild type tumor cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124347 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA511759 https://www.ebi.ac.uk/ena/browser/view/PRJNA511759 None [Overal design]Breast cancer SKBR3, MCF7, colon cancer SW620, HCT116 and lung cancer H1299, A549 cells were treated with ATO 5μM for 0, 6, 12, 24 and 36 hours. TP53 wild type MCF7, HCT116 and A549 cells were treated with the combination of ATO and TP53 inhibitor PFTα at 6h, 12h, 24h and 36 hours. Total RNA was collected and profiled to Affymetrix microarray.; [Treatment]'Breast cancer SKBR3, MCF7, colon cancer SW620, HCT116 and lung cancer H1299, A549 cells were treated with ATO 5μM for 0, 6, 12, 24 and 36 hours. TP53 wild type MCF7, HCT116 and A549 cells were treated with the combination of ATO and TP53 inhibitor PFTα at 6h, 12h, 24h and 36 hours'; [Growth]'Breast cancer SKBR3, MCF7, colon cancer SW620, HCT116 and lung cancer H1299, A549 cells were cultured on plates in 10% FBS.'; [Extraction]'Cellular RNA was isolated by Tri-Reagent using the manufacturer’s instructions. Qualified total RNA was further purified by RNeasy micro kit and RNase-Free DNase Set.'; [Cell type]'Source: ''time point: 0H; disease: lung cancer; agent: ATO; cell line: A549; ', 'time point: 6H; disease: lung cancer; agent: ATO; cell line: A549; ', 'time point: 12H; disease: lung cancer; agent: ATO; cell line: A549; ', 'time point: 24H; disease: lung cancer; agent: ATO; cell line: A549; ', 'time point: 36H; disease: lung cancer; agent: ATO; cell line: A549; ', 'time point: 6H; disease: lung cancer; agent: ATO and PFTalpha; cell line: A549; ', 'time point: 12H; disease: lung cancer; agent: ATO and PFTalpha; cell line: A549; ', 'time point: 24H; disease: lung cancer; agent: ATO and PFTalpha; cell line: A549; ', 'time point: 36H; disease: lung cancer; agent: ATO and PFTalpha; cell line: A549; ', 'time point: 0H; disease: lung cancer; agent: ATO; cell line: H1299; ', 'time point: 6H; disease: lung cancer; agent: ATO; cell line: H1299; ', 'time point: 12H.; disease: lung cancer; agent: ATO; cell line: H1299; ', 'time point: 24H.; disease: lung cancer; agent: ATO; cell line: H1299; ', 'time point: 36H.; disease: lung cancer; agent: ATO; cell line: H1299; ', 'time point: 0H; disease: colon cancer; agent: ATO; cell line: HCT116; ', 'time point: 6H; disease: colon cancer; agent: ATO; cell line: HCT116; ', 'time point: 12H; disease: colon cancer; agent: ATO; cell line: HCT116; ', 'time point: 24H; disease: colon cancer; agent: ATO; cell line: HCT116; ', 'time point: 36H; disease: colon cancer; agent: ATO; cell line: HCT116; ', 'time point: 12H; disease: colon cancer; agent: ATO and PFTalpha; cell line: HCT116; ', 'time point: 24H; disease: colon cancer; agent: ATO and PFTalpha; cell line: HCT116; ', 'time point: 36H; disease: colon cancer; agent: ATO and PFTalpha; cell line: HCT116; ', 'time point: 6H; disease: colon cancer; agent: ATO and PFTalpha; cell line: HCT116; ', 'disease: colon cancer; agent: ATO; cell line: SW620; ', 'time point: 0H; disease: breast cancer; agent: ATO; cell line: MCF7; ', 'time point: 6H; disease: breast cancer; agent: ATO; cell line: MCF7; ', 'time point: 12H; disease: breast cancer; agent: ATO; cell line: MCF7; ', 'time point: 24H; disease: breast cancer; agent: ATO; cell line: MCF7; ', 'time point: 36H; disease: breast cancer; agent: ATO; cell line: MCF7; ', 'time point: 6H; disease: breast cancer; agent: ATO and PFTalpha; cell line: MCF7; ', 'time point: 12H; disease: breast cancer; agent: ATO and PFTalpha; cell line: MCF7; ', 'time point: 24H; disease: breast cancer; agent: ATO and PFTalpha; cell line: MCF7; ', 'time point: 36H; disease: breast cancer; agent: ATO and PFTalpha; cell line: MCF7; ', 'time point: 0H; disease: breast cancer; agent: ATO; cell line: SKBR3; ', 'time point: 6h; disease: breast cancer; agent: ATO; cell line: SKBR3; ', 'time point: 12h; disease: breast cancer; agent: ATO; cell line: SKBR3; ', 'time point: 24h; disease: breast cancer; agent: ATO; cell line: SKBR3; ', 'time point: 36h; disease: breast cancer; agent: ATO; cell line: SKBR3; ' GSE98181 synthetic construct 48 Non-coding RNA profiling by array GPL21572 Circulating miRNA profiles from serum of women at high-risk for breast cancer 2017-04-25 Circulating microRNAs (c-miRNAs) have emerged as measurable biomarkers (liquid biopsies) for cancer detection. The goal of our study was to identify novel biomarkers to predict long-term breast cancer risk in cancer-free women. We evaluated the ability of c-miRNAs to identify women most likely to develop breast cancer by profiling miRNA from serum obtained long before diagnosis. 24 breast cancer cases and controls (matched for risk and age) were identified from women enrolled in the High-Risk Breast Program at the UVM Cancer Center. We used Affymetrix miRNA v4 microarrays to interrogate miRNAs (miRBase v20) in the serum of cancer-free women at high-risk for breast cancer. The 24 cases developed breast cancer at least 6 months (average of 3.2 years) and the 24 controls remain cancer-free. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98181 Development of a predictive miRNA signature for breast cancer risk among high-risk women. Oncotarget None https://doi.org/10.18632/oncotarget.22750 {Oncotarget (None): 10.18632/oncotarget.22750} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA384216 https://www.ebi.ac.uk/ena/browser/view/PRJNA384216 None [Overal design]24 cases and 24 matched controls; [Treatment]'Serum is obtained from coagulated whole blood samples by centrifugation at 3000 rpm for 10 minutes. Serum aliquots are stored at -80°C within 1 hour of blood draw. Serum samples did not undergo previous freeze/thaw cycles.'; [Growth]'not applicable'; [Extraction]'RNA was isolated from a 200μL serum aliquot using the miRNeasy Serum Plasma kit with ce-miR-39 spike-in (QIAGEN), QIAcube (QIAGEN) automation, and eluted with 14uL of nuclease-free water. Multiple serum aliquots from the same patient were processed simultaneously, RNA pooled, and stored in small aliquots to isolate sufficient RNA for downstream applications.'; [Cell type]'Source: ''tissue: serum; group: control; gender: female; ', 'tissue: serum; group: case; gender: female; ' GSE148848 Homo sapiens 30 Non-coding RNA profiling by array; Expression profiling by array GPL17077; GPL21576 microRNA expression profiling of paired primary and lymph node metastatic breast cancer patients, and gene expression profiling of MDA-MB-231 cells transfected with hsa-miR-205-5p and hsa-miR-214-3p compared to scrambled miRNA precursors 2020-04-17 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148848 MicroRNA Expression Profiling on Paired Primary and Lymph Node Metastatic Breast Cancer Revealed Distinct microRNA Profile Associated With LNM. Frontiers in oncology 4.137 https://doi.org/10.3389/fonc.2020.00756 {Frontiers in oncology (4.137): 10.3389/fonc.2020.00756} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA625952 https://www.ebi.ac.uk/ena/browser/view/PRJNA625952 None [Overal design]Refer to individual Series; [Treatment]'NA', 'MDA-MB-231 cells (0.168 x 10e6 cells/ml) were transfected with the selected miRNA precursors (pre-miR–negative control, hsa-miR-205-5p and hsa-miR-214-3p) purchased from Ambion. Cell transfection was conducted employing a reverse transfection protocol.'; [Growth]'NA', 'MDA-MB-231 cells were grown in DMEM supplemented with 10% fetal bovine serum, 1% NEAA, 1% L-glutamine, 100 mg/l penicillin, and 100 mg/l streptomycin.'; [Extraction]'Total RNA was extracted from FFPE sections using the recover all total nucleic acid isolation kit (Ambion Inc., Life Technologies, USA) according to the manufacturer’s protocol.', 'Total RNA were isolated from control and treated cells using Total RNA Purification Kit (Norgen-Biotek Corp., Canada) according to the manufacturer’s instructions. The concentrations of total RNA were measured using NanoDrop 2000 (Thermo-Scientific).'; [Cell type]'Source: ', 'Breast cancer cell line''tissue: Lymph node metastasis; ', 'tissue: Paired primary breast cancer; ', 'cell line: MDA-MB-231; cell type: Breast cancer cell line; miRNA: has-miR-205-5p precursor; ', 'cell line: MDA-MB-231; cell type: Breast cancer cell line; miRNA: has-miR-214-3p precursor; ', 'cell line: MDA-MB-231; cell type: Breast cancer cell line; miRNA: scrambled microRNA; ' GSE59055 Homo sapiens 9 Expression profiling by array GPL10558 A newly identified spliced isoform of metadherin differently regulates the global transcriptomic profile in MCF-7 breast cancer cells 2014-07-03 The current study analyzed the metadherin (MTDH)-mediated altered gene expression profiles in ER positive MCF-7 cells. Some of these altered gene expressions were further inter connected to various pathways which may eventually be recognized as drug targets or biomarkers in those breast cancers where MTDH plays a role in cancer progression/metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59055 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA254219 https://www.ebi.ac.uk/ena/browser/view/PRJNA254219 None [Overal design]To understand the global differential gene expression profile in MTDH-wild type and a newly identified MTDH-isoform knock down in malignant breast cancer cells. This data was compared to untreated breast cancer cells.; [Treatment]'MCF-7 cells were transfected with siRNA of either MTDH-WT or MTDH-isoform (200 pmols) for 24 h.'; [Growth]'MCF-7 cells were grown in DMEM supplemented with 10 % Foetal Bovine Serum, 2mM glutamine and Pen-Strep'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''cell line: MCF7; disease state: Breast adenocarcinoma, estrogen receptor-positive; genotype/variation: Control; ', 'cell line: MCF7; disease state: Breast adenocarcinoma, estrogen receptor-positive; genotype/variation: MTDH WT KD; ', 'cell line: MCF7; disease state: Breast adenocarcinoma, estrogen receptor-positive; genotype/variation: MTDH isoform KD; ' GSE45335 Homo sapiens 2 Expression profiling by high throughput sequencing GPL10999 Genome-wide methylation and expression analysis of two breast cancer cell lines [RNA-Seq] 2013-03-20 To improve our understanding of the relationships between methylation and expression we profiled mRNA expression and single-base resolution methylation levels for two breast cancer cell lines, MCF7 and T47D. Expression was profiled using RNA-seq. Methylation was assayed using Methyl-MAPS, which uses methylation-sensitive and -dependent restriction enzyme digests followed by high-throughput sequencing to identify methylation levels at individual CpGs (Edwards et al. 2010, Genome Research). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE45335 Discovering high-resolution patterns of differential DNA methylation that correlate with gene expression changes. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkt482 {Nucleic acids research (11.147) doi:10.1093/nar/gkt482}; {Oncogene (6.634) doi:10.1038/onc.2016.397}; 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA193492 https://www.ebi.ac.uk/ena/browser/view/PRJNA193492 https://www.ncbi.nlm.nih.gov/sra?term=SRP019817 [Overal design]RNA-Seq was used to generate mRNA expression profiles of MCF7 and T47D cells under standard growth conditions.; [Treatment]'none'; [Growth]'MCF7 and T47D cell lines were maintained in RPMI 1640 medium supplemented with 5% fetal bovine serum, 10 mmol/L HEPES, 4.5 g/L glucose, 2 mmol/L L-glutamine, 1 mmol/L sodium pyruvate, and 50 µg/ml gentamicin in a humidified 37°C incubator containing 5% carbon dioxide.'; [Extraction]'Total RNA (10 ug) was isolated from MCF7 and T47D cells, DNase treated, and twice oligo(dT) selected using the Dynabeads mRNA purification kit (Invitrogen).\nRNA-seq libraries were constructed using the NEBNext Kit from New England Biolabs. MCF7_1 and T47D_1 libraries were constructed with custom 4 bp barcodes and sequenced with an Illumina GAIIx (32 bp single-end reads). MCF7_2 and T47D_2 libraries were constructed with standard Illumina indexed primers and sequenced using Illumina HiSeq 2000 (42 bp single-end reads).'; [Cell type]'human breast cancer''cell line: MCF7; cell type: human breast cancer; ', 'cell line: T47D; cell type: human breast cancer; ' GSE41656 Homo sapiens 60 Expression profiling by array GPL6884 Gene expression analysis of a series of HER2+ of breast tumors 2012-10-17 Abstract Motivation Breast cancer is a heterogeneous disease with distinct subtypes. Even within these subtypes differences at the molecular level are present which are reflected in variable responses to chemotherapy. We set out to identify genes associated with chemotherapy resistance by analyzing a set of HER2-positive breast cancers. Methods We collected, gene expression profiled and analyzed 60 HER2-positive breast tumor biopsies, obtained from patients scheduled to undergo neoadjuvant therapy. In addition to conventional supervised approaches for the detection of reporters of resistance, we report on a novel approach specifically tailored to the detection of small groups of resistant samples that show aberrant gene expression patterns. Results We propose a novel analytical approach that takes heterogeneity in response into account. We show that this approach is more powerful than classical approaches for detecting small subgroups of samples showing aberrant expression in a controlled setting. We applied this approach to our 60 breast cancer samples prior to neoadjuvant chemotherapy, and generated candidate response reporter lists for each subtype. Discussion Using a novel analytical approach we report on the mRNA gene expression analysis of a cohort of breast cancers prior to neoadjuvant chemotherapy. An important characteristic of this approach is that it takes heterogeneity in neoadjuvant treatment response into account. Such approaches are needed to identify biomarkers for predicting treatment response. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41656 Identifying subgroup markers in heterogeneous populations. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkt845 {Nucleic acids research (11.147): 10.1093/nar/gkt845} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA177841 https://www.ebi.ac.uk/ena/browser/view/PRJNA177841 None [Overal design]We collected, gene expression profiled and analyzed 60 breast tumor biopsies, obtained from patients scheduled to undergo neoadjuvant therapy.; [Treatment]'None'; [Growth]'None'; [Extraction]'From the frozen biopsies approximately 30 sections of 30-μm thickness were used for total RNA isolation with RNABee (Campro Scientific, Amersfoort, The Netherlands). Isolated total RNA was subsequently DNase-treated by using the Qiagen RNase-free DNase kit and RNeasy spin columns (Qiagen, West Sussex, U.K.) and dissolved in RNase-free H2O.'; [Cell type]'Source: ''response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 0; ihc pr percentage: 0; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR+kl [(pathological) complete response breast, positive lymph nodes]; ihc er percentage: 100; ihc pr percentage: 100; intrinsic molecular subtype: LumA; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: PR+NR [Partial Response + No Response]; response: NOCR [No complete response]; ihc er percentage: 0; ihc pr percentage: 0; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: PR+NR [Partial Response + No Response]; response: NOCR [No complete response]; ihc er percentage: 0; ihc pr percentage: 0; intrinsic molecular subtype: Normal; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: PR+NR [Partial Response + No Response]; response: PD [progressive disease]; ihc er percentage: 100; ihc pr percentage: 0; intrinsic molecular subtype: LumB; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR+kl [(pathological) complete response breast, positive lymph nodes]; ihc er percentage: 40; ihc pr percentage: 0; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 80; ihc pr percentage: 0; intrinsic molecular subtype: Normal; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: PR+NR [Partial Response + No Response]; response: NOCR [No complete response]; ihc er percentage: 100; ihc pr percentage: 0; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: PR+NR [Partial Response + No Response]; response: NOCR [No complete response]; ihc er percentage: 100; ihc pr percentage: 50; intrinsic molecular subtype: LumB; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR+kl [(pathological) complete response breast, positive lymph nodes]; ihc er percentage: 0; ihc pr percentage: 0; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: NOCR [No complete response]; ihc er percentage: 0; ihc pr percentage: 0; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: PR+NR [Partial Response + No Response]; response: NOCR [No complete response]; ihc er percentage: 100; ihc pr percentage: 100; intrinsic molecular subtype: LumA; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 100; ihc pr percentage: 100; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR+kl [(pathological) complete response breast, positive lymph nodes]; ihc er percentage: 10; ihc pr percentage: 0; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: NA [Not Available]; response: NOCR [No complete response]; ihc er percentage: 100; ihc pr percentage: 100; intrinsic molecular subtype: LumA; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: NA [Not Available]; response: PD [progressive disease]; ihc er percentage: 0; ihc pr percentage: 0; intrinsic molecular subtype: Normal; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR+kl [(pathological) complete response breast, positive lymph nodes]; ihc er percentage: 100; ihc pr percentage: 1; intrinsic molecular subtype: LumB; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: NOCR [No complete response]; ihc er percentage: 100; ihc pr percentage: 100; intrinsic molecular subtype: LumA; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 100; ihc pr percentage: 50; intrinsic molecular subtype: LumA; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: PR+NR [Partial Response + No Response]; response: NOCR [No complete response]; ihc er percentage: 100; ihc pr percentage: 50; intrinsic molecular subtype: Basal; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: PR+NR [Partial Response + No Response]; response: NOCR [No complete response]; ihc er percentage: 50; ihc pr percentage: 0; intrinsic molecular subtype: LumB; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: PR+NR [Partial Response + No Response]; response: NOCR [No complete response]; ihc er percentage: 100; ihc pr percentage: 80; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 90; ihc pr percentage: 0; intrinsic molecular subtype: LumB; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: PR+NR [Partial Response + No Response]; response: NOCR [No complete response]; ihc er percentage: 100; ihc pr percentage: 10; intrinsic molecular subtype: Normal; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 50; ihc pr percentage: 5; intrinsic molecular subtype: LumA; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR+kl [(pathological) complete response breast, positive lymph nodes]; ihc er percentage: 70; ihc pr percentage: 10; intrinsic molecular subtype: LumA; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: NOCR [No complete response]; ihc er percentage: 100; ihc pr percentage: 0; intrinsic molecular subtype: Normal; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: PR+NR [Partial Response + No Response]; response: NOCR [No complete response]; ihc er percentage: 100; ihc pr percentage: 0; intrinsic molecular subtype: Normal; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 60; ihc pr percentage: 60; intrinsic molecular subtype: LumB; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 50; ihc pr percentage: 70; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 90; ihc pr percentage: 10; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR+kl [(pathological) complete response breast, positive lymph nodes]; ihc er percentage: 80; ihc pr percentage: 80; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 0; ihc pr percentage: 0; intrinsic molecular subtype: Normal; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR+kl [(pathological) complete response breast, positive lymph nodes]; ihc er percentage: 100; ihc pr percentage: 30; intrinsic molecular subtype: LumA; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: PR+NR [Partial Response + No Response]; response: NOCR [No complete response]; ihc er percentage: 100; ihc pr percentage: 100; intrinsic molecular subtype: Normal; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR+kl [(pathological) complete response breast, positive lymph nodes]; ihc er percentage: 100; ihc pr percentage: 30; intrinsic molecular subtype: LumB; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 0; ihc pr percentage: 0; intrinsic molecular subtype: Basal; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: NA [Not Available]; response: NE [Not evaluable]; ihc er percentage: 0; ihc pr percentage: 0; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: NOCR [No complete response]; ihc er percentage: 0; ihc pr percentage: 0; intrinsic molecular subtype: Normal; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 20; ihc pr percentage: 0; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 100; ihc pr percentage: NA; intrinsic molecular subtype: LumB; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ', 'response breast: pCR+npCR mamma [pathological complete response + near pathological complete response mamma]; response: CR [(pathological) complete response]; ihc er percentage: 100; ihc pr percentage: 50; intrinsic molecular subtype: Her2; treatment: PTC; clinical subtype: HER2; tissue: breast cancer tumor; ' GSE16231 Rattus norvegicus 10 Expression profiling by array GPL1355 Differentially expressed genes after treatment with adriamycin in DMBA-induced rat breast tumors 2009-05-26 The aim of this study was to compare the gene expression profile changes of DMBA-induced rat breast tumors after treatment with adriamycin. To this end, a cDNA microarray was performed (Affymetrix’s Rat Genome 230 2.0 array). This gene expression study was carried out on the tumor biopsy samples prior to adriamycin treatment, and compared with matched tumor biopsy samples after completion of the adriamycin treatment schedule. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE16231 Hydroxytyrosol inhibits growth and cell proliferation and promotes high expression of sfrp4 in rat mammary tumours. Molecular nutrition & food research 4.653 https://doi.org/10.1002/mnfr.201000220 {Molecular nutrition & food research (4.653): 10.1002/mnfr.201000220} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA115165 https://www.ebi.ac.uk/ena/browser/view/PRJNA115165 None [Overal design]Breast tumors were induced with a single oral dosage of 7,12-dimethylbenz(alpha)anthracene (100 mg/kg body weight) in female Sprague-Dawley rats and subsequently treated with adriamycin (1 mg/kg body weight/week for 6 weeks) intravenously through lateral tail vein. Gene expression analysis was performed in paired samples as follows: ADR final trucut tumor vs initial trucut tumor (ADR final vs basal). For this assay, 5 samples were chosen according to histopathologic criteria (Bloom-Richardson grade II). Gene expression profiling was carried out using Affymetrix’s GeneChip technology, using the Rat Genome 230 2.0 array from this provider. All the protocols and apparatus were recommended by Affymetrix. Total RNA from frozen mammary tumors was extracted by RNeasy Mini kit and homogenized by QIAshredder columns according to manufacturer’s instructions. The quality and quantity of the obtained RNA was checked out through agarose electrophoresis and later spectrophotometry at 260/280 nm. Biotinylated cRNA was synthesized following the IVT labeling kit from Affymetrix and purified by the GeneChip Sample Cleanup Module from Affymetrix. The quality and quantity of the obtained cRNA was again checked out through agarose electrophoresis and posterior spectrophotometry at 260/280 nm. After hybridization, slides were washed and scanned following the manufacturer’s standard protocol. Intensity values were normalized by Robust Multichip Average method and subsequently these were filtered to remove the control sequences and those with a hybridization signal close to background. The spike controls were: BioB, BioC, BioD and Cre; because BioB was the least abundant in the samples, it was used to estimate the sensitivity of the experiment. The housekeeping control was GAPDH. After non-supervised clustering using Pearson correlation coefficient, statistical significance of gene expression was estimated by Student’s T test for paired samples, using GeneSpring GX 7.3 software (Agilent).; [Treatment]'RNA was preserved using RNAlater (Quiagen) for 24h and frozen at -80ºC until RNA extraction protocol'; [Growth]'None'; [Extraction]'Total RNA was extracted using a RNeasy Mini Kit from Qiagen, and later homogenized with QIAshredder (Quiagen) columns. Quality and quantity was assessed by agarose electrophoresis and spectrophotometric analysis (Absorbance 260/280 nm)'; [Cell type]'Source: ''strain: Sprague-Dawley; gender: female; age: 12 weeks; tissue: Breast tumor. Trucut Biopsy of breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene before treatment with adriamycin. Such biopsy was taken when tumor had 2cm3 volume.; biopsy dimensions: 0.7 cm x 2.5 mm; treatment: none; sample: 09I1 (basal); ', 'strain: Sprague-Dawley; gender: female; age: 19 weeks; tissue: Breast tumor. Breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene at the moment of sacrifice.; treatment: adriamycin (1 mg/kg weight/week, for 6 weeks) through the lateral tail vein after trucut biopsy.; sacrifice: 7th week post-biopsy; sample: 09I1 (final); ', 'strain: Sprague-Dawley; gender: female; age: 12 weeks; tissue: Breast tumor. Trucut Biopsy of breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene before treatment with adriamycin. Such biopsy was taken when tumor had 2cm3 volume.; biopsy dimensions: 0.7 cm x 2.5 mm; treatment: none; sample: 11D2 (basal); ', 'strain: Sprague-Dawley; gender: female; age: 19 weeks; tissue: Breast tumor. Breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene at the moment of sacrifice.; treatment: adriamycin (1 mg/kg weight/week, for 6 weeks) through the lateral tail vein after trucut biopsy.; sacrifice: 7th week post-biopsy; sample: 11D2 (final); ', 'strain: Sprague-Dawley; gender: female; age: 12 weeks; tissue: Breast tumor. Trucut Biopsy of breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene before treatment with adriamycin. Such biopsy was taken when tumor had 2cm3 volume.; biopsy dimensions: 0.7 cm x 2.5 mm; treatment: none; sample: 12I1 (basal); ', 'strain: Sprague-Dawley; gender: female; age: 19 weeks; tissue: Breast tumor. Breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene at the moment of sacrifice.; treatment: adriamycin (1 mg/kg weight/week, for 6 weeks) through the lateral tail vein after trucut biopsy.; sacrifice: 7th week post-biopsy; sample: 12I1 (final); ', 'strain: Sprague-Dawley; gender: female; age: 12 weeks; tissue: Breast tumor. Trucut Biopsy of breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene before treatment with adriamycin. Such biopsy was taken when tumor had 2cm3 volume.; biopsy dimensions: 0.7 cm x 2.5 mm; treatment: none; sample: 29I1 (basal); ', 'strain: Sprague-Dawley; gender: female; age: 19 weeks; tissue: Breast tumor. Breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene at the moment of sacrifice.; treatment: adriamycin (1 mg/kg weight/week, for 6 weeks) through the lateral tail vein after trucut biopsy.; sacrifice: 7th week post-biopsy; sample: 29I1 (final); ', 'strain: Sprague-Dawley; gender: female; age: 12 weeks; tissue: Breast tumor. Trucut Biopsy of breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene before treatment with adriamycin. Such biopsy was taken when tumor had 2cm3 volume.; biopsy dimensions: 0.7 cm x 2.5 mm; treatment: none; sample: 43D1 (basal); ', 'strain: Sprague-Dawley; gender: female; age: 19 weeks; tissue: Breast tumor. Breast tumor chemically induced with 7,12-dimethylbenz(a)anthracene at the moment of sacrifice.; treatment: adriamycin (1 mg/kg weight/week, for 6 weeks) through the lateral tail vein after trucut biopsy.; sacrifice: 7th week post-biopsy; sample: 43D1 (final); ' GSE110651 Homo sapiens 147 Non-coding RNA profiling by array GPL21263 Prediction for the development of new distant metastases using serum microRNAs in patients with metastatic breast cancer treated with eribulin 2018-02-15 The combination of serum miRNAs could be a classifier for predicting the development of new distant metastasis in breast cancer patients during the treatment of eribulin https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE110651 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA434193 https://www.ebi.ac.uk/ena/browser/view/PRJNA434193 None [Overal design]Serum microRNA profiles and clinical characteristics of 147 woman with breast cancer; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted each from 300uL serum samples using 3D-Gene® RNA extraction reagent from liquid sample kit (Toray Industries, Inc.).'; [Cell type]'Source: ''disease state: metastatic breast cancer; age: 61; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 64; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 65; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 37; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 48; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 62; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 69; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 57; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 50; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 44; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 53; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 59; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 54; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 60; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 43; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 40; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 51; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 66; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 52; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 62; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 38; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 45; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 74; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 37; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 47; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 44; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 63; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 54; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 68; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 46; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 32; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 75; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 47; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 65; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 59; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 42; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 64; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 33; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 55; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 56; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 49; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 46; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 35; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 40; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 57; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 49; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 34; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 68; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 76; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 60; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 52; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 58; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 56; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 73; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 50; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 69; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 55; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 73; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 76; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 67; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 58; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 41; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 53; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 78; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 43; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 41; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 45; new distant metastasis: Yes; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 71; new distant metastasis: No; tissue: Serum; ', 'disease state: metastatic breast cancer; age: 48; new distant metastasis: Yes; tissue: Serum; ' GSE12080 Homo sapiens 16 Expression profiling by array GPL7025 Gene expression signature involved in estrogen receptor status and prognosis of breast cancers. 2008-07-11 Fine needle aspiration biopsies (FNABs) of breast cancers were taken before and after surgeries from 16 patients. The cDNA microarray data were used to determine the gene expression profile responding to patient's clinical finding and tumor's pathological changes. A gene profile was generated as Estrogen Receptor Gene Signature (ERGS). The ERGS was verified in a reference dataset and correlated with patient's prognosis significantly. Keywords: Breast cancer, fine needle biopsy, estrogen receptor, prognostic gene signature https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE12080 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA113339 https://www.ebi.ac.uk/ena/browser/view/PRJNA113339 None [Overal design]Dye-swap technical replicates were included both FNABs taken before and after surgeries for every patient, then the four replicated array data per patient were combined for analysis.; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA was extracted using RNAeasy Micro kit (Qiagen) then amplified using the MessageAmp aRNA kit (Ambion) according to the manufacturer's instructions."; [Cell type]'Source: ''' GSE110451 Homo sapiens 15 Expression profiling by high throughput sequencing GPL18573 Profiling in vivo Bone Lesion (IVBL) and Orthotopic tumors by Next Generation Sequencing 2018-02-10 Based on RNA-seq, we performed transcriptomic profiling to examine the differences between Orthotopic and IVBL (in vivo bone lesion). We found Calcium signalling is upregulated in IVBL and correlated to the expression of gap junctions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE110451 The Osteogenic Niche Is a Calcium Reservoir of Bone Micrometastases and Confers Unexpected Therapeutic Vulnerability. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2018.10.002 {Cancer cell (23.916): 10.1016/j.ccell.2018.10.002} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA433732 https://www.ebi.ac.uk/ena/browser/view/PRJNA433732 https://www.ncbi.nlm.nih.gov/sra?term=SRP132630 [Overal design]Orthotopic tumors and Bone lesions, all developed by MCF-7, are subject to NGS and then analyzed.; [Treatment]'None'; [Growth]'MCF-7 cells are cultured in DMEM with 10% FBS and then serve for mammary pad injection (Orthotopic tumor) or intra-illiac injection (IVBL tumor).'; [Extraction]'After homogenization, total RNA were extracted by Direct-zol RNA miniprep kit. . The first and second strand cDNA were prepared by SuperScript III First-Strand Synthesis System and NEBNext mRNA Second Strand Synthesis Module from at least 200ng total RNA for each sample. Illumina Nextera XT DNA Sample Prep Kit was used with 1 ng of dsDNA for the construction of sequencing libraries.\nRNA libraries were prepared for sequencing using nextera Illumina protocols'; [Cell type]'Source: ''tissue: xenograft bone lesion; derived from cell line: MCF-7; passage: P140-P142; reporter gene: Firefly Luciferase (MCF-7); ', 'tissue: xenograft breast tumor; derived from cell line: MCF-7; passage: P140-P142; reporter gene: Firefly Luciferase (MCF-7); ' GSE44836 Homo sapiens 26 Expression profiling by array GPL6480 Gene expression profile of breast cancer cells. 2013-03-04 We compared the gene expression profile of 26 breast cancer cell lines to identify variations associated with different phenotypes and molecular subtype. The panel includes 13 estrogen receptor negative (ER-) and 13 ER+ cell lines. Four of the ER- cell lines and 5 of the ER+ cell lines are HER2 positive. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE44836 Methylation of the claudin 1 promoter is associated with loss of expression in estrogen receptor positive breast cancer. PloS one 2.776 https://doi.org/10.1371/journal.pone.0068630 {PloS one (2.776): 10.1371/journal.pone.0068630} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA192571 https://www.ebi.ac.uk/ena/browser/view/PRJNA192571 None [Overal design]We have used 2-color gene expression arrays for two separate studies. The one described here compares the intensities of one color channel across 26 cell lines, as normalized signal intensities. The second color channel is not analyzed here and will be used in a separate study.; [Treatment]'None'; [Growth]'Cells were grown for three days changing media every day'; [Extraction]'Total RNA was isolated using TriZol (Invitrogen) followed by RNeasy Mini Kit (Qiagen) according to manufacturers’ manuals. RNA quality was assessed by Nanodrop-1000 spectrometer for OD260/280 and OD260/230 ratio and Bioanalyzer (Agilent Technologies).'; [Cell type]'Source: ''gender: Female; disease: Breast cancer; er: -; ', 'gender: Female; disease: Breast cancer; er: +; her2: +; ', 'gender: Female; disease: Breast cancer; er: +; ', 'gender: Female; disease: Breast cancer; er: -; her2: +; ' GSE149276 Homo sapiens 34 Expression profiling by high throughput sequencing GPL16791 Clinical characteristics and exploratory genomic analyses of germline BRCA1 or BRCA2 mutations in breast cancer 2020-04-24 gBRCA1/2 mutations increase the incidence of breast cancer (BC) by interrupting the homologous recombination repair (HRR) pathway. Although gBRCA1 and gBRCA2 BC have similar clinical profiles, different molecular characteristics have been observed. In this study, we conducted comprehensive genomic analyses and compared gBRCA1/2 BC. Sanger sequencing to identify gBRCA1/2 mutations was conducted in 2,720 patients, and gBRCA1 (n=128) and gBRCA2 (n=126) mutations were analyzed. Within that population, deep target sequencing (TS) and matched whole transcriptome sequencing (WTS) results were available for 46 and 34 patients, respectively. An internal database of breast-cancer patients with wildtype gBRCA was used to compile a TS (n=195) and WTS (n=137) reference dataset. Three specific mutation sites, p.Y130X (n=14) and p.1210Afs (n=13) in gBRCA1 and p.R294X (n=22) in gBRCA2, were comparably frequent. Immunohistochemistry subtyping determined that the incidence of triple negative BC was higher among those with a gBRCA1 mutation (71.9%), and estrogen receptor (ER)-positive BC was dominant in those with a gBRCA2 mutation (76.2%). gBRCA1/2 mutations were mutually exclusive with PIK3CA somatic mutations (P<0.05), and gBRCA1 frequently co-occurred with TP53 somatic mutations (P<0.05). The median tumor mutation burden was 6.53 per megabase (MB) in gBRCA1 and 6.44 per MB in gBRCA2. The expression of AR, ESR1, and PGR was significantly upregulated with gBRCA2 mutation compared with gBRCA1 mutation. gBRCA1 and gBRCA2 BC have similar clinical characteristics, but they have different molecular subtypes, co-altered somatic mutations, and gene expression patterns. Implications: Even though gBRCA1 and gBRCA2 mutations both alter HRR pathways, our results suggest that they generate different molecular characteristics and different mechanisms of carcinogenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE149276 Clinical Characteristics and Exploratory Genomic Analyses of Germline BRCA1 or BRCA2 Mutations in Breast Cancer. Molecular cancer research : MCR 4.484 https://doi.org/10.1158/1541-7786.MCR-19-1108 {Molecular cancer research : MCR (4.484): 10.1158/1541-7786.MCR-19-1108} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA627876 https://www.ebi.ac.uk/ena/browser/view/PRJNA627876 https://www.ncbi.nlm.nih.gov/sra?term=SRP258287 [Overal design]whole transcriptome sequencing of 34 breast cancer patients who have germline BRCA mutations by Illumina Hiseq 2500; [Treatment]'None'; [Growth]'None'; [Extraction]'Illumina TruSeq RNA Sample Prep Kit v2 was used with 1 ug of total RNA for the construction of sequencing libraries.\nSeqeuncing libraries were prepared using the TruSeq RNA Sample Preparation kit v2 (Illumina) using standard Illumina protocols.'; [Cell type]'Source: ''disease: breast cancer; age: 33 years; tissue: breast; ', 'disease: breast cancer; age: 31 years; tissue: breast; ', 'disease: breast cancer; age: 25 years; tissue: breast; ', 'disease: breast cancer; age: 35 years; tissue: breast; ', 'disease: breast cancer; age: 36 years; tissue: breast; ', 'disease: breast cancer; age: 38 years; tissue: breast; ', 'disease: breast cancer; age: 34 years; tissue: breast; ', 'disease: breast cancer; age: 47 years; tissue: breast; ', 'disease: breast cancer; age: 28 years; tissue: breast; ', 'disease: breast cancer; age: 49 years; tissue: breast; ', 'disease: breast cancer; age: 39 years; tissue: breast; ', 'disease: breast cancer; age: 46 years; tissue: breast; ', 'disease: breast cancer; age: 30 years; tissue: breast; ', 'disease: breast cancer; age: 29 years; tissue: breast; ', 'disease: breast cancer; age: 32 years; tissue: breast; ', 'disease: breast cancer; age: 41 years; tissue: breast; ' GSE168672 Homo sapiens 8 Expression profiling by high throughput sequencing GPL11154 Next Generation Sequencing identifies TAZ transcriptional targets in tumor derived isogenic cells 2021-03-10 To gain a broader perspective of the underlying biological processes used by TAZ-dependent (TAZDEP) and TAZ-independent (TAZIND) cells for the maintenance of their BCSC phenotypes, we performed an RNA-seq analysis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE168672 Identification of TAZ-Dependent Breast Cancer Vulnerabilities Using a Chemical Genomics Screening Approach. Frontiers in cell and developmental biology 5.206 https://doi.org/10.3389/fcell.2021.673374 {Frontiers in cell and developmental biology (5.206): 10.3389/fcell.2021.673374} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA713361 https://www.ebi.ac.uk/ena/browser/view/PRJNA713361 https://www.ncbi.nlm.nih.gov/sra?term=SRP310156 [Overal design]4 replicates of each isogenic line; [Treatment]'None'; [Growth]'TAZDEP and TAZIND cells were cultured in DMEM/F12 media (Corning, NY) supplemented with 5% horse serum (Invitrogen, MA), 1% Pen/Strep, 20 ng/mL EGF (ProSpec, NJ), 0.5 µg/mg hydrocortisone, 100 ng/mL cholera toxin, and 10 µg/mL insulin. TAZDEP were grown in presence of 2ug/ul doxycyclin'; [Extraction]'RNA was extracted from 60% confluent monolayers of cells, as described above.\nThe RNA samples were subjected to transcriptome sequencing (RNA-seq) with an Illumina HiSeq 2000 sequencer.'; [Cell type]'TAZ-dependent', 'TAZ-independent''cell type: TAZ-dependent; disease state: breast cancer; ', 'cell type: TAZ-independent; disease state: breast cancer; ' GSE99505 Homo sapiens 2 Methylation profiling by array GPL21145 Ginsenoside Rg3 epigenetically regulates cell-mediated immune pathway to inhibit proliferation of the MCF-7 breast cancer cell 2017-05-31 Genome wide DNA methylation profiling of estrogene receptor postive breast cancer cell line MCF-7, treating Ginsoenoside Rg3. The Illumina Infinium Human Methylation EPIC v1.0 B2 Bead chip was used to obtain DNA methylation profiles across approximately 850,000 CpGs. This profiling indicates that Ginsenoside Rg3 induces epigenetic and cellular changes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99505 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA388665 https://www.ebi.ac.uk/ena/browser/view/PRJNA388665 None [Overal design]Genomic DNA obtained from MCF-7 treated Ginsenoside Rg3; [Treatment]'None'; [Growth]'None'; [Extraction]'genomic DNA was extracted and purified from MCF-7 using ZR Dyet DNA/RNA kit (Zymo research) according to standard instructions'; [Cell type]'epithelial''cell line: MCF-7; cell type: epithelial; gender: female; disease: adenocarcinoma; ' GSE113178 Mus musculus 9 Expression profiling by high throughput sequencing GPL19057 Role of lncRNA BC030870 in mammary gland cell proliferation 2018-04-16 We investigated an uncharacterized lncRNA, BC030870, that displays an epithelial cell-restricted expression, is downregulated by TGF-β in mammary gland cells, and controls —among others— Cdkn1a (p21WAF1/Cip1) gene expression at both transcriptional and post-transcriptional levels. BC030870 encodes a functionally active microptide (EPRp) that interacts with proteins belonging to apical junctional complexes. We hypothesized that: 1. BC030870 operates at multiple levels to orchestrate gene networks able to control cell fate, proliferation, and adhesion/migration in epithelial mammary gland cells and 2. the reduced expression of BC030870 in a group of breast cancer cells plays a role in tumor growth and invasiveness. Thus, we wanted to define the transcriptomic changes induced by BC030870 over-expression and to verify the contribution of the EPRp to gene expression changes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113178 LncRNA EPR controls epithelial proliferation by coordinating Cdkn1a transcription and mRNA decay response to TGF-β. Nature communications 11.878 https://doi.org/10.1038/s41467-019-09754-1 {Nature communications (11.878) doi:10.1038/s41467-019-09754-1}; {Nucleic acids research (11.147) doi:10.1093/nar/gkaa628}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA450379 https://www.ebi.ac.uk/ena/browser/view/PRJNA450379 https://www.ncbi.nlm.nih.gov/sra?term=SRP140493 [Overal design]Comparison of the transcriptome changes caused by stable over-expression of either lncRNA BC030870 or a point mutant version unable to generate a small peptide.; [Treatment]'Cells have been stably transfected with pBICEP-based recombinant expression vector and selected with G418 to obtain transfectant pools'; [Growth]'NMuMG cultured in DMEM 10% FCS, 0.01 mg/ml'; [Extraction]'Total RNA was extracted using miRNeasy (Qiagen)\nLibraries were prepared according to TruSeq Stranded Total RNA illumina protocol , generating paired-end 75 base-pair reads on NextSeq_1_1_4'; [Cell type]'Source: ''cell line: NMuMg; genotype: mock; ', 'cell line: NMuMg; genotype: overexpressed full transcript; ', 'cell line: NMuMg; genotype: overexpressed point-mutant transcript; ' GSE103426 Homo sapiens 48 Expression profiling by array GPL16686 Expression profiling of MDA-MB-231 and MDA-MB-468 after ALDH1A3 manipulation, all-trans retinoic acid treatment, decitabine treatment 2017-09-04 Retinoids, derivatives of vitamin A, are key physiological molecules with regulatory effects on cell differentiation, proliferation and apoptosis. As a result, they are of interest for cancer therapy. Specifically, models of breast cancer have varied responses to manipulations of the retinoid signaling cascade. This study characterizes the transcriptional response of MDA-MB-231 and MDA-MB-468 breast cancer cells to retinaldehyde dehydrogenase 1A3 (ALDH1A3) and to all-trans retinoic acid (atRA). We demonstrate limited overlap between ALDH1A3-induced gene expression and atRA-induced gene expression in both cell lines, suggesting that the function of ALDH1A3 in breast cancer progression extends beyond its role as a retinaldehyde dehydrogenase. Our data reveals divergent transcriptional responses to atRA, which are largely independent of genomic retinoic acid response elements (RAREs) and consistent with the opposing responses of MDA-MB-231 and MDA-MB-468 to in vivo atRA treatment. We identify transcription factors associated with each gene set. Manipulation of one of the transcription factors (i.e. interferon regulatory factor 1; IRF1) demonstrates that it is the level of atRA-inducible and epigenetically regulated transcription factors that determine expression of target genes (e.g. CTSS, cathepsin S). This study provides a paradigm for complex, combinatorial responses of breast cancer models to atRA treatment, and illustrates the need to characterize RARE-independent responses to atRA in a variety of models. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE103426 Profiling of the transcriptional response to all-trans retinoic acid in breast cancer cells reveals RARE-independent mechanisms of gene expression. Scientific reports 4.011 https://doi.org/10.1038/s41598-017-16687-6 {Scientific reports (4.011): 10.1038/s41598-017-16687-6} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA401792 https://www.ebi.ac.uk/ena/browser/view/PRJNA401792 None [Overal design]Samples run in triplicate: MDA-MB-231 and MDA-MB-468 with or without ALDH1A3 expression; with or without atRA treatment; with or without decitabine treatment.; [Treatment]'None'; [Growth]'All cells grown in DMEM with 10% FBS, 1x antibiotic-antimycotic, 0.25 ug/mL puromycin.'; [Extraction]'RNA extracted with Trizol reagent and PureLink RNA kit (Invitrogen).'; [Cell type]'Source: ''cell line: MDA-MB-231; genotype/variation: MSCV scramble; atra tx: 0 nM; decitabine tx: 0 uM; replicate: 1; ', 'cell line: MDA-MB-468; genotype/variation: SMP scramble; atra tx: 100 nM; decitabine tx: 1 uM; replicate: 1; ', 'cell line: MDA-MB-468; genotype/variation: SMP ALDH1A3 kd; atra tx: 0 nM; decitabine tx: 1 uM; replicate: 1; ', 'cell line: MDA-MB-468; genotype/variation: SMP ALDH1A3 kd; atra tx: 100 nM; decitabine tx: 1 uM; replicate: 1; ', 'cell line: MDA-MB-468; genotype/variation: SMP scramble; atra tx: 0 nM; decitabine tx: 0 uM; replicate: 1; ', 'cell line: MDA-MB-468; genotype/variation: SMP scramble; atra tx: 100 nM; decitabine tx: 0 uM; replicate: 1; ', 'cell line: MDA-MB-468; genotype/variation: SMP ALDH1A3 kd; atra tx: 0 nM; decitabine tx: 0 uM; replicate: 1; ', 'cell line: MDA-MB-468; genotype/variation: SMP ALDH1A3 kd; atra tx: 100 nM; decitabine tx: 0 uM; replicate: 1; ', 'cell line: MDA-MB-231; genotype/variation: MSCV scramble; atra tx: 0 nM; decitabine tx: 0 uM; replicate: 2; ', 'cell line: MDA-MB-231; genotype/variation: MSCV scramble; atra tx: 100 nM; decitabine tx: 0 uM; replicate: 2; ', 'cell line: MDA-MB-231; genotype/variation: MSCV scramble; atra tx: 0 nM; decitabine tx: 1 uM; replicate: 2; ', 'cell line: MDA-MB-231; genotype/variation: MSCV scramble; atra tx: 100 nM; decitabine tx: 0 uM; replicate: 1; ', 'cell line: MDA-MB-231; genotype/variation: MSCV scramble; atra tx: 100 nM; decitabine tx: 1 uM; replicate: 2; ', 'cell line: MDA-MB-231; genotype/variation: MSCV ALDH1A3 overexpression; atra tx: 0 nM; decitabine tx: 0 uM; replicate: 2; ', 'cell line: MDA-MB-231; genotype/variation: MSCV ALDH1A3 overexpression; atra tx: 100 nM; decitabine tx: 0 uM; replicate: 2; ', 'cell line: MDA-MB-231; genotype/variation: MSCV ALDH1A3 overexpression; atra tx: 0 nM; decitabine tx: 1 uM; replicate: 2; ', 'cell line: MDA-MB-231; genotype/variation: MSCV ALDH1A3 overexpression; atra tx: 100 nM; decitabine tx: 1 uM; replicate: 2; ', 'cell line: MDA-MB-468; genotype/variation: SMP scramble; atra tx: 0 nM; decitabine tx: 1 uM; replicate: 2; ', 'cell line: MDA-MB-468; genotype/variation: SMP scramble; atra tx: 100 nM; decitabine tx: 1 uM; replicate: 2; ', 'cell line: MDA-MB-468; genotype/variation: SMP ALDH1A3 kd; atra tx: 0 nM; decitabine tx: 1 uM; replicate: 2; ', 'cell line: MDA-MB-468; genotype/variation: SMP ALDH1A3 kd; atra tx: 100 nM; decitabine tx: 1 uM; replicate: 2; ', 'cell line: MDA-MB-468; genotype/variation: SMP scramble; atra tx: 0 nM; decitabine tx: 0 uM; replicate: 2; ', 'cell line: MDA-MB-231; genotype/variation: MSCV scramble; atra tx: 0 nM; decitabine tx: 1 uM; replicate: 1; ', 'cell line: MDA-MB-468; genotype/variation: SMP scramble; atra tx: 100 nM; decitabine tx: 0 uM; replicate: 2; ', 'cell line: MDA-MB-468; genotype/variation: SMP ALDH1A3 kd; atra tx: 0 nM; decitabine tx: 0 uM; replicate: 2; ', 'cell line: MDA-MB-468; genotype/variation: SMP ALDH1A3 kd; atra tx: 100 nM; decitabine tx: 0 uM; replicate: 2; ', 'cell line: MDA-MB-231; genotype/variation: MSCV scramble; atra tx: 0 nM; decitabine tx: 0 uM; replicate: 3; ', 'cell line: MDA-MB-231; genotype/variation: MSCV scramble; atra tx: 100 nM; decitabine tx: 0 uM; replicate: 3; ', 'cell line: MDA-MB-231; genotype/variation: MSCV scramble; atra tx: 0 nM; decitabine tx: 1 uM; replicate: 3; ', 'cell line: MDA-MB-231; genotype/variation: MSCV scramble; atra tx: 100 nM; decitabine tx: 1 uM; replicate: 3; ', 'cell line: MDA-MB-231; genotype/variation: MSCV ALDH1A3 overexpression; atra tx: 0 nM; decitabine tx: 0 uM; replicate: 3; ', 'cell line: MDA-MB-231; genotype/variation: MSCV ALDH1A3 overexpression; atra tx: 100 nM; decitabine tx: 0 uM; replicate: 3; ', 'cell line: MDA-MB-231; genotype/variation: MSCV ALDH1A3 overexpression; atra tx: 0 nM; decitabine tx: 1 uM; replicate: 3; ', 'cell line: MDA-MB-231; genotype/variation: MSCV scramble; atra tx: 100 nM; decitabine tx: 1 uM; replicate: 1; ', 'cell line: MDA-MB-231; genotype/variation: MSCV ALDH1A3 overexpression; atra tx: 100 nM; decitabine tx: 1 uM; replicate: 3; ', 'cell line: MDA-MB-468; genotype/variation: SMP scramble; atra tx: 0 nM; decitabine tx: 1 uM; replicate: 3; ', 'cell line: MDA-MB-468; genotype/variation: SMP scramble; atra tx: 100 nM; decitabine tx: 1 uM; replicate: 3; ', 'cell line: MDA-MB-468; genotype/variation: SMP ALDH1A3 kd; atra tx: 0 nM; decitabine tx: 1 uM; replicate: 3; ', 'cell line: MDA-MB-468; genotype/variation: SMP ALDH1A3 kd; atra tx: 100 nM; decitabine tx: 1 uM; replicate: 3; ', 'cell line: MDA-MB-468; genotype/variation: SMP scramble; atra tx: 0 nM; decitabine tx: 0 uM; replicate: 3; ', 'cell line: MDA-MB-468; genotype/variation: SMP scramble; atra tx: 100 nM; decitabine tx: 0 uM; replicate: 3; ', 'cell line: MDA-MB-468; genotype/variation: SMP ALDH1A3 kd; atra tx: 0 nM; decitabine tx: 0 uM; replicate: 3; ', 'cell line: MDA-MB-468; genotype/variation: SMP ALDH1A3 kd; atra tx: 100 nM; decitabine tx: 0 uM; replicate: 3; ', 'cell line: MDA-MB-231; genotype/variation: MSCV ALDH1A3 overexpression; atra tx: 0 nM; decitabine tx: 0 uM; replicate: 1; ', 'cell line: MDA-MB-231; genotype/variation: MSCV ALDH1A3 overexpression; atra tx: 100 nM; decitabine tx: 0 uM; replicate: 1; ', 'cell line: MDA-MB-231; genotype/variation: MSCV ALDH1A3 overexpression; atra tx: 0 nM; decitabine tx: 1 uM; replicate: 1; ', 'cell line: MDA-MB-231; genotype/variation: MSCV ALDH1A3 overexpression; atra tx: 100 nM; decitabine tx: 1 uM; replicate: 1; ', 'cell line: MDA-MB-468; genotype/variation: SMP scramble; atra tx: 0 nM; decitabine tx: 1 uM; replicate: 1; ' GSE43522 Homo sapiens 2 SNP genotyping by SNP array; Genome variation profiling by SNP array GPL13829 Chromothripsis in AML 2013-01-15 This dataset contains data from two acute myeloid leukaemia (AML) specimens processed with the Illumina CytoSNP-12 SNP array platform. SNP array data showed evidence of chromothripsis in these two specimens. Each deletion in the mosaic specimen was present in the same proportion of cells, which supports the view that the many breaks occur as a single event. Complementary FISH studies highlighted the inclusion of centromeres from different chromosomes during the formation of the new chromosomes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43522 Chromothripsis under the microscope: a cytogenetic perspective of two cases of AML with catastrophic chromosome rearrangement. Cancer genetics 2.183 https://doi.org/10.1016/j.cancergen.2013.05.021 {Cancer genetics (2.183): 10.1016/j.cancergen.2013.05.021} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA186647 https://www.ebi.ac.uk/ena/browser/view/PRJNA186647 None [Overal design]Residual bone marrow specimens were chosen from patients who were determined to have a complex karyotype which included abnormalities of chromosomes 5 and 17, by routine cytogenetic examination.; [Treatment]'Stored at 4 degrees Celsius for 33 days (R4, Case 1) or 2 days (R13, Case 2), then -80 degrees Celsius; thawed before DNA extraction.'; [Growth]'None: specimen from bone marrow biopsy.'; [Extraction]'Qiagen DNeasy Cell and Tissue kit.'; [Cell type]'Source: ''tissue: bone marrow; primary tumor: acute myeloid leukaemia; tumor type: acute myeloid leukaemia; gender: male; lineage: myeloid; ', 'tissue: bone marrow; primary tumor: acute myeloid leukaemia; tumor type: therapy-related acute myeloid leukaemia after treatment for breast cancer; gender: female; lineage: myeloid; ' GSE86971 Mus musculus 2 Expression profiling by array GPL13684 cDNA expression profiling of 4T1 breast cancer cells isolated from tumor-draining lymph node (4T1LN) or primary tumors (4T1PT) 2016-09-15 Investigating the gene expression profile changes between 4T1LN and 4T1PT. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE86971 TGF-β1 secreted by Tregs in lymph nodes promotes breast cancer malignancy via up-regulation of IL-17RB. EMBO molecular medicine 10.624 https://doi.org/10.15252/emmm.201606914 {EMBO molecular medicine (10.624): 10.15252/emmm.201606914} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA343116 https://www.ebi.ac.uk/ena/browser/view/PRJNA343116 None [Overal design]Balb/c mice were injected with 4T1 cells at both site of 4th mammary fat pad. Three weeks later, mice were sacrificed and primary tumors and inguinal tumor-draining lymph nodes were harvested. Primary tumors from both 4th fat pads were excised, minced with scissors, and then digested in collagenase type I (150 U⁄ ml) plus hyaluronidase (50 U/ml) for 16 hr at humidified 37 °C incubator supplemented with 5% CO2. Inguinal tumor-draining LNs were excised and dissociated by mechanical disruption. Tissues were dissociated by 100 μm cell strainers from BD Biosciences (San Jose, CA, USA) and maintained in complete RPMI 1640 medium containing 60 μM 6-thioguanine (Sigma-Aldrich, St. Louis, MO, USA) and seeded into 10 cm dishes. After 10-14 days, cells were harvested and stained with APC-conjugated rat anti-mouse CD24 (#101814, Biolegend, San Diego, CA, USA) and PE-conjugated hamster anti-mouse CD29 antibodies (#102208, Biolegend, San Diego, CA, USA) for 30 mins at 4℃. The CD24+CD29+ 4T1 cell population was sorted on a FACS Aria II cell sorter. CD24+CD29+ 4T1 cell sorted from Inguinal tumor-draining LNs called 4T1LN cells, CD24+CD29+ 4T1 cell sorted from primary tumors called 4T1PT cells.; [Treatment]'No treatment.'; [Growth]'The single cell suspension were cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS), 2 mM L-glutamine, 1 mM non-essential, amino acids (NEAA), 1 mM sodium pyruvate, antibiotics/antimycotics, and 60 μM 6-thioguanine in a humidified 37°C incubator supplemented with 5% CO2.'; [Extraction]'RNA extraction by Trizol. RNA purity was checked by optical density of NanoDrop ND-1000 and agarose electrophoresis with the result of A260/A280≧1.8, no gDNA contamination. RNA integrity was measured by Agilent RNA 6000 Nano Assay (RIN≧7).'; [Cell type]'Source: ''originating cell line: 4T1; originating cell type: Breast cancer cell line; tissue: primary tumor; ', 'originating cell line: 4T1; originating cell type: Breast cancer cell line; tissue: tumor-draining lymph node; ' GSE55634 Homo sapiens 3 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Unbiased Capture Hi-C reveals the potential targets of breast cancer susceptibility loci 2014-03-05 Genome-wide association studies have identified over 70 common variants that are associated with breast cancer risk. Most of these variants map to non-protein-coding regions; several map to gene deserts, regions of several hundred kb lacking protein-coding genes. We hypothesized that gene deserts harbour long-range regulatory elements that can physically interact with target genes to influence their expression. To test this, we developed Capture Hi-C (CHi-C), which by incorporating a sequence capture step into a Hi-C protocol, allows high-resolution analysis of targeted regions of the genome. We used CHi-C to investigate long-range interactions at three breast cancer gene deserts mapping to 2q35, 8q24.21 and 9q31.2. We identified interaction peaks between putative regulatory elements ("bait fragments") within the captured regions and "targets" that included both protein-coding genes and long non-coding (lnc)RNAs, over distances of 6.6 kb to 2.6 Mb. Target protein-coding genes were IGFBP5, KLF4, NSMCE2 and MYC; target lncRNAs included DIRC3, PVT1 and CCDC26. For two gene deserts we were able to define a set of SNPs that were correlated with the published risk variant and that clustered within the bait end of an interaction peak. Preliminary functional analyses implicate one SNP (rs12613955; 2q35) as a potentially functional variant. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55634 Unbiased analysis of potential targets of breast cancer susceptibility loci by Capture Hi-C. Genome research 9.944 https://doi.org/10.1101/gr.175034.114 {Genome research (9.944): 10.1101/gr.175034.114} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA240252 https://www.ebi.ac.uk/ena/browser/view/PRJNA240252 https://www.ncbi.nlm.nih.gov/sra?term=SRP039464 [Overal design]Capture Hi-C was carried out in BT483, SUM44, and GM06990 cell lines to investigate breast cancer risk loci 2q35, 8q24.21 and 9q31.2.; [Treatment]'Cells were fixed in 2% formaldehyde for 5 minutes at room temperature followed by the addition of glycine to a final concentration of 150 mM.'; [Growth]'Grown in RPMI 1640 supplemented with 20% fetal bovine serum, 50U/ml penicillin, 50μg/ml streptomycin, 2mM L-Glutamine and 0.01mg/ml recombinant human insulin.', 'Grown in RPMI 1640 supplemented with 15% fetal bovine serum, 50U/ml penicillin, 50μg/ml streptomycin and 2mM L-Glutamine.', 'Grown in phenol-red-free RPMI 1640 supplemented with 10% fetal bovine serum, 50U/ml penicillin, 50μg/ml streptomycin, 2mM L-Glutamine and 1 nM Estradiol.'; [Extraction]'Each cross-linked cell aliquot (~20 million cells) was re-suspended in 50ml of permeabilisation buffer (10mM Tris-HCl p8, 10mM NaCl, 0.2% IGEPAL CA-630), supplemented with complete mini EDTA-free tablets and incubated on ice for 30 minutes with occasional mixing. SUM44 and GM06990 cells were lysed using 10 strokes of a dounce homogeniser. BT483 cells were lysed by incubating with trypsin (0.25%, Sigma-Aldrich, St. Louis, MO, USA) at 37°C for 5 minutes. Trypsin was inactivated by addition of 500μl FBS. Permeabilised cells were centrifuged for 6 minutes at 600g and washed three times in 1ml 1.3xNEBuffer 2. Nuclei were resuspended, and chromatin digestion and Hi-C library preparation were carried out as described by van Berkum and colleagues (Hi-C: a method to study the three-dimensional architecture of genomes J.Vis exp. 2010; (39): 1869) with the following modifications: (i) cells were split into three microcentrifuge tubes instead of five, (ii) restriction fragment overhangs were filled in with biotinylated dATP instead of biotinylated dCTP, (iii) dGTP was added to the reaction mixture for the removal of biotinylated dATP from unligated ends, (iv) we did not include an agarose gel size selection step, and (v) after PCR amplification (6-8 cycles) of the Hi-C library bound streptavidin beads the PCR product was pooled and subjected to target enrichment (below) before paired-end sequencing.\nTarget enrichment was performed based on the SureSelect protocol (Agilent, Santa Clara, CA, USA) but incorporating the following modifications: (i) Biotinylated Hi-C ditags bound to streptavidin-beads were amplified pre-hybridization directly from beads using 24 parallel 25μl PCR reactions cycles with six to eight cycles using Phusion High-Fidelity DNA polymerase to yield approximately 500ng total DNA. Subsequently, PCR products were pooled, purified using Agencourt Ampure XP beads (Beckman Coulter, Brea, CA, USA) and dried using a speedvac concentrator then resuspended in 34μl of water; and (ii) Enriched fragments were amplified post-hybridization again directly from the streptavidin beads, using 13 parallel 25μl reactions of six cycles of PCR. PCR products were again pooled and purified using Agencourt Ampure XP beads (Beckman Coulter, Brea, CA, USA).'; [Cell type]'Source: ''cell line: BT483; cell source: primary invasive ductal carcinoma; restriction enzyme: HindIII; ', 'cell line: GM06990; cell source: B-lymphocyte; restriction enzyme: HindIII; ', 'cell line: SUM44; cell source: plural effusion; restriction enzyme: HindIII; ' GSE120439 Mus musculus; Homo sapiens 24 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL18573; GPL19057 PTEN interacts with the transcription machinery on chromatin and regulates RNA polymerase II-mediated transcription.[RNA-seq and ChIP-seq] 2018-09-25 We demonstrate that PTEN interacts with the transcription machinery. Using ChIP-seq, we show that PTEN co-localizes with RNAPII and binds to chromatin in promoter and putative enhancer regions. We further show that loss of PTEN affects RNAPII occupancy in gene bodies and correlates with gene expression changes. Loss of PTEN also increased cells’ sensitivity to transcription inhibition via small molecules. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE120439 PTEN interacts with the transcription machinery on chromatin and regulates RNA polymerase II-mediated transcription. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkz272 {Nucleic acids research (11.147): 10.1093/nar/gkz272} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA493122 https://www.ebi.ac.uk/ena/browser/view/PRJNA493122 https://www.ncbi.nlm.nih.gov/sra?term=SRP162586 [Overal design]We interogate HeLa, MEF and MycOE mouse breast tumor cell lines for transcriptional changes after PTEN loss and correlate those with changes in PTEN, RNAPII, RNAPII Ser2P, RNAPII Ser5P occupancy at promoters, regulatory regions and in gene bodies.; [Treatment]'None'; [Growth]'None'; [Extraction]'ChIP-seq: Lysates were clarified from sonicated nuclei and prtein-DNA complexes were isolated with antibody\nRNA-seq: RNA was extracted from cell pellets using Qiagen RNeasy Kit.\nChIP-seq: 2-10 ng of DNA were subject to end-repair, A-tailing, and ligation with Illumina Truseq adapters using NEB enzymes (NEB), followed by size-selection of 300-400 bp and amplification for 10-15 cycles using the KAPA HiFi Library Amplification Kit (Kapa Biosystems).\nRNA-seq: Illumina TruSeq RNALibrary Prep Kit v2 (RS 122-2001) was used with 1 ug of total RNA for the construction of sequencing libraries'; [Cell type]'HeLa', 'primary mouse embryonic fibroblasts (passage 6-8)', 'mouse breast tumor cells''cell type: HeLa; growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: CRISPR-PTEN KO; ', 'cell type: HeLa; chip antibody: PTEN 6H2.1 (Millipore, 04-035); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; chip antibody: PTEN 138G6 (Cell Signaling, 9559); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; chip antibody: RNAPII (Santa Cruz, Sc-899); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; chip antibody: RNAPII Ser2P (abcam, ab5095); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; chip antibody: RNAPII Ser5P (abcam, ab5408); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; chip antibody: SPT5 (Bethyl Laboratories, A300-868A); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: PTEN WT; ', 'cell type: HeLa; chip antibody: PTEN 6H2.1 (Millipore, 04-035) and PTEN 138G6 (Cell Signaling, 9559); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: CRISPR-PTEN KO; ', 'cell type: HeLa; chip antibody: RNAPII (Santa Cruz, Sc-899); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: CRISPR-PTEN KO; ', 'cell type: HeLa; chip antibody: RNAPII Ser2P (abcam, ab5095); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: CRISPR-PTEN KO; ', 'cell type: HeLa; chip antibody: RNAPII Ser5P (abcam, ab5408); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: CRISPR-PTEN KO; ', 'cell type: HeLa; chip antibody: SPT5 (Bethyl Laboratories, A300-868A); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: CRISPR-PTEN KO; ', 'cell type: primary mouse embryonic fibroblasts (passage 6-8); chip antibody: n/a; growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin; genotype/variation: Pten WT; ', 'cell type: primary mouse embryonic fibroblasts (passage 6-8); chip antibody: RNAPII (Santa Cruz, Sc-899); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin, and 2mM L-glutamine; genotype/variation: Pten WT; ', 'cell type: primary mouse embryonic fibroblasts (passage 6-8); chip antibody: RNAPII (Santa Cruz, Sc-899); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin, and 2mM L-glutamine; genotype/variation: Pten Null; ', 'cell type: mouse breast tumor cells; chip antibody: n/a; growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin, and 2mM L-glutamine; genotype/variation: Pten WT; ', 'cell type: mouse breast tumor cells; chip antibody: RNAPII (Santa Cruz, Sc-899); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin, and 2mM L-glutamine; genotype/variation: Pten WT; ', 'cell type: mouse breast tumor cells; chip antibody: RNAPII (Santa Cruz, Sc-899); growth protocol: grown in DMEM supplemented with 10% FBS, penicillin and streptomycin, and 2mM L-glutamine; genotype/variation: Pten Null; ' GSE100403 Mus musculus 8 Expression profiling by high throughput sequencing GPL19057 A kinome-wide high-content siRNA screen identifies MEK5-ERK5 signaling as critical for breast cancer cell EMT and metastasis 2017-06-23 We have employed a high-content microscopy screen in combination with a kinome and phosphatome-wide siRNA library to identify signaling pathways underlying an EMT of murine mammary epithelial cells and breast cancer cells. This screen identified the MEK5-ERK5 axis as a critical player in TGFb-mediated EMT. Suppression of MEK5-ERK5 signaling completely prevented the morphological and molecular changes occurring during a TGFb-induced EMT and, conversely, forced highly metastatic breast cancer cells into a differentiated epithelial state. Inhibition of MEK5-ERK5 signaling also repressed breast cancer cell migration and invasion and substantially reduced lung metastasis without affecting primary tumor growth. The results suggest that the MEK5-ERK5 signaling axis plays an important role in the induction and maintenance of breast cancer cell migration and invasion and thus represents an exploitable target for the pharmacological inhibition of cancer cell metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE100403 A kinome-wide high-content siRNA screen identifies MEK5-ERK5 signaling as critical for breast cancer cell EMT and metastasis. Oncogene 6.634 https://doi.org/10.1038/s41388-018-0270-8 {Oncogene (6.634): 10.1038/s41388-018-0270-8} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA391573 https://www.ebi.ac.uk/ena/browser/view/PRJNA391573 https://www.ncbi.nlm.nih.gov/sra?term=SRP110236 [Overal design]We performed RNA-sequencing of 3 replicates of 2 different cell lines and 2 replicates of another cell line; [Treatment]'Lentiviral plasmids containing shRNAs against murine MEK5 and ERK5 and the Non-Targeting shCTRL vector were used. To produce lentiviral particles, HEK293T cells were transfected with the shRNA containing plasmids, the helper vectors pMDL and pREV and the envelope encoding plasmid pVSV. Virus-containing supernatant was conditioned for 2 days. 4T1 cells were infected with the virus containing supernatant and 8mg/mL polybrene. Then infected cells were selected with 4μg/ml puromycin'; [Growth]'4T1 cell lines were grown in Dulbecco’s Modified Eagle’s Medium supplemented with 10% fetal bovine serum, 2mM Glutamine, 100μg/ml penicillin-streptomycin at 37°C and 5% CO2 in a humidified incubator'; [Extraction]'Total RNA was isolated from 3 different cell lines in 3 replicates each using the RNeasy Mini Kit (Qiagen) according to the manufacturer’s instruction\nRNA quality control was performed with Bioanalyzer 2100 (Agilent) using the Eukaryote Total RNA Nano analysis kit from Labgene and RNA concentration was measured by Quanti-iTTM RiboGreen RNA assay kit (Thermo Fisher Scientific). 200ng of RNA was utilized for library preparation with the TruSeq Stranded total RNA kit plus Ribozero Gold (Illumina). The library quality check was performed using the DNF-473-33 - SS NGS Fragment analysis kit (Advanced Analytical Technologies Inc).'; [Cell type]'breast cancer cells''cell line: 4T1; cell type: breast cancer cells; ' GSE116870 Homo sapiens 6 Expression profiling by high throughput sequencing GPL18573 Oncogenic Notch promotes long-range regulatory interactions within hyperconnected 3D cliques [HCC1599_RNA-seq] 2018-07-10 Purpose: To investigate the impact of oncogenic Notch on the 3D genome organization of cancer cells. Methods: We generated cohesin HiChIP and 1D epigenomic data sets in two different Notch-dependent cancer cell types, triple-negative breast cancer (TNBC) and mantle cell lymphoma (MCL), in the Notch-on and -off states. Results: We report here that Notch transcription complexes control their direct target genes through two distinct regulatory modes: either through existing loops or by facilitating new long-range regulatory interactions. This combination of pre-existing and Notch-promoted loops coalesce enhancers and promoters to form highly interacting clusters, termed “3D cliques”. Notch preferentially activates enhancers and promotes looping interactions within highly connected 3D cliques that regulate key oncogenes. Conclusions: These observations suggest a general mechanism that oncogenic transcription factors can exploit to regulate the transcriptional outputs of cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE116870 Oncogenic Notch Promotes Long-Range Regulatory Interactions within Hyperconnected 3D Cliques. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2019.01.006 {Molecular cell (14.548): 10.1016/j.molcel.2019.01.006} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA480470 https://www.ebi.ac.uk/ena/browser/view/PRJNA480470 https://www.ncbi.nlm.nih.gov/sra?term=SRP152959 [Overal design]ChIP-seq, RNA-seq and HiChIP in Notch-on, -off, -recovery conditions in TNBC and MCL cell lines to profile Notch transcriptional complex binding, histone modification, Notch target genes and contact between regulatory elements.; [Treatment]'Cells were treated with the GSI compound E (1 μM, Calbiochem cat# 565790) for 72 hours, washed, and then cultured for 5 hours in media containing 1μM GSI (mock washout) or DMSO (washout) as previously described (Weng et al., 2006).'; [Growth]'HCC1599 (female) cells were grown in RPMI 1640 (Corning, cat# 10-040-CM) supplemented with 10% fetal bovine serum (Hyclone, cat# SH30070.03), 2 mM L-glutamine (Corning, cat# 25-005-CI), 100 U/mL and 100 μg/mL penicillin/streptomycin (Corning, cat# 30-002-CI), 100 mM nonessential amino acids (Gibco, cat# 11140-050), 1mM sodium pyruvate (Gibco, cat#11360-070) and 0.1mM of 2-mercaptoethanol (Sigma, cat# M6250).'; [Extraction]'Cells from GSI and washout conditions were washed with 1 x PBS (Corning, cat# 21031CV) and lysed with 350 μl RLT Plus buffer (Qiagen) supplemented with 10% 2-mercaptoethanol (Sigma, cat# M6250), vortexed briefly, snap-frozen on dry ice, and stored at -80°C. Subsequently, total RNA was isolated using the RNeasy Plus Micro Kit (Qiagen, cat# 74034).\nRNA integrity numbers were determined using TapeStation 2200 (Agilent), and all samples used for RNA-seq library preparation had RIN numbers greater than 9.5. 800 ng of total RNA was used and libraries were prepared using the SMARTer Standard Total RNA Sample Prep Kit-HI Mammalian (Clontech, cat# 634873). Libraries were single-end sequenced (75 bp) on a NextSeq 550.'; [Cell type]'Triple-negative breast cancer cell line''cell line: HCC1599; cell type: Triple-negative breast cancer cell line; drug treatment: GSI-washout; ', 'cell line: HCC1599; cell type: Triple-negative breast cancer cell line; drug treatment: GSI-mock-washout; ' GSE113486 Homo sapiens 972 Non-coding RNA profiling by array GPL21263 Circulating miRNA panels for specific and early detection in bladder cancer 2018-04-20 A serum miRNA combination could be a powerful classifier for the detection of patients with bladder cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113486 Circulating miRNA panels for specific and early detection in bladder cancer. Cancer science 4.751 https://doi.org/10.1111/cas.13856 {Cancer science (4.751): 10.1111/cas.13856} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA451225 https://www.ebi.ac.uk/ena/browser/view/PRJNA451225 None [Overal design]Serum microRNA profiles of 972 samples, which consist of 392 bladder cancer, 100 non-cancer control, and 480 other types of cancer patients.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted each from 300uL serum samples using 3D-Gene® RNA extraction reagent from liquid sample kit (Toray Industries, Inc.).'; [Cell type]'Source: ''tissue: Serum; Sex: Male; age: 59; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 50; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 71; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 66; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 74; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 81; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 65; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Female; age: 48; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 69; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 72; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 60; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 78; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 63; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 79; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 59; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 70; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 35; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 44; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 68; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Female; age: 70; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 73; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Female; age: 67; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 56; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 87; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Female; age: 56; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 38; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 71; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Female; age: 77; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 64; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 75; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 70; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 75; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 69; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Female; age: 75; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Female; age: 73; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Female; age: 71; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 70; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 47; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Female; age: 78; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Female; age: 87; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Female; age: 60; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 55; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 83; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 90; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 54; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Female; age: 65; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 52; disease status: Bladder Cancer; pathological tstage: =pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 79; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 48; disease status: Bladder Cancer; pathological tstage: >=pT2; pathological grade: high; ', 'tissue: Serum; Sex: Male; age: 86; disease status: Bladder Cancer; pathological tstage: 8 were considered for library preparation.\nLibraries were generated with the Illumina TruSeq RNA Library Preparation kit (RS-122-2001/2, Illumina Inc.).'; [Cell type]'Source: ', 'Mammary epithelial cells', 'Primary mouse mammary tumor cells''cell-type: HC11; sgrna: sgScr #1; ', 'cell-type: HC11; sgrna: sgTrps1 #1; ', 'cell-type: Mammary organoids; genotype/strain: Cdh1F/F;Trps1+/+; treatment: AdCre transduction, harvested after 14 days; ', 'cell-type: Mammary organoids; genotype/strain: Cdh1+/F;Trps1F/F; treatment: AdCre transduction, harvested after 14 days; ', 'cell-type: Mammary organoids; genotype/strain: Cdh1F/F;Trps1F/F; treatment: AdCre transduction, harvested after 14 days; ', 'cell-type: Mammary organoids; genotype/strain: Cdh1F/F;Trps1+/+; treatment: AdCre transduction, harvested after 28 days; ', 'cell-type: Mammary organoids; genotype/strain: Cdh1+/F;Trps1F/F; treatment: AdCre transduction, harvested after 28 days; ', 'cell-type: Mammary organoids; genotype/strain: Cdh1F/F;Trps1F/F; treatment: AdCre transduction, harvested after 28 days; ', 'cell line: HC11; cell type: Mammary epithelial cells; treatment: DMSO; ', 'cell line: HC11; cell type: Mammary epithelial cells; treatment: 300nM Trichostatin A (24 hours); ', 'cell type: Primary mouse mammary tumor cells; genotype/strain: WAP-cre;Cdh1F/F;Trps1F/F; ', 'cell type: Primary mouse mammary tumor cells; genotype/strain: WAP-cre;Cdh1F/F;Trps1+/+; ' GSE113826 Mus musculus 12 Expression profiling by array GPL6887 MMP14 empowers tumor-initiating breast cancer cells under hypoxic nutrient-depleted conditions 2018-04-30 Tumor-initiating cells (TICs) exist in breast cancer and are thought to be the cause of tumor initiation, progression, and relapse. In these processes, proteases play an important role. Additionally, conditions of the tumor milieu, including hypoxic nutrient-deprived as well as normoxic nutrient-rich environments, influence the tumor-promoting actions of neoplastic cells. Therefore, we investigated the role of proteases in TICs and their response to different environments by means of a generated immortalized TIC line. After assessing immortalized TIC tumorigenicity by limiting dilution assays in vivo and their characteristics in different environmental conditions, a transcriptome analysis was performed of iTICS cultured in hypoxic stem cell conditions and 1-7 days in normoxic standard condtitions. A high proteolytic signature was identified and further investigated by inhibitor treatment and shRNA mediated RNA interference of Mmp14. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113826 MMP14 empowers tumor-initiating breast cancer cells under hypoxic nutrient-depleted conditions. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 5.391 https://doi.org/10.1096/fj.201801127R {FASEB journal : official publication of the Federation of American Societies for Experimental Biology (5.391): 10.1096/fj.201801127R} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA454197 https://www.ebi.ac.uk/ena/browser/view/PRJNA454197 None [Overal design]Immortalized tumor-initiating cells (iTICs) were grown in hypoxic stem cell conditions (HSCC) or normoxic standard conditions till confluency of 80% on a 10 cm petridish. Subsequently, total RNA was extracted, analyzed for their quality (RIN), and hybridized to a Mouse WG-6 v2.0 Bead Chip (Illumina). To obtain an overview of expression profile over time iTICs are cultured in NSC, in addition to the HSCC replicates (3x), samples of iTICs cultured in NSC for 1, 2, 3, 4, 5, 6, and 7 days NSC were analyzed. The 7 day sample in NSC was also analyzed in triplicate while all other days in NSC were analyze as one replicate.; [Treatment]'To analyze iTICs gene expression profile in normoxic standart conditons (1 to 7 days), cells were transferred from hypoxic stem cell conditions into standard medium (DMEM base, Gibco) and an atmosphere of 21% O2, 5% CO2, and 92% N2 at 37°C.'; [Growth]'Immortalized tumor-initiating cells were cultured in hypoxic stem cell conditions, including a serum-free mammary stem cell medium (MEBM base, Lonza) with 2% Cultrex® supplement (Trevigen) and an atmosphere of 3% O2, 5% CO2, and 92% N2 at 37°C.'; [Extraction]"Total RNA was extracted using the peqGOLD Total RNA kit (Peqlab) following the manufacturer's instructions."; [Cell type]'Source: ''time: none; cell source: Immortalized tumor-initiating cells; replicate: rep 1; culture condition: hypoxic stem cell conditions; ', 'time: none; cell source: Immortalized tumor-initiating cells; replicate: rep 2; culture condition: hypoxic stem cell conditions; ', 'time: none; cell source: Immortalized tumor-initiating cells; replicate: rep 3; culture condition: hypoxic stem cell conditions; ', 'time: 1 day; cell source: Immortalized tumor-initiating cells; replicate: rep 1; culture condition: normoxic standard conditions; ', 'time: 2 days; cell source: Immortalized tumor-initiating cells; replicate: rep 1; culture condition: normoxic standard conditions; ', 'time: 3 days; cell source: Immortalized tumor-initiating cells; replicate: rep 1; culture condition: normoxic standard conditions; ', 'time: 4 days; cell source: Immortalized tumor-initiating cells; replicate: rep 1; culture condition: normoxic standard conditions; ', 'time: 5 days; cell source: Immortalized tumor-initiating cells; replicate: rep 1; culture condition: normoxic standard conditions; ', 'time: 6 days; cell source: Immortalized tumor-initiating cells; replicate: rep 1; culture condition: normoxic standard conditions; ', 'time: 7 days; cell source: Immortalized tumor-initiating cells; replicate: rep 1; culture condition: normoxic standard conditions; ', 'time: 7 days; cell source: Immortalized tumor-initiating cells; replicate: rep 2; culture condition: normoxic standard conditions; ', 'time: 7 days; cell source: Immortalized tumor-initiating cells; replicate: rep 3; culture condition: normoxic standard conditions; ' GSE104193 Homo sapiens 32 Expression profiling by high throughput sequencing GPL11154 Hypoxia-mediated translational activation of ITGB3 in breast cancer cells enhances TGF-β signalling and malignant features in vitro and in vivo 2017-09-25 We performed a polysomal RNA-Seq screen in non-malignant breast epithelial (MCF10A) and TNBC (MDA-MB-231) cells exposed to normoxic or hypoxic conditions and/or treated with an mTOR pathway inhibitor. Analysis of both the transcriptome and the translatome identified mRNA transcripts translationally activated or repressed by hypoxia in an mTOR-dependent or -independent manner. The mRNA populations of each sample were converted to cDNA libraries using the TruSeq protocol and then sequenced using a HiSeq 2000 machine. Paired-end reads were mapped against the reference human genome (GRCh38) with STAR v2.5.1b (ENCODE parameters for long RNA) and GENCODE v24 annotation. Gene quantification was performed using RSEM v1.2.28 with default parameters. Only protein-coding genes were included in the analysis. Normalization of the count matrix was performed with the TMM method of the edgeR R package. Polysomal RNA (P) and RNA total (T) fold changes across conditions were calculated with edgeR. Significant genes (FDR < 5% for MCF10A cells and FDR < 10% for MDA-MB-231 cells) in polysomes were selected for translational efficiency calculation (log2FC RNA polysomes/log2FC RNA total). Genes with a z-score > 1.5 were considered to have an increased translational efficiency and genes with a z-score < –1.5 were considered to have a decreased translational efficiency. GO enrichment analysis of significant genes was performed with the DAVID database. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE104193 Hypoxia-mediated translational activation of ITGB3 in breast cancer cells enhances TGF-β signaling and malignant features in vitro and in vivo. Oncotarget None https://doi.org/10.18632/oncotarget.23145 {Oncotarget (None): 10.18632/oncotarget.23145} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA412005 https://www.ebi.ac.uk/ena/browser/view/PRJNA412005 https://www.ncbi.nlm.nih.gov/sra?term=SRP118788 [Overal design]RNA-Seq profiles in polysomes vs total in Normoxia, Hypoxia, Hypoxia + PP242, Normoxia + PP242 in MCF10A and MDA-MB-231 cell lines; [Treatment]'Cells were maintained at 37°C in a 5% CO2 humidified incubator. To establish hypoxic conditions, cells were subjected to 0.5% O2 in 5% CO2/95% N2 and 100% humidity for 24 hours in a hypoxic chamber (INVIVO2 200; Ruskinn Technology, UK). PP242 was purchased from Selleckchem (#S2218), reconstituted in dimethyl sulfoxide (DMSO) and used at a final concentration of 2.5 μM for 3 hours'; [Growth]"MDA-MB-231 cells were maintained in Dulbecco's modified Eagle's medium (DMEM) (Invitrogen) supplemented with 10% heat-inactivated foetal bovine serum (FBS) (Life Technologies) and antibiotics (100 U/mL penicillin, 100 μg/mL streptomycin) (Life Technologies). MCF10A cells were maintained in DMEM supplemented with 10% FBS, 20 ng/mL EGF (#E9644; Sigma), 0.5 μg/mL hydrocortisone, 100 ng/mL cholera toxin (#C9903; Sigma) and 10 μg/mL insulin (#I9278; Sigma)."; [Extraction]"Polysomal mRNA was obtained by 10%–50% sucrose gradient sedimentation. Upon hypoxia or normoxia, with and without PP242 treatments, cells were washed twice with cold 1× phosphate-buffered saline (PBS) and lysed by incubation for 10 minutes on ice in polysome buffer: 1.5 mM KCl, 5 mM Tris-HCl pH 7.4, 2.5 mM MgCl2, 1% Triton X-100, 1% Na-deoxycholate, 100 μg/ml cycloheximide, 2.5 μl/mL RNAaseOut and 1× Complete Roche Protease Inhibitor. The cell lysate was centrifuged at 12,000 × g for 15 minutes at 4°C. One microgram of total protein from the supernatant was loaded onto a 10%–50% sucrose gradient, made with the BioComp Gradient Maker, and ultracentrifuged at 37,000 rpm (SW40 rotor) for 150 minutes at 4°C. The sucrose gradient was fractionated with the ISCP UV gradient fractionation system (BioComp), connected to a UV detector to monitor absorbance at 254 nm, and the polysome profile was recorded. Twelve fractions of 900 μl each were isolated and RNA was extracted using phenol:chloroform and ethanol precipitation followed by an RNeasy Mini Kit (Qiagen) for DNase treatment according to the manufacturer's instructions. Both total RNA and polysome-bound mRNA were analyzed on an Agilent Bioanalyzer to assess RNA integrity.\nThe RNASeq libraries were prepared from total RNA using the TruSeq™ RNA Sample Prep Kit v2 (Illumina Inc.,)."; [Cell type]'Source: ''cell line: MCF10A; treatment: Normoxia; fraction: Total mRNA; barcode: O097; replicate: Biological replicate 1; ', 'cell line: MCF10A; treatment: Hypoxia; fraction: Total mRNA; barcode: O098; replicate: Biological replicate 1; ', 'cell line: MCF10A; treatment: Normoxia+PP242; fraction: Total mRNA; barcode: O099; replicate: Biological replicate 1; ', 'cell line: MCF10A; treatment: Hypoxia+PP242; fraction: Total mRNA; barcode: O100; replicate: Biological replicate 1; ', 'cell line: MCF10A; treatment: Normoxia; fraction: Polysomal mRNA; barcode: O101; replicate: Biological replicate 1; ', 'cell line: MCF10A; treatment: Hypoxia; fraction: Polysomal mRNA; barcode: O102; replicate: Biological replicate 1; ', 'cell line: MCF10A; treatment: Normoxia+PP242; fraction: Polysomal mRNA; barcode: O103; replicate: Biological replicate 1; ', 'cell line: MCF10A; treatment: Hypoxia+PP242; fraction: Polysomal mRNA; barcode: O104; replicate: Biological replicate 1; ', 'cell line: MCF10A; treatment: Normoxia; fraction: Total mRNA; barcode: O105; replicate: Biological replicate 2; ', 'cell line: MCF10A; treatment: Hypoxia; fraction: Total mRNA; barcode: O106; replicate: Biological replicate 2; ', 'cell line: MCF10A; treatment: Normoxia+PP242; fraction: Total mRNA; barcode: O107; replicate: Biological replicate 2; ', 'cell line: MCF10A; treatment: Hypoxia+PP242; fraction: Total mRNA; barcode: O108; replicate: Biological replicate 2; ', 'cell line: MCF10A; treatment: Normoxia; fraction: Polysomal mRNA; barcode: O109; replicate: Biological replicate 2; ', 'cell line: MCF10A; treatment: Hypoxia; fraction: Polysomal mRNA; barcode: O110; replicate: Biological replicate 2; ', 'cell line: MCF10A; treatment: Normoxia+PP242; fraction: Polysomal mRNA; barcode: O111; replicate: Biological replicate 2; ', 'cell line: MCF10A; treatment: Hypoxia+PP242; fraction: Polysomal mRNA; barcode: O112; replicate: Biological replicate 2; ', 'cell line: MDA-MB-231; treatment: Normoxia; fraction: Total mRNA; barcode: U774; replicate: Biological replicate 1; ', 'cell line: MDA-MB-231; treatment: Hypoxia; fraction: Total mRNA; barcode: U775; replicate: Biological replicate 1; ', 'cell line: MDA-MB-231; treatment: Normoxia+PP242; fraction: Total mRNA; barcode: U776; replicate: Biological replicate 1; ', 'cell line: MDA-MB-231; treatment: Hypoxia+PP242; fraction: Total mRNA; barcode: U777; replicate: Biological replicate 1; ', 'cell line: MDA-MB-231; treatment: Normoxia; fraction: Polysomal mRNA; barcode: U778; replicate: Biological replicate 1; ', 'cell line: MDA-MB-231; treatment: Hypoxia; fraction: Polysomal mRNA; barcode: U779; replicate: Biological replicate 1; ', 'cell line: MDA-MB-231; treatment: Normoxia+PP242; fraction: Polysomal mRNA; barcode: U780; replicate: Biological replicate 1; ', 'cell line: MDA-MB-231; treatment: Hypoxia+PP242; fraction: Polysomal mRNA; barcode: U781; replicate: Biological replicate 1; ', 'cell line: MDA-MB-231; treatment: Normoxia; fraction: Total mRNA; barcode: U782; replicate: Biological replicate 2; ', 'cell line: MDA-MB-231; treatment: Hypoxia; fraction: Total mRNA; barcode: U783; replicate: Biological replicate 2; ', 'cell line: MDA-MB-231; treatment: Normoxia+PP242; fraction: Total mRNA; barcode: U784; replicate: Biological replicate 2; ', 'cell line: MDA-MB-231; treatment: Hypoxia+PP242; fraction: Total mRNA; barcode: U785; replicate: Biological replicate 2; ', 'cell line: MDA-MB-231; treatment: Normoxia; fraction: Polysomal mRNA; barcode: U786; replicate: Biological replicate 2; ', 'cell line: MDA-MB-231; treatment: Hypoxia; fraction: Polysomal mRNA; barcode: U787; replicate: Biological replicate 2; ', 'cell line: MDA-MB-231; treatment: Normoxia+PP242; fraction: Polysomal mRNA; barcode: U788; replicate: Biological replicate 2; ', 'cell line: MDA-MB-231; treatment: Hypoxia+PP242; fraction: Polysomal mRNA; barcode: U789; replicate: Biological replicate 2; ' GSE38234 Homo sapiens 16 Expression profiling by high throughput sequencing GPL11154 Genistein and bisphenol A exposure cause estrogen receptor 1 to bind thousands of binding sites in a cell type-specific manner 2012-05-24 To obtain an integrated view of gene regulation in response to environmental and endogenous estrogens on a genome-wide scale, we performed ChIP-seq, to identify estrogen receptor 1 (ER) binding sites, and RNA-seq in endometrial cancer cells exposed to bisphenol A (BPA; found in plastics), genistein (GEN; found in soybean), or 17β-estradiol (E2; an endogenous estrogen). GEN and BPA treatment induces thousands of ER binding sites and >50 gene expression changes, representing a subset of E2‑induced gene regulation changes. Genes affected by E2 were highly enriched for ribosome-associated proteins; however, GEN and BPA failed to regulate most ribosome-associated proteins and instead enriched for transporters of carboxylic acids. Treatment-dependent changes in gene expression were associated with treatment-dependent ER binding sites, with the exception that many genes up-regulated by E2 harbored a BPA-induced ER binding site, but failed to show any expression change after BPA treatment. GEN and BPA exhibited a similar relationship to E2 in the breast cancer line T-47D, where cell type specificity played a much larger role than treatment specificity. Overall, both environmental estrogens clearly regulate gene expression through ER on a genome-wide scale, although with lower potency resulting in less ER binding sites and less gene expression changes compared to the endogenous estrogen, E2. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE38234 Genistein and bisphenol A exposure cause estrogen receptor 1 to bind thousands of sites in a cell type-specific manner. Genome research 9.944 https://doi.org/10.1101/gr.135681.111 {Genome research (9.944): 10.1101/gr.135681.111} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA167511 https://www.ebi.ac.uk/ena/browser/view/PRJNA167511 https://www.ncbi.nlm.nih.gov/sra?term=SRP013389 [Overal design]RNA-seq of human cancer cell lines treated with estradiol, bisphenol A, genistein or DMSO (control); [Treatment]'Cells were treated with either 10 nM 17β-estradiol, 100 nM genistein, 100 nM bisphenol A or 0.02% DMSO (vehicle control) for 8 hours before harvesting.'; [Growth]'Both ECC-1 and T-47D were grown on phenol red-free RPMI-1640 supplemented with 10% dextran/charcoal treated fetal bovine serum for five days. RNA lysate was harvested from 100 mm dishes'; [Extraction]'mRNA was harvested using an mRNA-direct kit (Invitrogen), followed by DNase treatment. Non-directional libraries were then constructed as described in Gertz J, Varley KE, Davis NS, Baas BJ et al. Transposase mediated construction of RNA-seq libraries. Genome Res 2012 Jan;22(1):134-41.'; [Cell type]'Source: ''treatment: 8 hour 100 nM bisphenol A; replicate: 1; cell line: T-47D; ', 'treatment: 8 hour 0.02% DMSO; replicate: 1; cell line: T-47D; ', 'treatment: 8 hour 10 nM 17β-estradiol; replicate: 1; cell line: T-47D; ', 'treatment: 8 hour 100 nM genistein; replicate: 1; cell line: T-47D; ', 'treatment: 8 hour 100 nM bisphenol A; replicate: 2; cell line: T-47D; ', 'treatment: 8 hour 0.02% DMSO; replicate: 2; cell line: T-47D; ', 'treatment: 8 hour 10 nM 17β-estradiol; replicate: 2; cell line: T-47D; ', 'treatment: 8 hour 100 nM genistein; replicate: 2; cell line: T-47D; ', 'treatment: 8 hour 100 nM bisphenol A; replicate: 1; cell line: ECC-1; ', 'treatment: 8 hour 0.02% DMSO; replicate: 1; cell line: ECC-1; ', 'treatment: 8 hour 10 nM 17β-estradiol; replicate: 1; cell line: ECC-1; ', 'treatment: 8 hour 100 nM genistein; replicate: 1; cell line: ECC-1; ', 'treatment: 8 hour 100 nM bisphenol A; replicate: 2; cell line: ECC-1; ', 'treatment: 8 hour 0.02% DMSO; replicate: 2; cell line: ECC-1; ', 'treatment: 8 hour 10 nM 17β-estradiol; replicate: 2; cell line: ECC-1; ', 'treatment: 8 hour 100 nM genistein; replicate: 2; cell line: ECC-1; ' GSE32150 Homo sapiens 10 Expression profiling by array GPL4133 Elf5 inhibits epithelial mesenchymal transition in development and cancer metastasis through transcriptional repression of Snail2 2011-09-15 Elf5 (or ESE-2) is an ETS transcription factor that is abundantly expressed in the mammary epithelium, where it plays a critical role in dictating cell fate and lineage choices. These changes are in part mediated by alterations in the expression and activity of critical components of the Jak/Stat pathway. While the biological function of Elf5 in mammary gland development has been well characterized, its role in breast cancer remains to be elucidated. Here we show that loss of Elf5 leads to features associated with epithelial-mesenchymal transition (EMT) in the mouse mammary gland during pregnancy and lactation. These cellular changes in Elf5-null mammary epithelia are also reflected at the molecular level by the global enrichment of EMT-related gene signatures. ELF5 is expressed in higher level in weakly metastatic breast cancer cells that retained epithelial features compared to highly metastatic cells with mesenchymal features. ELF5 knockdown in T47D breast cancer cells resulted in EMT and increased migration. Conversely, ectopic expression of Elf5 revert mesenchymal-like MDA-MB-231 cells and its lung-tropic variant LM2 to an epithelial phenotype, with reduced migration, invasion and lung metastatic abilities. Finally, we showed that Elf5 binds directly to the promoter of the EMT transcriptional factor Snail2 (Slug) and repress its expression. Taken together, these data established a novel function for Elf5 in inhibiting EMT in normal mammary epithelium and in breast cancer through direct targeting of Snail2. This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32150 Elf5 inhibits the epithelial-mesenchymal transition in mammary gland development and breast cancer metastasis by transcriptionally repressing Snail2. Nature cell biology 17.728 https://doi.org/10.1038/ncb2607 {Nature cell biology (17.728): 10.1038/ncb2607} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA147651 https://www.ebi.ac.uk/ena/browser/view/PRJNA147651 None [Overal design]Refer to individual Series.; [Treatment]'LM2 cells were infected with lentivirus containing either Elf5 (in pLEX vector), and selected for 10 days with puromycin.', 'MDA-MB231cells were infected with lentivirus containing either wild type or mutant Elf5 (in pLEX vector), and selected for 10 days with puromycin.'; [Growth]'Standard cloning process was used to clone coding sequence of Elf5 or GFP in pLEX vector. Lentivirus were produced in H293T cells.or GFP control plasmid (pLEX vector),', 'Standard cloning process was used to clone coding sequence of Elf5 or DNA binding domain mutant Elf5 in pLEX vector. Lentivirus were produced in 293T cells.'; [Extraction]'Total RNA were extracted using RNAeasy mini-prep kit from Qiagen'; [Cell type]'Source: ''cell line: LM2 (MDA-MB231 subline); tissue: breast cancer; ', 'cell line: mixed; ', 'cell line: MDA-MB231; tissue: breast cancer; ' GSE95287 Homo sapiens 12 Expression profiling by array GPL20844 Expression profile of MCF7 and T47D human breast cancer cell lines upon treatment with the BET bromodomian inhibitor JQ1 2017-02-23 Expression profile of MCF7 and T47D human breast cancer cell lines upon treatment with the BET bromodomian inhibitor JQ1 https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95287 Bromodomain inhibition shows antitumoral activity in mice and human luminal breast cancer. Oncotarget None https://doi.org/10.18632/oncotarget.18255 {Oncotarget (None): 10.18632/oncotarget.18255} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA376563 https://www.ebi.ac.uk/ena/browser/view/PRJNA376563 None [Overal design]Two breast cancer cell lines (MCF7 and T47D) were treated with 1uM JQ1 or vehicle for 24 hours. Three biological replicates were obtained for each condition.; [Treatment]'Cells were treated with 1uM JQ1 or vehicle (DMSO) and incubated for 24 hours at 37ºC in a humidified incubator with 5%'; [Growth]'None'; [Extraction]"RNA was extracted using Maxwell ® RSC simply RNA Cell Kit (Promega) following the manufacturer's recommendations"; [Cell type]'Source: ''cell line: MCF7; agent: vehicle; ', 'cell line: MCF7; agent: JQ1; ', 'cell line: T47D; agent: vehicle; ', 'cell line: T47D; agent: JQ1; ' GSE51403 Homo sapiens 14 Expression profiling by high throughput sequencing GPL11154 RNA-seq differential expression studies: more sequence, or more replication? 2013-10-18 Motivation: RNA-seq is replacing microarrays as the primary tool for gene expression studies. Many RNA-seq studies have used insufficient biological replicates, resulting in low statistical power and inefficient use of sequencing resources. Results: We show the explicit trade-off between more biological replicates and deeper sequencing in increasing power to detect differentially expressed (DE) genes. In the human cell line MCF-7, adding more sequencing depth after 10M reads gives diminishing returns on power to detect DE genes, while adding biological replicates improves power significantly regardless of sequencing depth. We also propose a cost-effectiveness metric for guiding the design of large scale RNA-seq DE studies. Our analysis showed that sequencing less reads and perform more biological replication is an effective strategy to increase power and accuracy in large scale differential expression RNA-seq studies, and provided new insights into efficient experiment design of RNA-seq studies https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE51403 RNA-seq differential expression studies: more sequence or more replication? Bioinformatics (Oxford, England) 4.531 https://doi.org/10.1093/bioinformatics/btt688 {Bioinformatics (Oxford, England) (4.531): 10.1093/bioinformatics/btt688} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA222975 https://www.ebi.ac.uk/ena/browser/view/PRJNA222975 https://www.ncbi.nlm.nih.gov/sra?term=SRP031476 [Overal design]Treatment (10nM E2 treatment for 24h) and control MCF7 cells are both replicated 7 times, and collected for mRNA-seq. Reads are then subsampled for statistical analysis.; [Treatment]'Cells were hormone-deprived in phenol-free DMEM with 10% charcoal-stripped FBS 3 days before treatment with 10nM E2. mRNAs were collected 24hrs after treatment with Qiagen RNeasy mini kit.'; [Growth]"MCF7 breast cancer cells (ATCC HTB-22) were maintained in Dulbecco's modified Eagles's medium (DMEM), 10% fetal bovine serum (FBS), and antibiotics at 37oC in a 5% CO2 humidified atmosphere."; [Extraction]'Standard protocol of Qiagen RNeasy mini kit.\nStandard protocol of TrueSeq mRNA sample prep kit.'; [Cell type]'MCF7''treatment: 10nM E2 treatment for 24h; cell type: MCF7; ', 'treatment: Control ethanol 24h; cell type: MCF7; ' GSE98209 Homo sapiens 6 Expression profiling by high throughput sequencing GPL18573 eCLIP in immortalized human mammary epithelial cells 2017-04-25 The epithelial-to-mesenchymal transition (EMT) contributes to tumor heterogeneity and has been implicated in tumor initiation and metastasis. To systematically identify genes involved in EMT, we performed a genome-scale expression screen in human mammary epithelial cells and found a striking enrichment in RNA splicing factors. In particular, the RNA-binding proteins QKI and RBFOX1 were necessary and sufficient to promote EMT and stem-like states. Among the transcripts cooperatively regulated by both factors, we found that alternative splicing of the actin-binding protein FLNB plays an essential role in the regulation of EMT. The skipping of FLNB exon 30 and the elevated expression of QKI were strongly associated with EMT gene signatures in both basal B subtype breast cancer cell lines and basal-like breast cancer patient samples. These observations demonstrate that alternative splicing regulated by QKI and RBFOX1 plays an active role in promoting EMT in basal-like breast cancers. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE98209 An alternative splicing switch in FLNB promotes the mesenchymal cell state in human breast cancer. eLife 7.551 https://doi.org/10.7554/eLife.37184 {eLife (7.551): 10.7554/eLife.37184} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA384254 https://www.ebi.ac.uk/ena/browser/view/PRJNA384254 https://www.ncbi.nlm.nih.gov/sra?term=SRP105224 [Overal design]Immortalized human mammary epithelial cells stably overexpressing V5-tagged QKI or RBFOX1 were treated by UV crosslinking at 254nm with 400mJ/cm^2. Cells were processed as described in Van Nostrand et al (PMID: 27018577), with some slight modifications, as described in Li et al, 2017 (submitted).Immunoprecipitation was done using anti-V5 antibody (Life Technologies R96025) and for each protein, libraries were prepared from two replicates plus one size-matched input control for sequencing on the NextSeq 500 (single-end, 75bp).; [Treatment]'UV crosslinking (254nm) at 400mJ/cm^2'; [Growth]'None'; [Extraction]'Immunoprecipitation of RNA-protein complexes and purification of RNA were done as described in the ENCODE eCLIP protocol (Van Nostrand et al. 2016, PMID: 27018577 and ENCODE).\nLibraries were constructed as described in the ENCODE eCLIP protocol (Van Nostrand et al 2016, PMID: 27018577), with slight modifications as described in Li et al (submitted).'; [Cell type]'Immortalized mammary epithelial cells (HME)''cell type: Immortalized mammary epithelial cells (HME); genotype/variation: stably overexpressing V5-tagged QKI; treated with: UV crosslinking at 254nm with 400mJ/cm^2; ', 'cell type: Immortalized mammary epithelial cells (HME); genotype/variation: stably overexpressing V5-tagged RBFOX1; treated with: UV crosslinking at 254nm with 400mJ/cm^2; ' GSE166406 Homo sapiens 6 Non-coding RNA profiling by high throughput sequencing GPL18573 Effect of PAK5 gene on miRNA expression in MDA-MB-231 cells 2021-02-09 P21-activated kinase 5 (PAK5) plays an important role in tumors. Yet, the connection of PAK5 with miRNA biogenesis is so far unclear.In this work, we studied the change in microRNA profiles of breast cancer MDA-MB-231 cells as a result of overexpression of PAK5 protein. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE166406 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA700839 https://www.ebi.ac.uk/ena/browser/view/PRJNA700839 https://www.ncbi.nlm.nih.gov/sra?term=SRP305457 [Overal design]Total RNA was prepared from MDA-MB-231 cells with overexpression of Flag-PAK5 gene as well as from control MDA-MB-231(Flag vector) cells.; [Treatment]'Flag PAK5 and Falg vector lentivirus were obtained from Shanghai Genechem Co., Ltd. Virus supernatant was incubated on target cells for 24 hours, following the manufacturer’s instructions. Infected cells were selected in puromycin, as optimized for cell line.'; [Growth]"The human breast cancer cell lines MDA-MB-231 were obtained from Shanghai cell bank of CAS-Chinese Academy of Sciences. MDA-MB-231 cells were cultured in Leibovitz's L-15 Medium containing 10% FBS (fetal bovine serum). Cells were routinely maintained in a humidified chamber at 37°C and 5% CO2."; [Extraction]"Retinas were removed, flash frozen on dry ice, and RNA was harvested using Trizol reagent.\nTotal RNA was extracted from breast cancer cells using the TRIzol reagent (Invitrogen/Life Technologies) following the manufacturer’s protocol. Total RNA of each sample was used to prepare the miRNA sequencing library, which included the following steps: 1) 3'-adaptor ligation; 2) 5'-adaptor ligation; 3) cDNA synthesis; 4) PCR amplification; 5) size selection of ~135-155 bp PCR amplified fragments (corresponding to ~15-35 nt small RNAs). The libraries were denatured as single-stranded DNA molecules, captured on Illumina flow cells, amplified in situ as clusters and finally sequenced for 50 cycles on Illumina NextSeq per the manufacturer's instructions."; [Cell type]'breast cancer cells''cell line: MDA-MB-231; cell type: breast cancer cells; treatment: Flag vector was stably expressed in mammary adenocarcinoma MDA-MB-231 cells; ', 'cell line: MDA-MB-231; cell type: breast cancer cells; treatment: Flag-tagged PAK5 (Flag-PAK5) was stably expressed in mammary adenocarcinoma MDA-MB-231 cells; ' GSE33216 Homo sapiens 6 Genome binding/occupancy profiling by high throughput sequencing GPL9052; GPL11154 Genome-wide maps of H3K4me2 and DNase I hypersensitivity sites in prostate cancer cell line LNCaP and breast cancer cell line MCF-7. 2011-10-25 We report the high-throughput profiling of histone modification and DNase I hypersensitivity sites in prostate cancer and breaset cancer cells. We found that while AR binding is associated with nucleosome depletion, ER binding is not. We showed that a quantitative measure of DNase I hypersensitivity changes is a powerful tool in indentifying transcription factor cistromes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE33216 Differential DNase I hypersensitivity reveals factor-dependent chromatin dynamics. Genome research 9.944 https://doi.org/10.1101/gr.133280.111 {Genome research (9.944): 10.1101/gr.133280.111} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA149445 https://www.ebi.ac.uk/ena/browser/view/PRJNA149445 https://www.ncbi.nlm.nih.gov/sra?term=SRP009093 [Overal design]Examination of histone modification marked nucleosomes and Dnase I hypersensitivity in prostate cancer and breast cancer cells with and without hormone treatment.; [Treatment]'Cells were cultured in RPMI 1640 supplemented with 10% charcoal-stripe FBS for 3 days, and then treated with DHT or Ethanol for 4 hours for prostate cancer cells, treated with E2 or Ethanal for 45mins for breast cancer cells'; [Growth]'None'; [Extraction]"H3K4me2 ChIPed DNA or the size selected DNase I digested DNA was used for library preparation. Libraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit (Part# 0801-0303). Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation DNA was PCR amplified with Illumina primers for 18 cycles and library fragments of ~220 bp (for H3K4me2 ChIP-seq) or 200~300bp (for DNase-seq) (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the Genome Analyzer or HiSeq machine following the manufacturer's protocols."; [Cell type]'prostate cancer cells', 'breast cancer cells''cell line: LNCaP; cell type: prostate cancer cells; passages: 14-17; treatment: ethanol; sample type: DNase-seq; ', 'cell line: LNCaP; cell type: prostate cancer cells; passages: 14-17; treatment: DHT; sample type: DNase-seq; ', 'cell line: MCF-7; cell type: breast cancer cells; passages: 20-26; treatment: ethanol; sample type: DNase-seq; ', 'cell line: MCF-7; cell type: breast cancer cells; passages: 20-26; treatment: DHT; sample type: DNase-seq; ', 'cell line: MCF-7; cell type: breast cancer cells; passages: 20-26; treatment: ethanol; chip antibody: H3K4me2; sample type: Chromatin IP against H3K4me2; chip antibody manufacturer: Millipore; chip antibody catalog #: 07-030; chip antibody lot #: DAM1570816; ', 'cell line: MCF-7; cell type: breast cancer cells; passages: 20-26; treatment: E2; chip antibody: H3K4me2; sample type: Chromatin IP against H3K4me2; chip antibody manufacturer: Millipore; chip antibody catalog #: 07-030; chip antibody lot #: DAM1570816; ' GSE15523 Homo sapiens 31 Expression profiling by array GPL887; GPL1390 A Core MYC Gene Expression Signature is prominent in basal-like cancer 2009-04-02 BACKGROUND: The MYC oncogene contributes to induction and growth of many cancers but the full spectrum of the MYC transcriptional response remains unclear. METHODOLOGY/PRINCIPAL FINDINGS: Using microarrays, we conducted a detailed kinetic study of genes that respond to MYCN or MYCNDeltaMBII induction in primary human fibroblasts. In parallel, we determined the response to steady state overexpression of MYCN and MYCNDeltaMBII in the same cell type. An overlapping set of 398 genes from the two protocols was designated a 'Core MYC Signature' and used for further analysis. Comparison of the Core MYC Signature to a published study of the genes induced by serum stimulation revealed that only 7.4% of the Core MYC Signature genes are in the Core Serum Response and display similar expression changes to both MYC and serum. Furthermore, more than 50% of the Core MYC Signature genes were not influenced by serum stimulation. In contrast, comparison to a panel of breast cancers revealed a strong concordance in gene expression between the Core MYC Signature and the basal-like breast tumor subtype, which is a subtype with poor prognosis. This concordance was supported by the higher average level of MYC expression in the same tumor samples. CONCLUSIONS/SIGNIFICANCE: The Core MYC Signature has clinical relevance as this profile can be used to deduce an underlying genetic program that is likely to contribute to a clinical phenotype. Therefore, the presence of the Core MYC Signature may predict clinical responsiveness to therapeutics that are designed to disrupt MYC-mediated phenotypes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15523 A core MYC gene expression signature is prominent in basal-like breast cancer but only partially overlaps the core serum response. PloS one 2.776 https://doi.org/10.1371/journal.pone.0006693 {PloS one (2.776): 10.1371/journal.pone.0006693} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA115697 https://www.ebi.ac.uk/ena/browser/view/PRJNA115697 None [Overal design]reference X sample; [Treatment]'None', 'Sample was mock treated', 'Sample was treated with 0.8uM 4-hydroxytamoxifen', 'not treated'; [Growth]'None', 'DMEM + 10% FBS, 0.8ug/ml puromycin', 'DMEM + 10% FBS, 150 ug/ml hygromycin'; [Extraction]'Trizol, followed by RNeasy', 'Qiagen RNeasy protocol'; [Cell type]'human foreskin fibroblast cells (BJ cells)''cell type: human foreskin fibroblast cells (BJ cells); growth protocol: rapidly dividing when harvested; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with control virus (LCPX), selected and harvested at T= 0hr; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with control virus (LCPX), selected and harvested at T= 8hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with control virus (LCPX), selected and harvested at T= 48hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc, selected and harvested at T= 0hr; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc, selected and harvested at T= 2hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc, selected and harvested at T= 4hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc, selected and harvested at T= 8hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc, selected and harvested at T= 12hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc, selected and harvested at T= 24hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc, selected and harvested at T= 36hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc, selected and harvested at T= 48hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-Nmyc(delta-MBII), selected and harvested at T= 0hr; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc(delta-MBII), selected and harvested at T= 0hr; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc(delta-MBII), selected and harvested at T= 2hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc(delta-MBII), selected and harvested at T= 4hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc(delta-MBII), selected and harvested at T= 8hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc(delta-MBII), selected and harvested at T= 12hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc(delta-MBII), selected and harvested at T= 24hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc(delta-MBII), selected and harvested at T= 36hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LCPX-NMyc(delta-MBII), selected and harvested at T= 48hr after OHT treatment; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with control LXSH virus, selected and harvested weeks after viral transduction; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LXSH-NMyc, selected and harvested weeks after viral transduction; ', 'cell type: human foreskin fibroblast cells (BJ cells); treatment protocol: BJ cells were infected with LXSH-Nmyc(delta-MBII), selected and harvested weeks after viral transduction; ' GSE95529 Homo sapiens 23 Expression profiling by array GPL570 ESR1 mutations affect anti-proliferative responses to tamoxifen through enhanced cross-talk with IGF signaling 2017-02-28 The rediscovery of estrogen receptor (ESR1) mutations in metastatic breast cancer is current clinical scenario. We have modeled the three most frequent ESR1 mutations using stable lentiviral vectors in human breast cancer cell lines, and determined that they confer relative resistance to tamoxifen (Tam) in a cell-type specific manner due to distinct epigenetic changes. Resistance was only observed with concomitant engagement and activation of the insulin growth factor signaling pathway (IGF1R). The ESR1 mutants also exhibited enhanced binding with insulin growth factor receptor beta (IGF1Rβ). The selective estrogen degrader, fulvestrant, significantly reduced the anchorage-independent growth of ESR1 mutant-expressing cells, while the combination treatment with the mTOR inhibitor everolimus, restored Tam sensitivity. Since we detected relatively high frequencies of these three mutations in primary breast tumors, our results suggest that clinical targeted sequencing of both primary and metastatic tumors may be justified and comination therapies considered. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE95529 ESR1 mutations affect anti-proliferative responses to tamoxifen through enhanced cross-talk with IGF signaling. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-016-3829-5 {Breast cancer research and treatment (3.471): 10.1007/s10549-016-3829-5} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA377332 https://www.ebi.ac.uk/ena/browser/view/PRJNA377332 None [Overal design]2 cell lines: MCF7C and ZR75; 2 genotypes: WT or Y537S mutation; 2 treatments: Control or Tamoxifen; 23 samples in total, 8 groups; [Treatment]'breast cancer cell lines'; [Growth]'NA'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MCF7C; wt or y537s: WT; treatment: Control; ', 'cell line: MCF7C; wt or y537s: WT; treatment: Tamoxifen; ', 'cell line: MCF7C; wt or y537s: Y537S; treatment: Control; ', 'cell line: MCF7C; wt or y537s: Y537S; treatment: Tamoxifen; ', 'cell line: ZR75; wt or y537s: WT; treatment: Control; ', 'cell line: ZR75; wt or y537s: WT; treatment: Tamoxifen; ', 'cell line: ZR75; wt or y537s: Y537S; treatment: Control; ', 'cell line: ZR75; wt or y537s: Y537S; treatment: Tamoxifen; ' GSE15361 Homo sapiens 50 Expression profiling by array GPL7785 Molecular profiling of breast cancer cell lines defines relevant tumor models (gene expression) 2009-03-23 Summary: Breast cancer cell lines have been used widely to investigate breast cancer pathobiology and new therapies. Breast cancer is a molecularly heterogeneous disease, and it is important to understand how well and which cell lines best model that diversity. In particular, microarray studies have identified molecular subtypes (luminal A, luminal B, ERBB2-associated, basal-like and normal-like) with characteristic gene-expression patterns and underlying DNA copy number alterations (CNAs). Here, we studied a collection of breast cancer cell lines to catalog molecular profiles and to assess their relation to breast cancer subtypes. Whole-genome DNA microarrays were used to profile gene expression and CNAs in a collection of 52 widely-used breast cancer cell lines, and comparisons were made to existing profiles of primary breast tumors. Hierarchical clustering was used to identify gene-expression subtypes, and Gene Set Enrichment Analysis (GSEA) to discover biological features of those subtypes. Genomic and transcriptional profiles were integrated to discover within high-amplitude CNAs candidate cancer genes with coordinately altered gene copy number and expression. Transcriptional profiling of breast cancer cell lines identified one luminal and two basal-like (A and B) subtypes. Luminal lines displayed an estrogen receptor (ER) signature and resembled luminal-A/B tumors, basal-A lines were associated with ETS-pathway and BRCA1 signatures and resembled basal-like tumors, and basal-B lines displayed mesenchymal and stem-cell characteristics. Compared to tumors, cell lines exhibited similar patterns of CNA, but an overall higher complexity of CNA (genetically simple luminal-A tumors were not represented), and only partial conservation of subtype-specific CNAs. We identified 80 high-level DNA amplifications and 13 presumptive homozygous deletions, and the resident genes with concomitantly altered gene-expression, highlighting known and novel candidate breast cancer genes. Overall, breast cancer cell lines were genetically more complex than tumors, but retained expression patterns with relevance to the luminal-basal subtype distinction. The compendium of molecular profiles defines cell lines suitable for investigations of subtype-specific pathobiology, biomarkers and therapies, and provides a resource for discovery of new breast cancer genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15361 Molecular profiling of breast cancer cell lines defines relevant tumor models and provides a resource for cancer gene discovery. PloS one 2.776 https://doi.org/10.1371/journal.pone.0006146 {PloS one (2.776): 10.1371/journal.pone.0006146} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA123251 https://www.ebi.ac.uk/ena/browser/view/PRJNA123251 None [Overal design]HEEBO oligonucleotide microarrays from the Stanford Functional Genomics Facility were used to perform gene expression profiling of 50 human breast epithelial cell lines, in comparison to a universal RNA reference. Expression data were analyzed by hierarchical clustering to identify subgroups, and gene set enrichment analysis to identify subgroup-specific gene pathways.; [Treatment]'None'; [Growth]'None'; [Extraction]'not provided'; [Cell type]'Source: ', 'epithelial-like', 'fibroblast-like', 'normal breast fibroblasts''reference: Common Reference RNA; ', 'cell line: BT474; cell type: epithelial-like; ', 'cell line: MDA231; cell type: fibroblast-like; ', 'cell line: BT20; cell type: epithelial-like; ', 'cell line: SKBR3; cell type: epithelial-like; ', 'cell line: T47D; cell type: epithelial-like; ', 'cell line: 1394; cell type: normal breast fibroblasts; ', 'cell line: MCF7; cell type: epithelial-like; ', 'cell line: 1714; cell type: normal breast fibroblasts; ', 'cell line: 1299; cell type: normal breast fibroblasts; ', 'cell line: 1632; cell type: normal breast fibroblasts; ', 'cell line: BT549; cell type: fibroblast-like; ', 'cell line: MDA361; cell type: epithelial-like; ', 'cell line: UACC893; cell type: epithelial-like; ', 'cell line: MDA453; cell type: epithelial-like; ', 'cell line: MDA436; cell type: fibroblast-like; ', 'cell line: BT20; ', 'cell line: HCC70; ', 'cell line: HCC2218; ', 'cell line: HCC202; ', 'cell line: HCC2185; ', 'cell line: SUM149; ', 'cell line: HCC1937; ', 'cell line: MDA468; ', 'cell line: HCC1569; ', 'cell line: BT483; ', 'cell line: MCF10A; ', 'cell line: HCC2688; ', 'cell line: HCC3153; ', 'cell line: HCC1143; ', 'cell line: SUM52; ', 'cell line: HCC1500; ', 'cell line: SKBR3; ', 'cell line: HCC38; ', 'cell line: MDA134; ', 'cell line: HCC2157; ', 'cell line: HCC1428; ', 'cell line: HCC1419; ', 'cell line: HCC1187; ', 'cell line: HCC1599; ', 'cell line: HTERT; ', 'cell line: SUM190; ', 'cell line: SUM102; ', 'cell line: HCC1007; ', 'cell line: Cal51; ', 'cell line: HCC1395; ', 'cell line: MDA361; ', 'cell line: 184A1; ', 'cell line: HCC1954; ', 'cell line: HCC712; ', 'cell line: UACC893; ' GSE25231 Homo sapiens 91 Expression profiling by array GPL5826 Expression Profiling of Formalin-Fixed Parafin-Embedded Primary Breast Tumors DASL Cancer Panel 2010-11-09 HER2-positive and HER2-negative samples are compared within this DASL Cancer Panel Platform https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE25231 Expression profiling of formalin-fixed paraffin-embedded primary breast tumors using cancer-specific and whole genome gene panels on the DASL® platform. BMC medical genomics 2.568 https://doi.org/10.1186/1755-8794-3-60 {BMC medical genomics (2.568): 10.1186/1755-8794-3-60} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA142529 https://www.ebi.ac.uk/ena/browser/view/PRJNA142529 None [Overal design]Two-class comparison; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted using the Roche Hi-Pure RNA extraction kit in accordance with the prescribed protocol provided with the kit. Quality control was performed using a NanoDrop ND-100 spectrophotometer and an Agilent Bioanalyser.'; [Cell type]'Source: ''her2status: neg; subject id: c105; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c105; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c105; extract code: B; replicate number: 1; ', 'her2status: neg; subject id: c105; extract code: B; replicate number: 2; ', 'her2status: neg; subject id: c114; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c114; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c114; extract code: A; replicate number: 3; ', 'her2status: neg; subject id: c118; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c118; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c118; extract code: A; replicate number: 3; ', 'her2status: neg; subject id: c120; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c120; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c120; extract code: B; replicate number: 1; ', 'her2status: neg; subject id: c120; extract code: B; replicate number: 2; ', 'her2status: neg; subject id: c139; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c139; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c139; extract code: B; replicate number: 1; ', 'her2status: neg; subject id: c139; extract code: B; replicate number: 2; ', 'her2status: neg; subject id: c143; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c143; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c143; extract code: A; replicate number: 3; ', 'her2status: neg; subject id: c145; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c145; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c145; extract code: A; replicate number: 3; ', 'her2status: neg; subject id: c158; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c158; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c158; extract code: A; replicate number: 3; ', 'her2status: neg; subject id: c162; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c162; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c162; extract code: A; replicate number: 3; ', 'her2status: neg; subject id: c163; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c163; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c163; extract code: A; replicate number: 3; ', 'her2status: neg; subject id: c165; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c165; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c165; extract code: B; replicate number: 1; ', 'her2status: neg; subject id: c165; extract code: B; replicate number: 2; ', 'her2status: pos; subject id: c018; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c018; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c018; extract code: B; replicate number: 1; ', 'her2status: pos; subject id: c018; extract code: B; replicate number: 2; ', 'her2status: pos; subject id: c026; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c026; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c026; extract code: A; replicate number: 3; ', 'her2status: pos; subject id: c027; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c027; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c027; extract code: A; replicate number: 3; ', 'her2status: pos; subject id: c030; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c030; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c030; extract code: A; replicate number: 3; ', 'her2status: pos; subject id: c035; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c035; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c035; extract code: A; replicate number: 3; ', 'her2status: pos; subject id: c042; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c042; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c042; extract code: B; replicate number: 1; ', 'her2status: pos; subject id: c042; extract code: B; replicate number: 2; ', 'her2status: pos; subject id: c046; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c046; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c046; extract code: A; replicate number: 3; ', 'her2status: pos; subject id: c049; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c049; extract code: A; replicate number: 3; ', 'her2status: pos; subject id: c051; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c051; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c051; extract code: B; replicate number: 1; ', 'her2status: pos; subject id: c051; extract code: B; replicate number: 2; ', 'her2status: pos; subject id: c058; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c058; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c058; extract code: B; replicate number: 1; ', 'her2status: pos; subject id: c058; extract code: B; replicate number: 2; ', 'her2status: pos; subject id: c068; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c068; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c068; extract code: A; replicate number: 3; ', 'her2status: pos; subject id: c006; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c006; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c072; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c072; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c072; extract code: A; replicate number: 3; ', 'her2status: pos; subject id: c076; extract code: A; replicate number: 1; ', 'her2status: pos; subject id: c076; extract code: A; replicate number: 2; ', 'her2status: pos; subject id: c076; extract code: B; replicate number: 1; ', 'her2status: pos; subject id: c076; extract code: B; replicate number: 2; ', 'her2status: neg; subject id: c088; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c088; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c088; extract code: A; replicate number: 3; ', 'her2status: neg; subject id: c096; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c096; extract code: B; replicate number: 1; ', 'her2status: neg; subject id: c096; extract code: B; replicate number: 2; ', 'her2status: neg; subject id: c097; extract code: A; replicate number: 1; ', 'her2status: neg; subject id: c097; extract code: A; replicate number: 2; ', 'her2status: neg; subject id: c097; extract code: A; replicate number: 3; ' GSE53320 Homo sapiens 4 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Chromatinized PKC-q directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells 2013-12-13 Epithelial to mesenchymal transition (EMT) is activated during cancer invasion and metastasis, enriches for cancer stem cells (CSCs), and contributes to therapeutic resistance and disease recurrence. Signal transduction kinases play a pivotal role as chromatin-anchored proteins in eukaryotes. Here we report for the first time that protein kinase C-theta (PKC-q) regulates EMT by acting as a critical chromatin-anchored switch for inducible genes via TGF-β and the key inflammatory regulatory protein, NFkB. Chromatinized PKC-q exists as an active transcription complex and is required to establish a permissive chromatin state at signature EMT genes. Genome-wide analysis identifies a unique cohort of inducible PKC-q-sensitive genes that are directly tethered to PKC-q in the mesenchymal state. Collectively, we show that crosstalk between signaling kinases and chromatin is critical for eliciting inducible transcriptional programs that drive mesenchymal differentiation and CSC formation, providing novel mechanisms to target using epigenetic therapy in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53320 Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells. Molecular and cellular biology 3.735 https://doi.org/10.1128/MCB.01693-13 {Molecular and cellular biology (3.735): 10.1128/MCB.01693-13} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA231742 https://www.ebi.ac.uk/ena/browser/view/PRJNA231742 https://www.ncbi.nlm.nih.gov/sra?term=SRP034328 [Overal design]2 biological samples were analysed, Immunoprecipitated and total input samples were obtained from each biological treatment. 2 Technical replicates were performed (samples from the sample lib prep were run on two different lanes).; [Treatment]'Cells were left untreated or stimulated with PMA (0.65ng/ml) for 60h.'; [Growth]'Cells were cultured at 37C in low glucose DMEM (Gibco) and supplemented with 10% FCS, 2mM L-glutamine, and 0.1% PSN antibiotics.'; [Extraction]'ChIP samples were prepared with anti-PKC-theta (sc-212, SantaCruz), according to the protocol supplied by Upstate Biotechnology.\n10ng of PKC-theta immunoprecipitated ChIP-DNA, and the corresponding total input (TI), were used to prepare the ChIP-seq DNA library using the NEBNext® ChIP-Seq Library Prep Master Mix Set for Illumina® (New England BioLabs Inc, NEB#E6240L) according to the manufacturer’s instructions. ChIP-DNA size was selected with AMPure XP beads (Beckman Coulter, Inc., Part #: A63881). The selected DNA was repaired with NEBNext End Repair Enzyme Mix and Buffer, followed by treatment with Klenow fragment (3’à5’ exo-) to generate “A” base overhangs. Subsequent adaptor ligation of the dA-tailed DNA was performed with 1.5μM NEBNext adaptor primers, Quick Ligation Reaction Buffer, and Quick T4 DNA ligase. AMPure beads were used to isolate library fragments ranging between 175 and 225bp in size and the purified DNA was combined with the NEBNext High-Fidelity 2X PCR Master mix, 25μM Universal PCR primer, and 25μM index primer for multiplexing purposes (New England BioLabs Inc, NEBNext® Multiplex Oligos for Illumina®, NEB#E7335L). A total of 15 cycles were used for PCR amplification of the adaptor-ligated DNA. The resultant ChIP-DNA library was subjected to DNA purification with AMPure beads. The quality of the ChIP-DNA library was assessed on a Bioanalyzer. A total of 2nM was captured on the Illumina flow cell for cluster generation'; [Cell type]'Source: ''treatment: none; cell line: MCF7; chip antibody: PKCtheta (sc-212, SantaCruz); ', 'treatment: PMA; cell line: MCF7; chip antibody: PKCtheta (sc-212, SantaCruz); ', 'treatment: none; cell line: MCF7; chip antibody: Total input; ', 'treatment: PMA; cell line: MCF7; chip antibody: Total input; ' GSE35873 Mus musculus 8 Genome variation profiling by SNP array; Genome binding/occupancy profiling by SNP array GPL13147 Affymetrix SNP array data for breast cancer formation in mouse 2012-02-16 We investigated the CNAs in a four stage tumorigenesis model. This model included copy number analyses in non-transgenic NMRI mice (normal) and in transgenic SVT/t mice: non-malignant hyperplastic mammary glands and breast cancers, as well as breast cancer derived cell lines. We focused our research on copy number analyses to compare the genomic alterations that occur during tumorigenesis. We addressed the question, whether common predisposed chromosomal breakpoints could be seen to promote malignant transformation. We can report a characteristic increase of copy number alterations from normal to tumor stage in our model. Furthermore, we have identified chromosomal segments and found characteristic fragmentations. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE35873 SNP microarray analyses reveal copy number alterations and progressive genome reorganization during tumor development in SVT/t driven mice breast cancer. BMC cancer 2.933 https://doi.org/10.1186/1471-2407-12-380 {BMC cancer (2.933): 10.1186/1471-2407-12-380} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA151929 https://www.ebi.ac.uk/ena/browser/view/PRJNA151929 None [Overal design]Affymetrix SNP array analysis was performed with Mouse Diversity Genotyping Arrays (Affymetrix). DNA was extracted from frozen biopsies of mammary tumor samples of six mice and two cell lines. Normalization and allele summarization were performed with the BRLMM-P algorithm provided and copy number analysis was performed for the each sample using the average signal intensity of both normal samples as the reference for copy number inference.; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA was extracted using Purelink Genomic DNA Kit (K1820, Invitrogen) in accordance with the manufacturers protocol.'; [Cell type]'Source: ''genetic background: NMRI; tissue: normal mammary gland; ', 'genetic background: NMRI; transgene: WAP-SVT-t; tissue: non-malignant hyperplastic mammary glands; ', 'tissue: breast cancer tumor; ', 'cell line: 762TuD; phenotype: cytosine arabinoside sensitive; ', 'cell line: 762TuD; phenotype: cytosine arabinoside resistant; ' GSE56252 Mus musculus 14 Expression profiling by array GPL10787 The reprogramming of tumor stroma by HSF1 is a potent enabler of malignancy 2014-03-26 Stromal cells within the tumor microenvironment are essential for tumor progression and metastasis. Yet surprisingly little is known about the factors that drive the transcriptional reprogramming of stromal cells within tumors. We report that the transcriptional regulator Heat-Shock Factor 1 (HSF1) is activated in cancer-associated fibroblasts (CAFs) and is a potent enabler of malignancy. In CAFs, HSF1 drives a transcriptional program that complements, yet is completely different from, the program it drives in adjacent cancer cells. This CAF program is uniquely structured to support the malignant potential of cancer cells in a non-cell-autonomous way and involves two central stromal signaling molecules—TGFβ and stromal-derived factor 1 (SDF1). As clinical confirmation, in early stage breast and lung cancer high stromal HSF1 activation is strongly associated with poor patient outcome. Thus, cancers co-opt the ancient, multifaceted survival functions of HSF1 to orchestrate malignant progression in unexpected ways that have far-reaching therapeutic implications. Gene expression data https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE56252 The reprogramming of tumor stroma by HSF1 is a potent enabler of malignancy. Cell 36.216 https://doi.org/10.1016/j.cell.2014.05.045 {Cell (36.216): 10.1016/j.cell.2014.05.045} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA242748 https://www.ebi.ac.uk/ena/browser/view/PRJNA242748 None [Overal design]We used microarrays to examine the HSF1-dependent effect of co-culture on gene expression in cancer cells and fibroblasts. D2A1 mouse breast cancer cells were co-cultured with WT or Hsf1 null MEFs for 72h, afterwhich the two cell types were separated from each other by FACS and analyzed. Each cell type was also grown separately, as control.; [Treatment]'For profiling of cancer cells, MEFs were treated with 10 μg/ml mitomycin C for 2h before co-culture.'; [Growth]'In vitro cultured in DMEM with 10% FCS'; [Extraction]'Qiagen RNeasy kit'; [Cell type]'D2A1 tumor cells', 'Mouse Embryonic Fibroblasts''cell type: D2A1 tumor cells; genotype: not applicable; ', 'cell type: Mouse Embryonic Fibroblasts; genotype: Hsf1 +/+; ', 'cell type: Mouse Embryonic Fibroblasts; genotype: Hsf1 -/-; ' GSE148995 Homo sapiens 46 Genome binding/occupancy profiling by high throughput sequencing GPL20301 Cell-type-specific epigenomic variations associated with BRCA1 mutation in pre-cancer human breast tissues 2020-04-20 BRCA1 germline mutation carriers are predisposed to breast cancers. Epigenomic regulations have been known to strongly interact with genetic variations and potentially mediate biochemical cascades involved in tumorigenesis. Due to the cell-type specificity of epigenomic features, profiling of individual cell types is critical for understanding the molecular events in various cellular compartments within complex breast tissue. Here we report cell-type specific profiling of genome-wide histone modifications, including H3K27ac and H3K4me3 in basal, luminal progenitor, mature luminal, and stromal cells, extracted from pre-cancer BRCA1 mutation carriers and non-carriers, using a low-input technology. We discover that basal and stromal cells present the most substantial epigenomic differences between mutation carriers and non-carriers while luminal progenitor and mature luminal cells are relatively unchanged with the mutation. Furthermore, the epigenomic changes in basal cells due to BRCA1 mutation appear to facilitate their transformation into luminal progenitor cells. Our findings shed light on the pre-cancer epigenomic dynamics due to BRCA1 mutation and how they may contribute to eventual development of basal-like breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148995 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA626688 https://www.ebi.ac.uk/ena/browser/view/PRJNA626688 https://www.ncbi.nlm.nih.gov/sra?term=SRP257603 [Overal design]H3K27ac and H3K4me3 were profiled in four cell types from healthy breast tissues in women with and without the BRCA1 gene mutation. The cell types include basal cells (BCs), luminal progenitor cells (LPs), mature luminal cells (MLs), and stromal cells (SCs). We examined five non-carriers (BRCA1+/+: NC-1, NC-2, NC-3, NC-4, and NC-5) and three BRCA1 mutation carriers (BRCA1mut/+: MUT-1, MUT-2, and MUT-3). The profiling was conducted using MOWChIP-seq technology (Cao et al. Nature Methods, 12 (2015) 959-962; Zhu et al. Nature Protocols 14 (2019) 3366-3394).; [Treatment]'None'; [Growth]'None'; [Extraction]'Sorted samples containing 100K – 3M cells were used as the starting material and centrifuged at 1,600 g for 5 min and washed twice with 1 ml cold PBS. Cells were resuspended in 1 ml freshly made 1% formaldehyde and incubated at room temperature for 5 min on a shaker. Crosslinking was quenched by adding 50 µl of 2.5 M glycine and shaking for 5 min. The pellet was resuspended in 130 μl sonication buffer (10 mM Tris-HCl, pH 8.1, 1 mM EDTA, 0.1% SDS and 1× protease inhibitor cocktail) and sonicated with 105 W peak incident power, 5% duty factor, and 200 cycles per burst for 16 min using a Covaris S220 sonicator. The sheared sample was centrifuged in a 4 oC centrifuge at 16,100g for 10 min, and the supernatant was transferred to a new tube. Sheared chromatin was diluted with IP buffer (20 mM Tris-HCl, pH 8.0, 140 mM NaCl, 1 mM EDTA, 0.5 mM EGTA, 0.1% (w/v) sodium deoxycholate, 0.1% SDS, 1% (v/v) Triton X-100, with 1% freshly added PMSF and PIC) and diluted to contain chromatin from 50,000 cells (H3K27ac) or 10,000 cells (H3K4me3) in 50µL\nLibrary preparation was performed using the Accel-NGS 2S Plus DNA Library Kit (Swift Biosciences) using 8 μl of purified DNA per sample. 2.5 μl of the low EDTA TE buffer in the 50 μl amplification cycle reaction mix was replaced with 2.5 μl of 20x EvaGreen, and amplification was terminated after samples saw a >3000 RFU increase (BioRad CFX Connect). Amplified DNA was then eluted into 10 μl low EDTA TE buffer where 2 μl could be used in qPCR for preliminary quality control analysis, Kappa DNA quantification, and Tapestation fragment size analysis with the other 8 μl for library pooling. Libraries were pooled at 10 nM for sequencing by Illumina HiSeq 4000 with single-end 50 nt read.'; [Cell type]'Breast basal cells', 'Breast luminal progenitors', 'Breast mature luminal cells', 'Breast stromal cells''genotype: BRCA+/+; cell type: Breast basal cells; chip antibody: H3K27ac (abcam, Cat: ab4729, Lot: GR323132-1); ', 'genotype: BRCAmut/+; cell type: Breast basal cells; chip antibody: H3K27ac (abcam, Cat: ab4729, Lot: GR323132-1); ', 'genotype: BRCA+/+; cell type: Breast luminal progenitors; chip antibody: H3K27ac (abcam, Cat: ab4729, Lot: GR323132-1); ', 'genotype: BRCAmut/+; cell type: Breast luminal progenitors; chip antibody: H3K27ac (abcam, Cat: ab4729, Lot: GR323132-1); ', 'genotype: BRCA+/+; cell type: Breast mature luminal cells; chip antibody: H3K27ac (abcam, Cat: ab4729, Lot: GR323132-1); ', 'genotype: BRCAmut/+; cell type: Breast mature luminal cells; chip antibody: H3K27ac (abcam, Cat: ab4729, Lot: GR323132-1); ', 'genotype: BRCA+/+; cell type: Breast stromal cells; chip antibody: H3K27ac (abcam, Cat: ab4729, Lot: GR323132-1); ', 'genotype: BRCAmut/+; cell type: Breast stromal cells; chip antibody: H3K27ac (abcam, Cat: ab4729, Lot: GR323132-1); ', 'genotype: BRCA+/+; cell type: Breast basal cells; chip antibody: H3K4me3 (Millipore, Cat: 07-473, Lot: 2930138); ', 'genotype: BRCAmut/+; cell type: Breast basal cells; chip antibody: H3K4me3 (Millipore, Cat: 07-473, Lot: 2930138); ', 'genotype: BRCA+/+; cell type: Breast luminal progenitors; chip antibody: H3K4me3 (Millipore, Cat: 07-473, Lot: 2930138); ', 'genotype: BRCAmut/+; cell type: Breast luminal progenitors; chip antibody: H3K4me3 (Millipore, Cat: 07-473, Lot: 2930138); ', 'genotype: BRCA+/+; cell type: Breast mature luminal cells; chip antibody: H3K4me3 (Millipore, Cat: 07-473, Lot: 2930138); ', 'genotype: BRCAmut/+; cell type: Breast mature luminal cells; chip antibody: H3K4me3 (Millipore, Cat: 07-473, Lot: 2930138); ', 'genotype: BRCA+/+; cell type: Breast stromal cells; chip antibody: H3K4me3 (Millipore, Cat: 07-473, Lot: 2930138); ', 'genotype: BRCAmut/+; cell type: Breast stromal cells; chip antibody: H3K4me3 (Millipore, Cat: 07-473, Lot: 2930138); ', 'genotype: BRCA+/+; cell type: Breast basal cells; chip antibody: none; ', 'genotype: BRCAmut/+; cell type: Breast basal cells; chip antibody: none; ', 'genotype: BRCA+/+; cell type: Breast luminal progenitors; chip antibody: none; ', 'genotype: BRCAmut/+; cell type: Breast luminal progenitors; chip antibody: none; ', 'genotype: BRCA+/+; cell type: Breast mature luminal cells; chip antibody: none; ', 'genotype: BRCAmut/+; cell type: Breast mature luminal cells; chip antibody: none; ', 'genotype: BRCA+/+; cell type: Breast stromal cells; chip antibody: none; ', 'genotype: BRCAmut/+; cell type: Breast stromal cells; chip antibody: none; ' GSE107570 Homo sapiens 4 Expression profiling by array GPL10558 Regulation of breast cancer-induced osteoclstogenesis by mH2A1.2 involving EZH2-mediated H3K27me3 2017-12-01 In breast cancer metastasis soluble factors secreted by breast cancer cells trigger a cascade of events that stimulate osteoclast differentiation in the bone microenvironment. macroH2A is a unique histone variant with a C-terminal nonhistone domain and play a crucial role in modulating chromatin organization and gene transcription. To study the effect of macroH2A1.2, an isoform of macroH2A, on breast cancer-derived osteoclastogenesis, we performed gene expression array studies in wild type and mH2A1.2 knockout MDA-MB-468 cells . https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE107570 Regulation of Breast Cancer-Induced Osteoclastogenesis by MacroH2A1.2 Involving EZH2-Mediated H3K27me3. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2018.06.020 {Cell reports (7.815): 10.1016/j.celrep.2018.06.020} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA420642 https://www.ebi.ac.uk/ena/browser/view/PRJNA420642 None [Overal design]Total RNA was isolated from MDA-MB-468 cells in which mH2A1.2 gene have been depleted along with the wild type cells to study the differenetial regulation of various genes in each case.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Breast cancer cell line''cell line: MDA-MB-468; cell type: Breast cancer cell line; genotype/variation: wild type; ', 'cell line: MDA-MB-468; cell type: Breast cancer cell line; genotype/variation: mH2A1.2 knockout; ' GSE172215 Mus musculus; Homo sapiens 7 Expression profiling by array GPL16686; GPL23038 CD95 expression in triple negative breast cancer blocks induction of an inflammatory state through differential regulation of NF-κB Signaling 2021-04-16 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE172215 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA722468 https://www.ebi.ac.uk/ena/browser/view/PRJNA722468 None [Overal design]Refer to individual Series; [Treatment]'no stimulation'; [Growth]'The 4T1 cell line was cultured in RPMI supplemented with 8% heat-inactivated FCS (v/v) and 2 mM L-glutamine at 37°C/5% CO2.', 'cultured at 37°C/5% CO2 in DMEM supplemented with 8% heat-inactivated FCS and 2 mM L-glutamine'; [Extraction]'Cells were dissociated with trypsin/EDTA (0.05% trypsin; Gibco) for 5 min. Dissociated cells were washed twice in PBS. RNA was extracted using the NucleoSpin RNA XS extraction kit (Macherey–Nagel), according to the manufacturer’s recommendations.'; [Cell type]'Source: ''cell line: 4T1; genotype/variation: WT; ', 'cell line: 4T1; genotype/variation: KO; ', 'cell line: MDA-MB-231; genotype/variation: WT; ', 'cell line: MDA-MB-231; genotype/variation: KO; ' GSE108835 Homo sapiens 12 Expression profiling by array GPL16686 Gene expression analysis of human cancer associated fibroblasts (CAFs) stimulated with Platelet-Derived Growth Factor (PDGF)-CC 2018-01-05 This study is part of a larger effort set to determine the factors requried for the crosstalk between tumor cells and fibroblasts in breast cancer. Specifically, the primary aim of this microarray analysis is to detail the soluble factors secreted by cancer-asociated fibroblasts following stmulation with PDGF-CC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE108835 Microenvironmental control of breast cancer subtype elicited through paracrine platelet-derived growth factor-CC signaling. Nature medicine 30.641 https://doi.org/10.1038/nm.4494 {Nature medicine (30.641): 10.1038/nm.4494} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA428771 https://www.ebi.ac.uk/ena/browser/view/PRJNA428771 None [Overal design]CAF2 cells were either left untreated (control) or stimulated with human recombinant PDGF-C for 6 or 48 hours. Three (3) biological replicates for each of the three conditions were used for the analysis, for a total of 12 samples; [Treatment]'Cells were starved for 24 h in DMEM + 0,1 % BSA and stimulated with 100 ng/ml of PDGF-CC'; [Growth]'Cells were cultured in DMEM Glutamax (Invitrogen), supplemented with 1% Penicillin/Streptomycin and 10% fetal bovine serum at 37°C in a 5% CO2/95% air atmosphere'; [Extraction]'RNA was isolated following the RNeasy Mini Kit (Qiagen)'; [Cell type]'mammary fibroblast''cell line: CAF2; cell type: mammary fibroblast; treatment: unstimulated, 6h; ', 'cell line: CAF2; cell type: mammary fibroblast; treatment: stimulated, 6h; ', 'cell line: CAF2; cell type: mammary fibroblast; treatment: unstimulated, 48h; ', 'cell line: CAF2; cell type: mammary fibroblast; treatment: stimulated, 48h; ' GSE41194 Homo sapiens 50 Expression profiling by array GPL8300 Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 1) 2012-09-27 We used gene expression profiling of human DCIS and IBC to discover uniquely expressed genes that may also regulate progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41194 Differentially expressed genes regulating the progression of ductal carcinoma in situ to invasive breast cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-12-0636 {Cancer research (8.378): 10.1158/0008-5472.CAN-12-0636} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA176235 https://www.ebi.ac.uk/ena/browser/view/PRJNA176235 None [Overal design]RNA from human samples were extracted, purified, amplified, and evaluated for gene expression using Affymetrix U95Av2 gene expression arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'manual (macro) dissection of tumor epithelium to estimated >75% total cells using Ambion kit'; [Cell type]'Source: ''tissue: Breast; disease state: ductal carcinoma in situ; ', 'tissue: Breast; disease state: invasive breast cancer; ' GSE21068 Rattus norvegicus; Homo sapiens 12 Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by genome tiling array; Expression profiling by array GPL4135; GPL6325; GPL6326; GPL9052 Estrogen-mediated Epigenetic Repression of Large Chromosomal Regions through DNA Looping 2010-03-25 The current concept of epigenetic repression is based on one repressor unit corresponding to one silent gene. This notion, however, cannot adequately explain concurrent silencing of multiple loci observed in large chromosome regions. The long-range epigenetic silencing (LRES) can be a frequent occurrence throughout the human genome. To comprehensively characterize the influence of estrogen signaling on LRES, we analyzed transcriptome, methylome, and estrogen receptor alpha (ESR1)-binding datasets from normal breast epithelia and breast cancer cells. This ?omics? approach uncovered 11 large repressive zones (range: 0.35~5.98 megabases), including a 14-gene cluster located on 16p11.2. In normal cells, estrogen signaling induced transient formation of multiple DNA loops in the 16p11.2 region by bringing 14 distant loci to focal ESR1-docking sites for coordinate repression. However, the plasticity of this free DNA movement was reduced in breast cancer cells. Together with the acquisition of DNA methylation and repressive chromatin modifications at the 16p11.2 loci, an inflexible DNA scaffold may be a novel determinant used by breast cancer cells to reinforce estrogen-mediated repression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE21068 Estrogen-mediated epigenetic repression of large chromosomal regions through DNA looping. Genome research 9.944 https://doi.org/10.1101/gr.101923.109 {Genome research (9.944) doi:10.1101/gr.101923.109}; {PloS one (2.776) doi:10.1371/journal.pone.0013798}; 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA126731 https://www.ebi.ac.uk/ena/browser/view/PRJNA126731 https://www.ncbi.nlm.nih.gov/sra?term=SRP002398 [Overal design]ChIP-seq: E2-preexposed or DMSO-preexposed mammosphere-derived epithelial cells (MDECs); MCF-7 cells with 4hr of DMSO or E2 stimulation. MeDIP-chip: Methylated DNA from MCF7 cells was immunoprecipitated by the antibody against 5-methyl cytidine. The immunoprecipitated methylated DNA fragments were processed by the NimbleGen Methylation Microarray Service. Methylation analysis was performed on the NimbleGen Two-Array HG18 Promoter Set. mRNA profiling by array: Four sets of total RNA samples from the mammary gland of each 50-day-old rat with prepubertal exposure of BPA. Each sample set includes one BPA-exposed and one sesame oil-exposed rat RNA.; [Treatment]'None'; [Growth]'None'; [Extraction]"Lysates were clarified from sonicated nuclei and Pol II-DNA complexes were isolated with antibody. RNA Polymerase II ChIP Ab is from Santa Cruz (sc-899X). We use 10 ng per IP. Libraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit (Part# 0801-0303). Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation DNA was PCR amplified with Illumina primers for 15 cycles and library fragments of ~250 bp (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the Genome Analyzer following the manufacturer's protocols.", 'Methylated DNA from MCF7 cells was prepared according to the protocol published by Schubeler and coworkers (Weber et al. 2005). Briefly, high-quality genomic DNA was sheared to 300 bp (fragment size ranging from 200-600 bp) using Bioruptor. Fragmented DNA was heat denatured to produce single-stranded DNA to enhance the immunoselection step. Antibodies against 5-methyl cytidine (MAb-335MEC-500; Monoclonal Methyl DNA IP-grade; 1 μg/μl; Diagenode) were complexed to the magnetic beads (pan-mouse IgG Dynal Beads, Invitrogen). The immunoprecipitated methylated DNA fragments were processed by the NimbleGen Methylation Microarray Service (NimbleGen Systems, Inc. Madison, WI). Methylation analysis was performed on the NimbleGen Two-Array HG18 Promoter Set.', "Trizol extraction of total RNA was performed according to the manufacturer's instructions"; [Cell type]'mammosphere-derived epithelial cells (MDECs)', 'Source: ''patient: reduction mammoplasty patient #67; cell type: mammosphere-derived epithelial cells (MDECs); protocol: E2-preexposed; chip antibody: RNA Polymerase II (Santa Cruz, sc-899X, 10 ng per IP); ', 'patient: reduction mammoplasty patient #67; cell type: mammosphere-derived epithelial cells (MDECs); protocol: DMSO-preexposed; chip antibody: RNA Polymerase II (Santa Cruz, sc-899X, 10 ng per IP); ', 'patient: reduction mammoplasty patient #68; cell type: mammosphere-derived epithelial cells (MDECs); protocol: DMSO-preexposed; chip antibody: RNA Polymerase II (Santa Cruz, sc-899X, 10 ng per IP); ', 'patient: reduction mammoplasty patient #68; cell type: mammosphere-derived epithelial cells (MDECs); protocol: E2-preexposed; chip antibody: RNA Polymerase II (Santa Cruz, sc-899X, 10 ng per IP); ', 'cell line: MCF-7 breast cancer cell line; protocol: DMSO stimulation; chip antibody: RNA Polymerase II (Santa Cruz, sc-899X, 10 ng per IP); ', 'cell line: MCF-7 breast cancer cell line; protocol: E2 stimulation; chip antibody: RNA Polymerase II (Santa Cruz, sc-899X, 10 ng per IP); ', 'cell line: MCF-7 breast cancer cell line; antibody: anti-5-methyl cytidine (MAb-335MEC-500; Monoclonal Methyl DNA IP-grade; 1 μg/μl; Diagenode); ', 'cell line: MCF-7 breast cancer cell line; antibody: none; ', 'gender: Female; strain: Sprague Dawley CD; agent: BPA; tissue: the fourth abdominal mammary glands; age: 50-day-old; ', 'gender: Female; strain: Sprague Dawley CD; agent: sesame oil (control); tissue: the fourth abdominal mammary glands; age: 50-day-old; ' GSE63584 Homo sapiens 65 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL11154; GPL18573 Response and resistance to BET bromodomain inhibitors in triple negative breast cancer 2014-11-24 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE63584 Response and resistance to BET bromodomain inhibitors in triple-negative breast cancer. Nature 43.070 https://doi.org/10.1038/nature16508 {Nature (43.070): 10.1038/nature16508} 'genomic DNA', 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA268317 https://www.ebi.ac.uk/ena/browser/view/PRJNA268317 None [Overal design]Refer to individual Series; [Treatment]'Sonicated nuclear lysates were incubated with Biotin-JQ1 for 6 hour', 'Cells were treated with 500 nM JQ1 or DMSO for the indicated time', 'Cells were treated with 500nM JQ1 or DMSO for the indicated time'; [Growth]'Cells were growed with SUM medium'; [Extraction]'Whole cell extracts were sonicated to solubilize the chromatin. The chromatin extracts containing DNA fragments with an average size of 500 bp were precipitated using streptavidin conjugated beads. Purified precipitated DNA were prepared for sequencing according to a modified version of the Solexa Genomic DNA protocol. Fragmented DNA was end repaired and subjected to 18 cycles of LM-PCR using oligos provided by Illumina. Amplified fragments between 150 and 300bp (representing shear fragments between 50 and 200nt in length and ~100bp of primer sequence) were isolated by agarose gel electrophoresis and purified.', 'Whole cell extracts were sonicated to solubilize the chromatin. The chromatin extracts containing DNA fragments with an average size of 500 bp were immunoprecipitated using different antibodies. Purified immunoprecipitated DNA were prepared for sequencing according to a modified version of the Solexa Genomic DNA protocol. Fragmented DNA was end repaired and subjected to 18 cycles of LM-PCR using oligos provided by Illumina. Amplified fragments between 150 and 300bp (representing shear fragments between 50 and 200nt in length and ~100bp of primer sequence) were isolated by agarose gel electrophoresis and purified.', 'RNA-Seq libraries were generated on a Sciclone NGS instrument (Perkin Elmer) using Illumina TrueSeq reagents. Briefly, mRNA was enriched from 1 ug of total RNA, fragmented and reverse transcribed. Following 2nd strand synthesis, next generation sequencing libraries were obtained by end repair, A-tailing and adapter ligation reactions with reagents from the Illumina TrueSeq kit. Libraries were amplified and purified before sequencing on a HiSeq instrument.', 'total RNA was extracted using the\xa0standard QIAGEN RNeasy kit (74106). RNA concentrations were measured and quality controlled on\xa0a Bioanalyzer, RNA-Seq libraries were made using Illumina True-Seq RNA kits using the Sciclone\xa0NGSx workstation.'; [Cell type]'Source: ''cell line: SUM159R; sonicated nuclear lysates incubated with: Biotin-JQ1; dna fragments precipitated using: Streptavidin; barcode (already removed): TAGCTT; ', 'cell line: SUM159; sonicated nuclear lysates incubated with: Biotin-JQ1; dna fragments precipitated using: Streptavidin; barcode (already removed): GATCAG; ', 'cell line: SUM159R; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 2); drug treatment: DMSO; duration: 3 hour; barcode (already removed): TTAGGC; ', 'cell line: SUM159R; chip antibody: none; drug treatment: DMSO; duration: 3 hour; barcode (already removed): CTTGTA; ', 'cell line: SUM159R; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 2); drug treatment: JQ1; duration: 3 hour; barcode (already removed): TGACCA; ', 'cell line: SUM159R; chip antibody: H3K27AC (Abcam, catalog# ab4729, lot# GR184557-1); drug treatment: DMSO; duration: 3 hour; barcode (already removed): ACAGTG; ', 'cell line: SUM159R; chip antibody: H3K27AC (Abcam, catalog# ab4729, lot# GR184557-1); drug treatment: JQ1; duration: 3 hour; barcode (already removed): GCCAAT; ', 'cell line: SUM159; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 2); drug treatment: DMSO; duration: 3 hour; barcode (already removed): ATCACG; ', 'cell line: SUM159; chip antibody: none; drug treatment: DMSO; duration: 3 hour; barcode (already removed): GGCTAC; ', 'cell line: SUM159; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 2); drug treatment: JQ1; duration: 3 hour; barcode (already removed): CGATGT; ', 'cell line: SUM159; chip antibody: H3K27AC (Abcam, catalog# ab4729, lot# GR184557-1); drug treatment: DMSO; duration: 3 hour; barcode (already removed): TTAGGC; ', 'cell line: SUM159; chip antibody: H3K27AC (Abcam, catalog# ab4729, lot# GR184557-1); drug treatment: JQ1; duration: 3 hour; barcode (already removed): TGACCA; ', 'cell line: SUM159R; drug treatment: DMSO; duration: 24h; barcode (already removed): CCGTCC; ', 'cell line: SUM159R; drug treatment: DMSO; duration: 24h; barcode (already removed): AGTTCC; ', 'cell line: SUM159R; drug treatment: DMSO; duration: 3h; barcode (already removed): GCCAAT; ', 'cell line: SUM159R; drug treatment: DMSO; duration: 3h; barcode (already removed): CTTGTA; ', 'cell line: SUM159R; drug treatment: JQ1; duration: 24h; barcode (already removed): GTCCGC; ', 'cell line: SUM159R; drug treatment: JQ1; duration: 24h; barcode (already removed): ATGTCA; ', 'cell line: SUM159R; drug treatment: JQ1; duration: 3h; barcode (already removed): AGTCAA; ', 'cell line: SUM159R; drug treatment: JQ1; duration: 3h; barcode (already removed): AGTTCC; ', 'cell line: SUM159; drug treatment: DMSO; duration: 12h; barcode (already removed): AGTTCC; ', 'cell line: SUM159; drug treatment: DMSO; duration: 12h; barcode (already removed): ACAGTG; ', 'cell line: SUM159; drug treatment: DMSO; duration: 24h; barcode (already removed): CTTGTA; ', 'cell line: SUM159; drug treatment: DMSO; duration: 24h; barcode (already removed): ATGTCA; ', 'cell line: SUM159; drug treatment: DMSO; duration: 3h; barcode (already removed): CTTGTA; ', 'cell line: SUM159; drug treatment: DMSO; duration: 3h; barcode (already removed): CGATGT; ', 'cell line: SUM159; drug treatment: JQ1; duration: 12h; barcode (already removed): ATGTCA; ', 'cell line: SUM159; drug treatment: JQ1; duration: 12h; barcode (already removed): GCCAAT; ', 'cell line: SUM159; drug treatment: JQ1; duration: 24h; barcode (already removed): AGTCAA; ', 'cell line: SUM159; drug treatment: JQ1; duration: 24h; barcode (already removed): CCGTCC; ', 'cell line: SUM159; drug treatment: JQ1; duration: 3h; barcode (already removed): AGTCAA; ', 'cell line: SUM159; drug treatment: JQ1; duration: 3h; barcode (already removed): TGACCA; ', 'cell line: SUM149R; drug treatment: DMSO; duration: 12h; barcode (already removed): ACAGTG; ', 'cell line: SUM149R; drug treatment: JQ1; duration: 12h; barcode (already removed): CAGATC; ', 'cell line: SUM149R; drug treatment: JQ1; duration: 12h; barcode (already removed): GCCAAT; ', 'cell line: SUM149; drug treatment: DMSO; duration: 12h; barcode (already removed): GTCCGC; ', 'cell line: SUM149; drug treatment: DMSO; duration: 12h; barcode (already removed): GTGAAA; ', 'cell line: SUM149; drug treatment: JQ1; duration: 12h; barcode (already removed): CGATGT; ', 'cell line: SUM149; drug treatment: JQ1; duration: 12h; barcode (already removed): TGACCA; ', 'cell line: HCC1395; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: DMSO; duration: 12 hour; barcode (already removed): GATCAG; ', 'cell line: HCC1395; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: JQ1; duration: 12 hour; barcode (already removed): TAGCTT; ', 'cell line: HCC1395; chip antibody: none; drug treatment: DMSO; duration: 12 hour; barcode (already removed): TCCGTCTT; ', 'cell line: MDA436; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: DMSO; duration: 12 hour; barcode (already removed): GGCTAC; ', 'cell line: MDA436; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: JQ1; duration: 12 hour; barcode (already removed): CTTGTA; ', 'cell line: MDA436; chip antibody: none; drug treatment: DMSO; duration: 12 hour; barcode (already removed): TGTACCTT; ', 'cell line: SUM1315; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: DMSO; duration: 12 hour; barcode (already removed): CAGATC; ', 'cell line: SUM1315; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: JQ1; duration: 12 hour; barcode (already removed): ACTTGAAT; ', 'cell line: SUM1315; chip antibody: none; drug treatment: DMSO; duration: 12 hour; barcode (already removed): TAAGCGTT; ', 'cell line: SUM149R; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: DMSO; duration: 12 hour; barcode (already removed): TTAGGC; ', 'cell line: SUM149R; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: JQ1; duration: 12 hour; barcode (already removed): TGACCA; ', 'cell line: SUM149R; chip antibody: H3K27AC (Abcam, catalog# ab4729, lot# GR200563-2); drug treatment: DMSO; duration: 12 hour; barcode (already removed): CAGATC; ', 'cell line: SUM149R; chip antibody: H3K27AC (Abcam, catalog# ab4729, lot# GR200563-2); drug treatment: JQ1; duration: 12 hour; barcode (already removed): ACAGTG; ', 'cell line: SUM149R; chip antibody: none; drug treatment: DMSO; duration: 12 hour; barcode (already removed): TCTCGGTT; ', 'cell line: SUM149; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: DMSO; duration: 12 hour; barcode (already removed): ATCACGTT; ', 'cell line: SUM149; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: JQ1; duration: 12 hour; barcode (already removed): CGATGTTT; ', 'cell line: SUM149; chip antibody: H3K27AC (Abcam, catalog# ab4729, lot# GR200563-2); drug treatment: DMSO; duration: 12 hour; barcode (already removed): CTTGTA; ', 'cell line: SUM149; chip antibody: H3K27AC (Abcam, catalog# ab4729, lot# GR200563-2); drug treatment: JQ1; duration: 12 hour; barcode (already removed): CGATGT; ', 'cell line: SUM149; chip antibody: none; drug treatment: DMSO; duration: 12 hour; barcode (already removed): TGGTTGTT; ', 'cell line: SUM185; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: DMSO; duration: 12 hour; barcode (already removed): ACAGTGGT; ', 'cell line: SUM185; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: JQ1; duration: 12 hour; barcode (already removed): GCCAATGT; ', 'cell line: SUM185; chip antibody: none; drug treatment: DMSO; duration: 12 hour; barcode (already removed): ACAGTGGT; ', 'cell line: T47D; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: DMSO; duration: 12 hour; barcode (already removed): ATCACG; ', 'cell line: T47D; chip antibody: BRD4 (Bethyl, catalog# A301-985A, lot# 4); drug treatment: JQ1; duration: 12 hour; barcode (already removed): CGATGT; ', 'cell line: T47D; chip antibody: none; drug treatment: DMSO; duration: 12 hour; barcode (already removed): TTCTGTGT; ' GSE20700 Homo sapiens 6 Expression profiling by array GPL96 Multi-level Support Vector Regression analysis to identify condition-specific regulatory networks 2010-03-09 The identification of gene regulatory modules is an important yet challenging problem in computational biology. While many computational methods have been proposed to identify regulatory modules, their initial success is largely compromised by a high rate of false positives, especially when applied to human cancer studies. New strategies are needed for reliable regulatory module identification. We present a new approach, namely multi-level support vector regression (ml-SVR), to systematically identify conditionspecific regulatory modules. The approach is built upon a multi-level analysis strategy designed for suppressing false positive predictions. With this strategy, a regulatory module becomes ever more significant as more relevant gene sets are formed at finer levels. At each level, a two-stage support vector regression (SVR) method is utilized to help reduce false positive predictions by integrating binding motif information and gene expression data; a significant analysis procedure is followed to assess the significance of each regulatory module. We applied our method to breast cancer cell line data to identify condition-specific regulatory modules associated with estrogen treatment. Experimental results show that our method can identify biologically meaningful regulatory modules related to estrogen signaling and action in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE20700 Multilevel support vector regression analysis to identify condition-specific regulatory networks. Bioinformatics (Oxford, England) 4.531 https://doi.org/10.1093/bioinformatics/btq144 {Bioinformatics (Oxford, England) (4.531): 10.1093/bioinformatics/btq144} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA124893 https://www.ebi.ac.uk/ena/browser/view/PRJNA124893 None [Overal design]Three independent total RNA samples were extracted for each cell line (MCF-7 and MCF-7-stripped) and the samples were arrayed using Affymetrix GeneChip HG-U133A. MCF-7-stripped denotes estrogen-deprived MCF-7 human breast cancer cells, which were grown in the absence of estrogen for 96 hours. We analyzed the enriched motifs and their targets for the genes significantly down-regulated in MCF-7-stripped cells as compared to MCF-7 cells.; [Treatment]'Stripped cells were grown over 96 hours (4 successive days) in phenol-red free IMEM media supplemented with 5% Charcoal-Stripped Calf Serum. Every 24 hours the media was removed and replaced with fresh phenol-red free IMEM media supplemented with 5% Charcoal-Stripped Calf Serum (3 times total).'; [Growth]'Cells were grown in complete IMEM media supplemented with 5% Fetal Bovine Serum. Both Control and Treated cells were kept in a 37C incubator with 5% C02 and regulated humidity.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''gender: Female; age: 69 years; race: Caucasian; cell line: MCF-7; ' GSE148657 Homo sapiens 12 Expression profiling by high throughput sequencing GPL16791 Hyaluronan-CD44 signaling promotes pro-tumor inflammation in breast cancer 2020-04-14 We report the application of next-generation sequencing (NGS) technology for high-throughput profiling of RNA expression in human breast cancer cells. The goal of this study was to compare NGS-derived transcriptome profiling (RNA-seq) from cells expressing either wildtype or knockout CD44 to identify key downstream signaling events of HA-CD44 interactions. Methods: This experiment was repeated for a total of three times and replicate RNA samples were extracted and submitted for Illumina Sequencing. Twelve dual-indexed Illumina TruSeq stranded mRNA libraries were pooled for sequencing on 1 lane of a HiSeq 2500 using v4 chemistry to generate 2x50 bp paired-end reads. After applying the Benjamini-Hochberg multiple hypothesis adjustment to raw p-values, differentially expressed genes were identified requiring that they had a log2 fold change > 0 and an adjusted p-value ≤ 0.01. Results: A total of 1,530 and 320 genes were impacted by CD44 KO in the Hs578T cells and MDA-MB-231 cells, respectively. When comparing each of these data sets, 40 genes were differentially expressed in both Hs578T and MDA-MB-231 cells upon deletion of CD44. Conclusions: Gene ontology (GO) analysis revealed that CD44 KO in breast cancer cells altered expression of genes involved in both cell adhesion and cytokine activity. This study provides a framework for the application of NGS to compare differential gene expression between genetically edited mammalian cell populations. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE148657 Tumor Cell Associated Hyaluronan-CD44 Signaling Promotes Pro-Tumor Inflammation in Breast Cancer. Cancers 6.162 https://doi.org/10.3390/cancers12051325 {Cancers (6.162): 10.3390/cancers12051325} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA625295 https://www.ebi.ac.uk/ena/browser/view/PRJNA625295 https://www.ncbi.nlm.nih.gov/sra?term=SRP256345 [Overal design]Determining the effects of CD44 KO in 2 different human breast cancer cell lines. Three replicates were prepared for each of the four experimental conditions.; [Treatment]'CD44 was deleted from the Hs578T and MDA-MB-231 cells using CRISPR/Cas9 -based techniques and sorted to generate populations of CD44 knockout cells. Knockout was confirmed by flow cytometry and Western blot.'; [Growth]"Hs578T and MDA-MB-231 cells were grown per ATCC recommendations in Dulbecco's Modified Eagle's Medium, 10% fetal bovine serum, and 1% Pen/Strep."; [Extraction]'RNA was harvested using the RNeasy Mini Kit (Qiagen #74104) and 2000ng RNA was submitted per sample. Twelve dual-indexed Illumina TruSeq stranded mRNA libraries were pooled for sequencing on 1 lane of a HiSeq 2500 using v4 chemistry to generate 2x50 bp paired-end reads.\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'Breast cancer cell line''cell line: MDA-MB-231; cell type: Breast cancer cell line; cd44 status: knockout; ', 'cell line: MDA-MB-231; cell type: Breast cancer cell line; cd44 status: wild-type; ', 'cell line: Hs578T; cell type: Breast cancer cell line; cd44 status: knockout; ', 'cell line: Hs578T; cell type: Breast cancer cell line; cd44 status: wild-type; ' GSE144023 Homo sapiens 6 Expression profiling by array GPL17692 Expression data from MDA-MB-231 cells treated or not with AsiDNA 2020-01-21 Transcriptome analysis revealed a major change in gene expression with a large excess of genes down regulated in 3 independent AsiDNA-treated “evolved” populations as compared to three independent not-treated “naïve” populations The Achilles heel of anticancer treatments is intrinsic or acquired resistance. Among many targeted therapies, the DNA repair inhibitors show limited efficacy due to rapid emergence of resistance. We examined evolution of cancer cells and tumors treated with AsiDNA, a new DNA repair inhibitor targeting all DNA break repair pathways. Effects of AsiDNA or Olaparib were analyzed in various cell lines. Frequency of AsiDNA- and olaparib-resistant clones was measured after 2 weeks of continuous treatment in KBM7 haploid cells. Cell survivals were also measured after one to six cycles of 1-week treatment and 1-week recovery in MDA-MB-231 and NCI-H446. Transcriptomes of cell populations recovering from cyclic treatments or mock treatment were compared. MDAMB- 231 xenografted models were treated with three cycles of AsiDNA to monitor the effects of treatment on tumor growth and transcriptional modifications. No resistant clones were selected after AsiDNA treatment (frequency b 3x10−8) in treatment conditions that generate resistance to olaparib at a frequency of 7.2x10−7 resistant clones per treated cell. Cyclic treatments promote cumulative sensitivity characterized by a higher mortality of cells having undergone previous treatment cycles. This sensitization was stable, and transcriptome analysis revealed a major gene downregulation with a specific overrepresentation of genes coding for targets of DNA-PK. Such changes were also detected in tumor models which showed impaired growth after cycles of AsiDNA treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144023 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA602519 https://www.ebi.ac.uk/ena/browser/view/PRJNA602519 None [Overal design]MDA-MB-231 cells were treated or not with AsiDNA during 3 cycles of 1week treatement/1week release (6 total weeks), RNA was then extracted and hybridyzed on Affymetrix Human Gene 2.1 Arrays, 3 independant AsiDNA treated populations and 3 independant not-treated populations were analyzed.; [Treatment]'Cells were harvested and washed with PBS before RNA extraction from cell pellets.'; [Growth]'Cells were treated or not with AsiDNA during 6 total weeks before RNA extraction.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions"; [Cell type]'Source: ''tissue: breast cancer tumor cells; ' GSE102975 Mus musculus 4 Expression profiling by array GPL16570 Circulating adipose fatty acid binding protein promotes obesity associated breast cancer development 2017-08-23 It is still unclear that how obesity increases the risk of breast cancer. To address this question, we used mRNA microarrays to characterize mouse breast tumor EO771 cells treated with mouse recombinant A-FABP protein and compared the data from their controls. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE102975 Circulating Adipose Fatty Acid Binding Protein Is a New Link Underlying Obesity-Associated Breast/Mammary Tumor Development. Cell metabolism 22.415 https://doi.org/10.1016/j.cmet.2018.07.006 {Cell metabolism (22.415): 10.1016/j.cmet.2018.07.006} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA399690 https://www.ebi.ac.uk/ena/browser/view/PRJNA399690 None [Overal design]EO771 cells were seperated into A-FABP treated group (A-FABP+) and non A-FABP treated group (A-FABP-). They were treated with 100ng/ml recombinant mouse A-FABP and control PBS. Each condition was performed in duplicates.; [Treatment]'Always prepare mouse recombinant A-FABP immediatedly before use. Diltue the protein on a final concentration of 100ng/ml in culture medium.'; [Growth]'EO771 cells were cultured with RPMI 1640 at 37°C in a humidified incubator in an atmosphere of 5% CO2. Before the treatment with A-FABP, cells were cultured for 24 hours with 70% confluence as a minimum.'; [Extraction]"Directions for extraction and purifying total RNA from EO771 cells by the PureLink RNA Mini Kit are according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: EO771 cell line; ' GSE36309 Homo sapiens 6 Non-coding RNA profiling by array GPL7723 wqq_MDSC_miRNA Array 2012-03-06 Myeloid-derived suppressor cells (MDSCs) potently suppress the anti-tumor immune responses and also orchestrate the tumor microenvironment that favors tumor angiogenesis and metastasis. The immunosuppressive activity of MDSCs has been extensively investigated, however the molecular networks regulating the non-immunological functions of tumor-expanded MDSCs, are largely unknown. In this study, we identified microRNA-494 (miR-494), whose expression was dramatically induced by tumor-derived factors (TDFs), as an essential player, in regulating the non-immunological activity of MDSCs by targeting PTEN and activating the Akt pathway. TGF-beta 1 was found to be a main tumor-derived factor responsible for the up-regulation of miR-494 in MDSCs. Expression of miR-494 not only enhanced CXCR4-mediated MDSC chemotaxis but also altered the intrinsic apoptotic/survival signal by targeting PTEN, thus contributing to the accumulation of MDSCs in tumor tissues. Consequently, down-regulation of PTEN resulted in increased activity of the Akt pathway and the subsequent up-regulation of matrix metalloproteinases (MMPs) for facilitating tumor cell invasion and metastasis. Knock down of miR-494 significantly reversed the activity of MDSCs and inhibited the tumor growth and metastasis of 4T1 murine breast cancer in vivo. Collectively, our findings reveal that TGF-beta 1-induced miR-494 expression in MDSCs plays a critical role in the molecular events governing the accumulation and non-immunological functions of tumor-expanded MDSCs, and might be identified as a potential target in cancer therapy. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36309 MicroRNA-494 is required for the accumulation and functions of tumor-expanded myeloid-derived suppressor cells via targeting of PTEN. Journal of immunology (Baltimore, Md. : 1950) 4.718 https://doi.org/10.4049/jimmunol.1103505 {Journal of immunology (Baltimore, Md. : 1950) (4.718): 10.4049/jimmunol.1103505} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA153343 https://www.ebi.ac.uk/ena/browser/view/PRJNA153343 None [Overal design]BALB/c mice (female, 6- to 8-wk-old) were injected subcutaneously in the mammary fat pad with 100,000 4T1 tumor cells. Three weeks later, tumor-bearing animals were used for the indicated studies. Gr-1+ CD11b+ cells were isolated by immunomagnetic selection from the bone marrow of 4T1 tumor-bearing mice (n=3) and tumor-free BALB/c mice (n=3), then the miRNA expression profile were analyzed using miRCURY LNA™ microRNA Arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was harvested using TRIzol (Invitrogen) and the RNeasy mini kit (QIAGEN).'; [Cell type]'Source: ''strain: BALB/c; gender: female; age: 6-8 wk old; tumor stage: tumor-free mice; ', 'strain: BALB/c; gender: female; age: 6-8 wk old; tumor stage: tumor-bearing mice; ' GSE40206 Homo sapiens 80 Expression profiling by array GPL4133 Differential expression of genes and protein networks in the primary breast tumor that proceed to distant metastasis 2012-08-17 The presence or absence of lymph node metastasis plays a major role in the prediction of prognosis and subsequent patient management. However, good proportion of patients who display lymph node positivity remain disease free for 3 years or more, after the initial treatment, while a third of those who were lymph node negative at presentation, develop distant metastasis within the same period. We performed gene expression profiling on a cohort Indian breast cancer patients followed up for a period of 3-5 years and in comparison with a previously published Caucasian cohort data, we identified gene signatures that are associated with distant metastasis. This association was irrespective of the hormone receptor status. Our results show that the genes that signify immune system development and response are repressed, while factors for DNA replication are up regulated in patients who develop distant metastasis. A large number of genes encoding proteins involved in the mitotic spindle formation that belong to the TRIM28 protein network, are differentially regulated in the metastatic tumors. Also, there was a significant overlap of genes reported in a mouse model of bone metastasis, with patients who developed bone metastasis in our cohort. In conclusion, we present for the first time probable gene signatures that correlate with distant metastasis in breast cancer patients irrespective of nodal or hormone receptor status https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE40206 Activin-A signaling promotes epithelial-mesenchymal transition, invasion, and metastatic growth of breast cancer. NPJ breast cancer 32.43 https://doi.org/10.1038/npjbcancer.2015.7 {NPJ breast cancer (32.43): 10.1038/npjbcancer.2015.7} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA173465 https://www.ebi.ac.uk/ena/browser/view/PRJNA173465 None [Overal design]80 indian breast cancer patients(samples),comprising of 22ER+(estrogen receptor),and 55 ER-.PR(progesterone receptor) ,HER and NOD status are also given in corresponding sample title and array files; [Treatment]'None'; [Growth]'None'; [Extraction]"Total RNA extracted using Trizol following manufacturer's instructions"; [Cell type]'Source: ''tissue: normal breast tissues; ', 'tissue: tumor breast tissue; patient id: 45T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 46; size: 1x2x1; diag.: IDC-III; skin: Involved with ulcer; dsm: Very close to Tumour; nodal status: 10/10 nodes free; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', "tissue: tumor breast tissue; patient id: 67T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 60; size: 4x3x2; diag.: IDC- III moderate desmoplaria with focal DCIS; skin: Free; dsm: Free; nodal status: 7/11 metastases with Peri nodal spread.; last follow-up: 29/03/11; last follow-up notes: Advised RT, Patient didn't come further; other relevant investigations: Severe pain and advanced disease; follow-up period: 4yr.9m; ", 'tissue: tumor breast tissue; patient id: 147T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 53; size: 4x3x3; diag.: IDC-III with infiltrating margins, wide areas of necrosis; skin: Free; dsm: Free; nodal status: Free; last follow-up: 22.11.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 3yr.4m; ', 'tissue: tumor breast tissue; patient id: 162T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 52; size: 2x2x2; diag.: IDC-III with infiltrative margins; skin: Free; dsm: Free but clode to tumour; nodal status: 17/17 reactive changes; last follow-up: 2011-02-11; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 4yrs; ', "tissue: tumor breast tissue; patient id: 164T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 55; size: 4x3x3; diag.: IDC- III with infiltrating margins and moderate desmoplaria with focal DCIS; skin: Free; dsm: Free; nodal status: 2/14 metastases; last follow-up: 17.1.08; last follow-up notes: Plan for RT, But didn't turn up.; other relevant investigations: --------; follow-up period: 6months; ", 'tissue: tumor breast tissue; patient id: 168T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 34; size: 4x3x2.5; diag.: IDC-III stroma in minimal large area of necrosis; skin: Free; dsm: very close to tumour; nodal status: 12/12 are reactive; last follow-up: 2.7.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 3yrs; ', 'tissue: tumor breast tissue; patient id: 173T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 3+; age: 53; size: 7.5x3x4; diag.: IDC-III with predominantly high grade DCIS; skin: Free; dsm: Free; nodal status: 7/17 metsatasis; last follow-up: 4.2.08; last follow-up notes: Planed second line CT, Inj Docetaxel & carboplatin; other relevant investigations: Recurent tumour; follow-up period: 6months; ', 'tissue: tumor breast tissue; patient id: 176T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 45; size: 4x4x4; diag.: IDC-III with infiltrative margins,Necrosis& emboli , high grade DCIS seen; skin: Free; dsm: Free; nodal status: 6/10 nodes show metas with peri nodal spread; last follow-up: 24.10.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 3yr.2m; ', 'tissue: tumor breast tissue; patient id: 184T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 39; size: 3x2x2; diag.: IDC - III , fairly circumscribed with lymphocytic infiltrate, Medial margins shows a focal DCIS, Inferia of other margins are free; skin: Free; dsm: Free; nodal status: 12/12 Free; last follow-up: 2.3.12; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 4yr.5m; ', 'tissue: tumor breast tissue; patient id: 198T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 62; size: 2.5x2.5x2; diag.: IDC- III with infiltrating margins and mild lymphocytic response.; skin: Free; dsm: Free; nodal status: 10/10 Free; last follow-up: 29/9/08; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 8months; ', 'tissue: tumor breast tissue; patient id: 192T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 36; size: 5x4x3(Right), 2x1.5x1.5(left); diag.: IDC-III with medullary like areas(Both breasts); skin: Free; dsm: involved in Right; nodal status: 11/11 Free(Right), 1/12 metastases(left); last follow-up: 1.3.12; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 4yr.3m; ', 'tissue: tumor breast tissue; patient id: 236T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 38; size: 2x2x1.5; diag.: IDC -III with focal margins infiltrating predominantly circumscribed, lymphocytic response seen at the edge.; skin: Free; dsm: Free; nodal status: 9/9 Free; last follow-up: 11.2.11; last follow-up notes: completed 3 cycles of 2nd line CT; other relevant investigations: Multiple liver masses.; follow-up period: 2yr.3m; ', 'tissue: tumor breast tissue; patient id: 238T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 62; size: 2.5x2x2; diag.: IDC- III with sqvamoid areas and infiltrating margins,moderate lymphocytic response; skin: Free; dsm: Free; nodal status: 7/7 Free, 2/2 apical nodes Free; last follow-up: 22.2.11; last follow-up notes: Regular follow up,NAD; other relevant investigations: --------; follow-up period: 2yr.2m; ', 'tissue: tumor breast tissue; patient id: 239T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER; er: 0; pr: 0; her: 0; age: 45; size: 1x2x1.5; diag.: IDC- III with infiltrating margins, inferia margins shows tumour.; skin: Free; dsm: Free; nodal status: 9/16 Metastases; last follow-up: 11.10.10; last follow-up notes: No follow up after 11.10.10; other relevant investigations: --------; follow-up period: 2yrs; ', 'tissue: tumor breast tissue; patient id: 254T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 61; size: 2.5x2.5x2; diag.: IDC-III; skin: --------; dsm: --------; nodal status: 10/10 free; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 255T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 29; size: 2.5x2x2; diag.: IDC - III with margins fairly well circumscribed, stroma is minimal, larger areas of necrosis seen.; skin: Free; dsm: Free; nodal status: 15/15 Free; last follow-up: 2.12.10; last follow-up notes: Head ache/ Vomiting, Advised brain CT scan; other relevant investigations: Brain metastasis; follow-up period: 2yrs; ', 'tissue: tumor breast tissue; patient id: 256T; nod status: NOD0; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 56; size: 3x2x3; diag.: IDC-III, large areas of necrosis; skin: Free; dsm: Free; nodal status: 3/14 nodes metastasis; last follow-up: 23.10.09; last follow-up notes: NAD; other relevant investigations: Bilateral carcinoma; follow-up period: 9months; ', 'tissue: tumor breast tissue; patient id: 269T; nod status: NOD0; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 70; size: 3.5x3x3; diag.: IDC-III , Areas of necrosis, lymphatic emboli seen.; skin: Free; dsm: Free; nodal status: Not removed; last follow-up: 1.4.11; last follow-up notes: Advides RT, Patient did not come.; other relevant investigations: --------; follow-up period: 2yr.3m; ', 'tissue: tumor breast tissue; patient id: 292T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 30; size: 5x3x3.5; diag.: Medullary carcinoma grade - III; skin: Free; dsm: Free; nodal status: 8/10 show metastasis; last follow-up: 29.7.10; last follow-up notes: Passed away on August 2011; other relevant investigations: Brain metastases.; follow-up period: 8months; ', 'tissue: tumor breast tissue; patient id: 186T; nod status: NOD-; er status: ER+; pr status: PR+; her status: HER+; er: 3+3; pr: 2+3; her: 2+; age: 57; size: 2x2x2; diag.: IDC- III with focal DCIS and infiltrating margins and moderate desmoplaria; skin: Free; dsm: Free; nodal status: 10/10 free; last follow-up: 1.11.10; last follow-up notes: NAD, To continue Litrazol; other relevant investigations: --------; follow-up period: 3yrs; ', 'tissue: tumor breast tissue; patient id: 267T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER+; er: 4+3; pr: 4+3; her: 0; age: 75; size: 3x2x1.5; diag.: IDC- III with infiltrating margins; skin: Free; dsm: Free; nodal status: 12/12 Free; last follow-up: 1.4.11; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 2yr.1m; ', 'tissue: tumor breast tissue; patient id: 51T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER+; er: 4; pr: 4; her: 1+; age: 43; size: 4x2x3; diag.: IDC-III; skin: --------; dsm: --------; nodal status: 1/12 metastaic; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 277T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 3+; age: 43; size: 3x2.5x2; diag.: IDC-III witn infiltrating margins, lymphatic emboli seen; skin: Free; dsm: Free; nodal status: 12/12 Free; last follow-up: 21.11.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 1yr.7m; ', 'tissue: tumor breast tissue; patient id: 42T; nod status: NOD+; er status: ER-; pr status: PR+; her status: HER-; er: 0; pr: 0; her: 0; age: 35; size: 6x5x4; diag.: IDC III with focal infiltrating margins; skin: Free; dsm: Very close to tumour; nodal status: 4/10 lymph nodes show metastasis; last follow-up: 7.4.11; last follow-up notes: NAD; other relevant investigations: Chest wall recurrence; follow-up period: 5yrs; ', 'tissue: tumor breast tissue; patient id: 266T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER+; er: 1+1; pr: 3+3; her: 2 - 3+; age: 45; size: 2x2x2; diag.: IDC- III with infiltrating margins; skin: Free; dsm: Free; nodal status: 2/16 nodes show metastasis; last follow-up: 19.2.11; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 2yr.1m; ', 'tissue: tumor breast tissue; patient id: 251485053519-2; nod status: NOD+; er status: ER-; pr status: PR+; her status: HER-; er: 0; pr: 2; her: 0; age: 25; size: 6.5x6x3; diag.: IDC-III; skin: --------; dsm: --------; nodal status: POSITIVE; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 68T; nod status: NOD+; er status: ER-; pr status: PR+; her status: HER+; er: 0; pr: 4; her: 1; age: 60; size: 2.1x5.1x5; diag.: IDC-III; skin: --------; dsm: --------; nodal status: 3/10 meta; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 89T; nod status: NOD-; er status: ER-; pr status: PR+; her status: HER+; er: 0; pr: 2+1; her: 2+; age: 43; size: 6x6x5; diag.: IDC - III with infiltrating margins; skin: involved, upper dermis with ulceration; dsm: Free; nodal status: 10/10 Free; last follow-up: 5.9.08; last follow-up notes: Vomitings; other relevant investigations: Metastasis insternnum;She was Dead; follow-up period: 2yrs; ', 'tissue: tumor breast tissue; patient id: 235T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER+; er: 2+2; pr: 1+2; her: 2+, Advised FISH; age: 45; size: 3x2x1.5; diag.: IDC- III with focal DCIS and infiltrating margins; skin: Free; dsm: Free; nodal status: 2/16 Metastases with perinodal spread.; last follow-up: 9.8.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 2yr.2m; ', 'tissue: tumor breast tissue; patient id: 40T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 3; age: 70; size: 5x4x3; diag.: IDC - III with extensive DCIS, and with infiltrating margins; skin: Free; dsm: Involved; nodal status: 4/8 metastases; last follow-up: 13.08.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 4yrs; ', 'tissue: tumor breast tissue; patient id: 160T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 1; age: 28; size: 5x5x3; diag.: IDC-III with infiltrating margins; skin: Free; dsm: Free; nodal status: 5/11 show metastasis; last follow-up: 14.2.11; last follow-up notes: NAD; other relevant investigations: Recurrence chest wall & Bone metastasis; follow-up period: 3yr.5m; ', 'tissue: tumor breast tissue; patient id: 132T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER+; er: 3+3; pr: 3+3; her: 2; age: 29; size: 2.5x2x2; diag.: IDC-III with focal high grade DCIS and infiltrating margins - superior surgical margin shows involvement, other margins- free; skin: Free; dsm: Free; nodal status: 11/15 nodes show metastases.; last follow-up: 23.10.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 3yr.5m; ', 'tissue: tumor breast tissue; patient id: 25T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 3; age: 40; size: 6x2x3; diag.: Focal IDC with extensive high grade DCIS; skin: Free; dsm: Free; nodal status: 3/10 metastases with perinodal spread; last follow-up: 1.04.11; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 5yrs; ', 'tissue: tumor breast tissue; patient id: 295T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER+; er: 3+3; pr: 3+3; her: 1+; age: 63; size: 3.5x3x2.5; diag.: IDC-III with moderate lymphocytic response; skin: Free; dsm: Free; nodal status: 15/26 nodes show metastases.; last follow-up: --------; other relevant investigations: Passed away on 26/9/09; follow-up period: 4months; ', 'tissue: tumor breast tissue; patient id: 61T; nod status: NOD0; er status: ER+; pr status: PR+; her status: HER+; er: 3+3; pr: 3+3; her: 2; age: 60; size: 3x2x2; diag.: IDC -II with all margins free and dense fibrosis.; skin: --------; dsm: --------; nodal status: --------; last follow-up: 27.09.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 4yrs; ', 'tissue: tumor breast tissue; patient id: 59T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 3; age: 65; size: 4x2.5x2.5cm; diag.: IDC-III with infiltrative margins; skin: Free; dsm: Free; nodal status: 10/10 reactive; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 244T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 3+; age: 62; size: 3x2x2.5; diag.: IDC - III with dense lymphoplasmacytic and focally infilterate periphery around tumor cells.; skin: Free; dsm: Free; nodal status: 11/11 Free, Apical node- Free; last follow-up: 6.12.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 79T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 1+; age: 42; size: 3x2x2; diag.: IDC-III with margins circumscribed; skin: Free; dsm: Free; nodal status: 1 node +ve, 6/6 nodes -ve; last follow-up: 25.12.07; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 1yr.4m; ', 'tissue: tumor breast tissue; patient id: 155T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER+; er: 7; pr: 6; her: 1; age: 50; size: 3x3x2; diag.: IDC-III; skin: --------; dsm: --------; nodal status: 3/17 meta; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 60T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 3; age: 40; size: 4x4.5x3; diag.: IDC - III with infiltrating margin; skin: Free; dsm: Free; nodal status: 3/3 Neg., 3/3 extra nodes free; last follow-up: 1.04.11; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 4yr.8m; ', 'tissue: tumor breast tissue; patient id: 43T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER+; er: 2+2; pr: 3+3; her: 2; age: 65; size: 5x3x3; diag.: ILC - III - Bilateral breast, with focal insitu lobular; skin: Free; dsm: Positive - of right breast; nodal status: 7/7 metastases with perpheral nodal spread; last follow-up: 20.03.06; other relevant investigations: Multiple skeletal lesions; follow-up period: 3months; ', 'tissue: tumor breast tissue; patient id: 194T; nod status: NOD-; er status: ER+; pr status: PR-; her status: HER+; er: 4+3; pr: 0; her: 2; age: 50; size: 2x1.5x1; diag.: IDC - III with focal DCIS; skin: Free; dsm: close, but free; nodal status: 12/12 Free; last follow-up: 10.4.11; last follow-up notes: Patient did not come further; other relevant investigations: --------; follow-up period: 3yr.5m; ', 'tissue: tumor breast tissue; patient id: 151T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 45; size: 6x6x4; diag.: IDC-III; skin: --------; dsm: --------; nodal status: 5/13 meta; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 171T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 53; size: 3x3x2; diag.: IDC with infiltrating margins, stroma shows moderate desmoplasia with areas of necrosis; skin: Free; dsm: Free; nodal status: 9/9 reactive; last follow-up: 19.11.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 3yr.3m; ', 'tissue: tumor breast tissue; patient id: 179T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 23; size: 1.5x1x1; diag.: IDC III with focal DCIS and infiltrating margins, showing moderate lymphocytic response.; skin: Free; dsm: close to tumour, but free; nodal status: 11/11 Free; last follow-up: 6.11.07; last follow-up notes: Advised CT/RT, Patient refused.; other relevant investigations: --------; follow-up period: 2months; ', 'tissue: tumor breast tissue; patient id: 300T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 57; size: 4x3x2( diffused gray white areas); diag.: IDC- III with infiltrating margins, vascular emboli present; skin: Free; dsm: Free; nodal status: 2/15 nodes show metastasis; last follow-up: 3.1.11; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 1yr.2m; ', 'tissue: tumor breast tissue; patient id: 303T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 35; size: 3x3x2; diag.: IDC-III with circumscribed margins.; skin: Free; dsm: Free; nodal status: 17/17 nodes free; last follow-up: 11.11.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 1yr; ', 'tissue: tumor breast tissue; patient id: 304T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 34; size: 6x4x4; diag.: IDC-III with infiltrating margins. Moderate lymphocytic infiltrate seen, Dense Fibrosys; skin: Free; dsm: Free; nodal status: 11/11 Free; last follow-up: 11.5.10; other relevant investigations: --------; follow-up period: 6months; ', 'tissue: tumor breast tissue; patient id: 46T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 3; age: 40; size: 4x2x3; diag.: IDC - III with focal DCIS, margins circumscribed, with moderate lymphocytic infiltrate; skin: Free; dsm: Very close to DSM; nodal status: 8/8 free; last follow-up: 24.12.09; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 3yr.5m; ', 'tissue: tumor breast tissue; patient id: 57T-; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 3; age: 35; size: 5x5.5x3; diag.: IDC-III; skin: --------; dsm: --------; nodal status: 1/13 meta; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 92T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER+; er: 3+3; pr: 3+2; her: 3-Feb; age: 50; size: 4.5x3.5x3; diag.: IDC - III with focal DCIS; skin: Free; dsm: Involved. Stroma shows moderate desmoplasia; nodal status: 4/10 metastases with PNS.; last follow-up: 28.04.10; last follow-up notes: Skeletal metastases; other relevant investigations: bone metastases & multiple skeletal metastases; follow-up period: 3yr.8m; ', 'tissue: tumor breast tissue; patient id: 138T; nod status: NOD-; er status: ER-; pr status: PR+; her status: HER-; er: 0; pr: 1+3; her: 0; age: 51; size: 3x2.5x1.5; diag.: IDC - III with extensive DCIS, and with infiltrating margins; skin: Free; dsm: Close but free; nodal status: 9/9 Free; last follow-up: 1.04.11; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 4yrs; ', 'tissue: tumor breast tissue; patient id: 54T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER0; er: 0; pr: 0; her: Not done; age: 35; size: 5x4x3; diag.: IDC - III with focal DCIS, margins fairly circumscribed, with moderate lymphocytic infiltrate; skin: Free; dsm: Free; nodal status: 11/11 free; last follow-up: 1.04.11; other relevant investigations: --------; follow-up period: 4yr.3m; ', 'tissue: tumor breast tissue; patient id: 72T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 2; age: 55; size: 3.5x3.5x2.5; diag.: IDC -III, infiltrating margins were seen, Moderate Desmoplasia dermal lymphatic emboli were seen; skin: --------; dsm: Free; nodal status: 15/22 meta apical nodes \x96 adipose tissue; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 136T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER-; er: 3+3; pr: 3+3; her: 0; age: 80; size: 10x7x5.5; diag.: Neuro endocrine carcinoma- skin and margins fairly circumscribed, close to tumour but free; skin: involved; dsm: --------; nodal status: 3/17 metastases; last follow-up: 2007-10-10; last follow-up notes: Plan for RT, But patient not willing for RT/CT; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 166T; nod status: NOD-; er status: ER+; pr status: PR+; her status: HER-; er: 2+3; pr: 1+1; her: 0; age: 50; size: 3x2.5x1.5; diag.: IDC-III with infiltrating margins; skin: Free; dsm: Free; nodal status: 10/10 reactive; last follow-up: 28.11.07; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 3months; ', 'tissue: tumor breast tissue; patient id: 78T; nod status: NOD+; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 3; age: 82; size: 3x2 cms; diag.: IDC- III with focal high grade DCIS, margins infiltrating; skin: Free; dsm: Free; nodal status: 3/10 metastases; last follow-up: 24.03.07; last follow-up notes: Pain in operated site; other relevant investigations: --------; follow-up period: 7 months; ', 'tissue: tumor breast tissue; patient id: 193T; nod status: NOD+; er status: ER-; pr status: PR+; her status: HER-; er: 0; pr: 1+1; her: 0; age: 62; size: 2x2x1.5; diag.: IDC-III, margins fairly circumscrebed; skin: Free; dsm: Free; nodal status: 4/12 Metastases; last follow-up: 11.08.10; other relevant investigations: Supraclavicular node metastses.; follow-up period: 2yr.8m; ', 'tissue: tumor breast tissue; patient id: 180T; nod status: NOD-; er status: ER-; pr status: PR+; her status: HER+; er: 0; pr: 0; her: 3; age: 55; size: 5x4x3cm; diag.: IDC -III, with infiltrating margisn and focal DCIS; skin: Free; dsm: Free; nodal status: 14/14 free; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 82T; nod status: NOD-; er status: ER+; pr status: PR+; her status: HER+; er: 4+3; pr: 1+3; her: 0; age: 53; size: 4x4x2.5; diag.: IDC-III with infiltrating margins, vasculat emboli present with deposits in fat; skin: Free; dsm: Free; nodal status: Free; last follow-up: 2010-01-11; last follow-up notes: Passed away in November 2010; other relevant investigations: Developed veribral and liver metastasis; follow-up period: 4yrs; ', 'tissue: tumor breast tissue; patient id: 190T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 66; size: 2x1x1; diag.: DCIS high grade; skin: Free; dsm: --------; nodal status: 12/12 Free; last follow-up: 27.12.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 3yrs; ', 'tissue: tumor breast tissue; patient id: 210T; nod status: NOD-; er status: ER-; pr status: PR+; her status: HER0; er: 2+2; pr: 1+3; her: Cannot be evaluated; age: 36; size: 2x2x1.5; diag.: Residual DCIS tumour; skin: Tumour present in dermis; nodal status: 11/11 Free(Right), 1/12 metastases(left); last follow-up: 2011-01-07; other relevant investigations: --------; follow-up period: 3yr.5m; ', 'tissue: tumor breast tissue; patient id: 227T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER-; er: 0; pr: 0; her: 0; age: 40; size: 4.5x5x2; diag.: DCIS High grade (with one focus of invasion).; skin: Free; dsm: Free; nodal status: 15/15 Reactive; last follow-up: 30.12.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 2yrs; ', 'tissue: tumor breast tissue; patient id: 229T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER; er: 3+2; pr: 3+3; her: 0; age: 67; size: 2.5x2x1.5; diag.: IDC III with focal DCIS; skin: Free; dsm: Free; nodal status: 3/15 shows Metastases; last follow-up: 8.2.11; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 2yr.3m; ', 'tissue: tumor breast tissue; patient id: 233T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER-; er: 0; pr: 1+1; her: 3+; age: 40; size: 4x3.5x2.5; diag.: DCIS high grade with focal area of invasion.; skin: Free; dsm: Free; nodal status: 11/11 node & 2/2 apical nodes free; last follow-up: 2011-01-03; other relevant investigations: --------; follow-up period: 3yr.3m; ', 'tissue: tumor breast tissue; patient id: 268T; nod status: NOD-; er status: ER-; pr status: PR+; her status: HER+; er: 0; pr: 6; her: 3+; age: 40; size: --------; diag.: DCIS; skin: --------; dsm: --------; nodal status: 10/10 reactive; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 28T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 3; age: 60; size: 6.5x5x3; diag.: IDC-III; skin: --------; dsm: --------; nodal status: Negative; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 58T; nod status: NOD-; er status: ER-; pr status: PR+; her status: HER+; er: 0; pr: 3+3; her: 3+; age: 48; size: 3x3x3; diag.: IDC- III with infiltrating margins; skin: Free; dsm: Free; nodal status: 10/10 Free; last follow-up: 28.9.10; last follow-up notes: NAD; other relevant investigations: Blood in sputum; follow-up period: 4yrs; ', 'tissue: tumor breast tissue; patient id: 80T; nod status: NOD-; er status: ER-; pr status: PR-; her status: HER+; er: 0; pr: 0; her: 3; size: 2.2x2x2.5; diag.: IDC - III with focal high grade DCIS, Margins fairly circumscribed, lymphocytic infiltration seen at the periphery; skin: Free; dsm: Close but free; nodal status: 12/12 free; last follow-up: 02.09.09; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 3yr.2m; ', 'tissue: tumor breast tissue; patient id: 93T; nod status: NOD-; er status: ER-; pr status: PR+; her status: HER+; er: 0; pr: 2+3; her: 0; age: 74; size: 1.5x1x1; diag.: IDC - III with focal DCIS, and with infiltrating margins; skin: Free; dsm: Free; nodal status: 11/11 Free; last follow-up: --------; other relevant investigations: vertebra metastases; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 96T; nod status: NOD-; er status: ER0; pr status: PR0; her status: HER0; er: 3+3; pr: 3+2; her: 2+; size: 5x4x2.5; diag.: IDC III with infiltrating margins, and showing lymphocytic response.; skin: --------; dsm: Free; nodal status: 10/10 free; last follow-up: 1.04.11; last follow-up notes: NAD (To continue with Tamoxifen); other relevant investigations: --------; follow-up period: 4yr.5m; ', 'tissue: tumor breast tissue; patient id: 135T; nod status: NOD-; er status: ER+; pr status: PR+; her status: HER+; er: 4+3; pr: 3+3; her: 0; age: 58; size: 3x2.5x1.5; diag.: Mucinous carcinoma with neuro endocrine areas grade- III with infiltrating margins; skin: Free; dsm: close to tumour; nodal status: 11/11 free; last follow-up: 27.12.10; last follow-up notes: NAD(To continue with Letrozol); other relevant investigations: --------; follow-up period: 3yr.7m; ', "tissue: tumor breast tissue; patient id: 157T; nod status: NOD-; er status: ER+; pr status: PR+; her status: HER-; er: 2+3; pr: 3+3; her: 0; age: 53; size: 2x1x0.8; diag.: IDC - III with focal DCIS, and with infiltrating margins (both breasts); skin: Free; dsm: Free; nodal status: No nodes identified; last follow-up: Patient didn't turned up for adj treatment; other relevant investigations: --------; follow-up period: --------; ", 'tissue: tumor breast tissue; patient id: 159T; nod status: NOD-; er status: ER+; pr status: PR-; her status: HER-; er: 1+3; pr: 0; her: 0; age: 60; size: 3x2x1.5; diag.: IDC-III with infiltrating margins; skin: Free; dsm: Free; nodal status: 10/10 Free; last follow-up: 7.5.08; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 1yr; ', 'tissue: tumor breast tissue; patient id: 35T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER+; er: 1+3; pr: 1+3; her: 1; age: 40; size: 3x2x2x; diag.: IDC - III with focal DCIS; skin: --------; dsm: --------; nodal status: 5/11 metastases with perinodal spread; last follow-up: 28.09.06; last follow-up notes: Pain in left side of chest, due to advanced disease. Advised palliative treatments.; other relevant investigations: --------; follow-up period: 3months; ', 'tissue: tumor breast tissue; patient id: 70T; nod status: 2NOD+; er status: ER0; pr status: PR0; her status: HER0; er: 2+1; pr: 2+1; her: 1; age: 35; size: 4.5x3x1.5; diag.: IDC - III with high grade extensive DCIS, and infiltrating margins; skin: Free; dsm: Involved; nodal status: 2/10 metastases; last follow-up: 19.01.11; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 4yrs; ', 'tissue: tumor breast tissue; patient id: 75T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER-; er: 2+2; pr: 4+3; her: 0; age: 36; size: 5x4x3; diag.: IDC - III with focal high grade DCIS, and infiltrating margins; skin: Free; dsm: Free; nodal status: 4/10 metastases; last follow-up: 28.07.10; last follow-up notes: NAD; other relevant investigations: --------; follow-up period: 4yrs; ', "tissue: tumor breast tissue; patient id: 84T; nod status: NOD+; er status: ER0; pr status: PR0; her status: HER0; er: 4+3; pr: 3+2; her: 3+; age: 65; size: 3x1.5x1; diag.: IDC-III, with infiltrating margins; skin: involved; dsm: Free; nodal status: Free; last follow-up: 19.5.07; last follow-up notes: Advised RT, But patient didn't come further.; other relevant investigations: --------; follow-up period: 1yr; ", 'tissue: tumor breast tissue; patient id: 149T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER-; er: 6; pr: 6; her: 0; age: 50; size: 3.1x5.1x2; diag.: IDC-III; skin: --------; dsm: --------; nodal status: 6/12 meta; last follow-up: --------; other relevant investigations: --------; follow-up period: --------; ', 'tissue: tumor breast tissue; patient id: 150T; nod status: NOD+; er status: ER+; pr status: PR+; her status: HER-; er: 4+3; pr: 4+3; her: 0; age: 75; size: 6x6x4; diag.: IDC - III with margins focally infiltrative; skin: Dermis shows involvement; dsm: Free; nodal status: 4/7 metastases; last follow-up: 19.7.07; last follow-up notes: Patient discharged, didn\x92t turn up further.; other relevant investigations: --------; follow-up period: 1month; ' GSE25976 Homo sapiens 6 Expression profiling by array GPL6244 Expression profiles of CD24-/CD44+/ESA+ population in MDA-MB-231 and its highly metastatic variants. 2010-12-09 Breast cancer is a curable disease if it is diagnosed at an early stage. However, only little options are left once the tumor is metastasized to distant organs, and more than 90% of breast cancer death is attributed to metastatic disease. The process of metastasis is highly complex and involves many steps for successful colonization of tumor cells at a target organ. According to the cancer stem cell (CSC) theory, which still remains a hypothesis, these metastatic cells must have stem cell-like capability for their self-renewal in addition to their invasive ability. Therefore, it has been predicted that a “metastatic stem cell”, which is distinct from a cancer stem cell, must exist in the primary tumor mass. To identify genes that are involved in metastasis of CSCs, we isolated CSC populations from a well-established model cell line of breast cancer, MDA-MB231, and that of highly metastatic variants, 231BoM-1833 and 231BrM-2a, using CD24, CD44 and EpCAM (ESA), which have been identified as surface markers for CSCs in breast cancers. Overall yield of CSCs from these cells ranged from 2% to 4%. We then performed global expression profile analysis for these CSCs using the Affymetrix Human Gene 1.0ST array. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE25976 Hyaluronan synthase HAS2 promotes tumor progression in bone by stimulating the interaction of breast cancer stem-like cells with macrophages and stromal cells. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-11-1678 {Cancer research (8.378): 10.1158/0008-5472.CAN-11-1678} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA135451 https://www.ebi.ac.uk/ena/browser/view/PRJNA135451 None [Overal design]CSC populations (CD24-/CD44+/ESA+) from MDA-MB231, 231BoM-1833 and 231BrM-2a were isolated by magnetic-activated cell sorting (MACS) using specific antibodies to these surface markers. The total RNA was isolated from the CSC populations using the RNeasy RNA isolation kit (Qiagen). The RNA was then converted to cDNA and they were hybridized to the Human Gene 1.0ST chip (Affymetrix). The data was normalized using the RMA algorithm of the Expression Console software (Affymetrix). A comparison of transcriptional profiles was then performed in CSCs of highly metastatic cell lines (231BoM-1833 and 231BrM-2a) compared to the CSCs of MDA-MB-231.; [Treatment]'Stem cell population (CD24-/CD44+/ESA+) was isolated by MACS system (Miltenyi) using CD24, CD44 and ESA antibodies.'; [Growth]'Cells were grown in RPMI-1640 media with 10% FBS and antibiotics in 4% CO2 incubator.'; [Extraction]'Total RNA was extracted by using Qiagen RNeasy kit followed by DNase treatment and repulified by using Qiagen RNA cleanup kit.'; [Cell type]'Source: ''cell line: MDA-MB-231; ', 'cell line: 231BoM-1833; ', 'cell line: 231BrM-2a; ' GSE65398 Homo sapiens 96 Expression profiling by array GPL13158 Expression data from human carcinoma (MCF7) derived cells that have been exposed to insulin analogues 2015-01-28 Insulin analogues are designed to improve the pharmacokinetic parameters compared to regular human insulin. This provides a sustained control of blood glucose levels in diabetic patients. All novel insulin analogues are tested for their mitogenic side effects, however these assays do not take into account the molecular mode-of-action of different insulin analogues. Insulin analogues can bind the insulin receptor (INSR) and the insulin-like growth factor-1 receptor (IGF1R) with different affinities and consequently will activate different downstream signaling pathways. Here we used a panel of MCF7 human breast cancer cell lines that selectively express either one of the isoforms of the INSR (IRA or IRB) or the IGF1R. We sought to study the role of the different receptors (IRA, IRB and IGF1R) in the mitogenic signaling of insulin-like molecules (including insulin, glargine, X10 (or AspB10) and IGF1). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE65398 Alternative signaling network activation through different insulin receptor family members caused by pro-mitogenic antidiabetic insulin analogues in human mammary epithelial cells. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-015-0600-5 {Breast cancer research : BCR (5.676): 10.1186/s13058-015-0600-5} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA273881 https://www.ebi.ac.uk/ena/browser/view/PRJNA273881 None [Overal design]MCF7 IRA, MCF7 IRB or MCF7 IGF1R cells (as described in Arch Toxicol. 2014 Apr;88(4):953-66. doi: 10.1007/s00204-014-1201-2. Epub 2014 Jan 25.) were cultured in RPMI supplemented with 5% (v/v) CDFBS (Hyclone) and used for experiments. Cells have been exposed for 1 or 6 hours to 10 nM of the indicated insulin-like molecule. As a control sample a vehicle stimulation was performed that contained everything except the active compound.; [Treatment]'Prior to compound stimulation the cells were starved in 5% charcoal/dextran-stripped fetal bovine serum (CDFBS) containing medium. Stimulations included: insulin NPH (Insuman Basal, Sanofi Aventis), insulin glargine (Lantus, Sanofi Aventis), M1 (metabolite of glargine, Sanofi Aventis), M2 (metabolite of glargine, Sanofi Aventis), glulisine (Apidra, Sanofi Aventis), lispro (Humalog, Elly Lilly), Insulin X10 (not marketed, Novo Nordisk), aspart (B28Asp, Novo Nordisk), detemir (Levemir, Novo Nordisk) and IGF1 (Increlex, Ipsen). All insulin analogues were dissolved in their original vehicle solutions [18]. For the in vitro experiments 1000x stock concentrations were prepared. Except for the first exposure experiment (Figure 1C) in which a dose response of 10, 33 and 100 nM was used, all exposures have been performed with a concentration of 10 nM'; [Growth]'MCF7 IRA, MCF7 IRB or MCF7 IGF1R cells (as described in Arch Toxicol. 2014 Apr;88(4):953-66. doi: 10.1007/s00204-014-1201-2. Epub 2014 Jan 25.) were cultured in RPMI supplemented with 5% (v/v) CDFBS (Hyclone) and used for experiments. Cells have been exposed for 1 or 6 hours to 10 nM of the indicated insulin-like molecule. As a control sample a vehicle stimulation was performed that contained everything except the active compound.'; [Extraction]'RNA was isolated using the RNeasy® Plus Mini Kit (Qiagen, Venlo, the Netherlands) and RNA integrity and quality was assessed using the Agilent bioanalyser (Agilent Technologies, Palo Alto, CA, USA).'; [Cell type]'Source: ''cell line: MCF7; receptor: IRA; treatment: insulin; time point: 1 hr; ', 'cell line: MCF7; receptor: IRB; treatment: insulin; time point: 1 hr; ', 'cell line: MCF7; receptor: IGF1R; treatment: insulin; time point: 1 hr; ', 'cell line: MCF7; receptor: IRA; treatment: glargine; time point: 1 hr; ', 'cell line: MCF7; receptor: IRB; treatment: glargine; time point: 1 hr; ', 'cell line: MCF7; receptor: IGF1R; treatment: glargine; time point: 1 hr; ', 'cell line: MCF7; receptor: IRA; treatment: X10; time point: 1 hr; ', 'cell line: MCF7; receptor: IRB; treatment: X10; time point: 1 hr; ', 'cell line: MCF7; receptor: IGF1R; treatment: X10; time point: 1 hr; ', 'cell line: MCF7; receptor: IRA; treatment: IGF1; time point: 1 hr; ', 'cell line: MCF7; receptor: IRB; treatment: IGF1; time point: 1 hr; ', 'cell line: MCF7; receptor: IGF1R; treatment: IGF1; time point: 1 hr; ', 'cell line: MCF7; receptor: IRA; treatment: insulin; time point: 6 hrs; ', 'cell line: MCF7; receptor: IRB; treatment: insulin; time point: 6 hrs; ', 'cell line: MCF7; receptor: IGF1R; treatment: insulin; time point: 6 hrs; ', 'cell line: MCF7; receptor: IRA; treatment: glargine; time point: 6 hrs; ', 'cell line: MCF7; receptor: IRB; treatment: glargine; time point: 6 hrs; ', 'cell line: MCF7; receptor: IGF1R; treatment: glargine; time point: 6 hrs; ', 'cell line: MCF7; receptor: IRA; treatment: X10; time point: 6 hrs; ', 'cell line: MCF7; receptor: IRB; treatment: X10; time point: 6 hrs; ', 'cell line: MCF7; receptor: IGF1R; treatment: X10; time point: 6 hrs; ', 'cell line: MCF7; receptor: IRA; treatment: IGF1; time point: 6 hrs; ', 'cell line: MCF7; receptor: IRB; treatment: IGF1; time point: 6 hrs; ', 'cell line: MCF7; receptor: IGF1R; treatment: IGF1; time point: 6 hrs; ', 'cell line: MCF7; receptor: IRA; treatment: vehicle solution; time point: 1 hr; ', 'cell line: MCF7; receptor: IRB; treatment: vehicle solution; time point: 1 hr; ', 'cell line: MCF7; receptor: IGF1R; treatment: vehicle solution; time point: 1 hr; ', 'cell line: MCF7; receptor: IRA; treatment: vehicle solution; time point: 6 hrs; ', 'cell line: MCF7; receptor: IRB; treatment: vehicle solution; time point: 6 hrs; ', 'cell line: MCF7; receptor: IGF1R; treatment: vehicle solution; time point: 6 hrs; ' GSE32463 Mus musculus 9 Expression profiling by array GPL339 Gene expression profiling of mouse mammary tumorspheres, mammospheres, and mammospheres induced to differentiate 2011-09-28 Tumorpsheres and mammospheres were used to propagate mouse breast tumor-initiating cells and their normal stem/progenitor counterparts, respectively. Mammospheres induced to differentiate were used to model the more differentiated cells of the mouse mammary gland. We used microarrays to find differentrially expressed genes between tumorspheres, mammospheres, and mammospheres induced to differentiate https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32463 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA147875 https://www.ebi.ac.uk/ena/browser/view/PRJNA147875 None [Overal design]Primary cells were isolate from either mouse mammary glands (FVB/N) or mouse mammary tumors and placed in stem cell media (MMTV-Neu [N2O2]. Spheres were passaged every 7 days for 3-5 passages and harvested for RNA isolation; [Treatment]'None'; [Growth]'tumorspheres and mammospheres were passaged every 7 days in mouse stem cell media and harvested for RNA between passages 3-5. Mammospheres were placed in serum containing media and allowed to differentiate for 7 days.'; [Extraction]'Total RNA was isolated from tumorspheres, mammospheres or mammospheres induced to differentiate using an RNAeasy mini prep kit (QIAGEN, Hilden, Germany) according to the manufacturer’s protocol'; [Cell type]'Source: ''sample type: tumorspheres; ', 'strain: FVB/N; sample type: mammospheres; ', 'strain: FVB/N; sample type: mammospheres induced to differentiate in serum; ' GSE28040 Homo sapiens 2 Expression profiling by high throughput sequencing GPL9115 Accurate Identification of A-to-I RNA editing in human by transcriptome sequencing 2011-03-18 RNA editing enhances the diversity of gene products at the post-transcriptional level. Approaches for genome-wide identification of RNA editing face two main challenges: separating true editing sites from false discoveries and accurate estimation of editing levels. We developed an approach to analyze transcriptome sequencing data (RNA-Seq) for global identification of RNA editing in cells for which whole-genome sequencing data are available. We applied the method to analyze RNA-Seq data of a human glioblastoma cell line, U87MG. Around 10,000 DNA-RNA differences were identified, the majority being putative A-to-I editing sites. These predicted A-to-I events were associated with a low false discovery rate (~5%). Moreover, the estimated editing levels from RNA-Seq correlated well with those based on traditional clonal sequencing. Our results further facilitated unbiased characterization of the sequence and evolutionary features flanking predicted A-to-I editing sites and discovery of a conserved RNA structural motif that may be functionally relevant to editing. Genes with predicted A-to-I editing were significantly enriched with those known to be involved in cancer, supporting the potential importance of cancer-specific RNA editing. A similar profile of DNA-RNA differences as in U87MG was predicted for another RNA-Seq data set obtained from primary breast cancer samples. Remarkably, significant overlap exists between the putative editing sites of the two transcriptomes despite their difference in cell type, cancer type and genomic backgrounds. Our approach enabled de novo identification of the RNA editome, which sets the stage for further mechanistic studies of this important step of post-transcriptional regulation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28040 Accurate identification of A-to-I RNA editing in human by transcriptome sequencing. Genome research 9.944 https://doi.org/10.1101/gr.124107.111 {Genome research (9.944): 10.1101/gr.124107.111} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA137951 https://www.ebi.ac.uk/ena/browser/view/PRJNA137951 https://www.ncbi.nlm.nih.gov/sra?term=SRP009659 [Overal design]Examine mRNA expression in U87MG cells following ADAR1 or control siRNA knockdown; [Treatment]'50ng of ADAR1 siRNA and control siRNA were transfected respectively with lipofectamine RNAiMAX into 5x104 U87MG cells per single well of 6-well plate via reverse transfection and cells were harvested 48h following transfection. Total RNA was isolated using the RNeasy micro kit.'; [Growth]'U87MG cells were maintained in DMEM high glucose medium supplemented with pyruvate, L-glutamine, and 10% fetal bovine serum (FBS).'; [Extraction]'We used the standard Illumina protocol to prepare libraries for RNA-Seq (http://www.illumina.com/support/documentation.ilmn). Briefly, 10ug total RNA was first processed via poly-A selection and fragmentation. We generated first-strand cDNA using random hexamer-primed reverse transcription and subsequently used it to generate second-strand cDNA using RNase H and DNA polymerase. Sequencing adapters were ligated using the Illumina Paired-End sample prep kit. Fragments of ~200 bp were isolated by gel electrophoresis, amplified by 15 cycles of PCR and sequenced.'; [Cell type]'Source: ''cell line: U87MG; treatment: control siRNA; ', 'cell line: U87MG; treatment: ADAR1 siRNA; ' GSE23386 Homo sapiens 50 Expression profiling by array GPL6883; GPL8432 Clinical relevance of DNA microarray analyses using archival formalin-fixed paraffin-embedded breast cancer specimens 2010-08-02 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23386 Clinical relevance of DNA microarray analyses using archival formalin-fixed paraffin-embedded breast cancer specimens. BMC cancer 2.933 https://doi.org/10.1186/1471-2407-11-253 {BMC cancer (2.933): 10.1186/1471-2407-11-253} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA131263 https://www.ebi.ac.uk/ena/browser/view/PRJNA131263 None [Overal design]Refer to individual Series; [Treatment]'Breast cancer specimens were formalin fixed and paraffin embedded.', 'Breast cancer specimens were fresh fine needle aspirated biopsies.'; [Growth]'None'; [Extraction]'RNA was extracted with the RecoverAll Total Nucleic acid kit followed by DNase I treatment. Quality control was performed with the Agilent Bioanalyser.', 'RNA was extracted with RNeasy Micro kits. Quality control was performed with the Agilent Bioanalyser.'; [Cell type]'Source: ''tissue: breast cancer; age: 56; type: IDC; size: 1.2; grade: 2; positive node: 0(1); er: +; pr: +; her2: -; rin: 1.7; ', 'tissue: breast cancer; age: 47; type: IDC; size: 2.2; grade: 2; positive node: 1(12); er: +; pr: +; her2: -; rin: 2.3; ', 'tissue: breast cancer; age: 63; type: IDC; size: 2.4; grade: 2; positive node: 0(1); er: +; pr: +; her2: -; rin: 2.5; ', 'tissue: breast cancer; age: 76; type: IDC; size: 2.8; grade: 3; positive node: 0(3); er: +; pr: +; her2: -; rin: 2.5; ', 'tissue: breast cancer; age: 58; type: IDC; size: 10.6; grade: 2; positive node: 6(24); er: +; pr: +; her2: -; rin: 2.5; ', 'tissue: breast cancer; age: 50; type: IDC; size: 3.7; grade: 2; positive node: 0(2); er: +; pr: +; her2: -; rin: 2.4; ', 'tissue: breast cancer; age: 55; type: IDC; size: 1.9; grade: 2; positive node: 2(15); er: +; pr: +; her2: -; rin: 1.5; ', 'tissue: breast cancer; age: 68; type: IDC; size: 2; grade: 2; positive node: 4(17); er: +; pr: +; her2: -; rin: 2.7; ', 'tissue: breast cancer; age: 42; type: IDC; size: 2.6; grade: 2; positive node: 0(3); er: +; pr: +; her2: -; rin: 2.3; ', 'tissue: breast cancer; age: 64; type: IDC; size: 1.5; grade: 2; positive node: 0(4); er: +; pr: +; her2: -; rin: 2.1; ', 'tissue: breast cancer; age: 41; type: IDC; size: 1.6; grade: 3; positive node: 0(3); er: +; pr: +; her2: +; rin: 2.2; ', 'tissue: breast cancer; age: 37; type: IDC; size: 1.5; grade: 3; positive node: 0(18); er: +; pr: +; her2: +; rin: 2.1; ', 'tissue: breast cancer; age: 61; type: IDC; size: 2.2; grade: 3; positive node: 2(18); er: +; pr: -; her2: +; rin: 2.4; ', 'tissue: breast cancer; age: 43; type: IDC; size: 2.5; grade: 3; positive node: 0(5); er: +; pr: -; her2: +; rin: 2.4; ', 'tissue: breast cancer; age: 51; type: IDC; size: 1.6; grade: 3; positive node: 1(23); er: -; pr: -; her2: -; rin: 1.7; ', 'tissue: breast cancer; age: 54; type: IDC; size: 3.6; grade: 2; positive node: 0(11); er: -; pr: -; her2: -; rin: 2.4; ', 'tissue: breast cancer; age: 62; type: IDC; size: 1.6; grade: 3; positive node: 1(21); er: -; pr: -; her2: -; rin: 2.4; ', 'tissue: breast cancer; age: 47; type: IDC; size: 1.5; grade: 3; positive node: 0(4); er: -; pr: -; her2: -; rin: 2.3; ', 'tissue: breast cancer; age: 57; type: IDC; size: 2.9; grade: 2; positive node: 0(4); er: -; pr: -; her2: -; rin: 2.2; ', 'tissue: breast cancer; age: 44; type: IDC; size: 3.2; grade: 3; positive node: 0(1); er: -; pr: -; her2: +; rin: 2.7; ', 'tissue: breast cancer; age: 56; type: IDC; size: 1.4; grade: 3; positive node: 0(3); er: -; pr: -; her2: +; rin: 1.9; ', 'tissue: breast cancer; age: 76; type: IDC; size: 2.3; grade: 3; positive node: 2(20); er: -; pr: -; her2: +; rin: 2.3; ', 'tissue: breast cancer; age: 64; type: IDC; size: 2.3; grade: 3; positive node: 5(21); er: -; pr: -; her2: +; rin: 2.2; ', 'tissue: breast cancer; age: 73; type: IDC; size: 1.6; grade: 3; positive node: 0(2); er: -; pr: -; her2: +; rin: 2.4; ', 'tissue: breast cancer; age: 54; type: IDC; size: 2.9; grade: 3; positive node: 0(12); er: -; pr: -; her2: +; rin: 2.5; ', 'tissue: breast cancer; age: 44; type: IDC; size: 3.2; grade: 3; positive node: 0(1); er: -; pr: -; her2: +; rin: 6.7; ', 'tissue: breast cancer; age: 56; type: IDC; size: 1.2; grade: 2; positive node: 0(1); er: +; pr: +; her2: -; rin: 7.5; ', 'tissue: breast cancer; age: 41; type: IDC; size: 1.6; grade: 3; positive node: 0(3); er: +; pr: +; her2: +; rin: 9.3; ', 'tissue: breast cancer; age: 47; type: IDC; size: 2.2; grade: 2; positive node: 1(12); er: +; pr: +; her2: -; rin: 9.2; ', 'tissue: breast cancer; age: 63; type: IDC; size: 2.4; grade: 2; positive node: 0(1); er: +; pr: +; her2: -; rin: 7.0; ', 'tissue: breast cancer; age: 76; type: IDC; size: 2.8; grade: 3; positive node: 0(3); er: +; pr: +; her2: -; rin: 8.9; ', 'tissue: breast cancer; age: 51; type: IDC; size: 1.6; grade: 3; positive node: 1(23); er: -; pr: -; her2: -; rin: 8.3; ', 'tissue: breast cancer; age: 58; type: IDC; size: 10.6; grade: 2; positive node: 6(24); er: +; pr: +; her2: -; rin: 6.6; ', 'tissue: breast cancer; age: 54; type: IDC; size: 3.6; grade: 2; positive node: 0(11); er: -; pr: -; her2: -; rin: 6.9; ', 'tissue: breast cancer; age: 50; type: IDC; size: 3.7; grade: 2; positive node: 0(2); er: +; pr: +; her2: -; rin: 8.6; ', 'tissue: breast cancer; age: 56; type: IDC; size: 1.4; grade: 3; positive node: 0(3); er: -; pr: -; her2: +; rin: 6.9; ', 'tissue: breast cancer; age: 37; type: IDC; size: 1.5; grade: 3; positive node: 0(18); er: +; pr: +; her2: +; rin: 9.0; ', 'tissue: breast cancer; age: 55; type: IDC; size: 1.9; grade: 2; positive node: 2(15); er: +; pr: +; her2: -; rin: 9.4; ', 'tissue: breast cancer; age: 43; type: IDC; size: 2.5; grade: 3; positive node: 0(5); er: +; pr: -; her2: +; rin: 7.9; ', 'tissue: breast cancer; age: 73; type: IDC; size: 1.6; grade: 3; positive node: 0(2); er: -; pr: -; her2: +; rin: 6.5; ', 'tissue: breast cancer; age: 64; type: IDC; size: 1.5; grade: 2; positive node: 0(4); er: +; pr: +; her2: -; rin: 7.4; ', 'tissue: breast cancer; age: 61; type: IDC; size: 2.2; grade: 3; positive node: 2(18); er: +; pr: -; her2: +; rin: 8.3; ', 'tissue: breast cancer; age: 62; type: IDC; size: 1.6; grade: 3; positive node: 1(21); er: -; pr: -; her2: -; rin: 6.6; ', 'tissue: breast cancer; age: 68; type: IDC; size: 2; grade: 2; positive node: 4(17); er: +; pr: +; her2: -; rin: 7.2; ', 'tissue: breast cancer; age: 42; type: IDC; size: 2.6; grade: 2; positive node: 0(3); er: +; pr: +; her2: -; rin: 7.8; ', 'tissue: breast cancer; age: 76; type: IDC; size: 2.3; grade: 3; positive node: 2(20); er: -; pr: -; her2: +; rin: 5.6; ', 'tissue: breast cancer; age: 47; type: IDC; size: 1.5; grade: 3; positive node: 0(4); er: -; pr: -; her2: -; rin: 5.6; ', 'tissue: breast cancer; age: 54; type: IDC; size: 2.9; grade: 3; positive node: 0(12); er: -; pr: -; her2: +; rin: 8; ', 'tissue: breast cancer; age: 57; type: IDC; size: 2.9; grade: 2; positive node: 0(4); er: -; pr: -; her2: -; rin: 8.9; ', 'tissue: breast cancer; age: 64; type: IDC; size: 2.3; grade: 3; positive node: 5(21); er: -; pr: -; her2: +; rin: 8.8; ' GSE114572 Mus musculus 38 Expression profiling by high throughput sequencing GPL19057 PyMT-1099, a murine derived cell line is a breast cancer specific model for EMT 2018-05-17 Background: Epithelial-mesenchymal transition (EMT) has been implicated in metastasis, drug resistance, survival under stress and also conferring stem cell-like traits to cancer cells. However, several of the studies have been carried out using model systems that don’t appropriately recapitulate all stages of the dynamic process of EMT. Hence, there is a need to overcome this limitation by development of a model system that allows us to mimic each stage of EMT and accurately assess the plastic changes associated with it. Methods: We have derived a cancer cell line from the PyMT-MMTV model of breast cancer, named PyMT-1099 cells, and undertaken a detailed characterization of the morpho-genetic changes it undergoes during a TGF-induced EMT. Further, we have also performed high throughput transcriptomics on PyMT-1099 cells undergoing EMT in a high resolution kinetic of TGF treatment. Results: We show that PyMT-1099 cells undergo an EMT comparable to the classically used immortalized NMuMG cells as assessed by morphological, and marker expression changes on TGFtreatment. Further, PyMT-1099 cells can also migrate in vitro in response to TGF treatment. These cells are also tumorigenic and lead to metastasis formation when transplanted into immunocompromised mice. Conclusion: In this study we report the development of PyMT-1099 cells as an excellent tool to model and study breast cancer-associated EMT both in vitro and in vivo and show that these cells overcome the limitations posed by other cellular systems currently being used to study EMT https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE114572 PyMT-1099, a versatile murine cell model for EMT in breast cancer. Scientific reports 4.011 https://doi.org/10.1038/s41598-018-30640-1 {Scientific reports (4.011): 10.1038/s41598-018-30640-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA471818 https://www.ebi.ac.uk/ena/browser/view/PRJNA471818 https://www.ncbi.nlm.nih.gov/sra?term=SRP148095 [Overal design]RNA-Seq of TGFb-induced EMT and MET over a timecourse of 10 days in PyMT-1099 cells performed in biological duplicates; [Treatment]'For the EMT time-course, PyMT-1099 or NMuMG (E9) cells were treated with 2ng/ml TGF\uf062 for 2h, 6h, 12h, 24h, 36h, 48h, 72h, 96h, 7d or 10d. Untreated cells served as control. For the MET timecourse, TGF\uf062 was withdrawn from PyMT-1099 or NMuMG (E9) cells after 10d treatment. Cells were then seeded without TGF\uf062\uf020for 1, 2, 3, 4, 7 or 10d. 10d TGF\uf062 treated cells (MET d0) served as the control for MET experiment'; [Growth]'PyMT-1099 were cultured in Dulbecco’s modified Eagle’s medium (DMEM) (Sigma-Aldrich, D5671) supplemented with 10% Fetal Bovine Serum (FBS, 10%; Sigma-Aldrich), 2 mM glutamine (Sigma-Aldrich, G7513), 100 U penicillin (Sigma-Aldrich) and 0.1 mg/ml streptomycin (Sigma-Aldrich). All cell lines were grown at 37°C, 5% CO2, 95% humidity.'; [Extraction]'Total RNA was isolated from the samples above using the miRNeasy Mini Kit (Qiagen, 217004) with on-column DNAse digestion according to the manufacturer’s instructions. 5\uf06dg of RNA was then subjected to rRNA depletion using the Ribozero magnetic gold kit (Epicentre, MRZG12324) followed by concentrating it using the RNeasy MinElute Cleanup Kit (Qiagen, 74204).\nTotal RNA was isolated from the samples above using the miRNeasy Mini Kit (Qiagen, 217004) with on-column DNAse digestion according to the manufacturer’s instructions. RNA quality control was performed with an RNA ScreenTape on the Agilent 4200 TapeStation and the concentration measured by using the Quanti-iT RiboGreen RNA assay Kit (Life Technologies). 200 ng of RNA were subjected to rRNA depletion and utilized for library preparation with the\xa0Truseq Stranded Total RNA Library Prep kit with Ribo-Zero Gold (Illumina). Library QC was performed with a Fragment Analyzer (AATI) using the Standard Sensitivity NGS Fragment Analysis Kit (DNF-473). RNA-seq libraries were sequenced SR81 with NextSeq 500 High Output v2 kit (Illumina) on an Illumina NextSeq 500 using protocols defined by the manufacturer; primary data analysis was done using Illumina RTA Version: 2.4.11.'; [Cell type]'Source: ''strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 0h; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 2h; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 6h; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 12h; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 24h; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 36h; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 48h; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 60h; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 72h; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 96h; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 7d; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 10d; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 0d; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 1d; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 2d; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 3d; treatment: Tgfbeta; ', 'strain: MMTV-PyMT (FVB/N); tissue: Tumor developed in mammary gland 2/3; transgene: PyMT; time point: 4d; treatment: Tgfbeta; ' GSE7765 Homo sapiens 12 Expression profiling by array GPL96; GPL97 Dioxin-induced gene expression changes in MCF-7 human breast cancer cells 2007-05-09 MCF7 cells were treated with DMSO or 100 nM Dioxin for 16 hr. Gene expression changes were quantified by microarray analyses. Keywords: dose response https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7765 A proposed mechanism for the protective effect of dioxin against breast cancer. Toxicological sciences : an official journal of the Society of Toxicology 3.564 https://doi.org/10.1093/toxsci/kfm125 {Toxicological sciences : an official journal of the Society of Toxicology (3.564): 10.1093/toxsci/kfm125} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA99779 https://www.ebi.ac.uk/ena/browser/view/PRJNA99779 None [Overal design]HU133A and B arrays were used to quantify differences in RNA after treatment with 100 nM dioxin for 16 h. The experiment was repeated 3 times.; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen RNeasy kit'; [Cell type]'Source: ''' GSE71498 Homo sapiens 6 Expression profiling by array GPL18734 Arrayed gene expression analysis of the SETD1A depleted cancer cells 2015-07-29 Investigation of gene expression level changes in the SETD1A depleted cancer cells (shSETD1A), compared to the GFP depleted cancer cells (shGFP) as control. This analysis was performed to gain an understanding of the transcriptional changes induced by chromation modifications through H3K4 methyltransferase SETD1A. Key Word: SETD1A, Epigenetics https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE71498 SETD1A protects from senescence through regulation of the mitotic gene expression program. Nature communications 11.878 https://doi.org/10.1038/s41467-019-10786-w {Nature communications (11.878) doi:10.1038/s41467-019-10786-w}; {Nature communications (11.878) doi:10.1038/ncomms9257}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA291400 https://www.ebi.ac.uk/ena/browser/view/PRJNA291400 None [Overal design]This series represents a set of experiments performed using RNA isolated from SETD1A depleted cancer cells in human breast cancer MDA-MB-231 cells and lung cancer A549 cells.; [Treatment]'Lentiviral shRNA constructs were obtained from the RNAi Consortium shRNA Library at the Broad Institute. Conditioned medium containing infective lentiviral particles was generated by cotransfecting 3µg of each lentiviral vector, 3µg of pCMV d8.91 and 1µg pHCMV-G into 1×10*6 293T human embryonic kidney cells using FuGENE 6 transfection reagent (Roche Applied Science). Supernatants were collected 48 hr after transfection and filtered through a 0.45 µM membrane (Millipore). Cells were infected with each supernatants using 8µg/mL polybrene and selected with 2µg/mL puromycin. RNA was isolated 72 hr after lentiviral shRNA infection.'; [Growth]'Human breast (MDA-MB-231) and lung (A549) cancer cell lines (American Type Culture Collection, Manassas, VA, USA) were grown in Dulbeccco’s modified medium, which supplemented with 10% fetal bovine serum and penicillin/streptomycin (Pen/Strep). Both cell lines were maintained in 5% CO2 at 37°C.'; [Extraction]'Total RNA was extracted using the RNeasy Mini kit (Qiagen, Valencia, CA, USA) and the RNAprotect reagent (Qiagen) and DNA was removed by on-column DNase digestion with the RNase-Free DNase set (Qiagen). RNA was isolated 72 hr after lentiviral shRNA infection.'; [Cell type]'Source: ''cell line: Lung cancer cell line A549; genotype/variation: SETD1A depletion; ', 'cell line: Lung cancer cell line A549; genotype/variation: control; ', 'cell line: Breast cancer cell line MDA-MB-231; genotype/variation: SETD1A depletion; ', 'cell line: Breast cancer cell line MDA-MB-231; genotype/variation: control; ' GSE119090 Homo sapiens 6 Expression profiling by array GPL16956 lncRNA/mRNA expression profiling of miR-200c-overexpressing MDA-MB-231 cells 2018-08-27 MiR-200c is a well-studied miRNA that is involved in stemness, the epithelial-mesenchymal transition, chemoresistance, radioresistance, and invasion/metastasis of various cancer cells. To obtain an overview of the lncRNA/mRNA regulated by miR-200c signaling in breast-cancer cell lines, we performed global lncRNA/mRNA-expression profiling on MDA-MB-231-pGIPZ and MDA-MB-231-miR-200c cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE119090 Long noncoding RNA LINC02582 acts downstream of miR-200c to promote radioresistance through CHK1 in breast cancer cells. Cell death & disease 5.959 https://doi.org/10.1038/s41419-019-1996-0 {Cell death & disease (5.959): 10.1038/s41419-019-1996-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA488076 https://www.ebi.ac.uk/ena/browser/view/PRJNA488076 None [Overal design]Three independent cell-culture replicates from the total population of MDA-MB-231-pGIPZ and MDA-MB-231-miR-200c stable transfectants were used to generate total RNA. Total RNA was extracted using Trizol.; [Treatment]'None'; [Growth]'Cells were grown in RPMI 1640 medium supplemented with 10% fetal bovine serum.'; [Extraction]"Total RNA was extracted using the RNeasy Mini Kit according to manufacturer's instructions (Qiagen)."; [Cell type]'Source: ''cell line: MDA-MB-231; tissue: breast cancer cell line; transfection: pGIPZ-his plasmid; ', 'cell line: MDA-MB-231; tissue: breast cancer cell line; transfection: pGIPZ-his-miR-200c plasmid; ' GSE103001 Homo sapiens 44 Expression profiling by high throughput sequencing GPL11154 Stranded RNASeq of human mammary primary tumors ER+ and paired adjacent healthy tissues 2017-08-23 Non-coding RNAs (ncRNA) represent at least 1/5 of the mammalian transcript amount, and about 90% of the genome length is actively transcribed. Many ncRNAs have been demonstrated to play a role in cancer. Among them, natural antisense transcripts (NAT) are RNA sequences which are complementary and overlapping to those of protein-coding transcripts (PCT). NATs were punctually described as regulating gene expression, and are expected to act more frequently in cis than other ncRNAs that commonly function in trans. In this work, 22 breast cancers expressing estrogen receptors and their paired healthy tissues were analyzed by strand-specific RNA sequencing to highlight the potential role of NATs in gene regulations occurring in breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE103001 Transcriptome-wide analysis of natural antisense transcripts shows their potential role in breast cancer. Scientific reports 4.011 https://doi.org/10.1038/s41598-017-17811-2 {Scientific reports (4.011): 10.1038/s41598-017-17811-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA399721 https://www.ebi.ac.uk/ena/browser/view/PRJNA399721 https://www.ncbi.nlm.nih.gov/sra?term=SRP116023 [Overal design]22 primary invasive breast cancer carcinoma expressing estrogen receptors and their paired adjacent mammary healthy tissues were analyzed by strand-specific RNA sequencing on a Illumina HiSeq.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA were simultaneously extracted with DNA and miRNA using All Prep DNA/RNA/miRNA Universal kit (Qiagen) according to the manufacturer protocol.\nRNA-Sequencing libraries for 22 breast tumors and paired adjacent tissues were constructed from 500 ng of total RNA, using the TruSeq® Stranded Total RNA kit and Ribo-Zero rRNA Removal kit (Illumina). A step of chemical fragmentation generated RNA fragment of 180 pb.'; [Cell type]'Source: ''tissue nature: normal; tumor receptors: /; bloom: /; er subtype: /; tnm: /; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 2; er subtype: A; tnm: T2N1aM0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 3; er subtype: B; tnm: T2N2aM0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 2; er subtype: A; tnm: T2N0M0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 1; er subtype: A; tnm: T2N0M0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 3; er subtype: B; tnm: T1cN0M0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 3; er subtype: B; tnm: T2N1aM0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 2; er subtype: A; tnm: T2N1M0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 3; er subtype: B; tnm: T2N0M0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 2; er subtype: A; tnm: T1cN0M0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 2; er subtype: A; tnm: T1bN1bM0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 1; er subtype: A; tnm: T1cN0M0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 2; er subtype: B; tnm: T2N0M0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 3; er subtype: B; tnm: T2N3aM0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 2; er subtype: B; tnm: T1cN0M0; ', 'tissue nature: primary invasive breast carcinoma; tumor receptors: ER+/HER2-; bloom: 1; er subtype: A; tnm: T1cN1aM0; ' GSE26000 Homo sapiens 4 Expression profiling by array GPL11305 Altered antisense-to-sense transcript ratios in breast cancer: Agilent 2010-12-10 Transcriptome profiling studies suggest that a large fraction of the genome is transcribed and many transcripts function independent of their protein coding potential. The relevance of noncoding RNAs (ncRNAs) in normal physiological processes and in tumorigenesis is increasingly recognized. Here, we describe consistent and significant differences in the distribution of sense and antisense transcripts between normal and neoplastic breast tissues. Many of the differentially expressed antisense transcripts likely represent long ncRNAs. A subset of genes that mainly generate antisense transcripts in normal but not cancer cells is involved in essential metabolic processes. These findings suggest fundamental differences in global RNA regulation between normal and cancer cells that might play a role in tumorigenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26000 Altered antisense-to-sense transcript ratios in breast cancer. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1010559107 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1010559107} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA142363 https://www.ebi.ac.uk/ena/browser/view/PRJNA142363 None [Overal design]Global strand-specific transcriptome profilings of 4 samples in cancer from clinical breast tissue using Agilent Technologies Custom microarray.; [Treatment]'None'; [Growth]'None'; [Extraction]'polyA RNA were purified from four (N1 to N4) normal organoid and four breast tumor samples as described previously (PMID: 17349583).'; [Cell type]'Source: ''tissue: breast; disease state: cancer; ', 'tissue: breast; disease state: normal; ' GSE20181 Homo sapiens 176 Expression profiling by array GPL96 Letrozole (Femara) early and late responses to treatment 2010-02-03 In the present investigation, we have exploited the opportunity provided by neoadjuvant treatment of a group of postmenopausal women with large operable or locally advanced breast cancer (in which therapy is given with the primary tumour remaining within the breast) to take sequential biopsies of the same cancers before and after 10-14 days or 90 days treatment with letrozole. RNA extracted from the biopsies has been subjected to Affymetrix microarray analysis and the data from paired biopsies interrogated to discover genes whose expression is most influenced by oestrogen deprivation. Keywords: Timecourse between subjects https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE20181 Sequential changes in gene expression profiles in breast cancers during treatment with the aromatase inhibitor, letrozole. The pharmacogenomics journal None https://doi.org/10.1038/tpj.2010.67 {The pharmacogenomics journal (None) doi:10.1038/tpj.2010.67}; {Breast cancer research : BCR (None) doi:10.1186/bcr2611}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA125655 https://www.ebi.ac.uk/ena/browser/view/PRJNA125655 None [Overal design]Biopsies were taken from the same subjects at three timepoints: pretreatment, after 10-14 days Letrozol (2.5 mg/day, oral), and after 90 days Letrozol (2.5 mg/day, oral).; [Treatment]'None', 'breast biopsies were taken from subjects after 90 days Letrozol, 2.5 mg'; [Growth]'None'; [Extraction]"Biopsies were snap-frozen after collection and stored in liquid nitrogen. Frozen sections were taken prior to RNA extraction to confirm the presence of cancerous tissue within the specimens. Only samples in which the malignant component comprised at least 20% of the section area were used in further analyses. Immediately before RNA extraction the biopsies were pulverised using U2 micro-dismembranator U (Braun Biotech). Total RNA was extracted from the resultant frozen tissue powder using TRI-reagent (Sigma) according to the manufacturer's recommendations. Extracted RNA was additionally purified on RNeasy mini columns (Qiagen). RNA quantity and quality was verified on Bioanalyser 2100 (Agilent)."; [Cell type]'Source: ''', 'subject: 2; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 3; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 4; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 5; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 6; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 29; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 30; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 31; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 33; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 34; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 35; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 36; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 37; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 39; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 40; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 41; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 42; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 43; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 44; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 45; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 46; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 47; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 49; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 50; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 51; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 52; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 53; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 55; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 56; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 57; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 58; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 59; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 60; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 63; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 64; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 65; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 67; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 68; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 69; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 11; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 13; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 14; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 21; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 23; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 8; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 10; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 17; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 18; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 19; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 7; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 12; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 15; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 16; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 20; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 22; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 25; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 24; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 27; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 28; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ', 'subject: 9; gender: female; tissue: breast tumor; agent: Letrozol; dose: 2.5mg/day; administration: oral; time: 90 days; ' GSE86945 Homo sapiens 100 Expression profiling by array GPL17586 Transcriptome characterization of triple negative breast cancer [Italy] 2016-09-14 Triple negative breast cancer (TNBC) represents a challenging tumor type due to their poor prognosis and limited treatment options. It is well recognize that clinical and molecular heterogeneity of TNBC is driven in part by mRNA and lncRNAs. To stratify TNBCs, we profiled mRNAs and lncRNA in 158 adjuvant TNBC tumors using an Affymetrix microarray platform. Lehmann clustering analysis allowed us to identify TNBC subtypes featuring unique lncRNA expression patterns, disease free and overall survival rates and particular gene ontology enrichments (performed with GSEA algorithm). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE86945 WNT signaling modulates PD-L1 expression in the stem cell compartment of triple-negative breast cancer. Oncogene 6.634 https://doi.org/10.1038/s41388-019-0700-2 {Scientific reports (4.011) doi:10.1038/s41598-018-29708-9}; {Cancers (6.162) doi:10.3390/cancers11070911}; {Oncogene (6.634) doi:10.1038/s41388-019-0700-2}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA343045 https://www.ebi.ac.uk/ena/browser/view/PRJNA343045 None [Overal design]Breast cancer tumors were collected from the archives of the Fondazione IRCCS Istituto Nazionale dei Tumori of Milan (INT) after a carefully histopathological review by two training pathologist, according to the following criteria: adjuvant therapy and collection of the surgical sample without any treatment. We obtain triple negative tumors (ER-, PR- and Her2-) and tumors from other immunophenotype (ER+, PR+ or/and Her2+) by microdissection of tumoral cells for RNA extraction and hybridization on Affymetrix microarrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'From FFPE breast cancer tissues, total RNA was extracted with miRNeasy mini kit (Qiagen)'; [Cell type]'Source: ''tissue: Triple negative breast cancer; lehmann subtype: M; population: Italy Caucasian; ', 'tissue: Triple negative breast cancer; lehmann subtype: UNS; population: Italy Caucasian; ', 'tissue: Triple negative breast cancer; lehmann subtype: IM; population: Italy Caucasian; ', 'tissue: Triple negative breast cancer; lehmann subtype: BL1; population: Italy Caucasian; ', 'tissue: Triple negative breast cancer; lehmann subtype: LAR; population: Italy Caucasian; ', 'tissue: Triple negative breast cancer; lehmann subtype: BL2; population: Italy Caucasian; ', 'tissue: Triple negative breast cancer; lehmann subtype: MSL; population: Italy Caucasian; ', 'tissue: Triple negative breast cancer; lehmann subtype: NA; population: Italy Caucasian; ' GSE42948 Homo sapiens 53 Expression profiling by high throughput sequencing GPL10999 Two New Stromal Signatures Stratify Breast Cancers with Different Prognosis 2012-12-16 Purpose: Multiple studies from last decades have shown that the microenvironment of carcinomas plays an important role in the initiation, progression and metastasis of cancer. Our group has previously identified novel cancer stroma gene expression signatures associated with outcome differences in breast cancer by gene expression profiling of two tumors of fibroblasts as surrogates for physiologic stromal expression patterns. The aim of this study is to find additional new types of tumor stroma gene expression patterns. Results: 53 tumors were sequenced by 3SEQ with an average of 29 million reads per sample. Both the elastofibroma (EF) and fibroma of tendon sheath (FOTS) gene signatures demonstrated robust outcome results for survival in the four breast cancer datasets. The EF signature positive breast cancers (20-33% of the cohort) demonstrated significantly better outcome for survival. In contrast, the FOTS signature positive breast cancers (11-35% of the cohort) had a worse outcome. The combined stromal signatures of EF, FOTS, and our previously identified DTF, and CSF1 signatures characterize, in part, the stromal expression profile for the tumor microenvironment for between 74%-90% of all breast cancers. Conclusions: We defined and validated two new stromal signatures in breast cancer (EF and FOTS), which are significantly associated with prognosis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE42948 Next generation sequencing-based expression profiling identifies signatures from benign stromal proliferations that define stromal components of breast cancer. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr3586 {Breast cancer research : BCR (5.676): 10.1186/bcr3586} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA183925 https://www.ebi.ac.uk/ena/browser/view/PRJNA183925 https://www.ncbi.nlm.nih.gov/sra?term=SRP017575 [Overal design]Gene expression profiling by 3SEQ was performed on 8 additional types of fibrous tumors, to identify different fibrous tumor specific gene expression signatures. We then determined the significance of the fibrous tumor gene signatures in four publically available breast cancer datasets (GSE1456, GSE4922, GSE3494, NKI Dataset).; [Treatment]'Clinical tissue samples were formalin-fixed and paraffin-embedded (FFPE).'; [Growth]'None'; [Extraction]'Multiple 2mm-diameter cores were taken from diagnostic FFPE material for RNA isolation. Then, total RNA was extracted by using of RecoverAll Total Nucleic Acid Isolation Kit (Ambion).\nPoly(A)+RNA was selected and enriched with oligo(dT) using the Oligotex mRNA mini Kit (Qiagen). The Poly(A) RNA was heat sheared to 100~200nt fragments. The sheared RNA was then subjected to first and second strand cDNA synthesis, followed by additional steps of library construction as described previously. The libraries were sent to the Stanford Genomic Center to be sequenced for the first 36bp at the 5’end of mRNA fragments with Illumina GA IIx machines.'; [Cell type]'Source: ''tissue: Soft Tissue; tissue archive method: FFPE; stromal signature: DTF(3SEQ) signature; prognosis: UNCLEAR; ', 'tissue: Soft Tissue; tissue archive method: FFPE; stromal signature: SFT signature; prognosis: UNCLEAR; ', 'tissue: Soft Tissue; tissue archive method: FFPE; stromal signature: DFSP signature; prognosis: UNCLEAR; ', 'tissue: Soft Tissue; tissue archive method: FFPE; stromal signature: FC signature; prognosis: UNCLEAR; ', 'tissue: Soft Tissue; tissue archive method: FFPE; stromal signature: EF signature; prognosis: GOOD; ', 'tissue: Soft Tissue; tissue archive method: FFPE; stromal signature: IF signature; prognosis: UNCLEAR; ', 'tissue: Soft Tissue; tissue archive method: FFPE; stromal signature: PF signature; prognosis: UNCLEAR; ', 'tissue: Soft Tissue; tissue archive method: FFPE; stromal signature: NPAF signature; prognosis: UNCLEAR; ', 'tissue: Soft Tissue; tissue archive method: FFPE; stromal signature: FOTS signature; prognosis: BAD; ', 'tissue: Soft Tissue; tissue archive method: FFPE; stromal signature: NF signature; prognosis: UNCLEAR; ' GSE40730 Homo sapiens 8 Expression profiling by array GPL570 Genome-wide analysis of RNAs translationally regulated upon BRCA1 depletion in human mammary epithelial cells 2012-09-10 Loss of function of the tumor suppressor BRCA1 (Breast Cancer 1) protein is responsible for numerous familial and sporadic breast cancers. We previously identified PABP1 as a novel BRCA1 partner and showed that BRCA1 modulates translation through its interaction with PABP1. We showed that the global translation was diminished in BRCA1-depleted cells and increased in BRCA1-overexpressing cells. Our findings raised the question whether BRCA1 affects translation of all cytoplasmic cellular mRNAs or whether it specifically targets a subset of mRNAs. In the present study, we investigated which mRNAs are regulated by BRCA1 using a microarray analysis of polysome-associated RNAs from BRCA1-depleted MCF7 cells, a human breast cancer cell line. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE40730 BRCA1-Dependent Translational Regulation in Breast Cancer Cells. PloS one 2.776 https://doi.org/10.1371/journal.pone.0067313 {PloS one (2.776): 10.1371/journal.pone.0067313} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA174769 https://www.ebi.ac.uk/ena/browser/view/PRJNA174769 None [Overal design]We isolated mRNAs from the high-molecular-weight polysomes (fractions 12 to 18) and total cellular cytoplasmic mRNAs from the cytoplasmic fraction of MCF7 cells transiently expressing either siRNA directed against BRCA1 or control siRNA. Since we were interested in identifying the mRNAs that were translationally regulated by BRCA1, we determined the relative translatability of each mRNA. The relative translatability of an mRNA was determined by normalizing the change in abundance in polysomal mRNA to the change in abundance in total cytoplasmic mRNA for each mRNA.; [Treatment]'Extracts from MCF7 cells were prepared by lysis at 4°C in extraction buffer (50 mM Tris-HCl, pH 7.4, 25 mM KCl, 5 mM MgCl2, 250 mM sucrose, 0.7 % Nonidet-P40) and nuclei were removed by centrifugation (800 g, 10 min, 4°C). The supernatant was centrifuged (12 000 g, 10 min, 4°C) to eliminate mitochondria. The supernatant (cytoplasmic fraction) was layered onto a 11 ml linear sucrose gradient (10-40% sucrose supplemented with 50 mM Tris-HCl, pH 7.4, 25 mM KCl, 5 mM MgCl2, 10 mM DTE and 100µg/ml cycloheximide). After 2h of centrifugation at 250 000 g and at 4°C in a SW41Ti rotor (Beckman), 18 fractions of 600 µl were manually collected.'; [Growth]'MCF7 cells were plated at 1,8x10^6 cells per 10 cm diameter dish 24h before transfection. Cells were transfected with 200 pmol/dish of siRNA against BRCA1 or Control and 16 µL/dish of Lipofectamine 2000 (Life Technologies) using the protocol of the supplier. Cells were harvested 72 hours after transfection.'; [Extraction]"Approximately 20% of the total volume of the cytoplasmic fraction was used as a source for total cytoplasmic RNA by using Trizol (Life Technologies) extraction and isopropanol precipitation. Polysomal RNA was recovered from individual fractions 12 to 18 by Trizol extraction and isopropanol precipitation. Then 100 ng of RNA was amplified using GeneChip 3' IVT Express Kit from Affymetrix."; [Cell type]'Source: ''transfection: control; cell line: MCF7; fraction: total RNA; ', 'transfection: control; cell line: MCF7; fraction: polysomal RNA; ', 'transfection: BRCA1; cell line: MCF7; fraction: total RNA; ', 'transfection: BRCA1; cell line: MCF7; fraction: polysomal RNA; ' GSE146769 Homo sapiens 10 Expression profiling by high throughput sequencing GPL21290 KRAB domain of ZFP568 disrupts TRIM28-mediated abnormal interactions in cancer cells 2020-03-11 We observed changes in protein levels of EZH2, TRIM24, p53, and a substantial number of KRAB-ZF proteins in MCF7 cells upon introducing a peptide fragment containing the KRAB domain. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE146769 KRAB domain of ZFP568 disrupts TRIM28-mediated abnormal interactions in cancer cells. NAR cancer None https://doi.org/10.1093/narcan/zcaa007 {NAR cancer (None): 10.1093/narcan/zcaa007} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA611924 https://www.ebi.ac.uk/ena/browser/view/PRJNA611924 https://www.ncbi.nlm.nih.gov/sra?term=SRP252344 [Overal design]mRNA profiles of MCF7 cells expressing Krab domain, knockdown of TRIM28, and Vector alone, sh scrambled control were generated using deep sequencing, in duplicate; [Treatment]'None'; [Growth]'Stable gene expression Cells'; [Extraction]'Qiagen mRNA kit\nIllumina TruSeq Stranded total RNA kit according to the manufacturer’s protocol. The libraries were sequenced using 2x76 bases paired end protocol on Illumina HiSeq 3000 instrument. Two biological replicates per condition were sequenced, generating 45-58 million pairs of reads per sample. Each pair of reads represents a cDNA fragment from the library.'; [Cell type]'Source: ''cell line: MCF7; origin: Breast Cancer ER +ve; shRNA: empty vector; ', 'cell line: MCF7; origin: Breast Cancer ER +ve; shRNA: 2K fragment; ', 'cell line: MCF7; origin: Breast Cancer ER +ve; shRNA: sh scrambled Control; ', 'cell line: MCF7; origin: Breast Cancer ER +ve; shRNA: knockdown TRIM28; ', 'cell line: MCF7; origin: Breast Cancer ER +ve; shRNA: 1K fragment; ' GSE90505 Homo sapiens 70 Expression profiling by array GPL14550 Identification of interacting stromal properties in triple-negative breast cancer - Stromal Discovery Set 2016-11-25 Triple-negative breast cancer is a molecularly heterogeneous cancer that is difficult to treat. TNBC microenvironmental (stromal) heterogeneity has not been well characterized despite the key role that it may play in tumor progression. To address this challenge we investigated the transcriptome of tumor-associated stroma isolated from TNBCs (n=57). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE90505 Identification of Interacting Stromal Axes in Triple-Negative Breast Cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-16-3427 {Cancer research (8.378): 10.1158/0008-5472.CAN-16-3427} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA354938 https://www.ebi.ac.uk/ena/browser/view/PRJNA354938 None [Overal design]57 flash-frozen human primary breast cancer samples were subjected to laser capture microdissection to separately isolate tumor-associated and adjacent normal stromal components. RNA was isolated, subjected to 2 rounds of amplification, and hybridized on Agilent 8x60K microarrays along with a common reference two round-amplified commercially obtained Universal Human Reference RNA). For one sample each tumor-associated stroma and normal adjacent stroma, a second technical replicate was performed.; [Treatment]"Tissue compartments isolated from OCT-embedded frozen human tissue samples by laser capture microscopy following HistoGene staining and pathologist's evaluation"; [Growth]'None'; [Extraction]'Tumor epithelium and stroma were separately microdissected from tissue samples using a PixCell IIe LCM system (Arcturus). All microdissections were performed within three hours of tissue staining. Total RNA was extracted from each population of microdissected cells using an Arcturus PicoPure RNA Isolation Kit (Cat# 12204-01).'; [Cell type]'Source: ''sample type: Universal Human Reference RNA (Stratagene); ', 'event: FALSE; er: Negative; her2: NA; grade: High; lymph: Positive; chemo: Yes; tamoxifen: Yes; herceptin: No; age: 71; size: 25; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 55; size: 17; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 71; size: 24; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 56; size: 18; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: ND; tamoxifen: ND; herceptin: No; age: 34; size: 19; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 36; size: 16; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: NA; er: NA; her2: NA; grade: NA; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: NA; age: NA; size: NA; tissue.type: Normal-Stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: Yes; herceptin: No; age: 43; size: 18; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 41; size: 17; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: NA; er: NA; her2: NA; grade: High; lymph: Positive; chemo: NA; tamoxifen: NA; herceptin: NA; age: NA; size: 34; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: Yes; herceptin: No; age: 55; size: 10; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: No; age: 89; size: 25; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 61; size: 25; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: NA; er: NA; her2: NA; grade: High; lymph: Negative; chemo: NA; tamoxifen: NA; herceptin: NA; age: NA; size: 25; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: Intermediate; lymph: Negative; chemo: No; tamoxifen: NA; herceptin: No; age: 82; size: 90; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: NA; tamoxifen: NA; herceptin: NA; age: 54; size: 24; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: NA; tamoxifen: NA; herceptin: No; age: 54; size: 12; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 51; size: 12; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: NA; age: 58; size: 6; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 35; size: 38; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: NA; chemo: Yes; tamoxifen: No; herceptin: No; age: 66; size: 12; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: Yes; tamoxifen: No; herceptin: No; age: 38; size: 17; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: No; tamoxifen: No; herceptin: No; age: 83; size: 32; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: NA; age: 75; size: 28; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 64; size: 18; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: NA; chemo: No; tamoxifen: No; herceptin: No; age: 90; size: 32; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: Yes; tamoxifen: No; herceptin: No; age: 41; size: 31; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: Yes; tamoxifen: No; herceptin: No; age: 38; size: 60; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: Yes; tamoxifen: Yes; herceptin: No; age: 40; size: 25; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: No; tamoxifen: Yes; herceptin: No; age: 56; size: 19; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: Intermediate; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 57; size: 18; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: NA; tamoxifen: NA; herceptin: No; age: 57; size: 28; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: Intermediate; lymph: Negative; chemo: Yes; tamoxifen: Yes; herceptin: No; age: 47; size: 18; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: NA; chemo: Yes; tamoxifen: No; herceptin: No; age: 79; size: 21; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: No; tamoxifen: Yes; herceptin: No; age: 78; size: 35; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: Intermediate; lymph: Negative; chemo: Yes; tamoxifen: Yes; herceptin: No; age: 58; size: 15; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: Intermediate; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 60; size: 16; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: NA; age: 50; size: 22; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: NA; lymph: Negative; chemo: NA; tamoxifen: NA; herceptin: NA; age: 91; size: 40; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: Yes; tamoxifen: No; herceptin: No; age: 47; size: 17; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 47; size: 26; tissue.type: Tumor-stroma; replicate: TRUE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: NA; chemo: No; tamoxifen: No; herceptin: No; age: 55; size: 7; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: FALSE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 53; size: 32; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 64; size: 19; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: NA; er: NA; her2: NA; grade: High; lymph: Positive; chemo: NA; tamoxifen: NA; herceptin: NA; age: NA; size: 22; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: No; tamoxifen: No; herceptin: No; age: 75; size: 26; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: Yes; tamoxifen: No; herceptin: No; age: 43; size: 20; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: Yes; tamoxifen: No; herceptin: No; age: 55; size: 29; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: No; age: 64; size: 15; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: NA; chemo: Yes; tamoxifen: No; herceptin: No; age: 73; size: 12; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: No; tamoxifen: Yes; herceptin: No; age: 71; size: 21; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: Yes; tamoxifen: No; herceptin: No; age: 57; size: 35; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: Yes; tamoxifen: No; herceptin: No; age: 56; size: 39; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: Yes; tamoxifen: No; herceptin: No; age: 33; size: 32; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: Yes; tamoxifen: No; herceptin: No; age: 48; size: 48; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: Yes; tamoxifen: NA; herceptin: No; age: 72; size: 22; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: Negative; chemo: NA; tamoxifen: NA; herceptin: No; age: 82; size: 23; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: TRUE; er: Negative; her2: Negative; grade: High; lymph: Positive; chemo: Yes; tamoxifen: No; herceptin: No; age: 57; size: 48; tissue.type: Tumor-stroma; replicate: FALSE; ', 'event: NA; er: NA; her2: NA; grade: NA; lymph: NA; chemo: NA; tamoxifen: NA; herceptin: NA; age: NA; size: NA; tissue.type: Normal-Stroma; replicate: TRUE; ' GSE115784 Homo sapiens 6 Expression profiling by array GPL17586 Gene expression data from SKOV3 cell line with SND1 knockdown 2018-06-13 SND1 protein is a highly conserved protein of eukaryotic cells and is involved in a group of cellular biological processes, such as gene transcription, pre-mRNA splicing, cell cycle, DNA damage repair, proliferation and programmed cell death degradome, adipogenesis and cancerogenesis. SND1 can promote the metastasis and proliferation of breast cancer cells by down-regulating the miR-127 expression. Herein, we used microarrays to detail the potential molecular mechanism in the ovarian cancer tumorigenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE115784 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA476000 https://www.ebi.ac.uk/ena/browser/view/PRJNA476000 None [Overal design]Total RNA were extracted in SKOV3 cells transfection with shSND1 and pLKO-Vector respectively. cDNA was synthesized and hybridised to Affymetrix microarrays.; [Treatment]'no treatment'; [Growth]"SKOV3 stable cell lines of shSND1-#2 and pLKO-Vector was grown in McCoy's 5A with 10% fetal bovine serum."; [Extraction]"TRIzol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'SKOV3 pLKO-Vector stable cell line', 'SKOV3 pLKO-shSND1-#2 stable cell line''genotype/variation: normal; cell type: SKOV3 pLKO-Vector stable cell line; cell line: SKOV3; ', 'genotype/variation: SND1 knockdown; cell type: SKOV3 pLKO-shSND1-#2 stable cell line; cell line: SKOV3; ' GSE79242 Homo sapiens 6 Expression profiling by array GPL10558 MSI2 gene expression profile in breast cancer cell 2016-03-15 MSI2 is one of RNA Binding protein. To investigate the role of MSI2 in breast cancer cell (MCF7), we carried out microarray. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE79242 Musashi RNA-binding protein 2 regulates estrogen receptor 1 function in breast cancer. Oncogene 6.634 https://doi.org/10.1038/onc.2016.327 {Oncogene (6.634): 10.1038/onc.2016.327} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA315268 https://www.ebi.ac.uk/ena/browser/view/PRJNA315268 None [Overal design]MSI2 was silenced in MCF-7 cell (siCon=3, siMSI2=3); [Treatment]'Cells were treated with indicated lenti-viral vector'; [Growth]'The cells were grown in RPMI1640 media.'; [Extraction]'miRvana kit was used for RNA extraction'; [Cell type]'cancer cell''cell type: cancer cell; ' GSE11791 Homo sapiens 15 Expression profiling by array GPL570 Estrogen- and Myc-regulated genes in MCF-7 breast cancer cells 2008-06-16 Estrogen-responsive genes were identified by transcript profiling of estrogen-treated MCF-7 breast cancer cells. The gene expression profile generated after estrogen treatment was compared with that following inducible expression of c-Myc or c-Zip (a deletion mutant of c-Myc that lacks the N-terminal transactivation domains) in clonal MCF-7 cell lines. Keywords: Single time point https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE11791 Identification of functional networks of estrogen- and c-Myc-responsive genes and their relationship to response to tamoxifen therapy in breast cancer. PloS one 2.776 https://doi.org/10.1371/journal.pone.0002987 {PloS one (2.776): 10.1371/journal.pone.0002987} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA105991 https://www.ebi.ac.uk/ena/browser/view/PRJNA105991 None [Overal design]RNA was collected in three independent experiments, each including parental MCF-7 cells treated with 17b-estradiol (E2) or ethanol (EtOH), zinc-treated p∆MT-c-Myc cells, zinc-treated p∆MT-c-Zip cells and zinc-treated empty vector (p∆MT) cells. Cells were arrested for 48 h with 10 nM ICI 182780 and then treated for 6 h with either 100 nM E2 or ethanol vehicle, or 75 mM zinc for the stably transfected cell lines.; [Treatment]'Exponentially proliferating cells were growth arrested by pretreatment for 48 h with 10nM steroidal antiestrogen ICI 182780 and then treated with either 100nM E2 or 75 uM Zn (as ZnSO4). Vehicle controls for E2 or Zn were absolute ethanol and water respectively.'; [Growth]'None'; [Extraction]"Total RNA from three independent experiments was isolated from cells using the RNeasy mini kit (Qiagen Pty Ltd, Clifton Hill, Vic Australia) following the manufacturer's instructions."; [Cell type]'Source: ''' GSE84648 Homo sapiens 9 Expression profiling by array GPL6244 Targeted interference of sin3a-tgif1 function by SID decoy treatment inhibits WNT signaling and invasion in triple negative breast cancer cells 2016-07-20 Targeted interference of sin3a-tgif1 function by SID decoy treatment inhibits WNT signaling and invasion in triple negative breast cancer cells. MDA-MB-231 cells were treated with scrambled SID control, 2.5µM SID peptide or untreated for 24h. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE84648 Targeted interference of SIN3A-TGIF1 function by SID decoy treatment inhibits Wnt signaling and invasion in triple negative breast cancer cells. Oncotarget None https://doi.org/10.18632/oncotarget.11381 {Oncotarget (None): 10.18632/oncotarget.11381} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA330729 https://www.ebi.ac.uk/ena/browser/view/PRJNA330729 None [Overal design]Sub-confluent cultures of MDA-MB-231 cells were treated with scrambled SID control, 2.5µM SID peptide or untreated for 24h. Experiments were performed as three independent replicates.; [Treatment]'MDA-MB-231 cells were treated with scrambled SID control, 2.5µM SID peptide or untreated for 24h.'; [Growth]'MDA-MB-231 cell lines were maintained in DMEM supplemented with 10% FBS, 1% GlutaMAX (Invitrogen), 10mM HEPES, 1mM sodium pyruvate, non-essential amino acids and 1% antibiotic-antimycotic solution.'; [Extraction]'Total RNA was isolated using the ZR RNA MiniPrep Kit (Zymo Research). The concentration and quality of the total RNA was assessed on an Agilent 2100 BioAnalyzer (Agilent Technologies).'; [Cell type]'Breast cancer cell line''cell type: Breast cancer cell line; ' GSE15398 Homo sapiens 27 Expression profiling by array GPL570 Evaluation of methods for amplification of picogram amounts of total RNA for whole genome expression profiling 2009-03-25 For more than a decade, microarrays have been a powerful and widely used tool to explore the transcriptome of biological systems. However, the amount of biological material from cell sorting or laser capture microdissection is much too small to perform microarray studies. To address this issue, RNA amplification methods have been developed to generate sufficient targets from picogram amounts of total RNA to perform microarray hybridisation. In this study, four commercial protocols for amplification of picograms amounts of input RNA for microarray expression profiling were evaluated and compared. The quantitative and qualitative performances of the methods were assessed. Microarrays were hybridised with the amplified targets and the amplification protocols were compared with respect to the quality of expression profiles, reproducibility within a concentration range of input RNA, and sensitivity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15398 Evaluation of methods for amplification of picogram amounts of total RNA for whole genome expression profiling. BMC genomics 3.501 https://doi.org/10.1186/1471-2164-10-246 {BMC genomics (3.501): 10.1186/1471-2164-10-246} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA115879 https://www.ebi.ac.uk/ena/browser/view/PRJNA115879 None [Overal design]Four commercial protocols for amplification of picograms amounts of input RNA for microarray expression profiling were evaluated and compared. For each protocol, one RNA amplification was performed from 250 pg, and one from 500 pg of human universal RNA by two operators in two independent laboratories and compared to the amplified aRNA obtained from 2 µg and 100 ng RNA inputs following the standard protocol proposed by Affymetrix. A negative control (amplification without total RNA) and a positive control (if available) were included in each experimental batch. Samples indicating 50, 100, and 1000 pg RNA inputs correspond to 3 additional quantities of total RNA used to synthesise the cDNA target using the nugen protocol for comparison (250, 500 pg + 50, 100, 1000 pg).; [Treatment]'None'; [Growth]'None'; [Extraction]'not applicable', 'RNeasy Mini Kit (Qiagen)'; [Cell type]'Source: ''protocol: one cycle amplification kit from Affymetrix; ', 'protocol: two cycle amplification kit from Affymetrix; ', 'protocol: MessageAmp™ II aRNA Amplification (Ambion); ', 'protocol: RiboAmp™ HS RNA Amplification Kit (Arcturus); ', 'protocol: TargetAmp 2-Round Aminoallyl-aRNA Amplification_Epicentre; ', 'protocol: WT-Amplification™ Pico kit (Nugen); ' GSE155478 Homo sapiens 6 Expression profiling by array GPL22755 LncRNA expression data from BRCA drug-sensitive and drug-resistant cell lines 2020-07-31 Worldwide, breast cancer (BRCA) is the most common malignant tumor in women. Adriamycin (ADR) is considered one of the most effective agents for the treatment of BRCA, but its efficacy as a curative agent is compromised by intrinsic resistance and the acquisition of multidrug resistance characteristics during chemotherapy. The underlying mechanisms resulting in ADR resistance in BRCA remain poorly understood. Long non-coding RNA (lncRNA) are abnormally expressed in many cancers and are highly involved in its pathogenesis, including drug resistance. In order to systematically study the role of lncRNA in the resistance of BRCA cells to ADR, we used lncRNA expression microarray to establish gene expression profiles of ADR resistant cell lines and ADR sensitive cell lines. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE155478 LncRNA CBR3-AS1 regulates of breast cancer drug sensitivity as a competing endogenous RNA through the JNK1/MEK4-mediated MAPK signal pathway. Journal of experimental & clinical cancer research : CR 5.646 https://doi.org/10.1186/s13046-021-01844-7 {Journal of experimental & clinical cancer research : CR (5.646): 10.1186/s13046-021-01844-7} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA649906 https://www.ebi.ac.uk/ena/browser/view/PRJNA649906 None [Overal design]The ADR sensitive cell line MCF-7 and the ADR resistant cell line MCF-7/ADR were used for RNA extraction and hybridization on microarrays. We are trying to study the expression profile of lncRNA in BRCA cell lines and find the key factors that mediate breast cancer drug resistance.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was quantified by the NanoDrop ND-2000 (Thermo Scientific)and the RNA integrity was assessed using Agilent Bioanalyzer 2100 (Agilent Technologies).'; [Cell type]'breast cancer (BRCA) cell line''cell line: MCF-7/ADR; cell type: breast cancer (BRCA) cell line; phenotype: ADR resistant; ', 'cell line: MCF-7; cell type: breast cancer (BRCA) cell line; phenotype: ADR sensitive; ' GSE56022 Homo sapiens 22 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL11154; GPL16791 Ligand-dependent genomic function of glucocorticoid receptor in triple-negative breast cancer 2014-03-19 Glucocorticoids (GC) have been widely used as coadjuvants in the treatment of solid tumors, but GC treatment may be associated with poor pharmacotherapeutic response and/or prognosis. The genomic action of GC in these tumors is largely unknown. Here we find that dexamethasone (Dex, a synthetic GC) regulated genes in triple-negative breast cancer (TNBC) cells are associated with drug resistance. Importantly, these GC-regulated genes are aberrantly expressed in TNBC patients and associated with unfavorable clinical outcomes. Interestingly, in TNBC cells, Compound A (CpdA, a selective GR modulator) only regulates a small number of genes not involved in carcinogenesis and therapy resistance. Mechanistic studies using a ChIP-exo approach reveal that Dex- but not CpdA-liganded glucocorticoid receptor (GR) binds to a single glucocorticoid response element (GRE), which drives the expression of pro-tumorigenic genes. Our data suggest that development of safe coadjuvant therapy should consider the distinct genomic function between Dex- and CpdA-liganded GR. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE56022 Ligand-dependent genomic function of glucocorticoid receptor in triple-negative breast cancer. Nature communications 11.878 https://doi.org/10.1038/ncomms9323 {Nature communications (11.878): 10.1038/ncomms9323} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA242236 https://www.ebi.ac.uk/ena/browser/view/PRJNA242236 https://www.ncbi.nlm.nih.gov/sra?term=SRP040300 [Overal design]To study GR-regulated genes and define GRE in human genome, RNA-seq and GR ChIP-exo are performed in MDA-MB-231 cells before/after dex and CpdA stimulation. Each experiment includes two replicates.; [Treatment]'For hormone responsive experiments, MDA-MB-231 cells were maintained in phenol red-free RPMI medium with 5% charcoal-stripped FBS for 3 days, and then treated with vehicle and different ligands.'; [Growth]'The TNBC cell line MDA-MB-231 were obtained from the American Type Culture Collection, and cultured in DMEM 10% FBS.'; [Extraction]'After treatment with 100 nM Dex, 10 uM CpdA or vehicle for 1 h, MDA-MB-231 cells were crosslinked with 1% formaldehyde for 10 min. Sonicated chromatin was enriched by immunoprecipatation with an anti-GR antibody.\nFor ChIP-exo, T4 DNA polymerase, T4 PNK, and Klenow DNA Polymerase were used together for end polishing. The ligation step was performed with less reducing agent. Protein A Dynal magnetic beads were washed using modified RIPA buffer (50mM Tris-HCL pH 7.8, 1mM EDTA, 0.25% Na Deoxycholate, 1% NP-40, 0.5M LiCl). The library was amplified with only 10 or 12 PCR cycles, and prepared without gel-based size selection.', 'After treatment with 100 nM Dex, 10 uM CpdA or vehicle for 1 h, MDA-MB-231 cells were crosslinked with 1% formaldehyde for 10 min. Sonicated chromatin was enriched by immunoprecipatation with an anti-GR antibody. MDA-MB-231 cells were treated with 100 nM Dex, or 10 \uf06dM CpdA for 2h and 4h, respectively. RNA was extracted using the RNeasy Mini Kit.\nFor ChIP-exo, T4 DNA polymerase, T4 PNK, and Klenow DNA Polymerase were used together for end polishing. The ligation step was performed with less reducing agent. Protein A Dynal magnetic beads were washed using modified RIPA buffer (50mM Tris-HCL pH 7.8, 1mM EDTA, 0.25% Na Deoxycholate, 1% NP-40, 0.5M LiCl). The library was amplified with only 10 or 12 PCR cycles, and prepared without gel-based size selection. For RNA-seq, libraries were constructed using the Illumina Truseq RNA Sample Prep Kit according to the manufacturer’s protocol.'; [Cell type]'Source: ''cell line: MDA-MB-231; cancer: Breast adenocarcinoma; chip antibody: Glucocorticoid Receptor (D8H2) XP® Rabbit mAb #3660 from CST; ', 'cell line: MDA-MB-231; cancer: Breast adenocarcinoma; type: TNBC; ', 'cell line: MDA-MB-231; cancer: Breast adenocarcinoma; type: TNBC; chip antibody: c-Jun Antibody (H-79) from Santa Cruz Biotechnology; ', 'cell line: MDA-MB-231; cancer: Breast adenocarcinoma; type: TNBC; chip antibody: NFκB p65 Antibody (C-20) from Santa Cruz Biotechnology; ' GSE161146 Mus musculus; Homo sapiens 127 Expression profiling by high throughput sequencing; Other GPL18573; GPL19057; GPL20301; GPL24676 Bone invigorates metastatic seeding 2020-11-09 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE161146 The bone microenvironment invigorates metastatic seeds for further dissemination. Cell 36.216 https://doi.org/10.1016/j.cell.2021.03.011 {Cell (36.216): 10.1016/j.cell.2021.03.011} 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA675666 https://www.ebi.ac.uk/ena/browser/view/PRJNA675666 None [Overal design]Refer to individual Series; [Treatment]'cells were passaged every five days. For epz treatment, cells at passage 3 received a five-day treatment of 1uM ezh2 inhibitor, EPZ011989, under regular culture condition.'; [Growth]'SCP21 cells were transplanted into mammary fat pad, lung or bone via different injection routes, and inoculated in vivo for four weeks. Then the mammary fat pad tumors, lung metastases, and bone metastases were collected and subjected to tumor dissociation kit to generate single cell suspension. mRFP positive tumor cells were sorted by flow cytometry, and cultured in vitro on the petri dishes. if not specified, the total RNA subjected to sequencing was collected using TRIZOL with direct-zol RNA column purification kit from Zymo. the total RNAs were immediately shipped to Novogene, and the quality check, library preparation, and deep sequencing was performed by Novogene.', 'MDA-MB-231 FR and AT-3 FR cells were transduced with TLCV2-hgRNA A26 and selected by puromycin for 2 weeks. 1E5 barcoded cells were then implanted to the fourth pair of mammary fat pad of nude mice or C57BL/6 mice. 5 weeks later for MDA-MB-231 tumors or 18 days later for AT-3 tumors, the mammary tumors were resected and mice were give with a single dose of 5mg/kg doxycycline weekly for 5 cycles or 4 cycles through I.P. injection. 2 weeks after Dox treatment, the tissues with metastases were collected, and total DNA were exacted. For IIA injection model, 1E5 barcoded MDA-MB-231 cells were then delivered to bone via IIA. 2 weeks later, a single dose of 5mg/kg doxycycline weekly for 5 cycles was applied to the mice carrying bone metastases through I.P. injection. 3 weeks after Dox treatment, lung, right and left hindlimbhind limbs were collected, and total DNA were exacted. For in vitro treatment samples, cells were treated with 100μg/ml doxycycline for 2 hours and then rinsed by pre-warmed PBS twice to completely remove doxycycline and then allow to grow in vitro for 4 days. Then 1 million cells were collected for barcode sequencing and 0.5 million cells were seeded back to the petri dish and received another round of doxycycline treatment 24 hours later.'; [Extraction]"The metastatic lesions were dissected with ex vivo BLI imaging, and the uninvolved tissues were removed in the hood. The surgery tools were sterilized with a bead-sterilizer following by 70% isopropanol between different animals. The collected tissues were immediately subjected to the tumor dissociation kit and RFP positive cells were sorted and re-cultured in vitro. The total RNA were extracted using TRIZOL with directzol RNA isolation kit following the manufacturer's protocol.\nthe library construction was performed by Novogene.", 'The metastatic lesions were dissected with ex vivo BLI imaging, and the uninvolved tissues were removed. The surgery tools were sterilized with a bead-sterilizer following by 70% isopropanol between different lesions. The collected tissues was snap-frozen in the liquid nitrogen until DNA extraction. The tissues were then rinsed by the gDNA lysis buffer from Quick-DNA Miniprep Plus Kit (Zymo Research, D4068) and homogenized with Precellys Lysing Kit (Bertin Instruments, MK28-R). After the homogenization, samples were lysed at 55℃ for 3 h, followed by 0.33 mg/mL RNaseA treatment at 37℃ for 15 min. Nucleic acid was further extracted following the manufacturer’s instruction. The final DNA was assessed by NanoDrop 2000 (Thermo Scientific) and human/mouse DNA ratio was examined by q-PCR with primers targeting human and mouse GAPDH gene, respectively.\nBarcodes were amplified by two rounds of PCR. The first round of PCR was performed with 100 ng genomic DNA using Platinum Taq DNA Polymerase (Invitrogen) with Barcode-For and Barcode-Rev primers in 15 cycles. The second round of PCR were performed in a real-time setting and stopped in mid-exponential phase using PowerUp SYBR Green Master Mix (Thermo Fisher) with Barcode-P5-For and Barcode-P7-Rev primers. PCR products were then column-purified with QIAquick PCR purification Kit (QIAGEN) and assessed with Qubit. The NEBNext Multiplex oligos for Illumina (Dual index primer set 1,NEB, E7600S) and the NEB library preparation kit for Illumina (NEB, #E7645S) were used for library preparation as previously described (Kalhor et al., 2017).'; [Cell type]'breast cancer', 'Source: ''cell type: breast cancer; metastic sites: In vitro, navie parental cells; host: N.A.; mouse id: N.A.; ', 'cell type: breast cancer; metastic sites: mammary fat pad; host: Athymic Nude; mouse id: 326; ', 'cell type: breast cancer; metastic sites: mammary fat pad; host: Athymic Nude; mouse id: 327; ', 'cell type: breast cancer; metastic sites: mammary fat pad; host: Athymic Nude; mouse id: 328; ', 'cell type: breast cancer; metastic sites: lung; host: Athymic Nude; mouse id: 712; ', 'cell type: breast cancer; metastic sites: lung; host: Athymic Nude; mouse id: 713; ', 'cell type: breast cancer; metastic sites: lung; host: Athymic Nude; mouse id: 316; ', 'cell type: breast cancer; metastic sites: bone; host: Athymic Nude; mouse id: 320; ', 'cell type: breast cancer; metastic sites: bone; host: Athymic Nude; mouse id: 321; ', 'cell type: breast cancer; metastic sites: bone; host: Athymic Nude; mouse id: 322; ', 'cell type: breast cancer; metastic sites: bone; host: Athymic Nude; mouse id: 323; ', 'injected cell line: not injected; metastic sites: N.A.; host: N.A.; mouse id: N.A.; ', 'injected cell line: MDA-MB-231; metastic sites: Left Hindlimb; host: Athymic Nude; mouse id: 9928; ', 'injected cell line: MDA-MB-231; metastic sites: Lung; host: Athymic Nude; mouse id: 9928; ', 'injected cell line: MDA-MB-231; metastic sites: Right Hindlimb; host: Athymic Nude; mouse id: 9928; ', 'injected cell line: MDA-MB-231; metastic sites: Left Hindlimb; host: Athymic Nude; mouse id: 9934; ', 'injected cell line: MDA-MB-231; metastic sites: Lung; host: Athymic Nude; mouse id: 9934; ', 'injected cell line: MDA-MB-231; metastic sites: Right Hindlimb; host: Athymic Nude; mouse id: 9934; ', 'injected cell line: MDA-MB-231; metastic sites: Mammary fat pad; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Lung; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Liver; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Spleen; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Kidney; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Brain; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Right Hindlimb; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Left Hindlimb; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Right Forelimb; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Left Forelimb; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Sternum; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Spine; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Rib cage; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Skull; host: Athymic Nude; mouse id: 509; ', 'injected cell line: MDA-MB-231; metastic sites: Mammary fat pad; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Lung; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Liver; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Spleen; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Kidney; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Brain; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Right Hindlimb; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Left Hindlimb; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Right Forelimb; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Left Forelimb; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Sternum; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Spine; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Rib cage; host: Athymic Nude; mouse id: 510; ', 'injected cell line: MDA-MB-231; metastic sites: Skull; host: Athymic Nude; mouse id: 510; ', 'injected cell line: AT-3; metastic sites: Mammary fat pad; host: C57BL/6J; mouse id: 121; ', 'injected cell line: AT-3; metastic sites: Lung; host: C57BL/6J; mouse id: 121; ', 'injected cell line: AT-3; metastic sites: Liver; host: C57BL/6J; mouse id: 121; ', 'injected cell line: AT-3; metastic sites: Kidney; host: C57BL/6J; mouse id: 121; ', 'injected cell line: AT-3; metastic sites: Spleen; host: C57BL/6J; mouse id: 121; ', 'injected cell line: AT-3; metastic sites: Right Hindlimb; host: C57BL/6J; mouse id: 121; ', 'injected cell line: AT-3; metastic sites: Left Hindlimb; host: C57BL/6J; mouse id: 121; ', 'injected cell line: AT-3; metastic sites: Right Forelimb; host: C57BL/6J; mouse id: 121; ', 'injected cell line: AT-3; metastic sites: Rib cage; host: C57BL/6J; mouse id: 121; ', 'injected cell line: AT-3; metastic sites: Mammary fat pad; host: C57BL/6J; mouse id: 520; ', 'injected cell line: AT-3; metastic sites: Lung; host: C57BL/6J; mouse id: 520; ', 'injected cell line: AT-3; metastic sites: Liver; host: C57BL/6J; mouse id: 520; ', 'injected cell line: AT-3; metastic sites: Kidney; host: C57BL/6J; mouse id: 520; ', 'injected cell line: AT-3; metastic sites: Spleen; host: C57BL/6J; mouse id: 520; ', 'injected cell line: AT-3; metastic sites: Right Hindlimb; host: C57BL/6J; mouse id: 520; ', 'injected cell line: AT-3; metastic sites: Left Hindlimb; host: C57BL/6J; mouse id: 520; ', 'injected cell line: AT-3; metastic sites: Right Forelimb; host: C57BL/6J; mouse id: 520; ', 'injected cell line: AT-3; metastic sites: Left Forelimb; host: C57BL/6J; mouse id: 520; ', 'injected cell line: AT-3; metastic sites: Rib cage; host: C57BL/6J; mouse id: 520; ', 'injected cell line: AT-3; metastic sites: Sternum; host: C57BL/6J; mouse id: 520; ', 'injected cell line: AT-3; metastic sites: Skull; host: C57BL/6J; mouse id: 520; ' GSE134147 Homo sapiens 12 Expression profiling by high throughput sequencing GPL16791 MUC1-C ACTIVATES THE NURD COMPLEX IN DEDIFFERENTIATION OF TRIPLE-NEGATIVE BREASTCANCER CELLS 2019-07-11 The NuRD chromatin remodeling and deacetylation complex, which includes MTA1, MBD3, CHD4 and HDAC1 among other components, is of importance for development and cancer progression. The oncogenic MUC1-C protein activates EZH2 and BMI1 in the epigenetic reprogramming of triple-negative breast cancer (TNBC) cells. However, there is no known link between MUC1-C and chromatin remodeling complexes. The present studies demonstrate that MUC1-C binds directly to the MYC HLH/LZ domain. In turn, we identified a previously unrecognized MUC1-C®MYC pathway that regulates the NuRD complex. We show that MUC1-C/MYC complexes selectively activate the MTA1 and MBD3 genes and posttranscriptionally induce CHD4 expression in basal- and not luminal-type BC cells. The results further show that MUC1-C forms complexes with these NuRD components on the ESR1 promoter. In this way, silencing MUC1-C (i) decreased MTA1/MBD3/CHD4/HDAC1 occupancy and increased H3K27 acetylation on the ESR1 promoter, and (ii) induced ESR1 expression and downstream estrogen response pathways. We also demonstrate that targeting MUC1-C and these NuRD components induces expression of FOXA1, GATA3 and other markers associated with the luminal phenotype. These findings and results from gain-of-function studies support a model in which MUC1-C activates the NuRD complex in driving luminal®basal dedifferentiation and plasticity of TNBC cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE134147 MUC1-C Activates the NuRD Complex to Drive Dedifferentiation of Triple-Negative Breast Cancer Cells. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-19-1034 {Cancer research (8.378): 10.1158/0008-5472.CAN-19-1034} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA554094 https://www.ebi.ac.uk/ena/browser/view/PRJNA554094 https://www.ncbi.nlm.nih.gov/sra?term=SRP214243 [Overal design]BT-549 and SUM149 cells were transfected to stably express a control shRNA (CshRNA) or a MUC1shRNA. Total RNA was isolated from three different sets of the (i) BT-549/CshRNA and BT-549/MUC1shRNA cells, and (ii) SUM149/CshRNA and SUM149/MUC1shRNA cells. The RNA was used for RNA-seq library preparation.; [Treatment]'None'; [Growth]'Human BT-549 TNBC (ATCC) cells were cultured in RPMI1640 medium (Corning Life Sciences, Corning, NY, USA) containing 10% heat-inactivated fetal bovine serum (FBS; GEMINI Bio-Products, West Sacramento, CA, USA), 100 mg/ml streptomycin, 100 U/ml penicillin and 10 mg/ml insulin. SUM149 TNBC cells were grown in Ham’s F-12 medium (Corning) supplemented with 10 mM HEPES, 5% FBS, 100 mg/ml streptomycin, 100 U/ml penicillin, 5 mg/ml insulin and 1 mg/ml hydrocortisone.'; [Extraction]'Total RNA from cells cultured in triplicates was isolated using Trizol reagent (Invitrogen).\nTruSeq Stranded mRNA (Illumina, San Diego, CA, USA) was used for library preparation.'; [Cell type]'TNBC Breast Cancer Cell line (ER -ve, PR -ve, HER2/neu -ve)''cell line: BT-549; cell type: TNBC Breast Cancer Cell line (ER -ve, PR -ve, HER2/neu -ve); genotype: shRNA against MUC1-C; ', 'cell line: BT-549; cell type: TNBC Breast Cancer Cell line (ER -ve, PR -ve, HER2/neu -ve); genotype: Control; ', 'cell line: SUM149; cell type: TNBC Breast Cancer Cell line (ER -ve, PR -ve, HER2/neu -ve); genotype: Control; ', 'cell line: SUM149; cell type: TNBC Breast Cancer Cell line (ER -ve, PR -ve, HER2/neu -ve); genotype: shRNA against MUC1-C; ' GSE104760 Homo sapiens 25 Genome binding/occupancy profiling by high throughput sequencing GPL18573 SMAD3 and SOX4 binding profiling in human breast cell lines 2017-10-10 In order to identify genes co-bound by SOX4 and SMAD3 in the context of breast cancer, different breast cell lines (HMLEs, MDA-MB-231 or HCC-1954) were used. Due to low endogenous expression levels for SOX4 in HMLEs in untreated conditions, doxycycline-dependent SOX4 overexpression was obtained by transducing HMLE cells with pIINDUCER21-SOX4 vector..Cells were plated and SOX4 and SMAD3 chromatine-immunoprecipitation was performed in untreated conditions, TGF-beta (2.5ng/ml), doxycycline (0.5ug/ml) or both as indicated. Genome-wide binding sites for SOX4 and SMAD3 was identified in HMLEs, MAD-MB-231 and HCC-1954 cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE104760 SOX4 can redirect TGF-β-mediated SMAD3-transcriptional output in a context-dependent manner to promote tumorigenesis. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gky755 {Nucleic acids research (11.147) doi:10.1093/nar/gky755}; {eLife (7.551) doi:10.7554/eLife.27706}; 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA413781 https://www.ebi.ac.uk/ena/browser/view/PRJNA413781 https://www.ncbi.nlm.nih.gov/sra?term=SRP119661 [Overal design]SOX4 and SMAD3 ChIP-sequencing of different human mammary cells in the presence and absence of TGF-β; [Treatment]'Doxycicline, TGF-β or both'; [Growth]'Cell lines were grown according to manufacture]s protocol'; [Extraction]'Crosslink was performed with disuccinimidyl glutarate (DSG) (Thermo Scientifis) for 45 minutes followed by 30 minutes incubation with formaldehyde 1%. The reaction was blocked with glycine 100 mM. Shearing was performed using Covaris S2 (Covaris, Woburn, MA) for 8 min at maximum intensity. The sonicated chromatin was incubated O/N at 4°C in presence of 15µl of anti-SOX4 (CS-129-100, Diagenode) or 2µg of anti-SMAD3 (ab28379, abcam) coupled to A/G sepharose beads (Santa Cruz Biotechnology).\nKapa Hyper Prep Kit (Kapa Biosystems, Wilmington, MA) was used for End-repair, A-tailing and ligation of sequence adaptors. Samples were amplified by PCR and the libraries were size-selected in the 200-500 bp range.'; [Cell type]'Immortalized human mammary epithelial cells', 'human breast cell line''cell line: HMLE; cell type: Immortalized human mammary epithelial cells; immunoprecipitation: CS-129-100, Diagenode; ', 'cell line: HMLE; cell type: Immortalized human mammary epithelial cells; immunoprecipitation: ab28379, abcam; ', 'cell line: HMLE; cell type: Immortalized human mammary epithelial cells; immunoprecipitation: Input; ', 'cell line: MDA-MB-231; cell type: human breast cell line; immunoprecipitation: ab28379, abcam; ', 'cell line: MDA-MB-231; cell type: human breast cell line; immunoprecipitation: CS-129-100, Diagenode; ', 'cell line: MDA-MB-231; cell type: human breast cell line; immunoprecipitation: Input; ', 'cell line: HCC-1954; cell type: human breast cell line; immunoprecipitation: ab28379, abcam; ', 'cell line: HCC-1954; cell type: human breast cell line; immunoprecipitation: CS-129-100, Diagenode; ', 'cell line: HCC-1954; cell type: human breast cell line; immunoprecipitation: Input; ' GSE96641 Mus musculus 21 Expression profiling by high throughput sequencing GPL21103 Genome-wide Screen for Differentially Methylated Long Noncoding RNAs identifies Esrp2 and lncRNA Esrp2-as Regulated by Enhancer DNA Methylation with Prognostic Relevance for Human Breast Cancer 2017-03-15 The majority of long noncoding RNAs (lncRNAs) is still poorly characterized with respect to function, interactions with protein-coding genes, and mechanisms that regulate their expression. As for protein-coding RNAs, epigenetic deregulation of lncRNA expression by alterations in DNA methylation might contribute to carcinogenesis. To provide genome-wide information on lncRNAs aberrantly methylated in breast cancer we profiled tumors of the C3(1) SV40TAg mouse model by MCIp-seq (Methylated CpG Immunoprecipitation followed by sequencing). This approach detected 69 lncRNAs differentially methylated between tumor tissue and normal mammary glands, with 26 located in antisense orientation of a protein-coding gene. One of the hypomethylated lncRNAs, 1810019D21Rik (now called Esrp2-antisense (as)) was identified in proximity to the epithelial splicing regulatory protein 2 (Esrp2) that is significantly elevated in C3(1) tumors. ESRPs seem to have a dual role in carcinogenesis. Both gain and loss has been associated with poor prognosis in human cancers, but the mechanism regulating expression is not known. In-depth analyses indicate that coordinate overexpression of Esrp2 and Esrp2-as inversely correlates with DNA methylation. Luciferase reporter gene assays support co-expression of Esrp2 and the major short Esrp2-as variant from a bidirectional promoter, and transcriptional regulation by methylation of a proximal enhancer. Ultimately, this enhancer-based regulatory mechanism provides a novel explanation for tissue-specific expression differences and upregulation of Esrp2 during carcinogenesis. Knockdown of Esrp2-as reduced Esrp2 protein levels without affecting mRNA expression and resulted in an altered transcriptional profile associated with extracellular matrix (ECM), cell motility and reduced proliferation, whereas overexpression enhanced proliferation. Our findings not only hold true for the murine tumor model, but led to the identification of an unannotated human homolog of Esrp2-as which is significantly upregulated in human breast cancer and associated with poor prognosis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE96641 Genome-wide screen for differentially methylated long noncoding RNAs identifies Esrp2 and lncRNA Esrp2-as regulated by enhancer DNA methylation with prognostic relevance for human breast cancer. Oncogene 6.634 https://doi.org/10.1038/onc.2017.246 {Oncogene (6.634): 10.1038/onc.2017.246} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA379281 https://www.ebi.ac.uk/ena/browser/view/PRJNA379281 https://www.ncbi.nlm.nih.gov/sra?term=SRP101942 [Overal design]RNA Sequencing data of Esrp2-as knockdown and control in M6 cell lines and Esrp2-as overexpression and control in 3T3-L1 and M27H4 cell lines; [Treatment]'LNA antisense Gapmer-mediated knockdown of Esrp2-as in the M6 cell line, and overexpression of Esrp2-as in M27H4 and 3T3-L1 cell lines'; [Growth]'DMEM +10% FCS in a humidified atmosphere at 5% CO2 and 37°C'; [Extraction]'Total RNA isolation with RNeasy Mini Kit (Qiagen), ribodepletion with Ribo-Zero® Gold rRNA Removal Kit, purification with RNAeasy MinElute Kit (Qiagen)\nSureSelect Strand-Specific Library Preparation Kit'; [Cell type]'Source: ''cell line: M6; genotype/variation: Esrp2-as knockdown; ', 'cell line: M6; genotype/variation: empty vector control; ', 'cell line: M27H4; genotype/variation: Esrp2-as overexpression; ', 'cell line: M27H4; genotype/variation: empty vector control; ', 'cell line: 3T3-L1; genotype/variation: empty vector control; ', 'cell line: 3T3-L1; genotype/variation: Esrp2-as overexpression; ' GSE64363 Homo sapiens 2 Non-coding RNA profiling by high throughput sequencing GPL11154 Genome-wide miRNA profile of MCF7 cells overexpressing wild-type and mutant miR-222 2014-12-19 MCF7 cells were infected with retrovirus to overexpress wild-type and mutant miR-222 https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE64363 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA270829 https://www.ebi.ac.uk/ena/browser/view/PRJNA270829 https://www.ncbi.nlm.nih.gov/sra?term=SRP051374 [Overal design]Measure miRNA expression level in MCF7 cells after overexpressing wild-type and mutant miR-222; [Treatment]'None'; [Growth]'MCF7 cells were cultured in DMEM with 10% FBS and 1% Penicillin-Streptomycin.'; [Extraction]"MCF7 cells were collected with Trizol reagent (Invitrogen) following manufacturer's protocol. Small RNAs of 15-40 bases were gel-purified from 5 ug total RNA\nSmall RNAs of 15-40 bases were gel-purified from 5 ug total RNA with 10% acrylamide gel (American Bioanalytical AB13021). Purified small RNA was subjected to library preparation, similar to Illumina protocol with modification. Briefly, pre-adenylated primer was made following a published protocol (Chen, Y.-R., Zheng, Y., Liu, B., Zhong, S., Giovannoni, J. and Fei, Z. (2012) A cost-effective method for Illumina small RNA-Seq library preparation using T4 RNA ligase 1 adenylated adapters. Plant Methods, 8, 41.) using /5Phos/TGGAATTCTCGGGTGCCAAGG/3ddC/. Small RNA was ligated to the pre-adenylated primer with truncated T4 RNA ligase 2 (NEB M0242S). The 35-55 bases product was purified with 10% acrylamide gel and further went through a 5’ ligation reaction with primer: dGdTdTdCdAdGdAdGdTdTdCdTdAdCdA GUCCGACGAUC (Dharmacon) with T4 RNA ligase 1 (Fermentas EL0021). The 60-80 bases product was purified with 10% acrylamide gel and reverse transcribed with M-MLV reverse transcriptase (Invitrogen 28025-013) using primer: GCCTTGGCACCCGAGAATTCCA. The RT product was PCR amplified for 18 cycles with Phusion DNA polymerase (NEB M0530) using a universal primer: AATGATACGGCGACCACCGAGATCTACACGTT-CAGAGTTCTACAGTCCGA and a specific primer for each sample. 130-150nt small RNA libraries were purified with 8% acrylamide gel. Barcoded small RNA libraries were sequenced on a HiSeq2000 (Illumina).\nTruSeq Small RNA Library"; [Cell type]'Source: ''mir-222 overexpression: wild-type; ', 'mir-222 overexpression: mutant; ' GSE59230 Homo sapiens 12 Expression profiling by array GPL570 Regulation of gene expression by loss-of-YAP/TAZ in MDA-MB-231 breast cancer cells 2014-07-09 YAP1 (Yes-associated protein 1) and TAZ (transcriptional coactivator with PDZ-binding motif, or WWTR1) are nucleo-cytoplasmic shuttling proteins that can function in the nucleus as transcriptional coactivators. Their role in regulating gene transcription has been so far mainly investigated by overexpressing YAP1 or TAZ, while here we sought to determine which genes are regulated by endogenous levels of YAP/TAZ. To this end, we compared MCF10A cells transfected with a control non-targeting siRNA to cells transfected with two independent mixes of siRNA targeting both YAP and TAZ. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59230 Aerobic glycolysis tunes YAP/TAZ transcriptional activity. The EMBO journal 11.227 https://doi.org/10.15252/embj.201490379 {The EMBO journal (11.227): 10.15252/embj.201490379} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA254774 https://www.ebi.ac.uk/ena/browser/view/PRJNA254774 None [Overal design]MDA-MB-231 cells growing at low confluence in standard growth conditions were transfected with the indicated siRNAs (Dupont et al., Nature 2011). The following day, growth medium was renewed and cells were incubated for 24 more hours, and then harvested for total RNA extraction. 4 independent biological replicates were plated, transfected ans harvested in parallel for each siRNA.; [Treatment]"Cells were transfected on day 2 with siRNA oligonucleotides (final concentration 33nM) by using RNAi MAX (Life Technologies), following a direct transfection protocol as indicated by manifacturer's instructions. On day 3, medium was renewed. On day 4, cells were washed with 1XHBSS and harvested for RNA extraction."; [Growth]'Cells were seeded at low confluence on day 1 in standard growth medium (DMEM/F12 with 2mM Glutamine, 17.5mM D-glucose, without antibiotics, 10% Fetal Bovine Serum).'; [Extraction]"Trizol extraction of total RNA, followed by DNAseI digestion to reduce genomic DNA contaminations, was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MDA-MB-231; transfection: Control siRNA; ', 'cell line: MDA-MB-231; transfection: YAP/TAZ siRNA #1; ', 'cell line: MDA-MB-231; transfection: YAP/TAZ siRNA #2; ' GSE28580 Homo sapiens 9 Expression profiling by array GPL13158 RNA interference screening identifies the Insulin/IGF-1 receptor pathway as a mechanism of escape from hormone dependence in breast cancer 2011-04-13 A significant fraction of breast cancers exhibit de novo or acquired resistance to estrogen deprivation. A kinome-wide siRNA screen identified a role for Insulin Receptor (InsR) in the hormone-independent growth of ER+ breast cancer cells We used gene expression microarrays to identify genes and pathways that are altered by insulin stimulation of ER+ MCF-7 human breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28580 A kinome-wide screen identifies the insulin/IGF-I receptor pathway as a mechanism of escape from hormone dependence in breast cancer. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-11-1295 {Cancer research (8.378): 10.1158/0008-5472.CAN-11-1295} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA139131 https://www.ebi.ac.uk/ena/browser/view/PRJNA139131 None [Overal design]MCF-7 cells were treated with serum-free medium +/- insulin for 4 or 24 hrs prior to RNA harvest for analysis.; [Treatment]'Cells were seeded in 100 mm dishes in triplicate. The following day, cells were washed with PBS, and treated with serum-free IMEM. Twenty-four hrs later, cells were treated +/- 10 ug/mL insulin. RNA was harvested after 4 or 24 hrs of insulin stimulation.'; [Growth]'MCF-7 cells are maintained in IMEM + 10% FBS.'; [Extraction]'Trizol extraction followed by Qiagen RNeasy column clean-up with on-column DNase digestion'; [Cell type]'Source: ''cell line: MCF_7; treatment: serum-free medium x 48 hrs; ', 'cell line: MCF_7; treatment: serum-free medium x 44 hrs, then with 10 ug/mL insulin x 4 hrs; ', 'cell line: MCF_7; treatment: serum-free medium x 24 hrs, then with 10 ug/mL insulin x 24 hrs; ' GSE132436 Homo sapiens 24 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other GPL20795 NR2F2 study 2019-06-10 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132436 Cooperativity of co-factor NR2F2 with Pioneer Factors GATA3, FOXA1 in promoting ERα function. Theranostics 8.063 https://doi.org/10.7150/thno.34874 {Theranostics (8.063): 10.7150/thno.34874} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA548079 https://www.ebi.ac.uk/ena/browser/view/PRJNA548079 None [Overal design]Refer to individual Series; [Treatment]'MCF-7 cells were treated with vehicle or estrogen 10 nM for 12 h.', 'The MCF-7 cells were grown in the phenol red-free medium supplement with 10% charcoal/dextran-treated fetal bovine serum for 3 days, followed by treatment of vehicle or 10 nM estrogen for 12 hours.', 'DNA of MCF-7 cells with WT and NR2F2 KO were extracted using standard Illumina protocals.'; [Growth]'The MCF-7 cells were maintained in DMEM supplemented with 10% fetal bovinw serum at 37℃ incubator. Cells were incubated in Phenol red-free DMEM containing 2.5% charcoal/dextran treated FBS for three days.', 'The MCF-7 cells were maintained in DMEM supplemented with 10% fetal bovinw serum at 37℃ incubator.', 'The MCF-7 cells were maintained in DMEM supplemented with 10% fetal bovinw serum at 37℃ incubator'; [Extraction]'Lysates were clarified form sonicated nuclei and protein-DNA complexes were isolated with antibody.\nThe Chromatin immunoprecipitated DNA fragments (approx.10 ng in 30 µl water) are end repaired by using T4 DNA polymerase, Klenow DNA polymerase and T4 polynucleotide kinase in the presence of dNTPs. And an ‘A’ base is added to the 3’end of the blunt phosphorylated DNA fragments, using the polymerase activity of Klenow fragment. Then, adaptors (Adaptor oligo mix, Illumina) are ligated to the ends of the DNA fragments. The resulting DNA fragments are purified by MinElute column (QIAGEN). 300 ~ 500 bp DNA fragments are purified by using E-Gel SizeSelect agarose Gels (Invitrogen) according to manufacturer’s instruction. Size selected adaptor-modified DNA fragments are amplifiedand the resulting PCR products are purified by MinElute column (QIAGEN). The size and amount of DNA fragments (libraries) are validated by Bioanalyzer (Agilent)', "Trizol extraction of total RNA was performed according to the manufacturer's instructions.\nRNA libraries were prepared for sequencing using standard Illumina protocols", '50,000 sorted cells were washed with cold PBS and suspended in lysis buffer for 10-15 min on ice. DNA was purified using MinElute PCR Purification Kit (Qiagen). Transposed DNA was amplified using NEB Next High-Fidelity 2X PCR Master Mix and libraries were sequenced on HiSeq 4000\nDNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'breast cancer cell line', 'breast cell line''cell line: MCF-7; cell type: breast cancer cell line; genotype/variation: shCTRL; chip antibody: none; ', 'cell line: MCF-7; cell type: breast cancer cell line; genotype/variation: shCTRL; chip antibody: ERa (santa cruze, sc-543x,Lot # E3014 ); ', 'cell line: MCF-7; cell type: breast cancer cell line; genotype/variation: shCTRL; chip antibody: FOXA1 (Abcam,ab170933, Lot # GR3257262-1); ', 'cell line: MCF-7; cell type: breast cancer cell line; genotype/variation: shCTRL; chip antibody: H3K4me3 (active motif, 39915, Lot 17218007); ', 'cell line: MCF-7; cell type: breast cancer cell line; genotype/variation: shCTRL; chip antibody: H3K27ac (active motif, 39133, Lot 31814008); ', 'cell line: MCF-7; cell type: breast cancer cell line; genotype/variation: shCTRL; chip antibody: H3K4me1 (active motif, 39297, Lot 1518002); ', 'cell line: MCF-7; cell type: breast cancer cell line; genotype/variation: shNR2F2; chip antibody: none; ', 'cell line: MCF-7; cell type: breast cancer cell line; genotype/variation: shNR2F2; chip antibody: ERa (santa cruze, sc-543x,Lot # E3014 ); ', 'cell line: MCF-7; cell type: breast cancer cell line; genotype/variation: shNR2F2; chip antibody: FOXA1 (Abcam,ab170933, Lot # GR3257262-1); ', 'cell line: MCF-7; cell type: breast cancer cell line; genotype/variation: shNR2F2; chip antibody: H3K4me3 (active motif, 39915, Lot 17218007); ', 'cell line: MCF-7; cell type: breast cancer cell line; genotype/variation: shNR2F2; chip antibody: H3K27ac (active motif, 39133, Lot 31814008); ', 'cell line: MCF-7; cell type: breast cancer cell line; genotype/variation: shNR2F2; chip antibody: H3K4me1 (active motif, 39297, Lot 1518002); ', 'cell line: MCF-7; cell type: breast cancer cell line; chip antibody: none; ', 'cell line: MCF-7; cell type: breast cancer cell line; chip antibody: NR2F2 (active motif, 61213,Lot 10216002); ', 'cell line: MCF7; cell type: breast cell line; genotype/variation: wild type; treatment: vehicle for 12hr; ', 'cell line: MCF7; cell type: breast cell line; genotype/variation: NR2F2 KO; treatment: vehicle for 12hr; ', 'cell line: MCF7; cell type: breast cell line; genotype/variation: wild type; treatment: 10 nM estrogen for 12hr; ', 'cell line: MCF7; cell type: breast cell line; genotype/variation: NR2F2 KO; treatment: 10 nM estrogen for 12hr; ', 'cell line: MCF7; cell type: breast cancer cell line; genotype/variation: shCTRL; ', 'cell line: MCF7; cell type: breast cancer cell line; genotype/variation: shNR2F2; ' GSE50061 Homo sapiens 4 Expression profiling by array GPL14550; GPL17077 Gene expression in human breast cancer cell lines regulated by HIC1 gene 2013-08-21 This study aimed to further our understanding of the role that hypermethylatioted in cancer 1 (HIC1) plays in breast cancer progression. Microarrays were searched for some genes that had correlated expression with HIC1 mRNA. According to fold-change screening between restoring expression of HIC1 and its respective control cells in MDA-MB-231 cells, or HIC1 knockdown and its respective control cells in HBL100, both up-regulated and down-regulated genes were shown. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50061 HIC1 silencing in triple-negative breast cancer drives progression through misregulation of LCN2. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-13-2420 {Cancer research (8.378): 10.1158/0008-5472.CAN-13-2420} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA215902 https://www.ebi.ac.uk/ena/browser/view/PRJNA215902 None [Overal design]The restoring expression HIC1 in MDA-MB-231 cells were respectively noted as MDAMB-231-HIC1 and the respective controls were noted as MDA-MB-231-GFP cells. HIC1 knockdown in HBL100 cells were noted as HBL100-shHIC1 and the respective control HBL100-shCtrl cell.; [Treatment]'For restoring expression of HIC1 in MDA-MB-231 cells, human full-length HIC1 cDNA was inserted into lentivirus vector pHR-SIN-CSIGW. For the production of lentivirus, lenti-x cells were transfected with the PMD2.G, PSPAX2 and HIC1 expression vector using the lipofectamine 2000 (Invitrogen). After 48 hours, culture supernatants were collected and passed through 0.45µm filters, mixed with fresh media (1:1) and polybrene (8μg/ml) to infect target cells. For generation of a stable HIC1 knockdown cell line, GV248 lentiviral vectors expressing short hairpin RNAs targeting HIC1 were purchased from GeneChem Company (China, Shanghai). Lentiviruses were produced as described above and infected cells were selected by puromycin treatment at 1μg/ml.'; [Growth]'Human breast cancer cell lines MDA-MB-231 and the immortalized epithelial cells HBL-100 were maintained in DMEM (Hyclone), supplement with 10% FBS (GIBCO) and 1% penicillin/streptomycin. Cells were cultured at 37℃ water-saturated 5% CO2 atmosphere.'; [Extraction]'Total RNA was checked for a RIN number to inspect RNA integration by an Agilent Bioanalyzer 2100 (Agilent technologies, Santa Clara, CA, US).Qualified total RNA was further purified by RNeasy mini kit (Cat#74106, QIAGEN, GmBH, Germany) and RNase-Free DNase Set (Cat#79254, QIAGEN, GmBH, Germany).'; [Cell type]'human breast cancer cells''cell line: MDA-MB-231; cell type: human breast cancer cells; genotype/variation: control; ', 'cell line: MDA-MB-231; cell type: human breast cancer cells; genotype/variation: HIC1 overexpression; ', 'cell line: HBL100; cell type: human breast cancer cells; genotype/variation: control; ', 'cell line: HBL100; cell type: human breast cancer cells; genotype/variation: HIC1 knockdown; ' GSE149132 Homo sapiens 6 Expression profiling by high throughput sequencing GPL16791; GPL20301 Translational control of breast cancer plasticity 2020-04-22 Plasticity of neoplasia, whereby cancer cells attain stem-cell-like properties, is required for disease progression and represents a major therapeutic challenge. Hypoxia induces breast cancer cell plasticity and stem-cell-like phenotypes. Although this process is poorly understood, reports demonstrate that hypoxia induces the expression of stemness-factors including NANOG, SNAIL and NODAL. Moreover, both stem-cell-like phenotypes and elevated expression of stemness-factors have been linked to metastatic spread and chemoresistance. With the use of high through-put sequencing, we characterized the gene expression profiles of T47D breast cancer cells under normoxic and hypoxic conditions. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE149132 Translational control of breast cancer plasticity. Nature communications 11.878 https://doi.org/10.1038/s41467-020-16352-z {Nature communications (11.878): 10.1038/s41467-020-16352-z} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA627436 https://www.ebi.ac.uk/ena/browser/view/PRJNA627436 https://www.ncbi.nlm.nih.gov/sra?term=SRP257927 [Overal design]Transcriptomic profiles of T47D breast cancer cells treated with hypoxia with normoixa controls were generated via high throughput sequencing. Three replicates were collected.; [Treatment]'Cells were placed in a hypoxia incubation chamber set to 0.5% O2. Normoxia control cells were grown under normal tissue culture conditions.'; [Growth]'T47D cells were grown in adherent culture with RPMI media supplemented with 10% FBS'; [Extraction]'Total RNA was extracted using 5Prime RNA extraction kit\nLibraries were prepared using mRNA stranded library preparation from NEB'; [Cell type]'breast cancer cells''cell line: T47D; cell type: breast cancer cells; treatment: Control (20% O2); ', 'cell line: T47D; cell type: breast cancer cells; treatment: Hypoxia (0.5% O2, 48 hours); ' GSE133927 Homo sapiens 16 Expression profiling by high throughput sequencing GPL20301 RNA-Sequencing analysis of Meox1 siRNA knockdown in p53 and PTEN deficient triple negative breast cancer in vitro cell lines of BT-549 and MDA-MB-468 2019-07-08 The goal for this experiment was to analyze how knockdown of homeobox transcription factor Meox1 altered functional and mechanist biology of p53 and PTEN deficient triple negative breast cancer in vitro cell lines of claudin-low BT-549 and basal-like MDA-MB-468. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE133927 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA553144 https://www.ebi.ac.uk/ena/browser/view/PRJNA553144 https://www.ncbi.nlm.nih.gov/sra?term=SRP213607 [Overal design]Two different subtypes of triple negative breast cancer with p53 and PTEN deficiencies were utilized, claudin-low BT-549 and basal-like MDA-MB-468. For knocking down Meox1, siRNA transfection experiment was conducted with Negative Control siRNA and Meox1 siRNA, two biological replicates using Negative Control siRNA and Meox1 siRNA for each cell line were conducted. For RNA Seqeuncing, two technical replicates for each biological replicate were sequenced, making a total of 16 samples for sequencing.; [Treatment]'Cells were treated with 50nM Negative Control siRNA (Qiagen #1027281) and 50nM Meox1 siRNA (Qiagen #1027416, four different Meox1 siRNA pool mixture). Cells were transfected using Lipofectamine RNAiMAX Reagent (Invitrogen #13778-150), transfections were conducted according manufacturer protocol. Following 72 hours of siRNA transfection, cells were harvested to extract RNA.'; [Growth]'BT-549 cells were grown in RPMI Gibco Life Technologies base media supplemented with antibiotic-antimycotic, 10% fetal bovine serum, 0.85µg/mL insulin, 1mM sodium pyruvate, and 10mM HEPES. MDA-MB-468 cells were grown in DMEM Gibco Life Technologies base media supplemented with antibiotic-antimycotic, 10% fetal bovine serum, and 1mM sodium pyruvate.'; [Extraction]'RNA was extracted using RNeasy Kit (Qiagen #74104).\nLibraries were prepared by the University of Michigan DNA Core using just mRNA, non-strand-specific, polyA-selection, fragment lengths of ~120 nucleotides.'; [Cell type]'Source: ''cell line: triple negative breast cancer BT-549; genotype: Control; ', 'cell line: triple negative breast cancer BT-549; genotype: Meox1 knockdown; ', 'cell line: triple negative breast cancer MDA-MB-468; genotype: Control; ', 'cell line: triple negative breast cancer MDA-MB-468; genotype: Meox1 knockdown; ' GSE77843 Mus musculus 6 Expression profiling by array GPL4134 RAS signalling through PI3-Kinase controls cell migration via modulation of Reelin expression 2016-02-11 RAS signalling through Phosphoinositide 3-kinase (PI3-Kinase) has been shown to have an essential role in tumour initiation and maintenance. RAS also regulates cell motility and tumor invasiveness, but the role of direct RAS binding to PI3-Kinase in this remains uncertain. Here, we provide evidence that disruption of RAS interaction with PI3-Kinase p110adecreases cell motility and prevents activation of Rac GTPase. Analysis of gene expression in cells lacking RAS interaction with p110areveals increased levels of the extracellular matrix glycoprotein Reelin and activation of its downstream pathway resulting in upregulation of E-Cadherin expression. Induction of the Reelin / E-Cadherin axis is also observed in Kras mutant lung tumours that are regressing due to blockade of RAS interaction with PI3-Kinase. Furthermore, loss of Reelin correlates with decreased survival of lung and breast cancer patients. Reelin thus plays a role in restraining RAS and PI3-kinase promotion of cell motility and potentially tumour metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE77843 RAS signalling through PI3-Kinase controls cell migration via modulation of Reelin expression. Nature communications 11.878 https://doi.org/10.1038/ncomms11245 {Nature communications (11.878): 10.1038/ncomms11245} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA311715 https://www.ebi.ac.uk/ena/browser/view/PRJNA311715 None [Overal design]MEFs with or without RAS binding to p110a were seeded in a 10cm dish and left to attach during 24 hours. Full serum media was then removed and media with no FBS was added to the plates. Starvation was carried out during a period of 16 hours (over night starvation). Assay was performed in triplicates: for each genotype two diferent fibroblasts clones (and a mix of both of the clones) were used on the analysis. After starvation RNA was extracted using RNAsy kit (Quiagen). RNA was quantified and sent to Oxford Gene Technology microarray facility.; [Treatment]'None'; [Growth]'MEFs were grown on DMEM media supplemented with 10% FBS and antibiotics and kept at 10% CO2. On the day of the experiment media was replaced with FBS-free DMEM and left over night. Samples were then collected.'; [Extraction]'RNAsy Kit (Qiagen)'; [Cell type]'Inmortalized mouse embrionic fibroblasts''strain source: Pik3caRBD; cell line: B03; cell type: Inmortalized mouse embrionic fibroblasts; genotype/variation: wild type; clone id: Clone 1; ', 'strain source: Pik3caRBD; cell line: C01; cell type: Inmortalized mouse embrionic fibroblasts; genotype/variation: wild type; clone id: Clone 2; ', 'strain source: Pik3caRBD; cell line: B03; cell type: Inmortalized mouse embrionic fibroblasts; genotype/variation: wild type; clone id: Clone 1+2; ', 'strain source: Pik3caRBD; cell line: B02; cell type: Inmortalized mouse embrionic fibroblasts; genotype/variation: RBD-Mutant; clone id: Clone 1; ', 'strain source: Pik3caRBD; cell line: C05; cell type: Inmortalized mouse embrionic fibroblasts; genotype/variation: RBD-Mutant; clone id: Clone 2; ', 'strain source: Pik3caRBD; cell line: B02; cell type: Inmortalized mouse embrionic fibroblasts; genotype/variation: RBD-Mutant; clone id: Clone 1+2; ' GSE73960 Homo sapiens 2 Expression profiling by array GPL17077 CD24 suppresses malignant phenotype by downregulation of SHH transcription through STAT1 inhibition in breast cancer cells [HCC1937] 2015-10-13 We describe a relationship between CD24 and the Hedgehog (Hh) ligand Sonic Hedgehog (SHH), and reveal a role for this relationship in the induction of a malignant phenotype in breast cancer. Anchorage-dependent proliferation, anchorage-independent proliferation, invasiveness, and tumorigenicity in breast cancer cells (BCCs) transfected with siRNA and plasmid targeting Hh signaling, CD24, and STAT1 were investigated. CD24 siRNA-transfected BCCs demonstrated higher expression of SHH and GLI1, increased anchorage-independent proliferation, enhanced invasiveness and superior tumorigenicity compared with control. Conversely, CD24 forced-expressing BCCs possessed decreased SHH and GLI1 expression, anchorage-independent proliferation, and invasiveness. Suppression of SHH decreased invasiveness through inhibition of matrix metalloproteinase (MMP)-2 expression, GLI1 expression, anchorage-independent proliferation, tumorigenicity, and tumor volume in vivo in CD24 siRNA-transfected BCCs. DNA microarray analysis identified STAT1 as a connection between CD24 and SHH. CD24 siRNA-transfected BCCs with concurrent STAT1 inhibition exhibited decreased SHH expression, invasiveness, anchorage-independent proliferation, tumorigenicity, and tumor volume in vivo. Consistently, STAT1 over-expression induced elevated SHH expression, invasiveness, and anchorage-independent proliferation in BCCs. These results suggest that CD24 suppresses development of a malignant phenotype by down-regulating SHH transcription through STAT1 inhibition. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE73960 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA298588 https://www.ebi.ac.uk/ena/browser/view/PRJNA298588 None [Overal design]We focus on the BCSC marker CD24, and the Hh ligand SHH, and reveal a role for these molecules in the induction of a malignant phenotype in breast cancer.; [Treatment]"Following overnight attachment to a 6-well plate, 3.0 x 10^5 cells per well were transfected for 48 hours using Lipofectamine® RNAiMAX Reagent (Invitrogen by Life Technologies) according to the manufacturer's protocol. Sixteen hours after the medium change, siRNA-transfected cells were used for further experiments."; [Growth]'The culture condition for CD24-siRNA-treated HCC1937 cells was as following: RPMI1640 medium supplemented with 10% FCS, L-Gln and penicillin-streptomycin, 5% CO2/air.'; [Extraction]'Total RNA was isolated and purified from CD24-treated HCC1937 cells using High Pure RNA Isolation Kit (Roche, #11 828 665 001).'; [Cell type]'breast cancer cell line''cell line: HCC1937; cell type: breast cancer cell line; sirna: control; ', 'cell line: HCC1937; cell type: breast cancer cell line; sirna: CD24; ' GSE10800 Homo sapiens 63 Genome binding/occupancy profiling by genome tiling array GPL4910; GPL4911; GPL4912; GPL4913; GPL4914; GPL4915; GPL4916 Genome-wide Binding Site Mapping of Estrogen Receptor alpha and c-MYC in Breast Cancer Cells 2008-03-12 Estrogens are steroid hormones that play critical roles in the initiation, development, and metastasis of breast and uterine cancers. The estrogen (E2) response in breast cancer cells is predominantly mediated by the estrogen receptor-alpha (ER alpha), a ligand-activated transcription factor. ER alpha regulates transcription of target genes through direct binding to its cognate recognition sites, known as estrogen response elements (EREs), or by modulating the activity of other DNA-bound transcription factors at alternative DNA sequences. The proto-oncogene c-myc is upregulated by ER¦Á in response to E2 and encodes a transcription factor, c-MYC, which regulates a cascade of gene targets whose products mediate cellular transformation. This study aims at mapping the binding sites of these two transcription factors (ER alpha and c-MYC) in one ER alpha positive breast cancer cell line (MCF7 cell line). Keywords: ChIP-Chip Analysis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE10800 Genomic analysis of estrogen cascade reveals histone variant H2A.Z associated with breast cancer progression. Molecular systems biology 9.800 https://doi.org/10.1038/msb.2008.25 {Molecular systems biology (9.800): 10.1038/msb.2008.25} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA107383 https://www.ebi.ac.uk/ena/browser/view/PRJNA107383 None [Overal design]This series contains ChIP-on-Chip data sets for two transcription factors (ER alpha and c-MYC) and control samples (INPUT). All the experiments are done in triplicates. MCF7 Cells were E2-deprived for 3 days and then were treated with 10 nM E2 (45 minutes and 2 hours for mapping ER alpha and c-MYC binding sites, respectively) at 80% confluence.; [Treatment]'MCF7 Cells were E2-deprived for 3 days and then were treated with 10 nM E2 (45 minutes and 2 hours for mapping ER alpha and c-MYC binding sites, respectively) at 80% confluence. ~5x10^6 cells per ChIP were cross-linked with 1% formaldehyde for 10 minutes at 37oC then quenched with 125 mM glycine.'; [Growth]"MCF7 breast cancer cells (ATCC HTB-22) were grown in phenol-free Dulbecco's modified Eagles's medium, 10% fetal bovine serum, with supplemental bovine insulin (0.01 mg/ml), 2 mM L-glutamine, and antibiotics at 37oC in a 5% CO2 humidified atmosphere. Prior to hormone (E2 at 10 nM) or vehicle (100% EtOH) treatments, cells were changed to estrogen-depleted media for 72 hours by using 10% charcoal-stripped calf serum."; [Extraction]'According to the standard chromatin extraction protocol (Shang et al., 2000).'; [Cell type]'Source: ''' GSE47803 Homo sapiens 12 Expression profiling by array GPL6947 Co-regulated gene expression by estrogen receptor-α and liver receptor homolog-1 is a feature of the estrogen response in breast cancer cells 2013-06-10 Estrogen receptor α (ERα) is a nuclear receptor that is the driving transcription factor expressed in the majority of breast cancers. Recent studies have demonstrated that the liver receptor homolog-1 (LRH-1), another nuclear receptor, is ERα-regulated in breast cancer cells. Further, LRH-1 stimulates proliferation and promotes motility and invasion of breast cancer cells. To determine the mechanisms of LRH-1 action in breast cancer cells, we carried out gene expression microarray analysis following siRNA-mediated LRH-1 knockdown. Interestingly, gene ontology (GO) category enrichment analysis of the genes differentially regulated in the presence or absence of LRH-1 identified estrogen responsive genes as the most highly enriched GO categories. To further define LRH-1 target genes, we performed chromatin immunoprecipitation coupled to massively parallel sequencing (ChIP-seq) to identify genomic targets of LRH-1. Remarkably, ChIP-seq showed LRH-1 binding at many ERα binding sites. Analysis of select binding sites confirmed regulation of ERα-regulated genes by LRH-1 through binding to estrogen response elements, as exemplified by the TFF1/pS2 gene. Finally, LRH-1 over-expression stimulated ERα recruitment, whilst LRH-1 knockdown reduced ERα recruitment to ERα binding sites. Taken together, our findings establish a key role for LRH-1 in the regulation of ERα target genes in breast cancer cells and identify a mechanism in which co-operative binding of LRH-1 and ERα at estrogen response elements controls the expression of estrogen-responsive genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47803 Co-regulated gene expression by oestrogen receptor α and liver receptor homolog-1 is a feature of the oestrogen response in breast cancer cells. Nucleic acids research 11.147 https://doi.org/10.1093/nar/gkt827 {Nucleic acids research (11.147): 10.1093/nar/gkt827} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA207825 https://www.ebi.ac.uk/ena/browser/view/PRJNA207825 None [Overal design]MCF-7 cells were transfected with LRH-1 siRNA #2, #3, or with a non-targeting siRNA (siControl) for 72 hours. Following assessment of RNA integrity, four biological replicates for each siRNA treatment were used for microarray analysis.; [Treatment]"Cells were transfected with double-stranded RNA oligonucleotides using the Lipofectamine RNAiMax reverse transfection method (Invitrogen, UK), according to manufacturer's protocols. Two different siRNAs against LRH-1 were used: ON-TARGETplus siRNA J-003430-07 (siLRH-1_#2) and J-003430-08 (siLRH-1_#3) from Dharmacon. siGENOME Non-targeting siRNA (Dharmacon, cat. no.:D-001210-01) (siControl) was used as negative control. All siRNA experiments used the double-stranded RNA oligonucleotides at a final concentration of 80 nM."; [Growth]'MCF-7 cells were cultured in DMEM containing 10% FCS.'; [Extraction]"Total RNA was extracted using the RNeasy Kit from QIAGEN following manufacturer's instructions."; [Cell type]'Source: ''cell line: MCF-7; sirna knockdown: siControl; ', 'cell line: MCF-7; sirna knockdown: siLRH-1_#2; ', 'cell line: MCF-7; sirna knockdown: siLRH-1_#3; ' GSE43679 Homo sapiens 4 Genome variation profiling by SNP array GPL6801 Identification of DNA palindromes in the MCF-7 breast cancer cell line 2013-01-23 DNA palindromes are implicated as a causative agent in cancer formation due to their association with genomic instability and DNA amplification. However, the unique properties of palindromes render them refractory to current methods of analyses including PCR amplification and cloning into bacterial vectors. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43679 GAP-Seq: a method for identification of DNA palindromes. BMC genomics 3.501 https://doi.org/10.1186/1471-2164-15-394 {BMC genomics (3.501): 10.1186/1471-2164-15-394} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA187147 https://www.ebi.ac.uk/ena/browser/view/PRJNA187147 None [Overal design]Genomic DNA was isolated from 3 million cells. One microgram of genomic DNA was labeled using SNP6 core reagent kit and hybridized onto Genome-wide human SNP Array 6.0.; [Treatment]'None'; [Growth]'Cell lines were grown according to standard conditions.'; [Extraction]'Blood and Cell Culture DNA Midi Kit (QIAGEN)'; [Cell type]'breast cancer''cell type: breast cancer; cell line: MCF7; ', 'cell type: breast cancer; cell line: IMR90; ' GSE160018 Homo sapiens 8 Expression profiling by high throughput sequencing GPL18573 Adaptive responses of the HER2+ SKBR-3 and BT474m1 cell lines to lapatinib and JQ1 2020-10-25 SKBR-3 or BT474m1 HER2+ breast cancer cells were treated with either DMSO, 300nM lapatinib, 300nM JQ1, or lapatinib and JQ1 in combination for 48h. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE160018 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA671649 https://www.ebi.ac.uk/ena/browser/view/PRJNA671649 https://www.ncbi.nlm.nih.gov/sra?term=SRP288466 [Overal design]8 experimental samples; [Treatment]'RPMI supplemented with 10% FBS'; [Growth]'None'; [Extraction]'Total RNA was isolated using Qiagen RNeasy Plus kit.\n4 µg total RNA and 10 cycles of amplification were used for libraries constructed with KAPA Stranded mRNAseq kit.'; [Cell type]'Source: ''cell line: SKBR-3 HER2+; treatment: treated with DMSO for 48h; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: SKBR-3 HER2+; treatment: treated with 300nM lapatinib for 48h; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: SKBR-3 HER2+; treatment: treated with 300nM JQ1 for 48h; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: SKBR-3 HER2+; treatment: treated with 300nM lapatinib and 300nM JQ1 for 48h; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: BT474m1 HER2+; treatment: treated with DMSO for 48h; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: BT474m1 HER2+; treatment: treated with 300nM lapatinib for 48h; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: BT474m1 HER2+; treatment: treated with 300nM JQ1 for 48h; library preparation kit: Illumina TruSeq RNA library kit v2; ', 'cell line: BT474m1 HER2+; treatment: treated with 300nM lapatinib and 300nM JQ1 for 48h; library preparation kit: Illumina TruSeq RNA library kit v2; ' GSE61438 Homo sapiens 69 Non-coding RNA profiling by array GPL8179 Comparative microRNA profiling of sporadic and BRCA1 associated basal-like breast cancers 2014-09-15 Analysis of miRNA expression in grade 3 luminal, sporadic and BRCA1 associated basal-like breast cancers https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE61438 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA261072 https://www.ebi.ac.uk/ena/browser/view/PRJNA261072 None [Overal design]44 primary grade III breast cancer (11 BRCA1 basal, 16 sporadic basal, 17 luminal) and 13 normal breast FFPE (formalin fixed, paraffin embedded) specimens, plus 7 controls and 5 cell lines were analysed. The aim of the study was to derive grade-specific miRNA signatures for sporadic and BRCA1 basal-like breast cancers, and to ascertain an immunohistochemical profile regulated by BRCA1 specific miRNAs for potential diagnostic uses.; [Treatment]'None'; [Growth]'None'; [Extraction]'For primary tumours and normal breast tissue, 10μm thick sections were cut from FFPE tissue blocks. The sections were dewaxed in xylene, placed through 100% alcohol and allowed to dry. The samples were needle microdissected to ensure the proportion of tumour (or normal epithelium) was greater than 80%, prior to placement into lysis buffer (Agencourt Formapure kit, Beckman Coulter, Beverly, MA, USA). Tissue was digested as per kit protocol (incubate at 70oC for 1 hr, then add 20 µl of Proteinase K and incubate at 55oC for 1hr). Total RNA was extracted via a standard TRIZOL(Sigma)/chloroform protocol. For cell lines, total RNA was extracted using the total RNA protocol from the mirVana miRNA Isolation Kit (Ambion, TX, USA). All samples underwent DNase treatment with the Ambion DNA-free kit (Ambion, TX, USA).'; [Cell type]'Breast cancer cell line', 'FFPE breast cancer''cell type: Breast cancer cell line; breast cancer subtype: Luminal Cell Line; ', 'cell type: FFPE breast cancer; breast cancer subtype: BRCA1 basal; ', 'cell type: FFPE breast cancer; breast cancer subtype: Luminal; ', 'cell type: FFPE breast cancer; breast cancer subtype: Sporadic basal; ', 'cell type: FFPE breast cancer; breast cancer subtype: Normal; ', 'cell type: Breast cancer cell line; breast cancer subtype: Basal Cell Line; cell line: MDA-MB-231; ', 'cell type: Breast cancer cell line; breast cancer subtype: Sporadic basal; ', 'cell type: Breast cancer cell line; breast cancer subtype: Luminal Cell Line; cell line: MDA-MB-453; ', 'cell type: Breast cancer cell line; breast cancer subtype: Basal Cell Line; cell line: MDA-MB-468; ', 'cell type: Breast cancer cell line; breast cancer subtype: Basal Cell Line; cell line: HS578T; ', 'cell type: Breast cancer cell line; breast cancer subtype: Luminal Cell Line; cell line: MCF-7; ' GSE53734 Homo sapiens 8 Expression profiling by array GPL570 Disruption of Estrogen Signaling Enhances Invasiveness of Breast Cancer Cells by Attenuating a HER2-independent Gene Repression Program 2013-12-30 Disruption of Estrogen Signaling Enhances Invasiveness of Breast Cancer Cells by Attenuating a HER2-independent Gene Repression Program https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53734 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA232771 https://www.ebi.ac.uk/ena/browser/view/PRJNA232771 None [Overal design]In ER+ breast cancer cells, genes that were directly or indirectly repressed by E2, but not E2-activated genes, overlapped the gene overexpression signature of clinical progression of ductal carcinoma in situ to invasive ductal carcinoma. They also showed a strong collective functional bias toward tumor progression. In MCF-7 (ER+/PR+), ZR-75-1 (ER+/PR+) and BT474 (ER+/PR+/HER2 amplified) cells hormone depletion or tamoxifen treatment restored gene expression and invasiveness that were inhibited by E2.; [Treatment]'Cells were plated at 20% confluence in low glucose phenol red free medium supplemented with 5% charcoal stripped FBS and glutamine 48h prior to treatment. Cells were harvested 48 h after treatment with vehicle, E2 (1nM) or OH-Tam (100nM).'; [Growth]'Cells were routinely cultured at 37°C and in 5% CO2 in DMEM supplemented with FBS (10%), penicillin (100unit/ml), streptomycin (100μg/ml) and L-glutamine (2mM). Hormone depleted cells were grown in low glucose phenol-red free media supplemented with 5% charcoal-stripped FBS (v/v) and L-glutamine (2mM) for 48 hours before the experiments'; [Extraction]'Total RNA was prepared using the RNeasy Mini kit (Qiagen).'; [Cell type]'Source: ''cell line: MCF-7; treatment: vehicle; ', 'cell line: MCF-7; treatment: treated with 1 nM E2; ', 'cell line: MCF-7; treatment: treated with 100 nM 4-hydroxytamoxifen; ', 'cell line: MCF-7; treatment: treated with 1 nM E2 + 100 nM 4-hydroxytamoxifen; ' GSE39710 Homo sapiens 5 Genome variation profiling by genome tiling array GPL8887 Deletion of chromosome 13q and 14q is a common feature of tumors with BRCA2 mutations 2012-07-28 Genomic profiling to identify common features of breast tumors with BRCA2 mutations. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39710 Deletion of chromosomes 13q and 14q is a common feature of tumors with BRCA2 mutations. PloS one 2.776 https://doi.org/10.1371/journal.pone.0052079 {PloS one (2.776): 10.1371/journal.pone.0052079} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA171606 https://www.ebi.ac.uk/ena/browser/view/PRJNA171606 None [Overal design]Gene expression data and genomic profiling data were used to identify common features of breast tumors with BRCA2 mutations. The associated expression data and genomic data are either present in Array-express under accession number E-TABM-854 or undergoing submission.; [Treatment]'None'; [Growth]'None'; [Extraction]'Classic Phenol Chloroform extraction and ethanol precipitation'; [Cell type]'Source: ''diagnosis: breast cancer; tissue: BRCA2 tumor; ', 'diagnosis: breast cancer; tissue: BRCA2 Tumor; ' GSE178235 Homo sapiens 43 Methylation profiling by array GPL13534 Genome-wide DNA methylation analysis of HER2-positive breast cancer and stroma 2021-06-15 DNA methylation in HER2-positive breast cancers https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE178235 None None None None None 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA737795 https://www.ebi.ac.uk/ena/browser/view/PRJNA737795 None [Overal design]Multi-omics screening was conducted using laser capture microdissection-purified samples to explore response markers of HER2‑positive breast cancer to HER2‑directed therapy.; [Treatment]'None'; [Growth]'None'; [Extraction]'Specimen was obtained from each patient by core needle biopsy of a primary tumor before starting neoadjuvant therapy, and fixed using the PAXgene Tissue System (Qiagen, Hilden, Germany) and embedded in low-melting paraffin. Cancer cells or stroma cells were purified by the Leica LMD7000 system (Leica, Wetzlar, Germany) using 10 slices of 10-μm sections of block. This was conducted by an experienced pathologist (S. F.). Genomic DNA was extracted by a PAXgene DNA kit (Qiagen).'; [Cell type]'Source: ''gender: Female; age: 54; clinical tumor stage: T3; clinical nodal stage: N1; clinical stage: IIIA; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 48; clinical tumor stage: T2; clinical nodal stage: N0; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 56; clinical tumor stage: T3; clinical nodal stage: N3; clinical stage: IIIC; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 50; clinical tumor stage: T2; clinical nodal stage: N1; clinical stage: IIB; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 58; clinical tumor stage: T1; clinical nodal stage: N1; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade2a; ', 'gender: Female; age: 47; clinical tumor stage: T3; clinical nodal stage: N1; clinical stage: IIIA; histology: Invasive ductal carsinoma; er: Positive; pgr: Positive; chemotherapy effect: Grade1b; ', 'gender: Female; age: 65; clinical tumor stage: T1; clinical nodal stage: N1; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 49; clinical tumor stage: T2; clinical nodal stage: N1; clinical stage: IIB; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 64; clinical tumor stage: T1; clinical nodal stage: N1; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Positive; pgr: Positive; chemotherapy effect: Grade1a; ', 'gender: Female; age: 61; clinical tumor stage: T4; clinical nodal stage: N3; clinical stage: IIIC; histology: Invasive ductal carsinoma; er: Positive; pgr: Negative; chemotherapy effect: Grade2a; ', 'gender: Female; age: 59; clinical tumor stage: T2; clinical nodal stage: N1; clinical stage: IIB; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 67; clinical tumor stage: T2; clinical nodal stage: N2; clinical stage: IIIA; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 54; clinical tumor stage: T2; clinical nodal stage: N0; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 65; clinical tumor stage: T2; clinical nodal stage: N0; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 39; clinical tumor stage: T3; clinical nodal stage: N1; clinical stage: IIIA; histology: Invasive ductal carsinoma; er: Positive; pgr: Positive; chemotherapy effect: Grade2b; ', 'gender: Female; age: 58; clinical tumor stage: T4; clinical nodal stage: N1; clinical stage: IIIB; histology: Others; er: Positive; pgr: Positive; chemotherapy effect: Grade3; ', 'gender: Female; age: 66; clinical tumor stage: T2; clinical nodal stage: N2; clinical stage: IIIA; histology: Invasive ductal carsinoma; er: Positive; pgr: Negative; chemotherapy effect: Grade3 (rDCIS); ', 'gender: Female; age: 62; clinical tumor stage: T2; clinical nodal stage: N2; clinical stage: IIIA; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 68; clinical tumor stage: T2; clinical nodal stage: N3; clinical stage: IIIC; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 39; clinical tumor stage: T2; clinical nodal stage: N1; clinical stage: IIB; histology: Invasive ductal carsinoma; er: Positive; pgr: Positive; chemotherapy effect: Grade1b; ', 'gender: Female; age: 61; clinical tumor stage: T2; clinical nodal stage: N0; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Positive; pgr: Positive; chemotherapy effect: Grade1b; ', 'gender: Female; age: 54; clinical tumor stage: T2; clinical nodal stage: N0; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade2b; ', 'gender: Female; age: 63; clinical tumor stage: T2; clinical nodal stage: N1; clinical stage: IIB; histology: Invasive ductal carsinoma; er: Positive; pgr: Positive; chemotherapy effect: Grade1a; ', 'gender: Female; age: 71; clinical tumor stage: T2; clinical nodal stage: N0; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Positive; pgr: Negative; chemotherapy effect: Grade1a; ', 'gender: Female; age: 60; clinical tumor stage: T2; clinical nodal stage: N0; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Positive; pgr: Positive; chemotherapy effect: Grade1a; ', 'gender: Female; age: 56; clinical tumor stage: T2; clinical nodal stage: N1; clinical stage: IIB; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3; ', 'gender: Female; age: 54; clinical tumor stage: T3; clinical nodal stage: N2; clinical stage: IIIA; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade1b; ', 'gender: Female; age: 51; clinical tumor stage: T2; clinical nodal stage: N0; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Positive; pgr: Negative; chemotherapy effect: Grade3 (rDCIS); ', 'gender: Female; age: 52; clinical tumor stage: T2; clinical nodal stage: N0; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Positive; pgr: Negative; chemotherapy effect: Grade1b; ', 'gender: Female; age: 70; clinical tumor stage: T4; clinical nodal stage: N2; clinical stage: IIIB; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade1a; ', 'gender: Female; age: 29; clinical tumor stage: T2; clinical nodal stage: N0; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Positive; pgr: Positive; chemotherapy effect: Grade1a; ', 'gender: Female; age: 42; clinical tumor stage: T1; clinical nodal stage: N1; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Positive; pgr: Positive; chemotherapy effect: Grade1a; ', 'gender: Female; age: 68; clinical tumor stage: T2; clinical nodal stage: N0; clinical stage: IIA; histology: Invasive ductal carsinoma; er: Positive; pgr: Positive; chemotherapy effect: Grade1b; ', 'gender: Female; age: 36; clinical tumor stage: T2; clinical nodal stage: N1; clinical stage: IIB; histology: Invasive ductal carsinoma; er: Negative; pgr: Negative; chemotherapy effect: Grade3 (rDCIS); ' GSE113196 Homo sapiens 4 Expression profiling by high throughput sequencing GPL20301 Single Cell RNA sequencing of Adult Human Breast Epithelial Cells [Individual 4..7] 2018-04-16 Breast cancer arises from breast epithelial cells that acquire genetic alterations leading to subsequent loss of tissue homeostasis. Several distinct epithelial subpopulations have been proposed, but complete understanding of the spectrum of heterogeneity and differentiation hierarchy in the human breast remains elusive. Here, we used single-cell mRNA sequencing (scRNAseq) to profile the transcriptomes of 25,790 primary human breast epithelial cells isolated from reduction mammoplasties of seven individuals. Unbiased clustering analysis reveals the existence of three distinct epithelial cell populations, one basal and two luminal cell types, which we identify as secretory L1- and hormone-responsive L2-type cells. Pseudotemporal reconstruction of differentiation trajectories produc one continuous lineage hierarchy that closely connects the basal lineage to the two differentiated luminal branches. Our comprehensive cell atlas provides novel insights into cellular blueprint of the human breast epithelium and will form the foundation to understand how the system goes awry during breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113196 Profiling human breast epithelial cells using single cell RNA sequencing identifies cell diversity. Nature communications 11.878 https://doi.org/10.1038/s41467-018-04334-1 {Nature communications (11.878) doi:10.1038/s41467-018-04334-1}; {Communications biology (None) doi:10.1038/s42003-019-0554-8}; 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA450410 https://www.ebi.ac.uk/ena/browser/view/PRJNA450410 https://www.ncbi.nlm.nih.gov/sra?term=SRP140533 [Overal design]Droplet Based Single Cell RNA sequencing libraries were generated for 4 adult human women using the 10x Genomics Chromium Platform and sequenced on the Illumina HighSeq 4000; [Treatment]'Samples were washed in PBS (Corning 21-031-CV) and mechanically dissociated using a razor blade. Dissociated samples were digested overnight in DMEM (Corning 10-013-CV) with Collagenase Type I, 2 mg/mL (Life Technologies 17100-017). Viable organoids were separated using differential centrifugation and viably frozen in 50% FBS (Omega Scientific FB-12), 40% DMEM, and 10% DMSO (Sigma-Aldrich D8418) by volume.'; [Growth]'None'; [Extraction]'Viable organoids were thawed and washed using DMEM, and digested with 0.05% trypsin (Corning 25-052-CI) containing DNase (Sigma Aldrich D4263-5VL) to generate single cell suspension. Cells were stained for FACS using fluorescently labeled antibodies for CD31 (eBiosciences 48-0319-42), CD45 (eBiosciences 48-9459-42), EpCAM (eBiosciences 50-9326-42), CD49f (eBiosciences 12-0495-82), SytoxBlue (Life Technologies S34857). We only proceeded with samples showing at least 80% viability as measured using SytoxBlue in FACS\nflow cytometry sorted cells were washed in PBS with 0.04% BSA and reseupended at a concentration of approximately 1000 cells/µl. Library generation for 10x Genomics v1 chemistry was performed following the Chromium Single Cell 3’ Reagents Kits User Guide: CG00026 Rev B. Library generation for 10x Genomics v2 chemistry were performed following the Chromium Single Cell 3’ Reagents Kits v2 User Guide: CG00052 Rev B.'; [Cell type]'Source: ''Sex: female; tissue: Adult Human Breast Epithelium; ' GSE159391 Homo sapiens 4 Expression profiling by high throughput sequencing GPL18573 Targeted nanopore sequencing for the identification of ABCB1 promoter translocations in relapsed acute myeloid leukemia [RNAseq] 2020-10-12 Resistance to chemotherapy is the most common cause of treatment failure in acute myeloid leukemia and the drug efflux pump ABCB1 is a critical mediator. Here we demonstrate that in vitro daunorubicin exposure can induce activating ABCB1 promoter translocations in human myeloid cells, similar to those recently described in recurrent high-grade serous ovarian and breast cancer. We then develop a targeted nanopore sequencing approach that enables efficient identification of ABCB1 structural variants in high-grade serous ovarian cancer. Finally, we confirm that ABCB1high cases of relapsed AML are not characterized by ABCB1 promoter translocations but instead show high-level activity of native promoters, consistent with endogenous regulation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE159391 Targeted nanopore sequencing for the identification of ABCB1 promoter translocations in cancer. BMC cancer 2.933 https://doi.org/10.1186/s12885-020-07571-0 {BMC cancer (2.933): 10.1186/s12885-020-07571-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA668756 https://www.ebi.ac.uk/ena/browser/view/PRJNA668756 https://www.ncbi.nlm.nih.gov/sra?term=SRP287130 [Overal design]THP-1 cells were from DSMZ (Braunschweig, Germany) and cultured in RPMI 1640 medium (Sigma Aldrich) supplemented with 2mM L-Glutamine (Life Technologies, Carlsbad, CA) and 10% fetal bovine serum (Sigma Aldrich). Whilst under drug selection cells were counted and replated every third day. Cell lines were confirmed mycoplasma-free and authenticated by short tandem repeat DNA profiling. THP-1 were exposed to escalating doses of daunorubicin over 142 days, generating a resistant line (THP-1_R) which exhibited a 28.3-fold increase in daunorubicin IC50 compared with the sensitive parental cell line (THP-1_S). Total RNA was extracted from 5x10e5 cells using QIAshredder spin columns and an RNeasy® Plus Micro kit (Qiagen, Manchester, UK). RNA sequencing was performed using two replicates for both the sensitive (THP-1_S1 and THP-1_S2) and resistant (THP-1_R1 and THP-1_R2) lines. Prior to sequencing RNA integrity was checked using a 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA). PolyA libraries were prepared using a SureSelect PolyA kit (Agilent Technologies) and samples were then barcoded and pooled. Sequencing was performed using a NextSeq system (Illumina, San Diego, CA). Two replicates were sequenced for each cell line (THP-1_S and THP-1_R). A single run of 150bp paired-end sequencing produced a mean of 55.1M reads per sample.; [Treatment]'None'; [Growth]'THP-1 and derived cell lines were cultured in RPMI 1640 medium (Sigma Aldrich) supplemented with 2mM L-Glutamine (Life Technologies) and 10% fetal bovine serum (Sigma Aldrich).'; [Extraction]'Total RNA was extracted from sensitive or resistant K562 cells using QIAshredder spin columns and an RNeasy Plus Micro Kit (Qiagen, Manchester, UK) and its quality confirmed using an Agilent Bioanalyzer (Agilent Technologies, Santa Clara, CA).\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''cell line: THP-1_R; phenotype: Resistant; ', 'cell line: THP-1_S; phenotype: Sensitive; ' GSE94009 Homo sapiens 2 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Analysis of genome-wide occupancy of menin in T47D and MCF-10A cells 2017-01-24 We performed ChIP-seq using antibodies directed at menin in T47D and MCF-10A cells in order to assess the genome-wide presence of menin in these cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE94009 Enhancer-Mediated Oncogenic Function of the Menin Tumor Suppressor in Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2017.02.025 {Cell reports (7.815): 10.1016/j.celrep.2017.02.025} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA363054 https://www.ebi.ac.uk/ena/browser/view/PRJNA363054 https://www.ncbi.nlm.nih.gov/sra?term=SRP097686 [Overal design]T47D cells were synchronized in phenol red-free medium containing 10% charcoal dextran-treated fetal bovine serum (CDT medium). MCF-10A cells were cultured in DMEM. Menin ChIP-seq was performed.; [Treatment]'T47D cells were synchronized for 72 hrs in phenol red-free medium (DMEM) containing 10% charcoal dextran-treated fetal bovine serum (CDT medium). MCF-10A cells were not synchronized.'; [Growth]'Cells were maintained at 37oC and 5% CO2 in DMEM + 10% FBS and Pen-Strep.'; [Extraction]'Cells were crosslinked, lysed in a buffer containing sarkosyl and sonicated.\nThruPLEX-FD Prep kit, Rubicon Genomics'; [Cell type]'Source: ''chip antibody: anti-Menin(MEN1) (A300-115A,Bethyl); cell line: T47D; ', 'chip antibody: anti-Menin(MEN1) (A300-115A,Bethyl); cell line: MCF; ' GSE21475 Mus musculus 19 Expression profiling by array GPL6096 From mouse to humans: detecting preventing vaccination targets associated to breast cancer stem cells. Exon-level analysis 2010-04-22 TuBo cell line (E) was compared to passage 1 (P1), 2 (P2) and 3 (P3) mammospheres to detect specific transcription isoforms associated to cancer stem cell. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE21475 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA129519 https://www.ebi.ac.uk/ena/browser/view/PRJNA129519 None [Overal design]TuBo cell line (E) was compared to passage 1 (P1), 2 (P2) and 3 (P3) mammospheres. Exon-level transcription profiling was done using Affimetrix GeneChip® Exon 1.0 ST. Exon-level analysis is more complex than gene-level analysis. The number of probesets to be investigated is at least 10 times larger in number than gene-level probesets. Thus results, upon statistical analysis, are massively contaminated by type I statistical errors, i.e. false positive [Della Beffa et al. 2008]. Furthermore, exon-level probesets are based only on four probes, which makes exon-level signal summarization more noisy than gene-level, where signal summarization is based on the overall probes encompassed by all exons of a gene. To moderate these issues we have expanded the number of experimental replications: six for TuBo and passage 1 mammosphere, four for passage 3 mammosphere and three for passage 2 mammosphere. Furthermore, after data summarization with RMA and normalization with sketch quantile method, alternative splicing detection between epithelial and mammospheres passages, was assessed using MiDAS, a two way anova developed by Affymetrix for the detection of alternative splicing events. We considered suitable for further investigations the splicing events in common between the sets of exons detected as spliced in each of the following comparisons: E vs P1, E vs P2 and E vs P3.; [Treatment]'None'; [Growth]'The adherent TuBo epithelial cells were generated from a mammary carcinoma arising in a BALB/c mouse female transgenic for the activated rat ErbB2 oncogene (BALB-neuT) [Rovero et al. J Immunol, 2000. 165:5133-42] and were cultured in DMEM supplemented with 20% FCS (GIBCO, Grand Island, NY).', 'Single TuBo cells were plated in ultra low attachment flasks (Corning Life Sciences, Chorges, France) at 6 x 104 viable cells/ml in serum-free DMEM-F12 medium (Cambrex BioScience, Venviers, Belgium) supplemented with 20 ng/ml basic fibroblast growth factor (bFGF), 20 ng/ml epidermal growth factor (EGF), 5 μg/ml insulin, and 0.4% bovine serum albumin (BSA), all from Sigma-Aldrich (St. Louis, MO). Nonadherent spherical clusters of cells, named mammospheres, were collected by gentle centrifugation after 7 days.'; [Extraction]'Mirvana kit (Ambion)'; [Cell type]'adherent TuBo epithelial cells', 'non-adherent TuBo-derived mammospheres p1', 'non-adherent TuBo-derived mammospheres p2', 'non-adherent TuBo-derived mammospheres p3''strain: BALB/c; cell line: TuBo; cell type: adherent TuBo epithelial cells; ', 'strain: BALB/c; cell line: TuBo; cell type: non-adherent TuBo-derived mammospheres p1; ', 'strain: BALB/c; cell line: TuBo; cell type: non-adherent TuBo-derived mammospheres p2; ', 'strain: BALB/c; cell line: TuBo; cell type: non-adherent TuBo-derived mammospheres p3; ' GSE145787 Homo sapiens 5 Expression profiling by array GPL6244 Systems analysis of insulin and IGF1 receptors networks in breast cancer cells identifies commonalities and divergences in expression patterns 2020-02-24 Commonalities and dissimilarities between the IGF1R and INSR pathways Insulin and insulin-like growth factor-1 (IGF1), acting respectively via the insulin (INSR) and IGF1 (IGF1R) receptors, play key developmental and metabolic roles throughout life. In addition, both signaling pathways fulfill important roles in cancer initiation and progression. The inherent complexity of the INSR/IGF1R pathways, along with the well documented cross-talk between insulin-like ligands and receptors, translated into a disappointingly slow pace in the development of INSR/IGF1R-directed therapies in oncology. The present study was aimed at identifying mechanistic differences between INSR and IGF1R using a recently developed bioinformatics tool, the Biological Network Simulator (BioNSi). This application allows to import and merge multiple pathways and interaction information from the KEGG database into a single network representation. The BioNsi network simulation tool allowed us to exploit the availability of gene expression data derived from breast cancer cell lines with specific disruptions of the INSR or IGF1R genes in order to investigate potential differences in protein expression that might be linked to biological attributes of the specific receptor networks. Modeling-generated information was corroborated by experimental and biological assays. Our simulation analysis identified a number of commonalities and, most importantly, dissimilarities between the IGF1R and INSR pathways that were experimentally validated and that might help explain the basis for the biological differences between these networks. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE145787 Systems Analysis of Insulin and IGF1 Receptors Networks in Breast Cancer Cells Identifies Commonalities and Divergences in Expression Patterns. Frontiers in endocrinology 3.634 https://doi.org/10.3389/fendo.2020.00435 {Frontiers in endocrinology (3.634): 10.3389/fendo.2020.00435} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA608254 https://www.ebi.ac.uk/ena/browser/view/PRJNA608254 None [Overal design]MCF7 cells expression as baseline for a network simulation study; [Treatment]'Transfecion with plasmid containing a non-coding shRNA sequence (control shRNA) for various times'; [Growth]'MCF7 cells were seeded in 10-cm Petri dishes until reaching 100% confluence. The cells were washed with phosphate-buffered saline (PBS)'; [Extraction]'Total RNA was isolated using the TRIzol reagent (InVitrogen, Waltham, MA, USA), according to the RNA extraction guidelines for Affimetrix GeneChip Assays'; [Cell type]'Source: ''cell line: MCF7; ' GSE113362 Homo sapiens 20 Expression profiling by high throughput sequencing GPL16791 Activating Transcription Factor 4 modulated TGFb-induced aggresiveness in triple negative breast cancer vis SMAD2/3/4 and mTORC2 signaling 2018-04-19 Based on the identified stress-independent cellular functions of activating transcription factor 4 (ATF4), we reported enhanced ATF4 levels in MCF10A cells treated with TGFβ1. ATF4 is overexpressed in triple negative breast cancer (TNBC) patients, but its impact on patient survival and the underlying mechanisms remain unknown. We aimed to determine ATF4 effects on breast cancer patient survival and TNBC aggressiveness, and the relationships between TGFβ and ATF4. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113362 Activating Transcription Factor 4 Modulates TGFβ-Induced Aggressiveness in Triple-Negative Breast Cancer via SMAD2/3/4 and mTORC2 Signaling. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-17-3125 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-17-3125} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA450921 https://www.ebi.ac.uk/ena/browser/view/PRJNA450921 https://www.ncbi.nlm.nih.gov/sra?term=SRP141118 [Overal design]RNA seq analysis was carried out on 20 Triple Negative Breast Cancer Patient Derived Xenograft models; [Treatment]'PDX tumor fragments were transplanted into the cleared fat pad of 3- to 4-week-old SCID/Beige'; [Growth]'None'; [Extraction]'Total RNA was extracted from PDX samples using the RNeasy Mini kit (Life Technologies). Samples were then subject to poly(A) selection using oligo-dT beads (Life Technologies).\nIllumina TruSeq'; [Cell type]'Source: ''disease state: Triple Negative Breast Cancer; tissue: TNBC Patient Derived Xenograft (PDX); subtype: basal; ', 'disease state: Triple Negative Breast Cancer; tissue: TNBC Patient Derived Xenograft (PDX); subtype: HER2; ', 'disease state: Triple Negative Breast Cancer; tissue: TNBC Patient Derived Xenograft (PDX); subtype: basal/HER2; ' GSE79721 Homo sapiens 18 Expression profiling by array GPL10558 The BET-bromodomain inhibitor OTX015 (MK-8628) exerts in vitro and in vivo anti-tumor activity in triple-negative breast cancer models as single agent and in combination with everolimus 2016-03-30 assess the efficacy of OTX015 (MK-8628) BET inhibitor in vitro and in vivo triple negative breast cancer models https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE79721 The bromodomain inhibitor OTX015 (MK-8628) exerts anti-tumor activity in triple-negative breast cancer models as single agent and in combination with everolimus. Oncotarget None https://doi.org/10.18632/oncotarget.13814 {Oncotarget (None): 10.18632/oncotarget.13814} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA316847 https://www.ebi.ac.uk/ena/browser/view/PRJNA316847 None [Overal design]GEP analysis of 2 breast cancer cell lines with and without treatment at different timepoints; [Treatment]'treatment with OTX015 (MK-8628) BET inhibitor'; [Growth]'in vitro'; [Extraction]'RNA extraction was performed using a commercially available kit (RNeasy, Qiagen, Frederick,MD) according to the manufactures’ recommendations. RNA quality was confirmed based on a RNA integrity number >8 by use of an electrophoresis bioanalyzer (2100 Agilent Bioanalyser).'; [Cell type]'Source: ''cell line type: MDA-MB-231; treatment: [A] Control 4 h; ', 'cell line type: MDA-MB-231; treatment: [A] DMSO 4 h; ', 'cell line type: MDA-MB-231; treatment: [A] OTX 4 h; ', 'cell line type: MDA-MB-231; treatment: [A] Control 8 h; ', 'cell line type: MDA-MB-231; treatment: [A] DMSO 8 h; ', 'cell line type: MDA-MB-231; treatment: [A] OTX 8 h; ', 'cell line type: MDA-MB-231; treatment: [A] Control 24 h; ', 'cell line type: MDA-MB-231; treatment: [A] DMSO 24 h; ', 'cell line type: MDA-MB-231; treatment: [A] OTX 24 h; ', 'cell line type: MDA-MB-468; treatment: [B] Control 4 h; ', 'cell line type: MDA-MB-468; treatment: [B] DMSO 4 h; ', 'cell line type: MDA-MB-468; treatment: [B] OTX 4 h; ', 'cell line type: MDA-MB-468; treatment: [B] Control 8 h; ', 'cell line type: MDA-MB-468; treatment: [B] DMSO 8 h; ', 'cell line type: MDA-MB-468; treatment: [B] OTX 8 h; ', 'cell line type: MDA-MB-468; treatment: [B] Control 24 h; ', 'cell line type: MDA-MB-468; treatment: [B] DMSO 24 h; ', 'cell line type: MDA-MB-468; treatment: [B] OTX 24 h; ' GSE93837 Mus musculus 12 Expression profiling by array GPL6887 Whole genome transcriptional profile of PyMT/SIRT6 vs PyMT mammary tumors 2017-01-19 We compared the transcriptional profile of mammary tumors spontaneously developed in PyMT transgenic mice either bearing or not additional copies of the endogeneous SIRT6 gene. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93837 SIRT6 Suppresses Cancer Stem-like Capacity in Tumors with PI3K Activation Independently of Its Deacetylase Activity. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2017.01.065 {Cell reports (7.815): 10.1016/j.celrep.2017.01.065} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA362573 https://www.ebi.ac.uk/ena/browser/view/PRJNA362573 None [Overal design]We crossed genetically-engineered mice overexpressing functionally competent SIRT6 protein (Sirt6BAC mice) (Anderson et al., 2015) to PyMT mice. PyMT-transgenic females either bearing Sirt6BAC allele or wild-type were sacrified at 12 weeks of age. Mammary tumors spontaneously developd in these mice were excised and subject to micorarray analysis.; [Treatment]'Mice were sacrificed at 12 weeks of age and tissues were quickly removed, frozen in liquid nitrogen and subsequently stored at –80ºC'; [Growth]'Mice were housed in groups of 4-5 with food and water available ad libitum in light- and temperature-controlled environments. Care of mice was within the procedures approved by animal care and experimentation authorities of the Canton of Geneva, Switzerland'; [Extraction]'RNAs were extracted by Qiagen mRNA extract kits (RNeasy plus). Mircoarray analyses were performed by University of Texas Southwestern Medical Center at Dallas microarray Core facility (http://microarray.swmed.edu/) using Illumina Chip Mouse WG-6 v2.0 (Illumina, CA, USA)'; [Cell type]'Source: ''tissue: mammary tumor; age: 12 weeks-old; gender: female; strain/genotype: PyMT; ', 'tissue: mammary tumor; age: 12 weeks-old; gender: female; strain/genotype: PyMT/SIRT6; ' GSE66109 Homo sapiens 24 Expression profiling by array GPL19807 CCL171 BMP4 time course 2015-02-19 Methods: We used an ex vivo culture model and measured gene expression changes in human lung fibroblasts after stimulation with BMPs and their antagonists using HEEBO microarrays. The in vitro data were correlated with in vivo observations in published expression datasets of human lung adenocarcinomas. Results: We have systematically analyzed the response to BMP2, BMP4, BMP7 and their antagonists, gremlin and noggin, to define common and specific gene expression patterns. A BMP2 induced gene expression signature was defined, which is specific for stromal fibroblasts. Gene expression profiles from lung adenocarcinoma biopsies were analyzed to determine the prognostic significance of the Fibroblast specific BMP2 induced gene list. This gene list successfully segregated patients with different prognostic outcome in 3 datasets. In a small dataset (Garber et al.) there was a strong trend for a worse prognosis of patients with adenocarcinomas of all stages over-expressing the Fibroblast specific BMP2 induced gene list. In two larger datasets with stage I adenocarcinomas we observed a significantly worse disease-free (p=0.002, Lee et al. and p=0.002, Bhattacharjee et al.) and overall survival (p=0.0002). Conclusions: The effects of BMPs and their antagonists are heterogeneous in different cell types. The gene expression pattern induced by BMP2 in primary lung fibroblasts may predict outcomes of patients with lung adenocarcinomas. Experimental Factor Ontology https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE66109 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA275958 https://www.ebi.ac.uk/ena/browser/view/PRJNA275958 None [Overal design]time series design; [Treatment]'None', 'BMP stimulation experiments: For the experiment, 30?000 cells/cm2 were seeded in 3 ml of 5% FBS D-MEM and incubated for 6 h to allow attachment. The cells were washed extensively with phosphate-buffered saline and starved for 48 h in fresh low-serum D-MEM supplemented with 0.2% FBS. The cells were starved to reduce the effects of any stimulation from the regular cell culture medium. The medium was subsequently replaced with fresh low-serum D-MEM with or without 200 ng/ml BMP2 (human recombinant in Escherichia coli; Sigma Aldrich, St. Louis, MO, USA), 24 ng/ml BMP4, 200 ng/ml BMP7, 240 ng/ml Noggin or 1 ug/ml Gremlin. The cells were stimulated for 24 h, and the RNA was harvested to test the effects of BMP and their antagonists on mRNA expression patterns.'; [Growth]'None', "Primary human fibroblasts (CCL-171) and the human breast cancer cell lines MDA-MB-231 and T47D were obtained from the American Type Culture Collection (ATTC, Atlanta, Georgia, USA) on the 15. November 2005. After resuscitation the cells were propagated in Dulbecco's modified Eagle's medium (D-MEM, Invitrogen, Carlsbad, USA) supplemented with 10% heat-inactivated FBS (Invitrogen, Carlsbad, CA, USA), 4.5 g/l glucose, 4 mM L-glutamine, 100 U/ml penicillin and 100 ug/ml streptomycin (Gibco, Carlsbad, CA, USA). The cells were maintained by regular passages when confluence was reached and used for the experiments within 3-4 months. The study was approved by the Ethikkommission beider Basel, Switzerland (approval No. 271/05)."; [Extraction]'not provided', "RNA extraction and amplification: After aspirating the culture medium, the cell monolayer was washed once with phosphate-buffered saline. The cells were lysed in a buffer containing guanidine isothiocyanate (RLT buffer, QIAGEN, CA, USA). The total RNA was extracted with an RNeasy kit (QIAGEN, Valencia, CA, USA) according to the manufacturer?s instructions. The RNA concentration was measured with a NanoDrop system spectrophotometer (ND-1000 Spectrophotometer Technologies, Wilmington, NC, USA). The integrity of extracted RNA was assessed by electrophoresis in a 1% agarose gel in MOPS buffer. For mRNA amplification, an Amino Allyl MasageAmp II aRNA Amplification Kit was used (Ambion, Austin, TX, USA). The amplification of mRNA from 500 ng total RNA, purification of the cDNA, in vitro transcription and purification of aRNA were performed according to the manufacturer's instructions. The integrity and quantity of the amplified RNA were verified as described above."; [Cell type]'Source: ''reference: stratagene universal reference; ', 'cell line: CCL-171; ' GSE48159 Homo sapiens 4 Expression profiling by high throughput sequencing GPL9115; GPL11154 Mapping ERβ genomic binding sites reveals unique genomic features and identifies EBF1 as an ERβ interactor [Gro-Seq] 2013-06-20 The C4-12/Flag.ERβ cell line which stably expressed Flag.ERβ is used to study ERβ genomic functions without ERα interference. Mapping ERβ binding sites in these cells reveals ERβ unique distribution and motif enrichment patterns. Accompanying our mapping results, nascent RNA profiling is performed on cells at the same treatment time. The combined results allow the identification of ERβ target genes. Gene ontology analysis reveals that ERβ targets are enriched in differentiation, development and apoptosis. Concurrently, E2 treatment suppresses proliferation in these cells. Within ERβ binding sites, while the most prevalent binding motif is the canonical ERE, motifs of known ER interactors are also enriched in ERβ binding sites. Moreover, among enriched binding motifs are those of GFI, REST and EBF1, which are unique to ERβ binding sites in these cells. Further characterization confirms the association between EBF1 and the estrogen receptors, which favors the N-terminal region of the receptor. Furthermore, EBF1 negatively regulates ERs at the protein level. In summary, by studying ERβ genomic functions in our cell model, we confirm the anti-proliferative role of ERβ and discover the novel cross talk of ERβ with EBF1 which has various implications in normal physiology. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE48159 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA209071 https://www.ebi.ac.uk/ena/browser/view/PRJNA209071 https://www.ncbi.nlm.nih.gov/sra?term=SRP026204 [Overal design]C4-12/Flag.ERβ cells were treated with 10nM E2 (or ethanol as vehicle control) for 1 hour. Nuclei were extracted and processed with run-on assay. The resultant run-on RNA was reverse-transcribed to generate cDNA library which was subsequently sequenced by Illumina Genome Analyzer II or HiSeq2000. Two samples for each treatment were included in this experiment.; [Treatment]'None'; [Growth]'None'; [Extraction]'After 1 hour of E2 or Vehicle treatment, nuclei from C4-12/Flag-ERβ cells were extracted and processed with nuclear run-on assay.\nRun-on RNA was ligated with adapters and reverse transcribed to generate cDNA library.'; [Cell type]'Source: ''treatment: Vehicle; replicate: 1; ', 'treatment: Vehicle; replicate: 2; ', 'treatment: 10nM E2; replicate: 1; ', 'treatment: 10nM E2; replicate: 2; ' GSE34666 Mus musculus 35 Genome variation profiling by genome tiling array GPL13924 A novel preclinical mouse model of spontaneous breast cancer metastasis 2011-12-22 Metastatic disease remains one of the most urgent clinical challenges accounting for over 90% of cancer-related deaths. Yet, the identification of novel therapeutic targets to fight or prevent metastatic disease has been hampered by the limited availability of clinically relevant mouse models of metastasis formation. To address this caveat, we developed a novel preclinical mouse model of spontaneous metastatic breast cancer that recapitulates the key biological events of the metastatic cascade and mimics the clinical course of metastatic disease in humans. Exploiting the conditional K14cre;CdhF/F;Trp53F/F mouse model of de novo mammary tumor formation, we orthotopically transplanted K14cre;CdhF/F;Trp53F/F derived mouse invasive lobular carcinoma (mILC) fragments into mammary glands of wild-type syngeneic hosts. Once recipient mammary tumors were established, we mimicked the clinical setting and performed a mastectomy. Following surgery, recipient mice eventually succumbed to wide-spread clinically overt metastatic disease in lymph nodes, lungs and gastrointestinal tract. Using aCGH analyses, we explored the relationship between the genomic profiles of mammary donor tumors and paired recipient outgrowths and observed a strong correlation, indicating that the genomic profile of the parental K14cre;CdhF/F;Trp53F/F mILC is highly conserved in recipient mammary tumors. To investigate the genomic relationship between recipient mammary tumors and their metastases, we examined the correlation structure of genomic profiles derived from paired sets of primary tumors and metastases. Genomic profiles of clonally-related recipient mammary tumors were highly conserved in local and distant metastases, indicating that few genomic alterations occur during transition from a primary tumor to a distant site. To more thoroughly examine potential site-specific genomic alterations, we constructed so-called ‘delta-profiles’ by calculating the difference between the genomic profile of a recipient mammary tumor and its paired lymph node- and lung metastasis. Site-specific recurrent alterations were not observed in lymph node nor lung metastases. Taken together, these data show that genomic profiles of metastases are highly similar to those of parental recipient tumors and that, if changes occurred, they did not recur in different independent samples. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE34666 A preclinical mouse model of invasive lobular breast cancer metastasis. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-11-4208 {Cancer research (8.378): 10.1158/0008-5472.CAN-11-4208} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA151221 https://www.ebi.ac.uk/ena/browser/view/PRJNA151221 None [Overal design]We performed aCGH analyses on DNA isolated from K14cre;Cdh-/-;Trp53-/- derived donor mILCs (n=3) and their recipient mammary tumor outgrowths (n=10). Furthermore, we also analyzed genomic profiles derived from lung (n=10), tumor-draining (n=7) and distant lymph node metastases (n=5) isolated from the same recipient mice. DNA from each of these samples was hybridized against related donor splenic DNA.; [Treatment]'None'; [Growth]'None'; [Extraction]'Genomic DNA of tumor, metastasis and spleen samples was extracted by proteinase K lysis and organic extraction with phenol-chloroform.'; [Cell type]'Source: ''donor/recipient: Donor; tissue: Primary tumor; site: Mamma; related to donor: 1; mouse id: D1; ', 'tissue: spleen; derived from donor (id): 1; ', 'donor/recipient: Recipient; tissue: Primary tumor; site: Mamma; related to donor: 1; mouse id: R1a; ', 'donor/recipient: Recipient; tissue: Metastasis; site: Lung; related to donor: 1; mouse id: R1a; ', 'donor/recipient: Recipient; tissue: Metastasis; site: LN, renal; related to donor: 1; mouse id: R1a; ', 'donor/recipient: Recipient; tissue: Primary tumor; site: Mamma; related to donor: 1; mouse id: R1b; ', 'donor/recipient: Recipient; tissue: Metastasis; site: Lung; related to donor: 1; mouse id: R1b; ', 'donor/recipient: Recipient; tissue: Metastasis; site: LN, axillary; related to donor: 1; mouse id: R1b; ', 'donor/recipient: Recipient; tissue: Primary tumor; site: Mamma; related to donor: 1; mouse id: R1c; ', 'donor/recipient: Recipient; tissue: Metastasis; site: Lung; related to donor: 1; mouse id: R1c; ', 'donor/recipient: Recipient; tissue: Primary tumor; site: Mamma; related to donor: 1; mouse id: R1d; ', 'donor/recipient: Recipient; tissue: Metastasis; site: Lung; related to donor: 1; mouse id: R1d; ', 'donor/recipient: Recipient; tissue: Metastasis; site: LN, axillary; related to donor: 1; mouse id: R1d; ', 'donor/recipient: Donor; tissue: Primary tumor; site: Mamma; related to donor: 2; mouse id: D2; ', 'tissue: spleen; derived from donor (id): 2; ', 'donor/recipient: Recipient; tissue: Primary tumor; site: Mamma; related to donor: 2; mouse id: R2a; ', 'donor/recipient: Recipient; tissue: Metastasis; site: Lung; related to donor: 2; mouse id: R2a; ', 'donor/recipient: Recipient; tissue: Metastasis; site: LN, axillary; related to donor: 2; mouse id: R2a; ', 'donor/recipient: Recipient; tissue: Primary tumor; site: Mamma; related to donor: 2; mouse id: R2b; ', 'donor/recipient: Recipient; tissue: Metastasis; site: Lung; related to donor: 2; mouse id: R2b; ', 'donor/recipient: Recipient; tissue: Metastasis; site: LN, axillary; related to donor: 2; mouse id: R2b; ', 'donor/recipient: Recipient; tissue: Metastasis; site: LN, caudal; related to donor: 2; mouse id: R2b; ', 'donor/recipient: Recipient; tissue: Primary tumor; site: Mamma; related to donor: 2; mouse id: R2c; ', 'donor/recipient: Recipient; tissue: Metastasis; site: Lung; related to donor: 2; mouse id: R2c; ', 'donor/recipient: Donor; tissue: Primary tumor; site: Mamma; related to donor: 3; mouse id: D3; ', 'tissue: spleen; derived from donor (id): 3; ', 'donor/recipient: Recipient; tissue: Primary tumor; site: Mamma; related to donor: 3; mouse id: R3a; ', 'donor/recipient: Recipient; tissue: Metastasis; site: Lung; related to donor: 3; mouse id: R3a; ', 'donor/recipient: Recipient; tissue: Metastasis; site: LN, axillary; related to donor: 3; mouse id: R3a; ', 'donor/recipient: Recipient; tissue: Metastasis; site: LN, caudal; related to donor: 3; mouse id: R3a; ', 'donor/recipient: Recipient; tissue: Primary tumor; site: Mamma; related to donor: 3; mouse id: R3b; ', 'donor/recipient: Recipient; tissue: Metastasis; site: Lung; related to donor: 3; mouse id: R3b; ', 'donor/recipient: Recipient; tissue: Metastasis; site: LN, axillary; related to donor: 3; mouse id: R3b; ', 'donor/recipient: Recipient; tissue: Metastasis; site: LN, caudal; related to donor: 3; mouse id: R3b; ', 'donor/recipient: Recipient; tissue: Primary tumor; site: Mamma; related to donor: 3; mouse id: R3c; ', 'donor/recipient: Recipient; tissue: Metastasis; site: Lung; related to donor: 3; mouse id: R3c; ', 'donor/recipient: Recipient; tissue: Metastasis; site: LN, axillary; related to donor: 3; mouse id: R3c; ', 'donor/recipient: Recipient; tissue: Metastasis; site: LN, renal; related to donor: 3; mouse id: R3c; ' GSE85315 Homo sapiens 6 Genome binding/occupancy profiling by high throughput sequencing GPL15520; GPL18573 Genome-wide changes in H3K4me3 after MEN1 silencing in MCF-7 cells 2016-08-08 We performed ChIP-seq using H3K4me3 antibodies in MCF-7 cells after induction of small hairpin RNA's directed at the MEN1 mRNA or a control sequence. We demonstrate that at a selected group of loci H3K4me3 is affected by MEN1 silencing. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE85315 Enhancer-Mediated Oncogenic Function of the Menin Tumor Suppressor in Breast Cancer. Cell reports 7.815 https://doi.org/10.1016/j.celrep.2017.02.025 {Cell reports (7.815): 10.1016/j.celrep.2017.02.025} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA338157 https://www.ebi.ac.uk/ena/browser/view/PRJNA338157 https://www.ncbi.nlm.nih.gov/sra?term=SRP081088 [Overal design]Comparison of genome-wide H3K4me3 binding after ShMEN1 induction vs ShCtrl, in duplicate.; [Treatment]"MCF-7 cells that had been lentivirally infected with constructs for inducible expression of small hairpin RNA's directed against the MEN1 mRNA (ShMEN1#1) or a control sequnece were synchronized for 72 hrs in phenol red-free medium (DMEM) containing 10% charcoal dextran-treated fetal bovine serum (CDT medium). Expression of small hairpin RNA's was induced by adding 100 ng/ml for 72 hrs."; [Growth]'Cells were maintained at 37oC and 5% CO2 in DMEM + 10% FBS and Pen-Strep.'; [Extraction]'Cells were crosslinked, lysed in a buffer containing SDS and sonicated.\nThruPLEX-FD Prep kit, Rubicon Genomics'; [Cell type]'Source: ''chip antibody: H3K4me3 antibody Abcam (Ab8580); cell line: MCF-7; induced: ShCtrl; ', 'chip antibody: none; cell line: MCF-7; induced: ShCtrl; ', 'chip antibody: H3K4me3 antibody Abcam (Ab8580); cell line: MCF-7; induced: ShMEN1; ', 'chip antibody: none; cell line: MCF-7; induced: ShMEN1; ' GSE12814 Homo sapiens 33 Expression profiling by array GPL570 Identifying the molecular signature of the interstitial del(7q) subgroup of uterine leiomyomata using a paired analysis 2008-09-17 Uterine leiomyomata (UL), the most common neoplasm in reproductive-age women, have recurrent cytogenetic abnormalities including del(7)(q22q32). To develop a molecular signature, matched del(7q) and non-del(7q) tumors identified by FISH or karyotyping from 11 women were profiled with expression arrays. Our analysis using paired t-tests demonstrates this matched design is critical to eliminate confounding effects of genotype and environment that underlie patient variation. A gene list ordered by genome-wide significance showed enrichment for the 7q22 target region. Modification of the gene list by weighting each sample for percent of del(7q) cells to account for the mosaic nature of these tumors further enhanced the frequency of 7q22 genes. Pathway analysis revealed two of the 19 significant functional networks were associated with development and the most represented pathway was protein ubiquitination, which can influence tumor development by stabilizing oncoproteins and destabilizing tumor suppressor proteins. Array CGH (aCGH) studies determined the only consistent genomic imbalance was deletion of 9.5 megabases from 7q22-7q31.1. Combining the aCGH data with the del(7q) UL mosacism-weighted expression analysis resulted in a list of genes that are commonly deleted and whose copy number is correlated with significantly decreased expression. These genes include the proliferation inhibitor HPB1, the loss of expression of which has been associated with invasive breast cancer, as well as the mitosis integrity-maintenance tumor suppressor RINT1. This study provides a molecular signature of the del(7q) UL subgroup and will serve as a platform for future studies of tumor pathogenesis. Keywords: uterine leiomyomata, fibroids, del(7)(q22q32), gene expression, aCGH, microarray https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE12814 Identifying the molecular signature of the interstitial deletion 7q subgroup of uterine leiomyomata using a paired analysis. Genes, chromosomes & cancer 2.940 https://doi.org/10.1002/gcc.20692 {Genes, chromosomes & cancer (2.940): 10.1002/gcc.20692} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA111121 https://www.ebi.ac.uk/ena/browser/view/PRJNA111121 None [Overal design]Matched del(7q) and non-del(7q) tumors identified by FISH or karyotyping from each of eleven woman were profiled using Affymetrix GeneChip U133 Plus 2.0 oligonucleotide gene expression arrays.; [Treatment]'None'; [Growth]'None'; [Extraction]'Followed Affymetrix GeneChip Expression Analysis Technical Manual revision 4'; [Cell type]'Source: ''sample_type: del(7q) fibroid = 42.3% del(7q) nuclei by interphase FISH; ', 'sample_type: non-del(7q) fibroid based on interphase FISH; ', 'sample_type: myometrium; ', 'sample_type: del(7q) fibroid = 50% del(7q) nuclei by interphase FISH; ', 'sample_type: del(7q) fibroid = 80% del(7q) nuclei by interphase FISH; ', 'sample_type: del(7q) fibroid = 78% del(7q) nuclei by interphase FISH; ', 'sample_type: del(7q) fibroid = 25% del(7q) nuclei by interphase FISH; ', 'sample_type: del(7q) fibroid = 62% del(7q) nuclei by inteprhase FISH; ', 'sample_type: del(7q) fibroid = 52% del(7q) nuclei by interphase FISH; ', 'sample_type: non-del(7q) fibroid based on intephase FISH; ', 'sample_type: del(7q) fibroid = 34% del(7q) nuclei based on interphase FISH; ', 'sample_type: del(7q) fibroid = 37% del(7q) nuclei by interphase FISH; ', 'sample_type: del(7q) fibroid = 12% del(7q) nuclei by interphase FISH; ', 'sample_type: del(7q) fibroid = 71% del(7q) nuclei by interphase FISH; ' GSE66305 Homo sapiens 88 Expression profiling by array GPL570 Prospective biomarker analysis of the randomized CHER-LOB study evaluating the dual anti-HER2 treatment with chemotherapy plus trastuzumab and lapatinib as neoadjuvant therapy for HER2-positive breast cancer [expression] 2015-02-25 The CHER-LOB randomized phase II study showed that the combination of lapatinib and trastuzumab plus chemotherapy increases the pathologic complete remission (pCR) rate as compared to chemotherapy plus either trastuzumab or lapatinib. An extensive biomarker programme was prospectively planned to identify potential predictors of sensitivity to different treatments and evaluate treatment effect on tumor biomarkers. A mutation in PIK3CA exon 20 or 9 was documented in 20% of the cases. Overall, the pCR rates were similar in PIK3CA wild type and PIK3CA mutated patients (33.3% vs 22.7%; p=0.323). However, for patients receiving trastuzumab plus lapatinib, the probability of pCR was higher in PIK3CA wild type tumors (48.4% vs 12.5%; p=0.06). Ki67, pAKT and apoptosis measured on the residual disease were significantly reduced from baseline. The degree of Ki67 inhibition was significantly higher in patients receiving the dual anti-HER2 blockade. In conclusion, PIK3CA mutations seem to identify patients less likely to benefit from dual anti-HER2 inhibition. p95-HER2 and markers of PI3K pathway deregulation are not confirmed as markers of different sensitivity to trastuzumab or lapatinib. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE66305 Prospective Biomarker Analysis of the Randomized CHER-LOB Study Evaluating the Dual Anti-HER2 Treatment With Trastuzumab and Lapatinib Plus Chemotherapy as Neoadjuvant Therapy for HER2-Positive Breast Cancer. The oncologist 5.252 https://doi.org/10.1634/theoncologist.2015-0138 {The oncologist (5.252): 10.1634/theoncologist.2015-0138} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA276464 https://www.ebi.ac.uk/ena/browser/view/PRJNA276464 None [Overal design]121 HER2-positive breast cancer patients were randomly assigned to neoadjuvant chemotherapy plus either trastuzumab, lapatinib or both trastuzumab and lapatinib. Pre-treatment, fresh-frozen tissue samples were collected for genomic analyses. 88 samples passed quality control for RNA and were profiled with Affymetrix technology using the HG-U133 Plus 2.0 GeneChip array.; [Treatment]'CHER-LOB is a phase II, randomized, multicenter, trial in which 121 patients with primary HER2-positive breast cancer were randomized to receive preoperative chemotherapy with weekly paclitaxel times 12 followed by 4 courses of 3-weekly FEC (fluorouracil, epirubicin and cyclophosphamide) plus either trastuzumab (Arm A), lapatinib (Arm B) or the combination of trastuzumab and lapatinib (Arm C). The trial design, eligibility criteria, statistical analysis, and clinical results including response, surgery outcomes and treatment safety are described in details elsewhere.'; [Growth]'NA'; [Extraction]"Qiagen RNeasy (manufacturer's protocol)."; [Cell type]'Source: ''disease state: HER2-positive breast cancer; tissue: breast cancer; cher-lob arm: C; arm description: chemotherapy+trastuzumab+lapatinib; pcr (1=yes): 0; ', 'disease state: HER2-positive breast cancer; tissue: breast cancer; cher-lob arm: A; arm description: chemotherapy+trastuzumab; pcr (1=yes): 1; ', 'disease state: HER2-positive breast cancer; tissue: breast cancer; cher-lob arm: B; arm description: chemotherapy+lapatinib; pcr (1=yes): 1; ', 'disease state: HER2-positive breast cancer; tissue: breast cancer; cher-lob arm: C; arm description: chemotherapy+trastuzumab+lapatinib; pcr (1=yes): 1; ', 'disease state: HER2-positive breast cancer; tissue: breast cancer; cher-lob arm: B; arm description: chemotherapy+lapatinib; pcr (1=yes): 0; ', 'disease state: HER2-positive breast cancer; tissue: breast cancer; cher-lob arm: A; arm description: chemotherapy+trastuzumab; pcr (1=yes): 0; ' GSE144143 Mus musculus 6 Expression profiling by high throughput sequencing GPL19057 RNA-seq of murine breast cancer cell line AT3 infected with F. nucleatum 2020-01-23 Fusobacterium nucleatum (F. nucleatum) is implicated to exacerbate colorectal cancer. However, there is also evidence that the bacterium accumulates on other cancer types such as breast cancer. In order to better understand the transcriptional response of breast cancer cells to infection with F. nucleatum, we performed RNA-seq of the murine breast cancer cell AT3 with F. nucleatum. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144143 Breast cancer colonization by Fusobacterium nucleatum accelerates tumor growth and metastatic progression. Nature communications 11.878 https://doi.org/10.1038/s41467-020-16967-2 {Nature communications (11.878): 10.1038/s41467-020-16967-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA602883 https://www.ebi.ac.uk/ena/browser/view/PRJNA602883 https://www.ncbi.nlm.nih.gov/sra?term=SRP244361 [Overal design]Cells were seeded 2 days prior to infection and from this point on kept in an oxygen-controlled incubator (1% oxygen). The DMEM media was exchanged after 24h not containing otherwise used antibiotic mix. On the second day, AT3 cells were infected with F. nucleatum (m.o.i. of 10). Three biological replicates of infected and mock control samples were taken 24h after infection.; [Treatment]'AT3 cell were infected at a m.o.i. of 10 with F. nucleatum ATCC 23726 for 24h'; [Growth]'Cells were seeded in six-well plates 2 days prior to infection and kept in an oxygen-controlled incubator at 1% oxygen. The complete DMEM media was exchanged after 24h for complete DMEM without antibiotic.'; [Extraction]"Cells were washed 1x with PBS before total RNA extraction using the mirVana kit (Ambion) following the manufacturer's instructions\ninput of 500ng total RNA for oligo-dT capture beads for poly-A-mRNA enrichment for TruSeq Stranded mRNA Library Preparation Kit (Illumina) following manufacturer's instructions\nTruSeq Stranded mRNA Library Preparation Kit (Illumina)"; [Cell type]'Source: ''cell line: AT-3 Mouse Mammary Carcinoma Cell Line; infection: F. nucleatum; ', 'cell line: AT-3 Mouse Mammary Carcinoma Cell Line; infection: control; ' GSE9893 Homo sapiens 155 Expression profiling by array GPL5049 A gene expression signature predicting the recurrence of tamoxifen-treated primary breast cancer. 2007-12-14 A 36-gene classifier was constructed through expression profiling of 132 tumors from tamoxifen-treated patients using 70-mer oligonucleotide microarrays. The robustness of the signature was demonstrated using expression data from 83 independent tumors. The 36-gene signature was (i) more efficient to predict disease-free survival than the traditional histo-pathological prognostic factors, (ii) as effective as the Nottingham Prognostic Index or the "Adjuvant!" software, and (iii) the only independent prognostic factor. Comparison with several already published signatures demonstrated that the 36-gene signature was among the best to classify tumors. Keywords: Gene expression profiling; supervised analysis; molecular signature predictive of recurrence; univariate and multivariate analysis in relation to disease-free survival. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE9893 A gene expression signature that can predict the recurrence of tamoxifen-treated primary breast cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-07-1833 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-07-1833} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA103889 https://www.ebi.ac.uk/ena/browser/view/PRJNA103889 None [Overal design]In the study presented here, a cohort of 132 primary tumors from tamoxifen-treated patients followed up more than 5-years, was used to acquire expression profiles at the whole genome level by 70-mer oligonucleotide microarrays containing 22,680 probes (which represent 21,329 human specific genes). Supervised predictive analysis of microarrays allowed construction of a 36-gene molecular classifier whose robustness was assessed by using gene expression data from 83 independent tumors (including 23 tumors from our microarray platform and 60 tumors from the study by Ma et al., Cancer cell 2004; 5:607-616).; [Treatment]'None'; [Growth]'None'; [Extraction]'Frozen breast tumors (40 mg) were homogenized using the FastPrep System from Q-Biogene. Total RNA was extracted and cleaned up from the lysate with use of the Qiagen RNeasy Mini Kit. The RNA purity and integrity was controlled by way of the Bioanalyser 2100 (Agilent).'; [Cell type]'Source: ''' GSE113687 Homo sapiens 114 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by genome tiling array GPL11154; GPL18573; GPL21145 Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer 2018-04-25 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE113687 Epigenetic Switch-Induced Viral Mimicry Evasion in Chemotherapy-Resistant Breast Cancer. Cancer discovery 26.370 https://doi.org/10.1158/2159-8290.CD-19-1493 {Cancer discovery (26.370): 10.1158/2159-8290.CD-19-1493} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA453605 https://www.ebi.ac.uk/ena/browser/view/PRJNA453605 None [Overal design]Refer to individual Series; [Treatment]'None', 'Taxol-resistant cells were grown in presence of 20nM of Paclitaxel at all time. Parental cells (MDA-MB-436 and Hs 578T) were grown in DMEM with 1:1000 DMSO at all time.'; [Growth]'None', 'MDA-MB-436 and HS 578T cells were grown in DMSO supplemented with 10%FBS and Penicilin/Streptomycin (100 U/mL Penicilium and 100 μg/mL. Streptomycin). Taxane-resistant cells were generated upon long-term exposure to increasing concentrations of paclitaxel at a starting concentration 0.05 nM with increments (dose and time adjusted to the growth and survival of adapting cells), until the cytotoxic concentration of 10 to 20 nM was reached with the resistant cells growing at a similar rate than the parental cells (>6 months).'; [Extraction]'nor provided', 'RNA was extracted using the qiaquick purification kit\nRNA samples were quantified by qubit (Life Technologies) and quality by Agilent Bioananlyzer. Two hundred nanograms Total RNA from 42 samples were library prepared using TruSeq Stranded Total RNA kit (Illumina). RNA samples were ribosomal RNA depleted using Ribo-zero Gold rRNA beads, following purification the RNA was fragmented. The cleaved RNA fragments were copied into first strand cDNA using reverse transcriptase and random primers. This is followed by second strand cDNA synthesis using RNase H and DNA Polymerase I. A single “A” based were added and adapter ligated followed by purification and enrichment with PCR to create cDNA libraries.\nFinal cDNA libraries were size validated using Agilent Bioanalyzer and concentration validated by qPCR (Kapa Biosystems/Roche). All libraries were normalized to 10nM and pooled together, denatured with 0.2N NaOH and diluted to a final concentration of 1.4pM. 1.3ml of 1.4pM pooled libraries were loaded onto an Illumina NextSeq cartridge for cluster generation and sequencing on an Illumina Nextseq500 instrument (Illumina) using Paired-end 75bp protocol to achieve ~ 40 million reads per sample', "Lysates were clarified from sonicated nuclei and histone-DNA complexes were isolated with antibody.\nLibraries were prepared according to Illumina's instructions accompanying the DNA Sample Kit (Part# 0801-0303). Briefly, DNA was end-repaired using a combination of T4 DNA polymerase, E. coli DNA Pol I large fragment (Klenow polymerase) and T4 polynucleotide kinase. The blunt, phosphorylated ends were treated with Klenow fragment (32 to 52 exo minus) and dATP to yield a protruding 3- 'A' base for ligation of Illumina's adapters which have a single 'T' base overhang at the 3’ end. After adapter ligation DNA was PCR amplified with Illumina primers for 15 cycles and library fragments of ~250 bp (insert plus adaptor and PCR primer sequences) were band isolated from an agarose gel. The purified DNA was captured on an Illumina flow cell for cluster generation. Libraries were sequenced on the Genome Analyzer following the manufacturer's protocols.", "RNA was extracted using the qiaquick purification kit according to manufacturer's protocol\nRNA samples were quantified by qubit (Life Technologies) and quality by Agilent Bioananlyzer. All samples had RIN score >8 were library prepared using TruSeq Stranded mRNA kit (Illumina). Two hundred nanograms total RNa from 30 RNA samples were purified for polyA tail containing mRNA molecules using poly-T oligo attached magnetic beads , following purification the RNA was fragmented. The cleaved RNA fragments were copied into first strand cDNA using reverse transcriptase and random primers. This is followed by second strand cDNA synthesis using RNase H and DNA Polymerase I. A single “A” based were added and adapter ligated followed by purification and enrichment with PCR to create cDNA libraries.\nFinal cDNA libraries were size validated using Agilent Bioanalyzer and concentration validated by qPCR (Kapa Biosystems/Roche). All libraries were normalized to 10nM and pooled together, denatured with 0.2N NaOH and diluted to a final concentration of 8 pM. Pooled libraries were loaded onto cBot (Illumina) for cluster generation. Clustered flow cell was then sequenced Paired-end 100 cycles V3 using Illumina Hiseq2000 to achieve ~30 million reads per sample."; [Cell type]'Triple-negative breast cancer (TNBC)', 'TNBC''cell line: MDA-MB-436; cell type: Triple-negative breast cancer (TNBC); ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; treatment: DMSO 1:1000; replicate: GD_RNA_60 and 74; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive treated with paclitaxel 72h; treatment: UNC1999 3uM, 96h; replicate: GD_RNA_62 and 76; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: DMSO 1:1000; replicate: GD_RNA_65 and 79; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: UNC1999 3uM, 96h; replicate: GD_RNA_67 and 81; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: DMSO 1:1000; replicate: GD_RNA_68 and 82; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; treatment: UNC1999 3uM, 96h; replicate: GD_RNA_70 and 84; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive treated with paclitaxel 72h; treatment: DMSO 1:1000; replicate: GD_RNA_71 and 85; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: UNC1999 3uM, 96h; replicate: GD_RNA_73 and 87; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: DMSO 1:1000; replicate: GD_RNA_60 and 74; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: UNC1999 3uM, 96h; replicate: GD_RNA_62 and 76; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; treatment: DMSO 1:1000; replicate: GD_RNA_65 and 79; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive treated with paclitaxel 72h; treatment: UNC1999 3uM, 96h; replicate: GD_RNA_67 and 81; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: UNC1999 3uM, 96h; replicate: GD_RNA_70 and 84; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: DMSO 1:1000; replicate: GD_RNA_71 and 85; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; treatment: UNC1999 3uM, 96h; replicate: GD_RNA_73 and 87; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive treated with paclitaxel 72h; treatment: DMSO 1:1000; replicate: GD_RNA_60 and 46; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: UNC1999 3uM, 96h; replicate: GD_RNA_62 and 48; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: DMSO 1:1000; replicate: GD_RNA_65 and 51; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: UNC1999 3uM, 96h; replicate: GD_RNA_67 and 53; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; treatment: DMSO 1:1000; replicate: GD_RNA_68 and 54; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive treated with paclitaxel 72h; treatment: UNC1999 3uM, 96h; replicate: GD_RNA_70 and 56; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: DMSO 1:1000; replicate: GD_RNA_71 and 57; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; treatment: UNC1999 3uM, 96h; replicate: GD_RNA_73 and 59; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_31; antibody: none; agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_32; antibody: H3K4me1 (Abcam Ab8895); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_33; antibody: H3K4me3 (Millipore 05-1339); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_34; antibody: H3K27ac (Abcam Ab4729); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_35; antibody: H3K27me3 (Diagenode C15410069); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_43; antibody: none; agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_44; antibody: H3K4me1 (Abcam Ab8895); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_45; antibody: H3K4me3 (Millipore 05-1339); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_46; antibody: H3K27ac (Abcam Ab4729); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_47; antibody: H3K27me3 (Diagenode C15410069); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_49; antibody: none; agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_50; antibody: H3K4me1 (Abcam Ab8895); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_51; antibody: H3K4me3 (Millipore 05-1339); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_52; antibody: H3K27ac (Abcam Ab4729); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_53; antibody: H3K27me3 (Diagenode C15410069); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_55; antibody: none; agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_56; antibody: H3K4me1 (Abcam Ab8895); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_57; antibody: H3K4me3 (Millipore 05-1339); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_58; antibody: H3K27ac (Abcam Ab4729); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_59; antibody: H3K27me3 (Diagenode C15410069); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_1; antibody: none; agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_2; antibody: H3K4me1 (Abcam Ab8895); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_3; antibody: H3K4me3 (Millipore 05-1339); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_4; antibody: H3K27ac (Abcam Ab4729); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_ChIP_5; antibody: H3K27me3 (Diagenode C15410069); agent: DMSO; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_13; antibody: none; agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_14; antibody: H3K4me1 (Abcam Ab8895); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_15; antibody: H3K4me3 (Millipore 05-1339); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_16; antibody: H3K27ac (Abcam Ab4729); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_17; antibody: H3K27me3 (Diagenode C15410069); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_19; antibody: none; agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_20; antibody: H3K4me1 (Abcam Ab8895); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_21; antibody: H3K4me3 (Millipore 05-1339); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_22; antibody: H3K27ac (Abcam Ab4729); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_23; antibody: H3K27me3 (Diagenode C15410069); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_25; antibody: none; agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_26; antibody: H3K4me1 (Abcam Ab8895); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_27; antibody: H3K4me3 (Millipore 05-1339); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_28; antibody: H3K27ac (Abcam Ab4729); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_ChIP_29; antibody: H3K27me3 (Diagenode C15410069); agent: paclitaxel; cell line: MDA-MB-436; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_RNA_11 and 21; agent: 1:1000 DMSO; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive treated with paclitaxel 72h; replicate: GD_RNA_12 and 22; agent: 20nM Paclitaxel, 72h; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_13 and 23; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_14 and 24; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_15 and 25; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_RNA_16 and 26; agent: 1:1000 DMSO; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive treated with paclitaxel 72h; replicate: GD_RNA_17 and 27; agent: 20nM Paclitaxel, 72h; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_18 and 28; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_19 and 29; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_20 and 30; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_RNA_1 and 21; agent: 1:1000 DMSO; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive treated with paclitaxel 72h; replicate: GD_RNA_2 and 22; agent: 20nM Paclitaxel, 72h; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_3 and 23; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_4 and 24; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_5 and 25; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_RNA_6 and 26; agent: 1:1000 DMSO; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive treated with paclitaxel 72h; replicate: GD_RNA_7 and 27; agent: 20nM Paclitaxel, 72h; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_8 and 28; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_9 and 29; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_10 and 30; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_RNA_11 and 1; agent: 1:1000 DMSO; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive treated with paclitaxel 72h; replicate: GD_RNA_12 and 2; agent: 20nM Paclitaxel, 72h; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_13 and 3; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_14 and 4; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_15 and 5; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive; replicate: GD_RNA_16 and 6; agent: 1:1000 DMSO; ', 'cell type: TNBC; paclitaxel sensitivity: parental taxol-sensitive treated with paclitaxel 72h; replicate: GD_RNA_17 and 7; agent: 20nM Paclitaxel, 72h; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_18 and 8; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_19 and 9; agent: 20nM Paclitaxel; ', 'cell type: TNBC; paclitaxel sensitivity: Taxol-resistant; replicate: GD_RNA_20 and 10; agent: 20nM Paclitaxel; ' GSE27374 Homo sapiens 2 Methylation profiling by genome tiling array GPL9767 Methylation profile in breast cancer 2011-02-17 Agilent CpG microarray in combination with enriched methylated DNA by a MBD protein were carried out in each pool of genomic DNA from primary breast tumor and matched adjacent normal tissues. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE27374 Genome-wide identification of OTP gene as a novel methylation marker of breast cancer. Oncology reports 3.041 https://doi.org/10.3892/or.2012.1691 {Oncology reports (3.041): 10.3892/or.2012.1691} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA137279 https://www.ebi.ac.uk/ena/browser/view/PRJNA137279 None [Overal design]1.Common reference vs enriched methylated DNA in tumor 2. Common reference vs enriched methylated DNA in adjacent normal 3. Then compare two data indirectly; [Treatment]'None'; [Growth]'Common reference source : Normal placental gDNA without any history of malignancy was purchased from Biochain, Inc (CA, USA, Cat. No. D1234200).', 'tumor and nontumor source : Fresh-frozen tissue specimens were obtained from the School of Medicine, ChungNam National University, Daejeon, South Korea. All specimens and pertinent patient information were treated in accordance with the Institutional Review Board of the School of Medicine, ChungNam National University, Daejeon, South Korea. Each tumor specimen was histologically verified by a board-certified pathologist and archived for further DNA study.'; [Extraction]'Qiagen DNA mini kit\nIsolation of methylated DNA using MBD protein (for complete protocol see supplementary file on the Series record).'; [Cell type]'Source: ''tissue: reference control; ', 'tissue: nontumor breast; ', 'tissue: breast tumor; ' GSE41158 Homo sapiens 4 Expression profiling by array GPL6244 FBP1 expression in basal-like breast cancer MDA-MB231 and Hs578T cells 2012-09-26 FBP1 is a rate limiting enzyme in glucogenogenesis and FBP1 expression changes cells to oxidative phosphorylation. Expressing FBP1 in basal-like breast cancer cells, which lack the expression of this enzyme, will identify the genes involved in glycolysis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE41158 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA175939 https://www.ebi.ac.uk/ena/browser/view/PRJNA175939 None [Overal design]FBP1 was expressed in MDA-MB231 and Hs578T cells, stable clones were selected, and RNA was prepared for microarray analysis.; [Treatment]'Cells were trypinized and harvested when in log-growth phase.'; [Growth]'Cells were grown in DMEM/F12 plus 10%FBS in 5%CO2 at 37C.'; [Extraction]"Total RNA was extract from cells using Qiagene RNA purification kit following manfacturer's protocol"; [Cell type]'basal-like breast cancer''cell line: MDA-MB231; cell type: basal-like breast cancer; ', 'cell line: MDA-MB231; cell type: basal-like breast cancer; genotype/variation: expressing FBP1; ', 'cell line: Hs578T; cell type: basal-like breast cancer; ', 'cell line: Hs578T; cell type: basal-like breast cancer; genotype/variation: expressing FBP1; ' GSE10128 Homo sapiens 62 Genome variation profiling by genome tiling array GPL5772 Genomic copy number alterations as predictive markers of systemic recurrence in breast cancer 2008-01-10 Array CGH containing 4,044 human bacterial artificial chromosome clones was used to assess copy number changes in 31 pairs of clinicopathologically well matched recurred / nonrecurred breast cancer tissues. Keywords: array CGH https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE10128 DNA copy number alterations and expression of relevant genes in triple-negative breast cancer. Genes, chromosomes & cancer 2.940 https://doi.org/10.1002/gcc.20550 {Genes, chromosomes & cancer (2.940): 10.1002/gcc.20550} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA108977 https://www.ebi.ac.uk/ena/browser/view/PRJNA108977 None [Overal design]Array CGH containing 4,044 human bacterial artificial chromosome clones was used to assess copy number changes in 31 pairs of clinicopathologically well matched recurred / nonrecurred breast cancer tissues.; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA was extracted from each breast cancer tissue sample using the PureGene kit (Gentra Systems Inc., Minneapolis, MN, USA).', 'Channel 2 DNA was purchased from Promega Corporation: Human Genomic DNA, Female (#G1521)'; [Cell type]'Source: ''' GSE160773 Homo sapiens 23 Expression profiling by high throughput sequencing GPL24676 Bone invigorates metastatic seeding [RNA-seq] 2020-11-03 We herein examine the transciptioal alteration of a single cell derived MDA-MB-231 subline,SCP21. By retrieving tumor cells inoculated in different sites, we generated multiple mammary fat pad tumor, lung metastases or bone metastasis derived SCP21 sublines. RNA-sequencing uncovered the decreased expression of EZH2 target genes in bone metastases derived cells compared other organ entrained and parental SCP21 cells , suggesting enhanced EZH2 activity. Moreover, such phenotype is reversible upon in vitro culture. As a positive control, bone derived cells were also treated with EZH2 inhibitor, EPZ011989, to confirm the decreased level of EZH2 target genes upon EZH2 inhibition. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE160773 The bone microenvironment invigorates metastatic seeds for further dissemination. Cell 36.216 https://doi.org/10.1016/j.cell.2021.03.011 {Cell (36.216): 10.1016/j.cell.2021.03.011} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA674386 https://www.ebi.ac.uk/ena/browser/view/PRJNA674386 https://www.ncbi.nlm.nih.gov/sra?term=SRP291024 [Overal design]!0E4 SCP21 cells were implanted to mammary fat pad, lung or right hindlimb of 6 weeks old female nude mice. 4 weeks later, the tissues with tumors were dissected and subjected to tumor dissociation kit. RFP+ tumor cells were sorted by flow cytometry and culture on dishes to collect enough cells for subsequent analysis. The total RNA of SCP21 cells retrieved from different sites , and cultured in vitro for different passages, or treated with EZH2 inhibitor were sequenced, in pair-end way, using Illumina NovaSeq platform.; [Treatment]'cells were passaged every five days. For epz treatment, cells at passage 3 received a five-day treatment of 1uM ezh2 inhibitor, EPZ011989, under regular culture condition.'; [Growth]'SCP21 cells were transplanted into mammary fat pad, lung or bone via different injection routes, and inoculated in vivo for four weeks. Then the mammary fat pad tumors, lung metastases, and bone metastases were collected and subjected to tumor dissociation kit to generate single cell suspension. mRFP positive tumor cells were sorted by flow cytometry, and cultured in vitro on the petri dishes. if not specified, the total RNA subjected to sequencing was collected using TRIZOL with direct-zol RNA column purification kit from Zymo. the total RNAs were immediately shipped to Novogene, and the quality check, library preparation, and deep sequencing was performed by Novogene.'; [Extraction]"The metastatic lesions were dissected with ex vivo BLI imaging, and the uninvolved tissues were removed in the hood. The surgery tools were sterilized with a bead-sterilizer following by 70% isopropanol between different animals. The collected tissues were immediately subjected to the tumor dissociation kit and RFP positive cells were sorted and re-cultured in vitro. The total RNA were extracted using TRIZOL with directzol RNA isolation kit following the manufacturer's protocol.\nthe library construction was performed by Novogene."; [Cell type]'breast cancer''cell type: breast cancer; metastic sites: In vitro, navie parental cells; host: N.A.; mouse id: N.A.; ', 'cell type: breast cancer; metastic sites: mammary fat pad; host: Athymic Nude; mouse id: 326; ', 'cell type: breast cancer; metastic sites: mammary fat pad; host: Athymic Nude; mouse id: 327; ', 'cell type: breast cancer; metastic sites: mammary fat pad; host: Athymic Nude; mouse id: 328; ', 'cell type: breast cancer; metastic sites: lung; host: Athymic Nude; mouse id: 712; ', 'cell type: breast cancer; metastic sites: lung; host: Athymic Nude; mouse id: 713; ', 'cell type: breast cancer; metastic sites: lung; host: Athymic Nude; mouse id: 316; ', 'cell type: breast cancer; metastic sites: bone; host: Athymic Nude; mouse id: 320; ', 'cell type: breast cancer; metastic sites: bone; host: Athymic Nude; mouse id: 321; ', 'cell type: breast cancer; metastic sites: bone; host: Athymic Nude; mouse id: 322; ', 'cell type: breast cancer; metastic sites: bone; host: Athymic Nude; mouse id: 323; ' GSE162932 Homo sapiens 10 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL23227 O-GlcNAc regulates MTA1 transcriptional activity during breast cancer cells genotoxic adaptation 2020-12-09 Chromatin modifier metastatic tumor protein 1 (MTA1), closely correlated with the development and progression in breast cancer, has a fantastic role in multiple cellular processes, including gene expression and cell homeostasis. Although MTA1 is a stress-responsive gene, its role in genotoxic adaptation remains unexplored. Here, we demonstrate that O-GlcNAc modification promotes MTA1 to interact with chromatin and regulates target gene expression, contributing to breast cancer cell genotoxic adaptation. MTA1 is modified with O-GlcNAc residues at serine 237/241/246 in adriamycin adaptive breast cancer cells and that modification improves the genome-wide interactions of MTA1 with gene promotor regions by enhancing its association with nucleosome remodeling and histone deacetylation (NuRD) complex. Further, O-GlcNAc-modulated MTA1 chromatin-binding influences the specific transcriptional regulation of genes involved in the adaptation of breast cancer cells to genotoxic stress. We performed chromatin immunoprecipitation followed by sequencing (ChIP-seq) using anti-HA magnetic beads in HA-MTA1-WT or HA-MTA1-3A stably expressed MCF-7 cells. Next-generation sequencing libraries were generated and amplified for 15 cycles with BGISEQ kit. 100-300 bp DNA fragments were gel-purified and sequenced with BGISEQ-500 (BGI). Two biological replicates of the ChIP-seq were performed. We also analyzed gene expression in MTA1-WT and MTA1-3A expressed cells by RNA-seq. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE162932 None None None None None 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA683874 https://www.ebi.ac.uk/ena/browser/view/PRJNA683874 https://www.ncbi.nlm.nih.gov/sra?term=SRP297403 [Overal design]MTA1 ChIP-seq was performed in HA-MTA1-WT and HA-MTA1-3A expressed MCF-7 cells using anti-HA magnetic beads. Gene expression profiling of HA-MTA1-WT and HA-MTA1-3A expressed MCF-7 cells were performed by RNA-seq.; [Treatment]'MCF-7 cells were cultured in RPMI-1640 medium with 10% fetal calf serum. HA-tagged full-length wild type (WT) human MTA1 and O-GlcNAc amino acid sites mutant (human MTA1, Ser237/Ser241/Ser246 → Ala) MTA1 were subcloned into LvCGP04-Puro. Transfection of the MCF-7 cells was performed with Lentivirus according to the manufacturer’s instructions. The stably transfected cells were then selected by the addition of puromycin to the medium. ~2x10e7 cells were used as a unit of cells for each experiment.'; [Growth]'RPMI-1640 medium with 10% fetal calf serum.'; [Extraction]"HA-WT-MTA1 and HA-3A-MTA1 cells were maintained in RPMI-1640 medium with 10% fetal calf serum. Approximately 2 x 10e7 cells were used for ChIP-seq assay. For MTA1, HA-WT(wild type)-MTA1, or HA-3A(Ser237/Ser241/Ser246 → Ala)-MTA1 ChIP-seq, crosslinked chromatin complexes were immunoprecipitated with anti-HA-magnetic beads. For RNA-seq, total RNA was extracted from the WT-MTA1 and 3A-MTA1 cells using Trizol reagent (Invitrogen). RNA quality was checked by Agilent 2100 Bioanalyzer (Agilent Technologies, USA). RNA libraries were prepared for sequencing using standard BGI protocols.\nDNA-end repair, 3'-dA overhang and ligation of methylated sequencing adaptor. PCR amplification and size selection (usually 100-300bp, including adaptor sequence. Qualified library for sequencing. RNA-seq libraries were constructed using SMARTer cDNA library construction kit."; [Cell type]'Source: ''cell line: MCF-7; morphology type: epithelial type of breast cancer cell; chip antibody/selection: none; ', 'cell line: MCF-7; morphology type: epithelial type of breast cancer cell; chip antibody/selection: HA; ', 'cell line: MCF-7; morphology type: epithelial type of breast cancer cell; ' GSE87049 Homo sapiens 359 Expression profiling by array; Genome variation profiling by SNP array GPL6244; GPL6801 Analysis of somatic DNA copy number alterations and frequency of breast cancer intrinsic subtypes from Mexican women 2016-09-17 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE87049 None None None None None 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA343311 https://www.ebi.ac.uk/ena/browser/view/PRJNA343311 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA were extracted from the frozen tissue using the AllPrep DNA/RNA mini kit (Qiagen, Valencia, CA)', 'DNA from peripheral blood lymphocytes was extracted with the QIAamp DNA Blood Maxi Kit (Qiagen, Valencia, CA), according to manufacturer’s instructions'; [Cell type]'Source: ', 'Germinal cell fraction', 'Somatic cell fraction''molecular subtype: Luminal A; theraoy: Adjuvant; population: Mexico Hispanic; ', 'molecular subtype: Basal-like; theraoy: Adjuvant; population: Mexico Hispanic; ', 'molecular subtype: Luminal B; theraoy: Adjuvant; population: Mexico Hispanic; ', 'molecular subtype: HER2-enriched; theraoy: Adjuvant; population: Mexico Hispanic; ', 'molecular subtype: Normal-like; theraoy: Adjuvant; population: Mexico Hispanic; ', 'molecular subtype: NA; theraoy: Adjuvant; population: Mexico Hispanic; ', 'tissue: Buffy coat from peripheral blood; cell type: Germinal cell fraction; population: Mexican hispanic; ', 'tissue: Breast cancer tissue; cell type: Somatic cell fraction; population: Mexican hispanic; ' GSE163411 Homo sapiens 6 Expression profiling by high throughput sequencing GPL18573 MDA-MB-231-LM2 cells treated with sudemycin D6 (SD6) 2020-12-17 The objective is to identify gene expression patterns that occur after spliceosome inhibition in triple-negative breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE163411 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA686063 https://www.ebi.ac.uk/ena/browser/view/PRJNA686063 https://www.ncbi.nlm.nih.gov/sra?term=SRP298321 [Overal design]MDA-MB-231-LM2 cells were treated with vehicle (DMSO) or SD6 for 72 hours, in biological triplicate.; [Treatment]'Cells treated with SD6 or DMSO for 72h prior to collection in RNA lysis buffer.'; [Growth]'LM2 cells grown in media as described in manuscript.'; [Extraction]'RNA isolated using the RNeasy kit (Qiagen).\n~300 bp insert strand specific library with polyA selection (TruSeq Stranded mRNA kit, Illumina).'; [Cell type]'Source: ''cell line: MDA-MB-231-LM2; tissue: Immortalized cell line; treatment: Drug Treated; ', 'cell line: MDA-MB-231-LM2; tissue: Immortalized cell line; treatment: Vehicle Control; ' GSE165456 Mus musculus 4 Expression profiling by high throughput sequencing GPL21626 scRNAseq of MMTV-Neu primary site and lung cancer cells in early and late stage 2021-01-25 Cancer cells can disseminate from early-evolved primary lesions. It is thought that a state of early disseminated cancer cell (early DCC) dormancy would precede genetic maturation of DCCs and metastasis initiation. Here we reveal at single cell resolution a previously unrecognized role of mesenchymal- and pluripotency-like programs in coordinating early cancer cell spread and a long-lived dormancy program in early DCCs. We identify in early lesions and early DCCs, the transcription factor ZFP281 as an inducer of mesenchymal- and primed pluripotency-like programs, which is absent in advanced primary tumors and overt metastasis. ZFP281 not only controls the early spread of cancer cells but also locks early DCCs in a prolonged dormancy state by preventing the acquisition of an epithelial-like proliferative program. Thus, ZFP281-driven dormancy of early DCCs may be a rate-limiting step in metastatic progression functioning as a first barrier that DCCs must overcome to then undergo genetic maturation. This data set aims for a general characterization of the MMTV-Neu mouse model (primary site and lung DCCs) in early and late stages of cancer progression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE165456 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA694640 https://www.ebi.ac.uk/ena/browser/view/PRJNA694640 https://www.ncbi.nlm.nih.gov/sra?term=SRP303156 [Overal design]Single cell RNA profile of early and late breast cancer cells of MMTV-neu mice in the primary site (early lesions, EL; primary tumors, PT) and lungs (early lung disseminated cancer cells, eL DCCs; late lung DCCs, LL DDCs); [Treatment]'None'; [Growth]'MMTV-HER2/Neu mice were maintained on FvB background and bred and crossed in our facilities. All experimental procedures were approved by the Institutional Animal Care and Use Committee (IACUC) of Icahn School of Medicine at Mount Sinai.'; [Extraction]'Mammary glands of ‘early stage’ mice (EL), primary tumors from ‘late stage’ mice (PT) and lungs from ‘early’ and ‘late stage’ mice (eL and LL) were dissected and digested. After sorting, cancer cells (CD45- HER2+) were encapsulated using the 10X Chromium 3’ v2 and chemistry kit according to manufacturer instructions.\nSequencing, libraries were prepared according to manufacturer instructions. QC of cDNA and final libraries was performed by CyberGreen qPCR library quantification assay (KAPA). Samples were sequenced on an Illumina Nextseq 550 using the 75-cycle kit to a depth of 100 million reads per library.'; [Cell type]'Source: ''strain: FvB; age: 14-18 wk; tumor stage: No palpable tumor; tissue: lungs; cell tyoe: breast cancer cells; ', 'strain: FvB; age: >20 wk; tumor stage: With primary tumor(s); tissue: lungs; cell tyoe: breast cancer cells; ', 'strain: FvB; age: 14-18 wk; tumor stage: No palpable tumor; tissue: mammary gland; cell tyoe: breast cancer cells; ', 'strain: FvB; age: >20 wk; tumor stage: With primary tumor(s); tissue: breast tumor; cell tyoe: breast cancer cells; ' GSE119210 Mus musculus 2 Expression profiling by high throughput sequencing GPL21103 Targeting 17q23 amplicon to overcome the resistance to anti-HER2 therapy in HER2+ breast cancer 2018-08-29 Amplification of chromosome 17q23 is a frequent genomic event that occurs in ~ 11% of human breast cancers. The 17q23 amplification is enriched in HER2+ breast cancers, which is significantly correlated with poor clinical outcomes. Previous studies have identified the oncogenic phosphatase WIP1 gene in the amplicon, which functions as a master inhibitor in DNA damage response. While the possibility of any other protein-coding oncogenes in the WIP1-containing 17q23 amplicon was ruled out, our analysis of human breast cancer genomics uncovered an oncogenic microRNA gene, MIR21, in a majority of the WIP1-containing amplicons. Interestingly, DEAD-box helicase 5 (DDX5), co-amplified with WIP1 and MIR21 in the 17q23 amplicon, facilitates the essential processing of primary miR-21 transcripts. Accordingly, the 17q23 amplification results in aberrant expression of WIP1 and miR-21, which not only promotes breast tumorigenesis, but also leads to resistance to anti-HER2 therapies. Inhibiting WIP1 and miR-21 using small molecular inhibitor against WIP1 (GSK2830371) and anti-miR-21 oligonucleotides selectively inhibits the proliferation, survival and tumorigenic potential of HER2+ breast cancer cells harboring 17q23 amplification. However, the in vivo bioavailability of the two agents in their free form is poor. To overcome the resistance of trastuzumab-based therapies in vivo, we developed pH-sensitive nanoparticles for specific co-delivery of the two agents into breast tumors. The nanoparticles consist of four materials approved by the Food and Drug Administration (FDA) for medical use: Poly (d,l-lactide-co-glycolide) (PLGA), Pluronic F127 (PF127), chitosan, and 1,2-dipalmitoyl-sn-glycerol-3-phosphocholine (DPPC). Moreover, chitosan was modified with guanidine to form chitosan-guanidine (CG), which not only can improve the encapsulation efficiency of anti-miR-21 oligonucleotides but also effectively capture carbon dioxide (CO2) into the nanoparticle to achieve the ‘nano-bomb’ effect for triggered drug release under the reduced pH in tumors. The two agents (inhibitors of miR-21 and WIP1)-laden nanoparticles can be used to efficiently kill trastuzumab-resistant HER2+ breast cancer cells, leading to a profound reduction of the tumor growth in vivo. These results demonstrate the great potential of the combined treatment of WIP1 and miR-21 inhibitors for the HER2+ breast cancers resistant to anti-HER2-based therapies. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE119210 Targeting 17q23 amplicon to overcome the resistance to anti-HER2 therapy in HER2+ breast cancer. Nature communications 11.878 https://doi.org/10.1038/s41467-018-07264-0 {Nature communications (11.878): 10.1038/s41467-018-07264-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA488470 https://www.ebi.ac.uk/ena/browser/view/PRJNA488470 https://www.ncbi.nlm.nih.gov/sra?term=SRP159101 [Overal design]Primary MMTV-ErbB2 mouse mammary epithelial cells (8-wk old) were isolated as previously reported and then total mRNA was extracted using Direct-zol RNA extraction kit (duplicates, Zymo Research) and then submitted for deep sequencing. Deep sequence data were mapped, normalized and the differentially expressed genes were collected for pathway analysis.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total mRNA was extracted using Direct-zol RNA extraction kit (duplicates, Zymo Research)\nRNA libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'Source: ''mir21: WT; ', 'mir21: Knockout; ' GSE60716 synthetic construct; Homo sapiens 32 Expression profiling by array; Non-coding RNA profiling by array GPL10558; GPL18578; GPL19117 Cell-Independent MicroRNA Biogenesis 2014-08-25 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60716 Cancer exosomes perform cell-independent microRNA biogenesis and promote tumorigenesis. Cancer cell 23.916 https://doi.org/10.1016/j.ccell.2014.09.005 {Cancer cell (23.916): 10.1016/j.ccell.2014.09.005} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA259425 https://www.ebi.ac.uk/ena/browser/view/PRJNA259425 None [Overal design]Refer to individual Series; [Treatment]'Exosomes were extracted from cancer cells and added to the culture media of non-tumorigenic cells.'; [Growth]'Cells were grown for RNA as well as for extraction of exosomes for posterior RNA extraction in media with FBS depleted of exosomes.'; [Extraction]'Exosomes used for RNA extraction were resuspended in 500ul of Trizol and protocol as detailed by manufacturer. Cells were resuspended in 1000ul of Trizol and protocol as detailed by manufacturer.Cells were grown for RNA as well as for extraction of exosomes for posterior RNA extraction in media with FBS depleted of exosomes.'; [Cell type]'Breast cancer', 'breast epithelial', 'Source: ''cell line: MDA-MB-231; cell type: Breast cancer; treated with: none; ', 'cell line: MCf10A cells; cell type: breast epithelial; treated with: MDA-MB-231 exosomes; ', 'cell line: MCF10A cells; cell type: breast epithelial; treated with: none; ', 'cell line: MCF10A cells; cell type: breast epithelial; treated with: MDA-MB-231 exosomes that have a Dicer antibody inside; ', 'cell line source: MCF10A; cell/tissue type: breast epithelial cells; ', 'cell line source: MDA-MB-231; cell/tissue type: breast carcinoma cells; ', 'cell line source: MCF10A; cell/tissue type: breast epithelial exosomes; ', 'cell line source: MCF10AshDicer; cell/tissue type: breast epithelial exosomes; ', 'cell line source: MDA-MB-231; cell/tissue type: breast carcinoma exosomes; ', 'cell line source: MDA-MB-231shDicer; cell/tissue type: breast carcinoma exosomes; ', 'cell/tissue type: breast epithelial cells; ', 'cell/tissue type: cancer exosomes; ', 'cell/tissue type: normosomes; ' GSE117942 Homo sapiens 82 Expression profiling by high throughput sequencing GPL20301 RNA-seq of breast cancer cell lines post ligand treatment I 2018-07-31 Goal: study the impact of estrogen receptor ligands on gene expression in HR+ breast cancer cells Methods: RNA sequencing Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), promotes transcriptional activation of ER and mimics the transcriptional effect of natural ligand E2 for a subset of ER target genes, consistently across the seven breast cell lines (MCF-7, HCC1500, MDA-MB-330, EFM-19, T-47D, BT-474, and CAMA-1). Selective ER degraders (SERD) fulvestrant and GDC-0927 on the other hand do not induce, or induce very weakly the expression of ER target genes. The effect of GDC-0810 depends on the cellular context. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE117942 Therapeutic Ligands Antagonize Estrogen Receptor Function by Impairing Its Mobility. Cell 36.216 https://doi.org/10.1016/j.cell.2019.06.026 {Cell (36.216): 10.1016/j.cell.2019.06.026} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA483773 https://www.ebi.ac.uk/ena/browser/view/PRJNA483773 https://www.ncbi.nlm.nih.gov/sra?term=SRP155879 [Overal design]Duplicates results of RNA-Seq of seven cell lines treated with six different estrogen receptor ligands or DMSO for 24 hours; [Treatment]'Cells were treated with either 1 nM E2, or 1 M 4-OH tamoxifen, GDC-0810, fulvestrant, GNE-274 or GDC-0927 for 24 hours'; [Growth]'MCF7, HCC1500, Cama-1, MDA-MB-330, BT-474, EFM-19 and T47D cells were grown in hormone deprivation media for at least 3 days prior to treatment'; [Extraction]'Total RNA was extracted from duplicates using Qiagen RNeasy kit as per manufacturer’s protocol and quality control of RNA samples was done to determine their quantity and quality.\nApproximately 500 ng of total RNA was used as an input for library preparation using TruSeq RNA Sample Preparation Kit v2 (Illumina). In addition, RNA input of 100 ng was used for library preparation using TruSeq Stranded Total RNA Library Prep Kit (Illumina); The libraries were multiplexed and then sequenced on Illumina HiSeq4000 (Illumina) to generate 30M of single end 50 base pair reads'; [Cell type]'Source: ''cell line: MCF-7; ligand: DMSO; concentration: 0; time: 24h; ', 'cell line: MCF-7; ligand: E2; concentration: 1nM; time: 24h; ', 'cell line: MCF-7; ligand: 4-OH tamoxifen; concentration: 1uM; time: 24h; ', 'cell line: MCF-7; ligand: GDC-0810; concentration: 1uM; time: 24h; ', 'cell line: MCF-7; ligand: Fulvestrant; concentration: 1uM; time: 24h; ', 'cell line: HCC1500; ligand: DMSO; concentration: 0; time: 24h; ', 'cell line: HCC1500; ligand: E2; concentration: 1nM; time: 24h; ', 'cell line: HCC1500; ligand: 4-OH tamoxifen; concentration: 1uM; time: 24h; ', 'cell line: HCC1500; ligand: GDC-0810; concentration: 1uM; time: 24h; ', 'cell line: HCC1500; ligand: Fulvestrant; concentration: 1uM; time: 24h; ', 'cell line: MDA-MB-330; ligand: DMSO; concentration: 0; time: 24h; ', 'cell line: MDA-MB-330; ligand: E2; concentration: 1nM; time: 24h; ', 'cell line: MDA-MB-330; ligand: 4-OH tamoxifen; concentration: 1uM; time: 24h; ', 'cell line: MDA-MB-330; ligand: GDC-0810; concentration: 1uM; time: 24h; ', 'cell line: MDA-MB-330; ligand: Fulvestrant; concentration: 1uM; time: 24h; ', 'cell line: EFM-19; ligand: DMSO; concentration: 0; time: 24h; ', 'cell line: EFM-19; ligand: E2; concentration: 1nM; time: 24h; ', 'cell line: EFM-19; ligand: 4-OH tamoxifen; concentration: 1uM; time: 24h; ', 'cell line: EFM-19; ligand: GDC-0810; concentration: 1uM; time: 24h; ', 'cell line: EFM-19; ligand: Fulvestrant; concentration: 1uM; time: 24h; ', 'cell line: T-47D; ligand: DMSO; concentration: 0; time: 24h; ', 'cell line: T-47D; ligand: E2; concentration: 1nM; time: 24h; ', 'cell line: T-47D; ligand: 4-OH tamoxifen; concentration: 1uM; time: 24h; ', 'cell line: T-47D; ligand: GDC-0810; concentration: 1uM; time: 24h; ', 'cell line: T-47D; ligand: Fulvestrant; concentration: 1uM; time: 24h; ', 'cell line: BT-474; ligand: DMSO; concentration: 0; time: 24h; ', 'cell line: BT-474; ligand: E2; concentration: 1nM; time: 24h; ', 'cell line: BT-474; ligand: 4-OH tamoxifen; concentration: 1uM; time: 24h; ', 'cell line: BT-474; ligand: GDC-0810; concentration: 1uM; time: 24h; ', 'cell line: BT-474; ligand: Fulvestrant; concentration: 1uM; time: 24h; ', 'cell line: MCF-7; ligand: GDC-0927; concentration: 1uM; time: 24h; ', 'cell line: MCF-7; ligand: GNE-274; concentration: 1uM; time: 24h; ', 'cell line: HCC1500; ligand: GDC-0927; concentration: 1uM; time: 24h; ', 'cell line: HCC1500; ligand: GNE-274; concentration: 1uM; time: 24h; ', 'cell line: CAMA-1; ligand: DMSO; concentration: 0; time: 24h; ', 'cell line: CAMA-1; ligand: E2; concentration: 1nM; time: 24h; ', 'cell line: CAMA-1; ligand: 4-OH tamoxifen; concentration: 1uM; time: 24h; ', 'cell line: CAMA-1; ligand: GDC-0810; concentration: 1uM; time: 24h; ', 'cell line: CAMA-1; ligand: Fulvestrant; concentration: 1uM; time: 24h; ', 'cell line: CAMA-1; ligand: GDC-0927; concentration: 1uM; time: 24h; ', 'cell line: CAMA-1; ligand: GNE-274; concentration: 1uM; time: 24h; ' GSE74032 Homo sapiens 6 Expression profiling by array GPL17692 Estrogen receptor α promotes breast cancer by reprogramming cell metabolism [gene expression] 2015-10-14 Estrogen receptor α (ERα) is a key regulator of breast growth and breast cancer development. However, the role of ERα in metabolic reprogramming, a hallmark of cancer, is not well documented. In this study, using an integrated approach combining genome-wide mapping of chromatin bound ERα with estrogen induced transcript and metabolic profiling, we demonstrate that ERα reprograms metabolism upon estrogen stimulation, including changes in aerobic glycolysis, nucleotide and amino acid synthesis, and choline metabolism. We show, for the first time, that the ERα target gene choline phosphotransferase 1 (CHPT1) plays an essential role in estrogen induced increases in phosphatidylcholine (PtdCho) levels and that CHPT1 promotes tumorigenesis and proliferation. Furthermore, we show that CHPT1 is overexpressed in tumors compared to normal breast. We also demonstrate that ERα promotes aerobic glycolysis through increased expression of glycolytic genes. In conclusion, this study highlights the importance of ERα for metabolic alterations in breast cancer cells. Furthermore, overexpression of the ERα target CHPT1 in breast cancer supports its potential as a therapeutic target. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74032 Estrogen Receptor α Promotes Breast Cancer by Reprogramming Choline Metabolism. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-15-2910 {Cancer research (8.378): 10.1158/0008-5472.CAN-15-2910} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA298776 https://www.ebi.ac.uk/ena/browser/view/PRJNA298776 None [Overal design]Examination of E2 induced gene expression changes in T47D cells; [Treatment]'Cells were cultured in steroid depleted media for 48 h and treated with ethnaol or 10 nM 17β-estradiol for 6 h.'; [Growth]'Cells were maintained in 10% FBS containing media.'; [Extraction]'Total RNA was extracted using RNeasy Mini Kit (Qiagen, Valencia, CA).'; [Cell type]'breast cancer''cell line: T47D; cell type: breast cancer; ' GSE39130 Homo sapiens 65 Genome variation profiling by SNP array; SNP genotyping by SNP array GPL3718 Profiles of genomic instability in high-grade serous ovarian cancer (HGSC) predict treatment outcome 2012-07-05 Profiling of loss of heterozygosity (LOH) in HGSC, subcrouping HGSC by LOH-based clustering and comparing to the LOH profiles of triple-negative breast cancer [previously submitted; GSE19594]. Study for the correlation of LOH burdern and LOH-based subgroups to clinical response to platinum-based chemotherapy in patients suffered from HGSC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39130 Profiles of genomic instability in high-grade serous ovarian cancer predict treatment outcome. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-12-0857 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-12-0857} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA170063 https://www.ebi.ac.uk/ena/browser/view/PRJNA170063 None [Overal design]SNP data (Affymetrix GenChip 250K SNP Nsp) from 47 high grade serous ovarian cancer were generated and used for LOH and copy number analysis, LOH-based hierarchical clustering to subclassify HGSC, and comparison to the chromosomal alterations in high grade brest cancer. The associstion between LOH-based subgroups and LOH burden and clinical resposne to platinum-based chemotherapy was investigated. The results were validated in two independent public opening datasets.; [Treatment]'None'; [Growth]'None'; [Extraction]'DNA extracted by proteinase K disgestion-phenochloroform extraction or Qigen DNA extraction kit from ovarian cancer cells enriched from tumor tissues by needle-microdissection or from ascites by affinity enrichment with anti-EPCAM-conjugated beads.'; [Cell type]'Source: ''tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): Ascites; age: 62; residual disease: < 1cm; resistance: 0; progressed: 1; pfstx (months): 16.4; floh%: 36.9; bpm: 1; ', 'tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: III; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): Ascites; age: N/A; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 19.7; bpm: 0; ', 'tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: IV; grade: 3; grade h/l: H; primary site: ovarian; tso (tumor sample origin): Ascites; age: N/A; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 28.6; bpm: 0; ', 'tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: IV; grade: 3; grade h/l: H; primary site: peritoneal; tso (tumor sample origin): Ascites; age: N/A; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 44.7; bpm: 1; ', 'tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): Ascites; age: 52; residual disease: < 1 cm; resistance: 0; progressed: 1; pfstx (months): 9.8; floh%: 28.1; bpm: 1; ', 'tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): Ascites; age: 59; residual disease: < 1 cm; resistance: 0; progressed: 0; pfstx (months): 36; floh%: 13.0; bpm: 1; ', 'tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: N/A; grade: 3; grade h/l: H; primary site: endometrial; tso (tumor sample origin): Ascites; age: N/A; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 5.8; bpm: 0; ', 'tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: III; grade: 3; grade h/l: H; primary site: peritoneal; tso (tumor sample origin): Ascites; age: N/A; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 42.9; bpm: N/A; ', 'tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: N/A; grade: 3; grade h/l: H; primary site: ovarian; tso (tumor sample origin): Ascites; age: N/A; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 34.1; bpm: 0; ', 'tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: N/A; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): Ascites; age: N/A; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 48.3; bpm: N/A; ', 'tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: IIIC; grade: 2; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): Ascites; age: 67; residual disease: < 1 cm; resistance: 0; progressed: 1; pfstx (months): 9.2; floh%: 30.7; bpm: 0; ', 'tissue: ovarian cancer ascites; pathologic subtype: mix (S/E); Stage: III; grade: 3; grade h/l: H; primary site: ovarian; tso (tumor sample origin): Ascites; age: N/A; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 38.2; bpm: N/A; ', 'tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): Ascites; age: 54; residual disease: N/A; resistance: 1; progressed: 1; pfstx (months): 5; floh%: 6.8; bpm: 0; ', 'tissue: ovarian cancer ascites; pathologic subtype: Serous; Stage: IV; grade: 3; grade h/l: H; tso (tumor sample origin): Ascites; age: N/A; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 15.4; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Fallopian; tso (tumor sample origin): Omentum; age: 56; residual disease: < 1 cm; resistance: 0; progressed: 0; pfstx (months): 13.7; floh%: 50.6; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: III; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): L ovary; age: 43; residual disease: < 1 cm; resistance: 0; progressed: 1; pfstx (months): 17.4; floh%: 40.7; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): Omentum; age: 57; residual disease: < 1 cm; resistance: 0; progressed: 1; pfstx (months): 6.2; floh%: 14.9; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): R ovary; age: 59; residual disease: no; resistance: 0; progressed: 0; pfstx (months): 11; floh%: 41.2; bpm: 1; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Fallopian; tso (tumor sample origin): Omentum; age: 56; residual disease: < 1 cm; resistance: 0; progressed: 1; pfstx (months): 7.4; floh%: 12.3; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIB; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): L ovary; age: 82; residual disease: < 1 cm; resistance: 0; progressed: 0; pfstx (months): 9.7; floh%: 56.0; bpm: 1; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): L tube and ovary; age: 47; residual disease: < 1 cm; resistance: 0; progressed: 1; pfstx (months): 6.8; floh%: 24.6; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IV; grade: 2; grade h/l: H; primary site: Fallopian; tso (tumor sample origin): Omentum; age: 67; residual disease: < 1 cm; resistance: 0; progressed: 0; pfstx (months): 8.9; floh%: 2.1; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: mix (S/E); Stage: IV; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): R ovary; age: 60; residual disease: no; resistance: 0; progressed: 0; pfstx (months): 9.7; floh%: 9.9; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): L ovary; age: 77; residual disease: no; resistance: 0; progressed: 0; pfstx (months): 10; floh%: 9.9; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: III; grade: 3; grade h/l: H; primary site: Fallopian; tso (tumor sample origin): Omentum; age: 46; residual disease: < 1 cm; resistance: 0; progressed: 1; pfstx (months): 8.9; floh%: 12.8; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: II; grade: 3; grade h/l: H; primary site: ovarian; tso (tumor sample origin): uterus; age: 58; residual disease: no; resistance: 0; progressed: 1; pfstx (months): 15.5; floh%: 7.2; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): R ovary; age: 50; residual disease: no; resistance: 1; progressed: 1; pfstx (months): 5; floh%: 32.7; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Fallopian; tso (tumor sample origin): Omentum; age: 62; residual disease: < 1 cm; resistance: 1; progressed: 1; pfstx (months): 3.4; floh%: 21.2; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): Omentum; age: 72; residual disease: > 1 cm; resistance: 0; progressed: 1; pfstx (months): 7.4; floh%: 3.3; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIC; grade: 3; grade h/l: H; primary site: Fallopian; tso (tumor sample origin): R ovary; age: 60; residual disease: < 1 cm; resistance: 0; progressed: 0; pfstx (months): 12.9; floh%: 23.8; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): R ovary; age: 59; residual disease: < 1 cm; resistance: 1; progressed: 1; pfstx (months): 2.8; floh%: 26.6; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IC; grade: 2; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): R ovary; age: 73; residual disease: < 1 cm; resistance: 0; progressed: 0; pfstx (months): 7.2; floh%: 25.5; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIC; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): Omentum; age: 53; residual disease: < 1 cm; resistance: 0; progressed: 0; pfstx (months): 6.6; floh%: 3.6; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IIIA; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): R ovary; age: 62; residual disease: < 1 cm; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 22.0; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: IV; grade: 3; grade h/l: H; primary site: Ovarian; tso (tumor sample origin): Surface of right diaphragm; age: 69; residual disease: < 1 cm; resistance: 0; progressed: 0; pfstx (months): 2.0; floh%: 34.1; bpm: 1; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: N/A; grade: 3; grade h/l: H; primary site: Fallopian; tso (tumor sample origin): Omentum; age: 71; residual disease: < 1 cm; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 25.7; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: N/A; grade: N/A; grade h/l: H; primary site: Omentum; tso (tumor sample origin): Omentum; age: 51; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 33.9; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: N/A; grade: N/A; grade h/l: H; primary site: Omentum; tso (tumor sample origin): Omentum; age: 45; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 12.8; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: N/A; grade: N/A; grade h/l: H; primary site: Omentum; tso (tumor sample origin): Omentum; age: 67; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 17.3; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: N/A; grade: N/A; grade h/l: H; primary site: Ovary; tso (tumor sample origin): Ovary; age: 46; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 32.2; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: N/A; grade: N/A; grade h/l: H; primary site: Uterus; tso (tumor sample origin): Uterus; age: 55; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 48.9; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: N/A; grade: N/A; grade h/l: H; primary site: Ovary; tso (tumor sample origin): Ovary; age: 48; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 45.9; bpm: 1; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: N/A; grade: N/A; grade h/l: H; primary site: Omentum; tso (tumor sample origin): Omentum; age: 44; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 58.2; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: N/A; grade: N/A; grade h/l: H; primary site: Ovary; tso (tumor sample origin): Ovary; age: 65; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 22.7; bpm: 1; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: N/A; grade: N/A; grade h/l: H; primary site: Omentum; tso (tumor sample origin): Omentum; age: 60; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 18.8; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: mix (S/E); Stage: N/A; grade: N/A; grade h/l: H; primary site: Ovary; tso (tumor sample origin): Ovary; age: 80; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 42.9; bpm: 0; ', 'tissue: ovarian tumor tissue; pathologic subtype: Serous; Stage: N/A; grade: N/A; grade h/l: H; primary site: Ovary; tso (tumor sample origin): Ovary; age: 43; residual disease: N/A; resistance: N/A; progressed: N/A; pfstx (months): N/A; floh%: 37.6; bpm: 0; ', 'tissue: Blood (unpaired to tumors); ' GSE5764 Homo sapiens 30 Expression profiling by array GPL570 Analysis of microdissected invasive lobular and ductal breast carcinomas in relation to normal ductal and lobular cells 2006-09-05 The aim of our study was to identify gene expression profiles of ductal and lobular carcinomas in relation to normal ductal and lobular cells. We examined ten mastectomy specimens from postmenopausal breast cancer patients. Ductal and lobular tumor and normal cells were microdissected from cryosections. Fifty nanograms of total RNA were amplified and labeled by PCR and in vitro transcription. GCOS pairwise comparison algorithm and rank products have identified multiple genes that are differentially expressed in comparisons between ductal and lobular tumor and normal cell types. The results suggest that these genes are involved in epithelial-mesenchymal transition, TGFbeta and Wnt signaling. These changes are present in both tumor types but appear to be more prominent in lobular carcinomas. Keywords: cell type comparison https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE5764 Novel markers for differentiation of lobular and ductal invasive breast carcinomas by laser microdissection and microarray analysis. BMC cancer 2.933 https://doi.org/10.1186/1471-2407-7-55 {BMC cancer (2.933): 10.1186/1471-2407-7-55} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA97101 https://www.ebi.ac.uk/ena/browser/view/PRJNA97101 None [Overal design]Ten surgical specimens obtained by mastectomy from postmenopausal patients with invasive ductal (IDC) and lobular breast (ILC) carcinomas were investigated. Of these, 5 were IDCs and 5 were ILCs. Tumor and normal tissues from the same mammary gland were identified by an experienced pathologist, snap-frozen in liquid nitrogen and stored at -80ºC for further analysis. Microdissection, RNA isolation, amplification, labeling and microarray analysis are described in sample definitions. Samples from particular cell types (normal ductal, normal lobular, tumor ductal, tumor lobular - 10, 10, 5, 5 samples, respectively) were considered as biological replicates and were compared in between.; [Treatment]'None'; [Growth]'None'; [Extraction]'At least 1000 normal ductal cells were microdissected from cryosections using the VeritasTM Laser Capture Microdissection System (Arcturus Bioscience, Inc., USA) according to standard protocols. Caps with captured cells were directly placed in 100 ul lysis buffer (Qiagen, Hilden, Germany). Total cellular RNA was isolated (RNeasy® Micro Kit, Qiagen) according to manufacturer´s recommendations and subsequently quantified on a Nanodrop spectrophotometer (Nanodrop Technologies, Wilmington, DE, USA).'; [Cell type]'Source: ''' GSE101333 Mus musculus 6 Non-coding RNA profiling by high throughput sequencing GPL13112; GPL17021; GPL23703; GPL23704 Small RNA profiling in mouse mammary tumor virus (MMTV) infected cell cultures and induced mammary tumors 2017-07-12 Mouse mammary tumor virus (MMTV) is a complex retrovirus that induces breast cancer in mice in the absence of known virally-encoded oncogenes. Like other non-acute retroviruses, tumorigenesis by MMTV is thought to occur primarily through insertional mutagenesis, leading to the activation of cellular proto-oncogenes and outgrowth of selected cells. In this study, we investigated whether MMTV encodes microRNAs (miRNAs) and/or modulates host miRNAs that could contribute to tumorigenesis. We have applied high throughput small RNA sequencing to the analysis of MMTV-infected cells and MMTV-induced mammary tumors. Our results demonstrate that MMTV does not encode miRNAs. However, MMTV infected cells and MMTV-producing tumors have altered levels of several cellular miRNAs, including increases in the expression of members of the oncogenic miRNA cluster, miR-17-92. Notably, similar changes in levels of these miRNAs have been previously reported in human breast cancers. Combined, our results demonstrate that virally encoded miRNAs do not contribute to MMTV-mediated tumorigenesis, but that changes in specific host miRNAs in infected cells may contribute to virus replication and tumor biology. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE101333 MMTV does not encode viral microRNAs but alters the levels of cancer-associated host microRNAs. Virology 2.657 https://doi.org/10.1016/j.virol.2017.09.030 {Virology (2.657): 10.1016/j.virol.2017.09.030} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA394002 https://www.ebi.ac.uk/ena/browser/view/PRJNA394002 https://www.ncbi.nlm.nih.gov/sra?term=SRP111722 [Overal design]Six samples each, 2 cell lines, 2 glands, and 2 tumors.; [Treatment]'None'; [Growth]'None'; [Extraction]'Trizol\nTruSeq Small RNA Library Prep Kit'; [Cell type]'Source: ''strain: BALB/c; cell line: HC11; tissue: cell line; infection: uninfection; ', 'strain: BALB/c, C3H-MMTV; cell line: HC11; tissue: cell line; infection: C3H-MMTV; ', 'strain: BALB/c; tissue: gland; infection: uninfection; ', 'strain: BALB/c, HYB-MTV; tissue: tumor; infection: HYB-MTV; ' GSE55005 Homo sapiens 6 Expression profiling by high throughput sequencing GPL11154 mRNA profiling reveals determinants of trastuzumab efficiency in HER2-positive breast cancer 2014-02-13 The intention was to detect genes that are determining trastuzumab efficiency in HER2-positive breast cancer cell lines with different resistance phenotypes. While BT474 should be sensitive to the drug treatment, HCC1954 is expected to be resistant due to a PI3K mutation. The cell line BTR50 has been derived from BT474 and was cultured to be resistant as well. Based on RNA-Seq data, we performed differential expression analyses on these breast cancer cell lines with and without trastuzumab treatment. In detail, five separate tests were performed, namely resistant cells vs. wild type, i.e. HCC1954 and BTR50 vs. BT474, respectively, and untreated vs. drug treated cells. The significant genes of the first two tests should contribute to resistance. The significant genes of the test BT474 vs. its drug treated version should contribute to the trastuzumab effect. To exclude false positives from the combined gene set (#64), we removed ten genes that were also significant in the test BTR50 vs. its drug treated version. This way we ended up with 54 genes that are very likely to determine trastuzumab efficiency in HER2-positive breast cancer cell lines. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55005 mRNA profiling reveals determinants of trastuzumab efficiency in HER2-positive breast cancer. PloS one 2.776 https://doi.org/10.1371/journal.pone.0117818 {PloS one (2.776): 10.1371/journal.pone.0117818} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA238231 https://www.ebi.ac.uk/ena/browser/view/PRJNA238231 https://www.ncbi.nlm.nih.gov/sra?term=SRP037775 [Overal design]mRNA profiles of human breast cancer cell lines were generated by deep sequencing using Illumina HiSeq 2000. The cell lines BT474 and HCC1954 were analyzed with and without trastuzumab treatment. HCC1954 is known to be trastuzumab resistant. Additionally, the cell line BTR50 was generated as resistant version of BT474, and was analyzed with and without trastuzumab as well.; [Treatment]'For treatment experiments, 2x105 cells were seeded in T25 flasks and cultivated as recommended by ATCC.\nCells were treated with 20 μg/ml trastuzumab (Roche Diagnostics GmbH, Penzberg, Germany) or grown in full growth media without inhibitors.\nCell pellets were harvested after 72 h. The cells were incubated in the standard media 24 h before addition of trastuzumab or fresh full growth media.\nResistant cells (BTR50) were developed by culturing parental cells (BT474) in the presence of 20/50 µg trastuzumab (Roche) for around six month.\nParental cells were cultured in parallel to resistant ones without addition of trastuzumab.'; [Growth]"The cells were grown in a monolayer and collected as a cell pellet after trypsin treatment. RNA was harvested from cell pellet using the miRNeasy kit (Qiagen).\nThe human breast cancer cell lines BT474 and HCC1954 were obtained from the American Type Culture Collection (ATCC). The BT474 was cultured in Dulbecco's Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum, 0.01 mg/ml of insulin and 1% penicillin/streptomycin.\nThe human breast cancer cell line HCC1954 was cultured in RPMI media (Gibco) supplemented with 10% fetal bovine serum (Gibco). The medium was supplemented with 1% penicillin/streptomycin (Gibco).\nThe cells were cultured at 37°C in an atmosphere containing 5% CO2. Cells were harvested with trypsin-ethylenediamine tetraacetic acid (EDTA) (0.5 g/L trypsin; 0.2 g/L EDTA; Sigma)."; [Extraction]"Total RNA was isolated from cell lines BT474, BTR50 and HCC1954 using the Trizol (Invitrogen) method according to the manufacturer's recommendations.\nAfterwards, the samples were DNAse I (Sigma) treated in order to remove DNA contamination.\nRNA quality was determined using the Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA, USA) microfluidic electrophoresis.\nOnly samples with comparable RNA integrity numbers were selected for deep sequencing.\nLibrary preparation for RNA-Seq was performed using the TruSeq RNA Sample Preparation Kit (Illumina, Cat. N°RS-122-2002) starting from 800 ng of total RNA.\nAccurate quantitation of cDNA libraries was performed by using the QuantiFluor™ dsDNA System (Promega).\nThe size range of final cDNA libraries was determined applying the DNA 1000 chip on the Bioanalyzer 2100 from Agilent (280 bp).\ncDNA libraries were amplified and sequenced by using the cBot and HiSeq 2000 from Illumina (SR; 1x51 bp; 6 GB ca. 30-35 million reads per sample)."; [Cell type]'HER2-positive breast cancer''cell line: BT474; drug treatment: no drug; cell type: HER2-positive breast cancer; resistance: no trastuzumab resistance; ', 'cell line: BT474; drug treatment: trastuzumab; cell type: HER2-positive breast cancer; resistance: no trastuzumab resistance; ', 'cell line: HCC1954; drug treatment: no drug; cell type: HER2-positive breast cancer; resistance: trastuzumab resistance; ', 'cell line: HCC1954; drug treatment: trastuzumab; cell type: HER2-positive breast cancer; resistance: trastuzumab resistance; ', 'cell line: BTR50; drug treatment: no drug; cell type: HER2-positive breast cancer; resistance: induced trastuzumab resistance; ', 'cell line: BTR50; drug treatment: trastuzumab; cell type: HER2-positive breast cancer; resistance: induced trastuzumab resistance; ' GSE129915 Homo sapiens 15 Expression profiling by high throughput sequencing GPL11154 HMGA1 and FOXM1 synergistically regulate a common gene network modulating angiogenesis in breast cancer 2019-04-16 One of the factors involved in TNBC aggressiveness is HMGA1, a member of non-histone chromatin proteins. The High mobility group A1 is an architectural transcription factor which, by altering chromatin structure and interacting with transcription factors, can regulate the transcription of several genes. HMGA1 protein is defined as an oncofetal protein as it is highly expressed during the embryogenesis while its expression decreases or is absent in adults, and it is re-expressed in a variety of tumors, including breast cancer. Several works established that, in breast cancer, HMGA1 expression is correlated with high tumor grade and tumor metastasis, resistance to therapies and poor prognosis. The goal of this project is to find out in details, which are the genes that are modulated by HMGA1 in MDA-MB-231 triple negative breast cancer cell line model. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE129915 HMGA1 promotes breast cancer angiogenesis supporting the stability, nuclear localization and transcriptional activity of FOXM1. Journal of experimental & clinical cancer research : CR 5.646 https://doi.org/10.1186/s13046-019-1307-8 {Journal of experimental & clinical cancer research : CR (5.646): 10.1186/s13046-019-1307-8} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA533135 https://www.ebi.ac.uk/ena/browser/view/PRJNA533135 https://www.ncbi.nlm.nih.gov/sra?term=SRP192772 [Overal design]In order to identify the HMGA1-molecular partners involved in developing TNBC aggressiveness, we performed RNA sequencing analysis (RNA-Seq), on the MDA-MB-231 triple-negative cell line at 24 and 72 hours after HMGA1 silencing, looking for transcription factors as putative upstream regulators of HMGA1-gene networks.; [Treatment]'LipofectamineTM RNAiMAX reagent (Thermo Fisher Scientific) was used for transfection of 30 pmol of siRNA/35-mm dish, following the manufacturer instructions.'; [Growth]'MDA-MB-231 cell lines were routinely grown in high glucose DMEM, with 10% tetracycline-free FBS, 2mM L-Glutamine, 100 U/ml Penicillin and 100 µg/ml Streptomycin (Euroclone).'; [Extraction]'RNA extracts were collected at 24 and 72 hours after the silencing. Total RNA was isolated following the manufacturer’s instructions of the TRIzol reagent (Thermo Fisher Scientific), subjected to DNase-I (Thermo Fisher Scientific) treatment and subsequently purified using phenol-chloroform.\nLibraries were constructed with the Illumina TruSeq RNA kits pair reads.'; [Cell type]'Source: ''cell line: MDA-MB-231; treatment: No treatment; time: 0 Hours; ', 'cell line: MDA-MB-231; treatment: siHMGA1; time: 24 Hours; ', 'cell line: MDA-MB-231; treatment: siCTRL; time: 24 Hours; ', 'cell line: MDA-MB-231; treatment: siHMGA1; time: 72 Hours; ', 'cell line: MDA-MB-231; treatment: siCTRL; time: 72 Hours; ' GSE55374 Homo sapiens 36 Expression profiling by array GPL10558 Molecular changes in lobular breast cancers in response to endocrine therapy 2014-02-26 Invasive lobular cancer (ILC) accounts for approximately 10-15% of breast carcinomas and although it responds poorly to neoadjuvant chemotherapy, it appears to respond well to endocrine therapy. Pre- and on-treatment (after 2 weeks and 3 months) biopsies and surgical samples were obtained from 14 post-menopausal women with ER+ histologically confirmed ILC who responded to 3 months of neoadjuvant letrozole and were compared with a cohort of 14 responding infiltrating ductal carcinomas (IDCs) matched on clinicopathological features by gene expression profiling. Dynamic clinical response was assessed using periodic 3D ultrasound measurements performed during treatment and defined as a reduction of >70% in tumour volume by 3 months. The changes in gene expression in response to letrozole were highly consistent between responding ILC and IDC tumours, genes involved in proliferation were down-regulated and those involved with immune function and ECM remodelling were up-regulated. However, molecular differences between the histological subtypes were maintained upon treatment. This is the first study of molecular changes in ILC in response to endocrine therapy to date. The genes which change on letrozole are highly consistent between ILC and IDC. Differences in gene expression between ILC and IDC at diagnosis and are maintained at each time point on treatment. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE55374 Molecular changes in lobular breast cancers in response to endocrine therapy. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-14-0620 {Cancer research (8.378) doi:10.1158/0008-5472.CAN-14-0620}; {Journal of clinical oncology : official journal of the American Society of Clinical Oncology (None) doi:10.1200/JCO.2014.57.8963}; 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA239428 https://www.ebi.ac.uk/ena/browser/view/PRJNA239428 None [Overal design]14 Pre treatment, 10 two week and 14 three month on-treatment ILC and 14 Pre treatment, 14 two week and 14 three month on-treatment IDC samples from the same patients. Pre- and on-treatment samples from 7ILC & 6IDC patients were profiled on Illumina HT-12v4 (GPL10558) and samples from 7ILC and 8 IDC patients were profiled previously on Affymetrix U133A (GPL96) see GSE20181; [Treatment]'Patients were treated within a neoadjuvant protocol in which letrozole (Femara, 2.5mg; Novartis Pharma AG, Basel, Switzerland) was given daily'; [Growth]'Tumour biopsies were taken with a 14-guage needle before and approximately 2 weeks and 3 months following commencement of continuous letrozole treatment. Samples were snap-frozen in liquid nitrogen and frozen sections taken, stained with haematoxylin and eosin (H&E) and the cellularity and percentage presence of cancerous tissue within each specimen was assessed by a pathologist.'; [Extraction]'Biopsies were homogenised and RNA was extracted using the RNeasy Mini Kit with RNAse-free DNAse treatment (Qiagen). RNA quantity and quality was verified on a Bioanalyser 2100 with RNA 6000 Nano Kit (Agilent) and Nanodrop 2000c (Thermo Scientific).'; [Cell type]'Source: ''subject: patient 182; tissue: breat tumor ILC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 289; tissue: breat tumor ILC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 299; tissue: breat tumor ILC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 309; tissue: breat tumor ILC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 325; tissue: breat tumor ILC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 343; tissue: breat tumor ILC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 374; tissue: breat tumor ILC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 200; tissue: breat tumor IDC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 209; tissue: breat tumor IDC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 291; tissue: breat tumor IDC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 322; tissue: breat tumor IDC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 334; tissue: breat tumor IDC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 350; tissue: breat tumor IDC; treatment: pre-treatment; gender: Female; clinical response: Responder; ', 'subject: patient 299; tissue: breat tumor ILC; treatment: 2 wk endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 309; tissue: breat tumor ILC; treatment: 2 wk endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 343; tissue: breat tumor ILC; treatment: 2 wk endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 374; tissue: breat tumor ILC; treatment: 2 wk endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 200; tissue: breat tumor IDC; treatment: 2 wk endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 209; tissue: breat tumor IDC; treatment: 2 wk endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 291; tissue: breat tumor IDC; treatment: 2 wk endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 322; tissue: breat tumor IDC; treatment: 2 wk endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 334; tissue: breat tumor IDC; treatment: 2 wk endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 350; tissue: breat tumor IDC; treatment: 2 wk endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 182; tissue: breat tumor ILC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 289; tissue: breat tumor ILC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 299; tissue: breat tumor ILC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 309; tissue: breat tumor ILC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 325; tissue: breat tumor ILC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 343; tissue: breat tumor ILC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 374; tissue: breat tumor ILC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 200; tissue: breat tumor IDC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 209; tissue: breat tumor IDC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 291; tissue: breat tumor IDC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 322; tissue: breat tumor IDC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 334; tissue: breat tumor IDC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ', 'subject: patient 350; tissue: breat tumor IDC; treatment: 3 mo endocrine therapy; gender: Female; clinical response: Responder; ' GSE103624 Mus musculus 25 Other GPL16417 BRCA1 suppresses microhomology-mediated tandem duplications at Tus/Ter-stalled replication forks 2017-09-08 Small ~10 kb microhomology-mediated tandem duplications (“Group 1 TDs”) are abundant in BRCA1-linked but not BRCA2-linked breast cancer genomes. Here, we define the mechanism underlying this rearrangement signature. We show that BRCA1, but not BRCA2, suppresses TDs at a Tus/Ter site-specific chromosomal replication fork barrier in primary mammalian cells. BRCA1 has no equivalent role at chromosomal double strand breaks, indicating specificity for the stalled fork response. Two motor proteins—FANCM and the Bloom’s syndrome helicase—suppress Tus/Ter-induced TDs in BRCA1 mutants, revealing the existence of a multi-gene TD suppressor network. TDs arise by a “replication restart-bypass” mechanism terminated by end joining or microhomology-mediated template switching, the latter forming complex TD breakpoints. We show that solitary DNA ends form directly at Tus/Ter, implicating misrepair of these lesions in TD formation. We find that BRCA1 inactivation is strongly associated with Group 1 TDs in ovarian cancer. The Group 1 TD phenotype may be a general signature of BRCA1-deficient cancer https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE103624 Mechanism of tandem duplication formation in BRCA1-mutant cells. Nature 43.070 https://doi.org/10.1038/nature24477 {Nature (43.070): 10.1038/nature24477} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA403795 https://www.ebi.ac.uk/ena/browser/view/PRJNA403795 https://www.ncbi.nlm.nih.gov/sra?term=SRP117142 [Overal design]LAM-HTGTS from a Cas9/gRNA bait DSB 30kb away from the 1xGFP Ter array cassette inserted in the ROSA26 locus; [Treatment]'Genomic DNA was collected 48 hours after delivery of nuclease'; [Growth]'None'; [Extraction]'DNA was extracted overnight at 55degC in a lysis buffer containing: 200mM NaCl, 0.4% SDS, 100mM Tris-HCl pH7.5, 5mM EDTA pH8.0, 200ug/mL proteinase K, prior to DNA fragmentation\nLibraries were generated as described in Hu et al., 2016 Nature Protocols (PMC4895203) using RAG1 primers described in Frock et al., 2015 Nature Biotechnology (PMC4320661) and Illumina Miseq sequencing'; [Cell type]'Source: ''genotype: BRCA1del/exon11; sirna: FANCM; reporter: 4kb 1xGFP cassette in ROSA26; nuclease delivery: Transfection; Tus/nuclease/siRNA; treatment protocol: 48 hour culture post transfection; bait dsb: Cas9/US30kb_ROSA26 gRNA; growth protocol: MEF feeder; ES medium; extract_protocol (dna fragmentation/blocking methods): Sonication/ XbaI blocking; ', 'genotype: BRCA1del/exon11; sirna: BLM; reporter: 4kb 1xGFP cassette in ROSA26; nuclease delivery: Transfection; Tus/nuclease/siRNA; treatment protocol: 48 hour culture post transfection; bait dsb: Cas9/US30kb_ROSA26 gRNA; growth protocol: MEF feeder; ES medium; extract_protocol (dna fragmentation/blocking methods): Sonication/ XbaI blocking; ', 'genotype: BRCA1del/exon11; sirna: BRCA1; reporter: 4kb 1xGFP cassette in ROSA26; nuclease delivery: Transfection; Tus/nuclease/siRNA; treatment protocol: 48 hour culture post transfection; bait dsb: Cas9/US30kb_ROSA26 gRNA; growth protocol: MEF feeder; ES medium; extract_protocol (dna fragmentation/blocking methods): Sonication/ XbaI blocking; ', 'genotype: BRCA1del/exon11; sirna: Luciferase; reporter: 4kb 1xGFP cassette in ROSA26; nuclease delivery: Transfection; Tus/nuclease/siRNA; treatment protocol: 48 hour culture post transfection; bait dsb: Cas9/US30kb_ROSA26 gRNA; growth protocol: MEF feeder; ES medium; extract_protocol (dna fragmentation/blocking methods): Sonication/ XbaI blocking; ', 'genotype: BRCA1flox/exon11; sirna: BLM; reporter: 4kb 1xGFP cassette in ROSA26; nuclease delivery: Transfection; Tus/nuclease/siRNA; treatment protocol: 48 hour culture post transfection; bait dsb: Cas9/US30kb_ROSA26 gRNA; growth protocol: MEF feeder; ES medium; extract_protocol (dna fragmentation/blocking methods): Sonication/ XbaI blocking; ', 'genotype: BRCA1flox/exon11; sirna: BRCA1; reporter: 4kb 1xGFP cassette in ROSA26; nuclease delivery: Transfection; Tus/nuclease/siRNA; treatment protocol: 48 hour culture post transfection; bait dsb: Cas9/US30kb_ROSA26 gRNA; growth protocol: MEF feeder; ES medium; extract_protocol (dna fragmentation/blocking methods): Sonication/ XbaI blocking; ', 'genotype: BRCA1flox/exon11; sirna: FANCM; reporter: 4kb 1xGFP cassette in ROSA26; nuclease delivery: Transfection; Tus/nuclease/siRNA; treatment protocol: 48 hour culture post transfection; bait dsb: Cas9/US30kb_ROSA26 gRNA; growth protocol: MEF feeder; ES medium; extract_protocol (dna fragmentation/blocking methods): Sonication/ XbaI blocking; ', 'genotype: BRCA1flox/exon11; sirna: Luciferase; reporter: 4kb 1xGFP cassette in ROSA26; nuclease delivery: Transfection; Tus/nuclease/siRNA; treatment protocol: 48 hour culture post transfection; bait dsb: Cas9/US30kb_ROSA26 gRNA; growth protocol: MEF feeder; ES medium; extract_protocol (dna fragmentation/blocking methods): Sonication/ XbaI blocking; ' GSE47371 Homo sapiens 6 Expression profiling by array GPL10332 WWOX interacts with SMAD3 and modulates its transcriptional activity in breast cells 2013-05-24 WWOX expression is lost during tumor progression in many human malignancies including breast cancer. To understand the effects of loss of WWOX expression we analyzed the consequences of its silencing in normal human breast cells (MCF10F). WWOX silencing led to the formation of larger cell colonies, increased cell motility and decreased cell attachment. WWOX silenced cells demonstrated deregulated expression on genes involved in cell cycle, DNA damage response and cell motility. We detected an enrichment of targets activated by the SMAD3 transcription factor. Most notably expression of ANGPTL4, FST, PTHLH and SERPINE1 were all significantly increased upon WWOX silencing. Upregulation of these genes can be reversed by re-expressing WWOX in the previously silenced cells thus suggesting an inverse correlation between WWOX protein expression and SMAD3 transcriptional activity. Importantly, we demonstrate that WWOX physically interacts with SMAD3 protein via WW domain 1, that WWOX expression dramatically decreases SMAD3 occupancy at the ANGPTL4 and SERPINE1 promoters and significantly quenches activation of a TGFβ responsive reporter (3TP-LUX). Furthermore, WWOX expression leads to intracellular redistribution of SMAD3 protein levels redirecting protein availability from the nuclear to the cytoplasmic compartment. Interestingly, meta-analysis of gene expression breast cancer datasets indicate that WWOX and ANGPTL4 expression, encoding a secreted protein of key relevance in breast cancer lung metastatic cells, are inversely correlated and the WWOXlo/ANGPTL4hi cluster of tumors are enriched in triple-negative and basal-like sub-types. In summary, we demonstrate that WWOX modulates SMAD3 signaling in breast cells via direct WW-domain binding and potential cytoplasmic sequestration of SMAD3 protein. Since loss of WWOX expression increases with breast cancer progression and it behaves as an inhibitor of SMAD3 transcriptional activity these observations may help explain, at least in part, the paradoxical pro-tumorigenic effects of TGFβ signaling in advanced breast cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE47371 The cancer gene WWOX behaves as an inhibitor of SMAD3 transcriptional activity via direct binding. BMC cancer 2.933 https://doi.org/10.1186/1471-2407-13-593 {BMC cancer (2.933): 10.1186/1471-2407-13-593} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA205321 https://www.ebi.ac.uk/ena/browser/view/PRJNA205321 None [Overal design]We compared two independent shRNAs: shWWOX-A and shWWOX-B with 3 biological replicates each one, targeting different regions of the WWOX transcript as a means of ruling out any potential off-target effects.; [Treatment]'Cells were infected with the following shRNA-expressing GIPZ lentiviruses (Open Biosystems) at an MOI of 5: Scrambled control shRNA (#RHS4348), shWWOX-A (#V2LHS_255213 ) or shWWOX-B (#V2LHS_255229). Co-infection of shWWOX-A and shWWOX-B was indicated as “shWWOX”. Cells were infected according to manufacturer’s instructions. Cells were selected for three days with 2 μg/ml puromycin and WWOX protein level was assayed by western blot.'; [Growth]'MCF10 cells were cultured in DMEM/F12 supplemented with 5% fetal bovine serum, 100 μg/mL hydrocortisone, 10 μg/mL insulin, 20 ng/mL EGF, 1 ng/mL cholera toxin and 1% penicillin-streptomycin.'; [Extraction]'Total RNA was extracted from 3 biological replicates each of MCF10 Scr, MCF10 shWWOX-A and MCF10 shWWOX-B using the RNeasy Mini kit (Qiagen).'; [Cell type]'Source: ''cell line: MCF10F mammary epithelial cells; treatment: WWOX–silenced subline A; ', 'cell line: MCF10F mammary epithelial cells; treatment: scrambled control shRNA; ', 'cell line: MCF10F mammary epithelial cells; treatment: WWOX–silenced subline B; ' GSE29117 Mus musculus 28 Expression profiling by array GPL13502 Mammary carcinomas in WAP-SV40 transgenic mice [gene expression] 2011-05-06 Transgenic expression in mice of two synergistically acting SV40 early region encoded proteins, large (LT) and small (sT) tumor antigens, in the mammary epithelium recapitulates loss of p53 and Rb function and deregulation of PP2A-controlled mitogenic pathways in human breast cancer. In primiparous mice, WAP-promoter driven expression of SV40 proteins induces well and poorly differentiated mammary adenocarcinomas. We performed a correlative aCGH and gene expression analysis of 25 monofocal tumors, representing four histopathological grades, to explore the molecular traits of SV40-induced mammary tumors and to emphasize the relevance of this tumor model for human breast tumorigenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE29117 Low-grade and high-grade mammary carcinomas in WAP-T transgenic mice are independent entities distinguished by Met expression. International journal of cancer 4.982 https://doi.org/10.1002/ijc.27783 {International journal of cancer (4.982): 10.1002/ijc.27783} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA153973 https://www.ebi.ac.uk/ena/browser/view/PRJNA153973 None [Overal design]Gene expression analysis of 25 mammary carcinoma samples of two different WAP-SV40 mouse lines, T1 and NP8. Three involuted mammary gland tissues were included in the study as reference samples.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted using Trizol Reagent (Invitrogen) followed by DNA digestion (TURBO DNA-free; Ambion) according to the manufacturer’s instructions. Total RNA from tumor samples and normal mammary gland was cleaned up using RNeasy mini kit according to the manufacturer’s instructions (Qiagen).'; [Cell type]'Source: ''tumor: WAP-NP8 Mouse Mammary Carcinoma; strain: Balb/c; tumour grade: Grade 1; ', 'tumor: WAP-NP8 Mouse Mammary Carcinoma; strain: Balb/c; tumour grade: Grade 2; ', 'tumor: WAP-NP8 Mouse Mammary Carcinoma; strain: Balb/c; tumour grade: Grade 3; ', 'tumor: WAP-NP8 Mouse Mammary Carcinoma; strain: Balb/c; tumour grade: Grade 4; ', 'tumor: WAP-T1 Mouse Mammary Carcinoma; strain: Balb/c; tumour grade: Grade 3; ', 'tumor: WAP-T1 Mouse Mammary Carcinoma; strain: Balb/c; tumour grade: Grade 1; ', 'tumor: WAP-T1 Mouse Mammary Carcinoma; strain: Balb/c; tumour grade: Grade 2; ', 'tumor: WAP-T1 Mouse Mammary Carcinoma; strain: Balb/c; tumour grade: Grade 4; ', 'tissue: normal mammary gland; strain: BALB/c; tumour grade: Reference Tissue; ' GSE54331 Homo sapiens 371 Expression profiling by array GPL18189; GPL18190 Interleukin-6 is a Potential Therapeutic Target in Interleukin-6 Dependent Estrogen Receptor-alpha Positive Breast Cancer 2014-01-23 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54331 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA236212 https://www.ebi.ac.uk/ena/browser/view/PRJNA236212 None [Overal design]Refer to individual Series; [Treatment]'After establishment, the cells were grown in triplicate for 6 days in the absence or presence of 10 ng/ml IL-6, which was added on day 1. Sampling was performed on days 4, 5, and 6. Five additional conditions were investigated in duplicate: (i) 10 ng/ml IL-6 added on day 0 + 50 μg/ml siltuximab added on day 1 (ii) 10 ng/ml IL-6 added on day 1 + 50 μg/ml siltuximab added on day 1 (iii) 50 μg/ml siltuximab added on day 0 (iv) human marrow stromal cell-conditioned media (hMSC-CM) (v) hMSC-CM + 50 μg/ml siltuximab.'; [Growth]'Ten ERα-positive breast cancer cell lines, T47D, MDA-MB-134VI, BT474, BT-483, HCC1428, EFM-19, MCF-7, MDA-MB-175-VIIdsRed, MDA-MB-415 and ZR-751, were grown in TME-aligned 3D culture.'; [Extraction]'After culturing, the media overlay was removed by aspiration and 150 μl Qiazol (Qiagen) immediately added to the cells plus BME to achieve lysis. This mixture was combined with an additional 600 μl Qiazol and stored at -80 °C until RNA isolation. RNA isolation was performed using the miRNeasy 96 Kit (Qiagen). The RNA concentration of all the samples was determined on a Nanodrop-8000 UV-Vis Spectrophotometer (Thermo Scientific).', 'From each block four slices of 10 µm each were cut and transferred to a 1.5 ml Eppendorf tube. Paraffin was removed using Deparaffinization Solution (Qiagen). The tissue was then lyzed in proteinase K digestion (PKD) buffer (Qiagen). RNA isolation was continued using the RNeasy FFPE kit (Qiagen) according to the manufacturer’s instructions. The RNA concentration of all the samples was determined on a Nanodrop-8000 UV-Vis Spectrophotometer (Thermo Scientific). For a selection of samples, the RNA quality was determined with the RNA 6000 Nano LabChip on an Agilent 2100 Bioanalyzer (Agilent Technologies, Inc., Santa Clara, CA, USA) according to the manufacturer’s instructions. SenseRNA was generated from 200 ng of total RNA using the Sensation RNA Amplification Kit (Genisphere, Hatfield, PA, USA).'; [Cell type]'ERα-positive breast cancer cell line', 'Source: ''cell line: T47D; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 1; ', 'cell line: T47D; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 4; ', 'cell line: T47D; cell type: ERα-positive breast cancer cell line; treatment: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: T47D; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 4; ', 'cell line: T47D; cell type: ERα-positive breast cancer cell line; treatment: D0: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: T47D; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: T47D; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM; time point (day): 4; ', 'cell line: T47D; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM + 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: T47D; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 5; ', 'cell line: T47D; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 5; ', 'cell line: T47D; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 6; ', 'cell line: T47D; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 6; ', 'cell line: MDA-MB-134VI; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 1; ', 'cell line: MDA-MB-134VI; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 4; ', 'cell line: MDA-MB-134VI; cell type: ERα-positive breast cancer cell line; treatment: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MDA-MB-134VI; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 4; ', 'cell line: MDA-MB-134VI; cell type: ERα-positive breast cancer cell line; treatment: D0: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MDA-MB-134VI; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MDA-MB-134VI; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM; time point (day): 4; ', 'cell line: MDA-MB-134VI; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM + 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MDA-MB-134VI; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 5; ', 'cell line: MDA-MB-134VI; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 5; ', 'cell line: MDA-MB-134VI; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 6; ', 'cell line: MDA-MB-134VI; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 6; ', 'cell line: BT474; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 1; ', 'cell line: BT474; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 4; ', 'cell line: BT474; cell type: ERα-positive breast cancer cell line; treatment: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: BT474; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 4; ', 'cell line: BT474; cell type: ERα-positive breast cancer cell line; treatment: D0: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: BT474; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: BT474; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM; time point (day): 4; ', 'cell line: BT474; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM + 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: BT474; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 5; ', 'cell line: BT474; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 5; ', 'cell line: BT474; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 6; ', 'cell line: BT474; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 6; ', 'cell line: BT-483; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 1; ', 'cell line: BT-483; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 4; ', 'cell line: BT-483; cell type: ERα-positive breast cancer cell line; treatment: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: BT-483; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 4; ', 'cell line: BT-483; cell type: ERα-positive breast cancer cell line; treatment: D0: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: BT-483; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: BT-483; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM; time point (day): 4; ', 'cell line: BT-483; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM + 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: BT-483; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 5; ', 'cell line: BT-483; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 5; ', 'cell line: BT-483; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 6; ', 'cell line: BT-483; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 6; ', 'cell line: HCC1428; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 1; ', 'cell line: HCC1428; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 4; ', 'cell line: HCC1428; cell type: ERα-positive breast cancer cell line; treatment: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: HCC1428; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 4; ', 'cell line: HCC1428; cell type: ERα-positive breast cancer cell line; treatment: D0: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: HCC1428; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: HCC1428; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM; time point (day): 4; ', 'cell line: HCC1428; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM + 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: HCC1428; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 5; ', 'cell line: HCC1428; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 5; ', 'cell line: HCC1428; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 6; ', 'cell line: HCC1428; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 6; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 0; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 1; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 4; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 4; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: D0: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM; time point (day): 4; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM + 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 5; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 5; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 6; ', 'cell line: EFM-19; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 6; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 0; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 1; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 4; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 4; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: D0: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM; time point (day): 4; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM + 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 5; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 5; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 6; ', 'cell line: MCF-7; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 6; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 0; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 1; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 4; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 4; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: D0: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM; time point (day): 4; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM + 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 5; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 5; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 6; ', 'cell line: MDA-MB-175-VIIdsRed; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 6; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 0; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 1; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 4; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 4; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: D0: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM; time point (day): 4; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM + 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 5; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 5; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 6; ', 'cell line: MDA-MB-415; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 6; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 0; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 1; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 4; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 4; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: D0: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6 + D1: 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM; time point (day): 4; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: hMSC-CM + 50 ug/mL Siltuximab; time point (day): 4; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 5; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 5; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: untreated; time point (day): 6; ', 'cell line: ZR-751; cell type: ERα-positive breast cancer cell line; treatment: D1: 10 ng/mL IL-6; time point (day): 6; ', 'tissue type: FFPE tumor sample; panoptic il6: 9.77; ', 'tissue type: FFPE tumor sample; panoptic il6: 24.39; ', 'tissue type: FFPE tumor sample; panoptic il6: 21.39; ', 'tissue type: FFPE tumor sample; panoptic il6: 32.18; ', 'tissue type: FFPE tumor sample; panoptic il6: 21.14; ', 'tissue type: FFPE tumor sample; panoptic il6: 24.92; ', 'tissue type: FFPE tumor sample; panoptic il6: 22.72; ', 'tissue type: FFPE tumor sample; panoptic il6: 58.16; ', 'tissue type: FFPE tumor sample; panoptic il6: 13.63; ', 'tissue type: FFPE tumor sample; panoptic il6: 38.16; ', 'tissue type: FFPE tumor sample; panoptic il6: 28.05; ', 'tissue type: FFPE tumor sample; panoptic il6: 25.8; ', 'tissue type: FFPE tumor sample; panoptic il6: 37.25; ', 'tissue type: FFPE tumor sample; panoptic il6: 96.25; ', 'tissue type: FFPE tumor sample; panoptic il6: 49.59; ', 'tissue type: FFPE tumor sample; panoptic il6: 10.65; ', 'tissue type: FFPE tumor sample; panoptic il6: 41.08; ', 'tissue type: FFPE tumor sample; panoptic il6: 112.56; ', 'tissue type: FFPE tumor sample; panoptic il6: 803.75; ', 'tissue type: FFPE tumor sample; panoptic il6: 50.53; ' GSE75367 Homo sapiens 74 Expression profiling by high throughput sequencing GPL11154 HER2 expression identifies dynamic functional states within circulating breast cancer cells 2015-11-24 Circulating tumour cells in women with advanced oestrogen-receptor (ER)-positive/human epidermal growth factor receptor 2 (HER2)-negative breast cancer acquire a HER2-positive subpopulation after multiple courses of therapy. In contrast to HER2-amplified primary breast cancer, which is highly sensitive to HER2-targeted therapy, the clinical significance of acquired HER2 heterogeneity during the evolution of metastatic breast cancer is unknown. Here we analyse circulating tumour cells from 19 women with ER+/HER2- primary tumours, 84% of whom had acquired circulating tumour cells expressing HER2. Cultured circulating tumour cells maintain discrete HER2+ and HER2- subpopulations: HER2+ circulating tumour cells are more proliferative but not addicted to HER2, consistent with activation of multiple signalling pathways; HER2- circulating tumour cells show activation of Notch and DNA damage pathways, exhibiting resistance to cytotoxic chemotherapy, but sensitivity to Notch inhibition. HER2+ and HER2- circulating tumour cells interconvert spontaneously, with cells of one phenotype producing daughters of the opposite within four cell doublings. Although HER2+ and HER2- circulating tumour cells have comparable tumour initiating potential, differential proliferation favours the HER2+ state, while oxidative stress or cytotoxic chemotherapy enhances transition to the HER2- phenotype. Simultaneous treatment with paclitaxel and Notch inhibitors achieves sustained suppression of tumorigenesis in orthotopic circulating tumour cell-derived tumour models. Together, these results point to distinct yet interconverting phenotypes within patient-derived circulating tumour cells, contributing to progression of breast cancer and acquisition of drug resistance. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE75367 HER2 expression identifies dynamic functional states within circulating breast cancer cells. Nature 43.070 https://doi.org/10.1038/nature19328 {Nature (43.070): 10.1038/nature19328} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA304018 https://www.ebi.ac.uk/ena/browser/view/PRJNA304018 https://www.ncbi.nlm.nih.gov/sra?term=SRP066632 [Overal design]Seventy-four single candidate CTCs from two representative ER+/HER2- patients (BRx-42 and BRx-82) and 14 triple negative patients were isolated via micromanipulation and subjected to single-cell RNA-sequencing. Thirteen candidate CTCs expressed PTPRC at a level higher than 10 reads-per-million, so were deemed potential White Blood Cells and therefore dropped from further consideration. Expression profiles of CTCs expressing ERBB2 at a level greater than 10 RPM were compared with those expressing ERBB2 at a level less than 10 RPM.; [Treatment]'None'; [Growth]'None'; [Extraction]'Single CTCs were isolated from fresh whole blood following leukocyte depletion using the microfluidic CTC-iChip as described in PMID 23552373. Single cells were individually micromanipulated using a 10 μm transfer tip on an Eppendorf TransferMan NK 2 micromanipulator, transferred into PCR tubes containing RNA protective lysis buffer, and flash frozen in liquid nitrogen.\nWe used the Clontech SMARTer Ultra Low Input Kit for RNA v3 for cDNA synthesis and the Nextera XT kit for library construction. We spiked in a 1:50,000 dilution of the ERCC RNA Spike-In Mix, which is mix 1, before preparation with the SMARTer kit.', 'Single CTCs were isolated from fresh whole blood following leukocyte depletion using the microfluidic CTC-iChip as described in PMID 23552373. Single cells were individually micromanipulated using a 10 μm transfer tip on an Eppendorf TransferMan NK 2 micromanipulator, transferred into PCR tubes containing RNA protective lysis buffer, and flash frozen in liquid nitrogen.\nClontech SMARTer Ultra Low Input Kit for RNA v3 for cDNA synthesis and the Nextera XT kit for library construction'; [Cell type]'Source: ''donor: BRx-42; ptprc: low; erbb2: low; er: positive; pr: positive; her2: negative; ', 'donor: BRx-42; ptprc: low; erbb2: high; er: positive; pr: positive; her2: negative; ', 'donor: BRx-82; ptprc: high; erbb2: low; er: positive; pr: positive; her2: negative; ', 'donor: BRx-82; ptprc: low; erbb2: high; er: positive; pr: positive; her2: negative; ', 'donor: BRx-82; ptprc: low; erbb2: low; er: positive; pr: positive; her2: negative; ', 'donor: BRx-42; ptprc: high; erbb2: low; er: positive; pr: positive; her2: negative; ', 'donor: BRx-111; ptprc: low; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-129; ptprc: low; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-129; ptprc: high; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-131; ptprc: low; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-132; ptprc: low; erbb2: high; er: negative; pr: negative; her2: negative; ', 'donor: BRx-136; ptprc: low; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-136; ptprc: low; erbb2: high; er: negative; pr: negative; her2: negative; ', 'donor: BRx-139; ptprc: low; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-146; ptprc: high; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-146; ptprc: high; erbb2: high; er: negative; pr: negative; her2: negative; ', 'donor: BRx-16; ptprc: low; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-16; ptprc: high; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-170; ptprc: low; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-172; ptprc: low; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-172; ptprc: high; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-180; ptprc: high; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-180; ptprc: low; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-183; ptprc: low; erbb2: high; er: negative; pr: negative; her2: negative; ', 'donor: BRx-213; ptprc: low; erbb2: low; er: negative; pr: negative; her2: negative; ', 'donor: BRx-213; ptprc: low; erbb2: high; er: negative; pr: negative; her2: negative; ', 'donor: BRx-245; ptprc: low; erbb2: low; er: negative; pr: negative; her2: negative; ' GSE152315 Homo sapiens 1 Expression profiling by high throughput sequencing GPL24676 AR heterogeneity in TNBC MDA-MB-453 cells 2020-06-11 Triple-negative breast cancer (TNBC) is aggressive and difficult, and few targeted therapies are available to treat this patient population. The androgen receptor (AR) has emerged as a potential target in breast cancer. Newer generation AR inhibitors, such as Seviteronel (Sevi), are unique in their ability to inhibit AR both directly and by blocking upstream androgen synthesis. The purpose of this study was to investigate the pre-clinical activity of Sevi in TNBC and further explore the effectiveness of targeting both androgen biosynthesis and AR activity in combination with other downstream acting agents. AR overexpressing (AR+) TNBC cell lines, xenografts and androgen responsive patient-derived xenograft (PDX) models were using to show how effectively Sevi inhibits AR activity and cell/tumor proliferation. Single cell RNA-sequencing of the AR+ cell line MDA-MB-453 illustrated heterogeneity in AR levels and identified cell cycle pathway activation in ARHigh versus ARLow expressing cells. Combination treatment with the cell cycle CDK4/6 inhibitor abemaciclib and Sevi showed synergy in AR+ TNBC cells and increased effectiveness, compared to each drug alone, in an AR+ TNBC xenograft model. While cell cycle inhibitors have been approved for use in hormone-receptor positive breast cancer, our studies suggest that these drugs may be equally effective in AR+ TNBC cells, especially when combined with AR antagonists. Implications. These data suggest that targeting AR signaling at multiple points throughout the pathway may be an effective was to treat patients with AR+ TNBC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE152315 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA638948 https://www.ebi.ac.uk/ena/browser/view/PRJNA638948 https://www.ncbi.nlm.nih.gov/sra?term=SRP266972 [Overal design]TNBC androgen receptor (AR)-positive MDA-MB-453 cells were sequenced by single cell RNAseq to examine cell line heterogeneity, in particular differences in AR expression and genes associated with different levels of AR; [Treatment]'None, unstimulated'; [Growth]'Cells grown in DMEM media supplemented with 10% FBS'; [Extraction]'mRNA was extracted using the 10X Genomics Sample Preparation Protocol\nRNA libraries were prepared used Illumina HiSeq libraries according to manufacturer’s instructions for the TruSeq Stranded RNA kit'; [Cell type]'Source: ''treatment: None, unstimulated; cell line: MDA-MB-453 cells; ' GSE99508 Homo sapiens 8 Other GPL11154 Genome wide analysis of the transcription induced by estrogen and tamoxifen in MCF-7 cells 2017-05-31 The aim of this study is to understand the role of tamoxifen in the transcription regulation of estrogen receptor positive breast cancer cells using GRO-seq experiment. ER positive MCF-7 cells was depleted with lipid hormone in stripped culture media for 4 days, and stimulated with 17-β-estradiol (100nM), 4-OH-tamoxifen (1μM), and the combination of both for 40min. Each treatment was generated in duplicates. Then nuclei was isolated and used as the starting material for GRO-seq experiments. Sequencing data was analyzed and differential gene expression analysis was performed. A rapid induction of gene expression by 17-β-estradiol was observed as previous studies reported. While also a number of genes were also up-regulated by 4-OH-tamoxifen treatment which is considered as a ER antagnist. The data strongly indicate that as a recpressor of estrogen receptor induced transcription, tamoxifen could also perform as a partial agnist at the same time. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99508 DNA methylation at enhancers identifies distinct breast cancer lineages. Nature communications 11.878 https://doi.org/10.1038/s41467-017-00510-x {Nature communications (11.878): 10.1038/s41467-017-00510-x} 'nuclear RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA388671 https://www.ebi.ac.uk/ena/browser/view/PRJNA388671 https://www.ncbi.nlm.nih.gov/sra?term=SRP108366 [Overal design]Transcriptome profiling of hormone depleted MCF-7 cells treated with vehicle (control), 17-β-estradiol (100nM), 4-OH-tamoxifen (1μM) and combination of both for 40min. 2 replicates for each; [Treatment]'None'; [Growth]'None'; [Extraction]'5 ×10^6 nuclei were used for each run-on reaction, 2 biological replicates were produced for both vehicle and estrogen treatments. Br-UTP was incorporated into on-going transcription by run-on reaction which was performed at 30 degree for 5 min. Total RNA was extracted with TRIzol and fragmented with RNA Fragmentation Reagent. Fragmented RNA was purified with P-30 column, which was followed by T4 polynucleotide kinase treatment to dephosphorylate the 3’ end of RNA fragments. Br-UTP labeled RNA was enriched twice with anti-BrdU beads and precipitated overnight.\nPolyA tailing was done using E.coli Poly(A) Polymerase, followed by reverse transcription with oNTI-223-index: /5Phos/GATCGTCGGACTGTAGAACTCTGAAC/iSp18/TCAGACGTGTGCTCTTCCGATCTTTTTTTTTTTTTTTTTTTTVN which allows custom barcoding. Exonuclease I was used to remove excess oligo after reverse transcription. DNA-RNA duplex was purified with ChIP DNA Clean & Concentrator Kit followed by RNAse H treatment. cDNA was circularized amplified with oNTI-201: AATGATACGGCGACCACCGACAGGTTCAGAGTTCTACAGTCCGACG and oNTI-200: CAAGCAGAAGACGGCATACGAGATXXXXXXGTGACTGGAGTTCAGACGTGTGCTCTTCCGATCT(XXXXXX is barcode used for specific sample) for 12 to 14 cycles. Final PCR product was purified by running 10% TBE gel and cleaned up.'; [Cell type]'Source: ''tissue: mammary gland/breast; tumor type: breast adenocarcinoma; treatment: Vehicle; ', 'tissue: mammary gland/breast; tumor type: breast adenocarcinoma; treatment: Estrogen; ', 'tissue: mammary gland/breast; tumor type: breast adenocarcinoma; treatment: Tamoxifen; ', 'tissue: mammary gland/breast; tumor type: breast adenocarcinoma; treatment: Estrogen+tamoxifen; ' GSE87411 Homo sapiens 218 Expression profiling by array GPL6480 Z1031B Paired Gene Expression 2016-09-27 Agilent gene expression arrays were used to compare proliferation signatures between pre-treatment and 2-4 weeks post treatment samples from Z1031B patients. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE87411 Ki67 Proliferation Index as a Tool for Chemotherapy Decisions During and After Neoadjuvant Aromatase Inhibitor Treatment of Breast Cancer: Results From the American College of Surgeons Oncology Group Z1031 Trial (Alliance). Journal of clinical oncology : official journal of the American Society of Clinical Oncology 28.245 https://doi.org/10.1200/JCO.2016.69.4406 {Journal of clinical oncology : official journal of the American Society of Clinical Oncology (28.245): 10.1200/JCO.2016.69.4406} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA344680 https://www.ebi.ac.uk/ena/browser/view/PRJNA344680 None [Overal design]109 patients from clinical trial NCT00265759 with paired baseline (BL) and 2-4wk (2wk or M) post treatment arrays were analyzed. This series contains re-analyzed samples from GSE29442, GSE35186, and GSE35191.; [Treatment]'None'; [Growth]'patient biopsies were frozen and stored in oct compound'; [Extraction]'Trizol extractions followed by Dnase treatment and column purification.'; [Cell type]'Source: ''rna source: Total RNA from 10 human cell lines: 1_Adenocarcinoma, mammary gland 2_Hepatoblastoma, liver 3_Adenocarcinoma, cervix 4_Embryonal carcinoma, testis 5_Glioblastoma, brain 6_Melanoma 7_Liposarcoma 8_Histiocytic Lymphoma; macrophage; histocyte 9_ Lymphoblastic leukemia, T lymphoblast 10_Plasmacytoma; myeloma; B lymphocyte. Also, mRNA spiked in from MCF7 and ME16C.; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16723; bl ki67: 80.0%; eot ki67: 36.00%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16744; bl ki67: 75.0%; eot ki67: 6.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16745; bl ki67: 12.7%; eot ki67: 1.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16751; bl ki67: 11.0%; eot ki67: 2.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16754; bl ki67: 28.0%; eot ki67: 21.00%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16757; bl ki67: 16.0%; eot ki67: 2.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16779; bl ki67: 10.7%; eot ki67: 1.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16825; bl ki67: 10.3%; eot ki67: 2.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16847; bl ki67: 15.9%; eot ki67: 0.30%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16858; bl ki67: 5.0%; eot ki67: 0.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16880; bl ki67: 10.4%; eot ki67: 3.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16886; bl ki67: ~90%; eot ki67: 23.80%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16889; bl ki67: 45.0%; eot ki67: 17.80%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16895; bl ki67: 12.5%; eot ki67: 0.60%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16917; bl ki67: 9.1%; eot ki67: 16.20%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16918; bl ki67: 60.0%; eot ki67: 80.00%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16921; bl ki67: ~30%; eot ki67: 6.30%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16934; bl ki67: ~40%; eot ki67: 1.60%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16949; bl ki67: 25.9%; eot ki67: 9.30%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16956; bl ki67: 22.9%; eot ki67: 8.30%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16959; bl ki67: 10.8%; eot ki67: 2.30%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16965; bl ki67: ~70%; eot ki67: 26.60%; endocrine therapy response group: resistant; treatment course: surgery; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16970; bl ki67: 10.3%; eot ki67: 6.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16982; bl ki67: 12.1%; eot ki67: 0.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16984; bl ki67: 22.0%; eot ki67: 4.80%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16992; bl ki67: 21.4%; eot ki67: 10.10%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16993; bl ki67: 13.3%; eot ki67: 7.60%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16994; bl ki67: 11.90%; eot ki67: 0.80%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 16998; bl ki67: 13.60%; eot ki67: 0.90%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17032; bl ki67: 20.90%; eot ki67: 5.80%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17066; bl ki67: 30.00%; eot ki67: 12.50%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17070; bl ki67: 8.90%; eot ki67: 1.20%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17124; bl ki67: 30.0%; eot ki67: 2.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17143; bl ki67: 26.6%; eot ki67: 11.70%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17157; bl ki67: 39.8%; eot ki67: 27.40%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17170; bl ki67: 15.1%; eot ki67: 2.70%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17196; bl ki67: 21.4%; eot ki67: 6.70%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17232; bl ki67: 16.6%; eot ki67: 1.7%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17233; bl ki67: 1.9%; eot ki67: 0.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17240; bl ki67: 16.5%; eot ki67: 3.0%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17250; bl ki67: 24.3%; eot ki67: 32.10%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17277; bl ki67: 13.3%; eot ki67: 11.90%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17278; bl ki67: 14.3%; eot ki67: 1.40%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17292; bl ki67: 22.0%; eot ki67: 53.50%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17327; bl ki67: 12.2%; eot ki67: 15.00%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17328; bl ki67: 65.0%; eot ki67: 9.10%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17329; bl ki67: 53.3%; eot ki67: 22.90%; endocrine therapy response group: resistant; treatment course: surgery; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17331; bl ki67: 13.5%; eot ki67: 1.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17383; bl ki67: NA; eot ki67: 1.70%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17384; bl ki67: 0.7%; eot ki67: 14.40%; endocrine therapy response group: resistant; treatment course: surgery; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17407; bl ki67: 20.0%; eot ki67: 2.60%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17409; bl ki67: 90.0%; eot ki67: 22.40%; endocrine therapy response group: resistant; treatment course: chose to continue on AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17412; bl ki67: 24.0%; eot ki67: 3.20%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17423; bl ki67: 29.5%; eot ki67: 4.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17445; bl ki67: 16.1%; eot ki67: 4.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17467; bl ki67: 11.3%; eot ki67: <1%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17490; bl ki67: 3.3%; eot ki67: 3.0%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17494; bl ki67: 15.0%; eot ki67: 4.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17502; bl ki67: 65.0%; eot ki67: 17.00%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17518; bl ki67: 8.5%; eot ki67: 20.00%; endocrine therapy response group: resistant; treatment course: surgery; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17521; bl ki67: 16.7%; eot ki67: 0.30%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17522; bl ki67: 7.5%; eot ki67: 8.30%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17566; bl ki67: 75.0%; eot ki67: 35.0%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17584; bl ki67: 19.8%; eot ki67: 9.80%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17586; bl ki67: 9.0%; eot ki67: 5.70%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17601; bl ki67: 45.0%; eot ki67: 3.10%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17611; bl ki67: 8.6%; eot ki67: 1.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17612; bl ki67: 3.5%; eot ki67: 14.10%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17636; bl ki67: 9.2%; eot ki67: 3.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17646; bl ki67: 18.8%; eot ki67: 4.90%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17674; bl ki67: 15.9%; eot ki67: 0.80%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17675; bl ki67: 8.4%; eot ki67: 13.40%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17688; bl ki67: 13.4%; eot ki67: 2.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17714; bl ki67: 7.1%; eot ki67: 1.30%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17733; bl ki67: 12.4%; eot ki67: 2.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17738; bl ki67: 4.4%; eot ki67: 0.20%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17739; bl ki67: 14.3%; eot ki67: 7.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17746; bl ki67: 20.4%; eot ki67: 17.90%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17762; bl ki67: 11.8%; eot ki67: 4.10%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17776; bl ki67: NP; eot ki67: 10.30%; endocrine therapy response group: resistant; treatment course: off study; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17787; bl ki67: 11.7%; eot ki67: 1.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17807; bl ki67: 24.1%; eot ki67: 22.10%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17818; bl ki67: 33.6%; eot ki67: 2.10%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17823; bl ki67: 27.7%; eot ki67: 6.30%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17835; bl ki67: 1.0%; eot ki67: 3.70%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17860; bl ki67: 5.0%; eot ki67: 5.90%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17868; bl ki67: 2.5%; eot ki67: 3.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17881; bl ki67: 12.6%; eot ki67: 5.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17902; bl ki67: 24.4%; eot ki67: 3.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17910; bl ki67: 95.0%; eot ki67: >90%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17913; bl ki67: 4.8%; eot ki67: 24.70%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 17946; bl ki67: 6.5%; eot ki67: 6.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18025; bl ki67: 60-70%; eot ki67: 18.30%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18052; bl ki67: 50.0%; eot ki67: 25.20%; endocrine therapy response group: resistant; treatment course: switch to NAC; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18074; bl ki67: 6.7%; eot ki67: 0.20%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18091; bl ki67: 7.6%; eot ki67: 6.6%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18115; bl ki67: 28.5%; eot ki67: 6.20%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18145; bl ki67: ~50%; eot ki67: 11.40%; endocrine therapy response group: resistant; treatment course: chose to continue on AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18155; bl ki67: 18.2%; eot ki67: 5.40%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18156; bl ki67: 17.0%; eot ki67: 0.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18161; bl ki67: 3.6%; eot ki67: 1.80%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18182; bl ki67: 21.0%; eot ki67: 8.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18183; bl ki67: 5.6%; eot ki67: 1.70%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18184; bl ki67: ~30; eot ki67: 3.10%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18189; bl ki67: 6.1%; eot ki67: 3.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 18197; bl ki67: 7.1%; eot ki67: 0.60%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 21009; bl ki67: 0.3%; eot ki67: 1.00%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 21072; bl ki67: 0.3%; eot ki67: 6.50%; endocrine therapy response group: sensitive; treatment course: continue AI; ', 'tissue: breast cancer tissue; biopsy type: oct blocks from fine needle biopsies which contained at least 50% tumor cellularity; study id: Z1031B; studynum: 21080; bl ki67: 25.0%; eot ki67: 35.00%; endocrine therapy response group: resistant; treatment course: switch to NAC; ' GSE116744 Homo sapiens 27 Expression profiling by high throughput sequencing GPL11154 RNA-Seq analysis of long-term estrogen-deprived (LTED) MDA-MB-134VI (MM134) and SUM44PE (SUM44) ILC cell lines 2018-07-06 Background: Invasive lobular breast carcinoma (ILC) is a histological subtype of breast cancer that is characterized by loss of E-cadherin, and high expression of estrogen receptor alpha (ER). Many patients with ILC are effectively treated with adjuvant aromatase inhibitors (AIs), however, acquired AI resistance remains a significant problem. Methods: To identify underlying mechanisms of acquired antiestrogen resistance in ILC, we developed a total of 6 long-term estrogen-deprived (LTED) variant cell lines of the human ILC cell lines SUM44PE (SUM44; 2 lines) and MDA-MB-134VI (MM134; 4 lines). To better understand mechanisms of AI resistance in these models, we performed transcriptional profiling analysis by RNA-sequencing. Results: MM134 LTED cells expressed ER at decreased level and lost growth response to estradiol, while SUM44 LTED cells retained partial ER activity. Our transcriptional profiling analysis identified shared activation of lipid metabolism across all 6 independent models. However, the underlying basis of this signature was distinct between models. Oxysterols were able to promote the proliferation of SUM44 LTED cells, but not MM134 LTED. In contrast, MM134 LTED cells displayed high expression of the Sterol regulatory element-binding protein 1 (SREBP1), a regulator of fatty acid and cholesterol synthesis, and were hypersensitive to genetic or pharmacological inhibition of SREBPs. Several SREBP1 downstream targets involved in fatty acid synthesis, including FASN, were induced, and MM134 LTED cells were more sensitive to etomoxir, an inhibitor of the rate-limiting enzyme in β-oxidation, than their respective parental control cells. Conclusions: Our characterization of a unique series of AI-resistant ILC models identifies a lipogenic phenotype, including overexpression of SREBP1. This novel metabolic target deserves further study for the prevention and treatment of AI-resistance for patients with ILC. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE116744 Key regulators of lipid metabolism drive endocrine resistance in invasive lobular breast cancer. Breast cancer research : BCR 5.676 https://doi.org/10.1186/s13058-018-1041-8 {Breast cancer research : BCR (5.676): 10.1186/s13058-018-1041-8} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA480032 https://www.ebi.ac.uk/ena/browser/view/PRJNA480032 https://www.ncbi.nlm.nih.gov/sra?term=SRP152557 [Overal design]Parental and LTED MM134 and SUM44 cells were seeded in triplicates in 6-well plates. Parental cells were hormone deprived for three days before cell collection. RNA-Seq was carried out by Illumina HiSeq 2000. Raw sequence data were mapped to hg38 genome (ensembl release version 82) and gene counts were quantified with Salmon (version 0.6.0); [Treatment]'Parental and LTED MM134 and SUM44 cells were seeded in triplicates in 6-well plates. Parental cells were hormone deprived for three days before cell collection. For hormone deprivation, cells were washed twice daily for 3 days. For each wash, cells were rinsed twice with serum-free IMEM and then cultured in IMEM + 10% CSS. A minimum 1-hour interval was kept between two washes.'; [Growth]'None'; [Extraction]'RNA was isolated using Illustra RNAspin Mini Kit\nTruSeq Stranded Total RNA Library Prep Kit was used for library preparation according to Illumina standard protocols'; [Cell type]'Parental', 'long-term estrogen-deprived (LTED)''cell line: MM134; cell type: Parental; cell line type: Invasive lobular breast carcinoma; ', 'cell line: MM134; cell type: long-term estrogen-deprived (LTED); cell line type: Invasive lobular breast carcinoma; ', 'cell line: Sum44; cell type: Parental; cell line type: Invasive lobular breast carcinoma; ', 'cell line: Sum44; cell type: long-term estrogen-deprived (LTED); cell line type: Invasive lobular breast carcinoma; ' GSE80077 Homo sapiens 60 Expression profiling by array GPL571 Preoperative short-term hormone therapy for hormone receptor positive breast cancer 2016-04-08 Core needle biopsy (Cx) primary cancer specimens were collected at Okayama University Hospital in Japan from hormone receptor positive /HER2 negative patients that subsequently received two weeks of neoadjuvant hormone therapy. Thirty clinical TNM stage I and II women were enrolled in this study. The study was approved by the Institutional Review Board and all patients signed informed consent forms. Patients received preoperative hormone therapy daily for two weeks before surgery. Premenopausal patients received tamoxifen (40 mg) and postmenopausal patients received letrozole (2.5 mg). All patients underwent a mastectomy or breast-conserving surgery. Surgical samples after treatment were also collected. Hormone and HER2 receptor statuses were determined in the diagnostic Cx specimens before hormone therapy. Cases with ≥1% positive nuclear staining for estrogen receptors (ER) or progesterone receptors (PgR) with IHC were considered hormone receptor-positive. Cases with either 0 or 1 positive IHC staining for HER2 or with an HER2 gene copy number < 2.0 by fluorescent in situ hybridization (FISH) analysis were considered HER2−. Specimens for gene expression analysis were collected into RNA and later stored at -80°C. Gene expression profiling was performed using Affymetrix U133A gene chips. Expression data were normalized using the MAS5 algorithm, mean centered to 600, and log2 transformed before further analysis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE80077 Immunohistochemical Ki67 after short-term hormone therapy identifies low-risk breast cancers as reliably as genomic markers. Oncotarget None https://doi.org/10.18632/oncotarget.15385 {Oncotarget (None): 10.18632/oncotarget.15385} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA317765 https://www.ebi.ac.uk/ena/browser/view/PRJNA317765 None [Overal design]Thirty clinical TNM stage I and II women were enrolled in this study.; [Treatment]'Patients received preoperative hormone therapy daily for two weeks before surgery. Premenopausal patients received tamoxifen (40 mg) and postmenopausal patients received letrozole (2.5 mg). All patients underwent a mastectomy or breast-conserving surgery.'; [Growth]'Core needle biopsy (Cx) primary cancer specimens were collected at Okayama University Hospital in Japan from hormone receptor positive /HER2 negative patients that subsequently received two weeks of neoadjuvant hormone therapy. Thirty clinical TNM stage I and II women were enrolled in this study.'; [Extraction]'Specimens for gene expression analysis were collected into RNA and later stored at -80°C.'; [Cell type]'Source: ''paired: 7; pre.post.hormone: Pre; age at diagnosis: 45.4712328767123; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: 1~10%; pathological ihc her2: IHC 2;/FISH-; t cm: 2.6; cn: 0; m: 0; historogical grade: 2; histologic subtypes: Scirrhous carcinoma; type of hormone: TAM; type of operation: BT; ', 'paired: 9; pre.post.hormone: Pre; age at diagnosis: 57.9671232876712; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: 1~10%; pathological ihc her2: 1; t cm: 2.1; cn: 0; m: 0; historogical grade: 2; histologic subtypes: Solid-tubular carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 14; pre.post.hormone: Pre; age at diagnosis: 40.6191780821918; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: IHC 2;/FISH-; t cm: 4.8; cn: 0; m: 0; historogical grade: 2; histologic subtypes: Scirrhous carcinoma; type of hormone: TAM; type of operation: BT; ', 'paired: 16; pre.post.hormone: Pre; age at diagnosis: 57.1808219178082; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: 1; t cm: 1; cn: 0; m: 0; historogical grade: 2; histologic subtypes: Scirrhous carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 17; pre.post.hormone: Pre; age at diagnosis: 63.5150684931507; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: 1; t cm: 1.6; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Scirrhous carcinoma; type of hormone: AI; type of operation: BT; ', 'paired: 18; pre.post.hormone: Pre; age at diagnosis: 50.6191780821918; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >20; pathological ihc her2: IHC 2;/FISH-; t cm: 2.2; cn: 0; m: 0; historogical grade: Unknown; histologic subtypes: Solid-tubular carcinoma; type of hormone: TAM; type of operation: Bp; ', 'paired: 23; pre.post.hormone: Pre; age at diagnosis: 66.7150684931507; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: 0; t cm: 1.5; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Scirrhous carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 24; pre.post.hormone: Pre; age at diagnosis: 53.3917808219178; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: 10~50%; pathological ihc her2: 1; t cm: 1.3; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Papillotubular carcinoma; type of hormone: TAM; type of operation: Bp; ', 'paired: 27; pre.post.hormone: Pre; age at diagnosis: 46.0904109589041; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: 1; t cm: 1.2; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Papillotubular carcinoma; type of hormone: TAM; type of operation: Bp; ', 'paired: 28; pre.post.hormone: Pre; age at diagnosis: 46.1917808219178; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: 0; t cm: 0.8; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Scirrhous carcinoma; type of hormone: TAM; type of operation: BT; ', 'paired: 29; pre.post.hormone: Pre; age at diagnosis: 44.8547945205479; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: 0; t cm: 3.5; cn: 0; m: 0; historogical grade: 2; histologic subtypes: Scirrhous carcinoma; type of hormone: TAM; type of operation: BT; ', 'paired: 36; pre.post.hormone: Pre; age at diagnosis: 44.1945205479452; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: IHC 2;/FISH-; t cm: 2.7; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Papillotubular carcinoma; type of hormone: TAM; type of operation: Bp; ', 'paired: 52; pre.post.hormone: Pre; age at diagnosis: 69.1671232876712; ihc.er: Pos; ihc.pr: Neg; pathological ihc er: >50; pathological ihc pr: 0~1%; pathological ihc her2: 0; t cm: 1.8; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Scirrhous carcinoma; type of hormone: AI; type of operation: BT; ', 'paired: 53; pre.post.hormone: Pre; age at diagnosis: 72.2904109589041; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: 10~50%; pathological ihc her2: 1; t cm: 2.3; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Scirrhous carcinoma; type of hormone: AI; type of operation: BT; ', 'paired: 54; pre.post.hormone: Pre; age at diagnosis: 59.9123287671233; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: 10~50%; pathological ihc her2: IHC 2;/FISH-; t cm: 2.8; cn: 0; m: 0; historogical grade: 3; histologic subtypes: Scirrhous carcinoma; type of hormone: AI; type of operation: BT; ', 'paired: 55; pre.post.hormone: Pre; age at diagnosis: 81.8438356164384; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: IHC 2;/FISH-; t cm: 2.2; cn: 0; m: 0; historogical grade: 2; histologic subtypes: Scirrhous carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 56; pre.post.hormone: Pre; age at diagnosis: 83.2767123287671; ihc.er: Pos; ihc.pr: Neg; pathological ihc er: >50; pathological ihc pr: 0~1%; pathological ihc her2: 1; t cm: 0.9; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Scirrhous carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 65; pre.post.hormone: Pre; age at diagnosis: 69.6191780821918; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: IHC 2;/FISH-; t cm: 1.2; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Scirrhous carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 68; pre.post.hormone: Pre; age at diagnosis: 57.6328767123288; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: 1; t cm: 1.2; cn: 0; m: 0; historogical grade: 2; histologic subtypes: Scirrhous carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 73; pre.post.hormone: Pre; age at diagnosis: 66.8109589041096; ihc.er: Pos; ihc.pr: Neg; pathological ihc er: >50; pathological ihc pr: 0; pathological ihc her2: 1; t cm: 8; cn: 0; m: 0; historogical grade: 2; histologic subtypes: lobular carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 74; pre.post.hormone: Pre; age at diagnosis: 51.027397260274; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: 1; t cm: 1.4; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Tubular carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 76; pre.post.hormone: Pre; age at diagnosis: 88.2; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: 10~50%; pathological ihc her2: 1; t cm: 1.8; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Mucinous carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 79; pre.post.hormone: Pre; age at diagnosis: 71.7013698630137; ihc.er: Pos; ihc.pr: Neg; pathological ihc er: >50; pathological ihc pr: 0; pathological ihc her2: 0; t cm: 2.2; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Mucinous carcinoma; type of hormone: AI; type of operation: BT; ', 'paired: 83; pre.post.hormone: Pre; age at diagnosis: 46.4301369863014; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: IHC 2;/FISH-; t cm: 2.2; cn: 0; m: 0; historogical grade: 1; histologic subtypes: Papillotubular carcinoma; type of hormone: TAM; type of operation: Bp; ', 'paired: 86; pre.post.hormone: Pre; age at diagnosis: 47.3342465753425; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: 1; t cm: 3.5; cn: 0; m: 0; historogical grade: 1; histologic subtypes: lobular carcinoma; type of hormone: TAM; type of operation: BT; ', 'paired: 87; pre.post.hormone: Pre; age at diagnosis: 65.7068493150685; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: 1~10%; pathological ihc her2: 1; t cm: 4; cn: 0; m: 0; historogical grade: 3; histologic subtypes: Solid-tubular carcinoma; type of hormone: AI; type of operation: BT; ', 'paired: 91; pre.post.hormone: Pre; age at diagnosis: 48.1369863013699; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: >50; pathological ihc her2: 1; t cm: 2.2; cn: 0; m: 0; historogical grade: 2; histologic subtypes: Scirrhous carcinoma; type of hormone: TAM; type of operation: BT; ', 'paired: 92; pre.post.hormone: Pre; age at diagnosis: 59.7068493150685; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: 1~10%; pathological ihc her2: IHC 2;/FISH-; t cm: 1.1; cn: 0; m: 0; historogical grade: 2; histologic subtypes: Scirrhous carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 95; pre.post.hormone: Pre; age at diagnosis: 57.5917808219178; ihc.er: Pos; ihc.pr: Pos; pathological ihc er: >50; pathological ihc pr: 1~10%; pathological ihc her2: 1; t cm: 4.5; cn: 0; m: 0; historogical grade: 2; histologic subtypes: Scirrhous carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 104; pre.post.hormone: Pre; age at diagnosis: 72.8082191780822; ihc.er: Pos; ihc.pr: Neg; pathological ihc er: >50; pathological ihc pr: 0; pathological ihc her2: 1; t cm: 1.3; cn: 0; m: 0; historogical grade: 1; histologic subtypes: lobular carcinoma; type of hormone: AI; type of operation: Bp; ', 'paired: 7; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 9; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 14; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 16; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 17; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 18; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 23; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 24; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 27; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 28; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 29; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 36; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 52; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 53; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 54; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 55; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 56; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 65; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 68; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 73; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 74; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 76; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 79; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 83; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 86; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 87; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 91; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 92; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 95; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ', 'paired: 104; pre.post.hormone: Post; age at diagnosis: NA; ihc.er: NA; ihc.pr: NA; pathological ihc er: NA; pathological ihc pr: NA; pathological ihc her2: NA; t cm: NA; cn: NA; m: NA; historogical grade: NA; histologic subtypes: NA; type of hormone: NA; type of operation: NA; ' GSE81814 Homo sapiens 4 Expression profiling by high throughput sequencing GPL10999 Transcriptome of RA-responsive and RA-resistant breast cancer cell lines 2016-05-24 Retinoic acid (RA), the main active vitamin A metabolite, controls multiple biological processes such as cell proliferation and differentiation through genomic programs and kinase cascades activation. Several breast cancer cells respond to the antiproliferative effects of RA, but others are RA-resistant. In several cases resistance has been correlated to the amplification of the erb-b2 receptor tyrosine kinase 2 (ERBB2) gene, but the overall signaling and transcriptional pathways that are altered in such cells have not been elucidated. Here we compared two human breast cancer cell lines, the MCF7 cell line, which responds to the antiproliferative action of RA and the BT474 cell line, which is RA-resistant subsequent to ERBB2 amplification in a large-scale analysis of the phosphoproteins and in a genome-wide analysis of the RA-regulated genes. Using high-resolution nano-LC-LTQ-Orbitrap mass spectrometry associated to phosphopeptide enrichment, we found that several proteins involved in signaling and in transcription, are differentially phosphorylated after RA addition. The paradigm of these proteins is the RA receptor α (RARα), which was phosphorylated in MCF7 cells but not in BT474 cells. The panel of the RA-regulated genes was also different. Overall our results indicate that ERBB2 amplification interferes with the ability of RA to activate kinases with consequences on the phosphorylation of several proteins involved in transcription and thus on gene expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE81814 Phosphoproteome and Transcriptome of RA-Responsive and RA-Resistant Breast Cancer Cell Lines. PloS one 2.776 https://doi.org/10.1371/journal.pone.0157290 {PloS one (2.776): 10.1371/journal.pone.0157290} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA322613 https://www.ebi.ac.uk/ena/browser/view/PRJNA322613 https://www.ncbi.nlm.nih.gov/sra?term=SRP075643 [Overal design]Two human breast cancer cell lines were compared for their repertoire of genes regulated by retinoic acid (RA): the RA sensitive MCF7 cell line and the RA resistant B7474 cell line; [Treatment]'When cells were 80-90 % confluent, all-trans RA (10-6 M) (Sigma Aldrich)was added to two dishes and vehicle (0.1% ethanol) to the two others, after 24h in low (1%) serum medium conditions, without insulin and phenol red. Then the cells were scrapped for RNA extraction'; [Growth]'MCF-7 and BT474 human breast cancer cell lines were purchased from the American Type Culture Collection (ATCC) and cultured as monolayers under standard conditions.'; [Extraction]'Total RNA was extracted using the GenElute miniprep kit (Sigma)\nAfter isolation of total cellular RNA, a library of template molecules suitable for high throughput DNA sequencing was created following the Illumina “Truseq RNA sample preparation low throughput” protocol with some modifications. Briefly, mRNA was purified from 4 µg total RNA using oligo-dT magnetic beads and fragmented using divalent cations at 94°C for 8 minutes. The cleaved mRNA fragments were reverse transcribed to cDNA using random primers, then the second strand of the cDNA was synthesized using Polymerase I and RNase H. The next steps of RNA-Seq Library preparation were performed in a fully automated system using SPRIworks Fragment Library System I kit (ref A84801, Beckman Coulter, Inc) with the SPRI-TE instrument (Beckman Coulter, Inc). Briefly, in this system double stranded cDNA fragments were blunted, phosphorylated and ligated to indexed adapter dimers, and fragments in the range of ~200-400 bp were size selected. The automated steps were followed by PCR amplification (30 sec at 98°C; [10 sec at 98°C, 30 sec at 60°C, 30 sec at 72°C] x 12 cycles; 5 min at 72°C), then surplus PCR primers were removed by purification using AMPure XP beads (Agencourt Biosciences Corporation). DNA libraries were checked for quality and quantified using 2100 Bioanalyzer (Agilent). The libraries were loaded in the flow cell at 7pM concentration and clusters generated and sequenced in the Illumina Genome Analyzer IIX as single-end 54 base reads.'; [Cell type]'epithelial''cell type: epithelial; treatment: ethanol 4 hours; cell line: MCF7; ', 'cell type: epithelial; treatment: retinoic acid 10-7M 4hours; cell line: MCF7; ', 'cell type: epithelial; treatment: ethanol 4 hours; cell line: BT474; ', 'cell type: epithelial; treatment: retinoic acid 10-7M 4hours; cell line: BT474; ' GSE106890 Homo sapiens 8 Expression profiling by array GPL6244 Tamoxifen transcriptional regulation in human endometrial stromal cells (HESC) 2017-11-14 Tamoxifen (TAM), used for adjuvant therapy of breast cancer, also increases the risk of endometrial cancer. To compare TAM-induced transcriptional changes we examined human and monkey uterus, as well as cultured normal human mammary epithelial cells (NHMECs) and human endometrial stromal cells (HESCs). Uterine DNA from TAM-exposed women (n=15) and monkeys (Erythrocebus patas n=5, and Macaca fascicularis n=12) showed no difference in 5-methyl-cytosine (5-meC) levels compared to unexposed controls. Studies comparing NHMECs and HESCs exposed to 10 µM TAM for 48 hr showed cell-specific differences by microarray, with confirmation by RT-PCR. In TAM-exposed NHMECs there was significant up-regulation of interferon signaling and immune response pathways, while the TAM-exposed HESCs showed significant up-regulation of steroid and fatty acid biosynthesis pathways. Promoter region CpG islands of several genes highly up-regulated by TAM in each cell type (NHMECs: MX1 and STAT1; HESCs: PPARG, SREBF2, HMCGS and Prune2), were examined for 5-meC, but the levels (≤ 7%), were too low to measure accurately. We also examined several histone H3 lysine dimethylases by Western blot, and showed a significant depletion of total H3 histone, H3K4, H3K27 and H3K36 in TAM-exposed HESCs, with similar but non-significant changes in TAM-exposed NHMECs. Whereas TAM exposure had no discernible effect on 5-meC levels in primate uterus, TAM exposure induced up-regulation of different transcriptional pathways in NHMECs and HESCs, and concomitantly depleted H3 histone lysine dimethylase levels. Therefore, transcriptional dysregulation by TAM, including reduction of histone H3 dimethylase levels, may be related to TAM-induced endometrial carcinogenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE106890 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA418377 https://www.ebi.ac.uk/ena/browser/view/PRJNA418377 None [Overal design]Human endometrial stromal cells (HESCs) were exposed to 10 uM Tamoxifen (TAM) (n=4) or vehicle (n=4) for 48 hours.; [Treatment]'Treatment type: compound\nAgent: Tamoxifen (TAM)\nTreatment dose: 10 µM\nTreatment time: 48 hours\nIn-vitro treatment: Cells were exposed to 10 µM TAM for 48 hours.', 'Treatment time: 48 hours\nIn-vitro treatment: Cells were exposed to vehicle for 48 hours.'; [Growth]'None'; [Extraction]'RNase Easy Mini Kit\nOther: For isolation of RNA, the cells were lysed with 1.0 mL of TRIzol Reagent (Invitrogen Life Technologies) and RNA was extracted using the RNase Easy Mini Kit (Qiagen) according to the manufacturer’s protocol.'; [Cell type]'human endometrial stromal cells (HESC)''tissue: Endometrial tissue; cell type: human endometrial stromal cells (HESC); ' GSE124380 Homo sapiens 4 Expression profiling by high throughput sequencing GPL16791 Next generation sequencing analysis of transcriptomes in MDA-MB-231 and LM2-4175 cell lines 2018-12-26 LM2-4175 cell line was originally selected from MDA-MB-231,but has more aggressive characteristics in invasion, migration and metastasis. In addition, LM2 cell line specifically metastasizes to lung. To understand the melecular mechanisms of lung metastasis in breast cancer,we analyzed the RNA-seq data of MDA-MB-231 and LM2-4175 cell lines. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE124380 Comprehensive epigenetic analyses reveal master regulators driving lung metastasis of breast cancer. Journal of cellular and molecular medicine 4.658 https://doi.org/10.1111/jcmm.14424 {Journal of cellular and molecular medicine (4.658): 10.1111/jcmm.14424} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA511878 https://www.ebi.ac.uk/ena/browser/view/PRJNA511878 https://www.ncbi.nlm.nih.gov/sra?term=SRP174487 [Overal design]Total RNA from MDA-MB-231 and LM2-4175 cell lines was sequenced by HiSeq2500. Each cell line has two replicates.; [Treatment]'None'; [Growth]'The human breast cancer cell line MDA-MB-231 and LM2-4175 were cultured in DMEM (Thermo Fisher Scientific) supplemented with 10% FBS (Gibco BRL, Grand Island, NY, USA) at 37°C and 5% CO2 in a humidified incubator.'; [Extraction]'Cellular RNA was isolated by Tri-Reagent using the manufacturer’s instructions. Qualified total RNA was further purified by RNeasy micro kit and RNase-Free DNase Set.\nRNA sequencing libraries were prepared according to the IlluminaTruseq TM RNA sample prep Kit'; [Cell type]'Source: ''treatment: None; tissue: breast cancer cell line; cell line: MDA-MB-231; ', 'treatment: None; tissue: breast cancer cell line; cell line: LM2-4175; ' GSE30405 Homo sapiens 14 Expression profiling by array GPL6244 The ets transcription factor ELF5 suppresses the estrogen sensitive phenotype and contributes to antiestrogen resistance in luminal breast cancer. [human] 2011-07-05 The ets transcription factor ELF5 specifies the differentiation of mammary progenitor cells to establish the milk-secreting lineage. ER- and poor prognosis basal breast cancers arise from this progenitor cell and these cancers express high levels of Elf5. Knockdown of ELF5 expression in basal breast cancer cell lines, or forced expression in luminal breast cancer cell lines, resulted in reduced cell proliferation. Transcript profiling and chromatin immunoprecipitation revealed that the transcriptional activity of ELF5 specified the gene expression patterns that distinguish basal from luminal breast cancer, including suppression of FOXA1, GATA3 and ER, key estrogen-action genes. Tamoxifen treatment of luminal MCF7 cells upregulated Elf5 expression and cells that acquired resistance to Tamoxifen became dependent on ELF5 for proliferation. ELF5 is a regulator of breast cancer cell proliferation, transcriptionally specifies the basal molecular subtype and is utilised by ER+ breast cancer cells to escape proliferative arrest caused by Tamoxifen. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE30405 ELF5 suppresses estrogen sensitivity and underpins the acquisition of antiestrogen resistance in luminal breast cancer. PLoS biology 8.386 https://doi.org/10.1371/journal.pbio.1001461 {PLoS biology (8.386): 10.1371/journal.pbio.1001461} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA154827 https://www.ebi.ac.uk/ena/browser/view/PRJNA154827 None [Overal design]Elf5 was knocked down via siRNA in basal HCC1937 cell lines, in triplicate. Elf5 was induced in luminal T47D and MCF7 cell lines via a doxycycline inducible expression vector, in duplicate.; [Treatment]'HCC1937 cells were transiently knocked down with siRNA-vs-Elf5, or mock transfected with the transfection reagent of LF2000 and Optimem.', 'T47D and MCF7 cells were treated with doxycycline (Clontech) at 0.1 μg/ml, R5020 (Du Pont) at 10 nM or 17β-estradiol (Sigma) at 10 mM. Dox-containing medium was changed every 24 hours to ensure optimum Dox activity.'; [Growth]'Human breast, basal A carcinoma HCC1937 cell lines were also grown in 10% FBS RPMI medium.', 'Human breast carcinoma MCF7-EcoR and T47D-EcoR (Brummelkamp et al, 2002, Science 296) cell lines were grown in RPMI 1640 medium (Invitrogen) supplemented with 10 % Tet System Approved fetal bovine serum (FBS) (Clontech). Cells were infected with pHUSH-ProEX-based produced by the Platinum E cell line (Morita et al., 2000). Transient transfection with Elf5-containing plasmid constructs used FuGENE reagent (Roche) or Lipofectamine LTX (Invitrogen) according to manufacturer’s instructions. Cells were maintained in the presence of puromycin (Sigma) at a concentration of 1μg/ml for MCF7-EcoR and 2μg/ml for T47D-EcoR.'; [Extraction]'Total RNA was extracted with the RNeasy Minikit (Qiagen) and DNase-treated with the DNase kit (Qiagen) according to manufacturer’s instructions. RNA quality was assessed by RNA Nano LabChip analysis on an Agilent Bioanalyzer 2100 (Agilent Technologies).'; [Cell type]'Source: ''cell line: HCC1937; inducible vector: none; phenotype: basal; treatment: mock; batch: 1; ', 'cell line: HCC1937; inducible vector: none; phenotype: basal; treatment: siRNA to ELF5; batch: 1; ', 'cell line: MCF7; inducible vector: doxycycline inducible pHUSH ProEx vector containing ELF5; phenotype: luminal; treatment: vehicle; batch: 2; ', 'cell line: MCF7; inducible vector: doxycycline inducible pHUSH ProEx vector containing ELF5; phenotype: luminal; treatment: doxycycline; batch: 2; ', 'cell line: T47D; inducible vector: doxycycline inducible pHUSH ProEx vector containing ELF5; phenotype: luminal; treatment: vehicle; batch: 2; ', 'cell line: T47D; inducible vector: doxycycline inducible pHUSH ProEx vector containing ELF5; phenotype: luminal; treatment: doxycycline; batch: 2; ' GSE36586 Homo sapiens 14 Expression profiling by array GPL14550 Interplay between AP-1 and ERalpha in regulating gene expression and proliferation networks in breast cancer cells 2012-03-17 Estrogen receptor alpha (ERalpha) is a ligand-dependent transcription factor that plays an important role in breast cancer. Estrogen-dependent gene regulation by ERalpha can be mediated by interaction with other DNA-binding proteins, such as activator protein-1 (AP-1). The nature of such interactions in mediating the estrogen response in breast cancer cells remains unclear. Here we show that knockdown of c-Fos, a component of the transcription factor AP-1, attenuates the expression of 37% of all estrogen-regulated genes, suggesting that AP-1 is a fundamental factor for ERalpha-mediated transcription. Additionally, knockdown of c-Fos affected the expression of a number of genes that were not regulated by estrogen. Pathway analysis reveals that silencing of c-Fos downregulates an E2F1-dependent pro-proliferative gene network. Thus, modulation of the E2F1 pathway by c-Fos represents a novel mechanism by which c-Fos enhances breast cancer cell proliferation. Furthermore, we show that c-Fos and ERalpha can cooperate in regulating E2F1 gene expression by binding to regulatory elements in the E2F1 promoter. To start to dissect the molecular details of the cross-talk between AP-1 and estrogen signaling, we identify a novel ERalpha/AP-1 target, PKIB (cAMP-dependent protein kinase inhibitor-beta), which is overexpressed in ERalpha-positive breast cancer tissues. Knockdown of PKIB by siRNA results in drastic growth suppression of breast cancer cells. Collectively, our findings support AP-1 as a critical factor that governs estrogen-dependent gene expression and breast cancer proliferation programs. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE36586 Interplay between AP-1 and estrogen receptor α in regulating gene expression and proliferation networks in breast cancer cells. Carcinogenesis 4.004 https://doi.org/10.1093/carcin/bgs223 {Carcinogenesis (4.004): 10.1093/carcin/bgs223} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA153755 https://www.ebi.ac.uk/ena/browser/view/PRJNA153755 None [Overal design]MCF-7 cells were transfected with a control siRNA or with the pool of siRNAs targeting c-Fos for 72 h and were then treated with vehicle or E2 for 24 h, and global gene expression profiles were assessed. Three or four biological replicates were used for each group.; [Treatment]'MCF-7 cells were transfected with a control siRNA or with the pool of siRNAs targeting c-Fos. At 6h after transfection, the medium was changed into phenol red-free DMEM plus 2% charcoal-dextran-treated calf serum for 72 h and were then treated with vehicle or E2 for 24 h.'; [Growth]"The human breast cancer cell line MCF7 was maintained in Dulbecco's Modified Eagle's Medium (DMEM) supplemented with 10% fetal bovine serum (FBS) (Invitrogen) at 37°C, under a humidified atmosphere of 5% carbon dioxide."; [Extraction]"Total RNA was extracted using RNeasy Mini Kit (Qiagen) following the manufacturer's recommendations. RNA was quantified using a NanoDrop-1000 spectrophotometer and quality was monitored with the Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA)."; [Cell type]'breast cancer cells''cell line: MCF7; cell type: breast cancer cells; transfected with: pool of siRNAs targeting c-Fos for 72hr; treated with: vehicle for 24hr; ', 'cell line: MCF7; cell type: breast cancer cells; transfected with: pool of siRNAs targeting c-Fos for 72hr; treated with: E2 for 24hr; ', 'cell line: MCF7; cell type: breast cancer cells; transfected with: control siRNA for 72hr; treated with: vehicle for 24hr; ', 'cell line: MCF7; cell type: breast cancer cells; transfected with: control siRNA for 72hr; treated with: E2 for 24hr; ' GSE76485 Homo sapiens 8 Expression profiling by array GPL10558 MBNL1-dependent modulation of transcript stability 2016-01-04 In order to identify MBNL1-dependent changes in MBNL1 target transcript stability, MBNL1 levels in MDA-MB-231 breast cancer cells were stably knocked-down using short-hairpin RNAs. The cells were then treated with alpha-amanitin to inhibit transcription, RNA was isolated at 0 and 9 hours post-alpha-amanitin treatment, and the samples were transcriptomically profiled. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76485 Muscleblind-like 1 suppresses breast cancer metastatic colonization and stabilizes metastasis suppressor transcripts. Genes & development 8.990 https://doi.org/10.1101/gad.270645.115 {Genes & development (8.990): 10.1101/gad.270645.115} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA307560 https://www.ebi.ac.uk/ena/browser/view/PRJNA307560 None [Overal design]shRNAs targeting either MBNL1 or a control shRNA were stably expressed in MDA-MB-231 breast cancer cells. These cells were treated with 10ug/mL alpha-amanitin to inhibit transcription, and total RNA was isolated at 0 and 9 hours post-alpha-amanitin treatment.; [Treatment]'Alpha-amanitin was added to cells in complete growth media to a final concentration of 10ug/mL. RNA was isolated from cells 0 and 9 hours post-alpha-amanitin treatment.'; [Growth]'MDA-MB-231 cells were maintained at 37 degrees C, 5% CO2 and grown in DMEM supplemented with 10% FBS, 2mM L-glutamine, 1mM sodium pyruvate, 100 units/mL penicillin, 100 ug/mL streptomycin and 1ug/mL amphotericin B.'; [Extraction]"RNA was extracted with a spin-column based total RNA isolation kit (Norgen Biotek) including on-column DNase I treatment according to the manufacturer's protocol."; [Cell type]'breast cancer''Sex: female; cell line: MDA-MB-231; cell type: breast cancer; ' GSE33926 Homo sapiens 51 Expression profiling by array; Third-party reanalysis GPL7264 Molecular characteristics and metastasis predictor genes of triple-negative breast cancer 2011-11-23 This microarray dataset contains 51 triple-negative breast cancers with clinical and recurrence information for at least 3 years of follow-up and 106 luminal breast cancers (reanalyzed data from Series GSE24124, GSE9309, and GSE17040). A novel set of 45-gene signature that was statistically predictive of distant metastasis recurrence for triple-negative breast cancer was identified in this study. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE33926 Molecular characteristics and metastasis predictor genes of triple-negative breast cancer: a clinical study of triple-negative breast carcinomas. PloS one 2.776 https://doi.org/10.1371/journal.pone.0045831 {PloS one (2.776): 10.1371/journal.pone.0045831} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA148225 https://www.ebi.ac.uk/ena/browser/view/PRJNA148225 None [Overal design]Specimens of breast cancer tissue were collected and snap-frozen from breast cancer patients who had surgery between 1995 and 2008 at National Taiwan University Hospital (NTUH, Taipei, Taiwan). Clinicopathological information was obtained for all breast cancer patients along with informed consent. The AJCC/UICC TNM system was used for breast cancer staging classification.; [Treatment]'The breast tumor samples were excised, collected, and snap-frozen in liquid nitrogen immediately before RNA extraction.'; [Growth]'The breast tumor samples were immediately frozen by liquid nitrogen without any additional growth procedure before RNA extraction.'; [Extraction]'Trizol reagent combined with RNAeasy mini kit'; [Cell type]'Infiltrating Ductal Carcinoma (IDC)', 'Source: ''tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 1453; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 50; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 5.32; event of distant metastasis: 0; event of death: 0; ', 'sample type: Commercially-available reference; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 1621; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 49; ajcc stage: IIIA; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 3; distant metastasis-free (years): 2.54; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 1657; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 56; ajcc stage: IIIA; lymph node metastasis: 1; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 2; tumor size: 2; distant metastasis-free (years): 4.97; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 1661; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 47; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.84; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 1683; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 54; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 2; tumor size: 1; distant metastasis-free (years): 4.95; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 2461; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 60; ajcc stage: IIIA; lymph node metastasis: 1; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 1.24; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4353; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 45; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 0.00; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4355; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 53; ajcc stage: IIB; lymph node metastasis: 1; lymphovascular invasion: 0; grade: 2; mitotic count: 3; nuclear pleomorphism: 2; tubule formation: 2; tumor size: 2; distant metastasis-free (years): 3.30; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4359; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 69; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 6.15; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4361; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 85; ajcc stage: IIIA; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 3; distant metastasis-free (years): 1.20; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4363; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 56; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 5.42; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4365; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 33; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 0.39; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4367; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 66; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 2; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 2; tumor size: 1; distant metastasis-free (years): 0.00; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4369; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 27; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.59; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4371; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 54; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 2; mitotic count: 2; nuclear pleomorphism: 2; tubule formation: 2; tumor size: 1; distant metastasis-free (years): 4.67; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4373; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 52; ajcc stage: IIB; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 3; distant metastasis-free (years): 4.80; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4375; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 54; ajcc stage: IIA; lymph node metastasis: 1; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.76; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4377; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 55; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 4.46; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4379; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 60; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 4.47; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4381; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 57; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 2; mitotic count: 1; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 4.17; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4383; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 55; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.18; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4385; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 51; ajcc stage: IIIC; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 2; tumor size: 3; distant metastasis-free (years): 4.26; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4387; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 44; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.17; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4389; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 37; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 1.79; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4391; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 62; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 2; mitotic count: 2; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.14; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4393; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 51; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 2; mitotic count: 2; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 4.04; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4395; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 63; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 4.13; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4397; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 68; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 3.95; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4399; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 63; ajcc stage: IIIC; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 3; distant metastasis-free (years): 3.75; event of distant metastasis: 1; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4401; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 61; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 0.71; event of distant metastasis: 1; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4403; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 46; ajcc stage: IIB; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 3.82; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4405; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 65; ajcc stage: IIB; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 3.86; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4407; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 41; ajcc stage: IIIC; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 3; distant metastasis-free (years): 3.06; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4409; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 54; ajcc stage: IIB; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 1.64; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4411; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 58; ajcc stage: IIB; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 2; tumor size: 2; distant metastasis-free (years): 2.11; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 4413; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 49; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 2.82; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5307; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 61; ajcc stage: IIIB; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 1.04; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5317; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 83; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 3.53; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5323; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 38; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 2.86; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5325; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 52; ajcc stage: IIA; lymph node metastasis: 1; lymphovascular invasion: N/A; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 2.76; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5327; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 54; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 1; grade: 2; mitotic count: 1; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 2.79; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5329; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 51; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: 1; grade: N/A; mitotic count: N/A; nuclear pleomorphism: N/A; tubule formation: N/A; tumor size: 2; distant metastasis-free (years): 2.89; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5345; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 63; ajcc stage: I; lymph node metastasis: 0; lymphovascular invasion: 0; grade: 3; mitotic count: 3; nuclear pleomorphism: 2; tubule formation: 3; tumor size: 1; distant metastasis-free (years): 2.87; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5347; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 55; ajcc stage: IIB; lymph node metastasis: 1; lymphovascular invasion: N/A; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 2; tumor size: 2; distant metastasis-free (years): 1.45; event of distant metastasis: 1; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5357; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 57; ajcc stage: IIIC; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 5.53; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5393; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 38; ajcc stage: IIIC; lymph node metastasis: 1; lymphovascular invasion: N/A; grade: N/A; mitotic count: N/A; nuclear pleomorphism: N/A; tubule formation: N/A; tumor size: 2; distant metastasis-free (years): 7.05; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 5399; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 40; ajcc stage: IIIC; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 3.96; event of distant metastasis: 0; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 8571; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 54; ajcc stage: IIA; lymph node metastasis: 0; lymphovascular invasion: N/A; grade: N/A; mitotic count: N/A; nuclear pleomorphism: N/A; tubule formation: N/A; tumor size: 2; distant metastasis-free (years): 3.08; event of distant metastasis: 1; event of death: 0; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 8573; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 41; ajcc stage: IV; lymph node metastasis: 0; lymphovascular invasion: N/A; grade: 3; mitotic count: 3; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 2; distant metastasis-free (years): 0.13; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 8575; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 53; ajcc stage: IV; lymph node metastasis: 1; lymphovascular invasion: 1; grade: N/A; mitotic count: N/A; nuclear pleomorphism: N/A; tubule formation: N/A; tumor size: 3; distant metastasis-free (years): 0.11; event of distant metastasis: 1; event of death: 1; ', 'tissue type: breast tumor; cell type: Infiltrating Ductal Carcinoma (IDC); array id: 8577; er ihc: 0; pr ihc: 0; her-2/neu ihc: 0; age: 57; ajcc stage: IV; lymph node metastasis: 1; lymphovascular invasion: 1; grade: 3; mitotic count: 2; nuclear pleomorphism: 3; tubule formation: 3; tumor size: 3; distant metastasis-free (years): 0.00; event of distant metastasis: 1; event of death: 1; ' GSE84986 Homo sapiens 36 Expression profiling by high throughput sequencing GPL20301 53BP1 integrates DNA repair and p53-dependent cell fate decisions via distinct mechanisms 2016-07-29 The tumor suppressor protein 53BP1, a pivotal regulator of DNA double-strand break (DSB) repair, was first identified as a p53-interacting protein over two decades ago, however its direct contributions to p53-dependent cellular activities remain undefined. Here, we reveal 53BP1 stimulates genome-wide p53-dependent gene transactivation and repression events in response to ionizing radiation (IR) and synthetic p53 activation. 53BP1-dependent p53 modulation requires both auto-oligomerization and tandem-BRCT domain mediated bivalent interactions with p53 and the ubiquitin-specific protease USP28. Loss of these activities results in inefficient p53-dependent cell-cycle checkpoint and exit responses. Furthermore, we demonstrate 53BP1-USP28 cooperation to be essential for normal p53-promoter element interactions and gene transactivation-associated events, yet dispensable for 53BP1-dependent DSB repair regulation. Collectively, our data provides a mechanistic explanation for 53BP1-p53 cooperation in controlling anti-tumorigenic cell fate decisions, and reveal these activities to be distinct and separable from 53BP1’s regulation of DNA double-strand break repair pathway choice. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE84986 53BP1 Integrates DNA Repair and p53-Dependent Cell Fate Decisions via Distinct Mechanisms. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2016.08.002 {Molecular cell (14.548): 10.1016/j.molcel.2016.08.002} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA335834 https://www.ebi.ac.uk/ena/browser/view/PRJNA335834 https://www.ncbi.nlm.nih.gov/sra?term=SRP080321 [Overal design]We evaluated the transcriptional profiles of two 53BP1Δ cell lines and included a positive (WT) and a negative (p53Δ) controls. These cell lines were treated with Nutlin-3, ionising radiation or mock treated. Three independent replicates were included for each independent condition generating a total of 36 samples.; [Treatment]'Cells were either incubated with 4 uM Nutlin-3 for 8 h, irradiated at 5 Gy and subsequently incubated for 4 h or left untreated.'; [Growth]'Cells were cultured in Dulbecco’s Modified Eagle’s Medium supplemented with 10% fetal bovine serum (Firstlink), Pen-Strep and 2 mM L-Glutamine (Sigma-Aldrich) at 37 oC in 5% CO2'; [Extraction]'Trizol/chloroform-extracted total RNA was further purified with the RNeasy Mini Kit (Qiagen) incorporating a DNaseI step (Qiagen) to remove DNA contamination.\nLibraries were prepared from rRNA-depleted total RNA isolates and according to standard Illumina guidelines using in-house adapters (Lamble et al., 2013)'; [Cell type]'Source: ''cell line: MCF-7; genotype: wildtype; treatment: untreated; ', 'cell line: MCF-7; genotype: wildtype; treatment: IR; ', 'cell line: MCF-7; genotype: wildtype; treatment: Nutlin-3; ', 'cell line: MCF-7; genotype: p53_delta; treatment: untreated; ', 'cell line: MCF-7; genotype: p53_delta; treatment: IR; ', 'cell line: MCF-7; genotype: p53_delta; treatment: Nutlin-3; ', 'cell line: MCF-7; genotype: 53BP1_delta_1; treatment: untreated; ', 'cell line: MCF-7; genotype: 53BP1_delta_1; treatment: IR; ', 'cell line: MCF-7; genotype: 53BP1_delta_1; treatment: Nutlin-3; ', 'cell line: MCF-7; genotype: 53BP1_delta_2; treatment: untreated; ', 'cell line: MCF-7; genotype: 53BP1_delta_2; treatment: IR; ', 'cell line: MCF-7; genotype: 53BP1_delta_2; treatment: Nutlin-3; ' GSE35511 Homo sapiens 4 Expression profiling by array GPL570 Gene-expression profiling of ZNF217-overexpressing MDA-MB-231 cells 2012-02-02 To obtain an overview of the cellular functions regulated by ZNF217 signaling in breast-cancer cell lines, we performed global gene-expression profiling on MDA-MB-231-pcDNA6 and MDA-MB-231-ZNF217 cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE35511 ZNF217 is a marker of poor prognosis in breast cancer that drives epithelial-mesenchymal transition and invasion. Cancer research 8.378 https://doi.org/10.1158/0008-5472.CAN-11-3095 {Cancer research (8.378): 10.1158/0008-5472.CAN-11-3095} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA152321 https://www.ebi.ac.uk/ena/browser/view/PRJNA152321 None [Overal design]Two independent cell-culture replicates from the total population of MDA-MB-231-pcDNA6 and MDA-MB-231-ZNF217 stable transfectants were used to generate total RNA. Total RNA was extracted from cell culture using a Qiagen RNA extraction kit and RNA quality was assessed using the BioAnalyzer 2100™ (Agilent Technologies). Complex probes were produced from these RNA, then hybridized to Human genome U133 Plus 2.0 array according to the manufacturer’s recommendations (Affymetrix).; [Treatment]'None'; [Growth]'Cells were grown in DMEM medium supplemented with 10% fetal bovine serum and 20 µg/ml blasticidin'; [Extraction]"total RNA was extracted using the RNeasy Mini Kit according to manufacturer's instructions (Qiagen)."; [Cell type]'Source: ''tissue: cell line: MDA-MB-231; transfection: pcDNA6/V5-His plasmid; ', 'tissue: cell line: MDA-MB-231; transfection: pcDNA6/V5-His-ZNF217 plasmid; ' GSE58135 Homo sapiens 168 Expression profiling by high throughput sequencing GPL11154 Breast Cancer RNA-seq 2014-06-01 RNA-seq was performed on breast cancer cell lines and primary tumors https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58135 Recurrent read-through fusion transcripts in breast cancer. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-014-3019-2 {Breast cancer research and treatment (3.471): 10.1007/s10549-014-3019-2} 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA251383 https://www.ebi.ac.uk/ena/browser/view/PRJNA251383 https://www.ncbi.nlm.nih.gov/sra?term=SRP042620 [Overal design]RNA-seq was performed on 28 breast cancer cell lines, 42 Triple Negative Breast Cancer (TNBC) primary tumors, and 42 Estrogen Receptor Positive (ER+) and HER2 Negative Breast Cancer primary tumors, 30 uninovlved breast tissue samples that were adjacent to ER+ primary tumors, 5 breast tissue samples from reduction mammoplasty procedures performed on patients with no known cancer, and 21 uninvolved breast tissue samples that were adjacent to TNBC primary tumors.; [Treatment]'None'; [Growth]'De-identified fresh frozen breast cancer specimens, fresh frozen matched uninvolved breast tissue adjacent to tumors, and fresh frozen breast tissue specimens from reduction mammoplasty procedures were obtained from the University of Alabama at Birmingham’s Comprehensive Cancer Center Tissue Procurement Shared Facility. The specific aliquots of specimens provided for research were chosen based on their quality control by board certified pathologists. After identification by quality control, the uninvolved breast tissue aliquots were not further macro-dissected. The breast tumor specimens were macro-dissected by the pathologists at the Tissue Procurement Shared Facility to enrich for tumor cell content and remove adjacent normal tissue. The 28 breast cancer cell lines were cultured as described previously (Oliver et al. Effect of anti-DR5 and chemotherapy on basal-like breast cancer. Breast Cancer Res Treat. 2012 Jun;133(2):417-26).'; [Extraction]'The frozen breast tissue specimens were weighed, transferred to a 15 mL conical tube containing ceramic beads, and RLT Buffer (Qiagen) plus 1% BME was added so that the tube contained 35 uL of buffer for each milligram of tissue. The conical tubes containing tissue, ceramic beads and buffer were then shaken in a MP Biomedicals FastPrep machine until the tissue was visibly homogenized (90 seconds at 6.5 meters per second). The homogenized tissue was stored at -80°C. Total RNA was extracted from 5 million cultured cells or 350 uL of tissue homogenate (equivalent to 10 mg of tissue) using the Norgen Animal Tissue RNA Purification Kit (Norgen Biotek Corporation). Cell lysate was treated with Proteinase K before it was applied to the column and on-column DNAse treatment was performed according to the manufacturer’s instructions. Total RNA was eluted from the columns and quantified using the Qubit RNA Assay Kit and the Qubit 2.0 fluorometer (Invitrogen).\nRNA-seq libraries for each sample were constructed from 250 ng total RNA using the polyA selection and transposase-based non-stranded library construction (Tn-RNA-seq) described previously (Gertz et al. Transposase mediated construction of RNA-seq libraries.2012. Genome Res 22 (1):134-141). RNA-seq libraries were barcoded during PCR using Nextera barcoded primers according to the manufacturer (Epicentre). The RNA-seq libraries were quantified using the Qubit dsDNA HS Assay Kit and the Qubit 2.0 fluorometer (Invitrogen) and three barcoded libraries were pooled in equimolar quantities for sequencing. The pooled libraries were sequenced on an Illumina HiSeq 2000 sequencing machine using paired-end 50 bp reads and a 6 bp index read, and we obtained at least 50 million read pairs from each library.'; [Cell type]'Source: ''tissue: Breast Cancer Cell Line; ', 'tissue: ER+ Breast Cancer Primary Tumor; ', 'tissue: Triple Negative Breast Cancer Primary Tumor; ', 'tissue: Uninvolved Breast Tissue Adjacent to ER+ Primary Tumor; ', 'tissue: Reduction Mammoplasty - No known cancer; ', 'tissue: Uninvolved Breast Tissue Adjacent to TNBC Primary Tumor; ' GSE81313 Homo sapiens 61 Other GPL15520 Identification of shared TCR sequences from T cells in human breast cancer using emulsion RT-PCR 2016-05-11 We report the discovery of T cell receptors that are present and shared in multiple HLA-matched breast cancer patient tumors using a single cell emulsion based RT-PCR technique that pairs the alpha and beta TCR chains for high throughput analysis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE81313 Identification of shared TCR sequences from T cells in human breast cancer using emulsion RT-PCR. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1606994113 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1606994113} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA321261 https://www.ebi.ac.uk/ena/browser/view/PRJNA321261 https://www.ncbi.nlm.nih.gov/sra?term=SRP074899 [Overal design]Analysis of TCR sequences from 20 breast cancer patient tumors and blood, as well as 6 control HLA matched individuals; [Treatment]'CD8+ T cells were selected from bulk samples using a positive selection kit. CD* T cells were incubated overnight in 10U/ml of IL-2 prior to emulsion RT-PCR sequencing'; [Growth]'None'; [Extraction]'No extraction of RNA was performed, rather single cells were lysed within an emulsion droplet and RT-PCR was performed using TCR specific primers\nPCR amplicons were generated using primers containing the Read1, Read2, and Bridge priming sites as well as Illumina indicies (Read 2 side) and custom indicies on the Read 1 side\namplicon sequencing following RT-PCR of a specific gene(s)'; [Cell type]'Source: '"tumor stage: IIIA; illumina read 2 barcode: 5' - CGTGAT - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - CGTGAT - 3'; custom read 1 barcode: 5' - TGCANNNNNN - 3'; cell type isolated: CD8+ T cells; ", "sentinel ln tumor invasion: yes; illumina read 2 barcode: 5' - CGTGAT - 3'; custom read 1 barcode: 5' - GAGG - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IIA; illumina read 2 barcode: 5' - ACATCG - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - ACATCG - 3'; custom read 1 barcode: 5' - TGCANNNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IIB; illumina read 2 barcode: 5' - TGGTCA - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - TGGTCA - 3'; custom read 1 barcode: 5' - TGCANNNNNN - 3'; cell type isolated: CD8+ T cells; ", "sentinel ln tumor invasion: no; illumina read 2 barcode: 5' - TGGTCA - 3'; custom read 1 barcode: 5' - GAGG - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IIIA; illumina read 2 barcode: 5' - TGGTCA - 3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - GATCGC -3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IIIA; illumina read 2 barcode: 5' - ACATCG - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - CGTGAT - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "sentinel ln tumor invasion: yes; illumina read 2 barcode: 5' - CGTGAT - 3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - ACATCG - 3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IA; illumina read 2 barcode: 5' - ATCATC - 3'; custom read 1 barcode: 5' - GAGG - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - ATCATC - 3'; custom read 1 barcode: 5' - TGCANNNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IA; illumina read 2 barcode: 5' - ATCATC - 3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - ATCATC - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IA; illumina read 2 barcode: 5' - ATCATC - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "sentinel ln tumor invasion: no; illumina read 2 barcode: 5' - GATCGC -3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IIA; illumina read 2 barcode: 5' - ATCATC - 3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - ACATCG - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IA; illumina read 2 barcode: 5' - ACATCG - 3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - GCCTAA - 3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "sentinel ln tumor invasion: yes; illumina read 2 barcode: 5' - GCCTAA - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IA; illumina read 2 barcode: 5' - GATCGC -3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IIA; illumina read 2 barcode: 5' - CGTGAT - 3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IV; illumina read 2 barcode: 5' - GATCGC -3'; custom read 1 barcode: 5' - TGCANNNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - GATCGC -3'; custom read 1 barcode: 5' - GAGG - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IA; illumina read 2 barcode: 5' - TGGTCA - 3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "sentinel ln tumor invasion: yes; illumina read 2 barcode: 5' - TGGTCA - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IV; illumina read 2 barcode: 5' - GCCTAA - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IA; illumina read 2 barcode: 5' - GATCGC -3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - TGGTCA - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "sentinel ln tumor invasion: no; illumina read 2 barcode: 5' - TGGTCA - 3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IIA; illumina read 2 barcode: 5' - GCCTAA - 3'; custom read 1 barcode: 5' - TGCANNNNNN - 3'; cell type isolated: CD8+ T cells; ", "sentinel ln tumor invasion: no; illumina read 2 barcode: 5' - GCCTAA - 3'; custom read 1 barcode: 5' - ACGTNNNN - 3'; cell type isolated: CD8+ T cells; ", "sentinel ln tumor invasion: no; illumina read 2 barcode: 5' - CGTGAT - 3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "tumor stage: IA; illumina read 2 barcode: 5' - TGGTCA - 3'; custom read 1 barcode: 5' - TGCANNNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - GATCGC -3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - TGGTCA - 3'; custom read 1 barcode: 5' - GAGG - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - TGGTCA - 3'; custom read 1 barcode: 5' - GTACNNNNNNNN - 3'; cell type isolated: CD8+ T cells; ", "illumina read 2 barcode: 5' - CGTGAT - 3'; custom read 1 barcode: 5' - GAGG - 3'; cell type isolated: CD8+ T cells; " GSE30682 Homo sapiens 343 Expression profiling by array GPL6884 Search for a gene-expression signature of breast cancer local recurrence in young women 2011-07-14 Kreike et al, have constructed a gene-expression (GE) profile predictive for local recurrence (LR) after breast-conserving treatment (BCT) from a series of 165 patients . This study aimed to test this signature both internally (cross-platform) and externally on a independent series and to further explore the search for a GE signature of breast cancer LR in young women. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE30682 Search for a gene expression signature of breast cancer local recurrence in young women. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-11-1954 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-11-1954} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA144431 https://www.ebi.ac.uk/ena/browser/view/PRJNA144431 None [Overal design]The transcriptome of 343 primary breast cancer carcinoma were analyzed using Illumina HumanWG-6_v3 Arrays.; [Treatment]'Samples are individually processed (RNA isolation, followed by DNAse treatment and amplification) and equal quantities of each sample are combined to create a pool of amplified RNA.'; [Growth]'None'; [Extraction]'RNA Isolation with TRIZOL® Reagent (Cell pellets(A), tissues(A) or cell culture dishes(B) (A)RNA isolation from cell pellets or tissues'; [Cell type]'Source: ''origin: Dutch; age: 50; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 44; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: NA; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: p53-; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 39; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 31; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEIII; tubuleformation: NA; polymorphism: NA; mitoticindex: NA; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 49; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 49; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: Dutch; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: HT; histshape: NA; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: NA; dcisinside: NA; dcisoutside: NA; dcis: NA; dcisgrade: NA; lcis: NA; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 47; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 49; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 48; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 45; lr: 1; time2lr: 2.1; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: TNP; ', 'origin: Dutch; age: 43; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 50; lr: 1; time2lr: 5.1; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 37; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 47; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 49; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 39; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: NA; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: HER2; ', 'origin: Dutch; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 38; lr: 1; time2lr: 1.4; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEII; tubuleformation: NA; polymorphism: NA; mitoticindex: NA; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 42; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 46; lr: 1; time2lr: 3.4; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: Dutch; age: 42; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53+; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 43; lr: 1; time2lr: 2; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: NA; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 32; lr: 1; time2lr: 1.7; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 0; subtypebyge: HER2; ', 'origin: Dutch; age: 50; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: Dutch; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: NA; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: other type; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 45; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: NA; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 44; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 46; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: NA; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 0; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 39; lr: 1; time2lr: 5.9; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: other type; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: No DCIS outside; dcis: NA; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 44; lr: 1; time2lr: 5.7; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: NA; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEII; tubuleformation: NA; polymorphism: NA; mitoticindex: NA; dcisinside: NA; dcisoutside: NA; dcis: NA; dcisgrade: NA; lcis: NA; lvi: NA; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 44; lr: 1; time2lr: 2.2; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: other type; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: Dutch; age: 44; lr: 1; time2lr: 7.3; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 47; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: NA; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: NA; p53: p53+; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: Dutch; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEIII; tubuleformation: NA; polymorphism: NA; mitoticindex: NA; dcisinside: NA; dcisoutside: NA; dcis: NA; dcisgrade: NA; lcis: NA; lvi: NA; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 48; lr: 1; time2lr: 7.4; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 42; lr: 1; time2lr: 1; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: No DCIS outside; dcis: NA; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 50; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53+; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 41; lr: 1; time2lr: 4.6; pt: pT2-3; surgicalmargin: NA; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: TNP; ', 'origin: Dutch; age: 42; lr: 1; time2lr: 9.3; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: Dutch; age: 49; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 47; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 39; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 39; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 43; lr: 1; time2lr: 4.7; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: NA; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: Dutch; age: 44; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 50; lr: 1; time2lr: 2.1; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 50; lr: 1; time2lr: 3.1; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 42; lr: 1; time2lr: 0.8; pt: NA; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 39; lr: 1; time2lr: 6.2; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 44; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: other type; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 47; lr: 1; time2lr: 1.4; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: HER2; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: LVI present; lviquant: 1 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: LVI present; lviquant: 1 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: LVI present; lviquant: 1 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 49; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 36; lr: 1; time2lr: 3.1; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: French; age: 49; lr: 1; time2lr: 2.2; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 48; lr: 1; time2lr: 3.8; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 32; lr: 1; time2lr: 4.7; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 45; lr: 1; time2lr: 4.6; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: multinodular; histtype: other type; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: LVI present; lviquant: 1 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 30; lr: 1; time2lr: 0.8; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 38; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: Dutch; age: 39; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 40; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 48; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 42; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 47; lr: 1; time2lr: 2.5; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 43; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: NA; ht: NA; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: No DCIS outside; dcis: NA; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 29; lr: 1; time2lr: 2.1; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: Dutch; age: 40; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 46; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 40; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 42; lr: 1; time2lr: 4.1; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: Dutch; age: 45; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 50; lr: 1; time2lr: 0.8; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 44; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: NA; tubuleformation: NA; polymorphism: NA; mitoticindex: NA; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 48; lr: 1; time2lr: 3.3; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 44; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS+; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyg e: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 49; lr: 1; time2lr: 9.4; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 44; lr: 1; time2lr: 1.9; pt: pT1; surgicalmargin: marg-; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: multinodular; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 37; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEI; tubuleformation: tubule<10%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: NA; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: other type; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 46; lr: 1; time2lr: 3.3; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: LVI present; lviquant: 1 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 30; lr: 1; time2lr: 1.8; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 43; lr: 1; time2lr: 5.6; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: NA; dcis: NA; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEI; tubuleformation: tubule<10%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 42; lr: 1; time2lr: 2.2; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: LVI present; lviquant: 1 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 45; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 45; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 0; subtypebyge: HER2; ', 'origin: French; age: 44; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: LVI present; lviquant: 1 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 43; lr: 1; time2lr: 5; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 43; lr: 1; time2lr: 2.5; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEI; tubuleformation: tubule<10%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 41; lr: 1; time2lr: 2.5; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 39; lr: 1; time2lr: 1.8; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 37; lr: 1; time2lr: 2.3; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: HER2; ', 'origin: French; age: 42; lr: 1; time2lr: 5.7; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 23; lr: 1; time2lr: 1.1; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: TNP; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 48; lr: 1; time2lr: 4.6; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS+; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: LVI present; lviquant: 1 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: NA; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 47; lr: 1; time2lr: 6.7; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 42; lr: 1; time2lr: 2.3; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 36; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 46; lr: 1; time2lr: 1.2; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 40; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 35; lr: 1; time2lr: 1.3; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 40; lr: 1; time2lr: 1.2; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: HER2; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 26; lr: 1; time2lr: 1.5; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: NA; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 44; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 43; lr: 1; time2lr: 1.5; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 44; lr: 1; time2lr: 3.1; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 40; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 41; lr: 1; time2lr: 2.4; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: Dutch; age: 50; lr: 1; time2lr: 1.8; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: NA; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: Dutch; age: 41; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: multinodular; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 45; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS+; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 42; lr: 1; time2lr: 3.1; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: NA; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: NA; dcisgrade: NA; lcis: LCIS present; lvi: LVI present; lviquant: 1 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 42; lr: 1; time2lr: 2.2; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 48; lr: 1; time2lr: 5; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS low grade; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 43; lr: 1; time2lr: 2; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 49; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: French; age: 36; lr: 1; time2lr: 1.6; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEI; tubuleformation: tubule<10%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 49; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS+; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 37; lr: 1; time2lr: 4.5; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 30; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS+; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: NA; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS+; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: NA; tubuleformation: NA; polymorphism: NA; mitoticindex: NA; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: French; age: 28; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 43; lr: 1; time2lr: 2.9; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 35; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: French; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 44; lr: 1; time2lr: 1.6; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: multinodular; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 44; lr: 1; time2lr: 0.8; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: multinodular; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: TNP; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargi ndcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 43; lr: 1; time2lr: 6.7; pt: pT2-3; surgicalmargin: NA; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 46; lr: 1; time2lr: 4.2; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 28; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 39; lr: 1; time2lr: 3.3; pt: pT2-3; surgicalmargin: NA; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53+; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 40; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 30; lr: 1; time2lr: 4.9; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: NA; rttotaldose: NA; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: Dutch; age: 36; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: HER2; ', 'origin: Dutch; age: 29; lr: 1; time2lr: 8.3; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 47; lr: 1; time2lr: 4.6; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 47; lr: 1; time2lr: 0.3; pt: NA; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: NA; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 39; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53-; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 48; lr: 1; time2lr: 4.2; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: NA; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 42; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: TNP; ', 'origin: Dutch; age: 45; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 46; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 41; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 42; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: NA; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 33; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 35; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: multinodular; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 45; lr: 1; time2lr: 2; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 48; lr: 1; time2lr: 3.9; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 48; lr: 1; time2lr: 3.5; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEI; tubuleformation: tubule<10%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 44; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 36; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 50; lr: 1; time2lr: 7.2; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 38; lr: 1; time2lr: 3.5; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: HER2; ', 'origin: Dutch; age: 50; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: other type; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 45; lr: 1; time2lr: 4.5; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: LVI present; lviquant: 1 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 49; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 47; lr: 1; time2lr: 1.1; pt: pT1; surgicalmargin: marg-; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: NA; surgicalmargindcis: MargDCIS?; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 42; lr: 1; time2lr: 8; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: LCIS present; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: lobular; histgrade: EEI; tubuleformation: tubule<10%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 50; lr: 1; time2lr: 4.1; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: French; age: 48; lr: 1; time2lr: 9.3; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 46; lr: 1; time2lr: 4.2; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS+; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 39; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: TNP; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: HT; histshape: multinodular; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 47; lr: 1; time2lr: 1; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 39; lr: 1; time2lr: 4.2; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 50; lr: 1; time2lr: 1.7; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 1; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: French; age: 49; lr: 1; time2lr: 4.6; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: NA; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 33; lr: 1; time2lr: 2.2; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: other type; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 40; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: multinodular; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 50; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 49; lr: 1; time2lr: 5.6; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEI; tubuleformation: tubule<10%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 43; lr: 1; time2lr: 1.2; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 44; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 43; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 40; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 38; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: HER2; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 46; lr: 1; time2lr: 1.6; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: multinodular; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 44; lr: 1; time2lr: 1.6; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: French; age: 36; lr: 1; time2lr: 2.8; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEI; tubuleformation: tubule<10%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: HER2; ', 'origin: Dutch; age: 41; lr: 1; time2lr: 3.9; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: other type; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 47; lr: 1; time2lr: 5.9; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 38; lr: 1; time2lr: 3.3; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: NA; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 49; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 38; lr: 1; time2lr: 3.9; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 40; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 42; lr: 1; time2lr: 3.6; pt: pT2-3; surgicalmargin: NA; surgivalmargininv: NA; surgicalmargindcis: NA; pn: NA; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: HER2; ', 'origin: Dutch; age: 38; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: NA; surgicalmargindcis: MargDCIS?; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 48; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEI; tubuleformation: tubule<10%; polymorphism: polymorph1; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: HER2; ', 'origin: French; age: 44; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: F rench; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: NA; lvi: NA; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 44; lr: 1; time2lr: 4.8; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 23; lr: 1; time2lr: 6.5; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: multinodular; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 39; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 49; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 36; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 38; lr: 1; time2lr: 7.1; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: multinodular; histtype: other type; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 44; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 42; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 39; lr: 1; time2lr: 2.5; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: NA; tubuleformation: NA; polymorphism: NA; mitoticindex: NA; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 43; lr: 1; time2lr: 4; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS+; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: LVI present; lviquant: 1 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 35; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: French; age: 36; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: NA; tubuleformation: NA; polymorphism: NA; mitoticindex: NA; dcisinside: NA; dcisoutside: NA; dcis: NA; dcisgrade: NA; lcis: NA; lvi: NA; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: TNP; ', 'origin: Dutch; age: 38; lr: 1; time2lr: 5.2; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 49; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: multinodular; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 42; lr: 1; time2lr: 2.2; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 33; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: NA; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 35; lr: 1; time2lr: 9.4; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 45; lr: 1; time2lr: 7.2; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 37; lr: 1; time2lr: 1; pt: pT2-3; surgicalmargin: NA; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: NA; dcisinside: NA; dcisoutside: NA; dcis: NA; dcisgrade: NA; lcis: NA; lvi: NA; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 27; lr: 1; time2lr: 1.2; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: HER2; ', 'origin: Dutch; age: 49; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 39; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 46; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 37; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: Dutch; age: 50; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: Dutch; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule>90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 47; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 44; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 42; lr: 1; time2lr: 3.1; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 46; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 40; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: No DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: NA; dcisgrade: NA; lcis: NA; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 1; prolifbyge: 0; subtypebyge: LUMHER; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: multinodular; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: French; age: 45; lr: 1; time2lr: 3.9; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 45; lr: 1; time2lr: 1.9; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEIII; tubuleformation: NA; polymorphism: NA; mitoticindex: NA; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 45; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 50; lr: 1; time2lr: 2.8; pt: pT2-3; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: MargDCIS?; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: HT; histshape: stellate; histtype: lobular; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: lobular; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 47; lr: 1; time2lr: 1.3; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 40; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 48; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: NA; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 32; lr: 1; time2lr: 5.8; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: LCIS present; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 37; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 47; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 37; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 0; herbyge: 1; prolifbyge: 1; subtypebyge: LUMHER; ', 'origin: Dutch; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv+; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: multinodular; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53-; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 44; lr: 1; time2lr: 3.7; pt: pT1; surgicalmargin: NA; surgivalmargininv: NA; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 43; lr: 1; time2lr: 5.3; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: other type; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph1; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: NA; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: NA; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 34; lr: 1; time2lr: 1.1; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS intermed grade; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: French; age: 41; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: >66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: ductal; histgrade: EEII; tubuleformation: tubule<10%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 50; lr: 1; time2lr: 6; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEII; tubuleformation: tubule50-90%; polymorphism: polymorph3; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 1; prolifbyge: 0; subtypebyge: HER2; ', 'origin: French; age: 43; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: multinodular; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic2; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 45; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: no boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: sharply demarcated; histtype: other type; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ', 'origin: Dutch; age: 44; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: 2-5 LVI; p53: p53-; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: French; age: 36; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN+; rtboost: no boost; rttotaldose: <=66Gy; ct: ChT; ht: no HT; histshape: stellate; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: DCIS inside; dcisoutside: DCIS outside; dcis: DCIS; dcisgrade: DCIS high grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: NA; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 1; subtypebyge: LUMB; ', 'origin: Dutch; age: 44; lr: 0; time2lr: NA; pt: pT1; surgicalmargin: marg+; surgivalmargininv: MargInv-; surgicalmargindcis: MargDCIS-; pn: pN-; rtboost: boost; rttotaldose: <=66Gy; ct: no ChT; ht: no HT; histshape: NA; histtype: ductal; histgrade: EEI; tubuleformation: tubule50-90%; polymorphism: polymorph2; mitoticindex: mitotic1; dcisinside: NA; dcisoutside: NA; dcis: DCIS; dcisgrade: DCIS low grade; lcis: No LCIS; lvi: No LVI; lviquant: NA; p53: p53+; erbyge: 1; prbyge: 1; herbyge: 0; prolifbyge: 0; subtypebyge: LUMA; ', 'origin: Dutch; age: 47; lr: 0; time2lr: NA; pt: pT2-3; surgicalmargin: marg-; surgivalmargininv: MargInv-; surgicalmargindcis: NA; pn: pN+; rtboost: boost; rttotaldose: >66Gy; ct: ChT; ht: no HT; histshape: multinodular; histtype: ductal; histgrade: EEIII; tubuleformation: tubule<10%; polymorphism: polymorph3; mitoticindex: mitotic3; dcisinside: No DCIS inside; dcisoutside: No DCIS outside; dcis: No DCIS; dcisgrade: NA; lcis: No LCIS; lvi: NA; lviquant: >5 LVI; p53: p53-; erbyge: 0; prbyge: 0; herbyge: 0; prolifbyge: 1; subtypebyge: TNP; ' GSE130762 Homo sapiens 8 Expression profiling by high throughput sequencing GPL17303 Unlocking the transcriptomic potential of formalin-fixed paraffin embedded clinical tissues: Comparison of gene expression profiling approaches [AmpliSeq] 2019-05-06 Background: High-throughput transcriptomics has matured into a very well established and widely utilised research tool over the last two decades since the first mRNA profiling microarrays. Clinical datasets generated on a range of different platforms continue to be deposited in public repositories provide an ever-growing, valuable resource for reanalysis. Cost and tissue availability normally preclude processing samples across multiple technologies, making it difficult to directly evaluate performance, reliability and to what extent gene expression data from different platforms can be compared or integrated. Purpose: In this study, we describe our experiences using nine new and established mRNA profiling techniques including Lexogen QuantSeq, Qiagen QiaSeq, BioSpyder TempO-Seq, Ion AmpliSeq, Nanostring, Affymetrix Clariom S or U133A, Illumina BeadChip and Ion Total RNA-seq of formalin-fixed paraffin embedded (FFPE) and fresh frozen (FF) sequential patient-matched breast tumour samples. Results: The number of genes represented and reliability were found to vary between the platforms, but overall all methods provided data which were largely comparable. Crucially we found that it is possible to integrate data for combined analyses across FFPE/FF and platforms using established batch correction methods as required to increase cohort sizes. However, some platforms appear to be better suited to FFPE samples, particularly archival material. Overall, we illustrate that technology selection is a balance between required resolution, sample quality, availability and cost. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE130762 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA541297 https://www.ebi.ac.uk/ena/browser/view/PRJNA541297 https://www.ncbi.nlm.nih.gov/sra?term=SRP195588 [Overal design]Sequencing of patient-matched sets of human breast cancer biopsy samples using 9 different mRNA profiling platforms. We assess the feasibility of integrating data from FFPE or FF tissue sequenced using different platforms and compare these different technoolgies.; [Treatment]'None'; [Growth]'None'; [Extraction]"RNA was extracted from 2x20µm FFPE tissue sections using the RNeasy FFPE kit.\nAll samples were processed and libraries constructed following the manufacturer's guidelines in the Edinburgh Clinical Research Facility."; [Cell type]'Source: ''tissue: breast cancer; time point: early on-treatment biopsy; ', 'tissue: breast cancer; time point: pre-treatment biopsy; ', 'tissue: breast cancer; time point: late on-treatment biopsy; ' GSE99541 Homo sapiens 4 Other GPL16791 Phase Separation of Ligand-Activated Enhancers Licenses Cooperative Chromosomal Enhancer Assembly [HiC-seq] 2017-06-01 Detailed analysis of estrogen mediated enhancer landscape and chromosomal architectural changes specifically in human chromosome 21. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99541 Phase separation of ligand-activated enhancers licenses cooperative chromosomal enhancer assembly. Nature structural & molecular biology 12.109 https://doi.org/10.1038/s41594-019-0190-5 {Nature structural & molecular biology (12.109): 10.1038/s41594-019-0190-5} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA388867 https://www.ebi.ac.uk/ena/browser/view/PRJNA388867 https://www.ncbi.nlm.nih.gov/sra?term=SRP108500 [Overal design]in situ Hi-C experiments are designed to elucidate 3D chromatin landscape in human breast cancer cells (MCF7) under basal and estrogen treated conditions.; [Treatment]'MCF7 cells grown in phenol red free DMEM and charcoal stripped FBS were treated with estrogen for 60 before collecting the samples for ChIP-Seq. Control samples were treated with ICI 182,780, or ER alpha agonist'; [Growth]'MCF7, estrogen receptor alpha positive breast cancer cells were cultured in DMEM and 10%FBS under standard condition'; [Extraction]'Hi-C, samples were fixed for 10 minutes with 1% formaldehyde. Fixation was stopped by adding Glycine (0.125M). Samples were frozen at -80 degee Celcius till used. In situ Hi-C was essentially performed as described(Rao et al., 2014). Briefly, for each experiment, 2 x 10E6 cells, fixed for 10 minutes with 1 % formaldehyde/PBS and washed twice with PBS, permeabilized for 7 minutes at 62°C in a PCR cycler with 200 µl lysis buffer (0.5% SDS, 50 mM Tris-HCl pH=7.5, 10 mM NaCl, 1mM EDTA, and 1X protease inhibitors solution (Roche)) and pelleted at 2500x g for 5 minutes. Supernatant was removed and nuclei were resuspended in 25 µl 10% Triton X-100, 25 µl NEB 2 buffer, 195 µl water, and rotated for 15’ at 37°C. Chromatin was digested overnight at 37°C after adding 0.5 µl 1 M DTT and 4 µl 25 U/µl Mbo I and rotated at 8 RPM. MboI was inactivated by incubation at 62°C for 20 minutes. Nuclei were centrifuged for 5 minutes at 500 x g and 200 µl supernatant was discarded. Overhangs were filled in by adding 32 μL water, 5 μl of 10X NEBuffer2, 0.35 μl of 10 mM dATP, 0.35 μl of 10 mM dTTP, 0.35 μl of 10 mM dGTP, 7.5 μl 0.4 mM Biotin-14-dCTP (Invitrogen), 4 μl 10% Triton X-100, and 5 μl of 5 U/μl Klenow enzyme (Enzymatics) and rotating for 40 minutes at room temperature. The reaction was stopped by adding 2.5 µl 0.5 M EDTA. DNA was ligated under rotation overnight at 16°C in a total volume of 400 µl ligase mix containing 40ul 10x T4 DNA ligase buffer (Enzymatics), 36 µl 10 % Triton X-100, 5 µl 100x BSA (10 mg/ml), 1 µl (1200 U) T4 DNA ligase (Enzymatics). The reaction was terminated by adding 20 µl 0.5 M EDTA. Samples were digested for 15 minutes at 42°C with 1 µl 10 µg/µl RNase A. 33 μl of 5 M sodium chloride and 55 µl of 10% SDS were added and reverse crosslinked for 4 h at 65°C. Protein was digested with 10 μl of 20 mg/ml proteinase K (Life Technologies), incubated\u2028at 55°C for 120 minutes, shaking at 800 RPM, then 65°C for 90 minutes. DNA was extracted once with 600 µl phenol/chloroform/isoamylalcohol (25:24:1) Tris-buffered to pH 8.0 and once with 300 µl CHCl3, and precipitated overnight at -20°C with 1.5 µl 20 mg/ml glycogen and 1412 µl 100% ethanol overnight. DNA was pelleted for 20 minutes at 16000x g, 4°C and washed once with 1 ml 80% ethanol for 5 minutes, 8000x g, 4°C. Pellets were dissolved in 131 µl TT (0.05% Tween 20/10 mM Tris pH=8) each. DNA was sheared with 300 bp Covaris protocol in snap cap tube in a Covaris E220 at 10 % duty cycle, intensity 140 W, 200 cycles/burst for 80” total time. Large DNA fragments (>400 bp) were depleted with 5 µl Speedbeads and 6.45% PEG8000/2.5 M NaCl. Supernatant was transferred to fresh tubes and small DNA fragments were collected with 9.5% PEG8000 by adding an additional 60 µl PEG8000/2.5 M NaCl and 3 µl Speedbeads. DNA was eluted in 50ul TT for 5 minutes. DNA was captured with 50 µl 2x B&W buffer containing 0.2 % Tween 20 and 15 µl T1 Dynabeads (Invitrogen, washed twice with 1x B&W buffer (10 mM Tris-HCl pH 7.5, 01 mM EDTA, 2 M NaCl, then suspended in 51 µl 2x B&W buffer containing 0.2% Tween 20), rotating for 30 minutes at room temperature. Beads were washed once with 500 µl each of 1x B&W/0.1 % Triton-X100, once with TET (0.05% Tween 20/TE).\nHi-C library bound to beads were resuspend in 100 µl end repair mix (KAPA Library Preparation for Illumina) Incubated for 30 minutes at 20°C. Reaction was stopped by adding 2.5 µl 0.5 M EDTA. Beads were collected and washed twice with 150 µl 1x B&W/0.1% Triton-X100, once with 180 µl TET. Beads were resuspend in 50 ul A-tailing reaction mix (KAPA Library Preparation for Illumina), incubated 30 minutes at 30°C. Reaction was stopped by adding 1.5 µl 0.5 M EDTA. Beads were collected and washed twice with 150 µl 1x B&W/0.1% Triton-X100, once with 180 µl TET. Sequencing adapters were ligated to the bead-bound DNA in 100 µl 1x rapid ligation buffer (Enzymatics) containing 0.1% Tween 20, 2ul 1:20 Truseq adapters (Illumina), 1 µl (3000 U) T4 DNA ligase (Enzymatics) for 20 minutes at room temperature. The reaction was stopped with 5 µl 0.5 M EDTA, beads washed twice with 1x B&W, twice with 0.1% Tween 20/TE, then resuspended in 30 µl 0.033% Tween20/LoTE, (TE diluted 1:4 with water). Libraries were PCR-amplified using the 10 µl of the bead suspension as template for 10 cycles using KAPA HiFi, size-selected to 225-425 bp insert size using speedbeads PEG8000/2.5 M NaCl solutions, and paired-end sequenced on an Illumina HiSeq 2500.'; [Cell type]'Human breast cancer cells''cell line: MCF7; cell type: Human breast cancer cells; genotype/variation: wild type; treated with: ICI 182,780, an estrogen receptor alpha antagonist; Control; ', 'cell line: MCF7; cell type: Human breast cancer cells; genotype/variation: wild type; treated with: estrogen; Treatement; ' GSE147441 Homo sapiens 2 Non-coding RNA profiling by array GPL28301 The lncRNA microarray analysis in EZH2-overexpressing breast cancer cell MCF7 2020-03-24 To explore the potential target lncRNAs of EZH2 in breast cancer cells, we determined the lncRNA expression profiles in MCF7-control and MCF7-EZH2 overexpressing cells using lncRNA Microarray. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE147441 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA614636 https://www.ebi.ac.uk/ena/browser/view/PRJNA614636 None [Overal design]EZH2-overexpressing breast cancer cells MCF7 were used for treatment group. Empty vector was transfected into MCF7 cells using for control group. Then, total RNAs were extracted for lncRNA chip preparation and analysis.; [Treatment]'Empty vector and flag-EZH2 were transfected into breast cancer cell line MCF7 using Lipofectamine 2000 (Invitrogen).'; [Growth]'Breast cancer cells MCF7 were grown in Dulbecco’s modified Eagle’s medium (DMEM, Gibco; Thermo Fisher Scientific, Waltham, MA USA) supplemented with 10% fetal bovine serum (FBS) at 37°C under 5% CO2 in a humidified incubator.'; [Extraction]'Total RNA was isolated using TRIzol (Life Technologies) according to manufacturer’s instructions.RNA quality and quantity was measured by using Agilent 2200 Bioanalyzer.'; [Cell type]'breast cancer''cell line: MCF7; cell type: breast cancer; genotype/variation: EZH2 low; ', 'cell line: MCF7; cell type: breast cancer; genotype/variation: EZH2 high; ' GSE38829 Homo sapiens 4 Expression profiling by array GPL13667 Expression data from MCF7 and MCF7-LTED cells treated with YC-1 2012-06-20 To identify novel therapeutic opportunities for patients with acquired resistance to endocrine treatments in breast cancer, we applied a high-throughput drug screen. The IC50 values were determined for MCF7 and MCF7-LTED cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE38829 VAV3 mediates resistance to breast cancer endocrine therapy. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr3664 {Breast cancer research : BCR (5.676): 10.1186/bcr3664} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA169021 https://www.ebi.ac.uk/ena/browser/view/PRJNA169021 None [Overal design]MCF7 and LTED cells were treated with YC-1 for RNA extraction and hybridization on Affymetrix microarrays.; [Treatment]'MCF7 cells were treated with YC-1 (20 micrograms/L) and LTED cells were treated with YC-1 (2 micrograms/L) or vehicle (DMSO) for 48 hours.'; [Growth]'MCF7 cells were cultured and maintained in RPMI medium containing 10% FBS and 2 mM glutamine and LTED cells were cultured and maintained in RPMI medium containing 10% DCC-FBS (estrogen depleted) and 2 mM glutamine.'; [Extraction]"Trizol extraction of total RNA was performed according to manufacturer's instructions."; [Cell type]'Source: ''cell line source: Breast cancer; agent: none; cell line: MCF7; ', 'cell line source: Breast cancer; agent: YC-1 (20 micrograms/L); cell line: MCF7; ', 'cell line source: Breast cancer; agent: none; cell line: LTED; ', 'cell line source: Breast cancer; agent: YC-1 (2 micrograms/L); cell line: LTED; ' GSE16648 Homo sapiens 42 Expression profiling by array GPL570 Networking of differentially expressed genes in human cancer cell lines resistant to methotrexate 2009-06-16 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE16648 Networking of differentially expressed genes in human cancer cells resistant to methotrexate. Genome medicine 10.886 https://doi.org/10.1186/gm83 {Genome medicine (10.886): 10.1186/gm83} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA116233 https://www.ebi.ac.uk/ena/browser/view/PRJNA116233 None [Overal design]Refer to individual Series; [Treatment]'None'; [Growth]'None'; [Extraction]'RNeasy Mini Kit from Qiagen'; [Cell type]'colon cancer', 'breast cancer', 'pancreatic cancer', 'erythroblastic leukemia', 'osteosarcoma''cell line: HT29; cell type: colon cancer; methotrexate sensitivity: sensitive; ', 'cell line: HT29; cell type: colon cancer; methotrexate sensitivity: resistant; ', 'cell line: Caco2; cell type: colon cancer; methotrexate sensitivity: sensitive; ', 'cell line: Caco2; cell type: colon cancer; methotrexate sensitivity: resistant; ', 'cell line: MCF7; cell type: breast cancer; methotrexate sensitivity: sensitive; ', 'cell line: MCF7; cell type: breast cancer; methotrexate sensitivity: resistant; ', 'cell line: MDA-MB-468; cell type: breast cancer; methotrexate sensitivity: sensitive; ', 'cell line: MDA-MB-468; cell type: breast cancer; methotrexate sensitivity: resistant; ', 'cell line: MIA PaCa2; cell type: pancreatic cancer; methotrexate sensitivity: sensitive; ', 'cell line: MIA PaCa2; cell type: pancreatic cancer; methotrexate sensitivity: resistant; ', 'cell line: K562; cell type: erythroblastic leukemia; methotrexate sensitivity: sensitive; ', 'cell line: K562; cell type: erythroblastic leukemia; methotrexate sensitivity: resistant; ', 'cell line: Saos-2; cell type: osteosarcoma; methotrexate sensitivity: sensitive; ', 'cell line: Saos-2; cell type: osteosarcoma; methotrexate sensitivity: resistant; ' GSE26079 Homo sapiens 12 Expression profiling by array GPL6947 Genome-wide analysis gene expression in SUM-149 cells expressing AREG shRNA 2010-12-15 Results of knocking-down AREG expression in SUM-149 cells by lenitviral infection of shRNA vectors and measuring gene expression provides information as to what genes are regulated by AERG in inflammatory breast cancer cells. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE26079 Knock-down of amphiregulin inhibits cellular invasion in inflammatory breast cancer. Journal of cellular physiology 4.522 https://doi.org/10.1002/jcp.22620 {Journal of cellular physiology (4.522): 10.1002/jcp.22620} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA135213 https://www.ebi.ac.uk/ena/browser/view/PRJNA135213 None [Overal design]SUM-149 cells were infected with a single AREG shRNA virus (sh4) or three AREG shRNA viruses (shPld) and the non-silencing vector (shNS). Total RNA was collected and genome-wide analysis of expression was performed on RNA from each cell line.; [Treatment]'None'; [Growth]"SUM-149 cells were cultured in Ham's F-12 medium supplemented with fungizone (0.5 µg/mL), gentamicin (5 µg/mL), hydrocortisone (1 µg/mL), insulin (5 µg/mL, and 5% fetal bovine serum. Sh4, shPld, and shNS were cultured in the same media, but with the addition of puromycin (1mg/ml)."; [Extraction]'RNA was extracted with the QIAGEN Rneasy Plus kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with the Agilent Bioanylizer and the Agilent RNA 6000 Nano Kit.'; [Cell type]'Source: ''cell line: breast cancer SUM-149; disease state: triple negative inflammatory breast carcinoma; genotype/variation: control; ', 'cell line: breast cancer SUM-149; disease state: triple negative inflammatory breast carcinoma; genotype/variation: single AREG shRNA virus (sh4); ', 'cell line: breast cancer SUM-149; disease state: triple negative inflammatory breast carcinoma; genotype/variation: three AREG shRNA viruses (shPld); ', 'cell line: breast cancer SUM-149; disease state: triple negative inflammatory breast carcinoma; genotype/variation: non-silencing vector (shNS); ' GSE73958 Homo sapiens 48 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL16791 Target Gene Repression Based on Dismissal of Polymerase II from Estrogen Receptor Trans-bound Enhancers Is Associated With Clinical Outcome in Human Breast Cancer 2016-05-18 This SuperSeries is composed of the SubSeries listed below. Keywords: Genome binding/occupancy profiling by high throughput sequencing https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE73958 Dismissal of RNA Polymerase II Underlies a Large Ligand-Induced Enhancer Decommissioning Program. Molecular cell 14.548 https://doi.org/10.1016/j.molcel.2018.07.039 {Molecular cell (14.548): 10.1016/j.molcel.2018.07.039} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA322075 https://www.ebi.ac.uk/ena/browser/view/PRJNA322075 None [Overal design]Refer to individual Series; [Treatment]'For hormone treatments, cells were incubated at 37°C and 5% CO2 for at least 3 days in phenol red-free DMEM (GIBCO/Invitrogen) supplemented with 5% charcoal dextran-stripped FBS (GIBCO/Invitrogen). 17-β-Estradiol (E2; Steraloids, Inc.) was added to a final concentration of 100 nM. The ethanol (EtOH) vehicle control was 0.1% in all samples. Cloning, mutagenesis, and generation of ERα wild type and P-box mutation biotin-tagged inducible MCF7 stable cell lines were described in a previous paper. We performed biotin ChIP or biotin ChIP-seq experiments for ERα wild type (WT), and ERα P-box mutation stable cell lines following an earlier protocol. Briefly, cross-linked protein-DNA complexes were pulled down by M-280 Streptavidin Magnetic beads (Life Technologies, Cat# 11205D) and the washing was performed under much more stringent conditions that included 2 washes with 1% SDS in TE (20 min each) and two washes with 1% Triton X-100 in TE. The washed streptavidin beads were then subjected to AcTEV protease (Life Technologies, Cat# 12575-015) digestion twice for tagged protein and DNA complex elution before de-crosslinking at 65°C overnight.'; [Growth]"MCF7 cells were maintained at 37°C and 5% CO2 in Dulbecco's modified Eagle's medium (DMEM GIBCO/Invitrogen) with phenol red, supplemented with 10% fetal bovine serum (FBS, GIBCO/Invitrogen)."; [Extraction]'ChIP was performed as previously described. Briefly, cells were cross-linked with 1% formaldehyde at room temperature for 10 min. For KDM2A ChIP, cells were double cross-linked with 2mM DSG (ProteoChem Cat# C1104) for 45 min and then for another 15 min with 1% formaldehyde (Sigma, F8775). In both situations, the cross-linking was quenched with 0.125M glycine for 5 min. Chromatin was fragmented using a Bioruptor (Diagenode) for 30 min at high power, with an interval of 30 s between pulses to get 200-500bp fragments and precleared using 20 μl Protein G Dynabeads (Life Technologies, Cat# 10009D). Subsequently, the soluble chromatin was incubated with 2-5 μg antibodies at 4°C overnight. Immunoprecipitated complexes were collected using 20 μl Protein G Dynabeads per reaction. We performed biotin ChIP or biotin ChIP-seq experiments for BLRP-tagged KDM2A and ERα, and ERα P-box mutation stable cell lines following an earlier protocol. Briefly, cross-linked protein-DNA complexes were pulled down by M-280 Streptavidin Magnetic beads (Life Technologies, Cat# 11205D) and the washing was performed under much more stringent conditions that included 2 washes with 1% SDS in TE (20 min each) and two washes with 1% Triton X-100 in TE. The washed streptavidin beads were then subjected to AcTEV protease (Life Technologies, Cat# 12575-015) digestion twice for tagged protein and DNA complex elution before de-crosslinking at 65°C overnight.\nFor all ChIPs, after de-crosslinking overnight at 65°C, final ChIP DNA was extracted and purified using QIAquick spin columns (QIAGEN). The ChIP-seq libraries were constructed following Illumina’s ChIP-seq Sample prep kit. The library was amplified by 14 cycles of PCR.', 'GRO-seq experiments were performed as previously reported with a few modifications. Briefly, ∼10 millions of MCF7 cells treated with E2 for 1 hr were washed 3 times with cold PBS and then sequentially swelled in swelling buffer (10mM Tris-HCl pH7.5, 2mM MgCl2, 3mM CaCl2) for 10 min on ice, harvested, and lysed in lysis buffer (swelling buffer plus 0.5% NP-40, 20 units of SUPERase-In, and 10% glycerol). The resultant nuclei were washed two more times with 10ml lysis buffer and finally resuspended in 100 μl of freezing buffer (50mM Tris-HCl pH8.3, 40% glycerol, 5mM MgCl2, 0.1mM EDTA). For the run-on assay, resuspended nuclei were mixed with an equal volume of reaction buffer (10mM Tris-HCl pH 8.0, 5mM MgCl2, 1mM DTT, 300mM KCl, 20 units of SUPERase-In, 1% sarkosyl, 100 μM A/GTP, 100 µM biotin-11-C/UTP (Perkin-Elmer) and incubated for 5 min at 30°C. The resultant nuclear-run-on RNA (NRO-RNA) was then extracted with TRIzol® LS reagent (Life Technologies, Cat# 10296-028) following manufacturer’s instructions. NRO-RNA was fragmented to ∼200-500nt by alkaline base hydrolysis on ice for 30 min and and neutralized by adding 1× volume of 1 M Tris-HCl pH 6.8, Excessive salt and residual NTPs were removed by using P-30 column (Bio-Rad, Cat# 732-6250), followed by treatment with DNase I (Promega Cat# M6101) and antarctic phosphatase (NEB Cat# M0289L). Fragmented nascent RNA was bound to 10 µl of MyOne Streptavidin C1 dynabeads (Invitrogen, Cat# 65001) following the manufacturer’s instructions. The beads were washed twice in high salt (2 M NaCl, 50 mM Tris-HCl pH 7.5, 0.5% Triton X-100, 0.5 mM EDTA), once in medium salt (1M NaCl, 5 mM Tris-HCl pH 7.5, 0.1% Triton X-100, 0.5 mM EDTA), and once in low salt (5 mM Tris-HCl pH 7.5, 0.1% Triton X-100). Bound RNA was extracted from the bead using Trizol (Invitrogen, Cat# 15596-018) in two consecutive extractions, and the RNA fractions were pooled, followed by ethanol precipitation. The RNA fragments were then subjected to poly-A tailing reaction by poly-A polymerase (NEB, Cat# M0276L) for 30 min at 37°C. Subsequently, reverse transcription was performed using oNTI223 primer and superscript III RT kit (Life Technologies, Cat# 18080-044).\nThe cDNA products were separated on a 10% polyacrylamide TBE-urea gel and only those fragments migrating between 100-400bp were excised and recovered by gel extraction. Next, the first-strand cDNA was circularized by CircLigase (Epicenter, Cat# CL4115K) and relinearized by APE1 (NEB, Cat# M0282L). Finally, cDNA template was amplified by PCR using the Phusion High-Fidelity enzyme (NEB, Cat# M0530L) according to the manufacturer’s instructions. The oligonucleotide primers oNTI200 and oNTI201 were used to generate DNA library for deep sequencing and the primer sequences were described in previous paper.'; [Cell type]'human breast adenocarcinoma cell line', 'Source: ''cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; chip antibody: Dynabeads M-280 Streptavidin; ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; chip antibody: anti-H3K27Ac (Abcam, ab4729); ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; chip antibody: Input DNA; ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; chip antibody: anti-HA-tag (ab9110, abcam); ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; chip antibody: anti-NEDD4 (D17, sc-14482, Santa Cruz Biotechnology); ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; chip antibody: anti-Pol II (N-20, sc-899, Santa Cruz Biotechnology); ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; treatment: siCtrl_E2; ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; treatment: siCtrl_EtOH; ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; treatment: siKdm2a_E2; ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; treatment: siKdm2a_EtOH; ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; treatment: siKdm2a5utr_E2; ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; treatment: siKdm2a5utr_EtOH; ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; treatment: siKdm2a5utr_KDM2A_H212A_E2; ', 'cell type: human breast adenocarcinoma cell line; passages: 8-13; cell line: MCF7; treatment: siKdm2a5utr_KDM2A_WT_E2; ', 'tissue: mammary gland; cell line: breast adenocarcinoma cell line MCF7; passages: 8-13; treatment: E2; ', 'tissue: mammary gland; cell line: breast adenocarcinoma cell line MCF7; passages: 8-13; treatment: EtOH; ' GSE128775 Mus musculus 20 Expression profiling by high throughput sequencing GPL21103 Stochastic Changes in Gene Expression Promote Chaotic Dysregulation of Homeostasis in Clonal Breast Tumors 2019-03-25 Much remains unknown about the mechanisms contributing to molecular and cellular diversity in cancer. This diversity enables the evolutionary processes that govern tumor progression and contributes to treatment failures. In a previous study, we described atypical losses of heterozygosity at the DNA level in Her2/neu-driven breast tumors from first generation (F1) intercrossed mice. We now describe similar losses of heterozygosity at the level of gene expression. By quantitating each parental allele for genes expressed across a population of clonal tumors, we found variegated patterns of expression outliers in hundreds of genes, enriched in pathways typically co-opted by tumors. The frequency of outliers was correlated with transcriptional repression of a large set of homozygous genes. These findings reveal the potential for sporadic epigenetic errors that cause dysregulated cellular homeostasis and generate phenotypic variations available for clonal selection. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE128775 Stochastic changes in gene expression promote chaotic dysregulation of homeostasis in clonal breast tumors. Communications biology 0.12 https://doi.org/10.1038/s42003-019-0460-0 {Communications biology (0.12): 10.1038/s42003-019-0460-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA528873 https://www.ebi.ac.uk/ena/browser/view/PRJNA528873 https://www.ncbi.nlm.nih.gov/sra?term=SRP189304 [Overal design]Quantitation and characterization of germline-encoded BALB/c versus FVB/J allelic expression in breast tumors from [BALB/c x FVB/J] F1 mice.; [Treatment]'None'; [Growth]'None'; [Extraction]'miRNeasy\nTruSeq mRNA library prep kit'; [Cell type]'Source: ''strain: [BALB/c-neuT x FVB/J] F1; tissue: breast tumor; ' GSE58111 Homo sapiens 24 Expression profiling by high throughput sequencing GPL11154 Genome-wide analysis of transcriptome and translatome following eIF4A1 knockdown in MCF7 cells [RNA-Seq] 2014-05-30 To identify which genes were regulated by mRNA helicase activity, the effect of eIF4A1 knockdown on the MCF7 cell transcriptome and translatome was determined. eIF4A1-dependent mRNAs were highly enriched for several classes of genes with oncogenic potential, which leads to a model whereby dysregulation of mRNA unwinding contribues to the malignant phenotype in breast cancer cells via preferential translation of a subset of genes. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE58111 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA251350 https://www.ebi.ac.uk/ena/browser/view/PRJNA251350 https://www.ncbi.nlm.nih.gov/sra?term=SRP042616 [Overal design]Total, subpolysomal and polysomal RNA was isolated from MCF7 cells treated with either control siRNAs or siRNAs directed against eIF4A1 (48h post-transfection).; [Treatment]"Control ON-TARGETplus Non-targeting Pool and ON-TARGETplus SMART pool siRNAs targeting eIF4A1 were transfected into cells according to manufacturer's instructions (Thermo Scientific). DharmaFECT1 Transfection Reagent was used."; [Growth]'MCF7 cells were grown in DMEM 10% FBS under standard cell culture conditions.'; [Extraction]"Total RNA was extracted using TRIAZOL reagent. Subpolysomal and polysomal RNA was extracted using Guanidine HCl-ethanol precipitation, followed by LiCl precipitation. All samples were then repurified using miRNeasy kit (Qiagen).\nProcessing of total RNA following Illumina's standard\xa0TruSeq® RNA Sample Prep Kit-v2 protocol."; [Cell type]'Source: ''cell line: MCF7; ' GSE144234 Homo sapiens 4 Expression profiling by high throughput sequencing GPL20301 A SPEN Complex Serves as a Scaffold to Coordinate Multiple Epigenetic Regulatory Mechanisms in Breast Cancer Stem Cells 2020-01-24 There is substantial evidence that many cancers, including human breast cancer are hierarchically organized and driven by a cellular population that displays stem cell properties. These stem-like cells (CSC’s) mediate tumor metastasis and by virtue of their relative therapeutic resistance mediate tumor recurrence. Both normal and malignant stem cells are regulated through epigenetic mechanisms which involve DNA and histone modifications as well as noncoding RNAs. However, the mechanisms responsible for coordinating these multiple levels of epigenetic regulation in CSC’s remain elusive. Here, we identify a SPEN-Xist complex in breast CSC’s cells which, by virtue of inclusion of multiple epigenetic regulatory proteins, provides a scaffold for coordinating multiple levels of epigenetic regulation in these cells. Genetic knockdown of SPEN or XIST significantly reduces the CSC population as accessed by ALDH expression, sphere formation or tumor initiating capacity in xerograph models. Gene expression analysts suggests that the SPEN- XIST complex modulates multiple CSC regulatory pathways via the coordination of epigenetic modulatory proteins. This work has fundamental implications for understanding the epigenetic regulation of cancer stem cells as well as for developing strategies to target these cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144234 None None None None None 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA603096 https://www.ebi.ac.uk/ena/browser/view/PRJNA603096 https://www.ncbi.nlm.nih.gov/sra?term=SRP244697 [Overal design]Two control samples compared to two SHARP knockdown samples; [Treatment]'Cells were treated with either DMSO control or Doxycycline to induce siRNA knockdown of the SHARP gene'; [Growth]'SUM159 were grown in F12 with 5% FBS, Insulin, and Hydrocortisone'; [Extraction]'Total RNA was extracted with Qiagen columns\nStandard polyA RNA Illumina library construction'; [Cell type]'Source: ''cell line: SUM159; tissue: Breast Cancer Cell Line; treatment: DMSO-Control; ', 'cell line: SUM159; tissue: Breast Cancer Cell Line; treatment: Doxycyclin; ' GSE60322 Homo sapiens 8 Expression profiling by array GPL6244 Effect of knock down of LASP-1 on luminal breast cancer cells (MCF7) 2014-08-11 Nuclear LASP-1 has a direct correlation with the overall survival of breast cancer patients. Gene expression analysis of MCF7 human breast cancer cells cultured in 3D-Matrigel was performed. Up regulation of cell junction proteins, extracellular matrix proteins and down regulation of MMP 9 and 2 were observed. This corroborates well with the involvement of LASP-1 in cell migration and chemotaxis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60322 LASP-1: a nuclear hub for the UHRF1-DNMT1-G9a-Snail1 complex. Oncogene 6.634 https://doi.org/10.1038/onc.2015.166 {Oncogene (6.634): 10.1038/onc.2015.166} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA258028 https://www.ebi.ac.uk/ena/browser/view/PRJNA258028 None [Overal design]Non-silencing (control) and LASP-1 knock down MCF7 cells were cultured on 3D-Matrigel, total RNA was extracted and anlyzed - 4 biological replicates each. The first biological replicate was done as a pilot. Biological replicates 2-4 were run as a second set after pilot.; [Treatment]'Not applicable'; [Growth]'MCF cells (Non-silencing and LASP-1 knock down) were cultured on growth factor reduced Matrigel for 3 days to form spheroids.'; [Extraction]'Total RNA was quantitated from MCF7 spheroids using the QuBit RNA assay and were run on the Agilent Bioanalyzer.'; [Cell type]'Luminal breast cells''cell line: MCF7; cell type: Luminal breast cells; ' GSE123631 Homo sapiens 48 Expression profiling by high throughput sequencing GPL20301 BRCA2 abrogation triggers innate immune responses potentiated by treatment with PARP inhibitors 2018-12-11 Heterozygous germline mutations in BRCA2 predispose to breast and ovarian cancer. Contrary to non-cancerous cells, where BRCA2 deletion causes cell cycle arrest or cell death, BRCA2 inactivation in tumors is associated with uncontrolled cell proliferation. We set out to investigate this conundrum by exploring modalities of cell adaptation to loss of BRCA2 and focused on genome-wide transcriptome alterations. Human cells in which BRCA2 expression was inhibited using a doxycycline (DOX)-inducible shRNA for 4 or 28 days were subjected to RNA-seq analyses. Gene sets differentially expressed in BRCA2-deficient versus -proficient cells revealed a biphasic response to BRCA2 abrogation. The early, acute response consisted of downregulation of genes involved in cell cycle progression, DNA replication and repair and was associated with cell cycle arrest in G1. Surprisingly, the late, chronic response consisted exclusively of upregulation of innate immune response genes controlled by interferon. Activation of the cGAS-STING pathway detected in these cells further substantiated the concept that long-term BRCA2 abrogation triggers cell-intrinsic immune signaling. Importantly, we found that treatment with PARP inhibitors stimulated the interferon response in cells and tumors lacking BRCA2. We propose that PARP inhibitors suppress growth of BRCA2-deficient cells and tumors, in part, by activating interferon signaling. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE123631 BRCA2 abrogation triggers innate immune responses potentiated by treatment with PARP inhibitors. Nature communications 11.878 https://doi.org/10.1038/s41467-019-11048-5 {Nature communications (11.878): 10.1038/s41467-019-11048-5} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA509430 https://www.ebi.ac.uk/ena/browser/view/PRJNA509430 https://www.ncbi.nlm.nih.gov/sra?term=SRP173279 [Overal design]RNA-seq data in BRCA2-/- and BRCA2+/+ human non-small cell lung carcinoma H1299 and invasive ductal breast cancer MDA-MB-231 cells.; [Treatment]'For induction of shBRCA2, 2 µg/ml DOX (D9891, Sigma) was added to growth medium.'; [Growth]'Human non-small cell lung carcinoma H1299 cells and human invasive ductal breast cancer MDA-MB-231 cells, wild type (American Type Culture Collection) or carrying a doxycycline (DOX)-inducible BRCA2 shRNA4, were cultivated in monolayers in DMEM medium (Sigma) supplemented with 10% tetracycline free foetal bovine serum (Clontech).'; [Extraction]'Cells were collected for RNA extraction and processed using the RNeasy® Mini Kit (Qiagen, #74104) according to the manufacturer’s guidelines. RNA samples were quantified using RiboGreen (Invitrogen) on the FLUOstar OPTIMA plate reader (BMG Labtech) and the size profile and integrity analysed on the 2200 or 4200 TapeStation (Agilent, RNA ScreenTape).\nPoly(A) transcript enrichment and strand specific library preparation were performed using TruSeq Stranded mRNA kit (Illumina) following manufacturer’s instructions. Libraries were amplified (15 cycles) on a Tetrad (Bio-Rad) using in-house unique dual indexing primers27. Individual libraries were normalised using Qubit and size profile was analysed on the 2200 or 4200 TapeStation. Individual libraries were pooled together and pooled libraries were diluted to ~10 nM for storage. Each library aliquot was denatured and further diluted prior to loading on the sequencer.'; [Cell type]'Source: ''cell line: MDA-MB-231; genotype: WT; treatment: +DOX; time point: 4 days; ', 'cell line: MDA-MB-231; genotype: WT; treatment: +DOX; time point: 28 days; ', 'cell line: MDA-MB-231; genotype: shBRCA2; treatment: +DOX; time point: 4 days; ', 'cell line: MDA-MB-231; genotype: shBRCA2; treatment: +DOX; time point: 28 days; ', 'cell line: MDA-MB-231; genotype: WT; treatment: None; time point: 4 days; ', 'cell line: MDA-MB-231; genotype: WT; treatment: None; time point: 28 days; ', 'cell line: MDA-MB-231; genotype: shBRCA2; treatment: None; time point: 4 days; ', 'cell line: MDA-MB-231; genotype: shBRCA2; treatment: None; time point: 28 days; ', 'cell line: H1299; genotype: WT; treatment: +DOX; time point: 4 days; ', 'cell line: H1299; genotype: WT; treatment: +DOX; time point: 28 days; ', 'cell line: H1299; genotype: shBRCA2; treatment: +DOX; time point: 4 days; ', 'cell line: H1299; genotype: shBRCA2; treatment: +DOX; time point: 28 days; ', 'cell line: H1299; genotype: WT; treatment: None; time point: 4 days; ', 'cell line: H1299; genotype: WT; treatment: None; time point: 28 days; ', 'cell line: H1299; genotype: shBRCA2; treatment: None; time point: 4 days; ', 'cell line: H1299; genotype: shBRCA2; treatment: None; time point: 28 days; ' GSE59821 Homo sapiens 51 Other GPL11154; GPL15520; GPL16791 Restrictions in amino acid availability revealed by differential ribosome codon reading 2014-07-28 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE59821 Tumour-specific proline vulnerability uncovered by differential ribosome codon reading. Nature 43.070 https://doi.org/10.1038/nature16982 {Nature (43.070): 10.1038/nature16982} 'total RNA', 'polyA RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA256314 https://www.ebi.ac.uk/ena/browser/view/PRJNA256314 None [Overal design]Refer to individual Series; [Treatment]'Cells were treated with of harringtonine (2 μg/ml) for 5 min.', 'For inhibition of mTOR and nutrient starvation experiments, MCF10A cells were treated either with 250 nM of Torin 1 (Tocris Bioscience, Bristol, UK) or with EBSS medium (Sigma) for 2 hours, respectively.', 'For starvation experiments, cells were culture for 48hrs in glutamine-free DMEM (Life Technologies) supplemented with 10% dialyzed FBS in 5% CO2 at 37°C.', 'For samples which were ASNase treated: PC3 cells were treated with L-Asparaginase (Sigma) at 1U/ml for 48hrs in RPMI supplemented with 10% dialyzed FBS'; [Growth]'SUM1315 cells were culture in DMEM:F12 (1:1) medium supplemented with 5% FCS, EGF (10 ng/ml), and Insulin (5μg/ml)', 'MCF10A cells were cultured in DMEM/F12 1:1 medium supplemented with 5% horse serum, EGF (10 ng/ml), insulin (10 μg/ml), cholera toxin (100 ng/ml), and hydrocortisone (500 ng/ml) in 5% CO2 at 37°C.', 'All breast cancer cell lines were grown in DMEM supplemented with 10% FBS in 5% CO2 at 37°C.', 'PC3 cells were cultured in RPMI medium supplemented with 10% FBS', 'MCF7 cells were cultured in DMEM medium supplemented with 10% FBS', 'SUM159PT cells were cultured in DMEM/F12 1:1 medium supplemented with 5% FBS, insulin (5μg/ml), and hydrocortisone (1μg/ml).'; [Extraction]'Approximately 30e6 cells were treated with chloramphenicol (100μg/ml) for 15 minutes and cycloheximide (100μg/ml) for 5 minutes. Cells were lysed in buffer B (20 mM Tris-HCl, pH 7.8, 100mM KCl, 10mM MgCl2, 1% Triton X-100, 2mM DTT, 100 μg/ml chloramphenicol, 100 μg/ml cycloheximide, 1x Complete protease inhibitor). Lysates were centrifuged at 5000 rpm and the supernatant was treated with 2U/μl of RNase I (Ambion) for 40 minutes at room temperature. Lysates were fractionated on a linear sucrose gradient (7% - 47%) using the SW- 41Ti rotor at 36,000 rpm for 2hrs. Fractions enriched in mito-monosomes and cytosolic monosomes were identified by western blotting, pooled and treated with proteinase K (Roche) in 1% SDS. Released RPFs were purified using Trizol reagent (Invitrogen) following the manufacturer’s instructions.\nRNA was gel-purified on a denaturing 10% polyacrylamide urea (7 M) gel. A section corresponding to 30-33 nucleotides was excised, eluted and ethanol precipitated. The resulting fragments were 3′-dephosphorylated using T4 polynucleotide kinase (New England Biolabs Inc. Beverly, MA, USA) for 6 h at 37°C in 2-(N-morpholino)ethanesulfonic acid (MES) buffer (100 mM MES-NaOH, pH 5.5, 10 mM MgCl2, 10 mM β-mercaptoethanol, 300 mM NaCl). 3′ adaptor was added with T4 RNA ligase 1 (New England Biolabs Inc. Beverly, MA, USA) for 2.5 h at 37°C. Ligation products were 5′-phosphorylated with T4 polynucleotide kinase for 30 min at 37°C. 5′ adaptor was added with T4 RNA ligase 1 for 18 h at 22°C.', "RNA was harvested using Trizol reagent. Illumina TruSeq RNA Sample Prep Kit was used with 1 ug of total RNA for the construction of sequencing libraries.\nPoly(A) was isolated using the Oligotex mRNA mini kit (Qiagen). Libraries were prepared using the TruSeq RNA sample preparation kit (Illumina) following the manufacturer's instructions.", 'MCF7 GFP-RPL10a cells were treated with cycloheximide at a final conc of 10ug/m for 5 min. Cells were washed with cold PBS, scraped, and pelleted. Cell pellet was lysed with 1ml of NP40 lysis buffer (20mM Tris-HCl pH 7.8, 10mM MgCl2, 150mM KCl, 1% NP40, 2 mM DTT, 1X Complete protease Inhibitors, 100 ug/ml CHX) for 15 min, centrifuged for 10 min at 1300 g and 1ml of supernatant recovered. IP samples: (50ul/100ul) GFP-Trap_M beads (Chromotek) were washed for 3 times in 1ml of NP40 lysis buffer, resuspended in 3 ml of NP40 lysis buffer. 1ml of cleared lysate (cell line or tumor) was added to the beads and digested with RNAse I (100U/ul) for 1hr at RT under constant rotation. Beads were washed 3 times with of NP40 Lysis buffer and 3 times with NP40 wash buffer (20mM Tris-HCl pH 7.8, 10mM MgCl2, 350mM KCl, 1% NP40, 2 mM DTT, 1X Complete protease Inhibitors, 100 ug/ml CHX). Beads were resuspended in 300 ul of lysis buffer with 1% SDS and 15 ul of Proteinase K (Roche) and incubated for 1hr at 45C. Supernatant was recovered and resuspended in TriSure. RNA was isolated and libraries prepared according to the RP protocol.\nRNA was gel-purified on a denaturing 10% polyacrylamide urea (7 M) gel. A section corresponding to 30-33 nucleotides was excised, eluted and ethanol precipitated. The resulting fragments were 3′-dephosphorylated using T4 polynucleotide kinase (New England Biolabs Inc. Beverly, MA, USA) for 6 h at 37°C in 2-(N-morpholino)ethanesulfonic acid (MES) buffer (100 mM MES-NaOH, pH 5.5, 10 mM MgCl2, 10 mM β-mercaptoethanol, 300 mM NaCl). 3′ adaptor was added with T4 RNA ligase 1 (New England Biolabs Inc. Beverly, MA, USA) for 2.5 h at 37°C. Ligation products were 5′-phosphorylated with T4 polynucleotide kinase for 30 min at 37°C. 5′ adaptor was added with T4 RNA ligase 1 for 18 h at 22°C.', 'SUM-159 GFP-RPL10a cells were treated with cycloheximide at a final conc of 10ug/m for 5 min. Cells were washed with cold PBS, scraped, and pelleted. Cell pellet was lysed with 1ml of NP40 lysis buffer (20mM Tris-HCl pH 7.8, 10mM MgCl2, 150mM KCl, 1% NP40, 2 mM DTT, 1X Complete protease Inhibitors, 100 ug/ml CHX) for 15 min, centrifuged for 10 min at 1300 g and 1ml of supernatant recovered. For tumors preparation, each tumor was lysed in 1ml of NP40 lysis buffer in a tissue homogenizer. Tumor lysate was centrifuged at 1300g for 10 min and the supernatant was incubated with the beads. 85 ul per condition of GFP-Trap_M beads (Chromotek) were washed for 3 times in 1ml of NP40 lysis buffer, resuspended in 3 ml of NP40 lysis buffer. 1ml of cleared lysate (cell line or tumor) was added to the beads and digested with RNAse I (100U/ul) for 1hr at RT under constant rotation. Beads were washed 3 times with of NP40 Lysis buffer and 3 times with NP40 wash buffer (20mM Tris-HCl pH 7.8, 10mM MgCl2, 350mM KCl, 1% NP40, 2 mM DTT, 1X Complete protease Inhibitors, 100 ug/ml CHX). Beads were resuspended in 300 ul of lysis buffer with 1% SDS and 15 ul of Proteinase K (Roche) and incubated for 1hr at 45C. Supernatant was recovered and resuspended in TriSure. RNA was isolated and libraries prepared according to the RP protocol.\nRNA was gel-purified on a denaturing 10% polyacrylamide urea (7 M) gel. A section corresponding to 30-33 nucleotides was excised, eluted and ethanol precipitated. The resulting fragments were 3′-dephosphorylated using T4 polynucleotide kinase (New England Biolabs Inc. Beverly, MA, USA) for 6 h at 37°C in 2-(N-morpholino)ethanesulfonic acid (MES) buffer (100 mM MES-NaOH, pH 5.5, 10 mM MgCl2, 10 mM β-mercaptoethanol, 300 mM NaCl). 3′ adaptor was added with T4 RNA ligase 1 (New England Biolabs Inc. Beverly, MA, USA) for 2.5 h at 37°C. Ligation products were 5′-phosphorylated with T4 polynucleotide kinase for 30 min at 37°C. 5′ adaptor was added with T4 RNA ligase 1 for 18 h at 22°C.'; [Cell type]'Source: ''cell line: SUM1315; ', 'cell line: MCF10A; ', 'tissue: Kidney; ', 'tissue: kidney; ', 'cell line: MCF7; ', 'cell line: T47D; ', 'cell line: MDA-MB-231; ', 'cell line: Hs578t; ', "adapter sequence (3'): TGGAATTCTCGGGTGCCAAGGAACTCCAGTCACATCACGATCTCGTATGCCGTCTTCTGCTTG; cell line: PC3; agent: none; ", "adapter sequence (3'): TGGAATTCTCGGGTGCCAAGGAACTCCAGTCACATCACGATCTCGTATGCCGTCTTCTGCTTG; cell line: PC3; agent: L-Asparaginase; ", "adapter sequence (3'): TGGAATTCTCGGGTGCCAAGGAACTCCAGTCACATCACGATCTCGTATGCCGTCTTCTGCTTG; cell line: MCF7; protocol: sucrose gradient; ", "adapter sequence (3'): TGGAATTCTCGGGTGCCAAGGAACTCCAGTCACATCACGATCTCGTATGCCGTCTTCTGCTTG; cell line: MCF7; protocol: IP50; ", "adapter sequence (3'): TGGAATTCTCGGGTGCCAAGGAACTCCAGTCACATCACGATCTCGTATGCCGTCTTCTGCTTG; cell line: SUM159PT; ", "adapter sequence (3'): TGGAATTCTCGGGTGCCAAGGAACTCCAGTCACATCACGATCTCGTATGCCGTCTTCTGCTTG; cell line: MCF10A; ", "adapter sequence (3'): TGGAATTCTCGGGTGCCAAGGAACTCCAGTCACATCACGATCTCGTATGCCGTCTTCTGCTTG; tissue: normal; ", "adapter sequence (3'): TGGAATTCTCGGGTGCCAAGGAACTCCAGTCACATCACGATCTCGTATGCCGTCTTCTGCTTG; tissue: tumor; " GSE42667 Homo sapiens 2 Expression profiling by array GPL4133 Effect of cigarette smoke on gene expression in mammary epithelial cells [gene expression] 2012-12-02 Recent epidemiological studies demonstrate that both active and involuntary exposure to tobacco smoke increases the risk of breast cancer. Little is known, however, about the molecular mechanisms by which tobacco smoke contributes to breast carcinogenesis. To investigate these mechanisms we have analyzed gene expression and methylation in MCF 10A mammary epithelial cells chronically exposed to aqueous cigarette smoke extract (CSE). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE42667 Cigarette smoke induces epithelial to mesenchymal transition and increases the metastatic ability of breast cancer cells. Molecular cancer 10.679 https://doi.org/10.1186/1476-4598-12-90 {Molecular cancer (10.679): 10.1186/1476-4598-12-90} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA182598 https://www.ebi.ac.uk/ena/browser/view/PRJNA182598 None [Overal design]CSE was prepared weekly and added to the cell cultures at a concentration equivalent to 0.001 cigarettes/ml. Two clones were isolated after 13 weeks of treatment and expanded in the same concentration of CSE for 8 additional weeks. Mock-treated samples were prepared in parallel.; [Treatment]'None'; [Growth]'None'; [Extraction]'TriZol extraction followed by RNeasy kit (Qiagen) clean-up with on-column DNase treatment'; [Cell type]'epithelial''organ: mammary gland; breast; disease: fibrocystic disease; cell type: epithelial; growth properties: adherent; source: ATCC; treatment: control; ', 'organ: mammary gland; breast; disease: fibrocystic disease; cell type: epithelial; growth properties: adherent; source: ATCC; treatment: cigarette smoke extract (CSE); ' GSE76040 Homo sapiens 113 Expression profiling by array GPL17586 transCONFIRM gene expression analysis 2015-12-15 gene expression analysis ussing microarray analysis of a subset of primary tumors collected from patients that participated in the CONFIRM phase III study, which randomized post menopausal patients with ER+ metastatic breast cancer to fulvestrant 500mg and fulvestrant 250mg. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76040 TransCONFIRM: Identification of a Genetic Signature of Response to Fulvestrant in Advanced Hormone Receptor-Positive Breast Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-16-0148 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-16-0148} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA306048 https://www.ebi.ac.uk/ena/browser/view/PRJNA306048 None [Overal design]Primary tumor samples were collected from patients participating in the CONFIRM study.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted from FFPE tumor samples using Rneasy FFPE kits ( Qiagen) and amplified with WT-Ovation FFPE Sytem V2 ( NuGEN).'; [Cell type]'Source: ''tissue: primary breast cancer; age: 70; er (allred score): 4.5; pr (allred score): 3.8; ki67 (%): 19; her2: 3; ', 'tissue: primary breast cancer; age: 58; er (allred score): 8; pr (allred score): 0; ki67 (%): 15; her2: 0; ', 'tissue: primary breast cancer; age: 56; er (allred score): 8; pr (allred score): 8; ki67 (%): 11; her2: 0; ', 'tissue: primary breast cancer; age: 68; er (allred score): 5.5; pr (allred score): 5.3; ki67 (%): 10; her2: 3; ', 'tissue: primary breast cancer; age: 68; er (allred score): 3; pr (allred score): 5.5; ki67 (%): 21; her2: 0; ', 'tissue: primary breast cancer; age: 74; er (allred score): 3.5; pr (allred score): 0.8; ki67 (%): 7; her2: 0; ', 'tissue: primary breast cancer; age: 67; er (allred score): 8; pr (allred score): 0; ki67 (%): 6; her2: 0; ', 'tissue: primary breast cancer; age: 58; er (allred score): 2; pr (allred score): 2; ki67 (%): 2; her2: 2; ', 'tissue: primary breast cancer; age: 73; er (allred score): 8; pr (allred score): 6; ki67 (%): 40; her2: 0; ', 'tissue: primary breast cancer; age: 69; er (allred score): 8; pr (allred score): 8; ki67 (%): 32; her2: 0; ', 'tissue: primary breast cancer; age: 75; er (allred score): 0; pr (allred score): 0; ki67 (%): 9; her2: 0; ', 'tissue: primary breast cancer; age: 72; er (allred score): 8; pr (allred score): 0; ki67 (%): 41; her2: 0; ', 'tissue: primary breast cancer; age: 66; er (allred score): 7; pr (allred score): 8; ki67 (%): 17; her2: 0; ', 'tissue: primary breast cancer; age: 68; er (allred score): 8; pr (allred score): 7.7; ki67 (%): 13; her2: 0; ', 'tissue: primary breast cancer; age: 75; er (allred score): 7; pr (allred score): 5.5; ki67 (%): 44; her2: 0; ', 'tissue: primary breast cancer; age: 73; er (allred score): 8; pr (allred score): 0; ki67 (%): 18; her2: 0; ', 'tissue: primary breast cancer; age: 54; er (allred score): 7; pr (allred score): 6.3; ki67 (%): 41; her2: 0; ', 'tissue: primary breast cancer; age: 81; er (allred score): 8; pr (allred score): 6.8; ki67 (%): 49; her2: 3; ', 'tissue: primary breast cancer; age: 68; er (allred score): 8; pr (allred score): 3.8; ki67 (%): 8; her2: 0; ', 'tissue: primary breast cancer; age: 78; er (allred score): 6.7; pr (allred score): 6; ki67 (%): 22; her2: 0; ', 'tissue: primary breast cancer; age: 52; er (allred score): 5.3; pr (allred score): 0; ki67 (%): 9; her2: 0; ', 'tissue: primary breast cancer; age: 65; er (allred score): 2.7; pr (allred score): 0; ki67 (%): 25; her2: 0; ', 'tissue: primary breast cancer; age: 68; er (allred score): 8; pr (allred score): 5.5; ki67 (%): 24; her2: 0; ', 'tissue: primary breast cancer; age: 56; er (allred score): 8; pr (allred score): 5.5; ki67 (%): 8; her2: 1; ', 'tissue: primary breast cancer; age: 43; er (allred score): 4.8; pr (allred score): 0; ki67 (%): 19; her2: 1; ', 'tissue: primary breast cancer; age: 55; er (allred score): 8; pr (allred score): 3.5; ki67 (%): 18; her2: 0; ', 'tissue: primary breast cancer; age: 72; er (allred score): 8; pr (allred score): 2; ki67 (%): 19; her2: 1; ', 'tissue: primary breast cancer; age: 69; er (allred score): 4; pr (allred score): 7; ki67 (%): 7; her2: 3; ', 'tissue: primary breast cancer; age: 76; er (allred score): 5.5; pr (allred score): 0; ki67 (%): 45; her2: 1; ', 'tissue: primary breast cancer; age: 62; er (allred score): 5.5; pr (allred score): 5; ki67 (%): 18; her2: 0; ', 'tissue: primary breast cancer; age: 69; er (allred score): 8; pr (allred score): 5.8; ki67 (%): 21; her2: 2; ', 'tissue: primary breast cancer; age: 63; er (allred score): 8; pr (allred score): 2.7; ki67 (%): 22; her2: 0; ', 'tissue: primary breast cancer; age: 52; er (allred score): 0; pr (allred score): 0; ki67 (%): 5; her2: 3; ', 'tissue: primary breast cancer; age: 55; er (allred score): 4; pr (allred score): 3; ki67 (%): 2; her2: 0; ', 'tissue: primary breast cancer; age: 59; er (allred score): 3; pr (allred score): 5.3; ki67 (%): 4; her2: 0; ', 'tissue: primary breast cancer; age: 58; er (allred score): 4; pr (allred score): 2.5; ki67 (%): 0; her2: 3; ', 'tissue: primary breast cancer; age: 68; er (allred score): 8; pr (allred score): 4; ki67 (%): 30; her2: 0; ', 'tissue: primary breast cancer; age: 60; er (allred score): 7.3; pr (allred score): 6.3; ki67 (%): 26; her2: 0; ', 'tissue: primary breast cancer; age: 57; er (allred score): 7.3; pr (allred score): 0; ki67 (%): 13.2; her2: 0; ', 'tissue: primary breast cancer; age: 77; er (allred score): 6.3; pr (allred score): 5.8; ki67 (%): 8; her2: 0; ', 'tissue: primary breast cancer; age: 59; er (allred score): 6; pr (allred score): 2.5; ki67 (%): 11; her2: 0; ', 'tissue: primary breast cancer; age: 76; er (allred score): 7; pr (allred score): 4.3; ki67 (%): 0; her2: 0; ', 'tissue: primary breast cancer; age: 68; er (allred score): 6.8; pr (allred score): 8; ki67 (%): 9; her2: 0; ', 'tissue: primary breast cancer; age: 43; er (allred score): 4; pr (allred score): 8; ki67 (%): 24; her2: 0; ', 'tissue: primary breast cancer; age: 58; er (allred score): 6.7; pr (allred score): 3.7; ki67 (%): 27; her2: 0; ', 'tissue: primary breast cancer; age: 41; er (allred score): 0; pr (allred score): 0.5; ki67 (%): 92; her2: 0; ', 'tissue: primary breast cancer; age: 58; er (allred score): 0; pr (allred score): 0; ki67 (%): 52; her2: 0; ', 'tissue: primary breast cancer; age: 69; er (allred score): 8; pr (allred score): 2; ki67 (%): 0; her2: 1; ', 'tissue: primary breast cancer; age: 65; er (allred score): 8; pr (allred score): 6.3; ki67 (%): 24; her2: 3; ', 'tissue: primary breast cancer; age: 42; er (allred score): 7; pr (allred score): 4.5; ki67 (%): 33; her2: 0; ', 'tissue: primary breast cancer; age: 45; er (allred score): 7; pr (allred score): 8; ki67 (%): 16; her2: 0; ', 'tissue: primary breast cancer; age: 52; er (allred score): 8; pr (allred score): 8; ki67 (%): 12; her2: 1; ', 'tissue: primary breast cancer; age: 57; er (allred score): 6; pr (allred score): 3; ki67 (%): 35; her2: 0; ', 'tissue: primary breast cancer; age: 31; er (allred score): 7; pr (allred score): 6.7; ki67 (%): 10; her2: 1; ', 'tissue: primary breast cancer; age: 60; er (allred score): 8; pr (allred score): 4; ki67 (%): 2; her2: 0; ', 'tissue: primary breast cancer; age: 66; er (allred score): 0; pr (allred score): 0; ki67 (%): 0; her2: 0; ', 'tissue: primary breast cancer; age: 62; er (allred score): 0; pr (allred score): 0; ki67 (%): 58; her2: 3; ', 'tissue: primary breast cancer; age: 76; er (allred score): 7; pr (allred score): 8; ki67 (%): 15; her2: 0; ', 'tissue: primary breast cancer; age: 64; er (allred score): 7; pr (allred score): 0; ki67 (%): 5; her2: 1; ', 'tissue: primary breast cancer; age: 66; er (allred score): 5.8; pr (allred score): 2; ki67 (%): 0; her2: 0; ', 'tissue: primary breast cancer; age: 77; er (allred score): 7; pr (allred score): 1; ki67 (%): 16; her2: 1; ', 'tissue: primary breast cancer; age: 40; er (allred score): 5; pr (allred score): 8; ki67 (%): 17; her2: 0; ', 'tissue: primary breast cancer; age: 61; er (allred score): 3.5; pr (allred score): 5; ki67 (%): 2; her2: 0; ', 'tissue: primary breast cancer; age: 67; er (allred score): 7.3; pr (allred score): 0; ki67 (%): 5; her2: 0; ', 'tissue: primary breast cancer; age: 57; er (allred score): 6; pr (allred score): 7; ki67 (%): 4; her2: 0; ', 'tissue: primary breast cancer; age: 40; er (allred score): 8; pr (allred score): 8; ki67 (%): 51; her2: 0; ', 'tissue: primary breast cancer; age: 59; er (allred score): 4; pr (allred score): 7.8; ki67 (%): 11; her2: 0; ', 'tissue: primary breast cancer; age: 73; er (allred score): 7.5; pr (allred score): 7.8; ki67 (%): 10; her2: 0; ', 'tissue: primary breast cancer; age: 59; er (allred score): 0; pr (allred score): 0; ki67 (%): 0; her2: 0; ', 'tissue: primary breast cancer; age: 47; er (allred score): 4.5; pr (allred score): 0; ki67 (%): 6.8; her2: 0; ', 'tissue: primary breast cancer; age: 64; er (allred score): 8; pr (allred score): 5.5; ki67 (%): 40; her2: 0; ', 'tissue: primary breast cancer; age: 64; er (allred score): 6.3; pr (allred score): 5; ki67 (%): 12; her2: 0; ', 'tissue: primary breast cancer; age: 62; er (allred score): 7; pr (allred score): 0; ki67 (%): 7; her2: 0; ', 'tissue: primary breast cancer; age: 58; er (allred score): 1.8; pr (allred score): 8; ki67 (%): 22; her2: 0; ', 'tissue: primary breast cancer; age: 52; er (allred score): 5.3; pr (allred score): 3.7; ki67 (%): 3; her2: 0; ', 'tissue: primary breast cancer; age: 42; er (allred score): 7; pr (allred score): 0; ki67 (%): 17; her2: 1; ', 'tissue: primary breast cancer; age: 56; er (allred score): 8; pr (allred score): 6.7; ki67 (%): 4; her2: 0; ', 'tissue: primary breast cancer; age: 63; er (allred score): 4.5; pr (allred score): 8; ki67 (%): 6; her2: 0; ', 'tissue: primary breast cancer; age: 71; er (allred score): 6; pr (allred score): 6; ki67 (%): 16; her2: 0; ', 'tissue: primary breast cancer; age: 79; er (allred score): 7; pr (allred score): 0; ki67 (%): 19; her2: 3; ', 'tissue: primary breast cancer; age: 72; er (allred score): 8; pr (allred score): 7; ki67 (%): 21; her2: 0; ', 'tissue: primary breast cancer; age: 69; er (allred score): 0; pr (allred score): 0.7; ki67 (%): 1; her2: 0; ', 'tissue: primary breast cancer; age: 66; er (allred score): 1; pr (allred score): 6.5; ki67 (%): 5; her2: 0; ', 'tissue: primary breast cancer; age: 50; er (allred score): 6.4; pr (allred score): 1.6; ki67 (%): 43; her2: 0; ', 'tissue: primary breast cancer; age: 78; er (allred score): 8; pr (allred score): 0; ki67 (%): 0; her2: 2; ', 'tissue: primary breast cancer; age: 65; er (allred score): 8; pr (allred score): 3; ki67 (%): 2; her2: 1; ', 'tissue: primary breast cancer; age: 78; er (allred score): 8; pr (allred score): 5; ki67 (%): 17; her2: 1; ', 'tissue: primary breast cancer; age: 62; er (allred score): 6.5; pr (allred score): 8; ki67 (%): 20; her2: 3; ', 'tissue: primary breast cancer; age: 66; er (allred score): 8; pr (allred score): 3; ki67 (%): 20; her2: 0; ', 'tissue: primary breast cancer; age: 76; er (allred score): 8; pr (allred score): 0; ki67 (%): 20; her2: 0; ', 'tissue: primary breast cancer; age: 63; er (allred score): 8; pr (allred score): 2.3; ki67 (%): 3; her2: 0; ', 'tissue: primary breast cancer; age: 46; er (allred score): 1.3; pr (allred score): 0; ki67 (%): 0; her2: 0; ', 'tissue: primary breast cancer; age: 54; er (allred score): 7.3; pr (allred score): 1.2; ki67 (%): 62; her2: 3; ', 'tissue: primary breast cancer; age: 70; er (allred score): 8; pr (allred score): 3.3; ki67 (%): 32; her2: 1; ', 'tissue: primary breast cancer; age: 51; er (allred score): 4; pr (allred score): 4.5; ki67 (%): 30; her2: 0; ', 'tissue: primary breast cancer; age: 76; er (allred score): 7; pr (allred score): 2; ki67 (%): 3; her2: 0; ', 'tissue: primary breast cancer; age: 49; er (allred score): 8; pr (allred score): 8; ki67 (%): 22; her2: 0; ', 'tissue: primary breast cancer; age: 57; er (allred score): 8; pr (allred score): 8; ki67 (%): 8; her2: 0; ', 'tissue: primary breast cancer; age: 56; er (allred score): 8; pr (allred score): 0.5; ki67 (%): 26; her2: 1; ', 'tissue: primary breast cancer; age: 78; er (allred score): 6.5; pr (allred score): 0; ki67 (%): 8; her2: 0; ', 'tissue: primary breast cancer; age: 62; er (allred score): 4; pr (allred score): 6.3; ki67 (%): 0; her2: 0; ', 'tissue: primary breast cancer; age: 77; er (allred score): 4; pr (allred score): 3.3; ki67 (%): 13; her2: 0; ', 'tissue: primary breast cancer; age: 82; er (allred score): 8; pr (allred score): 8; ki67 (%): 8; her2: 0; ', 'tissue: primary breast cancer; age: 63; er (allred score): 7.8; pr (allred score): 6.5; ki67 (%): 2; her2: 0; ', 'tissue: primary breast cancer; age: 48; er (allred score): 1; pr (allred score): 2.5; ki67 (%): 1; her2: 0; ', 'tissue: primary breast cancer; age: 64; er (allred score): 8; pr (allred score): 7.3; ki67 (%): 40; her2: 1; ', 'tissue: primary breast cancer; age: 44; er (allred score): 4.5; pr (allred score): 8; ki67 (%): 4; her2: 1; ', 'tissue: primary breast cancer; age: 63; er (allred score): 7.8; pr (allred score): 6.8; ki67 (%): 18; her2: 1; ', 'tissue: primary breast cancer; age: 65; er (allred score): 3; pr (allred score): 8; ki67 (%): 27; her2: 0; ', 'tissue: primary breast cancer; age: 65; er (allred score): 8; pr (allred score): 2; ki67 (%): 41; her2: 3; ' GSE44024 Homo sapiens 4 Expression profiling by array GPL571 Effect of PIAS1 on gene expression 2013-02-01 To study the effect of PIAS1 on transcriptional regulation, we establishedstable PIAS1 shRNA knockdown cells in breast cancer cell line MDA-MB231. By comparing the expression profiles of control vs PIAS1 knockdown cells, we can identify potential PIAS1 target genes involved in breast tumorigenesis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE44024 PIAS1 regulates breast tumorigenesis through selective epigenetic gene silencing. PloS one 2.776 https://doi.org/10.1371/journal.pone.0089464 {PloS one (2.776): 10.1371/journal.pone.0089464} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA188331 https://www.ebi.ac.uk/ena/browser/view/PRJNA188331 None [Overal design]MDA-MB231 Control shRNA and PIAS1 shRNA2 cells were cultured in DMEM plus 10% FBS (DMEM) or SCM for 30 h, and total RNA was used for microarray.; [Treatment]'None'; [Growth]'MDA-MB231 Control shRNA and PIAS1 shRNA2 cells were cultured in DMEM plus 10% FBS (DMEM) or SCM for 30 h.'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Source: ''cell line: MDA-MB231; treatment: control shRNA; media: DMEM; ', 'cell line: MDA-MB231; treatment: control shRNA; media: SCM; ', 'cell line: MDA-MB231; treatment: PIAS1 shRNA; media: DMEM; ', 'cell line: MDA-MB231; treatment: PIAS1 shRNA; media: SCM; ' GSE61546 Homo sapiens 4 Expression profiling by array GPL10558 Telomerase promotes cell survival by suppression of long noncoding RNAs 2014-09-18 Human telomerase, hTERT, catalyzes telomere elongation using the hTR long noncoding RNA (lncRNA) template and confers replicative immortality, a hallmark of cancer. hTERT is reactivated in nearly 90% of cancers and telomere elongation was considered its sole role in tumorigenesis. However, evidence for telomere-independent hTERT cell phenotypes, which surprisingly require hTERT catalytic activity, is mounting. These phenotypes could profoundly impact our understanding and clinical exploitation of hTERT’s role in cancer, but their underlying mechanisms remain unclear. One mechanism was suggested by the demonstration of hTERT’s ability to bind an alternative lncRNA, RMRP, and synthesize double-stranded RNAs that are processed into Argonaute2-bound small interfering RNAs that suppress the lncRNA itself. Here we performed systematic lncRNA profiling to determine whether this is a general mode of hTERT action involving novel lncRNAs, and investigated the implications of hTERT-mediated lncRNA suppression for tumorigenesis. We found that hTERT’s telomere-independent catalytic activity increased cell survival resulting in luminal hyperplasia in a human breast acinar morphogenesis model. Using next-generation sequencing of Argonaute2-associated small RNAs, we discovered novel hTERT-downregulated lncRNAs. One such lncRNA, MEG3, could bind hTERT and was significantly downregulated in human breast carcinoma cell lines and tissues. MEG3 knockdown promoted survival and hyperplasia, consistent with early tumorigenesis, and ectopic MEG3 expression caused cell death and inhibited breast cancer cell proliferation. Microarray analysis identified Bcl2-interacting proteins, BEX1 and BNIPL, as MEG3 targets. BEX1 mediates cell death by decreasing phospho-Bcl2, and MEG3 or hTERT modulated phospho-Bcl2 levels. This pathway could, in part, underlie the observed phenotypes. Collectively, our findings show that hTERT can suppress multiple lncRNAs, including MEG3, and establish a novel mechanism of hTERT-mediated proliferative control that could facilitate tumorigenesis. Our mechanistic insights suggest that small RNA-directed diagnostic and therapeutic strategies will be relevant for targeting hTERT. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE61546 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA261437 https://www.ebi.ac.uk/ena/browser/view/PRJNA261437 None [Overal design]Primary human mammary epithelial cells (HMECs), derived from two human donors, were first stably retrovirally transduced with hTERT and then stably transfected with either empty vector control (Vector) or with MEG3. Cells were cultured in mitogen-limited conditions, and total RNA extracted on day 5. Statistical analyses were carried out between donor-paired samples (hTERT+Vector versus hTERT+MEG3).; [Treatment]'HMECs derived from two human donors were stably retrovirally transduced with hTERT, and thereafter stably transfected with either empty vector control or MEG3. Cells were plated in complete medium, switched to mitogen-limited medium after 24 h, and cultured for 4 more days.'; [Growth]'Cells were plated at 0.2 million cells per 100mm dish in Mammary Epithelial Basal Medium (MEBM) with supplements, including human epidermal growth factor (hEGF) and bovine pituitary extract. After 24h, cells were washed and cultured for 4 more days in mitogen-limitedl medium, which is MEBM without hEGF and bovine pituitary extract supplements. Total RNA was extracted on day 5.'; [Extraction]"Extraction of total RNA using TRIZOL reagent was carried out according to manufacturer's instructions, followed by overnight sodium acetate/ethanol precipitation and three ethanol washes for concentrating and purifying the RNA."; [Cell type]'Human mammary epithelial cells (HMEC)''cell type: Human mammary epithelial cells (HMEC); retrovirally transduced with: hTERT; stably transfected with: pCDNA; ', 'cell type: Human mammary epithelial cells (HMEC); retrovirally transduced with: hTERT; stably transfected with: MEG3; ' GSE86896 Homo sapiens 4 Expression profiling by high throughput sequencing GPL10999 Transcriptomic analyses for the CSC-like properties under monolayer and sphere culture conditions in 293T and MCF-7 cells 2016-09-13 In order to verify the CSC-like properties in 3D spheres of 293T cells as compared to monolayer, MCF-7 breast cancer cells under monolayer and sphere culture conditions were used as a control. Corresponding author: Chul Geun Kim, Department of Life Science, Hanyang University, Seoul 133-791, Korea (e-mail, cgkim@hanyang.ac.kr). https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE86896 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA342854 https://www.ebi.ac.uk/ena/browser/view/PRJNA342854 https://www.ncbi.nlm.nih.gov/sra?term=SRP089821 [Overal design]mRNA profiles of the 293T and MCF-7 cells [monolayer (mMCF-7 and m293T) and sphere (sMCF-7 and s293T) culture conditions] were generated by deep sequencing using Illumina GAIIx.; [Treatment]'For 3D-sphere culture, cells were plated at a density of 1×104 cells/mL in DMEM/F-12 medium (Hyclone) supplemented with B27 (Gibco), 10 ng/ mL bFGF (Gibco) and 20 ng/ mL EGF (Sigma) on 0.5% poly(2-hydroxyethyl methacrylate) (poly-HEMA; Sigma)-coated dishes.'; [Growth]'The human breast cancer cell line MCF-7 and human embryonic kidney cell line 293T were cultured in Dulbecco’s modified Eagle’s medium (Hyclone) containing 10% FBS (Hyclone), 100 U/mL penicillin (Sigma), and 100 µg/mL streptomycin (Sigma).'; [Extraction]'Total RNA was isolated from the cells [monolayer (mMCF-7 and m293T) and sphere (sMCF-7 and s293T) culture conditions] using the TRIzol reagent (Invitrogen, Carlsbad, CA, USA). RNA was treated with RNase-free DNase I (Promega, Madison, WI, USA) to eliminate DNA contamination. The RNA concentration and quality were determined using a NanoDrop® ND-1000 spectrophotometer (NanoDrop Technologies Inc., Wilmington, DE, USA) and the Agilent RNA Integrity number (RIN) (Schroeder et al., 2006) was evaluated using the Agilent 2100 Bioanalyzer and the Agilent RNA 6000 Nano kit (Agilent Technology, Santa Clara, CA, USA). The absorbance ratio at 260:280 nm for all samples was >1.8 and the RIN value was > 9. The integrity of RNA samples was also ascertained by the presence of distinct 28S and 18S ribosomal RNA bands in agarose gels after electrophoretic resolution.\nRNA libraries were prepared for sequencing using standard Illumina protocols.'; [Cell type]'Source: ''cell line: 293T; culture condition: monolayer (m) cultured cell; type: wild type (WT); ', 'cell line: MCF7; culture condition: monolayer (m) cultured cell; type: wild type (WT); ', 'cell line: 293T; culture condition: sphere (s) forming cell; type: wild type (WT); ', 'cell line: MCF7; culture condition: sphere (s) forming cell; type: wild type (WT); ' GSE50939 Homo sapiens 71 Expression profiling by array GPL4133; GPL16272 Tumor Intrinsic Subtype is Reflected in Cancer-Adjacent Benign Tissue 2013-09-17 Introduction: Overall survival of early-stage breast cancer (BC) patients is similar for those who undergo breast conserving therapy (BCT) and mastectomy, however, 10-15% of women undergoing BCT suffer ipsilateral breast tumor recurrence. The risk of recurrence may vary with age or breast cancer subtype. Understanding the gene expression of the cancer-adjacent tissue and/or stromal response to specific tumor subtypes is important for developing clinical strategies to reduce recurrence risk. Methods: We studied gene expression data in cancer-adjacent tissue from 158 BC patients. Complementary in vitro cocultures were used to study cell-cell communication between fibroblasts and specific breast cancer subtypes. Results: Our results suggest that intrinsic tumor subtypes are reflected in histologically normal cancer-adjacent tissue. Gene expression of cancer-adjacent tissues shows that triple negative (Claudin-low or Basal-like tumors) exhibit increased expression of genes involved in inflammation and immune response. While such changes could reflect distinct immune populations present in the microenvironment of different breast cancer subtypes, altered immune response gene expression was also observed in cocultures in the absence of immune cell infiltrates, emphasizing that these inflammatory mediators are secreted by breast-specific cells. In addition, while triple negative BCs are associated with upregulated immune response genes, Luminal breast cancers are more commonly associated with estrogen-response in adjacent tissues. Conclusions: Specific characteristics of BCs are reflected in the surrounding benign tissue. This commonality between tumor and surrounding tissue may underlie second primaries and local recurrences. Biomarkers derived from cancer-adjacent tissue may be helpful in defining personalized surgical strategies or in predicting recurrence risk. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50939 Tumor intrinsic subtype is reflected in cancer-adjacent tissue. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 5.057 https://doi.org/10.1158/1055-9965.EPI-14-0934 {Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology (5.057): 10.1158/1055-9965.EPI-14-0934} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA219415 https://www.ebi.ac.uk/ena/browser/view/PRJNA219415 None [Overal design]reference x sample; [Treatment]'None'; [Growth]'None'; [Extraction]'Qiagen Rneasy Mini'; [Cell type]'Source: ''reference: Stratagene Human Universal Reference that contained 1/10 added MCF7 and ME16C RNAs; ', 'distance to tumor: Peritumoral; er status: +; ', 'distance to tumor: Peritumoral; er status: -; ', 'distance to tumor: Remote; er status: +; ', 'distance to tumor: Remote; er status: -; ', 'distance to tumor: Peritumoral; tumor_subtype: LumB; ', 'distance to tumor: Peritumoral; tumor_subtype: Basal; ', 'distance to tumor: Peritumoral; tumor_subtype: Claudin; ', 'distance to tumor: Peritumoral; tumor_subtype: LumA; ', 'distance to tumor: Peritumoral; tumor_subtype: Her2; ' GSE104737 Mus musculus 12 Expression profiling by array GPL16570 Neo-Adjuvant Oncolytic Virotherapy Prior to Surgery Sensitizes Triple-Negative Breast Cancer to Immune Checkpoint Therapy 2017-10-09 Triple-negative breast cancer (TNBC) is an aggressive disease for which treatment options are limited and associated with severe toxicities. In this experiment we evaluated the response of 2 murine TNBC models to oncolytic Maraba virus infection. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE104737 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA413701 https://www.ebi.ac.uk/ena/browser/view/PRJNA413701 None [Overal design]Monolayers of 4T1 or EMT6 cells were treated at an MOI of 3 for 24h with either Maraba or UV-inactivated Maraba.; [Treatment]'Treatment done at MOI 3'; [Growth]'Cell grown in 10% FBS, virus grown in Vero cells'; [Extraction]'RNA was extracted using the RNeasy RNA extraction kit (Qiagen).'; [Cell type]'in-vitro cells''cell type: in-vitro cells; ' GSE29270 Homo sapiens 63 Expression profiling by array GPL4133 Molecular Characterization of Breast Carcinoma Associate fibroblasts 2011-05-12 Normal breast fibroblasts, breast cancer associated fibroblasts, fibroblasts taken at least 2cm from cancer margins and femur-derived human mesenchymal stem cells were profiled for comparative purposes https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE29270 A functional in vitro model of heterotypic interactions reveals a role for interferon-positive carcinoma associated fibroblasts in breast cancer. BMC cancer 2.933 https://doi.org/10.1186/s12885-015-1117-0 {BMC cancer (2.933): 10.1186/s12885-015-1117-0} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA139921 https://www.ebi.ac.uk/ena/browser/view/PRJNA139921 None [Overal design]Ex vivo cultured primary cells of different anatomical origin were expression profiled under low serum conditions: cancer-associated fibroblasts, fibroblasts from a distance of at least 2cm from the cancers' edge, fibroblasts from cancer-free breasts and mesenchymal stromal cells from the marrow of femurs. Biological Replicates= 46. Technical Replicates= 17; [Treatment]'None'; [Growth]'All samples were cultured in DMEM media with 2% fetal bovine serum and harvested at subconfluency'; [Extraction]'standard Agilent protocol'; [Cell type]'Source: ''tissue: breast carcinoma associated fibroblast; disease state: carcinoma; ', 'sample type: reference; ', 'tissue: breast counterpart fibroblast; ', 'tissue: breast fibroblast; disease state: normal; ', 'tissue: femur bone marrow aspirate; ' GSE76460 Homo sapiens 16 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL11154 The Chromatin-Looping Factor ZNF143 Engages at Looping Promoters to Favor the Estrogen Response in Breast Cancer 2015-12-31 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE76460 None None None None None 'total RNA', 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA307352 https://www.ebi.ac.uk/ena/browser/view/PRJNA307352 None [Overal design]Refer to individual Series; [Treatment]'MCF-7 cells were transfected with siZNF143 (Ambion siRNA ID: s15194) or a scrambled control siRNA and starved of oestrogen for 48hrs. They were stimulated with 10 nM 17-beta oestradiol for 3 hours prior to RNA extraction.', 'MCF-7 cells were starved of estrogen for 48hrs, then stimulated with 10 μM 17β oestradiol (E2) or vehicle (EtOH) for 45 minutes prior to cross-linking'; [Growth]'MCF-7 cells were grown in DMEM supplemented with 10% FBS and 1% P/S'; [Extraction]"RNA was harvested using Qiagen's Rneasy Plus Mini Kit\nRNA libraries were prepared for sequencing using standard Illumina protocols.", 'Chromatin was sonicated by biorupter and immunoprecipitated with anti-ZNF143 antibody. DNA was extracted using MinElute PCR purification kit (Qiagen 28004).\nLibrary construction was performed using New England Biolabs ChIP-seq library prep reagent set (E6200S)'; [Cell type]'Source: ''cell line: MCF-7; transfection: scrambled control siRNA; treatment: vehicle; ', 'cell line: MCF-7; transfection: scrambled control siRNA; treatment: 10 uM 17-beta oestradiol for 3 hours; ', 'cell line: MCF-7; transfection: siZNF143; treatment: vehicle; ', 'cell line: MCF-7; transfection: siZNF143; treatment: 10 uM 17-beta oestradiol for 3 hours; ', 'cell line: MCF-7; chip-antibody: ZNF143 (Novus Biologicals H00007702-M01); treatment: vehicle; ', 'cell line: MCF-7; chip-antibody: ZNF143 (Novus Biologicals H00007702-M01); treatment: 10 uM 17-beta oestradiol (E2); ' GSE149949 Mus musculus 5 Expression profiling by high throughput sequencing GPL17021 Characterization of estrogen, progesterone and the endocrine-disrupting chemical-induced mouse mammary gland reorganization via single-cell RNA-sequencing 2020-05-06 The mammary epithlium goes through the drastic reorganization during development, pregnancy, and menopause as well as by external hormones and its mimicry, which risks the gland for the specific type of breast cancer. Using a surgical menopausal (ovariectomized) mouse model, we assessed how mammary gland tissue was affected by 17β-estradiol (E2), progesterone (P4) and polybrominated diphenyl ethers (PBDEs). Then, we integrated the transcriptomes of 50K mouse and 24K human mammary epithelial cells from five different datasets and four individuals obtained by single-cell RNA sequencing (scRNAseq). The results indicated a putative trajectory originating from the embryonic mammary stem cells and differentiating into the three different epithelial lineage (Basal, Luminal alveolar, and Luminal hormone sensing) that were presumably sustained by unipotent progenitors in the postnatal glands. The identified lineage-specific gene sets inferred cells of origin of breast cancer using The Cancer Genome Atlas data and scRNAseq of human breast cancer. The comprehensive mammary cell atlas presented novel insights into the impact of the internal and external stimulati on the mammary epithelium in an unprecedented resolution. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE149949 Mammary cell gene expression atlas links epithelial cell remodeling events to breast carcinogenesis. Communications biology 0.12 https://doi.org/10.1038/s42003-021-02201-2 {Communications biology (0.12): 10.1038/s42003-021-02201-2} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA630686 https://www.ebi.ac.uk/ena/browser/view/PRJNA630686 https://www.ncbi.nlm.nih.gov/sra?term=SRP260243 [Overal design]Female BALB/cj mice were ovariectomized 20 weeks before treatment. They were treated with 5 different conditions for 1 week; 1)Vehicle, 2) E2, 3) E2 and PBDEs, 4) E2 and P4, and 5) E2, P4 and PBDEs, . The 4th mammary glands were harvested and single-cell RNA sequencing was performed.; [Treatment]'Special food with PBDEs mixture (BDE-47; 7.1 mg/kg, BDE-100; 0.4 mg/kg, and BDE-153; 0.9 mg/kg) was prepared (Research Diets, Inc, New Brunswick, NJ) and administered per oral to mimic environmental exposure of human to PBDEs via ingestion and diet. The composition was previously determined by us to achieve the relevant exposure with the ratio of the three congeners found in human blood (1 mg/kg/day, 0.056 mg/kg/day, and 0.126 mg/kg/day for BDE-47, -100, -153, respectively). Non-PBDE groups were fed with nutrient-matched special food with DMSO (Research Diets, Inc.). E2 (1 ug/animal) and P4 (0.1 mg/animal) were administered by daily intraperitoneal injection. DMSO was used as vehicle and injected in the control groups. The treatments started 20 weeks after ovariectomy and continued for 1 week.'; [Growth]'None'; [Extraction]"Mammary glands were digested using a mixture of Collagenase and DNAse I, and processed into a single-cell suspension for loading onto a Chromium Controller (10x Genomics).\nCell number and viability were measured using a TC20 Automated Cell Counter (BioRad). Single-cell RNA libraries were prepared according to the Chromium™ Single Cell 3' Reagent Kits v2 User Guide (10x Genomics). Approximately 4,000 cells were loaded on a Chromium single cell Controller instrument (10x Genomics) to generate single cell gel beads in emulsion (GEMs). The barcoded sequencing libraries were constructed using the Chromium Single-Cell 3′ Library Kit (10x Genomics) for enzymatic fragmentation, end-repair, A-tailing, adaptor ligation, ligation cleanup, sample index PCR, and PCR cleanup."; [Cell type]'Source: ''strain: BALB/cj; age: 30 weeks; treatment: Vehicle; ', 'strain: BALB/cj; age: 30 weeks; treatment: E2; ', 'strain: BALB/cj; age: 30 weeks; treatment: E2+PBDE; ', 'strain: BALB/cj; age: 30 weeks; treatment: E2+P4; ', 'strain: BALB/cj; age: 30 weeks; treatment: E2+P4+PBDE; ' GSE66665 Homo sapiens 8 Non-coding RNA profiling by high throughput sequencing GPL11154 A novel subclass of exon-derived microRNA is widespread in the mammalian genome 2015-03-09 Abstract: Argonaute-2, the primary effector molecule of the RNA Induced Silencing Complex, loads both canonical miRNAs and a wide variety of other non-canonical miRNA-like species that enable base pair mediated transcript regulation. Here, using ultra-deep RNA immunoprecipitation and sequencing of nuclear and cytoplasmic hAGO2 in human breast cancer-derived MCF-7 cells, we have identified over one thousand novel AGO2-associated small RNAs. These include a wide variety of isomiRs, in excess of 100 mirtron loci and H/ACA snoRNA and HY3 repeat-derived small RNAs. Unexpectedly, we also discovered 298 AGO2-loaded exon-derived miRNAs (emiRs). These conserved small RNAs are encoded within protein-coding exons and 3’UTRs, have a 5’ end adenosine bias (in contrast to the 5’ U observed in canonical miRNAs), are DICER-1 dependent, processed from mature mRNAs post-splicing and derived from a wide variety of genes involved in differentiation and development including SOX4, JUN, c-MYC and AGO2 itself. We find evidence of emiR expression in human brain and other peripheral tissues, and demonstrate that human emiRs are conserved and detected in murine Ago2 small RNA libraries. Five human emiR loci coincide with known Mendelian disease-causing mutations, and the expression of emiRs is altered in human breast cancer, which may indicate that these species can play a role in disease etiology and progression. We propose that emiRs are the small RNA complement to the competing endogenous RNA (ceRNA) system. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE66665 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA277698 https://www.ebi.ac.uk/ena/browser/view/PRJNA277698 https://www.ncbi.nlm.nih.gov/sra?term=SRP055991 [Overal design]Small RNAs and AGO2-bound small RNAs and in whole cell, nuclear and cytoplasmic compartments of MCF-7 cells.; [Treatment]'See sample description.'; [Growth]'MCF-7 cells were grown at 140 mm dishes in Invitrogen Gibco Minimal Essential Media (MEM – Invitrogen - 12360-038) supplemented with 10% heat inactivated FCS, 2 mM L-Glutamax (Invitrogen-35050-061), 50 units/mL of penicillin and 50 mg/mL of Streptomycin (Invitrogen-15070-063), 0.1 mM of non essential aminoacids (Invitrogen-11140-050), 1.0 mM Sodium Pyruvate (Invitrogen – 11360-070) and 10 mg/mL human insulin solution (Sigma – I9278).'; [Extraction]'RNA was extracted using the standard Invitrogen TRIzol procedure. RNA quality and yield was assessed on an Agilent 2100 Bioanalyzer using total RNA Pico Chip kit (Agilent). Cell equivalent amounts of RNA from nuclear and cytoplasmic fractions were used for all analyses, unless stated otherwise.\nLibraries were prepared using the TruSeq Small RNA kit v1.5'; [Cell type]'Source: ''cell line: MCF-7 human breast adenocarcinoma cell line; ip antibody: none; adaptor: TGGAATTCTCGGGTGCCAAGG; ', 'cell line: MCF-7 human breast adenocarcinoma cell line; ip antibody: Anti-Ago2 / eIF2C2 antibody - ChIP Grade (ab57113); adaptor: TGGAATTCTCGGGTGCCAAGG; ', 'cell line: MCF-7 human breast adenocarcinoma cell line; ip antibody: yes; adaptor: TGGAATTCTCGGGTGCCAAGG; ' GSE110659 Homo sapiens 6 Expression profiling by array GPL10558 MicroRNA-138: A Diagnostic Biomarker and Therapeutic Target for the Aggressive Basal-like subtype of Breast Cancer 2018-02-15 This study identifies miR-138 as a prognostic biomarker for basal breast carcinoma. Identification of differentially regulated genes upon miR-138 knockdown (AntagomiR-138) in basal breast cancer cell lines MDA-MB-231 https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE110659 MicroRNA-138 is a Prognostic Biomarker for Triple-Negative Breast Cancer and Promotes Tumorigenesis via TUSC2 repression. Scientific reports 4.011 https://doi.org/10.1038/s41598-019-49155-4 {Scientific reports (4.011): 10.1038/s41598-019-49155-4} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA434203 https://www.ebi.ac.uk/ena/browser/view/PRJNA434203 None [Overal design]Total RNA was extracted from MDA-MB-231 cells treated with scramble control and antimiR-138 expressing lentivirus; [Treatment]'MDA-MB-231 cells were transduced with 6 Transduction Units of scrambled or antimiR-138 control expressing lentivirus. Cells were harvested 72 hours post transduction.'; [Growth]'MDA-MB-231 cells were grown in complete medium containing DMEM and 10% FBS'; [Extraction]'Total RNA, including miRNA, was isolated using Exiqon RNA Isolation Kit'; [Cell type]'basal breast cancer cell line''cell line: MDA-MB-231; cell type: basal breast cancer cell line; transduced with: scamble control; time point: Day 3 post transduction; ', 'cell line: MDA-MB-231; cell type: basal breast cancer cell line; transduced with: antimiR-138; time point: Day 3 post transduction; ' GSE21719 Homo sapiens 12 Non-coding RNA profiling by array GPL5106 Identification of the receptor tyrosine kinase AXL in triple negative breast cancer as a novel target for the human miR-34a microRNA (miRNA study) 2010-05-06 Triple negative breast cancer (TNBC) is histologically characterized by the absence of the hormone receptors estrogen and progesterone, in addition to having a negative immunostain for HER-2. The aggressiveness of this disease and lack of targeted therapeutic options for treatment is of high clinical importance. MicroRNAs are short 21- to 23 nucleotide endogenous non-coding RNAs that regulate gene expression by binding to mRNA transcripts, resulting in either decreased protein translation or mRNA degradation. Dysregulated expression of miRNAs is now a hallmark of many human cancers. In order to identify a miRNA/mRNA interaction that is biologically relevant to the triple negative breast cancer genotype/phenotype, we initially conducted a miRNA profiling experiment to detect differentially expressed miRNAs in cell line models representing the triple negative (MDA-MB-231), ER+ (MCF7), and HER-2 overexpressed (SK-BR-3) histotypes. We identified human miR-34a expression as being >3-fold down (from its median expression value across all cell lines) in MDA-MB-231 cells, and identified AXL as a putative mRNA target using multiple miRNA/target prediction algorithms. The miR-34a/AXL interaction was functionally characterized through ectopic overexpression experiments with a miR-34a mimic. In reporter assays, miR-34a binds to the putative target site within the AXL 3’UTR to affect luciferase expression. We also observed degradation of AXL mRNA and decreased AXL protein levels, as well as cell signaling effects on AKT phosphorylation and phenotypic effects on cell migration. Finally, we present an inverse correlative trend in miR-34a and AXL expression for both cell line and patient tumor samples. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE21719 Identification of the receptor tyrosine kinase AXL in breast cancer as a target for the human miR-34a microRNA. Breast cancer research and treatment 3.471 https://doi.org/10.1007/s10549-011-1690-0 {Breast cancer research and treatment (3.471): 10.1007/s10549-011-1690-0} 'other' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA129373 https://www.ebi.ac.uk/ena/browser/view/PRJNA129373 None [Overal design]The small RNA (sRNA) fraction from four separate passages (biological replicates) of MCF7, SK-BR-3, MDA-MB-231, and MCF10A cells were extracted using Qiagen’s miRNeasy kit following the manufacturer’s instructions (Qiagen; Germantown, MD). Five micrograms of sRNA was labeled with either Cy3 (MCF10A) or Cy5 (breast cancer cell) fluorescent label (GE Healthcare; Piscataway, NJ) using the mirVana miRNA labeling kit (Ambion; Austin, TX). The labeled products were hybridized to miRVana miRNA Bioarrays V2 (Ambion, Austin, TX) and washed following the manufacturer’s protocol. Each array was comprised of 328 human miRNA probes in addition to 114 mouse and 46 rat miRNAs. The comparative hybridization for each breast cancer cell line to the reference MCF10A cell line control was conducted in quadruplicate (n=12 total arrays). Processed arrays were scanned for dual channel hybridization using a GenePix 4000B scanner (Molecular Devices; Sunnyvale, CA). Analyses were performed using BRB-Array Tools Version 3.8.1 (http://linus.nci.nih.gov/BRB-ArrayTools.html). Replicate spots for each miRNA were averaged within the array, background adjusted, and log2 normalized. Normalization was performed using a per chip median normalization method. Only those miRNAs with at least a 3-fold change in expression from its median value across all arrays, in at least 33% of all arrays tested, were retained. Samples and genes were hierarchical clustered with average linkage under the Euclidian distance similarity metric using the Cluster 3.0 (http://rana.stanford.edu/software) and Java TreeView 1.1.4r3 applications. MiRNA probes of mouse, rat, and manufacturer’s (Ambion) origins that passed the gene filter were excluded from future analyses.; [Treatment]'Cells were untreated.'; [Growth]'Cells were grown in RPMI 1640 basal medium + 10% FBS in a T75 flask at 37C with 5% carbon dioxide. Cells were harvested at 80-90% confluency for total RNA extraction.', 'Cells were grown in DMEM/F12 basal medium supplemented with 5% horse serum, 20 ng/ml final epidermal growth factor, 0.5 ug/ml final hydrocortisone, 100 ng/ml final cholera toxin, and 10 ug/ml final insulin in a T75 flask at 37C with 5% carbon dioxide. Cells were harvested at 80-90% confluency for total RNA extraction.'; [Extraction]"The small RNA fraction was extracted from these cells using Qiagen's miRNeasy kit by following the manufacturer's protocol."; [Cell type]'Source: ''estrogen receptor: negative; progesterone receptor: negative; her-2: negative; cell line: MB231; ', 'cell line: MCF10A; ', 'estrogen receptor: positive; progesterone receptor: positive; her-2: negative; cell line: MCF7; ', 'estrogen receptor: positive; progesterone receptor: negative; her-2: negative; cell line: MCF7; ', 'estrogen receptor: negative; progesterone receptor: negative; her-2: positive; cell line: SKBR3; ' GSE128397 Homo sapiens 1 Genome binding/occupancy profiling by high throughput sequencing GPL18573 Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [ChIP-seq] 2019-03-15 Long noncoding RNAs regulating diverse cellular processes implicate in many diseases. Here, we report the identification of a novel long intergenic noncoding RNA, Linc-ASEN, expressed in prematurely senescent cells, that associates with UPF1 and represses cellular senescence by reducing p21 production transcriptionally and post-transcriptionally. The Linc-ASEN-UPF1 complex suppressed p21 transcription by recruiting Polycomb Repressive Complex 1 (PRC1) and PRC2 to the p21 locus, and thereby preventing binding of the transcriptional activator p53 on the p21 promoter. Moreover, the Linc-ASEN-UPF1 complex repressed p21 expression post-transcriptionally by lowering p21 mRNA stability in association with DCP1A. Accordingly, Linc-ASEN levels were found inversely correlated with p21 mRNA levels in tumor tissues from patient-derived xenograft mice, in various human cancer tissues, and in aged mice tissues. Our studies reveal that Linc-ASEN prevents cellular senescence by reducing the transcription and stability of p21 mRNA in concert with UPF1, and suggest that Linc-ASEN might be a potential therapeutic target in processes influenced by senescence, including cancer. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE128397 A novel long noncoding RNA Linc-ASEN represses cellular senescence through multileveled reduction of p21 expression. Cell death and differentiation 8.086 https://doi.org/10.1038/s41418-019-0467-6 {Cell death and differentiation (8.086): 10.1038/s41418-019-0467-6} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA527317 https://www.ebi.ac.uk/ena/browser/view/PRJNA527317 https://www.ncbi.nlm.nih.gov/sra?term=SRP188573 [Overal design]Analysis of genome wide binding sites of UPF1 via ChIP-seq in MCF7 breast cancer cells.; [Treatment]'For ChIP, cells were lysed in NET-2 buffer containing 100 U of RNase Inhibitor (Invitrogen, Carlsbad, CA, USA) and preclearing with Protein A-Sepharose beads (GE Healthcare Bio-Science AB, Uppsala, Sweden). After preclearing, the lysates were immunoprecipitated with specific antibodies or IgG along with beads.'; [Growth]"MCF7 cells were cultulred in Dulbecco's modified Eagle's medium (DMEM) (WelGENE, Daegu, Korea) supplemented with 10% fetal bovine serum (Tissue Culture Biologies, Long Beach, CA, USA) and 1% penicillin and streptomycin solution (WelGENE) at 37°C in a 5% CO2 incubator."; [Extraction]'The DNAs and RNAs pulled down with proteins were purified by phenol-chloroform extraction and precipitated in ethanol.\nChIP-seq libraries were constructed using TruSeq Strandard library protocols.'; [Cell type]'epithelial''cell type: epithelial; tissue: mammary gland, breast; derived from metastatic site: pleural effusion; disease: adenocarcinoma; age: 69 years adult; chip antibody: Anti-RENT1 (UPF1) (Bethyl Laboratories, A301-902A); ' GSE89225 Homo sapiens 54 Expression profiling by high throughput sequencing GPL16791; GPL17303 Regulatory T cells exhibit distinct features in human breast cancer 2016-10-27 The goal of this study is to compare transcriptional profiles of regulatory T cells and conventional CD4 T cells in human breast cancer to regulatory T cells and conventional CD4 T cells in normal breast parenchyma and in peripheral blood. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE89225 Regulatory T Cells Exhibit Distinct Features in Human Breast Cancer. Immunity 21.522 https://doi.org/10.1016/j.immuni.2016.10.032 {Immunity (21.522): 10.1016/j.immuni.2016.10.032} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA350777 https://www.ebi.ac.uk/ena/browser/view/PRJNA350777 https://www.ncbi.nlm.nih.gov/sra?term=SRP092158 [Overal design]RNA sequencing of 2 different cell types in 3 different tissues; [Treatment]'Breast tumors and NBP were minced and enzymatically digested using Liberase TL for 20 minutes at 37C. The digested tissues were then passed through a 100uM filter and washed twice with FACS buffer prior to surface staining. PBMC were enriched for CD4 T cells through negative selection with RosetteSep antibody cocktails and washed twice with FACS buffer prior to surface staining. Lymphocytes were stained at 1 x 106 cells per ml for 20 minutes following Fc receptor blockade (BioLegend). Definitions used for cell sorting were as follows, conventional CD4+ T cells: CD45+CD3+CD4+CD8-CD25-, Treg cells: CD45+CD3+CD4+CD8-CD127-CD25high. Tissue Treg cells were largely of an activated phenotype and in order to provide a fair comparison to their blood counterparts blood Treg cells were defined as CD45+CD3+CD4+CD8-CD45RO+CD127-CD25high. , while resting Treg cells were defined as CD45+CD3+CD4+CD8-CD45RA+CD127-CD25high. Post sort purity was checked following every sort and was routinely > 95% pure for the sorted populations.'; [Growth]'Samples were collected from adult treatment-naïve women undergoing surgery for primary breast cancer. All samples were obtained after informed consent and approval from the Institutional Review Board (IRB) at Memorial Sloan Kettering Cancer Center. Normal breast parenchyma (NBP) was obtained from patients undergoing contralateral prophylactic mastectomies. Peripheral blood mononuclear cells (PBMCs) were obtained from patients prior to their surgical procedures and from buffy coats obtained from the New York Blood Center (NYBC). All cells were utilized immediately ex vivo.'; [Extraction]"Illumina TruSeq paired-end library preparation following manufacturer's protocols\nCells were sorted directly into Trizol LS (ThermoFisher) and stored at -80°C prior to RNA extraction. RNA was extracted and quantified and identical quantities of RNA from each sample were subjected to SMARTer amplification with 12-16 round of PCR was performed.", 'Iontorrent Ion ChIP-Seq Kit with end-repair process\nCells were sorted directly into Trizol LS (ThermoFisher) and stored at -80°C prior to RNA extraction. RNA was extracted and quantified and identical quantities of RNA from each sample were subjected to SMARTer amplification with 12-16 round of PCR was performed.'; [Cell type]'Regulatory T cells', 'Conventional CD4 T cells''tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: GTTTCG; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: AGTTCC; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: ACTTGA; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: GCCAAT; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: GGTAGC; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: GTGGCC; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: AGTCAA; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: TTAGGC; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: ACAGTG; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: GAGTGG; ', 'tissue: PBMC; cell type: Conventional CD4 T cells; cell activation: CD45RA+; cell category: naïve; ', 'tissue: PBMC; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; ', 'tissue: NBP; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: GTAGAG; ', 'tissue: NBP; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: GGCTAC; ', 'tissue: NBP; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: ATCACG; ', 'tissue: NBP; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: ATTCCT; ', 'tissue: NBP; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: CACGAT; ', 'tissue: NBP; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: CATGGC; ', 'tissue: breast tumor; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: GTGAAA; ', 'tissue: breast tumor; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: CGTACG; ', 'tissue: breast tumor; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; ', 'tissue: breast tumor; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: ATGTCA; ', 'tissue: breast tumor; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: GATCAG; ', 'tissue: breast tumor; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: CAGATC; ', 'tissue: breast tumor; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: TGACCA; ', 'tissue: breast tumor; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: ACTGAT; ', 'tissue: breast tumor; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: CAACTA; ', 'tissue: breast tumor; cell type: Conventional CD4 T cells; cell activation: CD45RO+; cell category: activated; barcode: CACTCA; ', 'tissue: PBMC; cell type: Regulatory T cells; cell activation: CD45RA+; cell category: naïve; ', 'tissue: PBMC; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; ', 'tissue: NBP; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: CCGTCC; ', 'tissue: NBP; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: TAGCTT; ', 'tissue: NBP; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: CTTGTA; ', 'tissue: NBP; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: ATGAGC; ', 'tissue: NBP; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: CACCGG; ', 'tissue: NBP; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: CAGGCG; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: GTCCGC; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: CGATGT; ', 'tissue: breast tumor; cell type: Regulatory T cells; cell activation: CD45RO+; cell category: activated; barcode: CAAAAG; ' GSE22783 Homo sapiens 12 Genome binding/occupancy profiling by genome tiling array; Expression profiling by array GPL570; GPL10648 Coupling p53 binding and nucleosome occupancy measurements at p53 binding sites 2010-07-07 We were interested to explain why p53 binds some high affinity sites in contrast to other high affinity sites that are not bound by p53. p53 binding was measured using p53 ChIP-CHIP and in parallel nucleosome occupancy was measured on these same sites Comparison between p53 binding and nucleosome occupancy at p53 predicted binding sites https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22783 p53 binds preferentially to genomic regions with high DNA-encoded nucleosome occupancy. Genome research 9.944 https://doi.org/10.1101/gr.103945.109 {Genome research (9.944): 10.1101/gr.103945.109} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA129117 https://www.ebi.ac.uk/ena/browser/view/PRJNA129117 None [Overal design]ChIP-CHIP of p53 from MCF7EcoR under Basal conditions and MCF7EcoR treated with NCS (Activated) and Mononucleosomal extraction from MCF7sip53, MCF7EcoR under Basal conditions and MCF7EcoR treated with NCS (Activated) Expression analysis of MCF7sip53 and MCF7EcoR treated with NCS (Activated); [Treatment]'no treatment', 'cells were treated with 200ng/ml NCS for 4 hours', 'For p53 activation, MCF7EcoR cells were treated with Neocarzinostatin (NCS (Sigma), 200ng/ml, 4h)'; [Growth]'Cells were grown in DMEM medium supplememted with 10%FCS, 1µg/ml puromycin and pen-strep', "MCF7 human breast cancer cells, stably transfected with shRNA against p53 or with empty vector were cultured in Dulbecco's modified Eagle's medium plus 10% FBS, 1% P/S and 1µg/ml Puromycin."; [Extraction]'Mononucleosome preperation: nuclei were isolated from 2.5*10^6 cells in lysis buffer (10mM Tris pH7.4, 10mM NaCl, 3mM MgCl2, 0.5% NP-40, 0.15mM Spermine, 0.5mM Spermidine) for 10 min on ice. Nuclei were washed once in wash buffer (10mM Tris pH7.4, 15mM NaCl, 60mM KCl, 0.15mM Spermine, 0.5mM Spermidine) followed by resuspension in MNase buffer (wash buffer+1mM CaCl2) followed by MNase digestion (1 unit/12 million cells, 10 min at 37ºC), Reaction was stopped by addition of EDTA to 0.01M, SDS and NaCl were added to a final concentration of 2% and 0.2M, respectively. Rnase (0.1mg) was added for 1hr at 37ºC. DNA was extracted using Qiagen PCR purification kit, seperated on a 1.5% agarose gel, and fragments of 150bp were excised and extraction using Qiagen gel extraction kit. In parallel, input DNA was isolated using Qiagen Dneasy Blood and tissue kit and sonicated in TE to ~500bp fragments, 1µg of nucleosomal DNA and input DNA were labeled and hybridized to Nimbelgen custom arrays as above.p53 ChIP was done using CM1 antibody and according to previously published protocol (Weinmann and Farnham,2002).', "RNA was extracted using the Qiagen Rneasy kit according to the manufacturer's instructions."; [Cell type]'Source: ''antibody: p53 (Novocastra, NCL-p53-CM1); cell line: MCF7EcoR; treatment: Control; ', 'cell line: MCF7EcoR; treatment: Control; ', 'antibody: p53 (Novocastra, NCL-p53-CM1); cell line: MCF7EcoR; treatment: NCS; ', 'cell line: MCF7EcoR; treatment: NCS; ', 'cell line: MCF7sip53; treatment: Control; ', 'cell line: MCF7sip53; treatment: control; ' GSE25519 Homo sapiens 2 Methylation profiling by genome tiling array GPL14671 Promoter methylation data: OHT/ICI-sensitive vs. -resistant cell lines 2010-11-20 MCF7 breast cancer cell lines: drug-resistant (OHT and ICI) cell lines vs. drug-sensitive (wild type) cell lines. Assessment of association between gene expression and methylation. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE25519 An empirical Bayes model for gene expression and methylation profiles in antiestrogen resistant breast cancer. BMC medical genomics 2.568 https://doi.org/10.1186/1755-8794-3-55 {BMC medical genomics (2.568): 10.1186/1755-8794-3-55} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA133775 https://www.ebi.ac.uk/ena/browser/view/PRJNA133775 None [Overal design]Two comparisons: OHT-resistant vs. wild type, and ICI-resistant vs. wild type. OHT: 4-hydroxytamoxifen ICI: fulvestrant ((ICI 182780) This submission represents the methylation component of the study.; [Treatment]'None'; [Growth]'Cells were maintained in MEM with 2 mmol/L L-glutamine, 0.1 mmol/L non-essential amino acids, 50 units/mL penicillin, 50 ug/mL streptomycin, 6 ng/mL insuliln, and 10% FBS.'; [Extraction]'Genomic DNA was isolated by using the Qiagen DNeasy Tissue kit.'; [Cell type]'breast cancer''cell line: MCF7; cell type: breast cancer; phenotype: OHT sensitive; ', 'cell line: MCF7; cell type: breast cancer; phenotype: OHT resistant; ', 'cell line: MCF7; cell type: breast cancer; phenotype: ICI sensitive; ', 'cell line: MCF7; cell type: breast cancer; phenotype: ICI resistant; ' GSE39720 Homo sapiens 3 Expression profiling by array GPL570 Time-course effect of estradiol and ERa17p on Early Gene expression in T47D cells 2012-07-30 ERα17p is a synthetic peptide corresponding to the sequence P295LMIKRSKKNSLALSLT311 of the estrogen receptor alpha (ERα) and initially synthesized to mimic its calmodulin binding site. ERα17p was subsequently found to elicit estrogenic responses in E2-deprived ERα-positive breast cancer cells, increasing proliferation and E2-dependent gene transcription. Surprisingly, in E2-supplemented media, ERα17p induced apoptosis and modified the actin network, influencing thereby cell motility. Here, we report that ERα17p induces a massive early (3h) transcriptional activity in breast cancer cell line T47D. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE39720 Whole transcriptome analysis of the ERα synthetic fragment P295-T311 (ERα17p) identifies specific ERα-isoform (ERα, ERα36)-dependent and -independent actions in breast cancer cells. Molecular oncology 5.962 https://doi.org/10.1016/j.molonc.2013.02.012 {Molecular oncology (5.962): 10.1016/j.molonc.2013.02.012} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA171552 https://www.ebi.ac.uk/ena/browser/view/PRJNA171552 None [Overal design]Cells after a 4h incubation with medium containing 10% charcoal stripped FBS were incubated with or without E2 (10-6M) or ERa17p in RPMI 1640 supplemented with 10% charcoal stripped FBS, for 3 hours. Total RNA was isolated using Nucleospin II columns (Macheray-Nagel, Dttren, Germany), according to the manufacturer’s instructions. RNA was labeled and hybridized according to the Affymetrix protocol (Affymetrix Gene-Chip Expression Analysis Technical Manual), using the HGU133A plus 2 chip, analyzing a total of 54675 transcripts. Signals were detected by an Affymetrix microarray chip reader.; [Treatment]'T47D cells were incubated with Estradiol or ERα17p for 3 hours after preincubation for 4 hours with medium containing 10% charcoal stripped FBS'; [Growth]'The human breast cancer cell line T47D was obtained from DSMZ (Braunschweig, Germany) and cultured in RPMI 1640 supplemented with 10% fetal bovine serum, at 37 °C, 5% CO2.'; [Extraction]'Total RNA was isolated using Nucleospin II columns (Macheray-Nagel, Dttren, Germany), according to the manufacturer’s instructions.'; [Cell type]'Source: ''cell line: T47D; protocol: ethanol treated cells (vehicle) 3h; ', 'cell line: T47D; protocol: estradiol treated cells 3h; ', 'cell line: T47D; protocol: ERα17p treated cells 3h; ' GSE40525 Homo sapiens 120 Non-coding RNA profiling by array GPL8227 miR-10b*, a master inhibitor of the cell cycle, is downregulated in human breast tumors 2012-08-31 Deciphering the molecular mechanisms involved in breast tumorigenesis has been the subject of extensive research in the last years; yet unpredictable response and development of resistance to adjuvant therapies remain major questions in the management of breast cancer patients. The power of miR expression signatures has emerged recently from several studies. Normal and breast tumor tissues can be discriminated by a miR signature as reported by Iorio et al (Iorio et al, 2005). Recent findings have also linked deregulated miR expression to breast cancer metastasis (Adorno et al, 2009; Huang et al, 2008; Tavazoie et al, 2008). Moreover, microRNAs are considering as a powerful tool in diagnosis and prognosis of breast cancer. In our study, we measured microRNA expression profiles from 64 primary breast cancer patients, comprising 56 matched tumor and adjacent peritumoral breast tissues, 5 tumor and 3 peritumor unmatched tissues. Our aim was to identify new microRNAs involved in the process of neoplastic transformation. The microarray data analysis identified, in every subgroup of breast cancers analyzed, a specific subset of microRNAs that were differentially expressed in tumor compared to peritumoral tissues. Among these miRs, we identified two (miR-10b* and miR-139-5p) that were down-regulated and three (miR-425, miR-454 and miR-301a) that were up-regulated for all three subtypes. We further show that microRNA-10b* is a master regulator of breast cancer cell proliferation. Two canonical CpG islands (5kb) upstream from the precursor sequence are hypermethylated in breast cancer tissues analyzed. Ectopic delivery of synthetic microRNA-10b* in breast cancer cell lines or into xenograft mouse breast tumors inhibits cell proliferation and impairs tumor growth in vivo, respectively. We identified and validated in vitro and in vivo three novel target mRNAs of miR-10b*, BUB1, PLK1 and CCNA2 genes, which play a remarkable role in cell cycle regulation and whose high expression in breast cancer patients reduced disease free survival, relapse free survival and metastasis free survival when compared to low expressors. This also suggests that restoration of microRNA-10b* expression might bear therapeutic promise. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE40525 miR-10b*, a master inhibitor of the cell cycle, is down-regulated in human breast tumours. EMBO molecular medicine 10.624 https://doi.org/10.1002/emmm.201201483 {EMBO molecular medicine (10.624): 10.1002/emmm.201201483} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA174219 https://www.ebi.ac.uk/ena/browser/view/PRJNA174219 None [Overal design]In exploring the potential involvement of miRs in breast tumorigenesis, we profiled the miRs expression of 64 primary breast cancer patients, comprising 56 matched tumor and adjacent peritumoral breast tissues, 5 tumor and 3 peritumor unmatched tissues, using the Agilent microarray platform. For 14 samples technical replicate were also performed.; [Treatment]'Following excision, tissue samples were immediately frozen in liquid nitrose and stored at -80° until RNA extraction.'; [Growth]'None'; [Extraction]"Breast tumor tissue (50-100 mg) was manually homogenized in 1 ml of TRI Reagent lysis reagent (Ambion) according to manufacturer's instructions."; [Cell type]'Source: ''tissue: Breast primary tumor; subtype (of tumor or matched tumor): HER2+; estrogen receptor status: neg; progesteron receptor status: neg; her2 status: pos; hystotype: IDC; grading: G3; tumor size: T2; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): HER2+; estrogen receptor status: neg; progesteron receptor status: neg; her2 status: pos; hystotype: IDC; grading: G3; tumor size: T3; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): HER2+; estrogen receptor status: neg; progesteron receptor status: neg; her2 status: pos; hystotype: ILC; grading: G3; tumor size: T2; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): HER2+; estrogen receptor status: neg; progesteron receptor status: neg; her2 status: pos; hystotype: IDC; grading: G3; tumor size: T2; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Basal-like; estrogen receptor status: neg; progesteron receptor status: neg; her2 status: neg; hystotype: ILC; grading: G3; tumor size: T2; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Basal-like; estrogen receptor status: neg; progesteron receptor status: neg; her2 status: neg; hystotype: IDC; grading: G3; tumor size: T1; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Basal-like; estrogen receptor status: neg; progesteron receptor status: neg; her2 status: neg; hystotype: IDC; grading: G3; tumor size: T2; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Basal-like; estrogen receptor status: neg; progesteron receptor status: neg; her2 status: neg; hystotype: IDC; grading: G2; tumor size: T1; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Basal-like; estrogen receptor status: neg; progesteron receptor status: neg; her2 status: neg; hystotype: IDC; grading: G3; tumor size: T2; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: IDC; grading: G3; tumor size: T3; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: IDC; grading: G2; tumor size: T2; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: IDC; grading: G3; tumor size: T2; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: IDC; grading: G2; tumor size: T1; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: IDC; grading: G2; tumor size: T2; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: pos; hystotype: IDC; grading: G3; tumor size: T2; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: IDC; grading: G3; tumor size: T2; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: ILC; grading: G2; tumor size: T2; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: neg; her2 status: neg; hystotype: IDC; grading: G2; tumor size: T2; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: neg; her2 status: neg; hystotype: IDC; grading: G2; tumor size: T1; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: neg; her2 status: neg; hystotype: IDC; grading: G1; tumor size: T2; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: IDC; grading: G3; tumor size: T1; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: IDC; grading: G2; tumor size: T2; nodal status: unknown; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: IDC; grading: G2; tumor size: T1; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: neg; her2 status: neg; hystotype: IDC; grading: G3; tumor size: T2; nodal status: N+; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: neg; her2 status: neg; hystotype: IDC; grading: G2; tumor size: T2; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: neg; her2 status: pos; hystotype: IDC; grading: G3; tumor size: T2; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: neg; her2 status: neg; hystotype: IDC; grading: G3; tumor size: T2; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: neg; her2 status: neg; hystotype: IDC; grading: G2; tumor size: T2; nodal status: unknown; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: IDC; grading: G1; tumor size: T2; nodal status: unknown; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: neg; her2 status: neg; hystotype: IDC; grading: G1; tumor size: T2; nodal status: N0; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: IDC; grading: G2; tumor size: T1; nodal status: unknown; ', 'tissue: Breast primary tumor; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: pos; progesteron receptor status: pos; her2 status: neg; hystotype: ILC; grading: G2; tumor size: T1; nodal status: N0; ', 'tissue: Peritumor breast tissue; subtype (of tumor or matched tumor): HER2+; estrogen receptor status: -; progesteron receptor status: -; her2 status: -; hystotype: -; grading: -; tumor size: -; nodal status: -; ', 'tissue: Peritumor breast tissue; subtype (of tumor or matched tumor): Basal-like; estrogen receptor status: -; progesteron receptor status: -; her2 status: -; hystotype: -; grading: -; tumor size: -; nodal status: -; ', 'tissue: Peritumor breast tissue; subtype (of tumor or matched tumor): Luminal; estrogen receptor status: -; progesteron receptor status: -; her2 status: -; hystotype: -; grading: -; tumor size: -; nodal status: -; ' GSE60479 Homo sapiens 6 Expression profiling by array GPL16686 Expression data in MDA-MB-231 cells treated with siATM, sip53 or control (SiNC) siRNA 2014-08-18 Ataxia-telangiectasia mutated (ATM) protein kinase regulates the DNA damage response and is associated with cancer suppression. Here, we used microarray to study global transcriptomic expression to identify tumor-promoting functions of ATM. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE60479 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA258379 https://www.ebi.ac.uk/ena/browser/view/PRJNA258379 None [Overal design]Human breast cancer MDA-MB-231 cells were transfected with siATM, sip53 or control siRNA followed by RNA extraction and hybridization on Affymetrix GeneChip Human Gene 2.0 ST array.; [Treatment]"Cells were treated with siATM, sip53 or control (siNC) siRNA by using Lipofectamine RNAiMAX (Invitrogen) following manufacturer's instructions."; [Growth]'Cells Were maintained in DMEM medium supplemented with 10% FBS, 100U/ml penicillin, 100mg/ml streptomycin and 2 Mm L-glutamine.'; [Extraction]'Cells were washed two times with iced PBS followed by extracting total RNA using RNeasy Mini kit (Qiagen).'; [Cell type]'Source: ''cell line: breast cancer MDA-MB-231 cells; treatment protocol: control siNC; ', 'cell line: breast cancer MDA-MB-231 cells; treatment protocol: siATM; ', 'cell line: breast cancer MDA-MB-231 cells; treatment protocol: sip53; ' GSE84104 Homo sapiens 5 Expression profiling by array GPL10558 Mitochondrial DNA drives tumor dormancy escape in ER+ breast cancer 2016-07-06 Although the estrogen receptor (ER) positive variant of breast cancer is touted as the most indolent and favorable, the majority of breast cancer deaths are in fact from this subtype. There are several features of this category of breast cancers that likely account for this outcome. The first is that metastatic relapse can occur many years after initial diagnosis of primary disease. The second is that once the cancer cells awaken into full-blown metastatic disease, they are largely resistant to ER-directed therapies (i.e. hormonal therapy, HT). The third is that when metastases do occur, they are invariably in many locations. This observation suggests that these dormant/sleeping metastatic cells are “globally” awakened as if by a “systemic” infection. We suggest that these three processes be not only linked, but underlie the lethal features of metastatic disease. We hypothesized that mtDNA is necessary for the escape from therapy induced tumor dormancy of luminal breast cancer cells https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE84104 Packaging and transfer of mitochondrial DNA via exosomes regulate escape from dormancy in hormonal therapy-resistant breast cancer. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.1704862114 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.1704862114} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA328027 https://www.ebi.ac.uk/ena/browser/view/PRJNA328027 None [Overal design]Total RNA was isolated after 2 months of treatment of breast cancer cell lines MCF7 cells with hormonal therapy (tamoxifen, 1uM) and biologically CTRL replicates are also present. Treatments with HT led to tumor dormancy in vitro. Samples for each group were processed for Illumina bead arrays (Illumina HT-12) by the MSKCC genomics core facility according to the specifications of the manufacturer.; [Treatment]'None'; [Growth]'None'; [Extraction]"RNeasy Mini Kit (Qiagen) extraction of total RNA was performed according to the manufacturer's instructions."; [Cell type]'Breast cancer cell line''cell line: MCF7; cell type: Breast cancer cell line; ' GSE42072 Homo sapiens 62 Non-coding RNA profiling by array GPL15018; GPL16249 Clinical Utility of Circulating MicroRNA Signatures for Breast Cancer Diagnosis (Gene expression) 2012-11-06 Purpose: There is a quest for novel non-invasive diagnostic markers for the detection of breast cancer. The goal of this study is to identify circulating microRNA signatures using a cohort of Asian Chinese breast cancer patients, and to compare microRNA profiles between tumour and serum samples. Experimental design: MicroRNAs from paired breast cancer tumours, normal tissue and serum samples derived from 32 patients were comprehensively profiled using microarrays (1300 microRNAs against tumour and normal tissues) or LNA RT-PCR panels (742 microRNAs against serum samples). Serum samples from healthy individuals (n=22) were also employed as normal controls. Significant serum microRNAs, identified by logistic regression, were validated in an independent set of serum samples from patients (n=82) and healthy controls (n=53). Results: The 20 most significant microRNAs differentially expressed in breast cancer tumours included miR-21, miR-10b, and miR-145, previously shown to be dysregulated in breast cancer. Interestingly, 16 of the 20 most significant microRNAs differentially expressed in serum samples were novel. MiR-1, miR-92a, miR-133a and miR-133b were identified as the most important diagnostic markers, and were successfully validated; receiver operating characteristic curves derived from combinations of these microRNAs exhibited areas under the curves of 0.944-0.946. Only seven microRNAs were overexpressed in both tumours and serum, suggesting that microRNAs may be released into the serum selectively. Conclusion: The clinical employment of microRNA signatures as a non-invasive diagnostic strategy is promising, but should be further validated for different subtypes of breast cancers. "_A" and "_B" are two tissue sections of the same sample; "_1" and "_2" represents 2 runs of the same sample; na = not available https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE42072 Identification of circulating microRNA signatures for breast cancer detection. Clinical cancer research : an official journal of the American Association for Cancer Research 8.911 https://doi.org/10.1158/1078-0432.CCR-12-3401 {Clinical cancer research : an official journal of the American Association for Cancer Research (8.911): 10.1158/1078-0432.CCR-12-3401} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA179164 https://www.ebi.ac.uk/ena/browser/view/PRJNA179164 None [Overal design]All tissue samples were histologically confirmed by a pathologist using hematoxylin and eosin staining of cryosectioned specimens. One tumour sample was rejected due to failure to detect any tumour cells. Except for two samples (with 30% and 40% tumour cells), all tumour tissues employed had a minimum of 60% tumour cells, as estimated microscopically. Overall, the breast cancer tumour samples had an average of 71% tumour cells. The criteria for adjacent normal tissue were absence of tumour cells and presence of epithelial cells. Hence, after histological confirmation, 31 breast cancer tumours and 23 matched normal tissues were employed for microRNA extraction and profiling using microarray.; [Treatment]'Cryosectioned frozen tissue'; [Growth]'None'; [Extraction]"RNA was extracted using mirVana kit (Life Technologies) following the manufacturer's recommendations. RNA was quantitated using the Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA)."; [Cell type]'Source: ''tissue: Breast tumour; tumour content: 60%; estrogen receptor: +; her2: na; node positivity: +; age: 69; ', 'tissue: Breast tumour; tumour content: 60%; estrogen receptor: +; her2: na; node positivity: -; age: 54; ', 'tissue: Breast tumour; tumour content: 80%; estrogen receptor: -; her2: na; node positivity: +; age: 48; ', 'tissue: Breast tumour; tumour content: 70%; estrogen receptor: +; her2: na; node positivity: +; age: 41; ', 'tissue: Breast tumour; tumour content: 30%; estrogen receptor: +; her2: -; node positivity: -; age: 47; ', 'tissue: Breast tumour; tumour content: 5%; estrogen receptor: +; her2: -; node positivity: -; age: 47; ', 'tissue: Breast tumour; tumour content: 60%; estrogen receptor: -; her2: na; node positivity: +; age: 59; ', 'tissue: Breast tumour; tumour content: 60%; estrogen receptor: +; her2: -; node positivity: -; age: 68; ', 'tissue: Breast tumour; tumour content: 95%; estrogen receptor: -; her2: +; node positivity: -; age: 36; ', 'tissue: Breast tumour; tumour content: 90%; estrogen receptor: +; her2: -; node positivity: -; age: 43; ', 'tissue: Breast tumour; tumour content: 80%; estrogen receptor: +; her2: +; node positivity: -; age: 37; ', 'tissue: Breast tumour; tumour content: 80%; estrogen receptor: +; her2: -; node positivity: +; age: 44; ', 'tissue: Breast tumour; tumour content: 60%; estrogen receptor: +; her2: -; node positivity: +; age: 28; ', 'tissue: Breast tumour; tumour content: 70%; estrogen receptor: +; her2: -; node positivity: +; age: 41; ', 'tissue: Breast tumour; tumour content: 80%; estrogen receptor: -; her2: +; node positivity: +; age: 46; ', 'tissue: Breast tumour; tumour content: 85%; estrogen receptor: +; her2: +; node positivity: +; age: 48; ', 'tissue: Breast tumour; tumour content: 60%; estrogen receptor: -; her2: +; node positivity: +; age: 38; ', 'tissue: Breast tumour; tumour content: 70%; estrogen receptor: -; her2: +; node positivity: +; age: 58; ', 'tissue: Breast tumour; tumour content: 70%; estrogen receptor: +; her2: -; node positivity: +; age: 47; ', 'tissue: Breast tumour; tumour content: 80%; estrogen receptor: +; her2: +; node positivity: -; age: 39; ', 'tissue: Breast tumour; tumour content: 80%; estrogen receptor: +; her2: +; node positivity: +; age: 43; ', 'tissue: Breast tumour; tumour content: 90%; estrogen receptor: -; her2: na; node positivity: -; age: 79; ', 'tissue: Breast tumour; tumour content: 80%; estrogen receptor: +; her2: +; node positivity: +; age: 50; ', 'tissue: Breast tumour; tumour content: 70%; estrogen receptor: +; her2: -; node positivity: +; age: 71; ', 'tissue: Breast tumour; tumour content: 60%; estrogen receptor: +; her2: +; node positivity: +; age: 65; ', 'tissue: Breast tumour; tumour content: 90%; estrogen receptor: -; her2: -; node positivity: -; age: 65; ', 'tissue: Breast tumour; tumour content: 40%; estrogen receptor: +; her2: +; node positivity: +; age: 49; ', 'tissue: Breast tumour; tumour content: 65%; estrogen receptor: +; her2: -; node positivity: +; age: 49; ', 'tissue: Breast tumour; tumour content: 60%; estrogen receptor: +; her2: +; node positivity: -; age: 42; ', 'tissue: Breast tumour; tumour content: 70%; estrogen receptor: +; her2: +; node positivity: -; age: 81; ', 'tissue: Breast tumour; tumour content: 80%; estrogen receptor: +; her2: +; node positivity: +; age: 36; ', 'tissue: Breast tumour; tumour content: 90%; estrogen receptor: -; her2: -; node positivity: +; age: 37; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 47; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 59; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 68; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 37; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 44; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 28; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 41; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 46; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 48; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 38; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 58; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 39; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 43; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 50; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 71; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 65; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 49; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 42; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 81; ', 'tissue: Adjacent normal tissue; tumour content: 0%; age: 36; ' GSE99063 Mus musculus; Homo sapiens 45 Expression profiling by high throughput sequencing GPL17303; GPL18635 CDK4/6 inhibition and tumor immunity 2017-05-18 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99063 CDK4/6 inhibition triggers anti-tumour immunity. Nature 43.070 https://doi.org/10.1038/nature23465 {Nature (43.070): 10.1038/nature23465} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA387162 https://www.ebi.ac.uk/ena/browser/view/PRJNA387162 None [Overal design]Refer to individual Series; [Treatment]'Abemaciclib concentration 500nM for MDA-MB_361 and MDA-MB453; 250nM for MCF7', 'Control vehicle or abemaciclib 90mg/kg daily by gavage', 'Abemaciclib 90mg/kg by gavage daily vs vehicle'; [Growth]'Cells were cultured in sterile dishes in media as described. Cells were plated at densities such that final density at time of RNA collection was between 60-70%.', 'Mice were induced with doxycyclin at age 6 weeks. Once tumors were established, mice were randomized to two groups with equal mean tumor volume.', 'Tumors were implanted orthotopically and treated once tumors reached appropriate size (see Methods of accompanying manuscript)'; [Extraction]'RNA was extracted using Macherey Nagel kit.\ncDNA libraries were constructed using\xa0the Ion AmpliSeq Transcriptome Human Gene Expression Kit (Thermo Fisher)\nThe Ion AmpliSeq Transcriptome Human Gene Expression Kit is designed for targeted amplification of over 20,000 human RefSeq genes. A short amplicon (~110 bp) is amplified for each targeted gene (Thermo Fisher).', 'Tumor tissue was snap frozen w hours after the 12th dose of treatment. Total RNA was extracted using the Macherey Nagel RNA Plus kit\ncDNA libraries were constructed using\xa0the Ion AmpliSeq AmpliSe DNA and RNA Library kit with custome primers(Thermo Fisher)\nAn Ion AmpliSeq™ Custom Panel was designed by the manufacturer (thermo Fisher) using Ion AmpliSeq™ Designer for targeted amplification of 3826 mouse genes , A short amplicon (~110 bp) is amplified for each target'; [Cell type]'Source: ''cell line: MDA-MB-361 breast carcinoma cell line; agent: control; ', 'cell line: MDA-MB-361 breast carcinoma cell line; agent: abemaciclib; ', 'cell line: MDA-MB-453 breast carcinoma cell line; agent: control; ', 'cell line: MDA-MB-453 breast carcinoma cell line; agent: abemaciclib; ', 'cell line: MCF7 breast carcinoma cell line; agent: control; ', 'cell line: MCF7 breast carcinoma cell line; agent: abemaciclib; ', 'tissue: mammary tumor; agent: control; ', 'tissue: mammary tumor; agent: abemaciclib; ', 'tissue: PDX tumor; agent: control; ', 'tissue: PDX tumor; agent: Abemaciclib; ' GSE69294 Homo sapiens 18 Expression profiling by array GPL10558 Active FOXO1 is a Key Determinant of Isoform-Specific Progesterone Receptor Transactivation and Senescence Programming 2015-05-27 The progesterone receptor specific gene targets were investigated in ovarian and breast cancer cell lines where FOXO1 was found to be a primary factor that cooperates with PR to activate cellular senescence genes (including p21) specifically in ovarian cells. ABSTRACT: Progesterone promotes differentiation coupled to proliferation and pro-survival in the breast, but inhibits estrogen-driven growth in the reproductive tract and ovaries. Herein, it is demonstrated, using progesterone receptor (PR) isoform-specific ovarian cancer model systems, that PR-A and PR-B promote distinct gene expression profiles that differ from PR-driven genes in breast cancer cells. In ovarian cancer models, PR-A primarily regulates genes independently of progestin, while PR-B is the dominant ligand-dependent isoform. Notably, FOXO1 and the PR/FOXO1 target-gene p21 (CDKN1A) are repressed by PR-A, but induced by PR-B. In the presence of progestin, PR-B, but not PR-A, robustly induced cellular senescence via FOXO1-dependent induction of p21 and p15 (CDKN2B). Chromatin immunoprecipitation (ChIP) assays performed on PR-isoform specific cells demonstrated that while each isoform is recruited to the same PRE-containing region of the p21 promoter in response to progestin, only PR-B elicits active chromatin marks. Overexpression of constitutively active FOXO1 in PR-A-expressing cells conferred robust ligand-dependent upregulation of the PR-B target genes GZMA, IGFBP1, and p21, and induced cellular senescence. In the presence of endogenous active FOXO1, PR-A was phosphorylated on Ser294 and transactivated PR-B at PR-B target genes; these events were blocked by the FOXO1 inhibitor (AS1842856). PR isoform-specific regulation of the FOXO1/p21 axis recapitulated in human primary ovarian tumor explants treated with progestin; loss of progestin sensitivity correlated with high AKT activity. IMPLICATIONS: This study indicates FOXO1 as a critical component for progesterone signaling to promote cellular senescence and reveals a novel mechanism for transcription factor control of hormone sensitivity. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE69294 Active FOXO1 Is a Key Determinant of Isoform-Specific Progesterone Receptor Transactivation and Senescence Programming. Molecular cancer research : MCR 4.484 https://doi.org/10.1158/1541-7786.MCR-15-0431 {Molecular cancer research : MCR (4.484): 10.1158/1541-7786.MCR-15-0431} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA285101 https://www.ebi.ac.uk/ena/browser/view/PRJNA285101 None [Overal design]The study contains 6 different sample groups measured in triplicate, for a total of 18 individual samples (18 arrays). From parental ES-2 human ovarian cancer cell lines, we created three stable clones expressing either (1) an empty vector pIRES-neo3, or (2) the wild type progesterone receptor isoform A (pIRES-neo3-PR-A), or (3) the wild type progesterone receptor isoform B (pIRES-neo3-PR-B). These three cell lines were treated with either (1) vehicle control (ethanol) or (2) R5020 10e-8 M for 24 hours before total RNA harvest. Thus, the experiment contains three cell lines and two treatments (6 sample groups), treated and analyzed in triplicate (18 microarrays). Standard Illumina HumanHT-12 V4.0 chip controls were used during hybridization.; [Treatment]'Samples treated in IMEM medium plus 5% DCC, with or without 10e-8 M R5020 for 24 hr.'; [Growth]"Samples grown in McCoy's 5A Modified medium supplemented with 10% charcoal-stripped fetal bovine serum (i.e., DCC), 100 units/mL penicillin, 100 μg/mL streptomycin, and 0.5 mg/mL of G418 sulfate before 1 day starvation in IMEM medium plus 5% DCC, then treated in IMEM medium plus 5% DCC for 24 hr."; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''parental cell line: ES-2; parental cell type: ovarian cancer cell line; stable vector integration: pIRES-neo3-empty; treatment: ethanol vehicle; time point: 24 hr; ', 'parental cell line: ES-2; parental cell type: ovarian cancer cell line; stable vector integration: pIRES-neo3-empty; treatment: R5020; time point: 24 hr; ', 'parental cell line: ES-2; parental cell type: ovarian cancer cell line; stable vector integration: pIRES-neo3-PRA; treatment: ethanol vehicle; time point: 24 hr; ', 'parental cell line: ES-2; parental cell type: ovarian cancer cell line; stable vector integration: pIRES-neo3-PRA; treatment: R5020; time point: 24 hr; ', 'parental cell line: ES-2; parental cell type: ovarian cancer cell line; stable vector integration: pIRES-neo3-PRB; treatment: ethanol vehicle; time point: 24 hr; ', 'parental cell line: ES-2; parental cell type: ovarian cancer cell line; stable vector integration: pIRES-neo3-PRB; treatment: R5020; time point: 24 hr; ' GSE93338 Homo sapiens 40 Expression profiling by array GPL570; GPL13667 Feasibility of Developing Reliable Gene Expression Modules from FFPE Derived RNA Profiled on Affymetrix Arrays 2017-01-09 This SuperSeries is composed of the SubSeries listed below. The reliability of differential expression analysis on FFPE expression profiles from Affymetrix arrays is questionable, due to the wide range of percent-present values reported in studies which profiled FFPE samples on Affymetrix arrays. Moreover the validity of externally defined gene-modules in FFPE microarray expression profiles is unknown. Using eight breast cancer tumors with available frozen and FFPE samples, five sample-matched data sets were generated from different combination of Affymetrix arrays, amplification-and-labeling kit and sample preservation method. The reliability of differential expression analysis was investigated by developing de novo ER/HER2 pathway gene-modules from matched data sets and validating it on external data set using ROC analysis. Spearman's rank correlation coefficient of module scores between matched FFPE-frozen expression profiles was used to measure reliability of externally defined gene-modules in FFPE expression profiles. Independent of array/amplification-kit/sample preservation method used, de novo ER/HER2 gene-modules derived from all matching data sets showed similar prediction performance during independent validation (AUC range; ER: 0.92-0.95, HER2: 0.88-0.91), except for de novo HER2 gene-module derived from FFPE data set with 3'IVT kit (AUC: 0.67-0.72). Further not all gene-module based biological signals present in frozen expression profiles can be recovered from matching FFPE microarray expression profiles using the currently available FFPE specific sample preparation kits. The gene-module based biological signal extracted from FFPE RNA, using microarrays, may not be as reliable as that from their frozen counterpart, if the sample preparation protocol used with FFPE RNA failed to recover relevant genes involved in the biological signal. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE93338 Feasibility of developing reliable gene expression modules from FFPE derived RNA profiled on Affymetrix arrays. PloS one 2.776 https://doi.org/10.1371/journal.pone.0203346 {PloS one (2.776): 10.1371/journal.pone.0203346} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA360624 https://www.ebi.ac.uk/ena/browser/view/PRJNA360624 None [Overal design]Refer to individual Series Using eight breast cancer tumors with available frozen and FFPE samples, five sample-matched data sets were generated from different combination of arrays , amplification-and-labeling kit and sample preservation method as listed below; 1) Two data set from matched FFPE and frozen samples profiled on HG-U133plus2 arrays with Affymetrix's 3'IVT kit (u133p2.3ivt array / 3ivt kit), 2) Two data set from matched FFPE and frozen samples profiled on HG-U219 arrays with Nugen's Ovation® FFPE WTA System and EncoreTM Biotin Module (u219.ovation arrays / ovation kit), and 3) a single data set from matched FFPE samples profiled on HG-U219 arrays with Affymetrix's SensationPlusTM FFPE Amplification and 3'IVT Labeling Kit (u219.sensation array / sensation kit). We consider the data set which profiled frozen samples on HG-U133plus2 array with 3'IVT kit as 100% truth and compared all other data sets to this reference data set. The eight BC tumors include two tumors from each Luminal-A, Luminal-B, HER2-amplified and Triple-Negative subtypes; [Treatment]'NA'; [Growth]'NA'; [Extraction]"Total RNA from frozen samples was extracted using TRIzol® Reagent according to Thermo Fisher Scientific's (Invitrogen) recommendations.", "Total RNA from FFPE sections was extracted using miRNeasy FFPE kit according to Qiagen's recommendation.", 'Total RNA from frozen samples was extracted using TRIzol® Reagent according to Thermo Fisher Scientific (Invitrogen) recommendations.', 'Total RNA from FFPE sections was extracted using miRNeasy FFPE kit according to Qiagen recommendation.'; [Cell type]'Source: ''tissue: breast tumor; er status: negative; her2 status: negative; tissue preservation method: Fresh-Frozen; ', 'tissue: breast tumor; er status: positive; her2 status: negative; tissue preservation method: Fresh-Frozen; ', 'tissue: breast tumor; er status: negative; her2 status: positive; tissue preservation method: Fresh-Frozen; ', 'tissue: breast tumor; er status: positive; her2 status: positive; tissue preservation method: Fresh-Frozen; ', 'tissue: breast tumor; er status: negative; her2 status: negative; tissue preservation method: FFPE; ', 'tissue: breast tumor; er status: positive; her2 status: negative; tissue preservation method: FFPE; ', 'tissue: breast tumor; er status: negative; her2 status: positive; tissue preservation method: FFPE; ', 'tissue: breast tumor; er status: positive; her2 status: positive; tissue preservation method: FFPE; ' GSE34149 Homo sapiens 22 Expression profiling by array GPL571; GPL10558 Phosphorylated and Sumoylation-Deficient Progesterone Receptors Drive Proliferative Gene Signatures During Breast Cancer Progression 2011-12-05 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE34149 Phosphorylated and sumoylation-deficient progesterone receptors drive proliferative gene signatures during breast cancer progression. Breast cancer research : BCR 5.676 https://doi.org/10.1186/bcr3211 {Breast cancer research : BCR (5.676): 10.1186/bcr3211} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA150063 https://www.ebi.ac.uk/ena/browser/view/PRJNA150063 None [Overal design]Refer to individual Series; [Treatment]'Cells were treated with 10e-9 M AP21967 durring the starvation with modified IMEM, and treated with 10e-8 M R5020 for 6 h'; [Growth]'T47D cells expressing inducible constructs were grown in minimal essential medium (5% FBS, 1% NEAA, 1% pennicilin/streptomycin, 6 ng/ml insulin, 200 ug/ml G418, 200 ug/ml hygromycin B) before being serum starved and AP21967 treated for 2 d, then treated with R5020'; [Extraction]"Trizol extraction of total RNA was performed according to the manufacturer's instructions.", 'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''tissue: breast; genotype: PR null; parental cell line: T47D-Y; inducer treatment: vehicle; ligand treatment: vehicle; ', 'tissue: breast; genotype: PR null; parental cell line: T47D-Y; inducer treatment: AP21967; ligand treatment: vehicle; ', 'tissue: breast; genotype: wild type PR; parental cell line: T47D-Y; inducer treatment: vehicle; ligand treatment: vehicle; ', 'tissue: breast; genotype: wild type PR; parental cell line: T47D-Y; inducer treatment: vehicle; ligand treatment: R5020; ', 'tissue: breast; genotype: wild type PR; parental cell line: T47D-Y; inducer treatment: AP21967; ligand treatment: vehicle; ', 'tissue: breast; genotype: wild type PR; parental cell line: T47D-Y; inducer treatment: AP21967; ligand treatment: R5020; ', 'tissue: breast; genotype: mutant K388R PR; parental cell line: T47D-Y; inducer treatment: vehicle; ligand treatment: vehicle; ', 'tissue: breast; genotype: mutant K388R PR; parental cell line: T47D-Y; inducer treatment: vehicle; ligand treatment: R5020; ', 'tissue: breast; genotype: mutant K388R PR; parental cell line: T47D-Y; inducer treatment: AP21967; ligand treatment: vehicle; ', 'tissue: breast; genotype: mutant K388R PR; parental cell line: T47D-Y; inducer treatment: AP21967; ligand treatment: R5020; ', 'tissue: breast; genotype: PR null; parental cell line: T47D-Y; ligand treatment: vehicle; ', 'tissue: breast; genotype: PR null; parental cell line: T47D-Y; ligand treatment: R5020; ', 'tissue: breast; genotype: wild type PR; parental cell line: T47D-Y; ligand treatment: vehicle; ', 'tissue: breast; genotype: wild type PR; parental cell line: T47D-Y; ligand treatment: R5020; ', 'tissue: breast; genotype: mutant K388R PR; parental cell line: T47D-Y; ligand treatment: vehicle; ', 'tissue: breast; genotype: mutant K388R PR; parental cell line: T47D-Y; ligand treatment: R5020; ' GSE62016 Mus musculus 18 Expression profiling by array GPL6246 Expression data comparing Rb/p53 and p53 deficient mammary tumors and normal mammary tissue 2014-10-02 To investigate the impact of combined Rb and p53 loss in mammary tumorigenesis, we used transgenic and viral approaches to delete Rb and p53 floxed alleles specifically in the mouse mammary epithelium. Although MMTV-Cre (NLST) targets stem/bi-potent progenitors in the mammary gland, a subset of MMTV-Cre:Rbf/f;p53f/f mice developed non-mammary tumors. Thus, freshly isolated primary mammary epithelial cells from these animals were transplanted into the mammary fat pads of immunodeficient mice and monitored for tumor formation. In addition, primary MECs were isolated from Cre-negative Rbf/f;p53f/f mice, infected with Ad-Cre followed by orthotopic transplantation. In all these cases, resulting tumors shared similar spindle-shape histology, expressed high levels of vimentin, a mesenchymal marker, but not E-cadherin, a luminal marker, and were classified as adeno-sacrcomatoid/spindle-cell/mesenchymal-like breast cancer. We used microarrays to detect differentially expressed genes in the Rb/p53 double-knock-out vs p53 single deletion or normal mammary tissue. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE62016 RB1 deficiency in triple-negative breast cancer induces mitochondrial protein translation. The Journal of clinical investigation 12.282 https://doi.org/10.1172/JCI81568 {The Journal of clinical investigation (12.282): 10.1172/JCI81568} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA262942 https://www.ebi.ac.uk/ena/browser/view/PRJNA262942 None [Overal design]Total RNA was extracted from tumors developed by double Trizol method and hybridized on Affymetrix microarrays; [Treatment]'Total RNA obtained from primary tumors and normal mammary tissue were used for microarray analysis to determine differentially regulated genes. Cluster analysis and pathway analysis based on gene expression were then performed to determine significant genes/pathways'; [Growth]'Samples from independent primary mammary tumors from MMTV-Cre:Rbp53,MMTV-Cre:p53, Ad-Cre:Rbp53 models and normal mammary tissue were frozen and kept in -80 degree.'; [Extraction]'Total RNA was extracted with Trizol reagent twice. Quality control was performed with Agilent Bioanalyser'; [Cell type]'Source: ''strain background: mixed; tumor model: MMTV-Cre (nulliparous); tissue: Primary mammary tumor Rbp53 deleted; ', 'strain background: mixed; tumor model: MMTV-Cre (Parous); tissue: Primary mammary tumor Rbp53 deleted; ', 'strain background: mixed; tumor model: MMTV-Cre (Transplant); tissue: Primary mammary tumor Rbp53 deleted; ', 'strain background: mixed; tumor model: Ad-CMVcre (Transplant); tissue: Primary mammary tumor Rbp53 deleted; ', 'strain background: mixed; tumor model: MMTV-Cre; tissue: Primary mammary tumor p53 deleted; ', 'strain background: mixed; tumor model: normal mammary tissue; tissue: normal mammary tissue; ' GSE13696 Homo sapiens 90 Genome variation profiling by SNP array GPL2004; GPL2005 Copy number profiling of 45 human breast cancer cell lines on Affymetrix 100K SNP arrays 2008-11-20 Breast cancer cell lines grown in full serum under standard conditions were profiled on Affymetrix GeneChip Mapping 100K Set Arrays Keywords: Mapping Array https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE13696 Genetic alterations and oncogenic pathways associated with breast cancer subtypes. Molecular cancer research : MCR 4.484 https://doi.org/10.1158/1541-7786.MCR-08-0107 {Molecular cancer research : MCR (4.484): 10.1158/1541-7786.MCR-08-0107} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA110451 https://www.ebi.ac.uk/ena/browser/view/PRJNA110451 None [Overal design]Profiling of cell lines grown under standard conditions; [Treatment]'None'; [Growth]'All cell lines were grown in DMEM or RPMI-1640 supplemented with 10% FBS'; [Extraction]"Qiagen DNA extraction kit was used according to the manufacturer's instructions"; [Cell type]'Source: ''' GSE45852 Homo sapiens 21 Genome binding/occupancy profiling by high throughput sequencing GPL11154 Tight coordination of protein translation and heat shock factor 1 activation supports the anabolic malignant state [ChIP-Seq] 2013-04-08 A unifying characteristic of aggressive cancers is a profound anabolic shift in metabolism to enable sustained proliferation and biomass expansion. The ribosome is centrally situated to sense metabolic states but whether it impacts systems that promote cellular survival is unknown. Here, through integrated chemical-genetic analyses, we find that a dominant transcriptional effect of blocking protein translation in cancer cells is complete inactivation of heat shock factor 1 (HSF1), a multifaceted transcriptional regulator of the heat-shock response and many other cellular processes essential for tumorigenesis. Translational flux through the ribosome reshapes the transcriptional landscape and links the fundamental anabolic processes of protein production and energy metabolism with HSF1 activity. Targeting this link deprives cancer cells of their energy and chaperone armamentarium thereby rendering the malignant phenotype unsustainable. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE45852 Tight coordination of protein translation and HSF1 activation supports the anabolic malignant state. Science (New York, N.Y.) 41.037 https://doi.org/10.1126/science.1238303 {Science (New York, N.Y.) (41.037): 10.1126/science.1238303} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA196591 https://www.ebi.ac.uk/ena/browser/view/PRJNA196591 https://www.ncbi.nlm.nih.gov/sra?term=SRP020615 [Overal design]We used ChIP-Seq to examine affect of rocaglates and cycloheximide on HSF1 genomic occupancy in MCF7 and M0-91 cancer cells.; [Treatment]'None'; [Growth]'None'; [Extraction]'Nuclear extracts were sonicated to solubilize the chromatin. The chromatin extracts containing DNA fragments with an average size of 500 bp were immunoprecipitated using different antibodies. Purified immunoprecipitated DNA were prepared for sequencing according to a modified version of the Solexa Genomic DNA protocol. Fragmented DNA was end repaired and subjected to 18 cycles of LM-PCR using oligos provided by Illumina. Amplified fragments between 150 and 300bp (representing shear fragments between 50 and 200nt in length and ~100bp of primer sequence) were isolated by agarose gel electrophoresis and purified.'; [Cell type]'breast cancer cell line', 'acute myelogenous leukemia cell line''cell type: breast cancer cell line; cell line: MCF7 cells; antibody: HSF1 (H-311, Santa Cruz, sc-9144, Lot# J0510); treatment: DMSO; ', 'cell type: breast cancer cell line; cell line: MCF7 cells; antibody: RNA Pol II (AB817, Abcam, Lot#36502-3); treatment: DMSO; ', 'cell type: breast cancer cell line; cell line: MCF7 cells; antibody: IGG (Santa Cruz, sc-2027, Lot# C2210); treatment: DMSO; ', 'cell type: breast cancer cell line; cell line: MCF7 cells; antibody: HSF1 (H-311, Santa Cruz, sc-9144, Lot# J0510); treatment: Cycloheximide (10 µM); ', 'cell type: breast cancer cell line; cell line: MCF7 cells; antibody: RNA Pol II (AB817, Abcam, Lot#36502-3); treatment: Cycloheximide (10 µM); ', 'cell type: breast cancer cell line; cell line: MCF7 cells; antibody: IGG (Santa Cruz, sc-2027, Lot# C2210); treatment: Cycloheximide (10 µM); ', 'cell type: acute myelogenous leukemia cell line; cell line: M0-91 cells; antibody: HSF1 (H-311, Santa Cruz, sc-9144, Lot# J0510); treatment: DMSO; ', 'cell type: acute myelogenous leukemia cell line; cell line: M0-91 cells; antibody: IGG (Santa Cruz, sc-2027, Lot# C2210); treatment: DMSO; ', 'cell type: acute myelogenous leukemia cell line; cell line: M0-91 cells; antibody: HSF1 (H-311, Santa Cruz, sc-9144, Lot# J0510); treatment: 27A (20 nM); ', 'cell type: acute myelogenous leukemia cell line; cell line: M0-91 cells; antibody: IGG (Santa Cruz, sc-2027, Lot# C2210); treatment: 27A (20 nM); ', 'cell type: acute myelogenous leukemia cell line; cell line: M0-91 cells; antibody: HSF1 (H-311, Santa Cruz, sc-9144, Lot# J0510); treatment: 27A (100 nM); ', 'cell type: acute myelogenous leukemia cell line; cell line: M0-91 cells; antibody: IGG (Santa Cruz, sc-2027, Lot# C2210); treatment: 27A (100 nM); ', 'cell type: acute myelogenous leukemia cell line; cell line: M0-91 cells; antibody: HSF1 (H-311, Santa Cruz, sc-9144, Lot# J0510); treatment: Cycloheximide (10 µM); ', 'cell type: acute myelogenous leukemia cell line; cell line: M0-91 cells; antibody: IGG (Santa Cruz, sc-2027, Lot# C2210); treatment: Cycloheximide (10 µM); ' GSE125511 Homo sapiens 9 Expression profiling by high throughput sequencing GPL18573 β-Caryophyllene Enhances the Transcriptional Upregulation of SREBP-dependent Lipid Biosynthesis in Breast Cancer Cells 2019-01-23 β-caryophyllene (BCP) exhibits anti-proliferative properties in cancer cells. Here, we examine the hypothesis that BCP induces membrane remodeling. Our data show that high concentrations of BCP increase membrane permeability of human breast cells (hBrC) causing detachment and cell death. At a “sub-lethal” concentration of BCP, we show that BCP induces a striking upregulation of genes involved in cholesterol biosynthesis, including the gene that encodes for HMGCoA reductase (HMGCR), the rate-determining step in cholesterol biosynthesis. In addition, stearoyl-CoA desaturase (SCD) is also upregulated which would lead to the enhanced formation of monounsaturated fatty acids, specifically oleate and palmitoleate from stearoyl CoA and palmitoyl CoA, respectively. These fatty acids are major components of membrane phospholipids and cholesterol esters. Together, these data suggest that cells respond to BCP by increasing the synthesis of components found in membranes. These responses could be viewed as a repair mechanism and/or as a mechanism to mount resistance to the cytotoxic effect of BCP. Blocking HMGCR enhances the cytotoxicity of BCP, suggesting that this may provide an additional therapeutic tool in controlling breast cancer cell growth, assuming that targeted specificity could be established. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE125511 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA516651 https://www.ebi.ac.uk/ena/browser/view/PRJNA516651 https://www.ncbi.nlm.nih.gov/sra?term=SRP181627 [Overal design]Examination of UFH-001 Triple Negative Breast Cancer cell line under hypoxic conditions (control) or in the presence of either 20uM or 200uM beta-caryophyllene (NOTE: The 3 hypoxia controls are duplicates of data submitted to GEO previously as part of another project - GSE123856); [Treatment]'All cells were exposed to hypoxia at the same time that cells were exposed (or not) to β-caryophyllene. Specifically, cells were provided fresh medium an hour before hypoxic treatment, along with the appropriate concentration β-caryophyllene (20μM, 200μM or vehicle control [DMSO]). Cells were were placed in humidified Billups Rothenberg Metabolic Chambers and exposed to 1% O2, 5% CO2 and balanced N2 for 16h at 37°C..'; [Growth]'UFH-001 cells were plated in 10 cm dishes at a density of 10,000 cells/mL and maintained in DMEM supplemented with 10% FBS. All cell lines were maintained at 37 °C in humidified air with 5% CO2. Experiments were conducted when cells achieved ~70% confluency'; [Extraction]"RNA was isolated from the UFH-001 cells using the Qiagen RNAeasy kit per manufacturer's protocols\nRNA libraries were prepared for sequencing using standard Illumina protocols"; [Cell type]'Triple Negative Breast Cancer Cells''cell line: UFH-001; cell type: Triple Negative Breast Cancer Cells; ' GSE73900 Mus musculus 6 Expression profiling by array GPL7202 Gene Regulation by microRNA-16 forced expression in ErbB-2 positive murine breast cancer cells. 2015-10-09 miR-16 is a potent tumor suppressor in ErbB-2 positive breast cancer. The primary objetive of this study was to identify previously uncharacterized putative mRNA targets of miR-16 in ErbB-2 postitive breast cancer cells. To achieve our objective we studied the effects of exogenously expressed miR-16 on the gene expression profile of primary cultures of ErbB-2 positive murine breast cancer tumors. The C4HD tumor line displays high levels of estrogen receptor and progesterone receptor, overexpresses ErbB-2 and ErbB-3, exhibits low ErbB-4 levels, and lacks EGF-R expression. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE73900 MiR-16 mediates trastuzumab and lapatinib response in ErbB-2-positive breast and gastric cancer via its novel targets CCNJ and FUBP1. Oncogene 6.634 https://doi.org/10.1038/onc.2016.151 {Oncogene (6.634): 10.1038/onc.2016.151} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA298360 https://www.ebi.ac.uk/ena/browser/view/PRJNA298360 None [Overal design]Primary cultures of the C4HD murine breast tumor were transfected with a miR-16 precursor (pre-miR-16) or a scrambled sequence (pre-miR-Control) that does not form any known mammalian miRNA. Three biological replicates were obtained for each experimental condition.; [Treatment]"miRNA precursors were obtained from Life Technologies and were used in accordance with the manufacturer's instructions. Briefly, 30 nM pre-miR-16 (AM17100) or a pre-miR-Control (AM17110) that does not form any known mammalian miRNA were transfected for 48hs using the siPORT NeoFx transfection reagent (Ambion)."; [Growth]"Hormone-dependent ductal tumors (C4HD) originated in mice treated with 40 mg medroxyprogesterone acetate (MPA) every 3 months for a year, and have been maintained by serial transplantation in animals treated with 40 mg s.c. MPA depot on the opposite flank to tumor inoculum. Primary cultures of epithelial cells from C4HD tumors, growing in MPA-treated mice, were performed as previously described. In brief, tumors were aseptically removed, minced and washed with DMEM/F12 (Dulbecco's modified Eagle's medium: Ham's F12, 1:1, without phenol red, 100 U/ml penicillin and 100\xa0μg/ml Streptomycin). The tissue was suspended in 5 ml of enzymatic solution\xa0[trypsin: 2.5 mg/ml, albumin: 5 mg/ml and collagenase type II (Gibco-BRL, Gaithersburg, MD): 239 U/ml]\xa0in phosphate buffered saline (PBS) and incubated at 37°C for 20 min, under continuous stirring. The liquid phase of the suspension was then removed and the undigested tissue was incubated with fresh enzymatic solution for 20 min. Enzyme action was stopped by adding DMEM/F12+5% heat inactivated fetal calf serum (FCS) (Gen S.A., Buenos Aires). Epithelial and fibroblastic cells were separated as already described. Briefly, the cell suspension was resuspended in 15 ml of DMEM/F12+10% FCS and allowed to sediment for 20 min. The upper 5 ml, corresponding to the fibroblastic fraction, was seeded in flasks, and the cells were allowed to attach during 1\xa0-\xa02 h after which the medium containing unattached cells was removed and replaced by fresh DMEM/F12+10% FCS. The sedimented cells, corresponding to the epithelial enriched fraction, were resuspended again in 15 ml of DMEM/F12+5% FCS and allowed to sediment for another 20 min. The upper 15 ml were discarded and this procedure was repeated until no fibroblasts were observed in the supernatant. Cells were plated in culture flasks with DMEM/F12+5% steroid-stripped FCS (ChFCS) and allowed to attach for 24\xa0-\xa048 h."; [Extraction]"Total RNA was extracted using the miRVANA Paris RNA Extraction Kit (Ambion, Austin, TX), following the manufacturer's instructions. RNA was quantified using a NanoDrop-2000 (Thermo Fisher Scientific) spectrophotometer and quality was monitored with the Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA)."; [Cell type]'primary cultures of the C4HD murine breast tumor''strain: BALB/c; gender: Female; transfection: pre-miR-Control; cell type: primary cultures of the C4HD murine breast tumor; ', 'strain: BALB/c; gender: Female; transfection: pre-miR-16; cell type: primary cultures of the C4HD murine breast tumor; ' GSE10905 Homo sapiens 79 Expression profiling by array GPL2507 Profiling BRCA1, BRCA2 and non-BRCA1/2 LCLs post-Irradiation 2008-03-20 The functional consequences of missense variants in disease genes are difficult to predict. We assessed if gene expression profiles could distinguish between BRCA1 or BRCA2 pathogenic truncating and missense mutation carriers and familial breast cancer cases whose disease was not attributable to BRCA1 or BRCA2 mutations (BRCAX cases). 72 cell lines from affected women in high-risk breast-ovarian families were assayed after exposure to ionising irradiation, including 23 BRCA1 carriers, 22 BRCA2 carriers, and 27 BRCAX individuals. A subset of 10 BRCAX individuals carried rare BRCA1/2 sequence variants considered to be of low clinical significance (LCS). BRCA1 and BRCA2 mutation carriers had similar expression profiles, with some subclustering of missense mutation carriers. The majority of BRCAX individuals formed a distinct cluster, but BRCAX individuals with LCS variants had expression profiles similar to BRCA1/2 mutation carriers. Gaussian Process Classifier predicted BRCA1, BRCA2 and BRCAX status with a maximum of 62% accuracy, and prediction accuracy decreased with inclusion of BRCAX samples carrying an LCS variant, and inclusion of pathogenic missense carriers. Similarly, prediction of mutation status with gene lists derived using Support Vector Machines was good for BRCAX samples without an LCS variant (82-94%), poor for BRCAX with an LCS (40-50%), and improved for pathogenic BRCA1/2 mutation carriers when the gene list used for prediction was appropriate to mutation effect being tested (71-100%). This study indicates that mutation effect, and presence of rare variants possibly associated with a low risk of cancer, must be considered in the development of array-based assays of variant pathogenicity. Keywords: cell type comparison, stress response https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE10905 BRCA1 and BRCA2 missense variants of high and low clinical significance influence lymphoblastoid cell line post-irradiation gene expression. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1000080 {PLoS genetics (5.224): 10.1371/journal.pgen.1000080} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA107315 https://www.ebi.ac.uk/ena/browser/view/PRJNA107315 None [Overal design]A cohort of 72 lymphoblastoid cell lines derived from patients who are carriers of different mutations: 23 BRCA1, 22 BRCA2, 27 non-BRCA1/2. 7 of the LCLs were regrown, treated and arrayed as replicate samples A-G; [Treatment]'24 hrs prior to treatment cells were counted and put at 500000 cells/ml. 10 ml Cells were treated with 10 Gy gamma irradation'; [Growth]'lymphoblastoid cell lines were removed from liquid nitrogen and grown for a minimum of 2 weeks prior to treatment with IR. LCLs were cultered in RPMI 1640 media with 15% fetal bovine serum, 1% penicillin-streptomycin and 1% glutamine'; [Extraction]'RNA was extracted 30 minutes after IR treatment using an RNeasy mini kit (Qiagen)'; [Cell type]'Source: ''' GSE118743 Mus musculus 22 Genome variation profiling by array GPL4092 Identification of Jun loss that promotes resistance to HDAC inhibitor Entinostat through Myc signaling in Luminal breast cancer [CGH] 2018-08-19 The histone deacetylase inhibitor Entinostat is in phase III trials for patients with metastatic estrogen receptor-positive breast cancer. Predictors of sensitivity and resistance, however, remain unknown. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE118743 Identification of Jun loss promotes resistance to histone deacetylase inhibitor entinostat through Myc signaling in luminal breast cancer. Genome medicine 10.886 https://doi.org/10.1186/s13073-018-0597-3 {Genome medicine (10.886): 10.1186/s13073-018-0597-3} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA486666 https://www.ebi.ac.uk/ena/browser/view/PRJNA486666 None [Overal design]A total of 8 cell lines and 9 mouse models of breast cancer were treated with Entinostat. Luminal cell lines were treated with or without Entinostat at their IC50 doses, and MMTV/Neu luminal mouse tumors were treated with Entinostat until progression. We investigated these models using gene expression profiling by microarray and copy number by arrayCGH. We also utilized the network-based Dawnrank algorithm, that integrates DNA and RNA data, to identify driver genes of resistance. The impact of a number of candidate drivers was investigated in The Cancer Genome Atlas and the METABRIC; [Treatment]'4 different treatments: Untreated, 3 week treatment, 6 week treatment, and Entinostat Progression'; [Growth]'None'; [Extraction]'genomic DNA isolated using Dneasy kit (Qiagen)'; [Cell type]'Source: ''characteristics: reference: DNA reference; ', 'cell line: MMTV-Neu; treatment: Untreated; ', 'cell line: MMTV-Neu; treatment: Entinostat 3wks; ', 'cell line: MMTV-Neu; treatment: Entinostat 6wks; ', 'cell line: MMTV-Neu; treatment: Entinostat Progression; ' GSE53024 Homo sapiens 3 Expression profiling by high throughput sequencing GPL9442 Architecture of Epigenetic Reprogramming Following Twist1 Mediated Epithelial-Mesenchymal Transition [RNA-seq] 2013-12-05 Purpose: to characterize epigenetic changes following Twist1 mediated Epithelial-Mesenchymal Transition in human Methods: we characterized the epigenetic and transcriptome landscapes using whole genome transcriptome analysis by RNA-seq, DNA methylation by digital restriction enzyme analysis of methylation (DREAM) and histone modifications by CHIP-seq of H3K4me3 and H3K27me3 in immortalized human mammary epithelial cells relative to cells induced to undergo EMT by Twist1. Results: EMT is accompanied by focal hypermethylation and widespread global DNA hypomethylation, predominantly within transcriptionally repressed gene bodies. At the chromatin level, the number of gene promoters marked by H3K4me3 increases by more than one fifth; H3K27me3 undergoes dynamic genomic redistribution characterized by loss at half of gene promoters and overall reduction of peak size by almost one-half. This is paralleled by increased phosphorylation of EZH2 at serine 21. Among genes with highly altered mRNA expression, 23.1% switch between H3K4me3 and H3K27me3 marks, and those point to the master EMT targets and regulators CDH1, PDGFRA and ESRP1. Strikingly, Twist1 increases the number of bivalent genes by more than two fold. Inhibition of the H3K27 methyltransferases EZH2 and EZH1, which form part of the PRC2 complex, results in blocking EMT and stemness properties. Conclusion: Our findings demonstrate that the EMT program requires epigenetic remodeling by the Polycomb/Trithorax complexes leading to increased cellular plasticity which suggests that its inhibition will prevent EMT, and the associated breast cancer metastasis. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53024 Architecture of epigenetic reprogramming following Twist1-mediated epithelial-mesenchymal transition. Genome biology 14.028 https://doi.org/10.1186/gb-2013-14-12-r144 {Genome biology (14.028): 10.1186/gb-2013-14-12-r144} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA230693 https://www.ebi.ac.uk/ena/browser/view/PRJNA230693 https://www.ncbi.nlm.nih.gov/sra?term=SRP033535 [Overal design]RNAseq profiles of human mammary epithelial cells before (HMLE_parental) and after Twist1 transfection (HMLE_Twist) were generated in monolayer (HMLE_Twist2D) and sphere culture by deep sequencing using SOLID; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was harvested using Trizol reagent.\nRNA libraries were prepared for sequencing using standard SoLID protocols'; [Cell type]'human mammary epithelial cells''cell type: human mammary epithelial cells; transfected with: none (parental); culture type: monolayer; ', 'cell type: human mammary epithelial cells; transfected with: Twist; culture type: monolayer; ', 'cell type: human mammary epithelial cells; transfected with: Twist; culture type: sphere; ' GSE15904 Mus musculus 126 Expression profiling by array GPL8321 Genetic Heterogeneity in Mouse Mammary Tumors 2009-04-30 Human cancers result from a complex series of genetic alterations resulting in heterogeneous disease states. Dissecting this heterogeneity is critical for understanding underlying mechanisms and providing opportunities for therapeutics matching the complexity. Mouse models of cancer have generally been employed to reduce this complexity and focus on the role of single genes. Nevertheless, our analysis of tumors arising in the MMTV-Myc model of mammary carcinogenesis reveals substantial heterogeneity, seen in both histological and expression phenotypes. One contribution to this heterogeneity is the substantial frequency of activating Ras mutations, the frequency of which can be changed by alterations in Myc. Additionally, we show that these Myc-induced mammary tumors exhibit even greater heterogeneity, revealed by distinct histological subtypes as well as distinct patterns of gene expression, than many other mouse models of tumorigenesis. Two of the major histological subtypes are characterized by differential patterns of cellular signaling pathways, including B-Catenin and Stat3 activities. We also demonstrate the predictive nature of this approach though examining metastatic potential. Together, these data reveal that a combination of histological and genomic analyses can uncover substantial heterogeneity in mammary tumor formation and therefore highlight aspects of tumor phenotype not evident in the population as a whole. Keywords: Transcription factor expression analysis https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE15904 Genetic heterogeneity of Myc-induced mammary tumors reflecting diverse phenotypes including metastatic potential. Proceedings of the National Academy of Sciences of the United States of America 9.580 https://doi.org/10.1073/pnas.0901250106 {Proceedings of the National Academy of Sciences of the United States of America (9.580): 10.1073/pnas.0901250106} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA116895 https://www.ebi.ac.uk/ena/browser/view/PRJNA116895 None [Overal design]20 MMTV-Neu Tumors, 25 Papillary MMTV-Myc T58A and 81 MMTV-Myc tumors of various histological subtypes were arrayed.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA from mouse mammary tumors was extracted using the Qiagen RNeasy Midi kit.'; [Cell type]'Source: ''tumor type: MMTV-Neu; ', 'tumor type: MMTV-Myc T58A; histological subtype: Papillary; ', 'tumor type: MMTV-Myc; histological subtype: EMT; ', 'tumor type: MMTV-Myc; histological subtype: Microacinar; ', 'tumor type: MMTV-Myc; histological subtype: Adenocarcinoma; ', 'tumor type: MMTV-Myc; histological subtype: Papillary; ', 'tumor type: MMTV-Myc; histological subtype: Mix; ', 'tumor type: MMTV-Myc; histological subtype: Squamous; ', 'tumor type: MMTV-Myc; histological subtype: Solid; ' GSE144964 Homo sapiens 20 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL16791 The HIF target MAFF promotes tumor invasion and metastasis through IL11 and STAT3 signaling 2020-02-07 Using RNA-sequencing and ChIP-sequencing, we identified direct target genes of the transcription factor MAFF in MDA-MB-231 under normoxia and hypoxia. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144964 The HIF target MAFF promotes tumor invasion and metastasis through IL11 and STAT3 signaling. Nature communications 11.878 https://doi.org/10.1038/s41467-021-24631-6 {Nature communications (11.878): 10.1038/s41467-021-24631-6} 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA605452 https://www.ebi.ac.uk/ena/browser/view/PRJNA605452 https://www.ncbi.nlm.nih.gov/sra?term=SRP247664 [Overal design]MDA-MB-231, a human breast cancer cell line, was treated either under normoxia or hypoxia. After ChIP or RNA extraction, sequencing was performed. After knocking down endogenous MAFF in MDA-MB-231, we overexpressed V5-tagged MAFF with mutations on shRNA target sites. Then nuclei was extracted and we proceeded to ChIP procedures using V5 antibody to further determine direct targets of MAFF.; [Treatment]'For ChIP-seq, cells were grown under normoxia or hypoxia (0.5% O2) for 24hours. For RNA-seq, cells were knocked down with siSCR or siMAFF and grown under normoxia or hypoxia (0.5% O2) for 24hours.', 'V5-tagged MAFF was overexpressed in MDA-MB-231 cells with stable MAFF knockdown using shRNA. Cells were crosslinked with 1% formalin and ChIP procedure was performed.'; [Growth]'MDA-MB-231 cells were grown in DMEM media with 10% FBS and 1% antibiotics', 'MDA-MB-231 cells were maintained in DMEM media with 10% FBS at 37°C, 21% O2 and 5% CO2.'; [Extraction]"For ChIP-seq, after fixation with 37% formaldehyde, nuclei was collected by sonication (Bioruptor, Diagenode). DNA-MAFF bound was immunoprecipitated with a MAFF-specific antibody. For RNA-seq, RNA was collected using a Rneasy kit (Qiagen)\nFor ChIP-seq, libraries were prepared using NEBNext ChIP-Seq Library Prep Master Mix set for Illumina (NEB #E6240) and NEBNext Multiplex Oligos for Illumina (NEB #E7730S). For RNA-seq, libraries were prepared using Illumina's TruSeq RNA library prep kit v2.\nChIP seq and RNA seq", '2x10^7 cell were crosslinked with 1% formaldehyde in CiA fixation buffer (50mM HEPES pH8, 1mM EDTA, 0.5mM EGTA, 100mM NaCl) for 10min. Then glycine was added to a final concentration of 125mM to stop the fixation. To collect nuclei cells were resuspended in CiA NP-Rinse 1 (50mM HEPES pH8, 140mM NaCl, 1mM EDTA, 10% glycerol, 0.5% NP40, 0.25% Triton X-10) and incubated in ice for 10min. Cells were washed with CiA NP-Rinse 2 (10mM Tris pH8, 1mM EDTA, 0.5mM EDTA, 200mM NaCl) and dissolved in Covaris shearing buffer (0.1% SDS, 1mM EDTA, 10mM Tris-HCl pH8). Cells were sonicated using Covaris S220 (Intensity 4, Duty Factor 5%, Cycle/Burst 200) for 420sec.\nLibraries were prepared using NEBNext Ultra II DNA Library Prep kit for Illumina (NEB #E7103) and NEBNext Multiplex Oligos for Illumina (NEB #E7730S). To control the quality of DNA libraries, the size and purity of samples were confirmed by Bioanalyzer.'; [Cell type]'Source: ', 'breast cancer cell line''origin: mammary gland/breast; derived from metastatic site: pleural effusion; disease: adenocarcinoma; antibody or sirna: MAFF antibody (MilliporeSigma #M8194); ', 'origin: mammary gland/breast; derived from metastatic site: pleural effusion; disease: adenocarcinoma; antibody or sirna: N/A; ', 'origin: mammary gland/breast; derived from metastatic site: pleural effusion; disease: adenocarcinoma; antibody or sirna: ONTARGET plus SMARTpool siRNAs; ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; hormone receptor: Triple negative; genotype/variation: endogenous MAFF knocked out, V5-tagged MAFF overexpressed; chip antibody: V5: CST 13202; ', 'cell line: MDA-MB-231; cell type: breast cancer cell line; hormone receptor: Triple negative; genotype/variation: endogenous MAFF knocked out, V5-tagged MAFF overexpressed; chip antibody: None; ' GSE123860 Homo sapiens 12 Expression profiling by high throughput sequencing GPL18573 MUC1-C represses the RASSF1A tumor suppressor and activated Kras signaling in human carcinoma cells 2018-12-14 RASSF1A encodes a tumor suppressor that inhibits RAS’RAF’MEK’ERK signaling and is one of the most frequently inactivated genes in human cancers. MUC1-C is an oncogenic effector of the cancer cell epigenome that is overexpressed in diverse carcinomas. We show here that MUC1-C represses RASSF1A expression in multiple types of KRAS wild-type and mutant cancer cells. Mechanistically, MUC1-C occupies the RASSF1A promoter in a complex with the ZEB1 transcriptional repressor. In turn, MUC1-C/ZEB1 complexes recruit DNA methyltransferase 3b (DNMT3b) to the CpG island in the RASSF1A promoter. Targeting MUC1-C, ZEB1 and DNMT3b thus decreases methylation of the CpG island and derepresses RASSF1A transcription. We also show that targeting MUC1-C downregulates KRAS signaling with decreases in MEK/ERK activation, which is of importance for RAS-mediated tumorigenicity. These findings define a previously unrecognized role for MUC1-C in suppression of RASSF1A and support targeting MUC1-C as an approach for inhibiting KRAS signaling. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE123860 MUC1-C represses the RASSF1A tumor suppressor in human carcinoma cells. Oncogene 6.634 https://doi.org/10.1038/s41388-019-0940-1 {Oncogene (6.634): 10.1038/s41388-019-0940-1} 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA510078 https://www.ebi.ac.uk/ena/browser/view/PRJNA510078 https://www.ncbi.nlm.nih.gov/sra?term=SRP173457 [Overal design]Using Lentiviral vector, a control shRNA hairpin and shRNA against MUC1-C were used to generate the stably silenced MUC1-C and control cell lines of BT-549 and A549 cells respectively. Total RNA were isolated from 3 different sets of control shRNA and MUC1-shRNA for both BT549 and A549 cell types and used for RNA-seq library preparation.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA were isolated using RNAeasy Plus Kit (Qiagen) as directed. Briefly the RNA isolation was done using up to 5 million cells form each cell lines, Cells were first lysed and homogenized using QIAshredder columns (Qiagen). The cell lysates were passed through a gDNA Eliminator spin column supplied in the kit, ethanol is added to the gDNA column flow-through as instructed, and the ethanol mixed samples were applied to individual RNeasy spin columns. RNA binds to the membrane and contaminants are washed away using different wash buffer supplied in the kit. The high-quality RNA is finally eluted in 50µl water and stored in -70 degree Celsius till further use.\nIllumina single end stranded'; [Cell type]'TNBC Breast Cancer Cell line (ER -ve, PR -ve, HER2/neu -ve)', 'Kras mutant Non-small Cells Lung Cancer''cell line: BT549; cell type: TNBC Breast Cancer Cell line (ER -ve, PR -ve, HER2/neu -ve); genotype/variation: control; ', 'cell line: BT549; cell type: TNBC Breast Cancer Cell line (ER -ve, PR -ve, HER2/neu -ve); genotype/variation: shRNA against MUC1-C; ', 'cell line: A549; cell type: Kras mutant Non-small Cells Lung Cancer; genotype/variation: control; ', 'cell line: A549; cell type: Kras mutant Non-small Cells Lung Cancer; genotype/variation: shRNA against MUC1-C; ' GSE102410 Homo sapiens 7 Genome binding/occupancy profiling by high throughput sequencing GPL9052 c-Jun/AP-1 overexpression reprograms ERα signaling related to tamoxifen response in ERα-positive breast cancer [ChIP-seq] 2017-08-09 A critical mechanism for transcription regulation by estrogen receptor α (ER) is the tethering of ER to DNA via other transcription factors, such as AP-1. However, genome-wide assessment of the overlap in chromatin binding repertoires of these two transcription factors has not been reported. Here, we show that the AP-1 transcription factor c-Jun interacts with ER and is recruited globally to ER binding regions. Interestingly, we identify differential motif enrichment between unique ER binding regions and unique c-Jun binding regions, with FoxA1 motif enriched in both sets of binding regions, whereas GATA3 motif only specifically enriched in the unique ER binding regions but not in the unique Jun binding regions. We demonstrate that the primary mechanism for estrogen/ER-dependent transcriptional responses is the tethering of ER to DNA under conditions where it cooperates with AP-1. We provide evidence that c-Jun overexpression causes reduced sensitivity to tamoxifen in ER+ breast cancer cells. Integrated omics data reveal TGFBI as one of the most perturbed genes regulated by c-Jun. TGFBI knockdown suppresses the growth of breast cancer cells and is critical for increasing the sensitivity of tamoxifen-resistant cells to tamoxifen. We show that TGFBI expression is elevated in breast cancer than in normal breast and the basal-like tumors express high levels of TGFBI. TGFBI expression is associated with poor patient survival in ER+ breast cancer receiving endocrine therapy, highlighting a role of AP-1 via TGFBI signaling as a major determinant of endocrine response in ER+ breast tumor. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE102410 c-Jun/AP-1 overexpression reprograms ERα signaling related to tamoxifen response in ERα-positive breast cancer. Oncogene 6.634 https://doi.org/10.1038/s41388-018-0165-8 {Oncogene (6.634): 10.1038/s41388-018-0165-8} 'genomic DNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA397714 https://www.ebi.ac.uk/ena/browser/view/PRJNA397714 https://www.ncbi.nlm.nih.gov/sra?term=SRP115104 [Overal design]Examination of E2 and Tamoxifen induced gene expression changes in MCF-7/c-Jun -Tet cells; [Treatment]'Cells were cultured in steroid depleted media for 72 h and treated with ethanol, 10 nM 17β-estradiol or 1μM Tamoxifen for 1 h. Cells were fixed with 1% formaldehyde for 10 minutes, then glycine-quenched and harvested'; [Growth]'Cells were maintained in DMEM supplemented with 10% FBS containing media in absence of tetracycline.'; [Extraction]'Lysates were clarified from sonicated nuclei, c-Jun and ERα complexes were isolated with antibody.\nChIP-seq libraries were prepared for sequencing using standard Illumina protocols'; [Cell type]'ERalpha-positive breast cancer cells''cell line: MCF-7; cell type: ERalpha-positive breast cancer cells; chip antibody: c-Jun (H-79, Santa Cruz); ', 'cell line: MCF-7; cell type: ERalpha-positive breast cancer cells; chip antibody: ERalpha (H-20, Santa Cruz); ', 'cell line: MCF-7; cell type: ERalpha-positive breast cancer cells; chip antibody: none; ' GSE74281 Homo sapiens 49 Expression profiling by array GPL14951 Systematic drug perturbations of cancer cells reveal diverse exit paths from the proliferative state 2015-10-22 Analysis of the time courses of gene expression profiles of breast cancer cell line MCF7 treated by 16 differentiation-inducing drugs at day 1, day 3 and day 5. The drugs are the screening results from the the JHCCL library (1,500 drugs). The hypothesis tested in the present study was that cancer cells exit the proliferative state via multiple paths. Results showed that cell state transition trajectories firstly diverged and later converged to a quiescient differentiated state https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE74281 None None None None None 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA299623 https://www.ebi.ac.uk/ena/browser/view/PRJNA299623 None [Overal design]MCF7 cells were cultured in 150mm dishes and treated 1/5/10 μM of each of the 16 drugs (see details in Table S1-2). 14 plates of cells were left untreated as control samples. Cells were collected after 1, 3 and 5 days of drug treatment in RNeasy (Qiagen) lysis buffer and RNA was isolated according to the manufacture’s protocol and sent to Vancouver Prostate Center for transcript profiling.; [Treatment]'None'; [Growth]'None'; [Extraction]'RNA was extracted with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser.'; [Cell type]'Source: ''tissue: Breast; cell line: MCF7; ' GSE166943 Homo sapiens 70 Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing GPL11154 YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation 2021-02-17 This SuperSeries is composed of the SubSeries listed below. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE166943 None None None None None 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA702446 https://www.ebi.ac.uk/ena/browser/view/PRJNA702446 None [Overal design]Refer to individual Series; [Treatment]'1-0.4 μM Tamoxifen (Sigma, H7904) + 2-4 μM AZD0530 (Selleck Chemicals, S1006) were used to induce the transformation.'; [Growth]'MCF-10A-ER-Src cells (Iliopoulos et al., 2009; Iliopoulos et al., 2010) were grown in DMEM/F12 without phenol red (Thermo Fisher Scientific, 11039-047) + 5% charcoal stripped FBS (Sigma, F6765) + 1% pen/strep (Thermo Fisher Scientific, 15140122)+20 ng/ml EGF (Peprotech, AF-100-15) + 0.5 μg/ml Hydrocortisone (Sigma, H-0888) + 0.1 μg/ml cholera toxin (Sigma, C-8052) + 10 μg/ml insulin (Sigma, 10516).\nMDA-MB-231 cells were grown in DMEM (Thermo Fisher Scientific, 11995-073) + 10% FBS (Sigma, TMS-013-B) + 1% pen/strep.', 'MCF-10A-ER-Src cells (Iliopoulos et al., 2009; Iliopoulos et al., 2010) were grown in DMEM/F12 without phenol red (Thermo Fisher Scientific, 11039-047) + 5% charcoal stripped FBS (Sigma, F6765) + 1% pen/strep (Thermo Fisher Scientific, 15140122)+20 ng/ml EGF (Peprotech, AF-100-15) + 0.5 μg/ml Hydrocortisone (Sigma, H-0888) + 0.1 μg/ml cholera toxin (Sigma, C-8052) + 10 μg/ml insulin (Sigma, 10516).'; [Extraction]'Cells were dual cross-linking with a mixture of 2 mM each of ethylene glycol bis (succinimidyl succinate) (EGS) and disuccinimidyl glutarate (DSG) and 1% formaldehyde. Chromatin was digested with 60 units MNase (New England Biolabs, M0247S) at 37 0C for 10 minutes and then sonicated using Branson Microtip Sonifier 450 (4X15 second at output 4.5 and duty cycle 60%) to the sizes mostly between 150-500 bp.\n50 μg chromatin, antibodies for transcription factors (listed in Table S6), and 15 μl Dynabead protein G (Thermo Fisher Scientific, 10004D) was used for the chromatin immunoprecipitation (ChIP)', 'RNA was prepared used mRNeasy Mini Kit (Qiagen, No. 217004).\nRNA-seq libraries were generated using TruSeq Ribo Profile Mammalian Kit (Illumina, RPHMR12126).'; [Cell type]'MCF10A ER-Src cells', 'MDA-MB-231 cells', 'Source: ''cell type: MCF10A ER-Src cells; transformation status: non-transformed; chip antibody: YAP (Bethyl Laboratories, A302-309A); ', 'cell type: MCF10A ER-Src cells; transformation status: transformed; chip antibody: YAP (Bethyl Laboratories, A302-309A); ', 'cell type: MCF10A ER-Src cells; transformation status: non-transformed; chip antibody: TAZ (Cell Signaling Technology, 4883s); ', 'cell type: MCF10A ER-Src cells; transformation status: transformed; chip antibody: TAZ (Cell Signaling Technology, 4883s); ', 'cell type: MCF10A ER-Src cells; transformation status: non-transformed; chip antibody: TEAD(Cell Signaling Technology, 13295 ); ', 'cell type: MCF10A ER-Src cells; transformation status: transformed; chip antibody: TEAD(Cell Signaling Technology, 13295 ); ', 'cell type: MCF10A ER-Src cells; transformation status: non-transformed; chip antibody: STAT3 (Cell Signaling Technology, 9139s); ', 'cell type: MCF10A ER-Src cells; transformation status: transformed; chip antibody: STAT3 (Cell Signaling Technology, 9139s); ', 'cell type: MCF10A ER-Src cells; transformation status: non-transformed; chip antibody: JUNB (Cell Signaling Technology, 3753s); ', 'cell type: MCF10A ER-Src cells; transformation status: transformed; chip antibody: JUNB (Cell Signaling Technology, 3753s); ', 'cell type: MDA-MB-231 cells; transformation status: --; chip antibody: YAP (Bethyl Laboratories, A302-309A); ', 'cell type: MDA-MB-231 cells; transformation status: --; chip antibody: TAZ (Cell Signaling Technology, 4883s); ', 'cell type: MDA-MB-231 cells; transformation status: --; chip antibody: TEAD(Cell Signaling Technology, 13295 ); ', 'cell type: MDA-MB-231 cells; transformation status: --; chip antibody: STAT3 (Cell Signaling Technology, 9139s); ', 'cell type: MDA-MB-231 cells; transformation status: --; chip antibody: JUNB (Cell Signaling Technology, 3753s); ', 'cell line: MCF10A ER-Src cells; transformation status: non-transformed; ', 'cell line: MCF10A ER-Src cells; transformation status: transformed; ', 'cell line: MDA-MB-231 cells; transformation status: --; ' GSE116831 Rattus norvegicus 52 Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing GPL20084 Deletion of Cdkn1b in ACI rats perturbs mammary progenitor cell proliferation and differentiation through non-cell-autonomous mechanisms 2018-07-09 Emerging data indicate that breast epithelial stem cells and progenitors, particularly those in the luminal epithelial cell lineage, are the cells-of-origin of breast carcinomas, and factors that influence breast cancer risk may alter the number and/or properties of these cells. We hypothesize that a subset of p27+ cells represent hormone-responsive progenitors that are quiescent due to the high activity of TGFβ signaling in these cells. The Estrogen-induced mammary tumor model in ACI inbred rats is physiologically relevant rodent model of breast cancer. In the present study we successfully generated Cdkn1b knockout ACI rats and performed comprehensive phenotypic assessment and RNAseq profiling using FACS sorted basal (CD24+CD29high) and luminal (CD24+CD29low) cell populations to characterize Cdkn1b+/+ and Cdkn1b-/- females in prepubertal and adult cohorts. We found that p27KO rats exhibited mammary differentiation phenotype and reduced numbers of mammary epithelial progenitor pool, Interestingly, p27 ablation has the most pronounced effect on luminal progenitor cell gene expression, and milk protein genes and pStat5 were dramatically upregulated, while PR and FoxA1 were greatly downregulated in Cdkn1b-/- luminal cells. Further characterization of mammary glands of prepubertal Cdkn1b knockout rats by fat pad transplantation illustrated p27 deletion in the mammary cancer susceptible ACI rat strain induced mammary epithelial cell differentiation through cell non-autonomous mechanisms. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE116831 Deletion of Cdkn1b in ACI rats leads to increased proliferation and pregnancy-associated changes in the mammary gland due to perturbed systemic endocrine environment. PLoS genetics 5.224 https://doi.org/10.1371/journal.pgen.1008002 {PLoS genetics (5.224): 10.1371/journal.pgen.1008002} 'polyA RNA', 'genomic DNA', 'total RNA' https://www.ncbi.nlm.nih.gov/bioproject/PRJNA480306 https://www.ebi.ac.uk/ena/browser/view/PRJNA480306 https://www.ncbi.nlm.nih.gov/sra?term=SRP152885 [Overal design]Bulk RNA-Seq: RNA-Seq of both Cdkn1b knockout and wild type ACI rat mammary glands, at various ages, and various FACS sorted cell types. ChIP-seq: ChIP-seq for PR of both Cdkn1b knockout and wild type 9 week old ACI rat mammary glands, with basal/myoepithelial and luminal FACS sorted cell types. Anti-PR antibody (H-190, Santa Cruz, cat# sc-7208). Bulk RNA-Seq: RNA-Seq of ACI and BN rats treated with and without E2, sorted for luminal and basal fractions of the mammary gland.; [Treatment]'None'; [Growth]'None'; [Extraction]'Total RNA was extracted using the RNeasy Mini Kit (Qiagen). The total RNA was measured by Aligent 2100 Bioanalyzer.\nRNA-seq libraries were prepared using Clontech Low Input mRNA Library (Clontech SMARTer) v4 kit from less than 10ng of purified total RNA according to the manufacturer’s protocol. The concentrations of finished dsDNA library were measured by Qubit Fluorometer, the size of library fragment was measured by Agilent TapeStation 2200, and RT-qPCR for adapted library molar concentration measurement according to manufacturer’s protocols. Uniquely indexed libraries were pooled in equimolar ratios and sequenced on an Illumina NextSeq500 with Single-End 75bp (SE75) reads by the Dana-Farber Cancer Institute Molecular Biology Core Facilities.', 'Single cell suspensions were obtained from dissociated mammary organoids, 1 × 107 cells were fixed with fixing buffer (50 mM HEPES-NaOH (pH 7.5), 100 mM NaCl, 1mM EDTA) containing 1% paraformaldehyde (Electron Microscopy Sciences, 15714) and crosslinked for 10 min at 37 °C. Crosslinking was quenched by adding glycine to a final concentration of 0.125 M. The cells were washed with ice-cold PBS, harvested in PBS. The nuclear fraction was extracted by first resuspending the pellet in 1 ml of lysis buffer (50 mM HEPES-NaOH (pH 8.0), 140 mM NaCl, 1mM EDTA, 10% glycerol, 0.5% NP-40, and 0.25% Triton X-100) for 10 min at 4 °C. Cells were pelleted, and washed in 1 ml of wash buffer (10 mM Tris-HCL (pH 8.0), 200 mM NaCl, 1 mM EDTA) for 10 min at 4 °C. Cells were then pelleted and resuspended in 1 ml of shearing buffer (10 mM Tris-HCl (pH 8), 1 mM EDTA, 0.1% SDS) and sonicated in a Covaris sonicator. Lysate was centrifuged for 5 min at 14,000 rpm to purify the debris. Then 100 µl of 10% Triton X-100 and 30 µl of 5M NaCl were added. The sample was then incubated with 20 µl of Dynabeads Protein G (LifeTechnologies,10003D) for 1 h at 4 °C. Primary antibodies were added to each tube and immunoprecipitation (IP) was conducted overnight in the cold room. Cross-linked complexes were precipitated with Dynabeads Protein G for 2 hr at 4 °C. The beads were then washed in low salt wash buffer (20 mM Tris-HCl pH 8, 150 mM NaCl, 10 mM EDTA, and 1% SDS) for 5 min at 4 °C, high salt wash buffer (50 mM Tris-HCl pH 8, 10 mM EDTA, and 1% SDS) for 5 min at 4 °C and LiCl wash buffer (50 mM Tris-HCl pH 8, 10 mM EDTA, and 1% SDS) for 5 min at 4 °C. DNA was eluted in elution buffer (100 mM sodium bicarbonate and 1% SDS). Cross-links were reversed overnight at 65 °C. RNA and protein were digested with 0.2 mg ml−1 RNase A for 30 min at 37 °C followed by 0.2 mg ml−1 Proteinase K for 1 h at 55 °C. DNA was purified with phenol-chloroform extraction and isopropanol precipitation.\nChIP-seq libraries were prepared using the Rubicon ThruPLEX DNA-seq Kit from 1 ng of purified ChIP DNA or input DNA according to the manufacturer’s protocol.'; [Cell type]'basal/myoepithelial (Cd24+ Cd29HIGH)', 'luminal progenitors (Cd24+ Cd29LOW Cd49b+)', 'mature luminal (Cd24+ Cd29LOW Cd49b- PNA-)', 'luminal progenitors (Cd24+ Cd29LOW PNA+)', 'luminal (Cd24+ Cd29LOW)', 'mammary cells', 'Basal', 'Luminal''strain: ACI; genotype: Cdkn1b-/-; age: 9 weeks; tissue: mammary gland; cell type: basal/myoepithelial (Cd24+ Cd29HIGH); ', 'strain: ACI; genotype: Cdkn1b-/-; age: 9 weeks; tissue: mammary gland; cell type: luminal progenitors (Cd24+ Cd29LOW Cd49b+); ', 'strain: ACI; genotype: Cdkn1b-/-; age: 9 weeks; tissue: mammary gland; cell type: mature luminal (Cd24+ Cd29LOW Cd49b- PNA-); ', 'strain: ACI; genotype: Cdkn1b-/-; age: 9 weeks; tissue: mammary gland; cell type: luminal progenitors (Cd24+ Cd29LOW PNA+); ', 'strain: ACI; genotype: Cdkn1b+/+; age: 9 weeks; tissue: mammary gland; cell type: basal/myoepithelial (Cd24+ Cd29HIGH); ', 'strain: ACI; genotype: Cdkn1b+/+; age: 9 weeks; tissue: mammary gland; cell type: luminal progenitors (Cd24+ Cd29LOW Cd49b+); ', 'strain: ACI; genotype: Cdkn1b+/+; age: 9 weeks; tissue: mammary gland; cell type: mature luminal (Cd24+ Cd29LOW Cd49b- PNA-); ', 'strain: ACI; genotype: Cdkn1b+/+; age: 9 weeks; tissue: mammary gland; cell type: luminal progenitors (Cd24+ Cd29LOW PNA+); ', 'strain: ACI; genotype: Cdkn1b+/+; age: 4 weeks; tissue: mammary gland; cell type: basal/myoepithelial (Cd24+ Cd29HIGH); ', 'strain: ACI; genotype: Cdkn1b+/+; age: 4 weeks; tissue: mammary gland; cell type: luminal (Cd24+ Cd29LOW); ', 'strain: ACI; genotype: Cdkn1b-/-; age: 4 weeks; tissue: mammary gland; cell type: luminal (Cd24+ Cd29LOW); ', 'strain: ACI; genotype: Cdkn1b-/-; age: 4 weeks; tissue: mammary gland; cell type: basal/myoepithelial (Cd24+ Cd29HIGH); ', 'strain: ACI; genotype: Cdkn1b+/+; age: 6 weeks; tissue: mammary gland; cell type: basal/myoepithelial (Cd24+ Cd29HIGH); ', 'strain: ACI; genotype: Cdkn1b+/+; age: 6 weeks; tissue: mammary gland; cell type: luminal (Cd24+ Cd29LOW); ', 'strain: ACI; genotype: Cdkn1b-/-; age: 6 weeks; tissue: mammary gland; cell type: basal/myoepithelial (Cd24+ Cd29HIGH); ', 'strain: ACI; genotype: Cdkn1b-/-; age: 6 weeks; tissue: mammary gland; cell type: luminal (Cd24+ Cd29LOW); ', 'strain: ACI; genotype: Cdkn1b+/+; age: 9 weeks; tissue: mammary gland; cell type: mammary cells; chip antibody: Anti-PR antibody (H-190, Santa Cruz, cat# sc-7208); ', 'strain: ACI; genotype: Cdkn1b+/+; age: 9 weeks; tissue: mammary gland; cell type: mammary cells; chip antibody: none (input); ', 'strain: ACI; genotype: Cdkn1b-/-; age: 9 weeks; tissue: mammary gland; cell type: mammary cells; chip antibody: Anti-PR antibody (H-190, Santa Cruz, cat# sc-7208); ', 'strain: ACI; genotype: Cdkn1b-/-; age: 9 weeks; tissue: mammary gland; cell type: mammary cells; chip antibody: none (input); ', 'strain: ACI; gender: Female; treatment: Control; tissue: mammary gland; cell type: Basal; ', 'strain: ACI; gender: Female; treatment: Control; tissue: mammary gland; cell type: Luminal; ', 'strain: ACI; gender: Female; treatment: E2; tissue: mammary gland; cell type: Basal; ', 'strain: ACI; gender: Female; treatment: E2; tissue: mammary gland; cell type: Luminal; ', 'strain: BN; gender: Female; treatment: Control; tissue: mammary gland; cell type: Basal; ', 'strain: BN; gender: Female; treatment: Control; tissue: mammary gland; cell type: Luminal; ', 'strain: BN; gender: Female; treatment: E2; tissue: mammary gland; cell type: Basal; ', 'strain: BN; gender: Female; treatment: E2; tissue: mammary gland; cell type: Luminal; '